Persius/hicric huggingface dataset:
Chronic liver disease overview

# Overview
Chronic liver disease is a liver disease of slow process and persisting over a long period of time, resulting in a progressive destruction of the liver.

# Treatment

## Medical Therapy
The treatment of chronic liver disease depends on the cause. While some conditions may be treated with medications, others may require surgery or a transplant. Transplant is required when the liver fails and there is no other alternative .
Because many chronic liver disorders have no cure, many people have been turning to alternative health care. Herbal supplements are widely used by many people with chronic liver disease. None of these herbs have ever been tested in randomized clinical trials and no one knows whether they work.  Some common herbs known to be potentially harmful in liver disease include black cohosh, ma huang, chaparral, comfrey, germander, greater celandine, kava, mistletoe, pennyroyal, skull cap and valerian.
Claire House Childrens Hospice
Claire House Children's Hospice is a children's hospice in England. The hospice provides care to children up to the age of 18 with life-threatening or life-limiting conditions. Services include specialist respite, palliative, terminal and bereavement care. The hospice is dedicated to enhancing the quality of life of its patients.
The hospice, which is located in Bebington on the Wirral, relies largely on goodwill to pay the 2 million annually needed to keep the hospice doors open.
The hospice has many celebrity supporters.  The most recognisable of these is Wayne Rooney and his girlfriend Coleen McLoughlin. Coleen has a sister who uses Claire House and she has been on Trevor McDonald to try to highlight the plight of children's hospices.
Most recently at Claire House a new Teenage Annex has been opened to provide respect, dignity, privacy and social interaction for all the people who use it.
Clindamycin phosphate warnings

# WARNINGS
Orally and parenterally administered clindamycin has been associated with severe colitis which may result in patient death. Use of the topical formulation of clindamycin results in absorption of the antibiotic from the skin surface. Diarrhea, bloody diarrhea, and colitis (including pseudomembranous colitis) have been reported with the use of topical and systemic clindamycin.
Studies indicate a toxin(s) produced by clostridia is one primary cause of antibiotic-associated colitis. The colitis is usually characterized by severe persistent diarrhea and severe abdominal cramps and may be associated with the passage of blood and mucus. Endoscopic examination may reveal pseudomembranous colitis. Stool culture for Clostridium difficile and stool assay for C. difficile toxin may be helpful diagnostically.
When significant diarrhea occurs, the drug should be discontinued. Large bowel endoscopy should be considered to establish a definitive diagnosis in cases of severe diarrhea.
Antiperistaltic agents such as opiates and diphenoxylate with atropine may prolong and/or worsen the condition. Vancomycin has been found to be effective in the treatment of antibiotic-associated pseudomembranous colitis produced by Clostridium difficile. The usual adult dosage is 500 milligrams to 2 grams of vancomycin orally per day in three to four divided doses administered for 7 to 10 days. Cholestyramine or colestipol resins bind vancomycin in vitro. If both a resin and vancomycin are to be administered concurrently, it may be advisable to separate the time of administration of each drug.
Diarrhea, colitis, and pseudomembranous colitis have been observed to begin up to several weeks following cessation of oral and parenteral therapy with clindamycin.
Cloxacillin Sodium description

# Description
Dicloxacillin sodium, USP is an antibacterial agent of the isoxazolyl penicillin series. It is a penicillinase-resistant, acid resistant semisynthetic penicillin suitable for oral administration.
Dicloxacillin sodium is chemically designated as 4-Thia-1-azabicyclo heptane-2-carboxylic acid, 6--carbonyl]-amino]-3,3-dimethyl-7-oxo-, monosodium salt, monohydrate,  and has the following structural formula:
Each capsule for oral administration contains dicloxacillin sodium equivalent to 250 or 500 mg of dicloxacillin. The inactive ingredient is magnesium stearate. The capsule shells contain FD&C Blue 1, titanium dioxide, and gelatin.
Clubfoot (patient information)
For the WikiDoc page for this topic, click here

# Overview
Clubfoot is when the foot turns inward and downward. It is a congenital condition, which means it is present at birth.

# What are the symptoms of Clubfoot?
The physical appearance of the foot may vary. One or both feet may be affected.
The foot turns inward and downward at birth, and is difficult to place in the correct position. The calf muscle and foot may be slightly smaller than normal.

# What causes Clubfoot?
Clubfoot is the most common congenital disorder of the legs. It can range from mild and flexible to severe and rigid.
The cause is not known, but the condition may be passed down through families in some cases. Risk factors include a family history of the disorder and being male. The condition occurs in about 1 out of every 1,000 live births.

# Who is at highest risk?
Risk factors include a family history of the disorder and being male. The condition occurs in about 1 out of every 1,000 live births.

# Diagnosis
The disorder is identified during a physical examination. A foot x-ray may be done.

# When to seek urgent medical care?
If your child is being treated for clubfoot, call your health care provider if:
- The toes swell, bleed, or change color under the cast
- The cast appears to be causing significant pain
- The toes disappear into the cast
- The cast slides off
- The foot begins to turn in again after treatment

# Treatment options
Treatment may involve moving the foot into the correct position and using a cast to keep it there. This is often done by an orthopedic specialist. Treatment should be started as early as possible -- ideally, shortly after birth -- when reshaping the foot is easiest.
Gentle stretching and recasting occurs every week to improve the position of the foot. Generally, five to 10 casts are needed. The final cast remains in place for 3 weeks. After the foot is in the correct position, a special brace is worn nearly full time for 3 months. Then it is used at night and during naps for up to 3 years.
Often, a simple outpatient procedure is needed to release a tightened Achilles tendon.
Some severe cases of clubfoot will require surgery if other treatments do not work, or if the problem returns. The child should be monitored by a doctor until the foot is fully grown. See: Clubfoot repair

# Where to find medical care for Clubfoot?
Directions to Hospitals Treating Clubfoot

# What to expect (Outlook/Prognosis)?
The outcome is usually good with treatment.

# Possible complications
Some defects may not be completely fixed. However, treatment can improve the appearance and function of the foot. Treatment may be less successful if the clubfoot is linked to other birth disorders.

# Sources
Coagulation factor II receptor
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Proteinase-activated receptor 1 (PAR1) also known as Protease-activated receptor 1 or coagulation factor II (thrombin) receptor is a protein that in humans is encoded by the F2R gene. PAR1 is a G protein-coupled receptor involved in the regulation of thrombotic response.  Proteolytic cleavage leads to the activation of the receptor.
PAR-1 has multifaceted effects and plays a key role in mediating the interplay between coagulation and inflammation, which is important in the pathogenesis of inflammatory and fibrotic lung diseases. It is involved both in disruption and maintaining of endothelial barrier integrity, through interaction with either thrombin or activated protein C, respectively.

# Ligands
Several selective antagonists for the PAR1 receptor have been developed, for use as anti-clotting agents for the treatment of heart disease.
- SCH-530,348
SCH530348 has been recently shown to attenuate the neutrophilic inflammatory response to Streptococcus pneumoniae by reducing levels of pro-inflamamtory cytokines such as IL-1 and chemokines CXCL1, CCL2 and CCL7.
Collision-induced dissociation
In mass spectrometry, collision-induced dissociation (CID), referred to by some as collisionally activated dissociation (CAD), is a mechanism by which to fragment molecular ions in the gas phase. The molecular ions are usually accelerated by some electrical potential to high kinetic energy in the vacuum of a mass spectrometer and then allowed to collide with neutral gas molecules (often helium, nitrogen or argon). In the collision some of the kinetic energy is converted into internal energy which results in bond breakage and the fragmentation of the molecular ion into smaller fragments. These fragment ions can then be analyzed by a mass spectrometer.
CID and the fragment ions produced by CID are used for several purposes. Partial or complete structural determination can be achieved. In some cases identity can be established based on previous knowledge without determining structure. Another use is in simply achieving more sensitive and specific detection. By looking for a unique fragment ion you can detect a given molecule in the presence of other molecules of the same nominal molecular mass, essentially reducing the background and increasing the limit of detection.
CID is used as part of tandem mass spectrometry for many experiments in proteomics. While CID is currently the most popular method for standard tandem mass spectrometry, there are other also other fragmentation methods for special purposes, for example electron transfer dissociation (ETD), electron capture dissociation (ECD) and Infrared multiphoton dissociation (IRMPD).

# Examples

## CID in a triple quadrupole
In a triple quadrupole mass spectrometer there are three quadrupole mass analyzers. The first quadrupole termed "Q1" can act as a mass filter and transmits a selected ion and accelerates it towards "Q2" which is termed a collision cell. The pressure in Q2  is higher and the ions collide with neutral gas in the collision cell and fragments by CID. The fragments are then accelerated out of the collision cell and enter Q3 which scans through the mass range, analyzing the resulting fragments (as they hit a detector).  This produces a mass spectrum of the CID fragments from which structural information or identity can be gained. Many other experiments using CID on a triple quadrupole exist such as precursor ion scans that determines where a specific fragment came from rather than what fragments are produced by a given molecule.

## CID in an FTMS ICR cell (SORI-CID)
SORI-CID (sustained off-resonance irradiation collision-induced dissociation) is a CID technique used in Fourier transform ion cyclotron resonance mass spectrometry which involves accelerating the ions in cyclotron motion (in a circle inside of an ion trap) and then increasing the pressure resulting in collisions that produce CID fragments. After the SORI-CID process is complete the pressure is reduced back to high vacuum and the analysis of the fragment ions is performed as usual.
Common palmar digital arteries
Three common palmar digital arteries (common volar digital arteries) arise from the convexity of the arch and proceed downward on the second, third, and fourth Lumbricales.
Each receives the corresponding volar metacarpal artery and then divides into a pair of proper volar digital arteries (aa. digitales volares propri; collateral digital arteries) which run along the contiguous sides of the index, middle, ring, and little fingers, deep to the corresponding digital nerves; they anastomose freely in the subcutaneous tissue of the finger tips and by smaller branches near the interphalangeal joints.
Each gives off a couple of dorsal branches which anastomose with the dorsal digital arteries, and supply the soft parts on the back of the second and third phalanges, including the matrix of the fingernail.
The proper volar digital artery for medial side of the little finger springs from the ulnar artery under cover of the Palmaris brevis.
Microvillous inclusion disease
Microvillous inclusion disease, also known as Davidson's disease, congenital microvillous atrophy and, less specifically, microvillous atrophy, is a rare genetic disorder of the small intestine that is inherited in an autosomal recessive pattern.

# Presentation
It is characterized by chronic, intractable diarrhoea in new-born infants, starting in the first few days of life.

# Prognosis
It is nearly always fatal unless, like short bowel syndrome patients, treated with parenteral nutrition or an intestinal transplant. The patient is often classified as being in "intestinal failure" and treated with the cohort of patients known as "short bowel syndrome" patients.

# Pathophysiology
It is caused by a congenital lack of apical microvilli in the epithelial cells of the small intestine.

# Diagnosis
Diagnosis in utero is currently not possible as the gene(s) involved in the disease are not known; diagnosis is made by biopsy of the small intestine.

## Biopsy
The appearance of microvillous inclusion disease on light microscopy is similar to celiac sprue; however, it usually lacks the intraepithelial lymphocytic infiltration characteristic of celiac sprue and stains positive for carcinoembryonic antigen (CEA).  
The definitive diagnosis is dependent on electron microscopy.

## Differential diagnosis
The differential diagnosis of chronic and intractable diarrhea is:
- Intestinal epithelial dysplasia
- Syndromatic diarrhea
- Immunoinflammatory enteropathy

# Genetic prevalence
File:Autorecessive.svg
Microvillous inclusion disease is thought to be extremely rare; only, approximately, two dozen cases have been identified in the medical literature.

# History
Microvillous inclusion disease was first described in 1978 by Davidson et al.  It was originally described as familial enteropathy.
Constantly fast dividing cells

# Overview
In cellular biology, constantly fast dividing cells are cells that spend little or no time in the quiescent G0 phase of the cell cycle, but regularly performs cell division.
This is the case for only a minority of cells in the body. Constantly dividing cell types include skin cells, cells in the gastrointestinal tract and blood cells in the bone marrow.
Many more types of cells in the body are constantly or regularily dividing, albeit at a very slow rate.
It is mainly not the segments of the cell cycle that go faster (i.e. G1 phase, S phase, G2 phase and M phase), but rather a short or absent G0 phase.

# Hazards
Constantly dividing cells have a higher risk of becoming malignant and develop cancer, dividing uncontrollably. This is why, on the other hand, muscle cancer is very rare, although constituting ~50% of body weight, since muscle cells are not constantly dividing cells.
In addition, cytotoxic drugs, used in treatment of cancer, work by inhibiting the proliferation of dividing cells, with the malignant cells as the desired target. However, this has the adverse effect of also striking against the cells normally dividing in the body, and thus impairing normal body function of skin, GI tract and bone marrow.
Coproporphyrinogen III oxidase
Coproporphyrinogen-III oxidase, mitochondrial (abbreviated as CPOX) is an enzyme that in humans is encoded by the CPOX gene. A genetic defect in the enzyme results in a reduced production of heme in animals. The medical condition associated with this enzyme defect is called hereditary coproporphyria.
CPOX, the sixth enzyme of the haem biosynthetic pathway, converts coproporphyrinogen III to protoporphyrinogen IX through two sequential steps of oxidative decarboxylation. The activity of the CPOX enzyme, located in the mitochondrial membrane, is measured in lymphocytes.

# Function
CPOX is an enzyme involved in the sixth step of porphyrin metabolism it catalyses the oxidative decarboxylation of coproporphyrinogen III to proto-porphyrinogen IX in the haem and chlorophyll biosynthetic pathways. The protein is a homodimer containing two internally bound iron atoms per molecule of native protein. The enzyme is active in the presence of molecular oxygen that acts as an electron acceptor. The enzyme is widely distributed having been found in a variety of eukaryotic and prokaryotic sources.

# Structure

## Gene
Human CPOX is a mitochondrial enzyme encoded by a 14 kb CPOX gene containing seven exons located on chromosome 3 at q11.2.

## Protein
CPOX is expressed as a 40 kDa precursor and contains an amino terminal mitochondrial targeting signal. After proteolytic processing, the protein is present as a mature form of a homodimer with a molecular mass of 37 kDa.

# Clinical significance
Hereditary coproporphyria (HCP) and harderoporphyria are two phenotypically separate disorders that concern partial deficiency of CPOX. Neurovisceral symptomatology predominates in HCP. Additionally, it may be associated with abdominal pain and/or skin photosensitivity. Hyper-excretion of coproporphyrin III in urine and faeces has been recorded in biochemical tests. HCP is an autosomal dominant inherited disorder, whereas harderoporphyria is a rare erythropoietic variant form of HCP and is inherited in an autosomal recessive fashion. Clinically, it is characterized by neonatal haemolytic anaemia. Sometimes, the presence of skin lesions with marked faecal excretion of harderoporphyrin is also described in harderoporphyric patients.
To date, over 50 CPOX mutations causing HCP have been described. Most of these mutations result in substitution of amino acid residues within the structural framework of CPOX. In terms of the molecular basis of HCP and harderoporphyria, mutations of CPOX in patients with harderoporphyria were demonstrated in the region of exon 6, where mutations in those with HCP were also identified.  As only patients with mutation in this region (K404E) would develop harderoporphyria, this mutation led to diminishment of the second step of the decarboxylation reaction during the conversion of coproporphyrinogen to protoporphyrinogen, implying that the active site of the enzyme involved in the second step of decarboxylation is located in exon 6.

# Interactions
CPOX has been shown to interact with the atypical keto-isocoproporphyrin (KICP) in human subjects with mercury (Hg) exposure.
Cowchock Wapner Kurtz syndrome
The Cowchock Syndrome or Cowchock Wapner Kurtz syndrome is a neuropathy which was named for the lead scientist of a team who did research on a family which was affected by this disease.  The research was published in 1985.
Cowchock Syndrome is a rare, X-linked recessive disorder.  It is caused by a defect in a particular gene on the X-chromosome.  According to the website Online Mendelian Inheritance in Man, it causes "motor sensory neuropathy," which results in muscle weakness. It also frequently causes deafness and mental retardation.
Also according to OMIM, defects in this same gene are also responsible for Charcot-Marie-Tooth disease.  Therefore, these two diseases are very closely related, although they exhibit some differences in the specific symptoms that were recorded.  (This similarity between the diseases has created some confusion for student researchers at DCHS who were investigating X-linked diseases, so other students should beware that there is not much information about Cowchock disease in particular - it is better to look for information about Charcot-Marie-Tooth disease).
References
Cowchock, F. S.; Duckett, S. W.; Streletz, L. J.; Graziani, L. J.; Jackson, L. G. : 
X-linked motor-sensory neuropathy type-II with deafness and mental retardation: a new disorder. Am. J. Med. Genet. 20: 307-315, 1985.
OMIM website.
Crouzonodermoskeletal syndrome
Crouzonodermoskeletal syndrome is a disorder characterized by the premature joining of certain bones of the skull (craniosynostosis) during development and a skin condition called acanthosis nigricans.
Some of the signs and symptoms of Crouzonodermoskeletal syndrome are similar to those seen with Crouzon syndrome. They include prematurely fused skull bones, which affect the shape of the head and face; wide-set, bulging eyes due to shallow eye sockets; eyes that do not point in the same direction (strabismus); a small, beaked nose; and an underdeveloped upper jaw. People with these conditions are generally of normal intelligence.
Several features distinguish Crouzonodermoskeletal syndrome from Crouzon syndrome. People with Crouzonodermoskeletal syndrome have acanthosis nigricans, a skin condition characterized by thick, dark, velvety skin in body folds and creases, including the neck and underarms. In addition, subtle changes may be seen in the bones of the spine (vertebrae). Noncancerous growths called cementomas may develop in the jaw during young adulthood.
Crouzonodermoskeletal syndrome is rare; the condition is seen in about 1 per million people.

# Genetics
Mutations in the FGFR3 gene cause Crouzonodermoskeletal syndrome. The protein made by the FGFR3 gene is a receptor that plays a role in the development and maintenance of bone and brain tissue. Researchers do not know how a mutation in FGFR3 leads to the characteristic features of this disorder, but changes in the receptor appear to disrupt the normal development of bones in the skull and affect skin pigmentation.
This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder.
In some cases, an affected person inherits the mutation from one affected parent. Other cases may result from new mutations in the gene. These cases occur in people with no history of the disorder in their family.
Current Procedural Terminology

# Overview
The Current Procedural Terminology (CPT) code set is maintained by the American Medical Association through the CPT Editorial Panel.  The CPT code set accurately describes medical, surgical, and diagnostic services and is designed to communicate uniform information about medical services and procedures among physicians, coders, patients, accreditation organizations, and payers for administrative, financial, and analytical purposes.  The current version is the CPT 2007.
There are three types of CPT codes:
- Category I CPT Code(s)
- Category II CPT Code(s)  Performance Measurement
- Category III CPT Code(s)  Emerging Technology
CPT is currently identified by the Centers for Medicare and Medicaid Services (CMS)  as Level 1 of the Health Care Procedure Coding System.

# Copyright
CPT is a registered trademark of the American Medical Association. The AMA holds copyright which prevents free use and distribution of codes.
Although the CPT system is mandated by the Centers for Medicare and Medicaid Services (CMS) and HIPAA, and the data for it appears in the Federal Register, the American Medical Association (AMA) maintains that their copyright of the CPT allows them to charge a license fee to anyone who wishes to associate RVU values with CPT codes. The AMA receives approximately $70 million annually from these fees, making them reluctant to allow the free distribution of tools and data that might help physicians calculate, record, or submit their fees accurately and fairly.