Persius/hicric huggingface dataset:
Anterior segment mesenchymal dysgenesis

# Overview
Anterior segment dysgenesis (ASD) is a failure of the normal development of the tissues of the anterior segment of the eye. It leads to anomalies in the structure of the mature anterior segment, associated with an increased risk of glaucoma and corneal opacity.
Peters' (frequently misspelled Peter's) anomaly  is a specific type of mesenchymal anterior segment dysgenesis, in which there is central corneal leukoma, adhesions of the iris and cornea, and abnormalities of the posterior corneal stroma, Descemet's membrane, corneal endothelium, lens, and anterior chamber.

# History
This congenital anomaly was first described by Albert Peters, a German ophthalmologist (1862-1938).

# Pathophysiology
Several gene mutations have been identified underlying these anomalies with the majority of ASD genes encoding transcriptional regulators. In this review, the role of the ASD genes, PITX2 and FOXC1, is considered in relation to the embryology of the anterior segment, the biochemical function of these proteins, and their role in development and disease aetiology. The emerging view is that these genes act in concert to specify a population of mesenchymal progenitor cells, mainly of neural crest origin, as they migrate anteriorly around the embryonic optic cup. These same genes then regulate mesenchymal cell differentiation to give rise to distinct anterior segment tissues. Development appears critically sensitive to gene dosage, and variation in the normal level of transcription factor activity causes a range of anterior segment anomalies. Interplay between PITX2 and FOXC1 in the development of different anterior segment tissues may partly explain the phenotypic variability and the genetic heterogeneity characteristic of ASD.
Atrioventricular septal defect overview

# Overview
Atrioventricular septal defect (AVSD), previously known as "common atrioventricular canal" (CAVC) or "endocardial cushion defect", is a congenital heart defect characterized by the deficiency in development of the atrioventricular septum of the heart. It is caused by an abnormal fusion of the superior and inferior endocardial cushions with the mid-portion of the atrial septum and the muscular portion of the ventricular septum. The malformation results in a hole in the heart between the mitral and triscupid valves. This lack of separation can cause hemodynamic complications.

# Classification
AVSD is classified as either complete, partial, or intermediate/transitional. Classification is based on the extent of loss of separation between the chambers of the heart. In partial AVSD, there is a defect in the primum or inferior part of the atrial septum but no direct intraventricular communication (ostium primum defect). In complete AVSD, there is a large ventricular component beneath either or both the superior or inferior bridging leaflets of the AV valve. In intermediate or transitional AVSD, the leaflets of the common AV valve are stuck to the ventricular septum causing a division of the two valves and resulting in a marginal sized hole between the ventricle. Transitional AVSDs are similar to partial AVSDs in behavior but visually appear more like a complete AVSD.

# Pathophysiology
AVSDs can result in significant changes in hemodynamics. A defect in the septum can result in blood freely traveling from the left side of the heart to the right side of the heart resulting in mixing of oxygenated and deoxygenated blood. This mixed blood is pumped back to the lungs and causes an increase in blood volume in the lungs resulting in hypertension, cardiomegaly, and damage to the blood vessels. A high pulmonary pressure can result in a pulmonary edema

# Epidemiology and Demographics
AVSDs account for approximately 5% of all congenital heart diseases. It is most commonly associated with patients with Down syndrome (trisomy 21) or heterotaxy syndromes. 45% of children with Down syndrome have some form of congenital heart disease. Of these, 3540% have AV septal defects.

# Diagnosis

## History and Symptoms
Most infants are largely asymptomatic and may only exhibit signs of failure to thrive. A clinical diagnosis often occurs based on the presence of a heart murmur and can be detected at any time, from fetal development to later in life. A fetal echocardiogram can detect the presence of a murmur during prenatal care. A cardiac catheterization can also used for diagnosis.

# Treatment

## Surgery
Surgical therapy is the most reliable method of treatment. An open heart surgery will separate the mitral and triscuspid valve and close the atrial and ventricular septal defects. Surgical therapy is not advised until a child is old enough to undergo surgery. A pulmonary artery banding surgery may be used to delay the necessity for surgery.
Brain-specific angiogenesis inhibitor 2
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Brain-specific angiogenesis inhibitor 2 is a protein that in humans is encoded by the BAI2 gene. It is a member of the adhesion-GPCR family of receptors.
BAI1, a p53-target gene, encodes brain-specific angiogenesis inhibitor, a seven-span transmembrane protein and is thought to be a member of the secretin receptor family. Brain-specific angiogenesis proteins BAI2 and BAI3 are similar to BAI1 in structure, have similar tissue specificities and may also play a role in angiogenesis.
Hypertrophic pulmonary osteoarthropathy
Synonyms and keywords: Pierre Marie-Bamberger disease; Bamberger-Marie disease; osteoarthropathia hypertrophicans; pulmonary hypertrophic osteodystrophy; pulmonary osteoarthropathy; hypertrophic pulmonary osteo-arthropathy

# Overview
Hypertrophic pulmonary osteoarthropathy is a medical condition combining clubbing and synovitis. This is the combination of clubbing and thickening of the periosteum (connective tissue lining of the bones) and synovium (lining of joints), and is often initially diagnosed as arthritis.
It is also known as "osteoarthropathia hypertrophicans".

# Historical Perspective
It is named for Eugen von Bamberger and Pierre Marie.

# Pathophysiology

## Associated Conditions
- Lung cancer

# Causes

## Causes in Alphabetical Order
- Mesothelioma
- Pleural fibroma

# Diagnosis

## Symptoms
Some of the symptoms include:
- Arthropathy
- Digital clubbing
- Gynaecomastia

## X-ray
- Pachydermoperiostosis
- The predominant radiographic periostitis, which is depicted as symmetric osseous thickening.
Periostitis mostly affects the tubular bones of the limbs, especially the radius, ulna, tibia, and fibula, although the pelvis, carpus, tarsus, metacarpals, metatarsals, and phalanges can be involved.
Periosteal proliferation is usually shaggy and associated with irregular excrescences and diaphyseal expansion.
- The predominant radiographic periostitis, which is depicted as symmetric osseous thickening.
- Periostitis mostly affects the tubular bones of the limbs, especially the radius, ulna, tibia, and fibula, although the pelvis, carpus, tarsus, metacarpals, metatarsals, and phalanges can be involved.
- Periosteal proliferation is usually shaggy and associated with irregular excrescences and diaphyseal expansion.
- Secondary hypertrophic osteoarthropathy
- Usually involves diaphyseal and metaphyseal periostitis.
- Usually involves diaphyseal and metaphyseal periostitis.
- Periosteal proliferation is usually single or laminated and regular or irregular.
- Laminated periostitis may have an onionskin appearance.
- Periarticular soft tissue swelling, clubbing, and clinical and radiologic features of an underlying primary lesion are often depicted.
- Digital clubbing associated with soft tissue swelling may be depicted on plain radiographs.
Hypertrophic osteoarthropathy in a patient with thymic carcinoma

## Other Imaging Findings

### Nuclear medicine
- Bone scan with technetium Tc 99mlabeled diphosphonate shows changes of HOA early and with sensitivity greater than that of other methods.
- Isotope uptake is symmetrically increased in the tubular bones along the cortical margins of the diaphysis and metaphysis.
- Uptake may be irregular, or it may create a double-stripe or parallel-track sign.
- Periarticular radionuclide uptake may be increased as a result of associated synovitis.
Bioinformatics tool gene transcriptions
Def. a "field of science in which biology, computer science, and information technology merge into a single discipline to analyse biological information using computers and statistical techniques" is called bioinformatics.
"To understand the gene function and regulation patterns of CsSODs, sequences of 1000 bp upstream regions from the translation start site of each CsSOD were identified from  CuGI and were subsequently determined using PlantCARE. The results showed that 59 types of cis-acting regulatory elements were found in the promoter region of CsSODs and all CsSOD promoters contained typical TATA and CAAT boxes, which are essential elements of the promoters ."

# Human genes
"Briefly, the mRNA sequences were obtained from the NCBI Reference Sequence Database (RefSeq) for human SIRT2 gene. The reference mRNA sequences was submitted to BLAST for comparison with the human genomic DNA sequence in the human genome database."

# Human promoter occurrences
"After noting the orientation of the alignment, the appropriate 5-Kb genomic DNA sequence upstream from the transcription start point corresponding to the promoter region of the gene was isolated and analyzed using a web-based bioinformatics tool TESS at . Because TESS results are model-based, the potential CArG sequence was verified by both using LALIGN () and visual confirmation."

# Acknowledgements
The content on this page was first contributed by: Henry A. Hoff.
Brain-specific angiogenesis inhibitor 1
Brain-specific angiogenesis inhibitor 1 is a protein that in humans is encoded by the BAI1 gene.  It is a member of the adhesion-GPCR family of receptors.

# Function
Angiogenesis is controlled by a local balance between stimulators and inhibitors of new vessel growth and is suppressed under normal physiologic conditions. Angiogenesis has been shown to be essential for growth and metastasis of solid tumors. In order to obtain blood supply for their growth, tumor cells are potently angiogenic and attract new vessels as results of increased secretion of inducers and decreased production of endogenous negative regulators.  BAI1 contains at least one 'functional' p53-binding site within an intron, and its expression has been shown to be induced by wildtype p53. There are two other brain-specific angiogenesis inhibitor genes, designated BAI2 and BAI3 which along with BAI1 have similar tissue specificities and structures, however only BAI1 is transcriptionally regulated by p53. BAI1 is postulated to be a member of the secretin receptor family, an inhibitor of angiogenesis and a growth suppressor of glioblastomas.

# Interactions
Brain-specific angiogenesis inhibitor 1 has been shown to interact with BAIAP3 and MAGI1.

# Model organisms
Model organisms have been used in the study of BAI1 function. A conditional knockout mouse line called Bai1tm2a(EUCOMM)Wtsi was generated at the Wellcome Trust Sanger Institute. Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Additional screens performed:  - In-depth immunological phenotyping - in-depth bone and cartilage phenotyping
Brain-specific angiogenesis inhibitor 3
Brain-specific angiogenesis inhibitor 3 is a protein that in humans is encoded by the BAI3 gene.
BAI1, a p53-target gene, encodes brain-specific angiogenesis inhibitor, a seven-span transmembrane protein and is thought to be a member of the secretin receptor family. Brain-specific angiogenesis proteins BAI2 and BAI3 are similar to BAI1 in structure, have similar tissue specificities and may also play a role in angiogenesis.
The adhesion GPCR BaI3 is an orphan receptor that has a long N-terminus consisting of one cub domain, five BaI Thrombospondin type 1 repeats, and one hormone binding domain.   BaI3 is expressed in neural tissues of the central nervous system.  BaI3 has been shown to have a high affinity for C1q proteins.  C1q added to hippocampal neurons expressing BaI3 resulted in a decrease in the number of synapses.
Cordarone tablet nonclinical toxicology

# Nonclinical Toxicology

## Carcinogenesis, Mutagenesis, Impairment of Fertility
Amiodarone HCl was associated with a statistically significant, dose-related increase in the incidence of thyroid tumors (follicular adenoma and/or carcinoma) in rats. The incidence of thyroid tumors was greater than control even at the lowest dose level tested, i.e., 5 mg/kg/day (approximately 0.08 times the maximum recommended human maintenance dose*).
Mutagenicity studies (Ames, micronucleus, and lysogenic tests) with Cordarone were negative.
In a study in which amiodarone HCl was administered to male and female rats, beginning 9 weeks prior to mating, reduced fertility was observed at a dose level of 90 mg/kg/day (approximately 1.4 times the maximum recommended human maintenance dose*).
- 600 mg in a 50 kg patient ( dose compared on a body surface area basis )
Calcifying epithelial odontogenic tumor

# Overview
The calcifying epithelial odontogenic tumor, also known as a Pindborg tumor or CEOT, is an odontogenic tumor.  It is more common in the posterior mandible of adults, typically in the 4th to 5th decades.  There may be a painless swelling, and it is often concurrent with an impacted tooth.  On radiographs, it appears as a radiolucency (dark area) and is known for sometimes having small radiopacities (white areas) within it.  In those instances, it is described as having a "driven-snow" appearance.  Microscopically, there are deposits of amyloid-like material.Clinicaly it has two types,the central and the peripheral.The central type of the CEOT occurs in individuals ranging in age from 20-60 years.2/3rd of the lesions are in jaws,more commonly in the molar area with a tendency to occur in the pre molar areas.It appears clinically to be a slowly enlarging painless mass.In the maxilla it can cause Proptosis,epistaxis and nasal air way obstruction.
The peripheral type is commonly found in the anterior region of the maxilla and occurs as a soft tissue swelling.
Histopathology will reveal prominent intercellular bridges and nuclear changes such as pleomorphism,hyperchromatism and prominent nucleoli.The mitotic figures are rare.Spread throughout the epithelium and connective tissue are spherical amorhpous calcifications.When clear cells are present with clear cytoplasms,then this variant is referred to as "Clear Cell Variant".
Carbenicillin indanyl sodium overdosage

# OVERDOSAGE
Geocillin is generally nontoxic. Geocillin when taken in excessive amounts may produce mild gastrointestinal irritation. The drug is rapidly excreted in the urine and symptoms are transitory. The usual symptoms of anaphylaxis may occur in hypersensitive individuals.
Carbenicillin blood levels achievable with Geocillin are very low, and toxic reactions as a function of overdosage should not occur systematically. The oral LD50 in mice is 3,600 mg/kg, in rats 2,000 mg/kg, and in dogs is in excess of 500 mg/kg. The lethal human dose is not known.
Although never reported, the possibility of accumulation of indanyl should be considered when large amounts of Geocillin are ingested. Free indole, which is a phenol derivative, may be potentially toxic. In general 815 grams of phenol, and presumably a similar amount of indole, are required orally before toxicity (peripheral vascular collapse) may occur. The metabolic by products of indole are nontoxic. In patients with hepatic failure it may be possible for unmetabolized indole to accumulate.
The metabolic by-products of Geocillin, indanyl sulfate and glucuronide, as well as free carbenicillin, are dialyzable.
Ceftriaxone Compatibility and Stability
Ceftriaxone has been shown to be compatible with Flagyl  IV (metronidazole hydrochloride). The concentration should not exceed 5 to 7.5 mg/mL metronidazole hydrochloride with ceftriaxone 10 mg/mL as an admixture. The admixture is stable for 24 hours at room temperature only in 0.9% sodium chloride injection or 5% dextrose in water (D5W). No compatibility studies have been conducted with the Flagyl  IV RTU  (metronidazole) formulation or using other diluents. Metronidazole at concentrations greater than 8 mg/mL will precipitate. Do not refrigerate the admixture as precipitation will occur.
Vancomycin, amsacrine, aminoglycosides, and fluconazole are physically incompatible with ceftriaxone in admixtures. When any of these drugs are to be administered concomitantly with ceftriaxone by intermittent intravenous infusion, it is recommended that they be given sequentially, with thorough flushing of the intravenous lines (with one of the compatible fluids) between the administrations.
Do not use diluents containing calcium, such as Ringers solution or Hartmanns solution, to reconstitute ceftriaxone for injection vials or to further dilute a reconstituted vial for IV administration. Particulate formation can result.
Ceftriaxone for injection solutions should not be physically mixed with or piggybacked into solutions containing other antimicrobial drugs or into diluent solutions other than those listed above, due to possible incompatibility (see WARNINGS).
Ceftriaxone for injection sterile powder should be stored at 20 to 25C (68 to 77F)  and protected from light. After reconstitution, protection from normal light is not necessary. The color of solutions ranges from light yellow to amber, depending on the length of storage, concentration and diluent used.
Ceftriaxone for injection intravenous solutions, at concentrations of 10, 20 and 40 mg/mL, remain stable (loss of potency less than 10%) for the following time periods stored in glass or PVC containers:
The following intravenous ceftriaxone for injection solutions are stable at room temperature (25C) for 24 hours, at concentrations between 10 mg/mL and 40 mg/mL: Sodium Lactate (PVC container), 10% Invert Sugar (glass container), 5% Sodium Bicarbonate (glass container), Freamine III (glass container), Normosol-M in 5% Dextrose (glass and PVC containers), Ionosol-B in 5% Dextrose (glass container), 5% Mannitol (glass container), 10% Mannitol (glass container).
After the indicated stability time periods, unused portions of solutions should be discarded.
NOTE: Parenteral drug products should be inspected visually for particulate matter before administration.
Ceftriaxone for injection reconstituted with 5% Dextrose or 0.9% Sodium Chloride solution at concentrations between 10 mg/mL and 40 mg/mL, and then stored in frozen state (-20C) in PVC or polyolefin containers, remains stable for 26 weeks.
Frozen solutions of ceftriaxone for injection should be thawed at room temperature before use. After thawing, unused portions should be discarded. DO NOT REFREEZE.
Cefuroxime axetil clinical pharmacology

# Absorption and Metabolism
After oral administration, cefuroxime axetil is absorbed from the gastrointestinal tract and rapidly hydrolyzed by nonspecific esterases in the intestinal mucosa and blood to cefuroxime. Cefuroxime is subsequently distributed throughout the extracellular fluids. The axetil moiety is metabolized to acetaldehyde and acetic acid.

# Pharmacokinetics
Approximately 50% of serum cefuroxime is bound to protein. Serum pharmacokinetic parameters for CEFTIN Tablets and CEFTIN for Oral Suspension are shown in Tables 1 and 2.
a  Mean values of 12 healthy adult volunteers.
b  Drug administered immediately after a meal.
a  Mean age = 23 months.
b  Drug administered with milk or milk products.
Comparative Pharmacokinetic Properties
A 250 mg/5 mL-dose of CEFTIN Suspension is bioequivalent to 2 times 125 mg/5 mL-dose of CEFTIN Suspension when administered with food (see Table 3). CEFTIN for Oral Suspension was not bioequivalent to CEFTIN Tablets when tested in healthy adults. The tablet and powder for oral suspension formulations are NOT substitutable on a milligram-per-milligram basis. The area under the curve for the suspension averaged 91% of that for the tablet, and the peak plasma concentration for the suspension averaged 71% of the peak plasma concentration of the tablets. Therefore, the safety and effectiveness of both the tablet and oral suspension formulations had to be established in separate clinical trials.
a  Mean values of 18 healthy adult volunteers.
Food Effect on Pharmacokinetics
Absorption of the tablet is greater when taken after food (absolute bioavailability of CEFTIN Tablets increases from 37% to 52%). Despite this difference in absorption, the clinical and bacteriologic responses of patients were independent of food intake at the time of tablet administration in 2 studies where this was assessed.
All pharmacokinetic and clinical effectiveness and safety studies in pediatric patients using the suspension formulation were conducted in the fed state. No data are available on the absorption kinetics of the suspension formulation when administered to fasted pediatric patients.
Renal Excretion
Cefuroxime is excreted unchanged in the urine; in adults, approximately 50% of the administered dose is recovered in the urine within 12 hours. The pharmacokinetics of cefuroxime in the urine of pediatric patients have not been studied at this time. Until further data are available, the renal pharmacokinetic properties of cefuroxime axetil established in adults should not be extrapolated to pediatric patients.
Because cefuroxime is renally excreted, the serum half-life is prolonged in patients with reduced renal function. In a study of 20 elderly patients (mean age = 83.9 years) having a mean creatinine clearance of 34.9 mL/min, the mean serum elimination half-life was 3.5 hours. Despite the lower elimination of cefuroxime in geriatric patients, dosage adjustment based on age is not necessary (see PRECAUTIONS: Geriatric Use).
Chloroquine phosphate drug interactions

# Drug Interactions

## Antacids and kaolin
Antacids and kaolin can reduce the absorption of chloroquine; an interval of at least 4 hours between intake of these agents and chloroquine should be observed.

## Cimetidine
Cimetidine can inhibit the metabolism of chloroquine, increasing its plasma level. Concomitant use of cimetidine should be avoided.

## Ampicillin
In a study of healthy volunteers, chloroquine significantly reduced the bioavailability of ampicillin. An interval of at least two hours between intake of this agent and chloroquine should be observed.

## Cyclosporine
After introduction of chloroquine (oral form), a sudden increase in serum cyclosporine level has been reported. Therefore, close monitoring of serum cyclosporine level is recommended and, if necessary, chloroquine should be discontinued.

## Mefloquine
Co-administration of chloroquine and mefloquine may increase the risk of convulsions.
The blood concentrations of chloroquine and desethylchloroquine (the major metabolite of chloroquine, which also has antimalarial properties) were negatively associated with log antibody titers. Chloroquine taken in the dose recommended for malaria prophylaxis can reduce the antibody response to primary immunization with intradermal human diploid-cell rabies vaccine.
Clindamycin phosphate adverse reactions

# ADVERSE REACTIONS
In 18 clinical studies of various formulations of CLEOCIN T using placebo vehicle and/or active comparator drugs as controls, patients experienced a number of treatment emergent adverse dermatologic events .
Orally and parenterally administered clindamycin has been associated with severe colitis which may end fatally.
Cases of diarrhea, bloody diarrhea and colitis (including pseudomembranous colitis) have been reported as adverse reactions in patients treated with oral and parenteral formulations of clindamycin and rarely with topical clindamycin (see WARNINGS).
Abdominal pain and gastrointestinal disturbances as well as gram-negative folliculitis have also been reported in association with the use of topical formulations of clindamycin.