Persius/hicric huggingface dataset:
Achromobacter xylosoxidans

# Overview
Achromobacter xylosoxidans is a Gram-negative, aerobic, oxidase- and catalase-positive, motile bacterium with peritrichous flagella, from the genus Achromobacter found in water environments and was isolated from patients (pulmonary). Achromobacter xylosoxidans can cause infections like bacteremia, especially for patients who suffer from cystic fibrosis. In 2013, the complete genome of an A. xylosoxidans isolate from CF patient was sequenced.

# Treatment
- Achromobacter xylosoxidans treatment,,,,,
- Preferred regimen: most active agents are Piperacillin-Tazobactam, Meropenem AND TrimethoprimSulfamethoxazole whereas Ceftazidime is more active than Cefepime
- Alternative regimen: Colistin inhaled, could also be considered
- Note : Achromobacter (formerly Alcaligenes) xylosoxidans is a newly emerging microorganism isolated with increased frequency from the lungs of patients with cystic fibrosis. Combination therapy has been recommended for the treatment of Achromobacter xylosoxidans pulmonary exacerbations in cystic fibrosis
Superior mesenteric artery
In human anatomy, the superior mesenteric artery (SMA) arises from the anterior surface of the abdominal aorta, just inferior to the origin of the celiac trunk, and supplies the intestine from the lower part of the duodenum to the left colic flexure and the pancreas.

# Location and path
It arises anterior to vertebra L1 in an adult. It is usually 1cm lower than the celiac trunk. It initially travels in an anterior/inferior direction, passing behind/under the neck of the pancreas and the splenic vein.  Located under this portion of the superior mesenteric artery, between it and the aorta, are the following:
- left renal vein - travels between the left kidney and the inferior vena cava (can be compressed by the SMA at this location, leading to the so-called nutcracker syndrome.
- the third part of the duodenum, part of the small intestines
- uncinate process of the pancreas - this is a small part of the pancreas that hooks around the SMA
The SMA typically runs to the left of the similarly named vein, the superior mesenteric vein. After passing the neck of the pancreas it starts giving off its branches.

# Branches
The middle, right, and ileocecal branches anastomose with each other to form a marginal artery along the inner border of the colon. This artery is completed by branches of the left colic which is a branch of the inferior mesenteric artery.

# Pathology
- Compared to other vessels of similar size, the SMA is largely spared the effects of atherosclerosis. This is likely due to protective haemodynamic conditions
- Occlusion of the SMA almost invariably leads to intestinal ischemia and often has devastating consequences; up to 80% of SMA occlusions lead to death.
- The SMA can compress the left renal vein, leading to the nutcracker syndrome and/or the third (horizontal) part of the duodenum, leading to SMA syndrome.

# Additional images
- The celiac artery and its branches; the stomach has been raised and the peritoneum removed.
- Abdominal part of digestive tube and its attachment to the primitive or common mesentery. Human embryo of six weeks.
- Posterior abdominal wall, after removal of the peritoneum, showing kidneys, suprarenal capsules, and great vessels.
- The anterior surfaces of the kidneys, showing the areas of contact of neighboring viscera.
- Front of abdomen, showing surface markings for arteries and inguinal canal.
Acyclovir clinical studies

# Clinical Studies
Initial Genital Herpes: Double-blind, placebo-controlled studies have demonstrated that orally administered ZOVIRAX significantly reduced the duration of acute infection and duration of lesion healing. The duration of pain and new lesion formation was decreased in some patient groups.
Recurrent Genital Herpes: Double-blind, placebo-controlled studies in patients with frequent recurrences (6 or more episodes per year) have shown that orally administered ZOVIRAX given daily for 4 months to 10 years prevented or reduced the frequency and/or severity of recurrences in greater than 95% of patients.
In a study of patients who received ZOVIRAX 400 mg twice daily for 3 years, 45%, 52%, and 63% of patients remained free of recurrences in the first, second, and third years, respectively. Serial analyses of the 3-month recurrence rates for the patients showed that 71% to 87% were recurrence free in each quarter.
Herpes Zoster Infections: In a double-blind, placebo-controlled study of immunocompetent patients with localized cutaneous zoster infection, ZOVIRAX (800 mg 5 times daily for 10 days) shortened the times to lesion scabbing, healing, and complete cessation of pain, and reduced the duration of viral shedding and the duration of new lesion formation.
In a similar double-blind, placebo-controlled study, ZOVIRAX (800 mg 5 times daily for 7 days) shortened the times to complete lesion scabbing, healing, and cessation of pain; reduced the duration of new lesion formation; and reduced the prevalence of localized zoster-associated neurologic symptoms (paresthesia, dysesthesia, or hyperesthesia).
Treatment was begun within 72 hours of rash onset and was most effective if started within the first 48 hours.
Adults greater than 50 years of age showed greater benefit.
Chickenpox: Three randomized, double-blind, placebo-controlled trials were conducted in 993 pediatric patients aged 2 to 18 years with chickenpox. All patients were treated within 24 hours after the onset of rash. In 2 trials, ZOVIRAX was administered at 20 mg/kg 4 times daily (up to 3,200 mg per day) for 5 days. In the third trial, doses of 10, 15, or 20 mg/kg were administered 4 times daily for 5 to 7 days. Treatment with ZOVIRAX shortened the time to 50% healing; reduced the maximum number of lesions; reduced the median number of vesicles; decreased the median number of residual lesions on day 28; and decreased the proportion of patients with fever, anorexia, and lethargy by day 2. Treatment with ZOVIRAX did not affect varicella-zoster virus-specific humoral or cellular immune responses at 1 month or 1 year following treatment.
Agarose gel loading buffer
Loading dye is mixed with DNA samples for use in agarose gel electrophoresis.  It generally contains a dye to assess how "fast" your gel is running and a reagent to render your samples denser than the running buffer (so that the samples sink in the well).

# Material

## Density
- Ficoll
- sucrose
- glycerol

## Colour
*sieving agarose

# Recipes for loading buffers
The precise amount of dye is not important. However, it is crucial that you prevent overlay of dye and expected DNA size. For example, if you are expecting a genotyping band of 200-400nt, you shouldn't use bromophenol blue since it  will obscure your product. In this case, you should use a larger dye like xylene cyanol.

## Ficoll & Orange G (6x)
- 1.5g Ficoll 400
- Orange G dye
- dH2O to 10mL
Add very small amounts of Orange G dye such that the loading dye is dark orange.  Store in small aliquots at 4C (room temperature is okay too). To use, add and mix 1/5th volume of loading dye to DNA solutions prior to loading into the wells of gels.

## Sucrose & xylene cyanol / bromophenol blue (6x)
- 4g sucrose
- 25mg bromophenol blue or xylene cyanol (0.25%)
- dH2O to 10mL
Add appropriate amount to DNA sample, e.g. 5l to 25l.
Store at 4C to avoid mould growing in the sucrose. 10mL of loading buffer will last for years.

## Glycerol & bromophenol blue (6x)
- 3ml glycerol (30%)
- 25mg bromophenol blue (0.25%)
- dH2O to 10mL
compare CSH protocols  (restricted access)

## Specific recipes
- Knight:Loading dye

# Links

## OWW
- Agarose gel electrophoresis
- Cresol Red

## External
- Methodsbook.net: xylene or bromophenol + sucrose DNA loading buffers File:2stars.png
- Bioron Company page on bromophenol + xylene + Ficoll DNA loading buffer File:2stars.png
Aicardi-Goutieres syndrome
Synonyms and keywords:  Cree encephalitis, pseudo-TORCH syndrome

# Overview
Aicardi-Goutieres syndrome is a rare genetic disorder.  It is a type of leukodystrophy and is usually fatal within the first few years.
It presents within the first few weeks of life.

# Historical Perspective
Aicardi-Goutieres syndrome was initially described by Jean Aicardi and Francoise Goutieres in 1984, based on observations of eight cases of early-onset progressive familial encephalopathy, with calcifications of the basal ganglia and chronic cerebrospinal fluid lymphocytosis.   Further clinical studies included 11 cases of early-onset progressive encephalopathy in a Cree community in Canada, described in 1988, which were given the name Cree encephalitis .

# Classification

# Pathophysiology

## Genetics
It is autosomal recessive and presents within the first few weeks of life.  Later work mapped the Aicardi-Goutieres syndrome to chromosome 3p21 and suggested that the two, along with the pseudo-TORCH (toxoplasmosis, rubella, cytomegalovirus, and herpes simplex virus types 1 and 2) syndrome were the same disorder.
The condition has been associated with TREX1.

# Epidemiology and Demographics
Aicardi-Goutieres syndrome is very rare, with only about 50 cases having been described.

# Treatment
Current treatment is supportive, involving management of seizures and spasticity associated with the syndrome.
Alagille syndrome overview

# Overview
Alagille syndrome is a multisystem genetic disorder that affects the liver, heart, eyes,face, skeleton, kidneys and vascular system.  Problems associated with the disorder generally become evident in infancy or early childhood.  The patients have a characteristic facial appearance. The disorder is  inherited in an autosomal dominant pattern, and the estimated prevalence of Alagille syndrome is 1 in every 70,000 live births. The clinical features are highly variable even within the family.
Alagille syndrome can be associated with congenital heart disease, particularly Tetralogy of Fallot.  The kidneys and central nervous system may also be affected. Cases of unilateral coronal craniosynostosis have also been described in association with this syndrome.

# Pathophysiology
This condition is inherited in an autosomal dominant pattern.

# Epidemiology and Demographics
The estimated prevalence of Alagille syndrome is 1 in every 70,000 live births.

# Natural History, Complications and Prognosis
Mortality is approximately 10%, with vascular accidents, cardiac disease, and liver disease accounting for most of the deaths. Vascular anomalies account for 34% of the mortality in this population .

# Diagnosis
The diagnosis is primarily clinical.

# Treatment
There is no known cure for Alagille's Syndrome. Most of the treatments available are aimed at improving the functioning of the heart, and reducing the effects of impaired liver function.
Aldose reductase inhibitor
Aldose reductase inhibitors are a class of drugs being studied as a way to prevent eye and nerve damage in people with diabetes.

# Mechanism
Their target, aldose reductase, is an enzyme that is normally present in many other parts of the body, and catalyzes one of the steps in the sorbitol(polyol) pathway that is responsible for fructose formation from glucose. Aldose reductase activity increases as glucose concentration rise in diabetes in those tissue that are not insulin sensitive, which includes the lenses, peripheral nerve and glomerulus. Sorbitol does not diffuse through cell membranes easily and therefore accumulates, causing osmotic damage which leads to retinopathy and neuropathy.

# Examples
Examples of aldose reductase inhibitors include:
- epalrestat
- ranirestat

# Diabetic cataract
Diabetic cataract formation follows an increase in sugars in the lens. The excess sugar within the lens is reduced by aldose reductase to its alcohol, but the lens capsule is relatively impermeable to sugar alcohols. Because of the excess sugar alcohol (polyol), the lens imbibes water, causing osmotic imbalance. Eventually, increased sodium and decreased potassium levels and decrease glutathione levels lead to cataract formation. Topical administration of aldose reductase inhibitors have been shown to prevent the cataract in rats.
Alveolar-arterial gradient

# Overview
The Alveolar-arterial gradient (A-a gradient), is a measure of the difference between the alveolar concentration of oxygen and the arterial concentration of oxygen. It is used in diagnosing the source of hypoxemia.

# Equation
A-a gradient = PAO2 - PaO2
Where:
- PAO2 = alveolar PO2 (calculated from the alveolar gas equation)
- PaO2 = arterial PO2 (measured in arterial blood A-a gradient)

# Values and meaning
The A-a gradient is useful in determining the source of hypoxemia. The measurement helps isolate the location of the problem as either intrapulmonary (within the lungs) or extrapulmonary (somewhere else in the body).
A normal A-a gradient is less than 10 mmHg, but can range from 5-20 mmHg. Normally, the A-a gradient increases with age. For every decade a person has lived, their A-a gradient is expected to increase by 1 mmHg. An abnormally increased A-a gradient suggests a defect in diffusion, V/Q (ventilation/perfusion ratio) defect, or right-to-left shunt.
Alveolar soft part sarcoma

# Overview
Alveolar soft part sarcoma (ASPS) is a very rare type of Soft tissue sarcoma - a slow growing tumor of an unknown origin that arises mainly in children and young adults. ASPS is highly angiogenic: it involves intensive growth of new blood vessels, that connect the tumor to the blood system and enable dissemination of tumor cells into the bloodstream. Tumor cells can then easily migrate into other parts of the body - typically the lungs, and the brain.
ASPS is a sarcoma, and that indicates that this cancer initially arises in soft tissues that connect, support, or surround other structures and organs of the body, rather than bones. Typically, ASPS arises in muscles and deep soft tissue of the thigh or the leg (lower extremities), but can also appear in the upper extremities: the hands, the neck, and the head. While ASPS is a soft tissue sarcoma, it can spread and grow inside the bones.
The term alveolar comes from the microscopic pattern, visible during the analysis of slides of ASPS under the microscope in histopathology. The tumor cells seem to be arranged in the same pattern as the cells of the small air sacks (alveoli) in the lungs. However, this is just a structural similarity. ASPS was first described and characterized in 1952.

# Very Rare
ASPS is an extremely rare cancer.  While sarcomas comprise about 1% of all newly diagnosed cancers, and 15% of all childhood cancers, ASPS comprises less than 1% of sarcomas.  According to the American Cancer Society, about 9530 new cases of soft tissue sarcoma will be diagnosed in the USA in 2006.  This predicts under 100 new cases of ASPS.  Such low numbers of occurrence seriously impede the search for a cure by making it hard to gather any meaningful statistics about the disease.  As a result, finding the best treatment option often involves making a lot of educated guesses.

# Primary Diagnosis
ASPS may exist in the patients body for a long time before being diagnosed. It can grow large and push aside surrounding tissues for a long time before causing any discomfort. Therefore, ASPS symptoms may either be a painless swelling, or a soreness caused by compressed nerves or muscles, affecting the range of motion in the area.

# What causes ASPS
Chromosomal analysis of ASPS shows the breaking and joining of two chromosomes in the tumor cells. A piece of chromosome X breaks and is joined to chromosome 17. This translocation creates a fusion between two genes named ASPL and TFE3, which results in the formation of an aberrant protein (termed fusion protein) that is not found in normal cells. Two sorts of fusions between chromosome X and chromosome 17 are found in different ASPS tumors: Type one, and type two. Dr. Ladanyi at Memorial Sloan-Kettering Cancer Center, in New York, has pioneered this work.

# Prognosis
Although ASPS displays a relativly indolent course, the ultimate prognosis is poor and is often characterized by late metastases.

# Notes
-  Christopherson WM, Foote FW, Stewart FW: Alveolar soft part sarcomas: structurally characteristic tumors of uncertain histogenesis. Cancer 1952, 5:100-111
American Legacy Foundation
The American Legacy Foundation (ALF) is a non-profit organization dedicated to preventing teen smoking and encouraging smokers to quit. Their vision is "Building a world where young people can reject tobacco and anyone can quit"
The organization is responsible for the truth anti-youth smoking ad campaign, which won an Effy Award in 2005, and the creation and continued funding of the Legacy Tobacco Documents Library (LTDL)
, a digital library hosted by the University of California, San Francisco.  The LTDL contains more than 7 million internal documents (40+ million pages) created by major tobacco companies related to their advertising, manufacturing, marketing, sales, and scientific research activities.
The American Legacy Foundation is a 501(c)(3) not-for-profit organization that was established in March 1998 as a result of the Master Settlement Agreement (MSA) between a coalition of attorneys general in 46 states and five United States territories and the tobacco industry. It is funded primarily by payments designated by the settlement.
Amikacin adverse reactions

# Adverse Reactions
All aminoglycosides have the potential to induce auditory, vestibular and renal toxicity and neuromuscular blockade (see WARNINGS box). They occur more frequently in patients with present or past history of renal impairment, of treatment with other ototoxic or nephrotoxic drugs and in patients treated for longer periods and/or with higher doses than recommended.
Toxic effects on the eighth cranial nerve can result in hearing loss, loss of balance, or both. Amikacin primarily affects auditory function. Cochlear damage includes high frequency deafness and usually occurs before clinical hearing loss can be detected.
Acute muscular paralysis and apnea can occur following treatment with aminoglycoside drugs.
Elevation of serum creatinine, albuminuria, presence of red and white cells, casts, azotemia, and oliguria have been reported. Renal function changes are usually reversible when the drug is discontinued. As would be expected with any aminoglycoside, reports of toxic nephropathy and acute renal failure have been received during postmarketing surveillance.
In addition to those described above, other adverse reactions which have been reported on rare occasions are skin rash, drug fever, headache, paresthesia, tremor, nausea and vomiting, eosinophilia, arthralgia, anemia, hypotension and hypomagnesemia. Macular infarction sometimes leading to permanent loss of vision has been reported following intravitreous administration (injection into the eye) of amikacin.
Ammonium bituminosulfonate
Ammonium bituminosulfonate (ichthyol or ichthammol, CAS#8029-68-3 ) is a product of natural origin obtained in the first step by dry distillation of sulfur-rich oil shale. It is used in medicine as a remedy for treating some forms of skin diseases, such as acne, eczema and psoriasis. It is commonly used in an ointment in 10% or 20% concentrate as a "drawing salve", also called "black ointment". Its dermatological action was discovered by Austrian physician Paul Gerson Unna.
From elementary analysis its composition was calculated to be C28H36S5O6(NH4)2. However, as a product from natural origin it is a mixture of many different compounds.
Chemically, it is a sulfonated shale oil. It can be presented in two forms: pale sulfonated shale oil (PSSO), and dark sulfonated shale oil (DSSO). DSSO is also sometimes called ichthammol. The last form is a thick reddish brown liquid, possessing a bituminous odor and taste. It is soluble in water and miscible with glycerin, but is nearly insoluble in strong alcohol or concentrated ether. It contains a large percentage of organically combined sulfur. Ichthyol is incompatible with acids, alkali carbonates or hydrates and alkaloidal salts.
Pharmacologically, PSSO and DSSO have anti-inflammatory, bactericidal and fungicidal properties. In otology, a mixture of glycerol and ichthammol (G & I) has been used for generations for the topical treatment of ear infections. It is efficient against Gram-positive organisms. The anti-inflammatory action is explained by its influence on the formation, secretion and effect of inflammation mediators.  DSSO is well tolerated and no indications of teratogenic, mutagenic or carcinogenic effects have been noted.
The European Medicines Agency recently published a Summary Report on ICHTHYOL-substances (synonym: bituminosulfonates) in course of the European Maximum Residue Limits (MRL) procedure (see report from June 2005) in veterinary medicine. The committee for Medicinal Products for Veterinary Use (CVMP) decided that because of good tolerance and safety there is no need to establish an MRL for ICHTHYOL-substances. As a result, ICHTHYOL-substances can be applied topically in all mammalian food producing species without restriction.
Amphotericin B description

# Description
ABELCET is a sterile, pyrogen-free suspension for intravenous infusion. ABELCET consists of amphotericin B complexed with two phospholipids in a 1:1 drug-to-lipid molar ratio. The two phospholipids, l--dimyristoylphosphatidylcholine (DMPC) and l--dimyristoylphosphatidylglycerol (DMPG), are present in a 7:3 molar ratio. ABELCET is yellow and opaque in appearance, with a pH of 5 - 7.
NOTE: Liposomal encapsulation or incorporation in a lipid complex can substantially affect a drugs functional properties relative to those of the unencapsulated or nonlipid-associated drug. In addition, different liposomal or lipid-complexed products with a common active ingredient may vary from one another in the chemical composition and physical form of the lipid component. Such differences may affect functional properties of these drug products.
Amphotericin B is a polyene, antifungal antibiotic produced from a strain of Streptomyces nodosus. Amphotericin B is designated chemically as -33--1,3,5,6,9,11,17,37-octahydroxy-15,16,18-trimethyl-13-oxo-14,39-dioxabicyclo nonatriaconta-19, 21, 23, 25, 27, 29, 31-heptaene-36-carboxylic acid.
It has a molecular weight of 924.09 and a molecular formula of C47H73NO17. The structural formula is:
ABELCET is provided as a sterile, opaque suspension in 20 mL glass, single-use vials. Each 20 mL vial contains 100 mg of amphotericin B (see DOSAGE AND ADMINISTRATION), and each mL of ABELCET contains:
Amphotericin B USP 5.0 mg
l--dimyristoylphosphatidylcholine (DMPC) 3.4 mg
l--dimyristoylphosphatidylglycerol (DMPG) 1.5 mg
Sodium Chloride USP 9.0 mg
Water for Injection USP, q.s. 1 mL.
Amplification (psychology)

# Overview
Amplification is to amplify physical symptoms based on psychological factors such as anxiety or depression: "somatosensory amplification refers to the tendency to experience somatic sensation as intense, noxious, and disturbing. What may be a minor 'twinge' or mild 'sorenes' to the stoic, is a severe, consuming pain to the amplifier."
Psychological state has been documented to effect the course of upper respiratory tract infection, post-infectious irritable bowel syndrome, and musculoskeletal pain.
Amplification is not recognized by the American Psychiatric Association.
The Somatosensory Amplification Scale (SAS) has been validated to measure amplification. The scale contains four items measured with a 5 item Likert scale:
- Sudden loud noises really disturb me
- I'm very uncomfortable when I'm in a place that is too hot or too cold
- I can't stand pain as well as most people can
- I find I'm often aware of various things happening in my body
- I'm quick to sense the hunger contractions in my stomach
Amplification is related to alexithymia. Amplification may also contribute to multiple-drug intolerance (if the adverse effects that are reported are non-specific). It is unclear whether amplification is related to observations that Type A personality trait may be associated with delayed recovery after organic illness.