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/index.php/Urinary_incontinence_resident_survival_guide

# Urinary incontinence resident survival guide Urinary incontinence is defined as an involuntary leakage of urine. The causes can be temporary or permanent. Most common reversible causes include dementia, delirium, infections, atrophic vaginitis, psychological, drugs, stool impaction. It is broadly classified into 5 types based on the characteristics on the urinary incontinence. The approach to the diagnosis of Urinary incontinence is based on a step-wise approach strategy. Below is an algorithm summarising the identification and diagnosis of different types of Urinary incontinence . The algorithm is developed and modified according to American Urological Evaluation (AUA) Guidelines. Shown below is an algorithm summarizing the diagnosis of Urinary incontinence according to The American Urological Association guidelines.

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# Urinary incontinence resident survival guide (pediatrics) Urinary incontinence in children is a very familiar finding and complaint amongst patients and their caregivers. It is broadly classified into physiological and pathological with its various subdivisions. The causes of urinary incontinence in children are identified based on the sub-classification of pathological incontinence. The focus is to eliminate any potential organic cause of incontinence and to classify and identify the type of functional incontinence using detailed history and non-invasive procedures. Identify any comorbidities which are mostly psychological occurring alongside incontinence. A fundamental diagnosis includes taking a detailed history using a standardized questionnaire. The primary aim of a physical examination is to look for possible organic causes of incontinence and comorbidities. Urinalysis is essential to rule out urinary tract infections. Ultrasonography is a useful tool when further diagnostics is required especially in situations of a likely organic cause or a lack of response to therapy. Uroflowmetry and urodynamic studies are additional diagnostic studies that can be employed. Urotherapy encompasses all non-pharmacological and non-surgical treatment methods employed in the treatment of urinary incontinence in children. Desmopressin and oxybutynin are common drugs used for the pharmacological management of urinary incontinence in children. Surgery is not routinely employed as a form of treatment, it might be of importance in correcting some organic causes of urinary incontinence in children.

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# Urinary retention Prognosis is generally good if condition is treated timely and with proper counseling about different complications, patients with retention who denied surgical treatment can be safely followed for at least 5 years without renal deterioration. The diagnosis of urinary retention is made through history including information about current prescription medications and use of over-the-counter medications and herbal supplements, physical exam, and lab test (to find the specific cause). Urinary retention is difficult to diagnose due to concomitant comorbidities and potential cognitive impairments. There are no specific diagnostic criteria for urinary retention. Lab test include Conclusion: Major criterion in the diagnosis of urinary retention is the drainage of a large volume of urine after catheterization with the relief of the pain.

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# Urinary retention resident survival guide Urinary retention is defined as an inability to pass urine, or incomplete emptying of the bladder. It is one of the most common presenting complaints encountered in the emergency department, and can be acute or chronic. It is commonly seen in males as compared to females due to benign prostate hyperplasia. If undiagnosed or left untreated, this condition can be life-threatening as it may lead to kidney damage and severe urosepsis. Acute urinary retention can be extremely uncomfortable, and is initially managed by urethral or suprapubic catheterization. Chronic urinary retention is often asymptomatic, not easily identified, and is linked to increased post void residual volume. A complete detailed history about current prescription, over the counter and herbal medications is necessary along with focused physical examination that must include neurological evaluation. Acute urinary retention is treated with immediate bladder decompression with intermittent urethral catheterization or suprapubic catheterization regardless of the cause and gender. Further management depend upon the cause of retention.

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/index.php/Urinary_tract_infection

# Urinary tract infection A urinary tract infection is an infection that involves any part of the urinary tract. It can result due to the invasion by a bacteria, virus, fungus or any other pathogen. The most common cause of a urinary tract infection is a bacterial infection. Depending on the site of the infection, a urinary tract infection can be classified as either upper or lower UTI. Lower UTI includes urethritis, prostatitis, asymptomatic bacteriuria, and cystitis (bladder infection), where as upper UTI may include pyelonephritis (infection of the kidneys) and rarely urethritis (infection of the ureters). Each subtype of urinary tract infection can also be subclassified on the basis of duration, etiology or therapeutic approach as acute, chronic, or recurrent and as uncomplicated or complicated infections. The urine is normally sterile, a urinary tract infection occurs when the normally sterile urinary tract is infected by bacteria, which leads to irritation and inflammation. Pyelonephritis and cystitis result mostly from ascending infections from the urethra (urethritis) but can also result from descending infections such as hematogenous spread, or by the lymphatic system. The condition more often affects women, but can affect either gender and all age groups. The pathogenesis of a complicated UTI may include obstruction and stasis of urine flow. Various factors are associated with the risk of developing a urinary tract infection. A common cause of the urinary tract infection in hospital settings is the urinary catheter placement. Diabetes, Crohn's disease, iatrogenic causes, endometriosis, pelvic inflammatory disease, urinary obstruction, and bladder incontinence are some risk factors for acquiring a urinary tract infection. A thorough physical exam is very helpful in differentiating upper from lower urinary tract infections. Patients with an uncomplicated urinary tract infections are usually well–appearing. The symptoms may include abnormal urine color (cloudy), blood in the urine, frequent urination or urgent need to urinate, dysuria, pressure in the lower pelvis or back, suprapubic pain, flank pain, back pain, fever, nausea, vomiting, and chills. Urinalysis and urine culture are very helpful laboratory tests in diagnosing a urinary tract infection. Pyuria and either white blood cells (WBCs) or red blood cells (RBCs) may be seen on urinalysis. Escherichia coli ("E. coli"), a bacterium found in the lower gastrointestinal tract is one of the most common culprits. The individual infection must be differentiated from various causes of dysuria such as cystitis, acute pyelonephritis, urethritis, prostatitis, vulvovaginitis, urethral strictures or diverticula, benign prostatic hyperplasia and neoplasms such as renal cell carcinoma and cancers of the bladder, prostate, and penis. Antimicrobial therapy is indicated in case of a symptomatic UTI. A large proportion of patients with acute uncomplicated urinary infections will recover without treatment within a few days or weeks. If left untreated, some patients may progress to develop recurrent infection, involve and infect other parts of the urinary tract, hematuria, and rarely renal failure. Prognosis is generally good for lower UTIs. The treatment of a UTI depends on the type of the disease, the disease course (acute uncomplicated versus complicated), history of the individual, and the rates of drug resistance in the community. Preventative measures to avoid a UTI include abstinence, being faithful, using a condom, using barrier contraception during sexual intercourse, urinating after intercourse, increasing fluid intake and frequency of urination, and use of estrogen among postmenopausal women.

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# Urinary tract infection in children In healthy people, urine in the bladder is sterile, no bacteria or other infectious organisms are present. The urethra that carries urine from the bladder out of the body contains no bacteria or too few to cause an infection. However, any part of the urinary tract can become infected. That is why any growth of typical urinary pathogens is considered clinically important if obtained by suprapubic aspiration. An infection anywhere along the urinary tract is called a urinary tract infection (UTI) and it is the 2nd most common infection in children. UTIs are caused by bacteria that enter the opening of the urethra and move upward to the urinary bladder and sometimes the kidneys. Rarely, in severe infections, bacteria may enter the bloodstream from the kidneys and cause infection of the bloodstream (sepsis) or infection of other organs. During infancy, boys are more likely to develop urinary tract infections. After infancy, girls are much more likely to develop them. children who have UTIs, however, more commonly have various structural abnormalities of their urinary system that make them more susceptible to urinary infection. These abnormalities include vesicoureteral reflux (VUR), which is an abnormality of the ureters that allows urine to pass backward from the bladder up to the kidney, and a number of conditions that block the flow of urine. The risk of renal scarring is greatest in infants and may be progressive if there is a delay in diagnosis and management of urinary tract infections in children. The aims of urinary tract infection management are to provide symptomatic relief and to prevent renal damage. In the meantime to be able to prevent the recurrences of urinary tract infection, evaluation and looking for any structural or functional predisposing factors. Treatment of underlying voiding dysfunction and constipation is important for the successful management of urinary tract infections in children. Since the early 1970s, occult bacteremia has been the major focus of concern for clinicians evaluating febrile infants who have no recognizable source of infection. With the introduction of effective conjugate vaccines against Haemophilus influenza type b and Streptococcus pneumoniae (which have resulted in dramatic decreases in bacteremia and meningitis), there has been increasing appreciation of the urinary tract as the most frequent site of the occult and serious bacterial infections. Because the clinical presentation tends to be nonspecific in infants and reliable urine specimens for culture cannot be obtained without invasive methods (urethral catheterization or suprapubic aspiration [SPA]), diagnosis and treatment may be delayed. Most experimental and clinical data support the concept that delays in the institution of appropriate treatment of pyelonephritis increase the risk of renal damage The urinary tract in healthy children is usually sterile. The urethra on the other hand is colonized with bacteria. UTI occurs with the entrance of pathogens into the urinary tract and subsequent adherence to it. Although normal voiding with intermittent urinary outflow usually clears pathogens within the bladder. In conditions with Urinary malformation, urine stasis, impaired urine flow lead to increase reservoir and gives more time to establish the infection and the adherence of bacteria to the uroepithelial mucosa being the main predisposing factors for the development of UTI. Congenital obstructive uropathy, "detrusor sphincter" dyssynergia syndrome is an infrequent bladder emptying that is also a cause of UTI. The second mechanism is the introduction of pathogens by way of a foreign body or instrument. Urinary infection is the third most common nosocomial infection after primary bloodstream infections and pneumonia in intensive care units. A recent prospective study estimates the incidence of nosocomial UTI as 0.6 case/1000 patient/day and newborns and infants are affected disproportionately. The infection is associated frequently with urethral catheterization. Escherichia coli accounts for 80 to 90% of UTI in children. Among febrile infants, unwell children, and older children with urinary symptoms 6%–8% will have a UTI. Symptoms and signs of pyelonephritis include fever, chills, rigor, flank pain, and costovertebral angle tenderness. Lower tract symptoms and signs include suprapubic pain, dysuria, urinary frequency, urgency, cloudy urine, malodorous urine, and suprapubic tenderness. A urinalysis and urine culture should be performed when UTI is suspected. While waiting for the culture results, prompt antibiotic therapy is indicated for symptomatic UTI based on clinical findings and positive urinalysis to eradicate the infection and improve clinical outcomes. The prevalence varies with age, peaking in young infants, toddlers, and older adolescents. UTI is more common in female and uncircumcised male infants. During toddler years, toilet training can lead to volitional holding and bladder stasis, promoting UTIs. Over 30% of children with UTI will have recurrent UTI. Common risk factors for recurrence include vesicoureteral reflux (VUR) and the bladder–bowel dysfunction. Older non-continent children (eg, developmental delay) also have more recurrent UTIs. Occult bacteremia should always be considered, although the probability of this diagnosis is much lower than UTI (less than 1 versus 7 percent) in fully immunized children with no other identifiable potential source for fever on physical examination. Urinary calculi, urethritis (including a sexually transmitted infection), dysfunctional elimination, and diabetes mellitus must be considered in verbal children with urinary tract problems. Structural abnormalities, neurologic deficiency, or behavioral voiding dysfunction resulting in residual urine in any part of the urinary tract also may influence the persistence of bacteriuria once established. Race seems to affect the incidence of UTI. In developed countries with adequate medical resources, UTI is more common in white girls than girls of other races. Although UTI occurs in children of all races and ethnicities, the incidence is low in African-American children. the risk for recurrence is proportional to the number of previous infections. Long-term antibiotic treatment is more likely if the child receives a diagnosis of vesicoureteral reflux or VUR. This birth defect results in the abnormal backward flow of urine from the bladder up the ureters, moving urine toward the kidneys instead of out the urethra. This disorder should be suspected in young children with recurring UTIs or any infant with more than one UTI with fever. Children with VUR have a higher risk of kidney infection. It creates an increased risk of kidney damage and, ultimately, kidney failure. Surgery is an option used in severe cases. Typically, children with mild or moderate VUR outgrow the condition. However, kidney damage or kidney failure may occur into adulthood. Fever is the most common presentation of UTI in young children, for this reason, the American Academy of Pediatrics (AAP) recommends UTI be ruled out in any child 2 months to 2 years of age with unexplained fever. The physical examination of children with UTI can be nonspecific. With the advent of ultrasonography, occasionally an anatomically abnormal genitourinary organ may be found during the initial evaluation (eg, hydronephrosis, xanthogranulomatous kidney, protruding ureterocele). An old-fashioned examination, however, still may reveal subtle information suggestive of the neurogenic bladder (eg, spinal anomalies, sacral dimples/pits/fat pads). A health care professional will look at the sample under a microscope for bacteria and white blood cells, which the body produces to fight infection. Bacteria also can be found in the urine of healthy children, so a bladder infection is diagnosed based on both your child's symptoms and lab test results. Currently, a second or third-generation cephalosporin and amoxicillin-clavulanate are drugs of choice in the treatment of acute uncomplicated UTI. Parenteral antibiotic therapy is recommended for infants ≤ 2 months and any child who is toxic-looking, hemodynamically unstable, immunocompromised, unable to tolerate oral medication, or not responding to oral medication. A combination of intravenous ampicillin and intravenous/intramuscular gentamycin or a third-generation cephalosporin can be used in those situations. Routine antimicrobial prophylaxis is rarely justified, but continuous antimicrobial prophylaxis should be considered for children with frequent febrile UTI.

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/index.php/Urinary_tract_infection_resident_survival_guide_(pediatrics)

# Urinary tract infection resident survival guide (pediatrics) Urinary tract infections (UTIs) are common in kids. UTIs occurs when bacteria (germs) get into the bladder (lower tract infection) or kidneys(upper tract). Abdominal pain and loin tenderness, with systemic features such as fever, anorexia, vomiting, lethargy and malaise are the signs of upper tract infection while lower abdominal or suprapubic pain, dysuria, urinary frequency and urgency are signs of lower tract infections. In younger children the typical signs are not clear and it is difficult to differentiation between upper and lower tract infection. Up to 8% of girls and 2% of boys will get a UTI by age 5. Prompt diagnosis and appropriate treatment are very important to reduce the morbidity associated with this condition. Urinary tract infections have two basic types, bladder infection and kidney infection. If the infection is in the bladder it is called cystitis and it causes pain and swelling in bladder. If the infection traveled up to the kidneys, it is called pyelonephritis which is serious and it may cause harm to the kidneys. UTI should be considered in any infant or child presenting with fever without an identifiable source of infection, because it can be associated with acute mortality (i.e. urosepsis) and/or chronic medical problems like renal scarring , hypertension, and chronic renal insufficiency,that is why urinalysis and urine culture should be done.The AAP (American Academy of pediatrics) recommendations for imaging after an initial febrile UTI were extensive and included renal and bladder ultrasound, voiding cystourethrography (VCUG) or radionuclide cystography in all children younger than two years of age

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/index.php/Urination

# Urination Urination, known by physiologists as micturition, or more simply as voiding, is the process of disposing urine from the urinary bladder through the urethra to the outside of the body. In healthy adults, the process of urination is under voluntary control; in infants and individuals with neurological injury, urination may occur as an involuntary reflex. Urination is often referred to as "peeing", a euphemism for "piss" which is considered more vulgar. It is also referred to as "weeing" in the UK. "To whiz" or "whizzing" is common in the U.S. Others of note are "tinkle" and "potty" - both of which are often used with children. The main organs involved in urination are the bladder and the urethra. The smooth muscle of the bladder, known as the detrusor, is innervated by sympathetic nervous system fibers from the lumbar spinal cord and parasympathetic fibers from the sacral spinal cord. Fibers in the pelvic nerves constitute the main afferent limb of the voiding reflex; the parasympathetic fibers to the bladder that constitute the excitatory efferent limb also travel in these nerves. Part of the urethra is surrounded by the external urinary sphincter, which is innervated by somatic fibers originating in the sacral cord, in an area termed Onuf's nucleus . Muscle bundles pass on either side of the urethra, and these fibers are sometimes called the internal urethral sphincter, although they do not encircle the urethra. Farther along the urethra is a sphincter of skeletal muscle, the sphincter of the membranous urethra (external urethral sphincter). The bladder epithelium is made up of a superficial layer of flat cells and a deep layer of cuboidal cells. The physiology of micturition and the physiologic basis of its disorders are subjects about which there is much confusion, especially at the supraspinal level. Micturition is fundamentally a spinobulbospinal reflex facilitated and inhibited by higher brain centers and, like defecation, subject to voluntary facilitation and inhibition. In healthy individuals, the lower urinary tract has two discrete phases of activity: the storage phase, when urine is stored in the bladder; and the voiding phase, when urine is released through the urethra. The state of the reflex system is dependent on both a conscious signal from the brain and the firing rate of sensory fibers from the bladder and urethra. At low bladder volumes, afferent firing is low, resulting in excitation of the outlet (the sphincter and urethra), and relaxation of the bladder. At high bladder volumes, afferent firing increases, causing a conscious sensation of urinary urge. When the individual is ready to urinate, he or she consciously initiates voiding, causing the bladder to contract and the outlet to relax. Voiding continues until the bladder empties completely, at which point the bladder relaxes and the outlet contracts to re-initiate storage. In infants, voiding occurs involuntarily (as a reflex). The ability to voluntarily inhibit micturition develops at the age of 2-3 years, as control at higher levels of the central nervous system develops. In the adult, the volume of urine in the bladder that normally initiates a reflex contraction is about 300-400 mL. During storage, bladder pressure stays low, because of the bladder's highly compliant nature. A plot of bladder (intravesical) pressure against the volume of fluid in the bladder (called a cystometrogram) will show a very slight rise as the bladder is filled. This phenomenon is a manifestation of the law of Laplace, which states that the pressure in a spherical viscus is equal to twice the wall tension divided by the radius. In the case of the bladder, the tension increases as the organ fills, but so does the radius. Therefore, the pressure increase is slight until the organ is relatively full. The bladder smooth muscle has some inherent contractile activity; however, when its nerve supply is intact, stretch receptors in the bladder wall initiate a reflex contraction that has a lower threshold than the inherent contractile response of the muscle. Action potentials carried by sensory neurons from stretch receptors in the urinary bladder wall travel to the sacral segments of the spinal cord through the pelvic nerves. Since bladder wall stretch is low during the storage phase, these afferent neurons fire at low frequencies. Low-frequency afferent signals cause relaxation of the bladder by inhibiting sacral preganglionic neurons and exciting lumbar sympathetic preganglionic neurons. Conversely, afferent input causes contraction of the sphincter through excitation of Onuf's nucleus, and contraction of the bladder neck and urethra through excitation of the sympathetic preganglionic neurons. As the bladder becomes full, afferent firing increases, yet the micturition reflex can be voluntarily inhibited until it is appropriate to begin voiding (e.g. a bathroom is reached). Bladder afferent signals ascend the spinal cord to the periaqueductal gray, where they project both to the pontine micturition center and to the cerebrum . At a certain level of afferent activity, the conscious urge to void becomes difficult to ignore. Once the voluntary signal to begin voiding has been issued, neurons in pontine micturition center fire maximally, causing excitation of sacral preganglionic neurons. The firing of these neurons causes the wall of the bladder to contract; as a result, a sudden, sharp rise in pressure in intravesical pressure occurs. The pontine micturition center also causes inhibition of Onuf's nucleus, resulting in relaxation of the external urinary sphincter. When the external urinary sphincter is relaxed urine flows from the urinary bladder when the pressure there is great enough to force urine to flow through the urethra. The micturition reflex normally produces a series of contractions of the urinary bladder. After urination, the female urethra empties by gravity. Urine remaining in the urethra of the male is expelled by several contractions of the bulbospongiosus muscle. The mechanism by which voluntary urination is initiated remains unsettled. One possibility is that the voluntary relaxation of the muscles of the pelvic floor causes a sufficient downward tug on the detrusor muscle to initiate its contraction. Another possibility is the excitation or disinhibition of neurons in the pontine micturition center, which causes concurrent contraction of the bladder and relaxation of the sphincter. There is an inhibitory area for micturition in the midbrain. After transection of the brain stem just above the pons, the threshold is lowered and less bladder filling is required to trigger it, whereas after transection at the top of the midbrain, the threshold for the reflex is essentially normal. There is another facilitatory area in the posterior hypothalamus. In humans with lesions in the superior frontal gyrus, the desire to urinate is reduced and there is also difficulty in stopping micturition once it has commenced. However, stimulation experiments in animals indicate that other cortical areas also affect the process. The bladder can be made to contract by voluntary facilitation of the spinal voiding reflex when it contains only a few milliliters of urine. Voluntary contraction of the abdominal muscles aids the expulsion of urine by increasing the pressure applied to the urinary bladder wall, but voiding can be initiated without straining even when the bladder is nearly empty. Voiding can also be consciously interrupted once it has begun, through a contraction of the perineal muscles and external sphincter can be contracted voluntarily, which will prevent urine from passing down the urethra. Need to urinate is experienced as an uncomfortable, full, feeling. It is highly correlated with the fullness of the bladder. In males the feeling of the need to urinate can be sensed at the end of the penis, even though the neural activity associated with a full bladder comes from the bladder itself. Post-micturition convulsion syndrome, the feeling of a shiver running down the spine following urination, occurs in more than 80% of men, but also occurs in more than 55% of women . Its explanation is unknown. There are three major types of bladder dysfunction due to neural lesions: (1) the type due to interruption of the afferent nerves from the bladder; (2) the type due to interruption of both afferent and efferent nerves; and (3) the type due to interruption of facilitatory and inhibitory pathways descending from the brain. In all three types the bladder contracts, but the contractions are generally not sufficient to empty the viscus completely, and residual urine is left in the bladder. Paruresis, also known as shy bladder syndrome, is an example of a bladder interruption from the brain that often causes total interruption until the person has left a public area. When the sacral dorsal roots are cut in experimental animals or interrupted by diseases of the dorsal roots such as tabes dorsalis in humans, all reflex contractions of the bladder are abolished. The bladder becomes distended, thin-walled, and hypotonic, but there are some contractions because of the intrinsic response of the smooth muscle to stretch. When the afferent and efferent nerves are both destroyed, as they may be by tumors of the cauda equina or filum terminale, the bladder is flaccid and distended for a while. Gradually, however, the muscle of the "decentralized bladder" becomes active, with many contraction waves that expel dribbles of urine out of the urethra. The bladder becomes shrunken and the bladder wall hypertrophied. The reason for the difference between the small, hypertrophic bladder seen in this condition and the distended, hypotonic bladder seen when only the afferent nerves are interrupted is not known. The hyperactive state in the former condition suggests the development of denervation hypersensitization even though the neurons interrupted are preganglionic rather than postganglionic. During spinal shock, the bladder is flaccid and unresponsive. It becomes overfilled, and urine dribbles through the sphincters (overflow incontinence). After spinal shock has passed, the voiding reflex returns, although there is, of course, no voluntary control and no inhibition or facilitation from higher centers when the spinal cord is transected. Some paraplegic patients train themselves to initiate voiding by pinching or stroking their thighs, provoking a mild mass reflex. In some instances, the voiding reflex becomes hyperactive. Bladder capacity is reduced, and the wall becomes hypertrophied. This type of bladder is sometimes called the spastic neurogenic bladder. The reflex hyperactivity is made worse by, and may be caused by, infection in the bladder wall. Due to the flexible and protruding nature of the penis, it is easy to control the direction of the urine stream. This makes it easy to urinate standing up, and most men urinate this way. The foreskin, if left in place during urination, may block the direct path of the outgoing stream by causing turbulence, resulting in a slower, but thicker stream of urine that may also dribble. Men who choose to retract their foreskin, or who have been circumcised, may have a more focused stream of urine that travels at the same speed it exits the urethra. When a man is done urinating, he will usually shake and/or gently squeeze his penis to expel the excess urine trapped in the opening of the foreskin or on the glans. This is known as "milking" the urethra. A common trick in expelling excess urine is gently pushing on the area behind the testicles (perineum). Trousers usually have a fly allowing men to urinate without lowering the whole trousers. The fly has buttons or a zipper. Either just the fly is opened or also the fastening at the waist. Additionally, the fly of the underpants is used or their front-side is lowered. All combinations are possible. Trousers without fly, like some jogging trousers, have usually an elastic waist band allowing lowering the front side like underpants. It is also possible for men to urinate sitting down. This is normally done when defecation has to take place as well. Some men also prefer to urinate this way. In women, the urethra opens straight into the vulva. Because of this, the urine does not exit at a distance from her body and is, therefore, hard to control. Because of surface tension in the urine, the easiest method is to just rely on gravity to take over once the urine has exited her body. This can easily be achieved if the woman is sitting down, although some women choose to squat or hover. Those alternative choices are sometimes made due to the perceived or actual unsanitary conditions at the location where the woman is urinating. When sitting, it helps if the woman leans forward and keeps her legs together, as this helps direct her stream downwards. When not urinating into a toilet, squatting is the easiest way for a woman to direct her urine stream. Some women use one or both hands to focus the direction of the urine stream, which is more easily achieved while in the squatting position. Women who wear pants/trousers/shorts will need to lower the garment to facilitate urination. Women wearing skirts or dresses only need to raise them to their waists to urinate, just lowering the underpants. While urinating in the squatting position, pants are often just lowered to the midst of the thighs, and some women lift the midst of the lowered underpants up. Some women hold the midst of their underpants or bikinipants to the side, so that they do not have to lower them. It is also possible for many women to urinate standing up by spreading their legs and pushing hard to avoid urine running down their legs. This technique for urinating while standing can be common when women often wear a sarong, skirt, or other such open bottomed garments, and either wear no underwear, or remove it. It is considered normal for women to urinate like this in many parts of Africa, whereas in contrast, it is not completely accepted in countries such as India where it also occurs in some areas. In Africa, even signs which forbid public urination often show a picture of a woman urinating while standing. . It is mostly in West Africa, like Ghana and Nigeria, that it is considered normal for a female to urinate standing up. In many other parts it is mostly occurring in the countryside or not at all. Though uncommon, it is possible for women to urinate standing up in a way similar to that of men. This may be done by spreading the labia minora open in a certain way and orienting the pelvis at an angle and rapidly forcing the urine stream out. An alternative method is to use a tool to assist. Occasionally, if a male's penis is damaged or removed, or a female's genitals/urinary tract is damaged, other urination techniques must be used. Most often in such cases, doctors will reposition the urethra to a location where urination can still be accomplished, usually in a position that would only promote urination while seated/squatting, though a permanent urinary catheter may rarely be used in some cases. Babies have no socialized control over urination within societies that do not practise elimination communication and instead use diapers. Toilet training is the process of learning to restrict urination to socially approved times and situations. Many young children suffer from nocturnal enuresis. It is socially more accepted and more hygienic for adults and older children to urinate in a toilet. Public toilets are often separate for men and women, and may be partitioned for reasons of cultural modesty. Public restrooms may have urinals for men. The etiquette associated with two or more males using adjoining urinals varies, however . Urinals for women, though rare, allow females to urinate while standing through the use of a special tool or through the finger-assist method . Urinals for either sex may have partitions between them in order to increase privacy. People with a mild form of paruresis, or "shy bladder syndrome," may have difficulty urinating in the presence of others and will consequently avoid using urinals directly adjacent to another person. Alternatively, they may opt for the privacy of a stall or simply avoid public restrooms altogether. A common transgression is urinating in the street (except at a public urinal). Often this is done after consumption of alcoholic beverage: the alcohol causes production of additional urine as well as a reduction of inhibitions. In New Orleans, urination on the street is sometimes referred to as a "New Orleans Piss". In most places, public urination is punishable by fine. Urination can also be seen as a sign of disrespect or contempt for someone or something. In popular culture, signs of a cartoon figure (sometimes Calvin) urinating on another object (usually a car brand) are common. In many countries and in many social classes even mentioning the need to urinate is seen as a social transgression, although the need is universal. Until recently in the UK many children were taught to say "I need a tidy" or "I need attention" when they needed to be taken to urinate. The abbreviations "tidy" or "tenny" were often used. Other euphemisms, such as 'Spending a penny" (a reference to coin-operated pay toilets); 'Going to see my aunt'; or 'Going to see a man about a dog' were used by adults. Even today adults may avoid stating that they need to urinate. Sometimes urination is done in a container such as a bottle, urinal, bedpan or chamber pot, e.g. in case of lying sick in bed, in the case that the urine has to be examined (for medical reasons, or for a drug test), or in the case that there is no toilet or it is inconvenient to go there, and no other possibility to dispose of the urine right away. See also Bedpan use and output measurement. For the latter application a more expensive solution (hence for special occasions while traveling etc.) is a special disposable bag containing absorbent material that solidifies the urine in 5 to 10 seconds, making it convenient and safe to keep. It can also be used for vomiting. As well, it is not uncommon for people who do not have access to toilets to simply urinate on the ground. The local flora such as a tree or bush can be used for added privacy.

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/index.php/Urine

# Urine Steven C. Campbell, M.D., Ph.D. Associate Editor(s)-in-Chief: Yazan Daaboul, M.D. Synonyms and keywords: Urinary findings; Urinary abnormalities; Findings on urine exam; Urine; Urine composition; Urine output Urine is a fluid produced by humans through the kidney, collected in the bladder, and excreted through the genital urethra. Urine formation helps to maintain the balance of minerals and other substances in the body. Urinary findings may be qualitative or quantitative. Qualitative urinary findings are often analyzed on urinalysis and urine culture. Quantitative urinary findings depends on urine output. A urinalysis (U) is an array of tests performed on urine and is one of the most common methods of medical diagnosis. A part of a urinalysis can be performed by using urine dipsticks, in which the test results can be read as color changes. Pyuria is defined as the presence of 10 or more white cells per cubic millimeter in a urine specimen, 3 or more white cells per high-power field of unspun urine, a positive result on Gram's stain of an unspun urine specimen, or a urinary dipstick test that is positive for leukocyte esterase

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/index.php/Urobilin

# Urobilin Urobilin is a yellow linear tetrapyrrole, resulting from the breakdown of haem, a cyclic tetrapyrrole. Urobilin is generated in intestines from urobilinogen. It is absorbed into blood stream and excreted in urine, giving urine its characteristic yellow color.

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/index.php/Urochrome

# Urochrome Urochrome is a pigment that causes the yellow color in urine. It is a breakdown product of the blood's hemoglobin and is removed by the kidneys. Depending on the amount of Urochome the urine might be darker.

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/index.php/Urocortin

# Urocortin Urocortin is a protein that in humans is encoded by the UCN gene. Urocortin belongs to the corticotropin-releasing factor (CRF) family of proteins which includes CRF, urotensin I, sauvagine, urocortin II and urocortin III. Urocortin is involved in the mammalian stress response, and regulates aspects of appetite and stress response. Urocortin is a peptide composed of 40 amino acids. Urocortin is composed of a single alpha helix structure. The human UCN gene contains two exons, and the entirety of the coding region is contained within the second exon. Urocortin is expressed widely in the central and peripheral nervous systems, with a pattern similar to that of CRF. Areas of similarity between urocortin and CRF expression include the supraoptic nucleus and the hippocampus. Urocortin is also expressed in areas distinct from CRF expression; these areas notably include the median eminence, the Edinger-Westphal nucleus, and the sphenoid nucleus. Additionally, Urocortin is expressed in peripheral tissues such as the heart. Urocortin is known to interact both with the CRF type 1 and CRF type 2 receptors. Furthermore, Urocortin is thought to be the primary ligand for the CRF type 2 receptor, as it has higher binding affinity for the CRF type 2 receptor than CRF. Additionally, urocortin interacts with CRF Binding Protein in the mammalian brain. Urocortin is closely related to CRF, which mediates the mammalian stress response. Urocortin is consequently implicated in a number of stress responses, primarily relating to appetite and food intake. Administration of urocortin to the central nervous system of mice and rats has been shown to decrease appetite. Additionally, central urocortin treatment increases anxiety-linked behaviors and increases motor activity in mice and rats. These general anxiety-linked behaviors are likely induced through the CRF type 1 receptor, and the appetite behaviors are likely induced through the CRF type 2 receptor. The reduction in appetite from urocortin treatment could be a result of suppression of gastric emptying and/or hypoglycemia, which have been shown to result from urocortin treatment. Urocortin expression is stimulated in response to osmotic stress; water deprivation in rats has been shown to induce urocortin expression in the supraoptic nucleus. Montane Voles and Meadow Voles are closely related species of voles which are regularly studied as a model for social and mating behavior. The distribution of urocortin-expressing neurons differs in meadow voles compared to montane voles, suggesting urocortin may also play a role in modulating social behavior in some species. Urocortin has been shown to induce increases in heart rate and coronary blood flow when applied peripherally. These effects are likely mediated through the CRF type 2 receptor, as this receptor is found in the cardiac atria and ventricles. Urocortin also functions to protect cardiovascular tissue from ischemic injury. Urocortin's cardiovascular effects separate it from other members of the CRF family, and likely represent its primary biological function. Urocortin is not present in all non-mammals; the closet analogue in teleost fish is urotensin I. However, in amphibian species such as Xenopus laevis, urocortin is expressed in tissues such as brain, pituitary, kidney, heart, and skin. Urocortin in Xenopus has been shown to increase cAMP accumulation and inhibit appetite

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/index.php/Urogenital_sinus

# Urogenital sinus The urogenital sinus (also known as the persistent cloaca) is a part of the human body only present in the development of the urinary and reproductive organs. It is the ventral part of the cloaca, formed after the cloaca separates from the rectum. It eventually becomes, among other things, the bladder.

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/index.php/Uroguanylin

# Uroguanylin Uroguanylin is a 16 amino acid peptide that is secreted by enterochromaffin cells in the duodenum and proximal small intestine. Guanylin acts as an agonist of the guanylyl cyclase receptor guanylate cyclase 2C (GC-C), and regulates electrolyte and water transport in intestinal and renal epithelia. Its sequence is H-Asn-Asp-Asp-Cys(1)-Glu-Leu-Cys(2)-Val-Asn-Val-Ala-Cys(1)-Thr-Gly-Cys(2)-Leu-OH. In humans, the uroguanylin peptide is encoded by the GUCA2B gene. Uroguanylin may be involved in appetite and perceptions of 'fullness' after eating meals, as suggested by a study into mice.

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/index.php/Urogynecologist

# Urogynecologist A Urogynecologist is a doctor whose specialty combines that of a gynecologist and a urologist, combining expertise in treating women's reproductive systems with that of treatment of the urinary tract.

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/index.php/Urokinase

# Urokinase Urokinase, also known as urokinase-type plasminogen activator (uPA), is a serine protease present in humans and other animals. The human urokinase protein was discovered, but not named, by McFarlane and Pilling in 1947. Urokinase was originally isolated from human urine, and it is also present in the blood and in the extracellular matrix of many tissues. The primary physiological substrate of this enzyme is plasminogen, which is an inactive form (zymogen) of the serine protease plasmin. Activation of plasmin triggers a proteolytic cascade that, depending on the physiological environment, participates in thrombolysis or extracellular matrix degradation. This cascade had been involved in vascular diseases and cancer progression. Urokinase is encoded in humans by the PLAU gene, which stands for "plasminogen activator, urokinase". The same symbol represents the gene in other animal species. The PLAU gene encodes a serine protease (EC 3.4.21.73) involved in degradation of the extracellular matrix and possibly tumor cell migration and proliferation. A specific polymorphism in this gene may be associated with late-onset Alzheimer disease and also with decreased affinity for fibrin-binding. The protein encoded by this gene converts plasminogen to plasmin by specific cleavage of an Arg-Val bond in plasminogen. This gene's proprotein is cleaved at a Lys-Ile bond by plasmin to form a two-chain derivative in which a single disulfide bond connects the amino-terminal A-chain to the catalytically active, carboxy-terminal B-chain. This two-chain derivative is also called HMW-uPA (high molecular weight uPA). HMW-uPA can be further processed into LMW-uPA (low molecular weight uPA) by cleavage of chain A into a short chain A (A1) and an amino-terminal fragment. LMW-uPA is proteolytically active but does not bind to the uPA receptor. Urokinase is a 411-residue protein, consisting of three domains: the serine protease domain, the kringle domain, and the growth factor domain. Urokinase is synthesized as a zymogen form (prourokinase or single-chain urokinase), and is activated by proteolytic cleavage between Lys158 and Ile159. The two resulting chains are kept together by a disulfide bond. The most important inhibitors of urokinase are the serpins plasminogen activator inhibitor-1 (PAI-1) and plasminogen activator inhibitor-2 (PAI-2), which inhibit the protease activity irreversibly. In the extracellular matrix, urokinase is tethered to the cell membrane by its interaction to the urokinase receptor. Elevated expression levels of urokinase and several other components of the plasminogen activation system are found to be correlated with tumor malignancy. It is believed that the tissue degradation following plasminogen activation facilitates tissue invasion and, thus, contributes to metastasis. This makes urokinase an attractive drug target, and, so, inhibitors have been sought to be used as anticancer agents. However, incompatibilities between the human and murine systems hamper clinical evaluation of these agents. Through its interaction with the urokinase receptor, urokinase affects several other aspects of cancer biology such as cell adhesion, migration, and cellular mitotic pathways. As of December 7, 2012, Mesupron, a small molecule serine protease inhibitor developed by the WILEX pharmaceutical company, has completed phase II trials. Mesupron appears to be safe when combined with chemotherapeutic drug Capecitabine for the progression-free survival in human breast cancer. Urokinase is effective for the restoration of flow to intravenous catheters blocked by clotted blood or fibrin (catheter clearance). Catheters are used extensively to administer treatments to patients for such purposes as dialysis, nutrition, antibiotic treatment and cancer treatment. Approximately 25% of catheters become blocked, meaning that affected patients cannot receive treatment until the catheter has been cleared or replaced. Urokinase is also used clinically as a thrombolytic agent in the treatment of severe or massive deep venous thrombosis, peripheral arterial occlusive disease, pulmonary embolism, acute myocardial infarction (AMI, heart attack), and occluded dialysis cannulas (catheter clearance). It is also administered intrapleurally to improve the drainage of complicated pleural effusions and empyemas. Urokinase is marketed as Kinlytic (formerly Abbokinase) and competes with recombinant tissue plasminogen activator (e.g., alteplase) as a thrombolytic drug. All plasminogen activators (urokinase, TPA) catalyze the production of plasmin, which in turn leads to the breakdown of the fibrin lattice structure in blood clots.  While there are commonalities in the mode of action for urokinase and TPA, urokinase has some advantages for treatment of peripheral clots (Pulmonary Embolism, Deep Vein Thrombosis, Peripheral arterial occlusive disease). Unlike TPA, which is activated by binding to the fibrin within clots, urokinase is not sequestered by fibrin and therefore does not specifically attack hemostatic clots.  This makes urokinase less likely to break down such hemostatic clots that are essential for ongoing blood vessel repair throughout the body.  Dissolution of these "good" clots can lead to serious adverse events through hemorrhagic bleeding.  Years of clinical study have confirmed the safety advantage of using urokinase. Consequently, urokinase has been preferentially used in deep venous thrombosis and peripheral arterial occlusive disease where it is administered directly to the site of the clot while TPA is preferred in AMI where peripheral bleeding is a secondary consideration.

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/index.php/Urologic_disease

# Urologic disease Diseases of other bodily systems also have a direct effect on urogenital function. For instance it has been shown that protein released by the kidneys in diabetes mellitus sensitises the kidney to the damaging effects of hypertension . Pre-renal failure refers to impairment of supply of blood to the functional nephrons including renal artery stenosis. Intrinsic renal diseases are the classic diseases of the kidney including drug toxicity and nephritis. Post-renal failure is outlet obstruction after the kidney, such as a renal stone or prostatic bladder outlet obstruction. Renal failure may require medication, dietary and lifestyle modification and dialysis. The causes of diseases of the body are common to the urinary tract. Structural and or traumatic change can lead to hemorrhage, functional blockage or inflammation. Colonisation by bacteria, protozoa or fungi can cause infection. Uncontrolled cell growth can cause neoplasia. For example: Biochemical blood tests determine the amount of typical markers of renal function in the blood serum, for instance serum urea and serum creatinine. Biochemistry can also be used to determine serum electrolytes. Special biochemical tests (arterial blood gas) can determine the amount of dissolved gases in the blood, indicating if pH imbalances are acute or chronic.

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/index.php/Urologicals

# Urology Urology is the specialty of medicine that focuses on the urinary tracts of males and females, and on the reproductive system of males. Medical professionals specializing in the field of urology are called urologists and are trained to diagnose, treat, and manage patients with urological disorders. The organs covered by urology include the kidneys, ureters, urinary bladder, urethra, and the male reproductive organs (testes, epididymis, vas deferens, seminal vesicles, prostate and penis). In men, the urinary system overlaps with the reproductive system, and in women the urinary tract opens into the vulva. In both sexes, the urinary and reproductive tracts are close together, and disorders of one often affect the other. Urology combines management of medical (i.e., non-surgical) problems such as urinary infections, and surgical problems such as the correction of congenital abnormalities and the surgical management of cancers. Such abnormalities within the genital region are called genitourinary disorders. As a discipline that involves the study of many organs and physiological systems, urology can be broken down into subfields. Many urologists, particularly those involved in research, choose an informal specialization in a particular field of urology.

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/index.php/Urophagia

# Urophagia Urophagia is generally considered harmless, as the urine of healthy individuals is sterile. However, a small risk exists if there is a disease present, or bacterial infection of the urethra. There may also be secondary effects, such as skin rashes in individuals sensitive to urine. The main dangers are the high salt and mineral content. The high salt content usually does not pose a problem if the urine is sufficiently diluted and not consumed in mass quantities. The effect of the high salt may be mitigated by drinking some water after consuming urine. The urine may be diluted if the person whose urine will be consumed drinks some water (or diet soda, see below) an hour or so before the act. Many people into BDSM drink beer before the act because it dilutes any unpleasant chemicals in the urine, and alcohol acts as a diuretic, stimulating the body to excrete more urine than it normally would. Since artificial sweeteners are excreted in urine, consuming artificial sweetener before urine play can lend a sweet taste to the urine. Drinking diet soda, or other beverages containing artificial sweetener, before urine play will have the dual effect of diluting the urine and sweetening it. However, if the taste of sugar is detected in an individual's urine, and it is known that artificial sweetener has not been consumed, this may be a sign of diabetes and a doctor should be consulted. Asparagus, on the other hand, gives urine an unpleasant smell with about 40%-79% of people. The participants should use caution or avoid drinking urine if one or both of them are taking vitamin or mineral supplements or medication, since many of these are excreted in urine. Urine of persons who are ill, or regularly take medication, should generally not be consumed. In special cases (e.g. chronic illness of the partner), a medical doctor should be consulted to clarify whether the urine of the chronically ill or medicated person may be consumed without endangering one's health, or not. It has been suggested that when a person is in desert survival or surrounded by salt water and devoid of drinking water that the person must resort to drinking his/her own urine if it is the only liquid available. As it tends to cause further dehydration due to the salts in it, drinking urine for survival is advised against by the US Army Field Manual , the head of the Texas Urological Society , and numerous survival instructors and guides while the Discovery Channel advises it In countries such as India and China, it is considered normal by some groups to drink your own urine for health and cosmetic purposes. This health branch of drinking urine is considered to be labeled as Urine therapy. Also, an old method of teeth-whitening during the Renaissance involved the consumption of urine, though it needn't be, and wasn't always necessarily, that of the user. In Roman times, there was a tradition among the Gauls to use urine to whiten teeth. A famous poem by the Roman poet Catullus, criticizing a Gaul named Egnatius, reads: Egnatius, because he has snow-white teeth, smiles all the time. If you're a defendant in court, when the counsel draws tears, he smiles: if you're in grief at the pyre of pious sons, the lone lorn mother weeping, he smiles. Whatever it is, wherever it is, whatever he's doing, he smiles: he's got a disease, neither polite, I would say, nor charming. So a reminder to you, from me, good Egnatius. If you were a Sabine or Tiburtine or a fat Umbrian, or plump Etruscan, or dark toothy Lanuvian, or from north of the Po, and I'll mention my own Veronese too, or whoever else clean their teeth religiously, I'd still not want you to smile all the time: there's nothing more foolish than foolishly smiling. Now you're Spanish: in the country of Spain what each man pisses, he's used to brushing his teeth and red gums with, every morning, so the fact that your teeth are so polished just shows you're the more full of piss. The Koryak people of Siberia drink urine in conjunction with their ceremonial use of the psychoactive Amanita muscaria (commonly known as fly agaric) mushroom. The active alkaloids are unchanged as they pass through the human body, allowing the urine to prolong the intoxicating effects of the mushroom.

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/index.php/Uroporphyrinogen_III_synthase

# Uroporphyrinogen III synthase Uroporphyrinogen III synthase EC 4.2.1.75 is an enzyme involved in the metabolism of the cyclic tetrapyrrole compound porphyrin. It is involved in the conversion of hydroxymethyl bilane into uroporphyrinogen III. This enzyme catalyses the inversion of the final pyrrole unit (ring D) of the linear tetrapyrrole molecule, linking it to the first pyrrole unit (ring A), thereby generating a large macrocyclic structure, uroporphyrinogen III. The enzyme folds into two alpha/beta domains connected by a beta-ladder, the active site being located between the two domains. A deficiency is associated with Gunther's disease, also known as congenital erythropoietic porphyria (CEP). This is an autosomal recessive inborn error of metabolism that results from the markedly deficient activity of uroporphyrinogen III synthase.

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/index.php/Uroscopy

# Uroscopy Uroscopy is the historic medical practice of visually examining a patient's urine for pus, blood, or other symptoms of disease. It dates back to ancient Egypt, Babylon, and India. It was particularly emphasized in Byzantine medicine. By modern medical standards, Uroscopy is considered to be a very limited means of obtaining evidence for the correct diagnosis of a patient's condition. In addition, many of the assumptions made by ancient physicians regarding uroscopy have proved to be quite incorrect and unscientific. However, visual examination of a patient's urine may provide preliminary evidence for a diagnosis, but is generally limited to conditions that affect the urinary system (such as infection (turbidity) or blood (infection or haemorrhage)). A uroscopy flask is a piece of glass that is circular at the bottom, while there is a thin neck at the top, and on top of that neck there is an opening for urine. In order for a doctor to examine a patients urine one would have to urinate into a uroscopy flask. A uroscopy flask is a glass bottle that must be transparent. If there is any color to the uroscopy flask, diagnosis could be wrong. In the process of uroscopy, color is very crucial to find diseases. If the uroscopy flask has a tint of color, the doctor may not be able effectively diagnose the patient. The glass must also have an even thickness throughout the flask. If the top is very thin glass and the bottom is thick glass, then the impurities in the top may look different from the top and bottom. While in all actuality they could be the very same impurities. The impurities in urine have varying shapes, uneven glass will corrupt the diagnosis. The uroscopy wheel is a diagram that linked the color of urine to a particular disease. It usually has twenty different uroscopy flasks with urine of different colors aligned around the boarder of the circle. Each flask has a line that connects it to a summary of a particular disease. This allowed doctors to have a quick reference guide to twenty different types of urine. The temperature at which the urine is examined is a very important factor to consider in the process of uroscopy. When a patient urinates, the urine will be warm, so it is necessary for it to stay warm for proper evaluation. The external temperature should be the same as the internal temperature. When the temperature of urine goes down the bubbles in it will change. Some of them will disappear, but some will remain. With the temperature decrease particles and impurities will be more difficult to evaluate. They will toward the middle of the flask, then sink to the bottom. They will all mix together, making it more difficult to see the impurities. Another problem with urine cooling is that it would become thicker. The longer that it had to cool down the more likely it was that the crystals in the it would bond together, causing it to thicken. This could lead to a false diagnosis, that is why doctors usually inspected the urine quickly. Richard Bright in the 19th century A.D. invented a technique that allowed doctors to examine a patients urine effectively after the temperature had dropped. The process involved heating water, then inserting the uroscopy flask containing cooled urine. This would heat the urine causing the crystals that formed during loss of temperature to break down. As a result the urine will become thin again. This process is very effective, but a doctor should "also be careful not to shake them much before you inspect them for you will move the particles and destroy the bubbles and dilute the deposits and confuse the situation," (The Late Greco-Roman and Byzantine Contribution to the Evolution of Laboratory Examinations of Bodily Excrement. Part1: Urine, Sperm, Menses and Stools, Pavlos C. Goudas). Since the identifying the color of the urine is essential for a proper diagnosis, the lighting is crucial. This is a very complicated step in the uroscopy test. The doctor must can not visually examine the urine in an overly lit location, because it will make the urine seem too bright. He can not examine the urine in a poorly lit location, because he will not be able to properly see the urine. So, he must examine the urine in both conditions. This is done to offset the effects of not enough light and too much light. After he examines in both conditions the doctor must use his best judgment, to make a diagnosis. Disease in which the pancreas does not function properly. Victims of this disease will have high glucose blood sugar. Victims may suffer from: cardiovascular disease (doubled risk), chronic renal failure (it is the main cause for dialysis in developed world adults), retinal damage which can lead to blindness and is the most significant cause of adult blindness in the non-elderly in the developed world, nerve damage, erectile dysfunction (impotence), to gangrene with risk of amputation of toes, feet, and even legs. Yellowish discoloration of the whites of the eyes, skin, and mucous membranes caused by deposition of bile salts in these tissues. It occurs as a symptom of various diseases, such as hepatitis, that affect the processing of bile. Also called icterus. The kidneys are supposed to filter wastes (especially urea) from the blood and excrete them, along with water, as urine. When they are not performing this task the patient is suffering from kidney disease. The medical field that studies the kidneys and diseases affecting the kidney is called nephrology, from the Ancient Greek name for kidney. Doctors would test urine by using a visual examination. If the urine had blood in it the patient was suffering from tumors in the urinary tract. Uroscopy was important to the Roman and Byzantine eras, because it allowed doctors to diagnose patients without technology. This was an era in which there was no microscope, stethoscope, or even thermometers. All that was needed was a uroscopy wheel, uroscopy flask, and an experienced doctor to be able to give a diagnosis. It was a very simple procedure that a doctor could determine a patients problem by simply tasting and/or looking at their urine. Uroscopy was also necessary, because the Hippocratic Oath did not allow doctors to perform any type of surgery. It stated "I will not cut for stone, even for patients in whom the disease is manifest . . ." (Hippocratic Oath). Doctors needed a different way to find out the problems with their patients. That is when the uroscopy test became involved. It followed the Hippocratic Oath and was a very effective test for that particular time period.

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/index.php/Urotensin-II

# Urotensin-II Urotensin-II (U-II) is a peptide ligand that is the strongest known vasoconstrictor. Because of the involvement of the UII system in multiple biological systems such as the cardiovascular, nervous, endocrine, and renal, it represents a promising target for the development of new drugs. U-II was initially isolated from the neurosecretory system of the Goby fish (Gillichthys mirabilis). For many years it was thought that U-II does not exhibit significant effects in mammalian systems; a view quickly overturned when it was demonstrated that Goby U-II produces slow relaxation of mouse anococcygeus muscle, in addition to contraction of rat artery segments. In 1998, the genes for Pre-pro U-II were found in mammals proving that the peptide U-II did exist in mammals. The U-II gene is located on chromosome 1p36. U-II peptide length varies between species due to the specific cleaving sites located at different spots depending on the species. In humans U-II length is 11 amino acids. The peptide sequence that is needed for biological function for both U-II and urotensin II-Related Peptide (URP) is known as the core. It is hexapeptide (-CYS-TYR-LYS-TRP-PHE-CYS-), and is connected at the two ends by a disulfide bond. Also just like URP the amino terminus can be modified without any loss in pharmacological activity suggesting that it is not needed for activation of the receptor. Unlike URP, U-II has an acidic amino acid (Glutamic or Aspartic) that precedes the core sequence. While the amino acid isn't necessary for the activation of urotensin II receptor the fact that it is conserved in different species suggests that it has a biological function that has not been discovered. U-II is an agonist for the urotensin-II receptor which is a G protein-coupled receptor that primarily activates the alpha subunit Gαq11. It activates PKC which then activates PLC which increases the intercellular calcium concentration. It is found in many peripheral tissues, blood vessels, and also the brainstem cholinergic neurons of the laterodorsal tegmental (LDT) and the pedunculopontine tegmental nuclei (PPT). It is also found in rat astrocytes. Pre-pro U-II in both humans and rats are primarily expressed in the motorneurons of the brainstem and spinal cord although it is also found in small amounts in other parts of the brain as well including the frontal lobe and the medulla oblongata. In humans U-II mRNA is also found in other peripheral tissues such as the heart, kidneys, adrenal gland, placenta, spleen, and thymus. When injected intracerebroventricularly (icv) U-II causes an increase in the corticotropin releasing factor by activating the hypothalamic paraventricular neurons. This leads to increased plasma levels of adrenocorticotropic hormones and adrenaline. Rats and mice exhibit many stress related behaviors when injected with U-II which were tested by the elevated plus maze which measures anxiety-like effects,and the hole-board test which measures head dipping which is also an anxiety-like behavior. U-II when injected icv in rats also leads to cardiovascular responses including raising mean arterial pressure (MAP) and causing tachycardia. When the arcuate nucleus, and the paraventricular nucleus, two different areas of the brain which are known to control blood pressure were injected with U-II simultaneously they caused an increase in blood pressure. When the two areas were injected separately it was discovered that U-II affected the excitatory neurons in the paraventricular nucleus and the inhibitory neurons of the arcuate nucleus. U-II when injected icv in both rats and mice also stimulates locomotion in familiar environments. This experiment was also tested in rainbow trout (Oncorhynchus mykiss) where a stimulatory effect was also observed.. Depression-like behavior was also observed when U-II was injected in the brain by using the forced swim test and the tail suspension test which are used to compare molecules that are thought to cause anti-depressive-like effects. U-II has a variety of effects on different tissues. In blood vessels it can cause contraction. In rat pancreas U-II inhibits insulin secretion. It also affects the kidneys including sodium transport, lipid and glucose metabolism, and natriuretic effects. Its has been linked to cardiac fibrosis and hypertrophy, heart failure, renal dysfunction, and diabetes.

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/index.php/Usher_syndrome

# Usher syndrome A leading cause of deaf-blindness, Usher syndrome (sometimes referred to as "Usher's syndrome") is a relatively rare genetic disorder that is associated with a mutation in any one of 10 genes. Other names for Usher syndrome include Hallgren syndrome, Usher-Hallgren syndrome, rp-dysacusis syndrome and dystrophia retinae dysacusis syndrome. Usher syndrome is incurable at present; however, using gene therapy to replace the missing gene, researchers have succeeded in reversing one form of the disease in knockout mice. This syndrome is characterized by deafness and a gradual vision loss. The hearing loss is associated with a defective inner ear, whereas the vision loss is associated with retinitis pigmentosa (rp), a degeneration of the retinal cells. Usually, the rod cells of the retina are affected first, leading to early night blindness and the gradual loss of peripheral vision. In other cases, there is early degeneration of the cone cells in the macula, leading to a loss of central acuity. In some cases, the foveal vision is spared, leading to "doughnut vision"; central and peripheral vision are intact, but there is an annulus around the central region in which vision is impaired. Usher syndrome has three clinical subtypes, denoted as I, II and III in decreasing order of severity. People with Usher I are born profoundly deaf, and begin to lose their vision in the first decade of life. They also exhibit balance difficulties and learn to walk slowly as children, due to problems in their vestibular system. People with Usher II are also born deaf, but do not seem to have noticeable problems with balance; they also begin to lose their vision later (in the second decade of life) and may preserve some vision even into middle age. People with Usher syndrome III are not born deaf, but experience a gradual loss of their hearing and vision; they may or may not have balance difficulties. Usher syndrome I and II are associated with a mutation in any one of six or three different genes, respectively, whereas only one mutation has been linked with Usher III. Since Usher syndrome is inherited in an autosomal recessive pattern, both males and females are equally likely to inherit Usher syndrome. Consanguinity of the parents is a risk factor. Since Usher syndrome mutations are recessive, if both parents have Usher syndrome in the same gene, all their children are overwhelmingly likely to have the same condition; by contrast, the children of a mixed marriage (one parent with Usher syndrome and the other with wild-type genes) are overwhelmingly likely to not have the condition, although they will be all carriers. First recognized in the 19th century, Usher syndrome was the first condition to demonstrate that phenotypes could be inherited in tandem; deafness and blindness are inherited together, but not separately. Animal models of this human disease (such as knockout mice and zebrafish) have been developed recently to study the effects of these gene mutations and to test potential cures for Usher syndrome. Usher syndrome is named after the British ophthalmologist Charles Usher, who examined the pathology and transmission of this illness in 1914 on the basis of 69 cases. However, it was first described in 1858 by Albrecht von Gräfe, a pioneer of modern ophthalmology. He reported the case of a deaf patient with retinitis pigmentosa, who had two brothers with the same symptoms. Three years later, one of his students, Richard Liebreich, examined the population of Berlin for disease pattern of deafness with retinitis pigmentosa. Liebreich noted that Usher syndrome is recessive, since the cases of blind-deafness combinations occurred particularly in the siblings of blood-related marriages or in families with patients in different generations. His observations supplied the first proofs for the coupled transmission of blindness and deafness, since no isolated cases of either could be found in the family trees. Usher syndrome is responsible for the majority of deaf-blindness. The word syndrome means that multiple symptoms occur together, in this case, deafness and blindness. It occurs in roughly 1 person in 23,000 in the United States, 1 in 28,000 in Norway and 1 in 12,500 in Germany. People with Usher syndrome represent roughly one-sixth of people with retinitis pigmentosa. Usher syndrome is inherited in an autosomal recessive pattern. "Recessive" means that both parents must contribute an appropriate gene for the syndrome to appear, and "autosomal" means that the gene is not carried on one of the sex chromosomes (X or Y), but rather on one of the 22 other pairs. (See the article on human genetics for more details.) The progressive blindness of Usher syndrome results from retinitis pigmentosa. The photoreceptors usually start to degenerate from the outer periphery to the center of the retina including the macula. The degeneration is usually first noticed as night blindness (nyctalopia); peripheral vision is gradually lost, restricting the visual field (tunnel vision), which generally progresses to complete blindness. The qualifier pigmentosa reflects the fact that clumps of pigment may be visible by an ophthalmoscope in advanced stages of degeneration. Although Usher syndrome has been classified clinically in several ways, the prevailing approach is to classify it into three clinical sub-types called Usher I, II and III in order of decreasing severity of deafness. Usher I and II are the more common forms; the fraction of people with Usher III is significant only in a few specific areas, such as Finland and Birmingham. As described below, these clinical subtypes may be further subdivided by the particular gene mutated; people with Usher I and II may have any one of six and three genes mutated, respectively, whereas only one gene has been associated with Usher III. The function of these genes is poorly understood as of yet. The hearing impairment associated with Usher syndrome is better understood: damaged hair cells in the cochlea of the inner ear inhibit electrical impulses from reaching the brain. People with Usher I are usually born deaf and often have difficulties in maintaining their balance owing to problems in the vestibular system. Babies with Usher I are usually slow to develop motor skills such as walking. Worldwide, the estimated prevalence of Usher syndrome type I is 3 to 6 per 100,000 people in the general population. Usher syndrome type I can be caused by mutations in any one of several different genes: CDH23, MYO7A, PCDH15, USH1C, and USH1G. These genes function in the development and maintenance of inner ear structures such as hair cells (stereocilia), which transmit sound and motion signals to the brain. Alterations in these genes can cause an inability to maintain balance (vestibular dysfunction) and hearing loss. The genes also play a role in the development and stability of the retina by influencing the structure and function of both the rod photoreceptor cells and supporting cells called the retinal pigmented epithelium. Mutations that affect the normal function of these genes can result in retinitis pigmentosa and vision loss. People with Usher II are generally hard-of-hearing rather than deaf, and their hearing does not degrade over time; moreover, they generally have a normal vestibular system. Usher syndrome type II occurs at least as frequently as type I, but because type II may be underdiagnosed or more difficult to detect, it could be up to three times as common as type I. Usher syndrome type II may be caused by mutations in any of three different genes: USH2A, GPR98 and DFNB31. The protein encoded by the USH2A gene, usherin, is located in the supportive tissue in the inner ear and retina. Usherin is critical for the proper development and maintenance of these structures, which may help explain its role in hearing and vision loss. The location and function of the other two proteins are not yet known. By contrast, people with Usher III experience a progressive loss of hearing and roughly half have vestibular dysfunction. The frequency of Usher syndrome type III is highest in the Finnish population, but it has been noted rarely in a few other ethnic groups. Mutations in only one gene, the CLRN1 gene, have been linked to Usher syndrome type III. The CLRN1 gene encodes Clarin-1, a protein that is important for the development and maintenance of the inner ear and retina. However, the protein's function in these structures, and how its mutation causes hearing and vision loss, is poorly understood as yet. Since Usher syndrome is incurable at present, it is helpful to diagnose children well before they develop the characteristic night blindness. Some preliminary studies have suggested that as many as 10% of congenitally deaf children may have Usher syndrome. However, a mis-diagnosis can have bad consequences, e.g., if the parents elect to give the child cochlear implants. The simplest approach to diagnosing Usher syndrome is to test for the characteristic chromosomal mutations. An alternative approach is electroretinography (ERG), although this is often disfavored for children, since its discomfort can also make the results unreliable. Parental consanguinity is a significant factor in diagnosis. Usher syndrome I may be indicated if the child is profoundly deaf from birth and especially slow in walking. Thirteen other syndromes may exhibit signs similar to Usher syndrome, including Alport syndrome, Alstrom syndrome, Bardet-Biedl syndrome, Cockayne syndrome, spondyloepiphyseal dysplasia congenita, Flynn-Aird syndrome, Friedreich ataxia, Hurler syndrome (MPS-1), Kearns-Sayre syndrome (CPEO), Norrie syndrome, osteopetrosis (Albers-Schonberg disease), Refsum's disease (phytanic acid storage disease), and Zellweger syndrome (cerebro-hepato-renal syndrome). Several genes have been associated with Usher syndrome using linkage analysis of patient families (Table 1) and DNA sequencing of the identified loci. A mutation in any one of these genes is likely to result in Usher syndrome. The clinical subtypes Usher I and II are associated with mutations in any one of six (USH1B-G) and three (USH2A,C-D) genes, respectively, whereas only one gene, USH3A, has been linked to Usher III so far. Two other genes, USH1A and USH2B, were initially associated with Usher syndrome, but USH2B has not been verified and USH1A was incorrectly determined and does not exist. Research in this area is ongoing. Using interaction analysis techniques it could be shown that the identified gene products interact with one another in one or more larger protein complexes. If one of the components is missing, this protein complex cannot fulfill its function in the living cell and it probably comes to the degeneration the same. The function of this protein complex has been suggested to participate in the signal transduction or in the cell adhesion of sensory cells. Since Usher syndrome results from the loss of a gene, gene therapy that adds the proper protein back ("gene replacement") may alleviate it, provided that the added protein becomes functional. Recent studies of mouse models have shown that one form of the disease — that associated with a mutation in myosin VIIa — can be alleviated by replacing the mutant gene using a lentivirus. However, some of the mutated genes associated with Usher syndrome encode very large proteins — most notably, the USH2A and GPR98 proteins, which have roughly 6000 amino-acid residues. Gene replacement therapy for such large proteins may be difficult.

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/index.php/Uterine

# Uterus The uterus or womb is the major female reproductive organ of most mammals, including humans. One end, the cervix, opens into the vagina; the other is connected on both sides to the fallopian tubes. The term uterus is commonly used within the medical and related professions, whilst womb is in more common usage. The plural of uterus is uteri. The main function of the uterus is to accept a fertilized ovum which becomes implanted into the endometrium, and derives nourishment from blood vessels which develop exclusively for this purpose. The fertilized ovum becomes an embryo, develops into a fetus and gestates until childbirth. Due to anatomical barriers such as the pelvis, the uterus is pushed partially into the abdomen due to its expansion during pregnancy. Even in pregnancy the mass of a human uterus amounts to only about a kilogram (2.2 pounds). The uterus is located inside the pelvis immediately dorsal (and usually somewhat rostral) to the urinary bladder and ventral to the rectum. Outside of pregnancy, its size in humans is several centimeters in diameter. The uterus is primarily supported by the pelvic diaphragm and the urogenital diaphragm. Secondarily, it is supported by ligaments and the peritoneum (broad ligament of the uterus) Other named ligaments near the uterus, i.e. the broad ligament, the round ligament, the suspensory ligament of the ovary, the infundibulopelvic ligament, have no role in the support of the uterus. The bilateral Müllerian ducts form during early fetal life. In males, MIF secreted from the testes leads to their regression. In females these ducts give rise to the Fallopian tubes and the uterus. In humans the lower segments of the two ducts fuse to form a single uterus, however, in cases of uterine malformations this development may be disturbed. The different uterine forms in various mammals are due to various degrees of fusion of the two Müllerian ducts.

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/index.php/Uterine_artery_embolization

# Uterine artery embolization Uterine artery embolization (UAE) or Uterine Fibroid Embolization (UFE) is a procedure where an interventional radiologist uses a catheter to deliver small particles that block the blood supply to the fibroids.

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/index.php/Uterine_cancer

# Uterine cancer History and Symptoms | Physical Examination | Staging | Laboratory Findings | Chest X Rays | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies

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/index.php/Uterine_didelphys

# Uterine didelphys Uterine didelphys is a rare type of deformity (1 in 1000 women) in the female reproductive organs in which some organs may be either split or duplicated. Typically, some of these "extra" organs are non-functional or semi-functional appendages, although on occasion they will be completely function in all normal respects, and often independently. A UK woman with two wombs gave birth to triplets in 2006. Hannah Kersey, of Northam in Devon, gave birth to a pair of identical twins from an egg that implanted into one womb and then divided, and to an infant from a single egg that implanted into the other womb. This was the first known birth of its kind.

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/index.php/Uterine_malformation

# Uterine malformation A uterine malformation is the result of an abnormal development of the Mullerian duct(s) during embryogenesis. Symptoms range from amenorrhea, infertility and pain, to normal functioning depending on the nature of the defect. Uterine malformations affect about 1% of the female population. A rudimentary uterus is an uterine remnant not connected to cervix and vagina and may be found on the other side of an unicornuate uterus. Uterine Didelphys is a rare type of deformity (1 in 1000 women) in the female reproductive organs in which some organs may be either split or duplicated. Typically, some of these "extra" organs are non-functional or semi-functional appendages, although on occasion they will be completely functional in all normal respects, and often independently. As the vagina is largely derived from the Mullerian ducts, lack of fusion of the two ducts can lead to the formation of a vaginal septum, or "double vagina", a condition sometimes called with a uterus didelphys or a uterine septum. Besides a physical examination, the physician will need imaging techniques to determine the character of the malformation: gynecologic ultrasonography, pelvic MRI, or hysterosalpingography. In addition, laparoscopy and/or hysteroscopy may be indicated. In some patients the vaginal development may be affected.

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/index.php/Uterine_transplant

# Uterine transplant ## Contents A uterine transplant is the transplantation of a uterus in order to replace one which has undergone necrosis. Though the procedure has significant potential, it has been performed only a few times. ## History In 1896 Knauer published the first study of ovarian transplantation and Grigor've that lead to the investigation of uterine auto-transplantation in 1918. Erslan, Hamernik and Hardy, in 1964 and 1966, were the first to perform an animal auto-transplantation of the uterus and subsequently deliver a pregnancy for that uterus (Erslan et al. 1966). With the availability of IVF in 1978, investigation of uterine transplantation was deferred (Confino et al. 1986). In 2000, a human uterine transplant was performed in Saudi Arabia by Dr. Wafa Fagee. Post-operatively, the patient had two spontaneous menstrual cycles, followed by amenorrhea; exploratory laparotomy confirmed uterine necrosis. The procedure has raised some moral and ethical concerns. ## Research Much of the animal research that has been investigated in the past have explored the feasibility of uterine auto transplantation and have neglected the role of uterine allo-transplantation as well as the influence of immunosuppressive therapy on fertility. Infertility and surrogacy, which also has been considered another alternative for infertility, have been subjected to legal, moral, ethical and religious restrains. This has then led for us as physicians to investigate cautiously the indications for human uterine transplants. The prime candidates for human uterine transplants are: ## Ethical and religious issues Due to the uterus' debatable status as a non-vital organ, debate over the ethicality of uterine transplants persists. Some groups consider the uterus a vital organ due to its ability to sustain the life of the fetus, and concerns exist that the successful transplantation of a uterus might give rise to birth defects should the recipient ever attempt to bear children. There is also religious debate surrounding the morality of uterine transplants, with a myriad of views which vary based on religion and personal preference. ## Successful transplants In Saudi Arabia in 2000, a uterine transplant was performed on a patient whose own uterus had hemorrhaged after childbirth. The transplanted uterus functioned for 99 days, however it ultimately needed to be removed after its failure due to blood clotting. Within the medical community there is some debate as to whether or not the transplant can truly be considered successful, however due to the operation's duration, general consensus favors success.

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/index.php/Uterine_venous_plexus

# Uterine venous plexus The uterine plexuses lie along the sides and superior angles of the uterus between the two layers of the broad ligament, and communicate with the ovarian and vaginal plexuses. They are drained by a pair of uterine veins on either side: these arise from the lower part of the plexuses, opposite the external orifice of the uterus, and open into the corresponding hypogastric vein.

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/index.php/Uteroglobin

# Uteroglobin SCGB1A1 is the founding member of the secretoglobin family of small, secreted, disulfide-bridged dimeric proteins found only in mammals. This antiparallel disulfide linked homodimeric protein is multifunctional and found in various tissues in various names such as: uteroglobin (UG, UGB), uteroglobin-like antigen (UGL), blastokinin, club-cell secretory protein (CCSP), Clara-cell 16 kD protein (17 in rat/mice), club-cell-specific 10 kD protein (CC10), human protein 1, urine protein 1 (UP-1), polychlorinated biphenyl-binding protein (PCB-BP), human club cell phospholipid-binding protein (hCCPBP), secretoglobin 1A member 1 (SCGB1A1).

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/index.php/Uterus_didelphys

# Uterus didelphys Uterus didelphys (sometimes also uterus didelphis) represents a uterine malformation where the uterus is present as a paired organ as the embryogenetic fusion of the mullerian ducts failed to occur. As a result there is a double uterus. Each uterus has a single horn linked to the ipsilateral fallopian tube that faces its ovary. The uterus is formed during embryogenesis by the fusion of the two mullerian ducts. This process usually fuses the two mullerian ducts into a single uterine body but fails to take place in these affected women who maintain their double mullerian systems. A didelphic uterus will have a double cervix and is usually associated with a double vagina. Causes for the failure to fuse are not known. Associated defects may affect the vagina, the renal system, and less common, the skeleton. The condition is less common than these other uterine malformations: arcuate uterus, septate uterus, and bicornuate uterus. It has been estimated to occur in 1/3,000 women. Women with the condition may be asymptomatic and unaware of having a double uterus. However, a study by Heinonen showed that certain conditions are more common. In his study of 26 women with a double uterus gynecological complaints included dysmenorrhea and dyspareunia. All patients displayed a double vagina. The fetal survival rate in 18 patients who delivered was 67.5%. Breech presentation was present in 43% and premature delivery common (21%). A pelvic examination will typically reveal a double vagina and a double cervix. Investigations are usually prompted on the basis of such findings as well as when reproductive problems are encountered. Helpful techniques to investigate the uterine structure are transvaginal ultrasonography and sonohysterography, hysterosalpingography, MRI, and hysteroscopy. More recently 3-D ultrasonography has been advocated as an excellent non-invasive method to evaluate uterine malformations. Patients with an double uterus may need special attention during pregnancy as premature birth and malpresentation are common. Cesarean section was preformed in 82% of patients reported by Heinonen. A number of twin gestations have occurred where each uterus carried its pregnancy separately. It is possible that the delivery occurs at different time, thus the delivery interval could be days or even weeks. A UK woman with a double uterus gave birth to triplets in 2006. Hannah Kersey, of Northam in Devon, gave birth to a pair of identical twins from an egg that implanted into one womb and then divided, and to an infant from a single egg that implanted into the other womb. This was the first known birth of viable triplets in a woman with a double uterus. . It is estimated that the possibility of such a birth is about 1 in 25 million. A triplet pregnancy in a woman with uterus didelphys was reported from Israel in 1981; one baby died in utero, and of the remaining babies, one was delivered at 27 weeks gestation and the other 72 days later.

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/index.php/Utilization_behavior

# Utilization behavior Utilization behavior is a frontal lobe disorder in which the patient has difficulty resisting their impulse to "utilize" objects which are in their visual field and within reach. Unlike other impulse-control disorders, patients with this disorder confabulate reasons for their actions.

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/index.php/Utrophin

# Utrophin The protein encoded by this gene is a component of the cytoskeleton. Utrophin was found during research into Duchenne's muscular dystrophy. The name is a contraction for ubiquitous dystrophin. The 900 kb gene for utrophin is found on the long arm of human chromosome 6. Utrophin was discovered due to its homology with dystrophin. It was found by screening a peptide containing the C-terminal domain of dystrophin against cDNA libraries. The homology varies over its full length from less than 30% in regions of the central rod structural domain to 85% (identity 73%) for the actin binding domain. The tertiary structure of utrophin contains a C-terminus that consists of protein–protein interaction motifs that interact with dystroglycan, a central rod region consisting of a triple coiled-coil repeat, and an actin-binding N-terminus. In normal muscle cells, utrophin is located at the neuromuscular synapse and myotendinous junctions. It is necessary for normal membrane maintenance, and for the clustering of the acetylcholine receptor. In adult humans, utrophin RNA is found ubiquitously, as the name implies, being abundant in the brain, kidney, liver, lung, muscle, spleen and stomach. In the human fetus during muscle differentiation, utrophin is found at the sarcolemma. It disappears when the fetus begins to express dystrophin. Utrophin expression is dramatically increased in patients with Duchenne's muscular dystrophy (and female carriers), both in those muscle fibers lacking dystrophin and in rare, revertant fibers that express dystrophin. No reports have yet associated mutation in the utrophin gene with disease, but it does not seem to play a critical role in development, since mice without utrophin develop normally.

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/index.php/Uvea

# Uvea (anatomy) The uvea (Lat. uva, grape), also called the uveal layer, uveal coat, uveal tract, or vascular tunic, is the pigmented middle of the three concentric layers that make up an eye. The name is possibly a reference to its almost black colour, wrinkled appearance and grape-like size and shape when stripped intact from a cadaveric eye. Its use as a technical term in anatomy and ophthalmology is relatively modern. The uvea lies between the corneosclera (outermost layer of the eye) and the retina (innermost layer/in the back of the eye). It is traditionally divided into 3 or 4 regions, the iris, ciliary body, pars plana and choroid. These distinctions are based on their different structures as seen under light microscopy, and continued use of these terms is appropriate in anatomical studies. For clinical use, the terms anterior uvea (ie, iris and ciliary body) and posterior uvea (ie, choroid) are now in common use, since diseases often spread beyond a single anatomical region of the uvea. In general the uvea consists of a pigmented, highly vascular loose fibrous tissue. The pigment is produced and held in numerous dendritic melanocytes, similar to normal dermal melanocytes. The blood vessels show patterns which are specific to the region of the uvea, and are described in more detail under iris, ciliary body, pars plana and choroid. The stroma also contains large nerves, which are branches of the posterior ciliary nerves. They enter the eye around the optic nerve, and run forwards in the uvea to reach their termination in the cilary body or iris. These parts of the uvea also contain smooth muscle. Broadly, the outer aspect of the posterior uvea lies directly against the sclera, but at the root of the iris, the uvea is reflected sharply towards the central axis, so that its outer surface becomes the anterior surface of the iris, which is in contact only with the aqueous humour. The inner aspect of the posterior uvea lies against Bruch's membrane, which separates it from the retina. On passing forwards beyond the ora serrata, Bruch's membrane and the retina are no longer present, and the inner relation of the uvea is a continuous epithelial sheet, represented in turn by the pars plana epithelium, the ciliary epithelium and the iris pigment epithelium. 1. nutrition and gas exchange. Uveal vessels directly perfuse the ciliary body and iris, to support their metabolic needs, and indirectly supply diffusible nutrients to the outer retina, cornea & lens, which lack any intrinsic blood supply. 2. light absorption. The uvea improves the contrast of the retinal image by reducing reflected light within the eye (analogous to the black paint inside a camera), and also absorbs outside light transmitted through the sclera, which is by no means opaque. In addition, some uveal regions have special functions of great importance, particularly secretion of the aqueous humour by the ciliary processes, control of accommodation (focus) by the ciliary body, and optimisation of retinal illumination by the iris's control over the pupil. Many of these functions are under the control of the autonomic nervous system. The pupil provides the neatest and most visible example of the neural feedback control in the body. This is subserved by a balance between the antagonistic sympathetic and parasympathetic divisions of the autonomic nervous system. Informal pharmacological experiments have been performed on the pupil for centuries, since the pupil is readily visible, and its size can be readily altered by drugs, even crude plant extracts, applied to the cornea. Pharmacological control over pupil size continues to be an important part of the treatment of some ocular diseases - see pupil, uveitis, acute glaucoma, chronic glaucoma. The normal uvea contains immune competent cells, particularly lymphocytes, and is prone to respond to inflammation by developing lymphocytic infiltrates. A rare disease called sympathetic ophthalmia may represent 'cross-reaction' between the uveal and retinal antigens (ie, the body's inability to distinguish between them, with resulting misdirected inflammatory reactions).

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/index.php/Uveitis_(patient_information)

# Uveitis (patient information) Uveitis specifically refers to inflammation of the uvea. The uvea consists of the iris, ciliary body, and choroid, and it provides most of the blood supply to the retina. Uveitis may occur in either eye or both eyes. Uveitis can have many causes, including injury to the eye, viruses, bacteria, parasites, and exposure to toxic substances such as acid. Uveitis can also be caused by inflammatory diseases, autoimmune disorders such as rheumatoid arthritis or ankylosing spondylitis, or genetics. However, in many cases the cause is unknown. People of all ages and both sexes can develop uveitis, although it is more common in women. Additionally, people are more likely to develop uveitis as they age . A complete medical history and comprehensive eye examination must be performed by an optometrist or ophthalmologist to properly diagnosis uveitis. Laboratory tests may be done to rule out infection or an autoimmune disorder. Call for an appointment with your health care provider if you have symptoms of uveitis (e.g. eye pain or reduced vision). Uveitis requires an urgent referral and thorough examination by an optometrist or ophthalmologist along with urgent treatment to control the inflammation. Generally speaking, uveitis is typically treated with glucocorticoid steroids, either as topical eye drops (prednisolone acetate) or oral therapy with corticosteroids. In addition to corticosteroids, topical cycloplegics, such as atropine or homatropine, may be used. In some cases an injection of PSTTA (posterior subtenon triamcinolone acetate) can also be given to reduce the swelling of the eye. Antimetabolite medications, such as methotrexate are often used for recalcitrant or more aggressive cases of uveitis. Experimental treatment with Infliximab or other anti-TNF's infusions may prove helpful. When left untreated, uveitis can lead to permanent vision loss. Additionally, a more serious, potentially life-threatening medical condition could worsen if the uveitis is caused by an underlying disorder that is left untreated. Uveitis is estimated to be responsible for approximately 10% of the blindness in the United States.

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/index.php/Uvulopalatopharyngoplasty

# Uvulopalatopharyngoplasty Uvulopalatopharyngoplasty (also known by the abbreviations UPPP and UP3) is a surgical procedure used to remove tissue in the throat. It involves the removal of tissues which may or may not include: Patients undergo the UPPP operation in two very different ways, with the majority of patients receiving UPPP as a stand-alone procedure. Other patients undergo UPPP as the first procedure in a stepped plan known as "The Stanford Protocol Operation". The way in which UPPP is administered greatly affects the overall prognosis of the intervention. Standard UPPP (The operation as a stand-alone surgical intervention) UPPP is typically administered to patients with obstructive sleep apnea in isolation. It is administered as a stand-alone procedure in the hope that the tissue that obstructs the patient's airway is localized in the back of the throat. The rationale is that, by removing the tissue, the patient's airway will be wider and breathing will become easier. The Role of UPPP in the "Stanford Protocol" Operation UPPP is also offered to sleep apnea patients who opt for a more comprehensive surgical procedure called "The Stanford Protocol", first attempted by Doctors Nelson Powell and Robert Riley of Stanford University. The Stanford Protocol is essentially a "cocktail" of surgeries that aim to address the entire airway and thereby treat (or possibly cure) sleep apnea. It has been found that obstructive sleep apnea usually involves multiple sites where tissue obstructs the airway; the base of the tongue is often involved. The Protocol successively addresses these multiple sites of obstruction. The Protocol operation involves two phases. First, the patient undergoes soft tissue surgeries, UPPP along with Genioglossus Advancement or Hyoid Suspension. After the first phase, the patient is given a sleep study and reassessed. The vast majority of patients fail the first phase, and the course of treatment may then proceed to Phase Two. Phase Two involves maxillomandibular advancement, a surgery which moves the jaw top (maxilla) and bottom (mandible) forward. The tongue muscle is anchored to the chin, and translation of the mandible forward pulls the tongue forward as well. If the procedure achieves the desired results, when the patient sleeps and the tongue relaxes, it will no longer be able to block the airway. Success is much better for Phase two than for Phase One- approximately 90 percent benefit from the second phase, and the success of the Stanford Protocol Operation therefore is due in large part to this second phase. Because of its high rate of complications, the role of UPPP in the Stanford Protocol operation is an important consideration that surgeons must weigh. Some surgeons, including Doctors Powell and Riley, feel that UPPP contributes to the overall success of the Stanford Protocol operation. This assertion is open to debate. In 2002, an Atlanta based surgical team, led by Dr. Jeffrey Prinsell, published results which have approximated those of the Stanford team when UPPP was not included in their mix of surgeries. The Effectiveness UPPP in Isolation When UPPP has been administered in isolation, the results have tended to be disappointing. As explained above, sleep apnea is often caused by multiple co-existing obstructions at various locations of the airway such as the nasal cavity, and particularly the base of the tongue. It has been the experience of some patients that their breathing improved immediately following the sugery, but that the improvements tended to deteriorate after about two years. Studies suggest that when UPPP is administered as a stand-alone procedure, it is effective in less than 40% of patients. The effectiveness of many of the studies on UPPP have been criticized for being methodologically unsound. Effectiveness of "The Stanford Protocol" Operation Over one thousand people have undergone The Stanford Protocol Operation and received follow-up PSG testing. The results have been that 60 to 70 percent of patients have been entirely cured. In approximately ninety percent of patients, a significant improvement can be expected. Laser-assisted uvulopalatopharyngoplasty (LAUP) became popular during the 1980s when it was aggressively marketed as a so-called "cure" for snoring. It was first emloyed by Yves Victor Kamami, a surgeon of the Marie-Louise Clinic in Paris, France, on people who were of slender build. Early results seemed favourable, and studies of flawed methodology were published. Longterm follow-up information was omitted entirely. The practice of using lasers to address snoring became widespread. During the late 1990s, researchers (including Finkelstein, Schmidt and others) published data which demonstrated that in a considerable number of cases, laser-assisted uvulopalatoplasty may also cause mild OSA in patients who formerly were nonapneic snorers, or lead to deterioration of existing apnea. These results are attributable to thermal damage inflicted by the laser beam. The laser may induce progressive palatal fibrosis, accompanied by medial traction of the posterior tonsillar pillars ie., scar tissue reduces the airspace in the pharynx leading to velopharyngeal insufficiency. The scar tissue can also make the airway more prone to collapse during sleep. LAUP can be a medically induced cause of sleep apnea. Despite adverse results, LAUP continues to be administered by a minority of surgeons. To this day, few if any patients who have undergone laser-assisted uvulopalatopharyngoplasty for primary (social) snoring have been provided with pre- and postoperative polysomnogram (sleep testing) or followup. An LAUP procedure typically costs between two and three thousand American dollars. It takes roughly thirty minutes and is usually done in a surgeon's office as an outpatient procedure. Typically a CO2 type laser is used. Radiofrequency surgical unit. Radiofrequency-assisted uvulopalatoplasty (RAUP) is similar to laser-assisted uvulopalatoplasty (LAUP). It is done with a radiofrequency (RF) instrument, instead of a laser . A special RF electrode is used to make two vertical cuts on either side of the uvula. These are joined by a horizontal cut and the uvula is removed. Occasionally, the edge of the soft palate is trimmed as well . One of the risks is that by cutting the tissues, excess scar tissue can "tighten" the airway and make it even smaller than it was before UPPP. Some individuals who have undergone UPPP as a stand alone procedure have written on internet forums that they experienced a worsening of their breathing following UPPP . Others have spoken of severe acid reflux.

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/index.php/V(D)J_recombination

# V(D)J recombination V(D)J recombination is a mechanism of genetic recombination that occurs in vertebrates, which randomly selects and assembles segments of genes encoding specific proteins with important roles in the immune system. This site-specific recombination reaction generates a diverse repertoire of T cell receptor (TCR) and immunoglobulin (Ig) molecules that are necessary for the recognition of diverse antigens from bacterial, viral, and parasitic invaders, and from dysfunctional cells such as tumor cells. Human antibody molecules (and B cell receptors) comprise heavy and light chains with both constant (C) and variable (V) regions that are encoded by three types of genes. Multiple genes for the variable regions are encoded in the human genome that contain three distinct types of segments. For example, the immunoglobulin heavy chain region contains 200 Variable (V) genes, 12 Diversity (D) genes, and 4 Joining (J) genes. The light chains also possess numerous V and J genes, but do not have D genes. By the mechanism of DNA rearrangement of these regional genes it is possible to generate an antibody repertoire >107 possible combinations. (200 x 12 x 4 = 9600, in addition to the 1000 possible light chain combinations) Most T cell receptors are composed of an alpha chain and a beta chain. The T cell receptor genes are similar to immunoglobulin genes in that they too contain multiple V, D and J genes in their beta chains (and V and J genes in their alpha chains) that are rearranged during the development of the lymphocyte to provide that cell with a unique antigen receptor. In the developing B cell, the first recombination event to occur is between one D and one J gene segment of the heavy chain locus. Any DNA between these two genes is deleted. This D-J recombination is followed by the joining of one V gene, from a region upstream of the newly formed DJ complex, forming a rearranged VDJ gene. All other genes between V and D segments of the new VDJ gene are now deleted from the cell's genome. Primary transcript (unspliced RNA) is generated containing the VDJ region of the heavy chain and both the constant mu and delta chains (Cμ and Cδ). (i.e. the primary transcript contains the segments: V-D-J-Cμ-Cδ). The primary RNA is processed to add a polyadenylation (poly-A) tail after the Cμ chain and to remove sequence between the VDJ segment and this constant gene segment. Translation of this mRNA leads to the production of the Ig μ heavy chain protein. The kappa (κ) and lamda (λ) chains of the immunoglobulin light chain loci rearrange in a very similar way, except the light chains lack a D segment. In other words, the first step of recombination for the light chains involves the joining of the V and J chains to give a VJ complex before the addition of the constant chain gene during primary transcription. Translation of the spliced mRNA for either the kappa or lamda chains results in formation of the Ig κ or Ig λ light chain protein. Assembly of the Ig μ heavy chain and one of the light chains results in the formation of membrane bound form of the immunglobulin IgM that is expressed on the surface of the immature B cell. During T cell development, the T cell receptor (TCR) chains undergo essentially the same sequence of ordered recombination events as that described for immunoglobulins. D-to-J recombination occurs first in the β chain of the TCR. This process can involve either the joining of the Dβ1 gene segment to one of six Jβ1 segments or the joining of the Dβ2 gene segment to one of six Jβ2 segments. DJ recombination is followed (as above) with Vβ-to-DβJβ rearrangements. All genes between the Vβ-Dβ-Jβ genes in the newly formed complex are deleted and the primary transcript is synthesized that incorporates the constant domain gene (Vβ-Dβ-Jβ-Cβ). mRNA transcription splices out any intervening sequence and allows translation of the full length protein for the TCR Cβ chain. The rearrangement of the alpha (α) chain of the TCR follows β chain rearrangement, and resembles V-to-J rearrangement described for Ig light chains (see above). The assembly of the β- and α- chains results in formation of the αβ-TCR that is expressed on a majority of T cells. The regional genes (V, D, J) are flanked by Recombination Signal Sequences (RSSs) that are recognized by a group of enzymes known collectively as the VDJ recombinase. RSSs are composed of seven conserved nucleotides (a heptamer) that reside next to the gene encoding sequence followed by a spacer (containing either 12 or 23 unconserved nucleotides) followed by a conserved nonamer (9 base pairs). The RSSs are present on the 3' side (downstream) of a V region and the 5' side (upstream) of the J region. These are the sides that will be involved in the joining. Only a pair of dissimilar spacer RSSs are efficiently recombined (i.e. one with a spacer of 12 nucleotides will be recombined with one that has a spacer containing 23 nucleotides). This is known as the 12/23 rule of recombination. VDJ recombinase refers to a collection of enzymes some of which are lymphocyte specific, and some that are expressed in many cell types. The initial steps of VDJ recombination are carried out by critical lymphocyte specific enzymes, called recombination activating gene-1 and -2 (RAG1 and RAG2). These enzymes associate with each other to recognize the RSS sequences and induce DNA cleavage at the RSS sequences. This cleavage only takes place on one strand of DNA, which leads to a nucleotide attack and creation of a hairpin loop. Other enzymes of the VDJ recombinase are expressed in multiple cell types and are involved in DNA repair following the activity of RAG1 and RAG2. One of these enzymes is called the DNA-dependent protein kinase complex (DNA-PK) that repairs double-stranded DNA. DNA-PK binds to each end of the broken DNA and recruits several other proteins, including Artemis nuclease, XRCC4 (X-ray repair cross-complementing factor 4), DNA ligase IV, Cernunnos (also called XLF or XRCC4-like factor), and any of several DNA polymerases. DNA-PK complexes on each DNA end phosphorylate (add phosphate groups to) each other, resulting in activation of Artemis. Artemis then breaks the hairpin loop that was formed by the RAG proteins . XRCC4 and Cernunnos act in concert with DNA-PK to align the two DNA ends with each other, and also help to recruit terminal transferase, which adds nucleotides randomly to the ends. DNA polymerases λ and μ insert additional nucleotides as needed to make the two ends compatible for joining. Ligase IV finally links DNA strands on opposite ends of the break to each other, completing the joining process. Because of the variability in the exact position of cleavage of the hairpin loop by Artemis, as well as the random nucleotide addition by terminal transferase, the final DNA sequence, and thus the sequence of the resulting antibody, is highly variable, even when the same two V, D, or J segments are joined. This great diversity allows VDJ recombination to generate antibodies even to microbes that neither the organism nor its ancestors have ever previously encountered.

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/index.php/V-erbA-related_gene

# V-erbA-related gene V-erbA-related protein 2 (EAR-2) also known as NR2F6 (nuclear receptor subfamily 2 group F member 6) is a protein that in humans is encoded by the NR2F6 gene. V-erbA-related protein 2 is a member of the nuclear receptor family of intracellular transcription factors. It was found that antigen receptor stimulation-induced NF-AT/AP-1 activity is regulated through the nuclear receptor NR2F6 (NR2F6 acts as a direct repressor of NF-AT/AP-1 transactivation) and that by preventing NR2F6 function, transcriptional activation of NF-AT/AP-1 is enhanced in immune cells which leads to an augmented immune response. NR2F6 impairs the formation of mature red blood cells in animals that over-express NR2F6 in their bone marrow. Mice that over expression of NR2F6 in their bone marrow cells have a block at the pro-erythroblast stage of blood cell development both in the bone marrow and in the spleen of animals that have excessive expression of NR2F6. So, when inhibition of differentiation of stem cell is desired, inhibition of differentiation is achieved through induction of increased NR2F6 activity. In situations where differentiation of stem cells into a cell of increased maturity is desired, inhibition of NR2F6 activity must be performed. It was found that expression of NR2F6 was consistently upregulated in neoplastic tissues in leukemic, ovarian cancer and endometrial cancer as compared to non-malignant tissues, while the silencing of NR2F6 induces a reduction of cancer cell proliferation, inhibiting clonogenicity and self-renewal of proliferating cancer cells, and induces differentiation.

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/index.php/VA

# Villous adenoma Villous adenoma (also known as adenomatous polyp) is a type of polyp that grows in the gastrointestinal tract; it occurs most commonly in the colon. Villous adenoma may result in malignanttransformation. Villous adenoma was first discovered by Helwig in 1946. Villous adenoma may be classified into flat, sessile, pedunculated and depressed subtypes. Villous adenoma arises from epithelial tissue, which is normally part of the lining of the colon. Genes associated with the development of villous adenoma include APC, TP53, K-ras, STK11 and SMAD4. The prevalence of villous adenoma is approximately 3.5 per 100,000 individuals worldwide. The most potent risk factors in the development of villous adenoma include familial syndromes such as Turcot syndrome, juvenile polyposis syndrome, and Cowden disease. Surgical removal is the mainstay of therapy for villous adenoma. Exploratory colonoscopy and cautery snare is the most common approach to the diagnosis and treatment of villous adenoma. Effective measures for the primary prevention of villous adenoma include periodic screening of patients with family history of familial adenomatous polyposis. Secondary prevention strategies include annual occult blood test and colonoscopy.

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/index.php/VAD

# Ventricular assist device Editor-In-Chief: C. Michael Gibson, M.S., M.D. Associate Editor(s)-in-Chief: Marv Slepian, M.D.; University of Arizona ; Juan A. Sanchez MD MPA , Chairman, The Stanley J. Dudrick Department of Surgery, Saint Mary's Hospital, Waterbury, CT, Tayebah Chaudhry , Syed Hassan A. Kazmi BSc, MD Ventricular assist device (VAD) is a mechanical device that provides Mechanical Circulatory Support (MCS) in patients with advanced heart failure. VAD therapy has shown improved outcome and survival in heart failure patients compared to pharmacological therapy alone. These devices are commonly used as a Bridge-to-Transplant (BTT) in heart transplant eligible patients or as a Destination Therapy (DT) in patients ineligible for heart transplant. VADs are indicated for either short-term use in patients recovering from heart attacks or heart surgery or for long-term use (months to years and in some cases for life) in patients suffering from end-stage heart failure. Over the years, significant development has been made to create miniaturized VADs with increased durability, reliability and lesser noise emission. Newer (third generation) VADs are Continuous Flow (CF) pumps with lesser complications compared to the older (first generation) VADs that were large and had pulsatile-flow pumps. Depending on the heart chamber that needs MCS, VADs can be used as Left Ventricular Assist Devices (LVADs), Right Ventricular Assist Devices (RVADs) or BiVentricular Assist Devices (BiVADs). Ongoing research in VAD development is being focused on eliminating the need for a driveline, better surgical approaches and strategies for telemetric assessment of device function and remote charging of batteries. VADs evolved over time after an external technology was used to provide cardiovascular support to a patient with Cardiopulmonary bypass (CPB) in an atrial septal defect repair surgery by John Gibbons. This lead to further interest and efforts to developing an artificial heart and later implantation of VAD in the late 1960s. Thoratec pneumatic VAD was the first Food and Drug Administration (FDA) approved VAD used as a BTT. This technology further evolved into HeartMate I, but more work needed to be done to develop newer LVADs with lesser complications. The Second and Third Generation VADs were designed to have a continuous flow rather than pulsatile. VADs are classified according to their operational characteristics. Most VADs operate on similar basic principle i.e., a cannula is inserted into the apex of the ventricle. Blood passes through this cannula to a pump and thence through a tube into the aorta (most commonly ascending aorta) in case of an LVAD or into the pulmonary artery in case of an RVAD. The pump is powered through a lead which connects it to a controller and power supply. In some cases there is also a tube to vent the pump to the outside air. Major distinguishing features between different VADs are the pumps (which vary substantially in method of operation, size and placement), the controller and the materials used for the pump and the associated parts (tubes, cannulas, lead between the pump and the controller/power supply). Unloading of the left ventricle post-LVAD implantation may result in septal shifts, leading to increased RV preload, decreased RV contractility and function. RVAD implantation may be necessary until RV function improves, at which point RVAD can be explanted. Bleeding is a common complication during the implantation procedure. Patients with Continuous Flow VADs are systemically anticoagulated with Warfarin, which further increases the risk of bleeding, particularly Gastro-intestial (GI) Bleed. Patients should be evaluated and if possible, treated preoperatively for GI bleeding sources such as colonic polyps, stomach ulcers and angiodysplasias. There is also a higher risk of bleeding post-LVAD implantation from degradation of Von-Willebrand Factor (VWF) by VAD rotors, which is reversible once LVAD is removed. There is an increased risk of thromboembolic events and Transient Ischemic Attacks (TIAs)in patients with Continous Flow VADs despite of systemic anticoagulation. If pump thrombosis develops, there might be an emergent need for pump exchange and moving the patient up on priority list of heart transplant. Infection at multiple sites of VAD circuit is a common complication. These sites include the VAD pocket where the VAD is implanted, the VAD itself or the cannulas that go from the ventricle to the VAD and from the VAD to the aorta. The most common infection site is the driveline which goes from the VAD through the skin to the VAD power source since it is a pathway from the external environment to the VAD interior. Common causative organisms in driveline infections are the skin flora such as Staphylococcus aureus and coagulase-negative staphylococci and in infection of internal components are Serratia, Klebsiella, and Enteroccocus species, Pseudomonas aeruginosa. Candida can cause up to ten percent of infections. Treatment includes debridement of infected tissue and administration of intravenous antibiotics. Explantantion of infected LVAD is sometimes necessary. Ventricular arrythmias is a common complication after LVAD implantation. It is thought to be from re-entrant circuits that are formed around the site of the inflow cannula in already damaged myocardium. Implantable cardioverter-defibrillator helps with these arrhythmias until the ventricles remodel as the time goes on. Anti-arrhythmic agents such as lidocaine or amiodarone are rarely necessary. Malfunction of different parts of VAD ( driveline, controller, pump) can cause the device to stop working. VADs are complex devices that need an expert to operate them in order to obtain optimal right and left ventricular hemodynamics. Recent developments in LVAD therapy have been made to provide short-term temporary MCS to patients in cardiogenic shock. Axillary artery is commonly being used for insertion of temporary VADs to allow for improved patient mobility. Most VADs currently being used are not fully implantable since they connect to an external power source, hence increasing the risk of infection. Fully implantable devices could reduce this risk of infection. The newest totally implantable LVAD (Leviticus FiVAD) uses the Jarvik VAD platform and is undergoing clinical trials.

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/index.php/VAPA

# VAPA VAMP-Associated Protein A ( or Vesicle-Associated Membrane Protein-Associated Protein A) is a protein that in humans is encoded by the VAPA gene. Together with VAPB and VAPC it forms the VAP protein family. They are integral endoplasmic reticulum membrane proteins of the type II and are ubiquitous among eukaryotes. VAPA is ubiquitously expressed in human tissues and is thought to be involved in membrane trafficking by interaction with SNAREs. in regulation of lipid transport and metabolism, and in the Unfolded Protein Response (UPR). The protein is divided in three different domains. First, an N-terminal beta-sheet with an immunoglobulin-like fold that shares homology with the Nematode major sperm protein (MSP). Secondly, a central coiled-coil domain. Then finally a C-terminal transmembrane domain (TMD) which is usually present in proteins of the t-SNARE superfamily and has been found in other proteins associated with vesicular transport. VAPA can form homo-dimers and also hetero dimers with VAPB by interactions through their (TMD). Because of its ubiquitous expression , the intracellular localisation and function of VAPA may vary between cell types. It is however mainly located in the ER , Golgi apparatus and the Vesicular Tubular Compartment or ER-Golgi Intermediate Compartment, an organelle of eukaryotic cells consisting in fused ER-derived vesicles that transports proteins from the ER to the Golgi apparatus. VAPA has been documented to interact with three different groups of proteins: proteins associated with vesicle traffic and fusion, proteins containing the FFAT motif and viral proteins. VAPA is able to bind a range of SNARE proteins including syntaxin1A, rbet1 and rsec22. It also binds to proteins associated with membrane fusion machinery such as alphaSNAP and NSF.These interaction suggest that VAPA could have a general role in the regulation of the function of these proteins that are mainly involved in membrane fusion VAP proteins binds with non-structural proteins of the hepatitis C virus NS5A and NS5B allowing the RNA replication machinery of the virus to set up on the lipid raft membrane of the host cell. VAPA also binds to several viral proteins from the Norovirus family and is important for the virus replication efficiency. The non-structural proteins NS1 and NS2 are able to bind VAPA thanks to sequence mimicry of the FFAT motif probably yielding the same advantage to viral replication as for hepatitis C virus. The N-terminal MSP-homologous part of VAPA is able to bind to the FFAT motif, a particular sequence motif shared by several lipid binding proteins including oxysterol-binding protein (OSBP). One of its proposed functions is to slow down the lipid flow back towards the ER when protein misfolding occurs, in order to reduce the amount of stress triggered by the UPR. The VAP would regulate this process by inhibiting membrane contact. The P56S SNP in the MSP domain of VAPB is involved in the onset of Lou Gehrig's disease also called amyotrophic lateral sclerosis (ALS) where the patient loses muscle control and function. The degenerescence of motor neurons observed in such condition could to be due to the inability of VAPB to regulate the lipid function around the ER and the subsequent consequences on cell function.

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# VAPRED Study ## Sponsor The purpose of this trial is to perform a prospective multicentric study to determine predictive ED score and D-dimer level in the evaluation of the thromboembolic event recurrence after anticoagulant treatment cessation

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/index.php/VCAP-AMP-VECP_regimen

# VCAP-AMP-VECP regimen VCAP-AMP-VECP regimen refers to a regimen consisting of with vincristine, cyclophosphamide, doxorubicin (adriamycin), and prednisone (VCAP), doxorubicin (adriamycin), ranimustine, and prednisone (AMP), and vindesine, etoposide, carboplatin, and prednisone (VECP) used to treat human T-lymphotropic virus type I-associated adult T-cell leukemia-lymphoma (ATLL)

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/index.php/VCHSR

# VCHSR VCHSR is a drug used in scientific research which acts as a selective antagonist of the cannabinoid receptor CB1. It is derived from the widely used CB1 antagonist rimonabant, and has similar potency and selectivity for the CB1 receptor, but has been modified to remove the hydrogen bonding capability in the C3 substituent region, which removes the inverse agonist effect that rimonabant produces at high doses, so that VCHSR instead acts as a neutral antagonist, blocking the receptor but producing no physiological effect of its own.

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/index.php/VDAC2

# VDAC2 Voltage-dependent anion-selective channel protein 2 is a protein that in humans is encoded by the VDAC2 gene on chromosome 10. This protein is a voltage-dependent anion channel and shares high structural homology with the other VDAC isoforms. VDACs are generally involved in the regulation of cell metabolism, mitochondrial apoptosis, and spermatogenesis. Additionally, VDAC2 participates in cardiac contractions and pulmonary circulation, which implicate it in cardiopulmonary diseases. VDAC2 also mediates immune response to infectious bursal disease (IBD). The three VDAC isoforms in human are highly conserved, particularly with respect to their 3D structure. VDACs form a wide β-barrel structure, inside of which the N-terminal resides to partially close the pore. The sequence of the VDAC2 isoform contains an abundance of cysteines, which allow for the formation of disulfide bridges and, ultimately, affect the flexibility of the β-barrel. VDACs also contain a mitochondrial targeting sequence for the protein's translocation to the outer mitochondrial membrane. In particular, VDAC2 possesses an N-terminal longer by 11 residues compared to the other two isoforms. VDAC2 belongs to the mitochondrial porin family and is expected to share similar biological functions to the other VDAC isoforms. VDACs generally are involved in cellular energy metabolism by transporting ATP and other small ions and metabolites across the outer mitochondrial membrane. In mammalian cardiomyocytes, VDAC2 promotes mitochondrial transport of calcium ions in order to power cardiac contractions. In addition, VDACs form part of the mitochondrial permeability transition pore (MPTP) and, thus, facilitate cytochrome C release, leading to apoptosis. VDACs have also been observed to interact with pro- or antiapoptotic proteins, such as Bcl-2 family proteins and kinases, and so may contribute to apoptosis independently from the MPTP. VDAC2 in particular has demonstrated a protective effect in cells undergoing mitochondrial apoptosis, and may even confer protection during aging. Furthermore, VDAcs have been linked to spermatogenesis, sperm maturation, motility, and fertilization. Though all VDAC isoforms are ubiquitously expressed, VDAC2 is majorly found in the sperm outer dense fiber (ODF), where it is hypothesized to promote proper assembly and maintenance of sperm flagella. It also localizes to the acrosomal membrane of the sperm, where it putatively mediates calcium ion transmembrane transport. The VDAC2 protein belongs to a group of mitochondrial membrane channels involved in translocation of adenine nucleotides through the outer membrane. These channels may also function as a mitochondrial binding site for hexokinase and glycerol kinase. The VDAC is an important constituent in apoptotic signaling and oxidative stress, most notably as part of the mitochondrial death pathway and cardiac myocyte apoptosis signaling. Programmed cell death is a distinct genetic and biochemical pathway essential to metazoans. An intact death pathway is required for successful embryonic development and the maintenance of normal tissue homeostasis. Apoptosis has proven to be tightly interwoven with other essential cell pathways. The identification of critical control points in the cell death pathway has yielded fundamental insights for basic biology, as well as provided rational targets for new therapeutics a normal embryologic processes, or during cell injury (such as ischemia-reperfusion injury during heart attacks and strokes) or during developments and processes in cancer, an apoptotic cell undergoes structural changes including cell shrinkage, plasma membrane blebbing, nuclear condensation, and fragmentation of the DNA and nucleus. This is followed by fragmentation into apoptotic bodies that are quickly removed by phagocytes, thereby preventing an inflammatory response. It is a mode of cell death defined by characteristic morphological, biochemical and molecular changes. It was first described as a "shrinkage necrosis", and then this term was replaced by apoptosis to emphasize its role opposite mitosis in tissue kinetics. In later stages of apoptosis the entire cell becomes fragmented, forming a number of plasma membrane-bounded apoptotic bodies which contain nuclear and or cytoplasmic elements. The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane breakdown and cellular disintegration. Apoptosis occurs in many physiological and pathological processes. It plays an important role during embryonal development as programmed cell death and accompanies a variety of normal involutional processes in which it serves as a mechanism to remove "unwanted" cells. The VDAC2 protein has been implicated in cardioprotection against ischemia-reperfusion injury, such as during ischemic preconditioning of the heart. Although a large burst of reactive oxygen species (ROS) is known to lead to cell damage, a moderate release of ROS from the mitochondria, which occurs during nonlethal short episodes of ischemia, can play a significant triggering role in the signal transduction pathways of ischemic preconditioning leading to reduction of cell damage. It has even been observed that during this release of reactive oxygen species, VDAC2 plays an important role in the mitochondrial cell death pathway transduction hereby regulating apoptotic signaling and cell death. The VDAC2 protein has been linked persistent pulmonary hypertension of the newborn (PPHN), which causes a large majority of neonatal morbidity and mortality, due to its role as a major regulator of endothelium-dependent nitric oxide synthase (eNOS) in the pulmonary endothelium. eNOS has been attributed with regulating NOS activity in response to physiological stimuli, which is vital to maintain NO production for proper blood circulation to the lungs. As a result, VDAC2 is significantly involved in pulmonary circulation and may become a therapeutic target for treating diseases such as pulmonary hypertension, VDAC2 may also serve an immune function, as it has been hypothesized to detect and induce apoptosis in cells infected by the IBD virus. IBD, the equivalent HIV in birds, can compromise their immune systems and even cause fatal injury to the lymphoid organ, Studies of this process indicate that VDAC2 interacts with the viral protein V5 to mediate cell death.

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/index.php/VDAC3

# VDAC3 Voltage-dependent anion-selective channel protein 3 (VDAC3) is a protein that in humans is encoded by the VDAC3 gene on chromosome 8. The protein encoded by this gene is a voltage-dependent anion channel and shares high structural homology with the other VDAC isoforms. Nonetheless, VDAC3 demonstrates limited pore-forming ability and, instead, interacts with other proteins to perform its biological functions, including sperm flagella assembly and centriole assembly. Mutations in VDAC3 have been linked to male infertility, as well as Parkinson's disease. The three VDAC isoforms in human are highly conserved, particularly with respect to their 3D structure. VDACs form a wide β-barrel structure, inside of which the N-terminal resides to partially close the pore. The sequence of the VDAC3 isoform contains an abundance of cysteines, which allow for the formation of disulfide bridges and, ultimately, affect the flexibility of the β-barrel. VDACs also contain a mitochondrial targeting sequence for the protein's translocation to the outer mitochondrial membrane. VDAC3 still yet possesses multiple isoforms, including a full-length form and shorter form termed VDAC3b. This shorter form is predominantly expressed over the full-length form at cell centrosomes. VDAC3 belongs to the mitochondrial porin family and is expected to share similar biological functions to the other VDAC isoforms. VDACs are involved in cell metabolism by transporting ATP and other small metabolites across the outer mitochondrial membrane. In addition, VDACs form part of the mitochondrial permeability transition pore (MPTP) and, thus, facilitate cytochrome C release, leading to apoptosis. VDACs have also been observed to interact with pro- or antiapoptotic proteins, such as Bcl-2 family proteins and kinases, and so may contribute to apoptosis independently from the MPTP. Nonetheless, experiments reveal a lack of pore-forming ability in the VDAC3 isoform, suggesting that it may perform different biological functions. Notably, though all VDAC isoforms are ubiquitously expressed, VDAC3 is majorly found in the sperm outer dense fiber (ODF), where it is hypothesized to promote proper assembly and maintenance of sperm flagella. Because the ODF membranes are not likely to support pore formation, VDAC3 may interact with protein partners to carry out other functions in the ODF. For instance, within cells, VDAC3 predominantly localizes to the centrosome and recruits Mps1 to regulate centriole assembly. In the case of localization to the mitochondria, VDAC3 interaction with Mps1 instead leads to ciliary disassembly. VDAC3 belongs to a group of mitochondrial membrane channels involved in translocation of adenine nucleotides through the outer membrane. These channels may also function as a mitochondrial binding site for hexokinase and glycerol kinase. The VDAC is an important constituent in apoptotic signaling and oxidative stress, most notably as part of the mitochondrial death pathway and cardiac myocyte apoptosis signaling. Programmed cell death is a distinct genetic and biochemical pathway essential to metazoans. An intact death pathway is required for successful embryonic development and the maintenance of normal tissue homeostasis. Apoptosis has proven to be tightly interwoven with other essential cell pathways. The identification of critical control points in the cell death pathway has yielded fundamental insights for basic biology, as well as provided rational targets for new therapeutics a normal embryologic processes, or during cell injury (such as ischemia-reperfusion injury during heart attacks and strokes) or during developments and processes in cancer, an apoptotic cell undergoes structural changes including cell shrinkage, plasma membrane blebbing, nuclear condensation, and fragmentation of the DNA and nucleus. This is followed by fragmentation into apoptotic bodies that are quickly removed by phagocytes, thereby preventing an inflammatory response. It is a mode of cell death defined by characteristic morphological, biochemical and molecular changes. It was first described as a "shrinkage necrosis", and then this term was replaced by apoptosis to emphasize its role opposite mitosis in tissue kinetics. In later stages of apoptosis the entire cell becomes fragmented, forming a number of plasma membrane-bounded apoptotic bodies which contain nuclear and or cytoplasmic elements. The ultrastructural appearance of necrosis is quite different, the main features being mitochondrial swelling, plasma membrane breakdown and cellular disintegration. Apoptosis occurs in many physiological and pathological processes. It plays an important role during embryonal development as programmed cell death and accompanies a variety of normal involutional processes in which it serves as a mechanism to remove "unwanted" cells. In addition, VDAC3 has been implicated in cardioprotection against ischemia-reperfusion injury, such as during ischemic preconditioning of the heart. Although a large burst of reactive oxygen species is known to lead to cell damage, a moderate release of ROS from the mitochondria, which occurs during nonlethal short episodes of ischemia, can play a significant triggering role in the signal transduction pathways of ischemic preconditioning leading to reduction of cell damage. It has even been observed that during this release of reactive oxygen species, VDAC3 plays an important role in the mitochondrial cell death pathway transduction hereby regulating apoptotic signaling and cell death. As VDAC3 is a regulator of sperm motility, male mice missing VDAC3 result in infertility. Mutations in VDAC3 are also associated with Parkinson's disease, as VDAC3 has been observed to target Parkin to defective mitochondria to eliminate them by mitophagy. Failure to eliminate these mitochondria result in the accumulation of reactive oxygen species, the commonly attributed cause of Parkinson's disease. In addition, it has been found that VDAC3-null mice were born at the expected mendelian ratio. Mutant females were fertile, but males were not due to markedly reduced sperm motility. The majority of epididymal axonemes showed structural defects, most commonly loss of a single microtubule doublet at a conserved position within the axoneme. In testicular sperm, the defect was only rarely observed, suggesting that instability of a normally formed axoneme occurred during sperm maturation. In contrast, tracheal epithelial cilia showed no structural abnormalities, but there was a reduced number of ciliated cells. In skeletal muscle, mitochondria were abnormally shaped, and the activities of respiratory chain complex enzymes were reduced. Citrate synthase activity was unchanged, suggesting an absence of mitochondrial proliferation that commonly occurs in response to respiratory chain defects.

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/index.php/VDRL

# Venereal disease research laboratory (VDRL) test The Venereal Disease Research Laboratory test (VDRL) is a nontreponemal serological screening for syphilis, the monitoring of the response to therapy, the detection of CNS involvement, and as an aid in the diagnosis of congenital syphilis. The basis of the test is that an antibody produced by a patient with syphilis reacts with an extract of ox heart (diphosphatidyl glycerol). It therefore detects anti-cardiolipin antibodies (IgG, IgM or IgA). Many other conditions can produce false positive results, including some viruses (mononucleosis, hepatitis), drugs, rheumatic fever, rheumatoid arthritis, lupus, and leprosy. The syphilis anti-cardiolipin antibodies are beta-2 glycoprotein independent, where as those that occur in the antiphospholipid antibody syndrome (associated to lupus for example) are beta-2 glycoprotein dependent, and this can be used to tell them apart in an ELISA assay. This test is very useful as the trend of titres are correlated to disease activity (i.e. falling titres indicate successful treatment). It has a very good sensitivity for syphilis, except in late tertiary form.

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/index.php/VEGFR1

# VEGFR1 Oncogene FLT belongs to the src gene family and is related to oncogene ROS (MIM 165020). Like other members of this family, it shows tyrosine protein kinase activity that is important for the control of cell proliferation and differentiation. The sequence structure of the FLT gene resembles that of the FMS gene (MIM 164770); hence, Yoshida et al. (1987) proposed the name FLT as an acronym for FMS-like tyrosine kinase.[supplied by OMIM] The ablation of VEGFR1 by chemical and genetic means has also recently been found to augment the conversion of white adipose tissue to brown adipose tissue as well as increase brown adipose angiogenesis in mice.

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/index.php/VEGF_receptor

# VEGF receptor VEGF receptors are receptors for vascular endothelial growth factor (VEGF). There are three main subtypes of VEGFR, numbered 1, 2 and 3. Also, they may be membrane-bound (mbVEGFR) or soluble (sVEGFR), depending on alternative splicing. Vascular endothelial growth factor (VEGF) is an important signaling protein involved in both vasculogenesis (the formation of the circulatory system) and angiogenesis (the growth of blood vessels from pre-existing vasculature). As its name implies, VEGF activity is restricted mainly to cells of the vascular endothelium, although it does have effects on a limited number of other cell types (e.g. stimulation monocyte/macrophage migration). In vitro, VEGF has been shown to stimulate endothelial cell mitogenesis and cell migration. VEGF also enhances microvascular permeability and is sometimes referred to as vascular permeability factor. All members of the VEGF family stimulate cellular responses by binding to tyrosine kinase receptors (the VEGFRs) on the cell surface, causing them to dimerize and become activated through transphosphorylation. The VEGF receptors have an extracellular portion consisting of 7 immunoglobulin-like domains, a single transmembrane spanning region and an intracellular portion containing a split tyrosine-kinase domain. VEGF-A binds to VEGFR-1 (Flt-1) and VEGFR-2 (KDR/Flk-1). VEGFR-2 appears to mediate almost all of the known cellular responses to VEGF. The function of VEGFR-1 is less well defined, although it is thought to modulate VEGFR-2 signaling. Another function of VEGFR-1 is to act as a dummy/decoy receptor, sequestering VEGF from VEGFR-2 binding (this appears to be particularly important during vasculogenesis in the embryo). In fact, an alternatively spliced form of VEGFR-1 (sFlt1) is not a membrane bound protein but is secreted and functions primarily as a decoy. A third receptor has been discovered (VEGFR-3), however, VEGF-A is not a ligand for this receptor. VEGFR-3 mediates lymphangiogenesis in response to VEGF-C and VEGF-D. In addition to binding to VEGFRs, TACO VEGF binds to receptor complexes consisting of both neuropilins and VEGFRs. This receptor complex has increased VEGF signalling activity in endothelial cells (blood vessels). Neuropilins (NRP) are pleitrophic receptors and therefore other molecules may interfere with the signalling of the NRP/VEGFR receptor complexes. For example, Class 3 semaphorins compete with VEGF165 for NRP binding and could therefore regulate VEGF-mediated angiogenesis. Some VEGFR antagonists (inhibitors) (for example lenvatinib, motesanib) are under investigation for treating various cancers. Pazopanib was approved for renal cell carcinoma in 2009. Regorafenib was approved for colorectal cancer in Sept 2012.

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/index.php/VF

# Ventricular fibrillation History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | EKG Examples | | Echocardiography and Ultrasound | CT-Scan Findings | MRI Findings | Other Imaging Findings | Other Diagnostic Studies

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# VGF VGF or VGF nerve growth factor inducible is a secreted protein and neuropeptide precursor that may play a role in regulating energy homeostasis, metabolism and synaptic plasticity. The protein was first discovered in 1985 by Levi et al. in an experiment with PC12 cells and its name is non-acronymic. VGF gene encodes a precursor which is divided by proteolysis to polypeptides of different mass, which have a variety of functions, the best studied of which are the roles of TLQP-21 in the control of appetite and inflammation. , and TLQP-62 as well as AQEE-30 in regulating depression-like behaviors and memory The expression of VGF and VGF-derived peptides is detected in a subset of neurons in the central and peripheral nervous systems and specific populations of endocrine cells in the adenohypophysis, adrenal medulla, gastrointestinal tract, and pancreas. VGF expression is induced by NGF, CREB and BDNF and regulated by neurotrophin-3. Physical exercise significantly increases VGF expression in mice hippocampal tissue and upregulates a neurotrophic signaling cascade thought to underlie the action of antidepressants. Changes in expression of discrete VGF fragments have been detected in different neurological and psychiatric conditions. In schizophrenia, one study has shown an increase in the VGF23-62 peptide and a subsequent small study demonstrated that drugs further increase the expression, pointing at a possible ameliorating action of the fragment. A decreased expression of VGF26-62 peptide was found in frontotemporal dementia and the expression of a fragment containing aminoacids 378-398 was found to be changing in amyotrophic lateral sclerosis and Alzheimer's disease. VGF expression has also been shown in damaged peripheral nerves, and it is thought to have a role in neuropathic pain. . In Glioblastoma, VGF has been shown to play autocrine and paracrine roles in feedback loops between differentiated glioblastoma cells and glioblastoma-specific cancer stem cells, promoting growth, survival and self-renewal.

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# VIP regimen VIP regimen refers to a regimen consisting of etoposide (vepesid), ifosfamide and cisplatin (platinol) used for the treatment of advanced-stage germ cell gonadal cancers and Thymoma.

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/index.php/VISA_(gene)

# VISA (gene) Double-stranded RNA viruses are recognized in a cell type-dependent manner by the transmembrane receptor TLR3 (MIM 603029) or by the cytoplasmic RNA helicases MDA5 (MIM 606951) and RIGI (ROBO3; MIM 608630). These interactions initiate signaling pathways that differ in their initial steps but converge in the activation of the protein kinases IKKA (CHUK; MIM 600664) and IKKB (IKBKB; MIM 603258), which activate NFKB (see MIM 164011), or TBK1 (MIM 604834) and IKKE (IKBKE; MIM 605048), which activate IRF3 (MIM 603734). Activated IRF3 and NFKB induce transcription of IFNB (IFNB1; MIM 147640). For the TLR3 pathway, the intermediary molecule before the pathways converge is the cytoplasmic protein TRIF (TICAM1; MIM 607601). For RIGI, the intermediary protein is mitochondria-bound IPS1 (Sen and Sarkar, 2005).[supplied by OMIM]

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/index.php/VO2_max

# VO2 max VO2 max is the maximum capacity to transport and utilize oxygen during incremental exercise. (The derivation is V̇ - volume per time, O2 - oxygen, max - maximum). It is also called maximal oxygen consumption or maximal oxygen uptake. It is also known as aerobic capacity, which reflects the physical fitness of a person. It is the maximal intake of oxygen that a person can take in at the moment of exhaustion, which is determined according to that person's age, height, weight, fitness level and basal metabolic rate. Expressed either as an absolute rate in litres of oxygen per minute (l/min) or as a relative rate in millilitres of oxygen per kilogram of bodyweight per minute (ml/kg/min), the latter expression is often used to compare the performance of endurance sports athletes. A less size-biased measure is to divide by <math>\sqrt {mass^2}</math> rather than mass. It has become a standard testing method for athletes, athletic and sportive people and even for airplane pilots, car race drivers, and individuals with jobs demanding them to be fit, in good shape and health. It is a part of cardiac and pulmonary screenings too. Accurately measuring VO2 max involves a physical effort sufficient in duration and intensity to fully tax the aerobic energy system. In general clinical and athletic testing, this usually involves a graded exercise test (either on a treadmill or on a cycle ergometer) in which exercise intensity is progressively increased while measuring ventilation and oxygen and carbon dioxide concentration of the inhaled and exhaled air. V̇O2 max is reached when oxygen consumption remains at steady state despite an increase in workload. Dr. Kenneth H. Cooper conducted a study for the United States Air Force in the late 1960s. One of the results of this was the Cooper test in which the distance covered running in 12 minutes is measured. An approximate estimate for VO2 max (in ml/min/kg) is: VO2 max varies considerably in the population. The average young untrained male will have a VO2 max of approximately 3.5 litres/minute and 45 ml/min/kg. The average young untrained female will score a VO2 max of approximately 2.0 litres/minute and 38 ml/min/kg.[citation needed] These scores can improve with training and decrease with age, though the degree of trainability also varies very widely. In sports where endurance is an important component in performance, such as cycling, rowing, cross-country skiing and running, world class athletes typically have high VO2 maximums. World class male athletes, cyclists and cross-country skiers typically exceed 80 ml/kg/min and a rare few may exceed 90 ml/kg/min for men and 70 ml/kg/min for women. Three time Tour de France winner Greg LeMond is reported to have had a VO2 max of 92.5 at his peak - one of the highest ever recorded, while cross-country skier Bjørn Dæhlie measured at an astounding 96 ml/kg/min. It should also be noted that Dæhlie's result was achieved out of season and that physiologist Erlend Hem who was responsible for the testing stated that he would not discount the possibility of the skier passing 100 ml/kg/min at his absolute peak. By comparison a competitive club athlete might achieve a VO2 max of around 70 ml/kg/min. World class rowers are physically very large endurance athletes and typically do not score as high on a per weight basis, but often score exceptionally high in absolute terms. Male rowers typically score VO2 maximums over 6 litres/minute, and some exceptional individuals have exceeded 8 l/min. To put this into perspective, thoroughbred horses have a VO2 max of around 180 ml/min/kg. Siberian dogs running in the Iditarod Trail Sled Dog Race sled race have VO2 values as high as 240 ml/min/kg.

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/index.php/VOC_contamination_of_groundwater

# VOC contamination of groundwater VOCs are responsible for a number of adverse health effects especially for nursing and pregnant mothers. Many of these compounds were not known to be harmful until the late 1960s and it was some time before regular testing of groundwater identified these substances in drinking water sources. Toluene is an organic compound which is mostly harmless to adults and is sometimes abused as an inhalant. Fetal Toluene Syndrome has been defined and resembles Fetal Alcohol Syndrome with resultant birth defects, but the U.S. Centers for Disease Control and Prevention have identified differentiating features between the two syndromes including FTS havinng the additional facial features of micrognathia, large anterior fontanel, down-turned mouth corners, hair patterning abnormalities, bifrontal narrowing of the face, and ear abnormalities. U.S. Marine Corps Base Camp Lejeune was built near Jacksonville, North Carolina in 1942. In 1982, the Marine Corps discovered volatile organic compounds (VOCs) in several drinking water wells that fed into two of the eight water systems. The sources were traced to Tetrachloroethylene (PCE) from a dry cleaner off the base and Trichloroethylene which had been used in vehicle maintenance on the base. These problems were addressed but there were concerns with nursing and pregnant mothers who may have been exposed previously. It wasn't until the late 1990s that the federal government tried to track down people who may have been exposed. Love Canal was an abandoned canal near Niagara Falls, New York which was used by the U.S. military and Occidental Petroleum as a chemical waste dumping ground. Numerous cases of cancer and birth defects were found from the 1950s to the 1970s. The primary VOC at Love Canal is toluene, which is found along with dioxins and other pollutants.

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/index.php/VPREB3

# VPREB3 The VPREB3 gene product is the human homologue of the mouse VpreB3 (8HS20) protein, and is specifically expressed in cell lines representative of all stages of B-lymphocyte differentiation. It is also related to VPREB1 and other members of the immunoglobulin supergene family. The VPREB3 protein apparently associates with membrane mu heavy chains early in the course of pre-B cell receptor biosynthesis. The precise function of VPREB3 is not known, but it may contribute to mu chain transport in pre-B cells. In humans, besides the bone marrow and secondary lymphoid tissues such as the tonsils, the VPREB3 protein is also present in Purkinje cells of the cerebellum and in the zona glomerulosa of the adrenal.

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/index.php/VPS25

# VPS25 It is a component of the endosome-associated complex ESCRT-II (Endosomal Sorting Complexes Required for Transport protein II). ESCRT (ESCRT-I, -II, -III) complexes orchestrate efficient sorting of ubiquitinated transmembrane receptors to lysosomes via multivesicular bodies (MVBs). ESCRT-II recruits the transport machinery for protein sorting at MVB. In addition, the human ESCRT-II has been shown to form a complex with RNA polymerase II elongation factor ELL in order to exert transcriptional control activity. ESCRT-II transiently associates with the endosomal membrane and thereby initiates the formation of ESCRT-III, a membrane-associated protein complex that functions immediately downstream of ESCRT-II during sorting of MVB cargo. ESCRT-II in turn functions downstream of ESCRT-I, a protein complex that binds to ubiquitinated endosomal cargo. ESCRT-II is a trilobal complex composed of two copies of vps25, one copy of vps22 and the C-terminal region of vps36. The crystal structure of vps25 revealed two winged-helix domains, the N-terminal domain of vps25 interacting with vps22 and vps36.

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/index.php/VPS4B

# VPS4B The protein encoded by this gene is a member of the AAA protein family (ATPases associated with diverse cellular activities), and is the homolog of the yeast Vps4 protein. In humans, two paralogs of the yeast protein have been identified. The former share a high degree of aa sequence similarity with each other, and also with yeast Vps4 and mouse Skd1 proteins. Mouse Skd1 (suppressor of K+ transport defect 1) has been shown to be a yeast Vps4 ortholog. Functional studies indicate that both human paralogs associate with the endosomal compartments, and are involved in intracellular protein trafficking, similar to Vps4 protein in yeast. The gene encoding this paralog has been mapped to chromosome 18; the gene for the other resides on chromosome 16.

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/index.php/VR-CHOP_regimen

# VR-CHOP regimen VR-CHOP regimen refers to a regimen consisting of velcade (bortezomib), rituximab, cyclophosphamide, hydroxydaunorubicin (doxorubicin), oncovin (Vincristine), prednisone used to treat previously untreated diffuse large B-cell lymphoma and mantle cell lymphoma. .

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/index.php/VSNL1

# VSNL1 This gene is a member of the visinin/recoverin subfamily of neuronal calcium sensor proteins. The encoded protein is strongly expressed in granule cells of the cerebellum where it associates with membranes in a calcium-dependent manner and modulates intracellular signaling pathways of the central nervous system by directly or indirectly regulating the activity of adenylyl cyclase. Alternatively spliced transcript variants have been observed, but their full-length nature has not been determined.

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/index.php/VS_ribozyme

# VS ribozyme The VS ribozyme is composed of 5 helices that form an H shape (helices II to VI). The first helix (I) contains the substrate cleavage site in the stem loop.

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/index.php/VTE

# Venous thromboembolism Editor-In-Chief: C. Michael Gibson, M.S., M.D. ; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD , Iqra Qamar M.D. , Anmol Pitliya, M.B.B.S. M.D. , Aravind Reddy Kothagadi M.B.B.S Venous thromboembolism (VTE) may be classified into deep vein thrombosis (DVT) and pulmonary embolism (PE). Pulmonary embolism may arise as a consequence of deep vein thrombosis as a result of embolization of the clot from deep veins of the legs. Pulmonary embolism (PE) is an acute obstruction of the pulmonary artery (or one of its branches). The obstruction in the pulmonary artery that causes a PE can be due to thrombus, air, tumor, or fat. Most often, pulmonary embolism is due to a venous thrombosis (blood clot from a vein), which has been dislodged from its site of formation in the lower extremities. It has then embolized to the arterial blood supply of one of the lungs. Deep vein thrombosis (also known as deep venous thrombosis or DVT and colloquially referred to as "economy class syndrome") is the formation of a blood clot ("thrombus") in a deep vein. Shown below is a list of predisposing factors for VTE. The risk factors are classified as moderate or weak depending on how strongly they are associated with a VTE.

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/index.php/VTE_prevention_resident_survival_guide

# Venous thromboembolism prevention resident survival guide Venous thromboembolism (VTE) is a disease associated with morbidity and mortality; therefore, thromboprophylaxis is indicated among specific categories of patients at elevated risk for VTE. VTE prophylaxis can be either pharmacological through the administration of medications such as low molecular weight heparin (LMWH) or fondaparinux among others, or mechanical through intermittent pneumatic compression or elastic stockings. The decision to administer VTE prophylaxis, the duration, and the choice of prophylaxis depend on the reason for hospitalization such as medical illness, non orthopedic surgery, or orthopedic surgery, as well as on the estimated risks of subsequent VTE and bleeding. Shown below is an algorithm depicting the indications and choices of VTE prophylaxis among acutely ill patients. If VTE prophylaxis is recommended, it should be administered for the period of immobilization or hospital stay. Do not extend the duration of the prophylaxis after the period of immobilization or hospital stay. If pharmacological anticoagulation is needed, the choice of the drug should be guided by the patient preference, readiness for compliance and the practicality of the administration of frequent doses. IMPROVE associative risk score assesses the risk of VTE among hospitalized medical patients. While the IMPROVE predictive score includes 4 independent risk factors for VTE which are present at admission, IMPROVE associative score includes 7 variables present either at admission or during hospitalization; however the timing of the presence of some of the factors compared to the onset of VTE is not available. Shown below is an algorithm depicting the choices for VTE prophylaxis among critically ill patients. Note that there is not a risk score to estimate the risk subsequent occurrence of VTE among critically ill patients. In addition, routine compression ultrasound screening for DVT is not recommended among critically ill patients. Do not extend the duration of the VTE prophylaxis after the period of immobilization or hospital stay. Shown below is an algorithm depicting VTE prophylaxis among cancer patients. Note that, cancer patients with indwelling central venous catheters do not require VTE prophylaxis with neither low molecular weight heparin, low dose unfractionated heparin or vitamin K antagonists. Shown below is an algorithm depicting the indications and choices of VTE prophylaxis among patients undergoing general and abdominal-pelvic surgeries. Note that inferior vena cava filter is not recommended. In addition, surveillance compression ultrasound should not be done to screen for VTE. Shown below is an algorithm depicting the indications and choices of VTE prophylaxis among patients with major trauma. Major trauma include traumatic brain or spine injury. Note that inferior vena cava filter is not recommended. In addition, surveillance compression ultrasound should not be done to screen for VTE. Shown below is an algorithm depicting VTE prophylaxis in patients undergoing major orthopedic surgeries which include total hip arthroplasty, total knee arthroplasty and hip fracture surgery. Among patients who are not at elevated risk of bleeding, LMWH is the first line choice for VTE therapy. Among patients who refuse LMWH injection or intermittent pneumatic compression device, apixaban or dabigatran can be administered. Do not consider inferior vena cava filter as VTE prophylaxis or screening with a compression ultrasound for VTE. There is no score to estimate the risk of bleeding in major orthopedic surgeries. However, some factors have been identified to increase the risk of bleeding in this category of patients. These factors include:

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/index.php/VWF

# Von Willebrand factor von Willebrand factor (VWF) (/ˌfʌnˈvɪlɪbrɑːnt/) is a blood glycoprotein involved in hemostasis. It is deficient or defective in von Willebrand disease and is involved in a large number of other diseases, including thrombotic thrombocytopenic purpura, Heyde's syndrome, and possibly hemolytic-uremic syndrome. Increased plasma levels in a large number of cardiovascular, neoplastic, and connective tissue diseases are presumed to arise from adverse changes to the endothelium, and may contribute to an increased risk of thrombosis.[citation needed] VWF is a large multimeric glycoprotein present in blood plasma and produced constitutively as ultra-large VWF in endothelium (in the Weibel-Palade bodies), megakaryocytes (α-granules of platelets), and subendothelial connective tissue. The basic VWF monomer is a 2050-amino acid protein. Every monomer contains a number of specific domains with a specific function; elements of note are: Monomers are subsequently N-glycosylated, arranged into dimers in the endoplasmic reticulum and into multimers in the Golgi apparatus by crosslinking of cysteine residues via disulfide bonds. With respect to the glycosylation, VWF is one of only a few proteins that carry ABO blood group system antigens. Multimers of VWF can be extremely large, >20,000 kDa, and consist of over 80 subunits of 250 kDa each. Only the large multimers are functional. Some cleavage products that result from VWF production are also secreted but probably serve no function. Von Willebrand Factor's primary function is binding to other proteins, in particular factor VIII, and it is important in platelet adhesion to wound sites. It is not an enzyme and, thus, has no catalytic activity. VWF plays a major role in blood coagulation. Therefore, VWF deficiency or dysfunction (von Willebrand disease) leads to a bleeding tendency, which is most apparent in tissues having high blood flow shear in narrow vessels. From studies it appears that VWF uncoils under these circumstances, decelerating passing platelets. Recent research also suggests that von Willebrand Factor is involved in the formation of blood vessels themselves, which would explain why some people with von Willebrand disease develop vascular malformations (predominantly in the digestive tract) that can bleed excessively. The biological breakdown (catabolism) of VWF is largely mediated by the enzyme ADAMTS13 (acronym of "a disintegrin-like and metalloprotease with thrombospondin type 1 motif no. 13"). It is a metalloproteinase that cleaves VWF between tyrosine at position 842 and methionine at position 843 (or 1605–1606 of the gene) in the A2 domain. This breaks down the multimers into smaller units, which are degraded by other peptidases. Hereditary or acquired defects of VWF lead to von Willebrand disease (vWD), a bleeding diathesis of the skin and mucous membranes, causing nosebleeds, menorrhagia, and gastrointestinal bleeding. The point at which the mutation occurs determines the severity of the bleeding diathesis. There are three types (I, II and III), and type II is further divided in several subtypes. Treatment depends on the nature of the abnormality and the severity of the symptoms. Most cases of vWD are hereditary, but abnormalities of VWF may be acquired; aortic valve stenosis, for instance, has been linked to vWD type IIA, causing gastrointestinal bleeding - an association known as Heyde's syndrome. In thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS), ADAMTS13 either is deficient or has been inhibited by antibodies directed at the enzyme. This leads to decreased breakdown of the ultra-large multimers of VWF and microangiopathic hemolytic anemia with deposition of fibrin and platelets in small vessels, and capillary necrosis. In TTP, the organ most obviously affected is the brain; in HUS, the kidney. Higher levels of VWF are more common among people that have had ischemic stroke (from blood-clotting) for the first time. Occurrence is not affected by ADAMTS13, and the only significant genetic factor is the person's blood group. High plasma VWF levels were found to be an independent predictor of major bleeding in anticoagulated atrial fibrillation patients. VWF is named after Erik Adolf von Willebrand, a Finnish physician who in 1926 first described a hereditary bleeding disorder in families from the land islands. Although Von Willebrand did not identify the definite cause, he distinguished von Willebrand disease (vWD) from hemophilia and other forms of bleeding diathesis. In the 1950s, vWD was shown to be caused by a plasma factor deficiency (instead of being caused by platelet disorders), and, in the 1970s, the VWF protein was purified. Recently, It has been reported that the cooperation and interactions within the Von Willebrand Factors enhances the adsorption probability in the primary haemostasis. Such cooperation is proven by calculating the adsorption probability of flowing VWF once it crosses another adsorbed one. Such cooperation is held within a wide range of shear rates.

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/index.php/VZV

# Varicella zoster virus For information about primary infection with VZV, visit chicken pox. For information about reactivation of primary VZV infection, visit shingles. For information about congenital Varicella Syndrome, click here. Varicella zoster virus or varicella-zoster virus (VZV) is one of eight herpes viruses known to infect humans and vertebrates. VZV only affects humans, and commonly causes chickenpox in children, teens and young adults and herpes zoster (shingles) in adults and rarely in children. VZV is known by many names, including chickenpox virus, varicella virus, zoster virus, and human herpesvirus type 3 (HHV-3). VZV infects the nerves and causes a wide variety of symptoms. After the primary infection (chickenpox), the virus goes dormant in the nerves, including the cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia. Many years after the patient has recovered from chickenpox, VZV can reactivate to cause a number of neurologic conditions. Primary Varicella Zoster Virus infection results in chickenpox (varicella), which may result in complications including encephalitis or pneumonia (either direct viral pneumonia or secondary bacterial pneumonia). Even when clinical symptoms of chickenpox have resolved, VZV remains dormant in the nervous system of the infected person (virus latency), in the trigeminal and dorsal root ganglia. In about 10–20% of cases, VZV reactivates later in life, producing a disease known as shingles or herpes zoster. VZV can also infect the central nervous system, with a 2013 article reporting an incidence rate of 1.02 cases per 100 000 inhabitants in Switzerland, and an annual incidence rate of 1.8 cases per 100,000 inhabitants in Sweden. For comparison, Amyotrophic lateral sclerosis (ALS) has an annual incidence rate of 0.2 to 2.4 per 100,000 population in industrialized countries. Other serious complications of varicella zoster infection include postherpetic neuralgia, Mollaret's meningitis, zoster multiplex, and inflammation of arteries in the brain leading to stroke, myelitis, herpes ophthalmics, or zoster sine herpete. In Ramsay Hunt syndrome, VZV affects the geniculate ganglion resulting in lesions that follow specific branches of the facial nerve. Symptoms may include painful blisters on the tongue and ear along with one sided facial weakness and hearing loss. Until the mid-1990s, infectious complications of the CNS caused by VZV reactivation were regarded as rare. The presence of rash, as well as specific neurological symptoms, were required to diagnose a CNS infection caused by VZV. Since 2000, PCR testing has become more widely used, and the number of diagnosed cases of CNS infection has increased. Classic textbook descriptions state that VZV reactivation in the CNS is restricted to immunocompromised individuals and the elderly, however, recent studies have found that most patients are immunocompetent, and less than 60 years old. Old references cite vesicular rash as a characteristic finding, however, recent studies have found that the rash is only present in 45% of cases. In addition, systemic inflammation is not as reliable an indicator as previously thought: the mean level of C-reactive protein and mean white blood cell count is within the normal range in patients with VZV meningitis. MRI and CT scans are usually normal in cases of VZV reactivation in the CNS. CSF pleocytosis, previously thought to be a strong indicator of VZV encephalitis, was absent in half of a group of patients diagnosed with VZV encephalitis by PCR. The frequency of CNS infections presented at the emergency room of a community hospital is not negligible, so a means of diagnosing cases is needed. PCR is not a foolproof method of diagnosis, but because so many other indicators have turned out to not be reliable in diagnosing VZV infections in the CNS, screening for VZV by PCR is recommended. Negative PCR does not rule out VZV involvement, but a positive PCR can be used for diagnosis, and appropriate treatment started (for example, antivirals can be prescribed rather than antibiotics). The introduction of DNA analysis techniques has shown some complications of varicella-zoster to be more common than previously thought. For example, sporadic meningoencephalitis (ME) caused by varicella-zoster was regarded as a rare disease, mostly related to childhood chickenpox. However, meningoencephalitis caused by varicella-zoster is increasingly recognized as a predominant cause of ME among immunocompetent adults in non-epidemic circumstances. Diagnosis of complications of varicella-zoster, particularly in cases where the disease reactivates after years or decades of latency, are difficult. A rash (shingles) can be present or absent. Symptoms vary, and there is significant overlap in symptoms with herpes-simplex symptoms. Although DNA analysis techniques such as Polymerase Chain Reaction can be used to look for DNA of herpesviruses in spinal fluid or blood, the results may be negative, even in cases where other definitive symptoms exist. Notwithstanding these limitations, the use of PCR has resulted in an advance in the state of the art in our understanding of herpesviruses, including VZV, during the 1990s and 2000s. For example, in the past, clinicians believed that encephalitis was caused by herpes simplex and that patients always died or developed serious long term function problems. People were diagnosed at autopsy or by brain biopsy. Brain biopsy is not undertaken lightly: it is reserved only for serious cases that cannot be diagnosed by less invasive methods. For this reason, knowledge of these herpes virus conditions was limited to severe cases. DNA techniques have made it possible to diagnose "mild" cases, caused by VZV or HSV, in which the symptoms include fever, headache, and altered mental status. Mortality rates in treated patients are decreasing. VZV is closely related to the herpes simplex viruses (HSV), sharing much genome homology. The known envelope glycoproteins (gB, gC, gE, gH, gI, gK, gL) correspond with those in HSV; however, there is no equivalent of HSV gD. VZV also fails to produce the LAT (latency-associated transcripts) that play an important role in establishing HSV latency (herpes simplex virus). VZV virions are spherical and 180–200 nm in diameter. Their lipid envelope encloses the 100 nm nucleocapsid of 162 hexameric and pentameric capsomers arranged in an icosahedral form. Its DNA is a single, linear, double-stranded molecule, 125,000 nt long. The capsid is surrounded by a number of loosely associated proteins known collectively as the tegument; many of these proteins play critical roles in initiating the process of virus reproduction in the infected cell. The tegument is in turn covered by a lipid envelope studded with glycoproteins that are displayed on the exterior of the virion, each approximately 8 nm long. The genome was first sequenced in 1986. It is a linear duplex DNA molecule, a laboratory strain has 124,884 base pairs. The genome has 2 predominant isomers, depending on the orientation of the S segment, P (prototype) and IS (inverted S) which are present with equal frequency for a total frequency of 90-95%. The L segment can also be inverted resulting in a total of four linear isomers (IL and ILS). This is distinct from HSV's equiprobable distribution, and the discriminatory mechanism is not known. A small percentage of isolated molecules are circular genomes, about which little is known. (It is known that HSV circularizes on infection.) There are at least 70 open reading frames in the genome. There are at least five clades of this virus. Clades 1 and 3 include European/North American strains; clade 2 are Asian strains, especially from Japan; and clade 5 appears to be based in India. Clade 4 includes some strains from Europe but its geographic origins need further clarification. Commonality with HSV1 and HSV2 indicates a common ancestor, five genes do not have corresponding HSV genes. Relation with other human herpes viruses is less strong, but many homologous and conserved gene blocks are still found. There are five principal clades (1-5) and four genotypes that do not fit into these clades. The current distribution of these clades is Asia (clades 1, 2, and 5) and Europe (clades 1, 3 and 4). Allocation of VZV strains to clades required a sequence of the whole virus genome. Practically all molecular epidemiological data on global VZV strain distribution obtained with the targeted sequencing of selected regions. Phylogenetic analysis of VZV genomic sequences resolves wild-type strains into 9 genotypes (E1, E2, J, M1, M2, M3, M4, VIII and IX). Complete sequences for M3 and M4 strains are unavailable, but targeted analyses of representative strains suggest they are stable, circulating VZV genotypes. Sequence analysis of VZV isolates identified both shared and specific markers for every genotype and validated a unified VZV genotyping strategy. Despite high genotype diversity no evidence for intra-genotypic recombination was observed. Five of seven VZV genotypes were reliably discriminated using only four single nucleotide polymorphisms (SNP) present in ORF22, and the E1 and E2 genotypes were resolved using SNP located in ORF21, ORF22 or ORF50. Sequence analysis of 342 clinical varicella and zoster specimens from 18 European countries identified the following distribution of VZV genotypes: E1, 221 (65%); E2, 87 (25%); M1, 20 (6%); M2, 3 (1%); M4, 11 (3%). No M3 or J strains were observed. Of 165 clinical varicella and zoster isolates from Australia and New Zealand typed using this approach, 67 of 127 eastern Australian isolates were E1, 30 were E2, 16 were J, 10 were M1, and 4 were M2; 25 of 38 New Zealand isolates were E1, 8 were E2, and 5 were M1. The mutation rate for synonymous and nonsynonymous mutation rates among the herpesviruses have been estimated at 1 × 10−7 and 2.7 × 10−8 mutations/site/year, respectively, based on the highly conserved gB gene. A live attenuated VZV Oka/Merck strain vaccine is available and is marketed in the United States under the trade name Varivax. It was developed by Merck, Sharp & Dohme in the 1980s from the Oka strain virus isolated and attenuated by Michiaki Takahashi and colleagues in the 1970s. It was submitted to the US Food and Drug Administration for approval in 1990 and was approved in 1995. Since then, it has been added to the recommended vaccination schedules for children in Australia, the United States, and many other countries. Varicella vaccination has raised concerns in some that the immunity induced by the vaccine may not be lifelong, possibly leaving adults vulnerable to more severe disease as the immunity from their childhood immunization wanes. Vaccine coverage in the United States in the population recommended for vaccination is approaching 90%, with concomitant reductions in the incidence of varicella cases and hospitalizations and deaths due to VZV. So far, clinical data has proved that the vaccine is effective for over 10 years in preventing varicella infection in healthy individuals and when breakthrough infections do occur, illness is typically mild. In 2007, the ACIP recommended a second dose of vaccine before school entry to ensure the maintenance of high levels of varicella immunity. In 2006, the United States Food and Drug Administration approved Zostavax for the prevention of shingles. Zostavax is a more concentrated formulation of the Varivax vaccine, designed to elicit an immune response in older adults whose immunity to VZV wanes with advancing age. A systematic review by the Cochrane Library shows that Zostavax reduces the incidence of shingles by almost 50%. photomicrograph reveals some of the cytoarchitectural histopathologic changes which you'd find in a human skin tissue specimen that included a chickenpox, or varicella zoster virus lesion (500x mag). From Public Health Image Library (PHIL). Hematoxylin-eosin (H&E)-stained photomicrograph reveals some of the cytoarchitectural histopathologic changes found in a human skin tissue specimen that included a varicella zoster virus lesion (50x mag). From Public Health Image Library (PHIL). Hematoxylin-eosin (H&E)-stained photomicrograph reveals some of the cytoarchitectural histopathologic changes found in a human skin tissue specimen that included a varicella zoster virus lesion (500x mag). From Public Health Image Library (PHIL). Hematoxylin-eosin (H&E)-stained photomicrograph reveals some of the cytoarchitectural histopathologic changes found in a human skin tissue specimen that included a varicella zoster virus lesion (1200x mag). From Public Health Image Library (PHIL). Back of boy who had manifested the maculopapular rash that was determined to be chickenpox, also known as varicella-zoster virus (VZV). From Public Health Image Library (PHIL). Chickenpox lesions on the skin of this patient's left breast and arm on day 6 of the illness. From Public Health Image Library (PHIL). Chickenpox lesions on the skin of this patient's breasts, arms, and torso at day 6 of the illness. From Public Health Image Library (PHIL). Chickenpox lesions on a patient's back, which were displaying the characteristic "cropping" distribution, or manifesting themselves in clusters. From Public Health Image Library (PHIL). Posterior view of a hospitalized man's neck, back and shoulders, who'd been assigned a bed in a smallpox ward, due to an initially misdiagnosed illness, which turned out to be chickenpox. From Public Health Image Library (PHIL). Pathologic changes seen on the surface of the right unilateral side of this elderly male patient's tongue and chin, represent a herpes outbreak due to the Varicella-zoster virus (VZV) pathogen. From Public Health Image Library (PHIL). Viewed from above, this image depicts a smallpox scab (left), and chickenpox scab (right) as a demonstration in comparative morphology. From Public Health Image Library (PHIL). This anteroposterior (AP) radiograph revealed bilateral pulmonary infiltrates throughout the entirety of each lung field in the case of a child with leukemia, as well as chickenpox pneumonia. From Public Health Image Library (PHIL). Image depicts three mounted chickenpox scabs seen from the side revealing the superficiality of these scabs when morphologically compared to a smallpox scab. From Public Health Image Library (PHIL). Volar surface of a patient's left forearm, including the palmar surface of the left hand upon which you'll note classic maculopapular rash of chickenpox. From Public Health Image Library (PHIL). Bilateral pulmonary infiltrates throughout the entirety of each lung field in the case of a child with leukemia, as well as chickenpox pneumonia. From Public Health Image Library (PHIL).

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/index.php/Vaccenic_acid

# Vaccenic acid Vaccenic acid is a trans fat found in the fat of ruminants and in dairy products. Its IUPAC name is trans-7-octadecenoic acid, and its lipid shorthand name is 18:1 trans-11. The name was derived from the Latin vacca (cow). Vaccenic acid was discovered in 1928 in animal fats and butter. It is the main trans fatty acid isomer present in milk fat. Mammals convert it into rumenic acid, a conjugated linoleic acid, where it shows anticarcinogenic properties. Its stereoisomer, Cis-Vaccenic acid is an Omega-7 fatty acid found in Sea Buckthorn (Hippophae rhamnoides) oil. Its IUPAC name is cis-7-octadecenoic acid, and its lipid shorthand name is 18:1 cis-11. In the April 2001 issue of THE JOURNAL OF INVESTIGATIVE DERMATOLOGY, Shinichiro Haze et al published an article entitled: "2-Nonenal, Newly Found in Human Body Odor Tends to Increase with Aging". In this article it was suggested that omega-7 unsaturated fatty acids, such as palmitoleic acid and vaccenic acid, found on the skin surface may be the cause of the phenomenon commonly known as "old person smell".

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# Vaccination Vaccination is the administration of agent-specific, but relatively harmless, antigenic components that can induce protective immunity against the corresponding infectious agent in those individuals who are vaccinated. In practice, the terms vaccination and immunization are often used interchangeably. Vaccination is highly effective in the prevention of some particular infections. Vaccines are safe and are associated with minimal adverse reactions. Vaccination can prevent illness, disability, and death from vaccine-preventable diseases, which includes cervical cancer, diphtheria, hepatitis B, measles, mumps, pertussis, pneumonia, polio, rotavirus diarrhea, rubella, and tetanus. Vaccines help develop immunity by imitating an infection. This type of infection, however, does not cause illness, though it does cause the immune system to produce T-lymphocytes and antibodies. Immunization currently prevents an estimated 2 to 3 million deaths every year. An additional 1.5 million deaths could be avoided, however, if global vaccination coverage is improved. An estimated 19.4 million infants worldwide are still missing out on basic vaccines. The material administered as a vaccine can either be live but weakened forms of pathogens such as bacteria or viruses; killed or inactivated forms of these pathogens; or purified material such as proteins. Benjamin Jesty is notable for being perhaps the first person recorded to have been vaccinated with cowpox in order to artificially induce immunity to smallpox during the epidemic of 1774. The term vaccination was first used by Edward Jenner, an English physician, 22 years later in 1796. Louis Pasteur further adapted this principle in his pioneering work in microbiology. Vaccination (vacca in latin means cow) is so named because the first vaccine was derived from a virus affecting cows—the relatively benign cowpox virus, which provides a degree of immunity to smallpox, a contagious and deadly disease. The World Health Organization coordinated the global effort to eradicate smallpox. The last naturally occurring case of smallpox occurred in Somalia in 1977. Passive immunization is a method of disease prevention that functions by transferring pre-made antibodies to a person at risk of acquiring a certain disease. This type of immunity could be acquired naturally during pregnancy, via trans-placental maternal antibodies' transfer to the fetus. Artificial passive immunization is normally given by pre-made immunoglobulins to a person at risk of acquiring a certain disease. Human immune globulin is obtained from normal, healthy people; it is a concentrated solution of antibodies, mainly IgG antibodies. Human immune globulin is given intra-muscularly (IM). Up to 48 hours is required for IGs to reach the maximum serum concentration and their half-life is about 3 weeks. The sooner administration occurs, the more effective the prevention. IGs only provide temporary protection. Diseases with available human immune globulins include: IV immune globulin contains larger amounts of human immune globulin and is administered via the IV route. Diseases that may be prevented or ameliorated by using IVIGs include: Hyperimmune globulin is derived from human plasma containing large amounts of antibodies. Those from whose plasma the globulin is derived are patients convalescing from natural infections or donors who are artificially immunized. Hyperimmune globulins are available for cytomegalovirus, varicella-zoster, hepatitis B, infant botulism, rabies, and tetanus. Live attenuated vaccines are produced by modifying a disease-producing (wild) virus or bacterium in a laboratory. The resulting vaccine organism retains the ability to replicate and produce immunity, but usually does not cause illness. These vaccines are produced by growing the virus in tissue cultures that will select for less virulent strains, or by mutagenesis or targeted deletions in genes required for virulence. Attenuated vaccines can not be used by immunocompromised individuals. Examples of live attenuated vaccines include measles, mumps, and rubella vaccine (MMR) and varicella (chickenpox) vaccine. Toxoid vaccines are effective against bacteria that produces toxins. The vaccines are weakened toxins produced by particular bacteria. The DTaP vaccine contains diphtheria and tetanus toxoids. ­Subunit vaccines contain only some parts of bacteria or virus, not the entire germ. Because these vaccines contain only the essential antigens and not all the other molecules that make up the germ, side effects are less common. The pertussis component of the DTaP vaccine is an example of a subunit vaccine. ­Conjugate vaccines are effective against bacteria that have polysaccharides in their cell wall components. Polysaccharides may cause less stimulation of immune system and result in a defective immune response. Conjugate vaccines are effective for these types of bacteria because they connect (or conjugate) the polysaccharides to antigens that the immune system responds to very well. This linkage helps the immature immune system react to the coating and develop an immune response. An example of this type of vaccine is the Haemophilus influenzae type B (Hib) vaccine. Anaphylaxis is rare but important among immediate reactions. Health care providers should be aware of its symptoms and signs and be prepared for prompt treatment. Other common but less serious immediate reactions include: Vaccine components such as gelatin, egg proteins, cow's milk, thimerosal, aluminum, and phenoxyethanol that are used as vaccine preservatives, and they may cause adverse reactions ranging from fever or skin reactions to severe reactions that may require skin testing before future administration.

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# Vaccination policy Vaccination policy refers to the policy a government practices in relation to vaccination. Vaccinations are voluntary in some countries and mandatory in some countries. Some governments pay all or part of the costs of vaccinations for vaccines in a national vaccination schedule. Vaccination policies aim to produce immunity to diseases. Besides individual protection from getting ill, with some vacccines vaccination policies aim also to provide herd immunity which is based on the idea that the pathogen will have trouble spreading when a significant part of the population has immunity against it. With some vaccines, a goal of vaccination policies is to eradicate the disease - make it disappear from Earth altogether. Victory is claimed for smallpox globally and getting rid of endemic measles, mumps and rubella in Finland. The World Health Organization coordinated the global effort to eradicate this disease. The last naturally occurring case of smallpox occurred in Somalia in 1977. In 1988, the governing body of W.H.O. targeted polio for eradication by the year 2000, but didn't succeed. The next eradication target would most likely be measles, which has declined since the introduction of measles vaccination in 1963. In an attempt to eliminate the risk of outbreaks of some diseases, at various times several governments and other institutions have instituted policies requiring vaccination for all people. For example, an 1853 law required universal vaccination against smallpox in England and Wales, with fines levied on people who did not comply. In the United States, the Supreme Court ruled in the 1905 case Jacobson v. Commonwealth of Massachusetts that the state could require individuals to be vaccinated for the common good. Common contemporary U.S. vaccination policies require that children receive common vaccinations before entering school. A few other countries also have some compulsory vaccinations. Compulsory vaccination is believed to have greatly reduced the rates of some infectious diseases. Beginning with early vaccination in the nineteenth century, these policies led to resistance from a variety of groups, collectively called anti-vaccinationists, who objected on ethical, political, medical safety, religious, and other grounds. Common objections are that compulsory vaccination represents excessive government intervention in personal matters, or that the proposed vaccinations are not sufficiently safe. Many modern vaccination policies allow exemptions for people who have compromised immune systems, allergies to the components used in vaccinations or strongly-held objections. In 1904 in the city of Rio de Janeiro, Brazil a government program of mandatory smallpox vaccination resulted in the so-called Vaccine Revolt, several days of rioting with considerable property damage and a number of deaths. Having compulsory vaccinations is connected with difficult policy issues where health authorities try to balance health of society and individual liberty and freedom of expression: "Vaccination is unique among de facto mandatory requirements in the modern era, requiring individuals to accept the injection of a medicine or medicinal agent into their bodies, and it has provoked a spirited opposition. This opposition began with the first vaccinations, has not ceased, and probably never will. From this realization arises a difficult issue: how should the mainstream medical authorities approach the anti-vaccination movement? A passive reaction could be construed as endangering the health of society, whereas a heavy handed approach can threaten the values of individual liberty and freedom of expression that we cherish." BMJ Most states in the U.S. mandate immunization, or obtaining exemption, before enrollment in public school. Exemptions are typically for people who have compromised immune systems, allergies to the components used in vaccinations, or strongly-held objections. Under occasional circumstances, the American Academy of Pediatrics considers parental refusal of immunization a form of child abuse and neglect. United States of America has mandatory vaccinations ar the state level - all states have laws requiring children to be vaccinated according to CDC schedules as a requisite for attending school. In practice there are religous and/or philosophical exemptions in all states. A significant number of vaccinations may be a requirement for school admission at various grades. This requirement exists primarily to reduce the number of diseases which are transmissible in the classroom, not as a comprehensive list of the vaccinations which may be appropriate for any given child.[citation needed] As a result, a school may require a vaccination for highly contagious diseases like HIB and chicken pox, which can cause significant school disruption during outbreaks, but is less likely to require vaccination against Hepatitis B, which is strictly a bloodborne pathogen and which cannot be caught through the kind of casual contact one encounters in a classroom. In the US, individual states have varying exemptions to compulsory vaccination that parents may claim for religious, ethical, or medical reasons.

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# Vaccine A vaccine is an antigenic preparation used to establish immunity to a disease. The term derives from Edward Jenner's use of cowpox ("vacca" means cow in Latin), which, when administered to humans, provided them protection against smallpox, the work which Louis Pasteur and others carried on. Vaccines are based on the concept of variolation originating in China, in which a person is deliberately infected with a weak form of smallpox. Jenner realized that milkmaids who had contact with cowpox did not get smallpox. The process of distributing and administrating vaccines is referred to as vaccination. Since vaccination was much safer, smallpox inoculation fell into disuse and was eventually banned in England in 1840. Vaccines can be prophylactic (e.g. to prevent or ameliorate the effects of a future infection by any natural or "wild" pathogen), or therapeutic (e.g. vaccines against cancer are also being investigated; see cancer vaccine). Note that while most vaccines are created using inactivated or attenuated compounds from micro-organisms, synthetic vaccines are composed mainly or wholly of synthetic peptides, carbohydrates or antigens. Some viral vaccines have been developed by use of cell lines derived from aborted fetuses ( http://www.lifecanada.org/html/science/Vaccines/ABriefHistoryofHumanDiploidCellStrains.pdf ) The immune system recognizes vaccine agents as foreign, destroys them, and 'remembers' them. When the virulent version of an agent comes along, the immune system is thus prepared to respond, by (1) neutralizing the target agent before it can enter cells, and (2) by recognizing and destroying infected cells before that agent can multiply to vast numbers. Vaccines have contributed to the eradication of smallpox, one of the most contagious and deadly diseases known to man. Other diseases such as rubella, polio, measles, mumps, chickenpox, and typhoid are nowhere near as common as they were just a hundred years ago. As long as the vast majority of people are vaccinated, it is much more difficult for an outbreak of disease to occur, let alone spread. This effect is called herd immunity. Polio, which is transmitted only between humans, is targeted by an extensive eradication campaign that has seen endemic polio restricted to only parts of four countries. The difficulty of reaching all children, however, has caused the eradication date to be missed twice by 2006. In order to provide best protection, children are recommended to receive vaccinations as soon as their immune systems are sufficiently developed to respond to particular vaccines, with additional 'booster' shots often required to achieve 'full immunity'. This has led to the development of complex vaccination schedules. In the United States, the Advisory Committee on Immunization Practices, which recommends schedule additions for the Center for Disease Control, recommends routine vaccination of children against: hepatitis A, hepatitis B, polio, mumps, measles, rubella, diphtheria, pertussis, tetanus, HiB, chicken pox, rotavirus, influenza, meningococcal disease and pneumonia. The large number of vaccines and boosters recommended (up to 24 injections by age two) has led to problems with achieving full compliance. In order to combat declining compliance rates, various notification systems have been instituted and a number of combination injections are now marketed (e.g., Prevnar and ProQuad vaccines), which provide protection against multiple diseases. Besides recommendations for infant vaccination boosters, many specific vaccines are recommended for repeated injections throughout life -- most commonly for measles, tetanus, influenza, and pneumonia. Pregnant women are often screened for continued resistance to rubella. In 2006, a vaccine was introduced against shingles, a disease caused by the chicken pox virus, which usually affects the elderly. Vaccine recommendations for the elderly concentrate on pneumonia and influenza, which are more deadly to that group. A number of vaccines, including those given to very young children, have contained thiomersal, a preservative that metabolizes into ethylmercury. It has been used in some influenza, DTP (diphtheria, tetanus and pertussis) vaccine formulations. Since 1997, use of thimerosal has been gradually diminishing in western industrialized countries after recommendations by medical authorities, but trace amounts of thimerosal remain in many vaccines and in some vaccines, thimerosal has not yet been phased out despite recommendations. Some states in USA have enacted laws banning the use of thimerosal in childhood vaccines. In the late 1990s, controversy over vaccines escalated in both the US and the United Kingdom when a study, published in the respected journal Lancet, by Dr. Andrew Wakefield suggested a possible link between bowel disorders, autism and the MMR vaccine, and urged further research. His report garnered significant media attention, leading to a drop in the uptake of the MMR vaccine in the United Kingdom and some other countries. In response to the controversies, a number of studies with larger sample sizes were conducted, and failed to confirm the findings. . In 2004, 10 of the 13 authors of the original Wakefield study retracted the paper's "interpretation", or conclusion, section, which had claimed: "Interpretation. We identified associated gastrointestinal disease and developmental regression in a group of previously normal children, which was generally associated in time with possible environmental triggers." The retraction of this claim stated that the data were insufficient to establish a causal link between MMR vaccine and autism. Wakefield was later found to have received £435,000 in fees from trial lawyers attempting to show the vaccine was dangerous . Also in 2004, the United States' Institute of Medicine reported that evidence "favors rejection" of any link between vaccines containing thimerosal, or MMR, and the development of autism . In 2004 and 2005, England and Wales experienced an increase in the incidence of mumps infections among adolescents and young adults. The age group affected were too old to have received the routine MMR immunisations around the time the paper by Wakefield et al was published, and too young to have contracted natural mumps as a child, and thus to achieve a herd immunity effect. With the decline in mumps that followed the introduction of the MMR vaccine, these individuals had not been exposed to the disease, but still had no immunity, either natural or vaccine induced. Therefore, as immunization rates declined following the controversy and the disease re-emerged, they were susceptible to infection. . This and similar examples indicate the importance of: There is opposition to any type of vaccination from some sectors of the community, particularly those who favor 'alternative' health care. Some skeptics claim that mass immunization is a eugenics program. Naturopaths and other alternative health care practitioners sometimes offer their own, alternative treatments to conventional vaccination. In Australia, a massive increase in vaccination rates was observed when the federal government made certain benefits (such as the universal 'Family Allowance' welfare payments for parents of children) dependent on vaccination. As well, children were not allowed into school unless they were either vaccinated or their parents completed a statutory declaration refusing to immunize them, after discussion with a doctor, and other bureaucracy. (Similar school-entry vaccination regulations have been in place in some parts of Canada for several years.) It became easier and cheaper to vaccinate one's children than not to. When faced with the annoyance, many more casual objectors simply gave in. Another vaccination controversy concerns smallpox. Since it has been eradicated, some suggest that the stores of smallpox virus should be destroyed. In an article on Newswise both sides debate the issue: "The destruction of remaining smallpox virus stocks is an overdue step forward for public health and security that will dramatically reduce the possibility that this scourge will kill again, either by accident or design, argues Edward Hammond of The Sunshine Project, an organisation seeking international consensus against biological weapons." "But John Agwunobi of the US Department of Health and Human Services believes that clandestine stocks almost certainly exist and that destroying the virus would be "irreversible and short sighted." Vaccines do not guarantee complete protection from a disease. Sometimes this is because the host's immune system simply doesn't respond adequately or at all. This may be due to a lowered immunity in general (diabetes, steroid use, HIV infection) or because the host's immune system does not have a B-cell capable of generating antibodies to that antigen. Even if the host develops antibodies, the human immune system is not perfect and in any case the immune system might still not be able to defeat the infection. Adjuvants are typically used to boost immune response. Adjuvants are sometimes called the dirty little secret of vaccines in the scientific community, as not much is known about how adjuvants work. Most often aluminium adjuvants are used, but adjuvants like squalene are also used in some vaccines and more vaccines with squalene and phosphate adjuvants are being tested. The efficacy or performance of the vaccine is dependent on a number of factors: One challenge in vaccine development is economic: many of the diseases most demanding a vaccine, including HIV, malaria and tuberculosis, exist principally in poor countries. Although some contend pharmaceutical firms and biotech companies have little incentive to develop vaccines for these diseases, because there is little revenue potential, the number of vaccines actually administered has risen dramatically in recent decades. This increase, particularly in the number of different vaccines administered to children before entry into schools may be due to government mandates, rather than economic incentive. Most vaccine development to date has relied on 'push' funding by government and non-profit organizations, of government agencies, universities and non-profit organizations. Many researchers and policymakers are calling for a different approach, using 'pull' mechanisms to motivate industry. Mechanisms such as prizes, tax credits, or advance market commitments could ensure a financial return to firms that successfully developed a HIV vaccine. If the policy were well-designed, it might also ensure people have access to a vaccine if and when it is developed. Statistics from the government agencies of the U.S., the British Commonwealth and the U.K. show that between the 1800s and the time various vaccines were introduced, the incidences of the diseases for which vaccines were provided were reduced by 70%-90%. For some, this prompts the question as to whether the reduction in the morbidity and mortality due to these diseases is owed to improved sewage systems, food refrigeration, improved home and work environments, and the introduction of antibiotics, all of which occurred during the same period. In order to extend shelf life and reduce production and storage costs, thimerosal, a preservative containing about 49% of a form of mercury called ethylmercury, was used routinely until recent years. Thimerosal has been phased out in the U.S. in all but a few flu vaccines (it has been phased out earlier in other countries, e.g. Denmark in 1992), but may be used in stages of manufacture. Parents wishing to avoid this preservative, most common in multi-dose containers of influenza vaccine, may specifically ask for thimerosal-free alternatives that contain only trace amounts. A study published in the September 2007 New England Journal of Medicine reported no causal association between early exposure to mercury from thimerosal-containing vaccines and neurological problems by the age of 7 to 10 years old.

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# Vaccine Safety Datalink The Vaccine Safety Datalink Project (VSD) was established in 1990 by the United States Centers for Disease Control and Prevention (CDC) to study the adverse side effects of vaccines. Four large health maintenance organizations, including Kaiser Permanente, were initially recruited to provide the CDC with medical data on vaccination histories, health outcomes, and subject characteristics. The VSD database contains data compiled from surveillance on more than seven million Americans, including about 500,000 children from birth through age six years (2% of the U.S. population in this age group). The VSD data-sharing program is now being administered by the National Center for Health Statistics Research Data Center. The data sharing guidelines have been revised to include comments from interested groups as well as recommendations from the Institute of Medicine (IOM). Data from the Vaccine Safety Datalink Project have been utilized to address a number of vaccine safety concerns; examples include a study clarifying the risk of anaphylaxis after vaccine administration and several studies finding no link between thimerosal-containing vaccines and autism.

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# Vaccine controversy A vaccine controversy is a dispute over the morality, ethics, effectiveness, or safety of vaccination. Medical opinion is that the benefits of preventing suffering and death from infectious diseases greatly outweigh the risks of adverse effects following immunization. Some vaccination critics say that vaccines are ineffective against disease, that vaccine safety studies are inadequate, or raise other objections. Some religious groups oppose vaccination as a matter of doctrine, and some political groups oppose mandatory vaccination on the grounds of individual liberty. Mass vaccination campaigns were essential components of strategies that led to the eradication of smallpox, which once killed as many as every seventh child in Europe, and the near-eradication of polio. As a more modest example, incidence of invasive disease with Haemophilus influenzae, a major cause of bacterial meningitis and other serious disease in children, has decreased by over 99% in the U.S. since the introduction of a vaccine in 1988. Fully vaccinating all U.S. children born in a given year from birth to adolescence saves an estimated 33,000 lives and prevents an estimated 14 million infections. Vaccines are a cost-effective and preventive way of promoting health, compared to the treatment of acute or chronic disease. In the U.S. during the year 2001, routine childhood immunizations against seven diseases were estimated to save over $40 billion per birth-year cohort in overall social costs including $10 billion in direct health costs, and the societal benefit-cost ratio for these vaccinations was estimated to be 16.5. Incomplete vaccine coverage increases the risk of disease for the entire population, including those who have been vaccinated. One study found that doubling the number of unvaccinated individuals would increase the risk of measles in vaccinated children anywhere from 5–30%. A second study provided evidence that the risk of measles and pertussis increased in vaccinated children proportionally to the number of unvaccinated individuals among them, again highlighting the evident efficacy of widespread vaccine coverage for public health. In several countries, reductions in the use of some vaccines were followed by increases in the diseases' morbidity and mortality. According to the Centers for Disease Control and Prevention, continued high levels vaccine coverage are necessary to prevent resurgence of diseases which have been nearly eliminated. An anti-vaccination campaign motivated by religious objections, by concerns about effectiveness, and by concerns about individual rights, led to the vaccination rate in Stockholm dropping to just over 40%, compared to about 90% elsewhere in Sweden. A major smallpox epidemic then started in 1873. It led to a rise in vaccine uptake and an end of the epidemic. A 1974 report ascribed 36 reactions to whooping cough (pertussis) vaccine, a prominent public-health academic claimed that the vaccine was only marginally effective and questioned whether its benefits outweigh its risks, and extended television and press coverage caused a scare. Vaccine uptake in the UK decreased from 81% to 31% and pertussis epidemics followed, leading to deaths of some children. Mainstream medical opinion continued to support the effectiveness and safety of the vaccine; public confidence was restored after the publication of a national reassessment of vaccine efficacy. Vaccine uptake then increased to levels above 90% and disease incidence declined dramatically. In the vaccination moratorium period that occurred when Sweden suspended vaccination against whooping cough (pertussis) from 1979 to 1996, 60% of the country's children contracted the potentially fatal disease before the age of ten years; close medical monitoring kept the death rate from whooping cough at about one per year. Pertussis continues to be a major health problem in developing countries, where mass vaccination is not practiced; the World Health Organization estimates it caused 294,000 deaths in 2002. An outbreak at a religious community and school in The Netherlands illustrates the effect of measles in an unvaccinated population. The population in the several provinces affected had a high level of immunization with the exception of one of the religious denominations who traditionally do not accept vaccination. The three measles-related deaths and 68 hospitalizations that occurred among 2961 cases in the Netherlands demonstrate that measles can be severe and may result in death even in industrialized countries. From late 1999 until the summer of 2000, there was a measles outbreak in North Dublin, Ireland. At the time, the national immunization level had fallen below 80%, and in part of North Dublin the level was around 60%. There were more than 100 hospital admissions from over 300 cases. Three children died and several more were gravely ill, some requiring mechanical ventilation to recover. In the early 2000s, conservative religious leaders in northern Nigeria, suspicious of Western medicine, advised their followers to not have their children vaccinated with oral polio vaccine. The boycott was endorsed by the governor of Kano State, and immunization was suspended for several months. Subsequently, polio reappeared in a dozen formerly polio-free neighbors of Nigeria, and genetic tests showed the virus was the same one that originated in northern Nigeria: Nigeria had become a net exporter of polio virus to its African neighbors. People in the northern states were also reported to be wary of other vaccinations, and Nigeria reported over 20,000 measles cases and nearly 600 deaths from measles from January through March 2005. In 2006 Nigeria accounted for over half of all new polio cases worldwide. Outbreaks continued thereafter; for example, at least 200 children died in a late-2007 measles outbreak in Borno State. A 2005 measles outbreak in Indiana was due to children whose parents had refused to have them vaccinated. Most cases of pediatric tetanus in the U.S. occur in children whose parents objected to their vaccination. Since the inception of vaccination in the late 18th century, opponents have argued that vaccines do not work, that they are dangerous, that individuals should rely on personal hygiene instead, or that mandatory vaccinations violate individual rights or religious principles. Some vaccine critics claim that there have never been any benefits to public health from vaccination. They argue that all the reduction of communicable diseases which were rampant in conditions where overcrowding, poor sanitation, almost non-existent hygiene and a yearly period of very restricted diet existed, are reduced because of changes in conditions excepting vaccination. Other critics argue that immunity given by vaccines is only temporary and requires boosters, whereas those who survive the disease become permanently immune. As discussed below, the philosophies of some alternative medicine practitioners are incompatible with the idea that vaccines are effective. Children who survive diseases like diphtheria develop a natural immunity that lasts longer than immunity developed via vaccination. Even though the overall mortality rate is much lower with vaccination, the percentage of adults protected against the disease may also be lower. Vaccination critics argue that for diseases like diphtheria the extra risk to older or weaker adults may outweigh the benefit of lowering the mortality rate among the general population. Few deny the vast improvements vaccination has made to public health; a more common concern is their safety. All vaccines may cause side effects, and immunization safety is a real concern. Controversies in this area revolve around the question of whether the risks of adverse events following immunization outweigh the benefits of preventing adverse effects of common diseases. Critics point out that lack of evidence of harm is not the same as evidence of safety. If individual or multiple vaccinations were to "weaken the immune system", as some vaccine critics contend, then one would expect an increase in hospitalizations for other infections following immunization. A large epidemiological study, involving all 805,206 children born in Denmark between 1990 and 2001, found no evidence that multiple-antigen vaccines, nor the increasing number of vaccinations given to children, led to a higher rate of infections. A 2006 study of health data from the Canadian province of Ontario (where influenza vaccines have been free since 2000), found a correlation between receiving a vaccination and developing Guillain-Barré syndrome (GBS) in individuals, but no increase of GBS in the general population corresponding to vaccination popularity. The authors concluded, "individuals who receive the influenza vaccine should be advised of the potential risk for GBS". Aluminum compounds are used in many vaccines as immunologic adjuvants, to stimulate the immune system and increase the response of the vaccine. Although these vaccines can elicit redness, itching, and low-grade fever, and aluminum as such is considered neurotoxic for humans, its use in vaccines has not been associated with serious adverse events. In some cases aluminum-containing vaccines are associated with macrophagic myofasciitis (MMF), localized microscopic lesions containing aluminum salts that persist up to 8 years. However, recent case-controlled studies have found no specific clinical symptoms in individuals with biopsies showing MMF, and there is no evidence that aluminum-containing vaccines are a serious health risk or justify changes to immunization practice. The organic mercury content of thiomersal in child vaccines has been alleged to contribute to autism, and thousands of parents in the United States have pursued legal compensation from a federal fund. In July 1999, the Centers for Disease Control (CDC) and the American Academy of Pediatrics (AAP) asked vaccine makers to remove thiomersal from vaccines as quickly as possible, and thiomersal has been phased out of most U.S. and European vaccines. However, the 2004 Institute of Medicine (IOM) panel favoured rejecting any causal relationship between thiomersal-containing vaccines and autism. The CDC and the AAP followed the precautionary principle, which assumes that there is no harm in exercising caution even if it later turns out to be unwarranted, but their 1999 action sparked confusion and controversy that has diverted attention and resources away from efforts to determine the causes of autism. The current scientific consensus is that there is no convincing scientific evidence that thiomersal causes or helps cause autism. In the UK, the MMR vaccine was the subject of controversy after publication of a 1998 paper by Andrew Wakefield, et al., reporting a study of 12 children mostly with autism spectrum disorders with onset soon after administration of the vaccine. During a 1998 press conference, Wakefield suggested that giving children the vaccines in three separate doses would be safer than a single vaccination. This suggestion was not supported by the paper, and several subsequent peer-reviewed studies have failed to show any association between the vaccine and autism. Wakefield has been heavily criticized on scientific grounds and for triggering a decline in vaccination rates, as well as on ethical grounds for the way the research was conducted. In 2004 the MMR-and-autism interpretation of the paper was formally retracted by 10 of Wakefield's 12 co-authors. The CDC, the IOM of the National Academy of Sciences, and the UK National Health Service have all concluded that there is no evidence of a link between the MMR vaccine and autism. A systematic review by the Cochrane Library concluded that there is no credible link between the MMR vaccine and autism, that MMR has prevented diseases that still carry a heavy burden of death and complications, that the lack of confidence in MMR has damaged public health, and that design and reporting of safety outcomes in MMR vaccine studies are largely inadequate. There is evidence that schizophrenia is associated with prenatal exposure to rubella, influenza, and toxoplasmosis infection. For example, one study found a seven-fold increased risk of schizophrenia when mothers were exposed to influenza in the first trimester of gestation. This may have public health implications, as strategies for preventing infection include vaccination, antibiotics, and simple hygiene. When weighing the benefits of protecting the woman and fetus from influenza against the potential risk of vaccine-induced antibodies that could conceivably contribute to schizophrenia, influenza vaccination for women of reproductive age still makes sense, but it is not known whether vaccination during pregnancy helps or harms. The CDC's Advisory Committee on Immunization Practices, the American College of Obstetricians and Gynecologists, and the American Academy of Family Physicians all recommend routine flu shots for pregnant women, for several reasons: Critics allege that the profit motive explains why vaccination is required, and that vaccine makers cover up or suppress information, or generate misinformation, about safety or effectiveness. Compulsory vaccination policies have provoked opposition at various times from people who say that governments should not infringe on the freedom of an individual to choose medications, even if the choice increases the risk of disease to others. If a vaccination program successfully reduces the disease threat, it may reduce the perceived risk of disease enough so that an individual's optimal strategy is to refuse vaccination at coverage levels below those optimal for the community. If many exemptions are granted to mandatory vaccination rules, the resulting free rider problem may cause loss of herd immunity, substantially increasing risks even to vaccinated individuals. Vaccination has been opposed on religious grounds ever since it was introduced, even when vaccination is not compulsory. Early Christian opponents argued that if God had decreed that someone should die of smallpox, it would be a sin to thwart God's will via vaccination. Opposition continues to the present day, on various grounds. For example, the Family Research Council, a conservative U.S. Christian group, opposes mandatory vaccination for diseases typically spread via sexual contact, arguing that the possibility of disease deters sexual promiscuity. Many governments allow parents to opt out of their children's otherwise-mandatory vaccinations for religious reasons; some parents falsely claim religious beliefs to get vaccination exemptions. Many forms of alternative medicine are based on philosophies that oppose vaccination and have practitioners who voice their opposition. These include anthroposophy, some elements of the chiropractic community, non-medically trained homoeopaths, and naturopaths. Historically, chiropractic strongly opposed vaccination based on its belief that all diseases were traceable to causes in the spine, and therefore could not be affected by vaccines; Daniel D. Palmer, the founder of chiropractic, wrote, "It is the very height of absurdity to strive to 'protect' any person from smallpox or any other malady by inoculating them with a filthy animal poison." Vaccination remains controversial within chiropractic. The American Chiropractic Association and the International Chiropractic Association support individual exemptions to compulsory vaccination laws, and a 1995 survey of U.S. chiropractors found that about a third believed there was no scientific proof that immunization prevents disease. The Canadian Chiropractic Association supports vaccination; however, surveys in Canada in 2000 and 2002 found that only 40% of chiropractors supported vaccination, and that over a quarter opposed it and advised patients against vaccinating themselves or their children. Although most chiropractic writings on vaccination focus on its negative aspects, antivaccination sentiment is espoused by what appears to be a minority of chiropractors. Several surveys have shown that some practitioners of homeopathy, particularly lay homeopaths, advise patients against vaccination. For example, a survey of registered homeopaths in Austria found that only 28% considered immunization to be an important preventive measure, and 83% of homeopaths surveyed in Sydney, Australia did not recommend vaccination. Many practitioners of naturopathy also oppose vaccination. The U.S. Vaccine Injury Compensation Program (VICP) was created to provide a federal no-fault system for compensating vaccine-related injuries or death. It was established after a scare in the 1980s over the DPT vaccine: even though claims of side effects were later generally discredited, large jury awards had been given to some claimants of DPT vaccine injuries, and most DPT vaccine makers had ceased production. Claims against vaccine manufacturers must be heard first in the vaccine court. By 2008 the fund had paid out 2,114 awards totaling $1.7 billion. Thousands of autism-related claims are pending before the court, and have not yet been resolved. Religious arguments against inoculation were advanced even before the work of Edward Jenner; for example, in a 1772 sermon entitled "The Dangerous and Sinful Practice of Inoculation" the English theologian Rev. Edward Massey argued that diseases are sent by God to punish sin and that any attempt to prevent smallpox via inoculation is a "diabolical operation". Some anti-vaccinationists still base their stance against vaccination with reference to their religious beliefs. After Jenner's work, vaccination became widespread in the United Kingdom in the early 1800s. Variolation, which had preceded vaccination, was banned in 1840 because of its greater risks. Public policy and successive Vaccination Acts first encouraged vaccination and then made it mandatory for all infants in 1853, with the highest penalty for refusal being a prison sentence. This was a significant change in the relationship between the British state and its citizens, and there was a public backlash. After an 1867 law extended the requirement to age 14 years, its opponents focused concern on infrigement of individual freedom, and eventually a 1898 law allowed for conscientious objection to compulsory vaccination. In the 19th century, the city of Leicester in the UK achieved a high level of isolation of smallpox cases and great reduction in spread compared to other areas. The mainstay of Leicester's approach to conquering smallpox was to decline vaccination and put their public funds into sanitary improvements. Bigg's account of the public health procedures in Leicester, presented as evidence to the Royal Commission, refers to erysipelas, an infection of the superficial tissues which was a complication of any surgical procedure. In the U.S., President Thomas Jefferson took a close interest in vaccination, alongside Dr. Waterhouse, chief physician at Boston. Jefferson encouraged the development of ways to transport vaccine material through the Southern states, which included measures to avoid damage by heat, a leading cause of ineffective batches. Smallpox outbreaks were contained by the latter half of the 19th century, a development widely attributed to vaccination of a large portion of the population. Vaccination rates fell after this decline in smallpox cases, and the disease again became epidemic in the 1870s (see smallpox). Anti-vaccination activity increased again in the U.S. in the late 19th century. After a visit to New York in 1879 by William Tebb, a prominent British anti-vaccinationist, the Anti-Vaccination Society of America was founded. The New England Anti-Compulsory Vaccination League was formed in 1882, and the Anti-Vaccination League of New York City in 1885. In the early 19th century, the anti-vaccination movement drew members from across a wide range of society; more recently, it has been reduced to a predominantly middle-class phenomenon. Arguments against vaccines in the 21st century are often similar to those of 19th-century anti-vaccinationists.

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# Vaccine critic The concept can be identified from viewing various of the anti-vaccination websites and is referred to in a Journal of the Royal Society of Medicine (2005) review describing the differences between contemporary anti-vaccination campaigns and those before 1907 . Vaccine critics should be distinguishable from anti-vaccinationists by being in favour of some specific immunisations for some specific people in some specific circumstances, and explaining those clearly.

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# Vaccine injury A vaccine injury is an injury caused by vaccination. Historically, allegations of vaccine injuries have come in waves, and have been closely related to litigation, and publicity surrounding that litigation. Allegations of vaccine injuries in recent decades have appeared in litigation in the United States , and in the United Kingdom.[citation needed] Numerous legislative bills have been introduced in the United States to shield pharmaceutical companies from liabilities stemming from vaccine injury claims. Globally, billions of dollars have been paid out to the families of alleged victims, and potential cumulative liability many times that amount has been estimated. Some adverse events following vaccination, as with all pharmaceutical interventions, are widely recognized as very rare events. Nearly 5,000 U.S. families of autistic children have lodged claims for compensation from a federal fund, saying that their health problems were caused by common childhood vaccines. Large scientific studies have found no association, and no autism claim has been paid from the fund so far. In 1998, concerns arising from allegations of a possible link between MMR vaccines and autistic spectrum disorders arose after the publication of a controversial paper, by Dr. Andrew Wakefield, et al, in the Lancet. This described an alleged novel inflammatory bowel disease, later named autistic enterocolitis by Wakefield. The interpretation of this link, however, was later retracted. Others, including Bernard Rimland, had earlier expressed concerns about a possible relationship between vaccines and an increase in autism diagnoses. In 1988, the National Vaccine Injury Compensation Program (VICP) went into effect to compensate individuals and families of individuals who have been injured by covered childhood vaccines. The VICP was adopted in response to an earlier scare over the pertussis portion of the DPT vaccine. These claims were later generally discredited, but some U.S. lawsuits against vaccine makers won substantial awards; most makers ceased production, and the last remaining major manufacturer threatened to do so. It uses a no-fault alternative dispute resolution system for resolving vaccine injury claims. Funding for claims of harm after 1988 comes from a patient fee of 75 cents per vaccination. To win an award, a claimant must show a causal connection; if medical records show a child has one of several listed adverse effects soon after vaccination, the assumption is that it was caused by the vaccine. The proof standard is the civil-law preponderance of the evidence, showing that causation was more likely than not. Claims that are denied can be pursued in regular lawsuits, though this is rare. Some claimants are having some luck suing thimerosal makers instead of vaccine makers, filing class-action suits, or demanding monitoring for vaccinated children who do not show signs of autism. The VICP covers all vaccines listed on the Vaccine Injury Table maintained by the Secretary of Health and Human Services. From 1988 until 2007-08-31, 5,222 claims relating to autism, and 2,816 non-autism claims, were made to the VICP. 893 of these claims, all non-autism-related, were compensated, with 1,154 non-autism and 327 autism claims dismissed; awards (including attorney's fees) totaled $806 million. The VICP also applies to claims for injuries suffered before 1988; there were 4,264 of these claims of which 1,189 were compensated with awards totaling $903 million. In 1988, the National Childhood Vaccine Injury Act (NCVIA) was enacted "to ensure an adequate supply of vaccines, stabilize vaccine costs, and establish and maintain an accessible and efficient forum for individuals thought to be injured by childhood vaccines." This followed extensive litigation against vaccine manufacturers, most of whom withdrew from production on grounds that the cost of lawsuits outweighed any profit in making them. The VICP is administered jointly by the U.S. Department of Health and Human Services (HHS), the U.S. Court of Federal Claims, and the U.S. Department of Justice (DOJ). As of February, 2003, 3,482 vaccine victims have received compensation totaling over $1.4 billion. For vaccine injuries ruled to have been sustained after its enactment, the NCVIA allows 'reasonable compensation' for past and future unreimbursable medical, custodial care, and rehabilitation costs, lost earnings, reasonable legal fees, and places a cap of $250,000 for actual and projected pain, suffering and emotional distress. The HHS is represented by the DOJ in hearings before a "special master", who makes initial decision for compensation under the VICP. A special master is appointed by the judges of the Court. Decisions can be appealed to the Court, then to the US Court of Appeals for the Federal Circuit, and then to the Supreme Court. The U.S. Department of Health and Human Services set up a trust fund in 1988 to compensate people damaged by vaccination. By 2007, the fund had paid out $1.8 billion to 1,500 claimants. The vaccines covered by the compensation scheme are those aimed at protecting against diphtheria, tetanus, pertussis (whooping cough), measles, mumps, rubella (German measles), polio, hepatitis B, varicella (chicken pox), Hemophilus influenzae type b, and rotavirus. Pneumococcal vaccine is expected to be covered soon. The Vaccine Adverse Event Reporting System (VAERS) is a passive surveillance program administered jointly by the Food and Drug Administration (FDA) and the Centers for Disease Control (CDC). VAERS is intended to track adverse events associated with vaccines. VAERS collects and analyzes information from reports of adverse events (possible side effects) that occur after the administration of US licensed vaccines. The program's success in tracking vaccine injuries has been questioned by some, who allege medical practitioners frequently fail to make reports. Others say that it may overstate possible injuries since many neurological problems in childhood may manifest at around the ages when vaccines are routinely administered. The Vaccine Safety Datalink (VSD) is comprised of databases from seeral organizations containing information regarding health outcomes for millions of US citizens and to enhance assessment of vaccine injuries. It was designed to allow for such things as comparisons between vaccinated and unvaccinated populations, and for the identification of possible groups at risk for adverse events. In 2003, parents of over 1,000 United Kingdom children diagnosed with autistic spectrum disorders, alleging the MMR vaccine was the culprit, were dealt a major setback by decision by the Legal Services Commission to withdraw legal aid. This followed advice to the commission by the lawyers representing the parents themselves that the lawsuit had no reasonable prospects of success. Under the Vaccine Damage Payment Scheme (VDPS), it is thought that thousands of unsuccessful claims have been made. The maximum payment per claim is currently £100,000. Disabled vaccine injury patients are allowed to file a claim up to the age of 21. The 'disability threshold' before payments are granted is 60%. The scheme covers vaccinations for illnesses such as tetanus, measles, tuberculosis and meningitis C. As of 2005, the British government had paid out £3.5 million to vaccine injury patients since 1997.

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# Vaccinia Vaccinia virus (VACV or VV) is a large, complex, enveloped virus belonging to the poxvirus family. It has a linear, double-stranded DNA genome approximately 190 kbp in length, and which encodes for approximately 250 genes. The dimensions of the virion are roughly 360 × 270 × 250 nm. Vaccinia virus is well-known for its role as a vaccine that eradicated the smallpox disease, making it the first human disease to be successfully eradicated by mankind. This endeavour was carried out by the World Health Organization under the Smallpox Eradication Program. Post eradication of smallpox, scientists study Vaccinia virus to use as a tool for delivering genes into biological tissues (gene therapy and genetic engineering). Moreover, due to recent concerns about smallpox resurfacing as a possible agent for bioterrorism, scientists have renewed their interests in studying Vaccinia virus. Vaccinia virus is closely related to the virus that causes cowpox; historically the two were often considered to be one in the same. The precise origin of Vaccinia virus is unknown, however, due to the lack of record-keeping as the virus was repeatedly cultivated and passaged in research laboratories for many decades. The most common notion is that Vaccinia virus, cowpox virus, and Variola virus (the causative agent of smallpox), were all derived from a common ancestral virus. There is also speculation that Vaccinia virus was originally isolated from horses. Vaccinia virus is unique among DNA viruses because it replicates only in the cytoplasm of the host cell, outside of the nucleus. Therefore, the large genome is required for encoding various enzymes and proteins involved in viral DNA replication and gene transcription. During its replication cycle, VV produces four infectious forms which differ in their outer membranes: intracellular mature virion (IMV), the intracellular enveloped virion (IEV), the cell-associated enveloped virion (CEV) and the extracellular enveloped virion (EEV). Although the issue remains contentious, the prevailing view is that the IMV consists of a single lipoprotein membrane, while the CEV and EEV are both surrounded by two membrane layers and the IEV has three envelopes. The IMV is the most abundant infectious form and is thought to be responsible for spread between hosts. On the other hand, the CEV is believed to play a role in cell-to-cell spread and the EEV is thought to be important for long range dissemination within the host organism. Vaccinia contains within its genome several proteins that give the virus resistance to interferons. K3L is a protein with homology to the protein eukaryotic initiation factor 2 (eIF-2alpha). K3L protein inhibits the action of PKR, an activator of interferons. E3L is another protein encoded by Vaccinia. E3L also inhibits PKR activation; and is also able to bind to double stranded RNA. A Vaccinia virus infection is very mild and is typically asymptomatic in healthy individuals, but it may cause a mild rash and fever. Immune responses generated from a Vaccinia virus infection protects the person against a lethal smallpox infection. For this reason, Vaccinia virus was, and is still being used as a live-virus vaccine against smallpox. Unlike vaccines that use weakened forms of the virus being vaccinated against, the Vaccinia virus vaccine cannot because it does not contain the smallpox virus. However, certain complications and/or vaccine adverse effects occasionally arise. The chance of this happening is significantly increased in people who are immunocompromised. Approximately one in one million individuals will develop a fatal response to the vaccination. Currently, the vaccine is only administered to health care workers or research personnel who have a high risk of contracting Vaccinia virus, and to the military personnel of the United States of America. Due to the present threat of smallpox-related bioterrorism, there is a possibility the vaccine may have to be widely administered again in the future. Therefore, scientists are currently developing novel vaccine strategies against smallpox which are safer and much faster to deploy during a bioterrorism event. On September 1, 2007, the U.S. Food and Drug Administration (FDA) licensed a new vaccine ACAM2000 against smallpox which can be produced quickly upon need. Manufactured by Acambis Inc. of Cambridge, England, and Cambridge, Massachusets, the U.S. Centers for Disease Control and Prevention stockpiled 192.5 million doses of the new vaccine (derived from the old Dryvax, and made using a pox virus vaccinia). The original vaccine for smallpox, and the origin of the idea of vaccination, was cowpox, reported on by Edward Jenner in 1796. The Latin term used for cowpox was variolae vaccinae, essentially a direct translation of "cow-related pox". That term lent its name to the whole idea of vaccination. When it was realized that the virus used in smallpox vaccination was not, or was no longer, the same as the cowpox virus, the name 'vaccinia' stayed with the vaccine-related virus. (See OED.) In March 2007, a 2-year-old Indiana boy and his mother contracted the life-threatening vaccinia infection from the boy's father. The boy developed the telltale rash over 80 percent of his body after coming into close contact with his father, who was vaccinated for smallpox before being deployed overseas by the United States Army. The United States military resumed smallpox vaccinations in 2002. The child acquired the infection due to eczema, which is a known risk factor for vaccinia infection. The boy was treated with intravenous immunoglobulin, cidofovir, and an experimental drug being developed by SIGA Technologies. On April 19, 2007, he was sent home with no after effects except for possible scarring of the skin.

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# Vaccinia Immune Globulin Vaccinia immune globulin (VIG) is made from the pooled blood of individuals who have been inoculated with the smallpox vaccine. The antibodies these individuals developed in response to the smallpox vaccine are removed and purified. This results in VIG. It can be administered intravenously. It is used to treat individuals who have developed progressive vaccinia after smallpox vaccination. It was also used along with cidofovirinfor the 2003 Midwest monkeypox outbreak as concomitant therapy to reduce the serious side effects of smallpox vaccine. For a small percentage of the population, the smallpox vaccine either doesn't "take" or it produces adverse events. These include postvaccinial central nervous system disease, progressive vaccinia, eczema vaccinatum, accidental implantations, "generalized vaccinia," and the common erythematous and/or urticarial rashes. In the late 1940s, Dr. Henry Kempe suggested that the solution to the complications of the smallpox vaccine was to provide antibodies in the form of gamma globulin. Kempe noted that for some infants, the smallpox vaccine failed to "take." Kempe believed this failure might be due to the high levels of maternal antibodies to vaccinia in the infants' blood. It appeared to Kempe, that the presence of the antibodies blocked viral replication and therefore a transfusion of antibodies from people who were immune due to vaccination, would help those in whom vaccination had failed.

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# Vacuole Vacuoles are found in the cytoplasm of most plant cells and some animal cells. Vacuoles are membrane-bound compartments within some eukaryotic cells that can serve a variety of secretory, excretory, and storage functions. Vacuoles and their contents are considered to be distinct from the cytoplasm, and are classified as ergastic according to some authors. Vacuoles are especially conspicuous in most plant cells. Vacuoles also play a major role in autophagy, maintaining a balance between biogenesis (production) and degradation (or turnover), of many substances and cell structures. They also aid in destruction of invading bacteria or of misfolded proteins that have begun to build up within the cell. The vacuole is a major part in the plant and animal cell. Some protists and macrophages use food vacuoles as a stage in phagocytosis—the intake of large molecules, particles, or even other cells, by the cell for digestion. They are also called "storage sacs." A contractile vacuole is used to pump excess water out of the cell to reduce osmotic pressure and keep the cell from bursting, which is referred to as cytolysis or osmotic lysis. In budding yeast cells, vacuoles act as storage compartments of amino acids and detoxification compartments. Under conditions of starvation, proteins are degraded in vacuoles; this is called autophagy. First, cytoplasms, mitochondrion, and small organelles are covered with multiplex plasma membranes called autophagosomes. Next, the autophagosomes fuse the vacuoles. Finally, the cytoplasms and the organelles are degraded. In a vacuole of budding yeast, black particles sometimes appear, called a dancing body. The dancing body moves actively in the vacuole and appears and disappears within 10 minutes to several hours. In previous research, it was suggested but not proven that the main component of the dancing body is polyphosphate acid. But the main component has been determined to be crystallized sodium polyphosphate and its function has been studied. It is thought that its function is to supply and store phosphates in budding yeast cells. Most mature plant cells have one or several vacuoles that typically occupy more than 30% of the cell's volume, and that can occupy as much as 90% of the volume for certain cell types and conditions. A vacuole is surrounded by a membrane called the tonoplast. This vacuole houses large amounts of a liquid called cell sap, composed of water, enzymes, inorganic ions (like K+ and Cl-), salts (such as calcium), and other substances, including toxic byproducts removed from the cytosol to avoid interference with metabolism. Toxins present in the vacuole may also help to protect some plants from predators. Transport of protons from cytosol to vacuole aids in keeping cytoplasmic pH stable, while making the vacuolar interior more acidic, allowing degradative enzymes to act. Although having a large central vacuole is the most common case, the size and number of vacuoles may vary in different tissues and stages of development. Cells of the vascular cambium, for example, have many small vacuoles in winter, and one large one in summer. Aside from storage, the main role of the central vacuole is to maintain turgor pressure against the cell wall. Proteins found in the tonoplast control the flow of water into and out of the vacuole through active transport, pumping potassium (K+) ions into and out of the vacuolar interior. Due to osmosis, water will diffuse into the vacuole, placing pressure on the cell wall. If water loss leads to a significant decline in turgor pressure, the cell will plasmolyse. Turgor pressure exerted by vacuoles is also helpful for cellular elongation: as the cell wall is partially degraded by the action of auxins, the less rigid wall is expanded by the pressure coming from within the vacuole. Vacuoles can help some plant cells to reach considerable size. Another function of a central vacuole is that it pushes all contents of the cell's cytoplasm against the cellular membrane, and thus keeps the chloroplasts closer to light. Vacuoles in animals are a part of the processes of exocytosis and endocytosis. Exocytosis is the extrusion process of proteins from the Golgi apparatus initially enter secretory granules, where processing of prohormones to the mature hormones occurs before exocytosis, and also allows the animal cell to rid waste products. Endocytosis is the reverse of exocytosis. There are various types. Phagocytosis ("cell eating") is the process by which bacteria, dead tissue, or other bits of material visible under the microscope are engulfed by cells. The material makes contact with the cell membrane, which then invaginates. The invagination is pinched off, leaving the engulfed material in the membrane-enclosed vacuole and the cell membrane intact. Pinocytosis ("cell drinking") is essentially the same process, the difference being that the substances ingested are in solution and not visible under the microscope Hydropic (vacuolar) changes are of importance of identifying various pathologies, such as the reversible cell swelling in renal tubules caused by hypoperfusion of the kidneys during open heart surgery.

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# Vasovagal syncope Vasovagal syncope is the most common type of syncope (fainting). There are a number of different syncope syndromes which all fall under the umbrella of vasovagal syncope. The common element among these conditions is the central mechanism leading to loss of consciousness. The differences among them are in the factors which trigger this mechanism. You do not need to be bradycardic to have heightened vagal tone. Vagal episodes are common following procedures such as cardiac catheterization, and this chapter discusses the management of this complication. Regardless of the trigger, the mechanism of syncope is similar in the various vasovagal syncope syndromes. In it, the nucleus tractus solitarius of the brainstem is activated directly or indirectly by the triggering stimulus, resulting in simultaneous enhancement of parasympathetic nervous system (vagal) tone and withdrawal of sympathetic nervous system tone. One account for these physiological responses is the Bezold-Jarisch Reflex. This reflex involves a variety of cardiovascular and neurological processes, which can be summarized as follows: Prolonged upright posture results in some degree of pooling of blood in the lower extremities that can lead to diminished intracardiac volume. This phenomenon is accentuated if the individual is dehydrated. The resultant arterial hypotension is sensed in the carotid body baroreceptors, and afferent fibers from these receptors trigger autonomic signals that increase cardiac rate and contractility. However, pressure receptors in the wall and trabeculae of the underfilled left ventricle may then sense stimuli, indicating high-pressure C-fiber afferent nerves from these receptors. They may respond by sending signals that trigger paradoxical bradycardia and decreased contractility, resulting in additional and relatively sudden arterial hypotension. People with vasovagal syncope typically have recurrent episodes, usually when exposed to a specific trigger. The initial episode often occurs when the person is a teenager, then recurs in clusters throughout his or her life. Prior to losing consciousness, the individual frequently experiences a prodrome of symptoms such as lightheadedness, nausea, sweating, ringing in the ears, and visual disturbances. These last for at least a few seconds before consciousness is lost, which typically happens when the person is sitting up or standing. When they pass out, they fall down; and when in this position, effective blood flow to the brain is immediately restored, allowing the person to wake up. In addition to the mechanism described above, a number of other medical conditions may cause syncope. Making the correct diagnosis for loss of consciousness is one of the most difficult challenges that a physician can face. The core of the diagnosis of vasovagal syncope rests upon a clear description by the patient of a typical pattern of triggers, symptoms, and time course. Also is pertinent to differentiate lightheadedness, vertigo and hypoglycemia as other causes Treatment for vasovagal syncope focuses on avoidance of triggers, restoring blood flow to the brain during an impending episode, and measures which interrupt or prevent the pathophysiologic mechanism described above.

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# Vagifem Vagifem is an estrogen replacement consisting of estradiol and is used primarily after menopause to relieve symptoms of atrophic vaginitis such as vaginal dryness, soreness, and itching. It is available as vaginal tablets, and as such, the route of administration is per vagina.

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# Vagina The vagina, (from Latin, literally "sheath" or "scabbard" ) is the cylinder tubular tract leading from the uterus to the exterior of the body in female placental mammals and marsupials, or to the cloaca in female birds, monotremes, and some reptiles. Female insects and other invertebrates also have a vagina, which is the terminal part of the oviduct. The Latinate plural (rarely used in English) is vaginae. In common speech, the term "vagina" is often used inaccurately to refer to the vulva or female genitals generally; strictly speaking, the vagina is a specific internal structure and the vulva is the exterior genitalia only. The human vagina is an elastic muscular canal that extends from the cervix to the vulva. Although there is wide anatomical variation the average vagina is 6 to 7 inches (15 to 18 cm) in length; its elasticity allows it to stretch during sexual intercourse and during birth to offspring. The vagina connects the superficial vulva to the cervix of the deep uterus. If the woman stands upright, the vaginal tube points in an upward-backward direction and forms an angle of slightly more than 45 degrees with the uterus. The vaginal opening is at the caudal end of the vulva, behind the opening of the urethra. Above the vagina is Mons Veneris. The vagina, along with the inside of the vulva, is reddish pink in color, as with most healthy internal mucous membranes in mammals. Vaginal lubrication is provided by the Bartholin's glands near the vaginal opening and the cervix. The membrane of the vaginal wall also produces moisture, although it does not contain any glands. Before and during ovulation, the cervix produces cervical mucus, which provides a favorable environment for sperm to survive. The hymen is a membrane which is situated at the opening of the vagina. As with many female animals, the hymen covers the opening of the vagina from birth until it is ruptured during activity. The hymen may rupture during sexual or non-sexual activity; the presence or absence of a hymen does not indicate prior sexual activity. The vagina provides a path for menstrual blood and tissue to leave the body. In modern societies, tampons, menstrual cups, and sanitary towels may be used to absorb or capture these fluids. The concentration of the nerve endings that lie close to the entrance of a woman's vagina can provide pleasurable sensation during sexual activity, when stimulated in a way that the particular woman enjoys. During sexual arousal and particularly stimulation of the clitoris, the walls of the vagina self-lubricate, reducing friction during sexual activity. An erogenous zone referred to commonly as the G-spot is located at the anterior wall of the vagina, about five centimeters in from the entrance. Some women experience intense pleasure if the G-spot is stimulated appropriately during sexual activity. A G-Spot orgasm may be responsible for female ejaculation, leading some doctors and researchers to believe that G-spot pleasure comes from the Skene's glands, a female homologue of the prostate, rather than any particular spot on the vaginal wall. Some researchers deny the existence of the G-spot. During childbirth, the vagina provides the route to deliver the baby from the uterus to its independent life outside the body of the mother. During birth, the vagina is often referred to as the birth canal. The vagina is remarkably elastic and stretches to many times its normal diameter during vaginal birth. The vagina is self-cleansing and therefore usually needs no special treatment. Since a healthy vagina is colonized by a mutually symbiotic flora of microorganisms that protect its host from disease-causing microbes, any attempt to upset this balance may cause many undesirable outcomes, including abnormal discharge and yeast infection. The acidity of a healthy vagina due to lactic acid secreted by symbiotic microorganisms retards the growth of many strains of dangerous microbes. The vagina is examined during gynecological exams, often using a speculum, which holds the vagina open for visual inspection of the cervix or taking of samples (see pap smear). The presence of unusual lumps in the wall or base of the vagina is always abnormal. The most common of these is Bartholin's cyst. The cyst, which can feel like a pea, is formed by a blockage in glands which normally supply the opening of the vagina. This condition is easily treated with minor surgery or silver nitrate. Other less common causes of small lumps or vesicles are herpes simplex. They are usually multiple and very painful with a clear fluid leaving a crust. They may be associated with generalized swelling and are very tender. Lumps associated with cancer of the vaginal wall are very rare and the average age of onset is seventy years . The most common form is squamous cell carcinoma, then cancer of the glands or adenocarcinoma and finally, and even more rarely, melanoma. The great majority of vaginal discharges are normal or physiological and include blood or menses (from the uterus), the most common, and clear fluid either as a result of sexual arousal or secretions from the cervix. Other noninfective causes include dermatitis, discharge from foreign bodies such as retained tampons or foreign bodies inserted by curious children. Non-sexually transmitted discharges occur from bacterial vaginosis and thrush or candidiasis. The final group of discharges include sexually transmitted diseases, gonorrhoea, Chlamydia and Trichomonas. The discharge from thrush is slightly pungent and white, that from Trichomonas more foul and greenish and that from foreign bodies resembles the discharge of gonorrhea, greyish or yellow and purulent (like pus). All sores involve a break down in the walls of the fine membrane of the vaginal wall. The most common of these are abrasions and small ulcers caused by trauma. While these can be inflicted during rape most are actually caused by excessive rubbing from clothing or improper insertion of a sanitary tampon. The typical ulcer or sore caused by syphilis is painless with raised edges. These are often undetected because they occur mostly inside the vagina. The sores of herpes which occur with vesicles are extremely tender and may cause such swelling that passing urine is difficult. In the developing world a group of parasitic diseases also cause vaginal ulceration such as Leishmaniasis but these are rarely encountered in the West. HIV/AIDS can be contracted through the vagina during intercourse but is not associated with any local vaginal or vulval disease . All the above local vulvovaginal diseases are easily treated. Often only shame prevents patients from presenting for treatment

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# Vaginal birth after caesarean Vaginal birth after caesarean (VBAC) refers to the practice of delivering a baby vaginally (naturally) after a previous baby has been delivered through caesarean section (surgically). . A caesarian section leaves a scar in the wall of the uterus. This scar is weaker than the normal uterine wall, so if the woman goes in labor in a subsequent pregnancy there is a higher than normal risk of a ruptured uterus, a catastrophic complication. Because of this risk an attempt at normal vaginal delivery was for most of the 20th century considered unacceptably risky. This opinion was challenged by many studies showing that many women with previous caesaran sections did have successful vaginal deliveries. In the 1980s and 1990s there was a strong movement to encourage attempts at vaginal delivery after caesarean section. For a while some regulatory bodies in the US monitored the percentage of those women with previous caesareans who were offered vaginal delivery, using this number as a measure of the quality of obstetrical care. Studies in the 1990s confirmed that vaginal delivery after previous caesaran section was indeed much riskier than average. The American College of Obstetrics and Gynecology issued guidelines which identify VBAC as a high-risk delivery requiring the availabilty of an anesthesiologist, an obstetrician, and on operating room on standby (Int J Gyn Obs; 1999; vol 66, p197). In the 1990s the rate at which VBAC was tried fell from 26% to 13%. According to the American Pregnancy Association, 90% of women who have undergone cesarean deliveries are candidates for VBAC. From 60-80% of women opting for VBAC will successfully give birth vaginally. The decision to have a trial of VBAC is made by the mother with the advice of her obstetrician. The decision is guided by an assessment of the known risk factors for complications. In general, an attempt at VBAC is safe if there are no other identified risk factors. Risks of cesarean section include a higher chance of re-hospitalization after birth, infertility, and uterine rupture in the next birth.[citation needed] The risk of uterine rupture in a VBAC is 0.2% to 1.5%. Because of the risks involved, many health insurance companies will not support VBAC. Today only about 10% of eligible women in the United States try VBAC. It is also difficult to find a hospital or doctor willing to do a VBAC because of ACOG's insistence on stringent safety guidelines. The doctor of a VBAC patient is required to be at the hospital throughout the entire labor, and an anesthesiologist needs to be immediately available. The risk of infection doubles if vaginal delivery is attempted but results in another cesarean. . All complications of cesarean section are more likely and more severe if it is done as an emergency after a failed attempt at vaginal delivery rather than as a planned operation. The benefits of a VBAC are as follows. There is less medical risk to the mother and the baby than a repeat cesarean. There is less blood loss and therefore fewer transfusions are needed. There is less risk of infection for the mother and the infant. It is less costly to have a VBAC and the recovery time is shorter. A VBAC can also often help the mother mentally. Women are often depressed or angry about the first cesarean and see a VBAC as righting a past wrong. The mother and infant have more time for immediate bonding, and nursing is often easier. VBAC is not uncommon today. The medical practice until the late 1970s was "once a caesarean, always a caesarean" but a consumer-driven movement supporting VBAC changed the medical practice. Rates of VBAC rose in the 80s and early 90s, they have fallen since.

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/index.php/Vaginal_cancer

# Vaginal cancer History and Symptoms | Physical Examination | Staging | Laboratory Findings | X Ray | CT | MRI | Ultrasound | Other Imaging Findings | Other Diagnostic Studies

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/index.php/Vaginal_discharge

# Vaginal discharge Vaginal discharge is a common patient complaint that is paired with anxiety regarding sexually transmitted diseases. If a STD is detected, a search for all other STDs should be done. Advise the infected patient to inform all sexual partners of their diagnosis.Also there is normal vaginal discharge depends on periodic hormonal change Vaginal discharge is a common complaint in primary care which can be a subjective complaint or an objective finding. So, it is important to differentiate between normal physiological discharge and pathological discharge. Vaginal discharge is a mixture of liquid, cells, and bacteria that lubricate and protect the vagina. It is produced by the cells of the vagina and cervix. Normal vaginal discharge changes with the menstrual cycle, such as the character of the discharge is clearer with a stretchable consistency around ovulation, then may be thicker and slightly yellow during the luteal phase. Normal healthy discharge should not be associated with symptoms such as itching, redness and swelling, and does not have a strong odor. It is important to take complete history and ask about the associated symptoms like dysuria, dyspareunia, lower abdominal pain, itching, and fever. While considering the causes, it is necessary to distinguish between infectious and non-infectious. The infectious causes are infection with Candida albicans, Trichomonas vaginalis, Gardnerella vaginalis, Chlamydia trachomatis, Neisseria gonorrhea, Herpes Simplex Virus. Diagnosis must be confirmed by laboratory tests and cultures. Non-infectious causes include puberty, menstrual cycle, foreign body, cervical cancer, vaginal cancer, diabetes etc. Treatment depends on the cause of the discharge.

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/index.php/Vaginal_discharge_resident_survival_guide

# Vaginal discharge resident survival guide Vaginal discharge is a common complaint in primary care which can be a subjective complaint or an objective finding. So, it is important to differentiate between normal physiological discharge and pathological discharge. Vaginal discharge is a mixture of liquid, cells, and bacteria that lubricate and protect the vagina. It is produced by the cells of the vagina and cervix. Normal vaginal discharge changes with the menstrual cycle, such as the character of the discharge is clearer with a stretchable consistency around ovulation, then may be thicker and slightly yellow during the luteal phase. Normal healthy discharge should not be associated with symptoms such as itching, redness and swelling, and does not have a strong odor. It is important to take complete history and ask about the associated symptoms like dysuria, dyspareunia, lower abdominal pain, itching, and fever. While considering the causes, it is necessary to distinguish between infectious and non-infectious. The infectious causes are infection with Candida albicans, Trichomonas vaginalis, Gardnerella vaginalis, Chlamydia trachomatis, Neisseria gonorrhea, Herpes Simplex Virus. Diagnosis must be confirmed by laboratory tests and cultures. Non-infectious causes include puberty, menstrual cycle, foreign body, cervical cancer, vaginal cancer, diabetes etc. Treatment depends on the cause of the discharge.

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/index.php/Vaginal_flatulence

# Vaginal flatulence Vaginal flatulence (flatus vaginalis in Latin) is an emission or expulsion of air from the vagina, often during or after sexual intercourse or (less often) other sexual acts, stretching or exercise. The sound is somewhat comparable to flatulence from the anus but does not involve waste gases and thus often has no specific odor associated. Vaginal gas that involves strong odor or fecal matter may be a result of colovaginal fistula, a serious condition involving a tear between the vagina and colon, which can result from surgery, child birth, diseases (such as Crohn's disease), and other causes. This condition can lead to urinary tract infection and other complications. A doctor should be consulted if symptoms of colovaginal fistula occur. Air which is forced into the vagina, especially by blowing in order to cause vaginal flatulence during cunnilingus, can cause an air embolism. This is a potentially life-threatening condition for a woman and also for her child if she is pregnant at the time. Queef (onomatopoeia), pussy fart, and vart are slang terms which refer to vaginal flatulence. The term fanny fart is also commonly used in Britain and Australia. .

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/index.php/Vaginal_flora

# Vaginal flora The human vaginal region has a higher concentration of bacteria, than any other part of the body, save the colon . The bacteria of the vaginal flora were discovered by the gynecologist Albert Döderlein in 1892. Primarily, these bacteria consist of lactobacilli , and are collectively referred to as the vaginal flora. The amount and type of bacteria present have significant implications for a woman's overall health. These bacteria and the lactic acid they produce, in combination with fluids secreted during sexual arousal, are greatly responsible for the characteristic odor associated with the vaginal area. During menstruation, the concentration of vaginal flora is observed to decline. The effect of tampon use on vaginal flora is debated, but safe application of sterile tampons appears not to significantly modify the balance of bacterial presence. A healthy vaginal flora aids in the prevention of yeast infections and other possible problems by occupying the chemical resources otherwise utilized by pathogen organisms. However, harmful bacteria or an imbalance in bacteria can lead to infection. One method of reducing the risk of infection in the local area of the urethra is to urinate immediately after sex. Additionally, exclusive use of sterile contraceptives can assist in prevention of infection.

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/index.php/Vaginal_lubrication

# Vaginal lubrication Vaginal lubrication is the naturally produced lubricating fluid that reduces friction during sexual intercourse. It is often produced on occasions of women's sexual arousal. Vaginal dryness is the condition in which this lubrication is insufficient. The lubrication fluid contains water, pyridine, squalene, urea, acetic acid, lactic acid, complex alcohols and glycols, ketones, and aldehydes. The fluid is typically clear and more resembling of male pre-ejaculate than male ejaculate. It can vary in consistency, texture, color, and odor, depending on sexual arousal, the time of the menstrual cycle, the presence of an infection, and diet. Vaginal fluid is slightly acidic and can become more acidic with certain sexually transmitted diseases. The normal pH of vaginal fluid is between 3.8 and 4.5, whereas male semen is typically between 7.2 and 8.0 (a neutral substance has a pH of 7.0) . Certain medications, including some over-the-counter antihistamines, as well as life events such as pregnancy, lactation, menopause, aging or diseases such as diabetes, will inhibit lubrication. Medicines with anticholinergic or sympathomimetic effects will dry out the "mucosal" or wet tissues of the vagina. Such medicines include many common drugs for allergic, cardiovascular, psychiatric, and other medical conditions. Safe sex educators warn that the vaginal fluids of a woman who is infected with HIV or other STIs can transmit the disease, even in the absence of direct penile-vaginal sexual intercourse, so direct contact is discouraged. When natural lubrication is insufficient, penetrative intercourse may be uncomfortable or painful. A personal lubricant applied to the vaginal opening and/or the penis can prevent this discomfort. More rarely, a vaginal suppository may be inserted prior to intercourse. Oil-based lubricants can weaken latex and reduce the effectiveness of condoms, latex gloves, or dental dams as either forms of birth control or for protection from sexually transmitted diseases, so water- or silicone-based lubricants are often used instead.

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/index.php/Vaginal_process

# Processus vaginalis In males, it precedes the testis in their descent down within the gubernaculum, and closes. This closure occurs at any point from a few weeks before birth, to a few weeks after birth. The remaining portion around the testes becomes the tunica vaginalis. There is the potential for an inguinal hernia to develop, although not all people with a patent processus vaginalis will develop one. The more patent the processus vaginalis, the more likely the patient is to develope a hernia.

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/index.php/Vaginal_prolapse

# Vaginal prolapse Vaginal prolapse is characterized by a portion of the vaginal canal protruding from the opening of the vagina. The condition usually occurs when the pelvic floor collapses as a result of childbirth and is inherent among tall Caucasian women. Vaginal prolapse was first discovered in era of the pharaohs, about 1500 years before Christ. Then MRI/surgery was developed by Hippocrates to treat/diagnose vaginal prolapse over the centuries, different treatment modalities, some of which we can currently seem strange Vaginal prolapse may be classified according to Uterine cervical elongation that found in patients undergoing hysterectomy for pelvic organ prolapse, Cervical elongation grades and prolapse stages are correlated. Vaginal prolapse is classified as physiological uterine cervical elongation based on corpus/cervix ratio to (grade 0, CCR>1.5) grade I (CCR>1 and ≤1.5) grade II (CCR>0.5 and ≤1), and grade III (CCR≤0.5) The pathogenesis of Pelvic organ prolapse like vaginal prolapse is not fully understood. It is thought that vaginal prolapse is characterized by two main theories predominate: either the fibromuscular layer of the vagina develops a defect/tears away from its supports, or its tissues are stretched and attenuated, Pelvic organ prolapse is a hernia of the vaginal wall. The utero-sacral ligaments and the arcus tendineus of the pelvic fascia lose their elasticity. Atrophic levator anii muscles do not play their trempoline, active support anymore To the pelvic floor. That is related to the aging of these structures but also to excessive mechanical strains -pregnancy, delivery, dyschesia, physical practices-. Moreover, postural disorders lead to a direct orientation of these strains on the genital slit Prolapse and urinary incontinence often occur concomitantly and cystocele, rectocele, enterocele, uterine descent or vaginal vault prolapse may also be present. The pathophysiology of prolapse encompasses direct and indirect injury, metabolic abnormalities and chronic high intra-abdominal pressure. Anterior vaginal wall prolapse may present as stress incontinence A new minimally invasive surgical procedure is effective in restoring a woman's anatomy to the condition before childbirth with a two weeks recovery period. It is performed vaginally using a laparoscope and surgical mesh to repair the cystocele and rectocele and a laser to tighten the vaginal canal, which create a natural support for the uterus [./Vaginal_prolapse#cite_note-pmid:_8934045-35 ]

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/index.php/Vaginal_ring

# Vaginal ring Vaginal rings (also known as intravaginal rings, or V-Rings) are 'doughnut-shaped' polymeric drug delivery devices designed to provide controlled release of drugs to the vagina over extended periods of time. Several vaginal ring products are currently available, including: General - Vaginal rings are easily inserted and removed. Vaginal walls hold them in place. Although their exact location within the vagina is not critical for clinical efficacy, rings commonly reside next to the cervix. Rings are typically left in place during intercourse, and most couples report no interference or discomfort. In many cases, neither partner feels the presence of the ring. Rings can be removed prior to intercourse, but in the case of the contraceptive Nuvaring only for one to three hours in order to maintain efficacy of birth control. Issues have been raised about the biodegradability of the product given the recent concern about pollution and use of plastics, especially of the poly(ethylene-co-vinyl+) archetypes.[citation needed]

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/index.php/Vaginal_septum

# Vaginal septum A longitudinal vaginal septum develops during embryogenesis when there is an incomplete fusion of the lower parts of the two mullerian ducts. As a result there is a double vagina. There may be associated duplications of the more cranial parts of the mullerian derivatives, a double cervix, and either a uterine septum or uterus didelphys (double uterus). The person with a longitudinal vaginal septum may be asymptomatic and not aware of the condition. If dyspareunia is a problem a simple resection of the septum could be performed. A transverse septum can form during embryogenesis when the mullerian ducts fuse improperly to the urogenital sinus. A complete transverse will block menstrual flow and is a cause of primary amenorrhea. The accumulation of menstrual debris behind the septum is termed cryptomenorrhea. Some transverse septa are incomplete and may lead to dysparunia or obstruction in labor. A surgical incision will relieve the situation. Transverse vaginal septum must be differentiated from other diseases that cause latency in secondary sexual characteristics development, such as constitutional delay of puberty, hypopituitarism, delayed puberty, and chromosomal abnormalities. Chromosomal abnormalities are Turner's syndrome, and Noonan's syndrome.

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/index.php/Vaginal_venous_plexus

# Vaginal venous plexus The vaginal plexuses are placed at the sides of the vagina; they communicate with the uterine, vesical, and hemorrhoidal plexuses, and are drained by the vaginal veins, one on either side, into the hypogastric veins.

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/index.php/Vaginectomy

# Vaginectomy Vaginectomy is a medical procedure to remove all or part of the vagina. It is usually used as a treatment for vaginal cancer. Vaginectomy is also used as part of some types of female-to-male sex reassignment surgery. An operation under which the whole vagina is removed is called a radical vaginectomy. If only the upper part of the vagina is removed then the operation is called a partial vaginectomy. The doctor will decide depending the severity of the case and the affected areas.

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/index.php/Vaginismus

# Vaginismus Vaginismus (the German equivalent of the word Vaginism) is a condition which affects a woman's ability to engage in any form of vaginal penetration, including sexual penetration, insertion of tampons, and the penetration involved in gynecological examinations. This is the result of a conditioned reflex of the pubococcygeus muscle, which is sometimes referred to as the 'PC muscle'. The reflex causes the muscles in the vagina to tense suddenly, which makes any kind of vaginal penetration -- including sexual penetration -- either painful or impossible. A vaginismic woman does not consciously control the spasm. The vaginismic reflex can be compared to the response of the eye shutting when an object comes towards it. The severity of vaginismus varies from woman to woman. The conditioned reflex can create a vicious circle for vaginismic women. One example: if a teenage female learns that the first time she engages in penetrative sex that it will be painful, she may develop vaginismus because she expects pain. If she then attempts to engage in penetrative sex, the muscle spasm will make penetrative sex painful. This and each further attempt at sexual penetration confirms her fear of pain and may worsen the condition. Naturally, penetration may be extremely painful without vaginismus or psychological prerequisite as well. Primary vaginismus occurs when a woman has never been able to have penetrative sex or achieve any kind of vaginal penetration. It is commonly discovered in teenagers and women in their early twenties, as this is when many young women in the Western world will initially attempt to use tampons, have penetrative sex, or undergo a pap smear. Women who have vaginismus may not be aware of their condition until they attempt vaginal penetration. It may be confusing for a woman to discover she has vaginismus. She may believe that vaginal penetration should be naturally easy, or she may be unaware as to the reason for her condition. Secondary vaginismus occurs when a woman who has previously been able to achieve penetration develops vaginismus. This may be due to physical causes such as a yeast infection or trauma during childbirth, or it may be due to psychological causes. The treatment for secondary vaginismus is the same as for primary vaginismus, although, in these cases, previous experience with successful penetration can assist in a more rapid resolution of the condition. There are a variety of factors that can contribute to vaginismus. These may be psychological or physiological, and the treatment required can depend on the reason that the woman has developed the condition. As each case is different, an individualized approach to treatment is useful. The condition will not necessarily become more severe if left untreated, unless the woman is continuing to attempt penetration, despite feeling pain. Some women may choose to refrain from seeking treatment for their condition. According to the Cochrane Collaboration review of the scientific literature, "In spite of encouraging results reported from uncontrolled case series there is very limited evidence from controlled trials concerning the effectiveness of treatments for vaginismus. Further trials are needed to compare therapies with waiting list control and with other therapies." Although few controlled trials have been carried out, many serious scientific studies have tested and proved the efficacy of the treatment of vaginismus. In all cases where the systematic desensitization method was used, success rates were close to 90-95% and even 100%. For an example of one of these studies, see Nasab, M., & Farnoosh, Z., or for a basic review, see Reissing's literature review. (links below) According to Ward and Ogden's qualitative study on the experience of vaginismus for women (1994), the three highest ranked causes for vaginismus are usually fear of painful sex, strict religious upbringing where sex was viewed as wrong or not discussed, and early childhood traumatic experiences (not necessarily sexual in nature). It is important to address the psychological aspects of the problem as well as the actual muscle spasm. A woman may choose to address the issue on her own terms, or she may avail the help of a therapist. Many people -- even some professionals -- are not aware of the emotional difficulties associated with vaginismus, which can include low self-esteem, fears, and depression. Women with this condition may wish to seek an understanding professional who has previous experience with women who experience vaginismus. A therapist who has a positive attitude towards sex and the human body may be beneficial. Physical treatment of the internal spasms may include sensate focus exercises, exploring the vagina through touch, and desensitization with vaginal dilators. Dilating involves inserting objects, usually phallic in shape, into the vagina. In treating the spasms through dilation, the objects used gradually increase in size as the woman progresses. Medical dilators may be obtained online, though they may be expensive. If a woman suspects she has vaginismus, sexual penetration is likely to remain painful or impossible until her vaginismus is addressed. Women with vaginismus may be able to engage in other sexual activities, as long as penetration is avoided. Sexual partners of vaginismic women may come to believe that vaginismic women do not want to engage in penetrative sex at all, though this may not be true. Many vaginismic women do wish to engage in penetrative sex, but are deterred by the pain and emotional distress that comes with each attempt. Women with vaginismus may not realize that most women who do not have vaginismus usually do experience pain or discomfort if they attempt sexual penetration without prior sexual arousal. Most women acknowledge sexual arousal as integral to painless sexual penetration so self-exploration of the vaginal area through masturbation can be beneficial in addressing vaginismus. One of the problems that can come with vaginismus is that a woman may be fearful to engage in sexual activity, due to the fear of pain with any kind of vaginal penetration. Solo masturbation, with or without penetration, can alleviate this fear, as well as the psychological pressure to 'perform' sexually or become aroused quickly, with a partner. Despite popular belief, orgasm need not be the goal of masturbation. The reason may be to simply increase comfort with the genital area, to explore various sensations through genital and clitoral touch, and to become aware of those sensations which are relaxing and pleasurable. Sexual arousal causes changes in the shape and color of the vulva, as well as in the vaginal lubrication produced. As a woman becomes more aware of her individual sexual response, she can learn which sensations are best for bringing her to a state of arousal. She will then be better equipped to teach her partner(s) which sensations feel best for her. A wide range of emotions may surface during masturbation and other forms of genital exploration. Some women have negative associations with their genitals, including fears that their genitals are dirty, smelly, oddly shaped, or ugly. These associations can lead to negative emotions arising during any kind of sexual expression, including masturbation, and these emotions can take time to process. Especially in the case of a vaginismic woman, feelings of shame, inadequacy or of being 'defective' can be deeply troubling. Relaxation, patience and self-acceptance are vital to a pleasurable experience. The process of addressing vaginismus requires time, patience, and a focused personal intention to heal. In almost all cases it can be successfully treated.

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/index.php/Vaginitis

# Vaginitis Vulvovaginitis, a common condition for which women seek medical care, accounts for greater than 10% of visits made to providers of women's health care. It is characterized by symptoms that cause itching, irritation, burning, and abnormal vaginal discharge. The three most common causes of vaginal discharge in women within the reproductive age group are bacterial vaginosis, candida vulvovaginitis, and trichomoniasis. All patients with vulvovaginitis present with common symptoms like vaginal discharge, itching, and dysuria. Diagnosis of vulvovaginitis requires a detailed history of the patient's symptoms, as well as her sexual history, both of which facilitate an accurate diagnosis. Physical examination of the external genitalia and speculum examination should focus on documenting the nature of the discharge, the presence of any vulvar or labial lesions, foreign body, presence of cervical inflammation, cervical lesions, and any cervical motion or adnexal tenderness with a bimanual examination. It is essential to rule out pelvic inflammatory disease and cervical lesions as the cause of vaginal discharge. Estimation of vaginal pH and vaginal smear wet mount examination constitute the initial diagnostic test, which helps differentiate among common etiologies. Treatment of vulvovaginitis includes medical therapy targeted against the causative pathogen and counseling on hygiene, voiding techniques, and sexual practices. The prognosis is good in most patients, though a minority of patients experience recurrence.

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/index.php/Vaginoplasty

# Vaginoplasty Vaginoplasty is any surgical procedure whose purpose is to treat vaginal structural defects, affect aesthetic considerations, or to partially or totally construct or reconstruct a vagina. The term vaginoplasty is used to describe any such vaginal surgery, while the term neovaginoplasty is more specifically used to refer to procedures of partial or total construction or reconstruction of the vulvovaginal complex. There are many different vaginoplasty techniques. Some involve the use of autologous biological tissue from other parts of the body of the patient to construct areas of vagina. Areas that may be used include oral mucosa, skin flaps, skin grafts, the vaginal labia, penile skin and/or tissue, scrotal skin, intestinal mucosa, and others. Neovaginoplasty is a reconstructive surgery procedure used to construct or reconstruct a vaginal canal and mucous membrane. These may be absent in a woman, due either to congenital disease such as vaginal atresia or to an acquired cause, such as trauma or cancer. Some transwomen opt for vaginoplasty as part of their gender transition. The outcome of neovaginoplasty is variable. It usually allows sexual intercourse, although sensation is not always present. In genetic women, menstruation and fertilization are assured when the uterus and ovaries have preserved a normal function. In a few cases, vaginal childbirth is possible. Most neovaginoplasty procedures are performed on transsexual women. The penile inversion technique was perfected by the late Georges Burou during his pioneering work in sex reassignment surgery. For the creation of the male-to-female neovagina, there is also the possibility of using penile skin flaps (so-called penile inversion), as well as the "Suporn technique" and "Wilson method". In the 1990s and continuing to the present, neovaginal construction has been further advanced by Toby R. Meltzer, M.D., whose technique involves the use of both penile and scrotal tissue to form the vaginal vault, and has yielded more reliable sexual sensation, maintenance of vaginal depth, and a stronger pelvic floor by maintaining a nearly intact levitor ani muscle complex. Meltzer creates a neurologically sensate clitoris, constructed from a penile glans pedicle, with its attached blood supply and nerves. During a secondary procedure using Meltzer's technique, he forms a labia hood for the clitoris using the inverted Y plasty suturing method, leaving only a single midline incision scar. When the transwoman is ready, there are two steps to Sexual Reassignment Surgery. The first procedure is called Vaginoplasty. Vaginoplasty is the procedure that essentially turns the penis into the vagina. It is often followed several months later by the Labiaplasty. The Labiaplasty refines the labia or external female genitalia. During Vaginoplasty "the right spermatic cord is clamped and ligated. The primary incision is continued up the ventral side of the shaft of the penis. [Then] the anterior flap is developed from the skin of the penis. The urethra is dissected from the shaft. The corpora cavernosa are separated to assure a minimal stump. [After that] the anterior flap [is] perforated to position the urethral meatus. The skin flaps are sutured and placed in position in the vaginal cavity. [When that is completed], the preservation of the vaginal cavity is assured by the use of a suitable vaginal form." Finally the vagina is complete. When a patient receives Labiaplasty, a frequently used procedure, labia and a clitoral hood are created. This is often performed a few months after the first part of the procedure. In some cases, labiaplasty is an elective procedure to improve appearance after a one-stage Vaginoplasty. Labiaplasty (2000). Even after SRS there are many complications that range from minor to major. There are the minor complications which include infections, bleeding and loss of grafted skin. "The more serious complications include major infections or bleeding, and damage to the bladder. There is a possibility of damage to the prostate or major nerves during the dissection to form the vagina." While undergoing this surgery the most severe complication is the formation of a vaginal-rectal fistula. This occurs when the doctor accidentally cuts through the rectal wall during vaginal cavity dissection. As a result, excrement bypasses the anal stricture and exits through the vagina. This prevents proper healing. This process can be remedied through a long process of surgeries and many months of wearing of a colostomy bag. Because of the embarrassment, the complication often goes untreated, leading to serious infections. The Vecchietti procedure is a laparoscopic procedure that has been shown to result in a vagina that is comparable to a normal vagina in patients with Mullerian agenesis. With colovaginoplasty, sometimes called a colon section, a vagina is created by cutting away a section of the sigmoid colon and using it to form a vaginal lining. This surgery is performed on females with androgen insensitivity syndrome, congenital adrenal hyperplasia, vaginal agenesis, Müllerian agenesis, and other intersexed conditions, where non-invasive forms of lengthening the vagina cannot be done and, mostly, on male-to-female transsexuals as an alternative to penile inversion with or without an accompanying skin graft (usually from either the thigh or abdomen). Penile inversion is a surgical technique for genital reassignment (sex change) used to construct a neo-vagina from a penis for transwomen, sometimes also for intersex people. It is one of two main sorts of vaginoplasty, along with colovaginoplasty. The erectile tissue of the penis is removed, and the skin, with its blood and nerve supplies still attached (a flap technique first used by Sir Harold Gillies in 1951), is used to create a vestibule area and labia minora, and inverted into a cavity created in the pelvic tissue. Part of the tip (glans) of the penis, still connected to its blood and nerve supplies, is usually used to construct a clitoris, the urethra is shortened to end at a place that is appropriate for a female anatomy. There are two ways to create a clitoris for a transsexual woman. The most common method is to remove the head or glans of the penis, and use some of that tissue to function in the position of a biological woman's clitoris. Some transsexual women have the entire penis head used as their clitoris. Some transsexual women have spongiform from their urethras to function as the neoclitoris. The success rate for the creation of a clitoris for transsexual women varies greatly. If the relocation of the glans penis is successful then the transsexual woman may have a sensate neoclitoris capable of orgasm. The glans penis tissue does not resemble a biological woman's clitoris. Most transsexual women's bodies readily accept the relocation of glans penile tissue in the area of a biological woman's clitoris. However, as with all surgeries nothing is perfect and there have been cases of the glans penis neoclitoris bleeding and even falling off entirely. There are many SRS surgeons who do not attempt any creation of a neoclitoris for their transsexual patients. Instead they allow the transwoman to orgasm with the penile lined vagina. Some SRS surgeons do not agree with using the head of the penis to create a neoclitoris. They prefer to either use urethral spongiform or make no attempt at the creation of a clitoris at all. Some SRS surgeons take the head of the penis and surgically place it inside the body in the position of a cervix. The late Stanley Biber preferred this method. Many transsexual women like the glans penis being inside their bodies because it can be greatly stimulated during vaginal penetration. The transsexual activist and playwright Kate Bornstein has indicated in her book 'Gender Outlaw: On Men, Women and The Rest Of Us' that her glans penis was placed inside her body in the position of a cervix. She reports enjoying vaginal penetration and that the use of dildos greatly stimulates her now internalized penis head. Labiaplasty is a plastic surgery procedure involving the labia, any of four folds of tissue of the vulva. Labiaplasty may be performed alone or as part of vaginoplasty. Labiaplasty - Cosmetic Vaginal Surgery (sometimes spelled labioplasty ) is plastic surgery of the Labia majora and/or the Labia minora, the external folds of the female genital organs (Vulva). The procedure involves reshaping or reduction of the labia. Labiaplasty is a plastic surgery procedure involving the labia, any of four folds of tissue of the vulva . Labiaplasty may be performed alone or as part of vaginoplasty. Labiaplasty may be undertaken for functional reasons, aesthetic reasons, or a combination of the two, although the cosmetic surgery's definition of "functional reasons" has yet to be explained to the rest of society: having large labia does not prevent the "function" of the vagina, and in fact because labiaplasty can make sex painful and prevent orgasm, labiaplasty can actually decrease the functionality of the vagina for sexual pleasure. The procedure is frequently performed to reduce the size of one or both sets of labia. It may also be used to repair the labia following disease or injury, or to reshape after childbirth. Labiaplasty does not improve the "function" of the vagina, but can in fact decrease or eliminate sensory perception of the genitals. Complications from the surgery, outside of those complications from any surgery (scarring, infection), include a loss of sensation of the clitoris, an inability to achieve orgasm, and pain from intercourse. Labia Majora (outer lips) Reduction - This common anatomical variation may be worsened by childbirth or by weight gain or loss. The Labia Majora may become stretched out, most commonly in the shape of flaps or "wings". Labia Minora (inner lips) Reduction - Cosmetic surgeons say that overly large labia minora can also result in constant irritation in tight pants, though this has largely been descried as myth by medical professionals. Women are often pressured into having labiaplasty by partners who are confused about the realistic proportions of unique women; because the side effects can be so devastating (including loss of sensation or pain during sex), most medical professionals who do not have a financial stake in cosmetic surgery advise against the procedure at all costs. Non-reconstructive vaginoplasty or "vaginal rejuvenation" is used to restore vaginal tone and appearance, largely by removing excess tissue and tightening supportive structures. The popularity of surgery to improve the cosmetic appearance of a female's genitalia has increased in North America over the last few years. The term "designer vagina" refers to an idealized image of female sex organs attained through vaginoplasty. In recent years laser has been introduced to assist in the procedure. The rejuvenation procedure is intended to reduce or undo effects of age and childbearing. The American College of Obstetricians and Gynecologists, however, warns that this procedure lacks supporting data regarding safety and efficacy. Indeed, vaginal rejuvenation surgery can lead to decreased sensory perception of the clitoris and the rest of the genital area, potentially to such an extent as to prevent the possibility of orgasm, and can lead to complications such as infection, adhesions, and scarring.

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# Vagovagal reflex Vagovagal reflex refers to gastrointestinal tract reflex circuits where afferent and efferent fibers of the vagus nerve coordinate responses to gut stimuli via the dorsal vagal complex in the brain. The vagovagal reflex controls contraction of the gastrointestinal muscle layers in response to distension of the tract by food. This reflex also allows for the accommodation of large amounts of food in the gastrointestinal tracts. The parasympathetic vagus nerve composed of both afferents and efferents carries signals from stretch receptors, osmoreceptors, and chemoreceptors to dorsal vagal complex where the signal may be further transmitted to autonomic centers in the medulla. Efferent fibers of the vagus then carry signals to the gastrointestinal tract up to 2/3 of the Tranverse Colon (coinciding with the second GI watershed point). The vagovagal reflex is active during the receptive relaxation of the stomach in response to swallowing of food (prior to it reaching the stomach). When food enters the stomach a "vagovagal" reflex goes from the stomach to the brain, and then back again to the stomach causing active relaxation of the smooth muscle in the stomach wall. If vagal innervation is interrupted then intra-gastric pressure increases. The vagal afferents are activated during the gastric phase of digestion when the corpus and fundus of the stomach are distended secondary to the entry of a food bolus. The stimulation of the mechanical receptors located in the gastric mucosa stimulates the vagus afferents. The completion of the reflex circuit by vagus efferents leads to the stimulation of postganglionic muscarinic nerves. These nerves release acetylcholine to stimulate two end effects. One, the parietal cells in the body of the stomach are stimulated to release H+. Two, the ECL cells of the lamina propria of the body of the stomach are stimulated to release histamine. Vagal stimulation of the peptidergic neurons, occurring simultaneously, leads to the release of gastrin-releasing-peptide. Finally, the Delta cells are inhibited to reduce the inhibition of gastrin release.

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# Vagus nerve The vagus nerve (also called pneumogastric nerve or cranial nerve X) is the tenth of twelve paired cranial nerves, and is the only nerve that starts in the brainstem (within the medulla oblongata) and extends, through the jugular foramen, down below the head, to the neck, chest and abdomen. The medieval Latin word vagus means literally "Wandering" (the words vagrant, vagabond, and vague come from the same root). It is also called the pneumogastric nerve since it innervates both the lungs and the stomach. The vagus descends from the spinal cord in the carotid sheath, lateral to the carotid artery. It carries on past the aortic arch to dip inferiorly behind the left bronchus. Here it forms the pulmonary plexus, after giving rise to the recurrent laryngeal nerve. The vagus nerve supplies motor parasympathetic fibers to all the organs except the suprarenal (adrenal) glands, from the neck down to the second segment of the transverse colon. The vagus also controls a few skeletal muscles, namely: This means that the vagus nerve is responsible for such varied tasks as heart rate, gastrointestinal peristalsis, sweating, and quite a few muscle movements in the mouth, including speech (via the recurrent laryngeal nerve) and keeping the larynx open for breathing. It also receives some sensation from the outer ear, via the Auricular branch (also known as Alderman's nerve) and part of the meninges. Parasympathetic innervation of the heart is mediated by the vagus nerve. The right vagus innervates the sinoatrial node. Parasympathetic hyperstimulation predisposes those affected to bradyarrhythmias. The left vagus when hyperstimulated predisposes the heart to atrioventricular (AV) blocks. At this location Otto Loewi first proved that nerves secrete substances called neurotransmitters which have effects on receptors in target tissues. Loewi described the substance released by the vagus nerve as vagusstoff, which was later found to be acetylcholine. Drugs that inhibit the muscarinic cholinergic receptor (anticholinergics) such as atropine and scopolamine are called vagolytic because they inhibit the action of the vagus nerve on the heart, gastrointestinal tract and other organs. Anticholinergic drugs increase heart rate and are used to treat bradycardia (slow heart rate) and asystole, which is when the heart has no electrical activity. Anticholinergic drugs relax the detrusor muscle and cause constipation which again involves the vagus nerve. Vagus nerve stimulation (VNS) therapy using a pacemaker-like device implanted in the chest is a treatment used since 1997 to control seizures in epilepsy patients and has recently been approved for treating drug-resistant cases of clinical depression. A convenient, non-invasive VNS device that stimulates an afferent branch of the vagus nerve is also being developed and will soon undergo trials. A degree of intermittent VNS can be achieved by daily breathing exercises (for example, Pranayama) over a period of several weeks. In some patients, such proactive relaxation exercises have been found to correlate with lower blood pressure and lower heart rate and more stable moods.[citation needed] The Valsalva maneuver may activate the vagus nerve and is a "natural" way to achieve the same effect in some patients. Patients with atrial fibrillation, supraventricular tachycardia and other illnesses may be trained to perform the valsalva maneuver (or find it for themselves). Vagotomy (cutting of the vagus nerve) is a now-obsolete therapy that was performed for peptic ulcer disease. Vagotomy is currently being researched as a less invasive alternative weight loss procedure to gastric bypass surgery . The procedure curbs the feeling of hunger and is sometimes performed in conjunction with putting bands on patients's stomachs, resulting in average weight loss of 43% at six months with diet and exercise . Five pencil-sized scars are the result of the procedure. Activation of the vagus nerve typically leads to a reduction in heart rate, blood pressure, or both. This occurs commonly in the setting of gastrointestinal illness such as viral gastroenteritis or acute cholecystitis, or in response to other stimuli, including carotid sinus massage, Valsalva maneuver, or pain from any cause, particularly having blood drawn. When the circulatory changes are great enough, vasovagal syncope results. Relative dehydration tends to amplify these responses. Excessive activation of the vagal nerve during emotional stress, which is a parasympathetic overcompensation of a strong sympathetic nervous system response associated with stress, can also cause vasovagal syncope because of a sudden drop in blood pressure and heart rate. Vasovagal syncope affects young children and women more often. It can also lead to temporary loss of bladder control under moments of extreme fear. Research has shown that women who have complete transection of the spinal cord can experience orgasms through the vagus nerve, which can go from the uterus, cervix and probably the vagina to the brain. The patient complains of hoarse voice, difficulty in swallowing (dysphagia), pain during swallowing(odynophagia) and choking when drinking fluid. There is also loss of gag reflex. Uvula deviates away from the side of lesion and there is failure of palate elevation.

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/index.php/Valaciclovir

# Valaciclovir The recommended dosage of Valaciclovir for the treatment of herpes zoster is 1 gram orally 3 times daily for 7 days. Therapy should be initiated at the earliest sign or symptom of herpes zoster and is most effective when started within 48 hours of the onset of zoster rash. No data are available on efficacy of treatment started greater than 72 hours after rash onset. See Instructions for Administration for further dosing and administration information. Most Recent Articles on Valaciclovir Review Articles on Valaciclovir Articles on Valaciclovir in N Eng J Med, Lancet, BMJ WikiDoc State of the Art Review Textbook Information on Valaciclovir Return to top Patient Information from National Library of Medicine Patient Resources on Valaciclovir Discussion Groups on Valaciclovir Patient Handouts on Valaciclovir Blogs on Valaciclovir Valaciclovir in the News Valaciclovir in the Marketplace Return to top

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# Valaciclovir detailed information Valaciclovir (INN) or valacyclovir (USAN) is an antiviral drug used in the management of herpes simplex and herpes zoster (shingles). It is a prodrug, being converted in vivo to aciclovir. It is marketed by GlaxoSmithKline under the trade name Valtrex or Zelitrex. Valaciclovir is a prodrug that is converted by esterases to the active drug aciclovir via hepatic first-pass metabolism, that was created by scientist Christine Moraski. Aciclovir is selectively converted into a monophosphate form by viral thymidine kinase, which is far more effective (3000 times) in phosphorylation than cellular thymidine kinase. Subsequently, the monophosphate form is further phosphorylated into the active triphosphate form, aciclo-GTP, by cellular kinases. Aciclo-GTP is a very potent inhibitor of viral DNA polymerase; it has approximately 100 times higher affinity to viral than cellular polymerase. Its monophosphate form also incorporates into the viral DNA, resulting in chain termination. It has also been shown that the viral enzymes cannot remove aciclo-GMP from the chain, which results in inhibition of further activity of DNA polymerase. Aciclo-GTP is fairly rapidly metabolised within the cell, possibly by cellular phosphatases. Activity is predominantly active against HSV, and to a lesser extent VZV. It is only of limited efficacy against EBV and CMV. It is inactive against latent viruses in nerve ganglia. To date, resistance to valaciclovir has not been clinically significant. Mechanisms of resistance in HSV include deficient viral thymidine kinase; and mutations to viral thymidine kinase and/or DNA polymerase, altering substrate sensitivity. Common adverse drug reactions (≥1% of patients) associated with valaciclovir therapy are the same as for aciclovir, its active metabolite, and include: nausea, vomiting, diarrhoea and/or headache. Infrequent adverse effects (0.1–1% of patients) include: agitation, vertigo, confusion, dizziness, oedema, arthralgia, sore throat, constipation, abdominal pain, rash, weakness and/or renal impairment. Rare adverse effects (<0.1% of patients) include: coma, seizures, neutropenia, leukopenia, tremor, ataxia, encephalopathy, psychotic symptoms, crystalluria, anorexia, fatigue, hepatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis and/or anaphylaxis. Valaciclovir is contraindicated in immuno-suppressed patients such as those infected with HIV as it may cause thrombotic thrombocytopenic purpura and hemolytic uremic syndromes resulting in kidney failure. Aciclovir is preferred in these patients.

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