Persius/hicric huggingface dataset:
Mycobacterium avium subspecies paratuberculosis
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Mycobacterium avium subspecies paratuberculosis is a pathogenic bacteria in the genus Mycobacteria.  It is often abbreviated Map, M. paratuberculosis, or M. avium sub. paratuberculosis. The type strain is ATCC 19698 (equivalent to CIP 103963  or DSM 44133).

# Pathophysiology
Map causes Johne's disease in cattle and other ruminants, and it has long been suspected as a causative agent in Crohn's disease in humans; this connection is controversial.
Recent studies have shown that Map present in milk can survive pasteurization, which has raised human health concerns due to the widespread nature of Map in modern dairy herds. Map is heat resistant and it is capable of sequestering itself inside white blood cells, which may contribute to its persistence in milk. It has also been reported to survive chlorination in municipal water supplies.
Even though Map is hardy, it is slow growing and fastidious, which means it is difficult to culture. Many negative studies for Map presence in living tissue, food, and water have used culture methods to determine whether the bacteria is present. Due to recent advances in our knowledge of the bacterium, some or all of these studies may need to be re-evaluated on the basis of culture methodology.
Map, like most mycobacteria, is difficult to treat. It is not susceptible to anti-tuberculosis drugs (which can generally kill Mycobacterium tuberculosis), but can only be treated with a combination of antibiotics such as Rifabutin and a macrolide such as Clarithromycin.  Treatment regimes can last years.

## Crohn's disease
MAP is recognized as a multi-host mycobacterial pathogen with a proven specific ability to initiate and maintain systemic infection and chronic inflammation of the intestine of a range of histopathological types in many animal species including primates.
On the assumption that Map is a causative agent in Crohn's, the Australian biotechnology company Giaconda is seeking to commercialise a combination of Rifabutin, clarithromycin and clofazimine as a potential drug therapy for Crohn's. As of April 2007, Giaconda received United States FDA IND approval for this medication, now called Myoconda.

# Genome
The genome of Map strain K-10 was sequenced in 2005 and found to consist of a single circular chromosome of 4,829,781 base pairs.
Necrotizing enterocolitis (patient information)
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# Overview
Necrotizing enterocolitis is the death of intestinal tissue. It most often affects premature or sick babies.

# What are the symptoms of Necrotizing enterocolitis?
Symptoms may come on slowly or suddenly, and may include:
- Abdominal distention
- Blood in the stool
- Diarrhea
- Feeding intolerance
- Lethargy
- Temperature instability
- Vomiting

# What causes Necrotizing enterocolitis?
- Necrotizing enterocolitis occurs when the lining of the intestinal wall dies and the tissue falls off.
- The cause for this disorder is unknown.
- However, it is thought that a decrease in blood flow to the bowel keeps the bowel from producing mucus that protects the gastrointestinal tract.
- Bacteria in the intestine may also be a cause.
- This disorder usually develops in an infant that is already ill or premature, and most often develops while the infant is still in the hospital.
- Those with a higher risk for this condition include:
- Premature infants
- Infants who are fed concentrated formulas
- Infants in a nursery where an outbreak has occurred
- Infants who have received blood exchange transfusions

# When to seek urgent medical care?
If any symptoms of necrotizing enterocolitis develop, especially in an infant that has recently been hospitalized for illness or prematurity, go to the emergency room or call the local emergency number (such as 911).

# Diagnosis
- Abdominal x-ray
- Stool for occult blood test (guaiac)
- Elevated white blood cell count in a CBC
- Thrombocytopenia (low platelet count)
- Lactic acidosis

# Treatment options
- In an infant suspected of having necrotizing enterocolitis, feedings are stopped and gas is relieved from the bowel by inserting a small tube into the stomach.
- Intravenous fluid replaces formula or breast milk. Antibiotic therapy is started.
- The infant's condition is monitored with abdominal x-rays, blood tests, and blood gases.
- Surgery will be needed if there is a hole in the intestines or peritonitis (inflammation of the abdominal wall). The dead bowel tissue is removed and a colostomy or ileostomy is performed. The bowel is then reconnected several weeks or months later when the infection and inflammation have healed.

# Where to find medical care for Necrotizing enterocolitis?
Directions to Hospitals Treating Necrotizing enterocolitis

# What to expect (Outlook/Prognosis)?
- Necrotizing enterocolitis is a serious disease with a death rate approaching 25%.
- Early, aggressive treatment helps improve the outcome.

# Possible complications
- Intestinal perforation
- Intestinal stricture
- Peritonitis
- Sepsis

# Source
Oxytetracycline hydrochloride adverse reactions

# Adverse Reactions
Glossitis, stomatitis, proctitis, nausea, diarrhea, vaginitis, and dermatitis, as well as reactions of an allergic nature, may occur during oxytetracycline HCl therapy, but are rare. If adverse reactions, individual idiosyncrasy, or allergy occur, discontinue medication. Rare instances of esophagitis and esophageal ulcerations have been reported in patients receiving capsule forms of drugs in the tetracycline class. Most of these patients took medications immediately before going to bed. (See Dosage and Administration.)
With oxytetracycline therapy bulging fontanels in infants and benign intracranial hypertension in adults have been reported in individuals receiving full therapeutic dosages. These conditions disappeared rapidly when the drug was discontinued.
As in all sulfonamide therapy, the following reactions may occur: nausea, vomiting, diarrhea, hepatitis, pancreatitis, blood dyscrasias, neuropathy, drug fever, skin rash, injection of the conjunctiva and sclera, petechiae, purpura, hematuria and crystalluria. The dosage should be decreased or the drug withdrawn, depending upon the severity of the reaction.
PCI in The Patient with Impaired Renal Function
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# 2011 and 2009 ACCF/AHA/SCAI Guidelines for Percutaneous Coronary Intervention (DO  NOT EDIT)

## Contrast-Induced Acute Kidney Injury (DO  NOT EDIT)

## PCI in Chronic Kidney Disease (DO  NOT EDIT)

## Angiography in Patients With Chronic Kidney Disease (DO NOT EDIT)
Pathophysiology of Saphenous Vein Graft Disease
Several factors contribute to stenosis of saphenous vein grafts, including intimal hyperplasia, plaque formation, and graft remodeling.  Additionally, arterialization of the graft accelerates atherosclerosis.  Furthermore, atheroma found in SVGs are more friable (easily break into small pieces) and more prone to thrombus than plaques found in native vessels.  Another reason why SVGs are more susceptible to thrombotic occlusion is that they lack side branches.

# Saphenous Vein Graft Aneurysms
It  is also known as SVGA, aortocoronary saphenous vein graft aneurysms,  saphenous vein graft aneurysm disease and saphenous vein graft  aneurysmal dilatation.
- Atherosclerosis
- Hypertension
- Mycotic
- Postoperative mediastinitis
- Previous aneurysms
- Torn sutures

# Amyloidosis of Saphenous Coronary Bypass Grafts
Amyloid has been associated with accelarated disease in saphenous vein grafts.    

# Rupture of the Saphenous Vein Coronary Artery Bypass Grafts
Aspergillus species causing a necrotizing vasculitis have been associated with rupture of a saphenous vein grafts.

# Phlebitis in the Implanted SVG
Acute postoperative phlebitis is a rare complication of SVG implantation which can be associated with SVG thombosis, and a purulent pericarditis and mediastinitis.

# Potential for Pre-Operative SVG Failure
It should be noted that studies of SVGs that are not implanted show that about 1% of veins are already stenosed by > 50% before implantation.
Penicillin G procaine dosage and administration

# Dosage and Administration
Streptococcal Infections Group AInfections of the upper-respiratory tract, skin and soft-tissue infections, scarlet fever, and erysipelas.
The following doses are recommended:
- Adults and pediatric patients over 60 lbs. in weight: 2,400,000 units.
- Pediatric patients from 30 to 60 lbs.: 900,000 units to 1,200,000 units.
- Pediatric patients under 30 lbs.: 600,000 units.
NOTE: Treatment with the recommended dosage is usually given at a single session using multiple IM sites when indicated. An alternative dosage schedule may be used, giving one-half (1/2) the total dose on day 1 and one-half (1/2) on day 3. This will also insure the penicillinemia required over a 10-day period; however, this alternate schedule should be used only when the physician can be assured of the patient's cooperation.
Pneumococcal Infections (except pneumococcal meningitis)
600,000 units in pediatric patients and 1,200,000 units in adults, repeated every 2 or 3 days until the temperature is normal for 48 hours. Other forms of penicillin may be necessary for severe cases.

## Method of Administration
Bicillin C-R is intended for Intramuscular Injection ONLY. Do not inject into or near an artery or nerve, or intravenously or admix with other intravenous solutions. (See WARNINGS section).
Administer by DEEP INTRAMUSCULAR INJECTION in the upper, outer quadrant of the buttock. In neonates, infants and small children, the midlateral aspect of the thigh may be preferable. When doses are repeated, vary the injection site.
Because of the high concentration of suspended material in this product, the needle may be blocked if the injection is not made at a slow, steady rate.
Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration whenever solution and container permit.
Portal hypertensive gastropathy medical therapy

# Overview

# Medical Therapy

## Pharmacotherapies
Several treatment options have been developed for portal hypertensive gastropathy.
- Beta-blockers: The first is the use of beta-blockers, which reduce portal pressures.  Non-selective beta blockers (such as propranolol and nadolol have been used to decrease the pressure of the portal vein in patients with esophageal varices, and have been shown to regress portal hypertensive gastropathy that has been worsened by medical treatment of varices.  Propranolol has also been evaluated in patients with chronic cirrhosis and portal hypertensive gastropathy 
- Anti fibrinolytics:  Other medications that primarily treat bleeding, including anti-fibrinolytic medications such as tranexamic acid have also been used in case reports of patients with portal hypertensive gastropathy.  These medications work by stabilizing deposits of fibrin at sites that ordinarily would bleed.
- Octreotide:  Finally, octreotide, an analogue of somatostatin that leads to vasoconstriction of the portal circulation, can be used for active bleeding due to portal hypertensive gastropathy.
- Sucralfate:  Sucralfate, a coating medication has also been used, but evidence is from animal models.

## Endoscopy
Portal hypertensive gastropathy can also be treated with endoscopic treatment delivered through a fibre-optic camera into the stomach.  Argon plasma coagulation and electrocautery have both been used to stop bleeding from ectatic vessels, and to attempt to obliterate the vessels, but have limited utility if the disease is diffuse.
Post-chemotherapy cognitive impairment overview

# Overview
In medicine, post-chemotherapy cognitive impairment (also known as chemotherapy-induced cognitive dysfunction or, colloquially, as chemo brain or chemo fog) describes the cognitive impairment that can result from chemotherapy treatment. Approximately 20-30% of people who undergo chemotherapy experience some level of post-chemotherapy cognitive impairment. The phenomenon first came to light because of the large number of breast cancer survivors who complained of changes in memory, fluency, and other cognitive abilities that impeded their ability to function as they had pre-chemotherapy.
Although the causes (and indeed, existence) of post-chemotherapy cognitive impairment have been a subject of debate, recent studies have confirmed that post-chemotherapy cognitive impairment is a real, measurable side-effect of chemotherapy treatment, at least in some patients. A UCLA study published in October 2006 showed that the brains of breast cancer survivors who were treated with chemotherapy have to work harder to perform tasks than survivors whose treatment was surgical.   Even more recently, Japanese researchers have demonstrated that a year after treatment, the brains of cancer survivors treated with chemotherapy had physically shrunk; those of people not treated with chemotherapy had not.
Post-chemotherapy cognitive impairment comes as a surprise to many cancer survivors. Often, survivors think their lives will return to normal when the cancer is gone, only to find that the lingering effects of post-chemotherapy cognitive impairment impede their efforts. Working, connecting with loved ones, carrying out day-to-day tasksall can be very challenging for an impaired brain. Although post-chemotherapy cognitive impairment appears to be temporary, it can be quite long-lived, with some cases lasting 10 years or more.
Sandbox Urinary tract infection medical therapy

# Overview
Most uncomplicated UTIs can be treated with oral antibiotics such as trimethoprim, cephalosporins, nitrofurantoin, or a fluoroquinolone (e.g. ciprofloxacin, levofloxacin). These are usually taken for 3 days in young adults, and 5 days in elderly. Whilst co-trimoxazole was previously internationally used (and continues to be used in the U.S.), the additional of the sulphonamide gave little additional benefit compared to the trimethoprim component alone, but was responsible for its both high incidence of mild allergic reactions and rare but serious complications.
If the patient has symptoms consistent with pyelonephritis, intravenous antibiotics may be indicated. Regimens vary, usually Aminoglycosides (such as Gentamicin) are used in combination with a beta-lactam, such as Ampicillin or Ceftriaxone. These are continued for 48 hours after fever subsides. The patient may then be discharged home on oral antibiotics for a further 5 days.
If the patient makes a poor response to IV antibiotics (marked by persistent fever, worsening renal function), then imaging is indicated to rule out formation of an abscess either within or around the kidney, or the presence of an obstructing lesion such as a stone or tumor. The gold-standard imaging modality is CT scan.

# Empiric Therapy for Acute Pyelonephritis (Outpatient & Inpatient) Adapted from Clin Infect Dis. 2011;52(5):e103-20.

# Empiric Therapy for Acute Pyelonephritis (Pregnancy) Adapted from European Association of Urology's Guidelines on Urological Infections 
==Empiric Therapy for Acute Cystitis== Adapted from Clin Infect Dis. 2011;52(5):e103-20.
Saphenous Vein Graft Intervention Complications
As with all medical procedures, complications for SVG intervention can occur.  Risk factors for complications include: older graft age (>3-5 years), the presence of thrombus, and diffuse disease.
Although PCI with stenting is effective for focal lesions, there is uncertainty regarding the best treatment for diffusely degenerated SVGs.  In these cases, it is often a better choice to abandon the graft and intervene on the native vessel instead.
As mentioned above, prevention of no reflow should be attempted with embolic protection devices, pretreatment using nitroprusside and the avoidance of high-pressure inflations and unnecessary pre/post-dilation and oversizing.  However, in the event that no reflow develops, it should be aggressively managed with intracoronary vasodilators (i.e. diltiazem, nicardipine, adenosine, and nitroprusside).
Secondary Prevention Guidelines Recommendations

# Secondary Prevention Guidelines Recommendations

## 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS Guideline on the Management of Patients With Extracranial Carotid and Vertebral Artery Disease (DO NOT EDIT)

### Smoking Cessation (DO NOT EDIT)

### Treatment of Hypertension (DO NOT EDIT)

### Control of Hyperlipidemia (DO NOT EDIT)

### Management of Diabetes Mellitus in Patients With Atherosclerosis of the Extracranial Carotid or Vertebral Arteries (DO NOT EDIT)

### Antithrombotic Therapy in Patients With Extracranial Carotid Atherosclerotic Disease Not Undergoing Revascularization (DO NOT EDIT)
Star related lipid transfer domain containing 3
StAR related lipid transfer domain containing 3 (STARD3) is a protein that in humans is encoded by the STARD3 gene. STARD3 also known as metastatic lymph node 64 protein (MLN64) is a late endosomal integral membrane protein involved in cholesterol transport. STARD3 creates membrane contact sites between the endoplasmic reticulum and late endosomes where it moves cholesterol.

# Function
This gene encodes a member of a subfamily of lipid trafficking proteins that are characterized by a C-terminal steroidogenic acute regulatory domain and an N-terminal metastatic lymph node 64 domain. The encoded protein localizes to the membranes of late endosomes and may be involved in exporting cholesterol. Alternative splicing results in multiple transcript variants..
STARD3 is involved in cholesterol transport from the endoplasmic reticulum to late endosomes where the protein is anchored. 
The closest homolog to STARD3 is the steroidogenic acute regulatory protein (StAR/StarD1), which initiates the production of steroids by moving cholesterol inside the mitochondrion.  Thus, MLN64 is also proposed to move cholesterol inside the mitochondria under certain conditions to initiate StAR-independent steroidogenesis, such as in the human placenta which lacks StAR yet produces steroids. This functional role is supported by evidence that MLN64 expression can stimulate steroid production in a model cell system.
A recent study indicates that this protein also specifically binds lutein in the retina.

# Structure
STARD3 is a multi-domain protein composed of a N-terminal MENTAL (MLN64 N-terminal) domain, a central FFAT motif (two phenylalanines in an acidic tract), and a C-terminal StAR-related transfer domain (START) lipid transport domain.
The MENTAL domain of STARD3 is similar to the protein STARD3 N-terminal like protein (STARD3NL) also known as MLN64 N-terminal homologue (MENTHO).  This domain is composed of 4 transmembrane helices which anchor the protein in the limiting membrane of late endosomes. This domain binds cholesterol and associates with the same domain in STARD3NL.
The FFAT motif is a short protein sequence motif which binds to the ER proteins VAP-A, VAP-B and MOSPD2 proteins.
The START domain of STARD3 is homologous to the StAR protein. X-ray crystallography of the C-terminus indicates that this domain forms a pocket that can bind cholesterol.  This places STARD3 within the StarD1/D3 subfamily of START domain-containing proteins.

# Tissue distribution
STARD3 is expressed in all tissues in the body at various levels.  In the brain, MLN64 is detectable in many but not all cells. Many malignant tumors highly express STARD3 as a result of its gene being part of a Her2/erbB2-containing gene locus that is amplified.

# Pathology
Loss of STARD3 has little effect in mice. At the cellular level, changes in STARD3 can disrupt trafficking of endosomes and cause accumulation of cholesterol in late endosomes.
The heart in systemic lupus erythematosus (SLE)

# Overview

# Histopathological Findings
Image courtesy of Professor Peter Anderson DVM PhD and published with permission  PEIR, University of Alabama at Birmingham, Department of Pathology
- Lupus Erythematosus Libman Sacks Endocarditis: Gross natural color mitral valve small lesions but cause much trouble in form of TIAs and terminally multiple hemorrhagic brain infarcts
- Lupus Erythematosus, Libman Sacks Endocarditis: Micro low mag trichrome stain thickened valve leaflet with small mural fibrin deposit. A 19yo female with cerebral lupus in form of TIAs due to this lesion.
- Lupus Erythematosus, Libman Sacks Endocarditis: Micro low mag, elastic van Gieson stain, mitral valve thickened, leaflet with small mural fibrin deposit that caused TIAs in 19yo female
- Lupus Erythematosus Myocardial Necrosis Due To Libman Sacks: Micro low mag H&E focal myocardial necrosis due to embolism from Libman Sacks lesion on mitral valve 19yo female with TIAs due to mitral lesion
- Lupus Erythematosus Focal Myocardial Scar Due To Libman Sacks Embolism: Micro low mag H&E focal scar in myocardium due to embolism
- Lupus Erythematosus Myocardial Scar Due to Libman Sacks Embolism: Micro low mag H&E scar with portion of embolus in small artery
- Lupus Erythematosus Myocardial Necrosis Due to Libman Sacks: Micro low mag H&E well shown focal myocardial necrosis due to embolism from mitral Libman Sacks lesion
- Lupus Erythematosus Libman Sacks Endocarditis: Micro high mag H&E atrial surface of mitral valve with small fibrin thrombus representing Libman Sacks lesion 10yo female
- Lupus Erythematosus Libman Sacks Endocarditis: Micro low mag H&E mitral valve lesion with easily seen mural thrombi and focal necrobiosis of collagen in thickened valve leaflet 19yo female
- Myocarditis: Micro high mag H&E focal myofiber necrosis typical for this diagnosis but this is case of lupus erythematosus with Libman Sacks lesion and brain emboli and heart emboli did she also have viral myocarditis? This lesion is typical for the diagnosis
Urinary tract infection resident survival guide

# Overview
A urinary tract infection (UTI) is a bacterial infection that affects any part of the urinary tract.

# Causes

## Life Threatening Causes
- Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
- Urinary tract infection does not have life threatening causes.

## Common Causes
- Escherichia coli
- Klebsiella pneumonia
- Neisseria gonorrhea
- Proteus mirabilis
- Pseudomonas aeruginosa
- Staphylococcus saprophyticus
- Urinary catheterization

# Management
Shown below is an algorithm depicting the initial approach to UTI.

## Diagnosis and Treatment
An algorithm using symptoms/physical finding in diagnosis and treatment of UTIs.

# Do's
- TMP-SMX should only be used in the second trimester of pregnancy.

# Dont's
- Don't use fluoroquinolones empirically for treatment of acute uncomplicated cystitis.
- Do not give fluoroquinolones in pregnancy.
- Don't give TMP-SMX in first trimester or near term of pregnancy.