Persius/hicric huggingface dataset:
Amphotericin B lipid complex 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, 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
Antibody-Directed Enzyme Prodrug Therapy

# Overview
ADEPT (Antibody-directed enzyme prodrug therapy) is a strategy to overcome the problems of lack of tumor selectivity. An antibody designed/developed against a tumor antigen is linked to an enzyme and injected to the blood, resulting in selective binding of the enzyme in the tumor. When the discrimination between tumor and normal tissue enzyme levels is sufficient, a prodrug is administrated into the blood circultion, which is converted to an active cytotoxic drug by the enzyme, only within the tumor. Selectivity is achieved by the tumor specificity of the antibody and by delaying prodrug administration until there is a large differential between tumor and normal tissue enzyme levels.
ADEPT has shown antitumor activity in animal tumor models of human choriocarcinoma and colonic and breast carcinoma.

# ADEPT history
The first pilot-scale clinical trial of ADEPT was carried out at Charing Cross Hospital, London, using an anti-CEA F(ab)2 antibody conjugated to the bacterial enzyme carboxypeptidase G2 (CPG2).
The antibody used in the first ADEPT clinical trial was of murine origin and the enzyme was bacterial. Host antibodies to both components of the AEC were present in the blood of all non-immunosuppressed patients by day 10 after AEC infusion . Several patients received cyclosporin since it had been shown in rabbits that this could delay the appearance of host antibodies to soluble proteins .
A subsequent, small-scale trial at the Royal Free Hospital, London, used the same agents as in the Charing Cross Hospital trial but the protocol was modified to provide additional pharmacokinetic data and most patients received only a single course of treatment .

# Other versions of directed enzyme prodrug therapy (DEPT)
There are several other strategies to use prodrug/enzyme systems for cancer therapy, including gene-directed enzyme prodrug therapy (GDEPT), virus-directed enzyme prodrug therapy (VDEPT), PDEPT (Polymer-Directed Enzyme Prodrug Therapy), LEAPT (Lectin-directed enzyme-activated prodrug therapy), and CDEPT (Clostridial-directed enzyme prodrug therapy).
Laboratory diagnosis of viral infections

# Overview
In the diagnostic laboratory virus infections are confirmed by several methods that include:
- Growth of the virus in a cell culture from a specimen taken from the patient.
- Detection of virus-specific antibodies in the blood.
- Detection of virus antigens
- Detection of virus nucleic acids
- Observation of virus particles by electron microscopy.
- Hemagglutination assay

# Cell culture
When growing virus in a cell culture, the cells affected with virus will evolve morphologic changes, often specific for the type of virus involved.

# Antibody detection
When the adaptive immune system of a vertebrate encounters a virus, it produces specific antibodies which bind to the virus and render it non-infectious. This is called humoral immunity. Two types of antibodies are important. The first called IgM is highly effective at neutralizing viruses but is only produced by the cells of the immune system for a few weeks. The second, called, IgG is produced indefinitely. The presence of IgM in the blood of the host is used to test for acute infection, whereas IgG indicates an infection sometime in the past. Both types of antibodies are measured when tests for immunity are carried out.

# Antigen detection
Detection of virus antigens can be done by ELISA in tissues and fluids.
Other techniques are:
- immunofluorescence
- immunoperoxidase

# Hemagglutination assay
Many viruses attach to molecules present on the surface of red blood cells. A consequence of this is that - at certain concentrations - a viral suspension may bind together (agglutinate) the red blood cells thus preventing them from settling out of suspension. Usefully, agglutination is rarely linked to infectivity, attenuated viruses can therefore be used in assays.

# Nucleic acid detection
Detection of virus encoded DNA and RNA is done with polymerase chain reaction.  Nucleic acid hybridization with virus-specific probes detects specific viruses.
Approach to a patient with hypercalcemia
Introduction
- Hypercalcemia is a relatively common clinical problem. Among all causes of hypercalcemia, primary hyperparathyroidism and malignancy are the most common, accounting for greater than 90 percent of cases.  
- Hypercalcemia : Serum total calcium above 10.6 mg/dl.
- This topic card will discuss how to approach a hypercalcemic patient.
History and physical examination :
- Signs and symptoms related to the Hypercalcemia itself :
- Signs and symptoms related to the cause of Hypercalcemia.
Diagnostic approach : See algorithm.
- Step one: Serum total calcium level.
- Step two : Correction of serum calcium level for albumin level to exclude pseudohypercalcemia (facticious Hypercalcemia) by the following equation :
- Step three : Serum parathyroid hormone level(PTH) : To distinguish PTH-dependent from PTH-independent Hypercalcemia.
- Step four (A) : In PTH-dependent cases do the following :
- Step four (B) : In PTH-independent cases do serum phosphate level.
- Step five (A):  If serum phosphate level is low, do Parathyroid-hormone related peptide (PhRP) level : to assess for Hypercalcemia of malignancy.
- Step five (B) : If serum phosphate level is high do the following :
Clinical Clues :
- The degree of hypercalcemia also may be useful diagnostically.
- PhRP is usually not necessary for diagnosis since most patients have clinically apparent malignancy at the time of Hypercalcemia.
- There appears to be a higher incidence of primary hyperparathyroidism in patients with malignancy than in the general population . Thus, despite the increased cost, it is reasonable to order an intact PTH assay as part of the routine evaluation for hypercalcemia even in a patient with known malignant disease.
- Vitamin D metabolites :
- Other tests that can be helpful :
References
Gait disturbance resident survival guide
Synonyms and Keywords: gait disturbance management, gait disturbance workup, gait disturbance approach, approach to disequilibrium, approach to imbalance

# Overview
Gait disturbance refers to an impaired sense or absence of balance or equilibrioception that primarily occurs during standing or walking. Gait disturbance usually occurs without any cephalic sensations like headache, nausea, and vomiting. It may also causes dizziness, but it is typically a more complex category with more continuous symptoms in comparison to the other causes of dizziness, like presyncope and vertigo.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions that may result in death or permanent disability within 24 hours if left untreated.
- Intoxications
- Head trauma
- Carbon monoxide poisoning

## Common Causes
- Osteoarthritis
- Pelvic girdle pain
- Ataxia
- Hip dysplasia
- Polio
- Multiple sclerosis
- Cerebellar lesions
- Cerebellar degeneration
- Parkinson's disease

# Diagnosis
Shown below is an algorithm summarizing the diagnosis of Gait disturbance according to the American Academy of Neurology guidelines:

# Treatment
Treat the underlying cause.
- To view the specific treatment of Ataxia click here.
- To view the specific treatment of Multiple sclerosis click here.
- To view the specific treatment of Polio click here.
- To view the specific treatment of Osteoarthritis click here.
- To view the specific treatment of Hip dysplasia click here.

# Do's
- Perform a top-down visual orientation evaluation to assess symmetry, quantity, and quality of arm swing; pelvic rotation; knee motion; pelvic tilt; and lateral trunk shift.
- Perform a bottom-up orientation evaluation to assess ankle, subtalar, midfoot, and hallux motion symmetry, quantity, and quality.
- Perform a thorough evaluation of gait, measuring gait on a level surface, change in gait speed, gait with horizontal head turns, gait with vertical head turns, gait with pivot turn, step over obstacle, gait with narrow base of support, gait with eyes closed, ambulating backwards, and steps.
- Be aware of the patients' surroundings and be always aware for possible falls.
- Three-dimensional analysis systems may be used as a tool as it is currently the gold standard for measuring spatiotemporal variables and joint kinematics.
- Innovative pressure measurement technology may provide unique insight on mechanical dysfunctions and gait abnormalities.

# Don'ts
- Do not delay brain imaging when TBI is suspected.
- Do not perform walking tests in patients with severe acute gait disturbance.
Atovaquone proguanil labels and packages

# Labels And Packages
Principal Display Panel
NDC 0173-0675-01
MALARONE
(atovaquone and proguanil HCl)
Tablets
Each tablet contains 250 mg atovaquone and 100 mg proguanil HCl.
Rx only
100 Tablets
See accompanying prescribing information for Dosage and Administration.
Store at 25oC (77oF); excursions permitted to 15o to 30oC (59oto 86oF) (see USP Controlled Room Temperature).
Do not use if printed safety seal under cap is broken or missing.
GlaxoSmithKline
Research Triangle Park, NC 27709
Made in Canada
Rev. 3/10
A079205
Principal Display Panel
NDC 0173-0676-01
MALARONE
(atovaquone and proguanil HCl)
Pediatric Tablets
Each tablet contains 62.5 mg atovaquone and 25 mg proguanil HCl.
Rx only
100 Tablets
See accompanying prescribing information for Dosage and Administration.
Store at 25oC (77oF); excursions permitted to 15o to 30oC (59oto 86oF) (see USP Controlled Room Temperature).
Do not use if printed safety seal under cap is broken or missing.
GlaxoSmithKline
Research Triangle Park, NC 27709
Made in Canada
Rev. 3/10
A079206
Autoregressive integrated moving average

# Overview
In statistics, an autoregressive integrated moving average (ARIMA) model is a generalisation of an autoregressive moving average or (ARMA) model.  These models are fitted to time series data either to better understand the data or to predict future points in the series.  The model is generally referred to as an ARIMA(p,d,q) model where p, d, and q are integers greater than or equal to zero and refer to the order of the autoregressive, integrated, and moving average parts of the model respectively.
Given a time series of data X_t where t is an integer index and the X_t are real numbers, then an ARMA(p,q) model is given by
where L is the lag operator, the \phi_i are the parameters of the autoregressive part of the model, the \theta_i are the parameters of the moving average part and the \varepsilon_t are error terms.  The error terms \varepsilon_t are generally assumed to be independent, identically distributed variables sampled from a normal distribution with zero mean.
An ARIMA(p,d,q) process is obtained by integrating an ARMA(p,q) process.  That is,
where d is a positive integer that controls the level of differencing (or, if d=0, this model is equivalent to an ARMA model).  Conversely, applying term-by-term differencing d times to an ARMA(p,q) process gives an ARIMA(p,d,q) process.  Note that it is only necessary to difference the AR side of the ARMA representation, because the MA component is always I(0).
It should be noted that not all choices of parameters produce well-behaved models.  In particular, if the model is required to be stationary then conditions on these parameters must be met.
Some well-known special cases arise naturally.  For example, an ARIMA(0,1,0) model is given by:
which is simply a random walk.
A number of variations on the ARIMA model are commonly used.  For example, if multiple time series are used then the X_t can be thought of as vectors and a VARIMA model may be appropriate.  Sometimes a seasonal effect is suspected in the model.  For example, consider a model of daily road traffic volumes.  Weekends clearly exhibit different behaviour from weekdays.  In this case it is often considered better to use a SARIMA (seasonal ARIMA) model than to increase the order of the AR or MA parts of the model.  If the time-series is suspected to exhibit long-range dependence then the d parameter may be replaced by certain non-integer values in a Fractional ARIMA (FARIMA also sometimes called ARFIMA) model.
Bannayan-Riley-Ruvalcaba syndrome causes

# Overview
Bannayan-Riley-Ruvalcaba syndrome (BRRS) is caused by a mutation in the phosphatase and tensin homolog (PTEN) gene.

# Causes
Genetic Cause
- Bannayan-Riley-Ruvalcaba syndrome (BRRS) is caused by a mutation in the phosphatase and tensin homolog (PTEN) gene.
- Different types of mutations occurs in PTEN gene and are as follows:
Germline intragenic mutations in PTEN gene
Gross gene deletions in PTEN gene
Mutations in the PTEN gene promoter region results in heterozygous germline mutations
Deletion in exons 1-5 of PTEN gene
- Germline intragenic mutations in PTEN gene
- Gross gene deletions in PTEN gene
- Mutations in the PTEN gene promoter region results in heterozygous germline mutations
- Deletion in exons 1-5 of PTEN gene
Basic Interpersonal Communicative Skills
Basic Interpersonal Communicative Skills (BICS) are language skills needed to interact in social situations, for example, when speaking to a friend on the telephone. BICS refers primarily to context-bound, face-to-face communication, like the language first learned by toddlers and preschoolers, which is used in everyday social interaction.
We use this language skill in face-to-face interactions, rather than in dealing with academic tasks.
This term is often credited to Jim Cummins research related to language acquisition and learning.  The other term that is often used in conjunction with this term is Cognitive Academic Language Proficiency (CALP). CALP refers to the highly abstract, decontextualized communication that takes place in the classroom, especially in the later elementary grades. CALP involves the language of learning, which enables children to problem-solve, hypothesize, imagine, reason and project into situations with which they have no personal experience. It is a prerequisite for learning to read and write and for overall academic success. The implications of the BICS and CALP concepts for children are that the second language or language of the classroom needs to be sufficiently well developed for her or him to be able to meet the cognitive demands of the academic setting. Students typically are thought to acquire BICS in 2-3 years but take 5-7 years to develop the CALP needed to be on the same level with their native speaking counterparts in the classroom.

# Further reading
- One Language or Two?: Answers to Questions about Bilingualism in Children
Betainehomocysteine S-methyltransferase
In the field of enzymology, a betaine-homocysteine S-methyltransferase also known as betaine-homocysteine methyltransferase (BHMT) is a zinc metallo-enzyme that catalyzes the transfer of a methyl group from trimethylglycine and a hydrogen ion from homocysteine to produce dimethylglycine and methionine respectively:
- Trimethylglycine (methyl donor) + homocysteine (hydrogen donor)  dimethylglycine (hydrogen receiver) + methionine (methyl receiver)
This enzyme belongs to the family of transferases, specifically those transferring one-carbon group methyltransferases. This enzyme participates in the metabolism of glycine, serine, threonine and also methionine.

# Isozymes
In humans, there are two isozymes, BHMT and BHMT2, each encoded by a separate gene.

# Tissue distribution
BHMT is expressed most predominantly in the liver and kidney.

# Clinical significance
Mutations in the BHMT gene are known to exist in humans. Anomalies may influence the metabolism of homocysteine , which is implicated in disorders ranging from vascular disease, autism, and schizophrenia to neural tube birth defects such as spina bifida.
Branched chain amino acid transaminase 1
Branched chain amino acid transaminase 1 is a protein that in humans is encoded by the BCAT1 gene. It is the first enzyme in the Branched-chain amino acid (BCAA) degradation pathway and facilitates the reversible transamination of BCAAs and glutamate. BCAT1 resides in the cytoplasm, while its isoform, BCAT2, is found in the mitochondria.

# Function
This gene encodes the cytosolic form of the enzyme branched-chain amino acid transaminase. This enzyme catalyzes the reversible transamination of branched-chain alpha-keto acids (BCKAs) to the branched-chain amino acids (BCAAs) Valine, Leucine and Isoleucine, which are essential for cell growth. In humans, its primary role is the deamination of BCAAs, as humans lack the enzymes for de novo synthesis of BCKAs. The respective cofactors are alpha-ketoglutarate and glutamate. The respective reactions are:
L-leucine + 2-oxoglutarate = 4-methyl-2-oxopentanoate + L-glutamate
L-isoleucine + 2-oxoglutarate = (S)-3-methyl-2-oxopentanoate + L-glutamate
L-valine + 2-oxoglutarate = 3-methyl-2-oxobutanoate + L-glutamate 
Cells can further degrade BCKAs by the Branched-chain keto acid dehydrogenase complex from which the carbon backbones of each BCAA may enter distinct degradation pathways.
The oncogenic transcription factor Myc is frequently reported to drive BCAT1 expression.

# Clinical significance
Two different clinical disorders have been attributed to a defect of branched-chain amino acid transamination: hypervalinemia and hyperleucine-isoleucinemia. As there is also a gene encoding a mitochondrial form of this enzyme (BCAT2), mutations in either gene may contribute to these disorders.
Overexpression of BCAT1 has been associated with a variety of cancers, among them glioblastoma, breast cancer, acute myeloid leukemia, gastric cancer and chronic myeloid leukemia.
Bullous pemphigoid (patient information)
For the WikiDoc page for this topic, click here

# Overview
Bullous pemphigoid is a skin disorder characterized by large blisters.

# What are the symptoms of Bullous pemphigoid?
Some people may have no symptoms, others may have mild redness and irration.
In severe cases, they are multiple blisters, called bullae. The blisters are usually located on the arms, legs, or middle of the body. About one-third of persons with bullous pemphigoid also develop blisters in the mouth. The blisters may break open and form ulcers or open sores.
Other symptoms may include:
- Itching
- Rashes
- Mouth sores
- Bleeding gums

# What causes Bullous pemphigoid?
The cause is not known, but may be related to immune system disorders, certain other diseases, or use of some medications.

# Who is at highest risk?
Bullous pemphigoid usually occurs in elderly persons and is rare in young people. Symptoms come and go. In most patients, the condition goes away within 6 years.

# Diagnosis
Tests that may be done to help diagnose this condition include:
- Blood tests
- Skin lesion biopsy

# When to seek urgent medical care?
Call your doctor for an appointment if you have:
- Unexplained blisters on your skin
- An itchy rash that continues despite home treatment

# Treatment options
Power anti-inflammatory medicines called corticosteroids may be prescribed. Some corticosteroids are taken by mouth, while others require a shot (injection). In persons with early forms of the disease, corticosteroid creams may be used.
Your doctor may prescribe chemotherapy or medicines to help suppress the immune system.
Antibiotics called tetracyclines may be useful in mild cases. Niacin (a B complex vitamin) is sometimes given along with tetracycline.

# Where to find medical care for Bullous pemphigoid?
Directions to Hospitals Treating Bullous pemphigoid

# What to expect (Outlook/Prognosis)?
Bullous pemphigoid usually responds well to treatment. Most patients may stop taking medicine after several years. However, the disease sometimes returns after treatment is stopped.

# Possible complications
Skin infection is the most common complication.

# Sources
Carbenicillin indanyl sodium description

# Description
Geocillin, a semisynthetic penicillin, is the sodium salt of the indanyl ester of Geopen (carbenicillin disodium). The chemical name is: 1-(5-Indanyl)-N-(2-carboxy-3,3-dimethyl-7-oxo-4-thia-1-azabicyclo hept-6-yl)-2-phenylmalonamate monosodium salt.
The structural formula is:
The empirical formula is: C26H25N2NaO6S and mol. wt. is 516.55.
Geocillin tablets are yellow, capsule-shaped and film-coated, made of a white crystalline solid. Carbenicillin is freely soluble in water. Each Geocillin tablet contains 382 mg of carbenicillin, 118 mg of indanyl sodium ester. Each Geocillin tablet contains 23 mg of sodium.
Inert ingredients are: glycine; magnesium stearate and sodium lauryl sulfate. May also include the following: hydroxypropyl cellulose; hypromellose; opaspray (which may include Blue 2 Lake, Yellow 6 Lake, Yellow 10 Lake, and other inert ingredients); opadry light yellow (which may contain D&C Yellow 10 Lake, FD&C Yellow 6 Lake and other inert ingredients); opadry clear (which may contain other inert ingredients).