Persius/hicric huggingface dataset:
Hypertriglyceridemia (patient information)
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# Overview
Familial hypertriglyceridemia is a common disorder passed down through families in which the level of triglycerides (a type of fat) in a person's blood are higher than normal. The condition is not associated with a significant increase in cholesterol levels.

# What are the symptoms of Hypertriglyceridemia?
You may not notice any symptoms. People with the condition may have coronary artery disease at an early age.

# What causes Hypertriglyceridemia?
Familial hypertriglyceridemia is caused by a genetic defect, which is passed on in an autosomal dominant fashion. This means that if you get a bad copy of the gene from just one of your parents, you will have the condition.
Some people with this condition also have high levels of very low density lipoprotein (VLDL). The reason for the rise in triglycerides and VLDL is not understood.
Familial hypertriglyceridemia does not usually become noticeable until puberty or early adulthood. Obesity, hyperglycemia (high blood glucose levels), and high levels of insulin are often also present and may cause even higher triglyceride levels.
Familial hypertriglyceridemia occurs in about 1 in 500 individuals in the United States. Risk factors are a family history of hypertriglyceridemia or a family history of heart disease before the age of 50.

# Who is at highest risk?
Family members with history of hypertriglyceridemia are at increased risk of having the condition.

# When to seek urgent medical care?
You may not notice any symptoms. People with the condition may have coronary artery disease at an early age.

# Diagnosis
People with a family history of this condition should have blood tests to check very low density lipoprotein (VLDL) and triglyceride levels. Blood tests usually show a mild to moderate increase in triglycerides (about 200 to 500 mg/dL). A coronary risk profile may also be done.

# Treatment options
The goal of treatment is to control conditions that can raise triglyceride levels such as obesity, hypothyroidism, and diabetes.
Your doctor may tell you not to drink alcohol. Because certain birth control pills can raise triglyceride levels, you should carefully discuss their use with your doctor.
Treatment also involves avoiding excess calories and foods high in saturated fats and carbohydrates. See also: Heart disease and diet
If high triglyceride levels persist despite diet changes, medication may be needed. Nicotinic acid, gemfibrozil (Lopid), and fenofibrate have been shown to lower triglyceride levels in people with this condition.

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

# What to expect (Outlook/Prognosis)?
Persons with this condition have an increased risk of coronary artery disease and pancreatitis. Losing weight and keeping diabetes under control helps improve the outcome.

# Possible complications
- Pancreatitis
- Coronary artery disease

# Prevention
Screening family members for high triglycerides may detect the disease early.

# Sources
Insulin-like growth factor binding protein
The Insulin-like growth factor binding protein serves as a carrier protein for Insulin-like growth factor 1.
Approximately 98% of IGF-1 is always bound to one of 6 binding proteins (IGF-BP). IGFBP-3, the most abundant protein, accounts for 80% of all IGF binding. IGF-1 binds to IGFBP-3 in a 1:1 molar ratio.
IGF-BP also binds to IGF-1 inside the liver, allowing growth hormone to continuously act upon the liver to produce more IGF-1. This is important because proliferating IGF-1 + IGF-BP complex allow growth of the femur and the muscle.
There are seven genes:
- IGFBP1
- IGFBP2
- IGFBP3
- IGFBP4
- IGFBP5
- IGFBP6
- IGFBP7
Infantile free sialic acid storage disease
Infantile free sialic acid storage disease (ISSD) is a lysosomal storage disease caused when sialic acid, a kind of charged sugar, is unable to be transported out of the lysosomal membrane and instead, accumulates in the tissue and free sialic acid is excreted in the urine. Mutations in the SLC17A5 (solute carrier family 17 (anion/sugar transporter), member 50) gene cause all forms of sialic acid storage disease.  The SLC17A5 gene is located on the long (q) arm of chromosome 6 between positions 14 and 15. This gene provides instructions for producing a protein called sialin that is located mainly on the membranes of lysosomes, compartments in the cell that digest and recycle materials.
ISSD is the most severe form of the sialic acid storage diseases. Babies with this condition have severe developmental delay, weak muscle tone (hypotonia), and failure to gain weight and grow at the expected rate (failure to thrive). They may have unusual facial features that are often described as "coarse," seizures, bone malformations, enlarged liver and spleen (hepatosplenomegaly), and an enlarged heart (cardiomegaly).
ISSD is a rare autosomal recessive disorder and affects 1 in 528,000 live births worldwide.

# Symptoms
Symptoms present by eight months of age and are marked by developmental delay followed by neurological complications such as seizures, involuntary eye movements, and ataxia, involuntary muscle movements and failure to gain weight and grow at the expected rate (failure to thrive).  Babies with this condition also have and enlarged liver and spleen (hepatosplenomegaly) and enlarged heart (cardiomegaly).

# Diagnosis and Testing
A diagnosis can be made by measuring cultured tissue samples for increased levels of free sialic acid. Prenatal testing is also available for known carriers of this disorder.

# Treatment
There is no treatment for ISSD. Treatment is limited to controlling the symptoms of this disorder such as administering anti-convulsant medication to control seizure episodes.
Interferon-induced transmembrane protein 5
Interferon-induced transmembrane protein 5 is a gene that encodes a membrane protein thought to play a role in bone mineralization.

# Genomics
The gene is located on the short arm of the Crick strand of chromosome 11 (11p15.5). It is located with a cluster of interferon inducible genes but is itself not interferon inducible. The gene is 1,327 bases in length and encodes a protein of 132 amino acids with a predicted molecular weight of 14378 Daltons. Expression in adults is bone specific and highest in osteoblasts.
The homolog in the mouse is located on chromosome 7. A homolog is also known to be present in lizards.

# Evolution
The gene first appeared in bony fish and its bone specific expression appears to be limited to therian mammals.

# Biochemistry
The protein has two transmembrane domains. It associates with FK506 binding protein 11.

# Clinical
Mutations in the gene are associated with osteogenesis imperfecta type 5.
Interferon alfacon-1 clinical pharmacology

# Clinical Pharmacology

## Pharmacodynamics
Interferons induce pleiotropic biologic responses which include antiviral, antiproliferative, and immunomodulatory effects, regulation of cell surface major histocompatibility antigen (HLA class I and class II) expression and regulation of cytokine expression.
Analysis of INFERGEN-induced cellular products (induction of 2'5' OAS and -2 microglobulin) after treatment in these subjects revealed a statistically significant, dose-related increase in the area under the curve (AUC) for the levels of 2'5' OAS or -2 microglobulin induced over time. Concentrations of 2'5' OAS were maximal at 24 hours after dosing, while serum levels of -2 microglobulin appeared to reach a maximum 24 to 36 hours after dosing. The dose-response relationships observed for 2'5' OAS and -2 microglobulin were indicative of biological activity after subcutaneous injection administration of 1 mcg to 9 mcg INFERGEN.

## Pharmacokinetics
The pharmacokinetic properties of INFERGEN have not been evaluated in patients with chronic hepatitis C. Pharmacokinetic profiles were evaluated in normal, healthy volunteer subjects after subcutaneous injection of 1 mcg, 3 mcg, or 9 mcg INFERGEN. Plasma levels of INFERGEN after subcutaneous injection administration of any dose were too low to be detected by either enzyme-linked immunosorbent assay (ELISA) or by inhibition of viral cytopathic effect.

### Renal Dysfunction
Patients with creatinine clearance <50 mL/min should not be treated with ribavirin .Pharmacodynamics
Interferons induce pleiotropic biologic responses which include antiviral, antiproliferative, and immunomodulatory effects, regulation of cell surface major histocompatibility antigen (HLA class I and class II) expression and regulation of cytokine expression.
Analysis of INFERGEN-induced cellular products (induction of 2'5' OAS and -2 microglobulin) after treatment in these subjects revealed a statistically significant, dose-related increase in the area under the curve (AUC) for the levels of 2'5' OAS or -2 microglobulin induced over time. Concentrations of 2'5' OAS were maximal at 24 hours after dosing, while serum levels of -2 microglobulin appeared to reach a maximum 24 to 36 hours after dosing. The dose-response relationships observed for 2'5' OAS and -2 microglobulin were indicative of biological activity after subcutaneous injection administration of 1 mcg to 9 mcg INFERGEN.
12.3 Pharmacokinetics
The pharmacokinetic properties of INFERGEN have not been evaluated in patients with chronic hepatitis C. Pharmacokinetic profiles were evaluated in normal, healthy volunteer subjects after subcutaneous injection of 1 mcg, 3 mcg, or 9 mcg INFERGEN. Plasma levels of INFERGEN after subcutaneous injection administration of any dose were too low to be detected by either enzyme-linked immunosorbent assay (ELISA) or by inhibition of viral cytopathic effect.
Renal Dysfunction
Patients with creatinine clearance <50 mL/min should not be treated with ribavirin .
Interferon alfacon-1 indications and usage

# Indications And Usage

## Chronic Hepatitis C
INFERGEN (interferon alfacon-1) is indicated for treatment of chronic hepatitis C in patients 18 years of age or older with compensated liver disease. This indication is based on clinical trials conducted using INFERGEN as monotherapy prior to the time that combination treatment was the standard of care and on a single trial evaluating INFERGEN in combination with ribavirin in patients who failed to respond to previous treatment with a pegylated interferon and ribavirin.
The following points should be considered when initiating treatment with INFERGEN:
- Use of monotherapy with an interferon such as INFERGEN for the treatment of hepatitis C is not recommended unless a patient is unable to take ribavirin.
- The safety and efficacy of the combination of INFERGEN/ribavirin in treatment-naive patients or in patients co-infected with HBV or HIV-1 have not been evaluated.
- Patients with the following characteristics are less likely to benefit from retreatment with combination therapy: response of 850,000 IU/mL), African American race, and/or presence of cirrhosis.
- No safety and efficacy data are available for treatment of longer than one year.
Left ventricular outflow tract obstruction
Synonyms and keywords: LV outflow tract obstruction; LVOT obstruction

# Overview
Left ventricular outflow tract obstruction refers to any functional or anatomic obstruction of flow out of the left ventricle.

# Causes
- Aortic stenosis
- Hypertrophic obstructive cardiomyopathy
- Stress cardiomyopathy
- Subvalvular aortic stenosis
- Supravalvular aortic stenosis

# 2008 ACC/AHA Guidelines for the Management of Adults With Congenital Heart Disease (DO NOT EDIT)

## Evaluation of the Unoperated Patient (DO NOT EDIT)

## Medical Therapy (DO NOT EDIT)

## Catheter Interventions for Adults With Valvular Aortic Stenosis (DO NOT EDIT)
Lacrimal gland tumor (patient information)
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# Overview
A lacrimal gland tumor is a tumor in the glands that release tears. These glands are located above and to the side of each eye. The tumor can be harmless (benign) or cancer (malignant).

# What are the symptoms of Lacrimal gland tumor?
- Double vision
- Fullness in one eyelid or the side of the face
- Pain

# Diagnosis
A head and neck or eye (orbital) specialist will perform an examination and evaluate vision. Tests may include a CT or MRI scan.

# Treatment options
Often patients need surgery to remove the tumor. Cancerous tumors may need additional treatment.

# Where to find medical care for Lacrimal gland tumor?
Directions to Hospitals Treating Lacrimal gland tumor

# What to expect (Outlook/Prognosis)?
If lacrimal gland tumor is not treated, the child may be permanently unable to fully move the elbow. With treatment, there is usually no permanent damage.
The outlook is generally excellent for noncancerous growths. The outlook for cancer depends on the type of cancer and stage at which it is discovered.

# Sources
Lanoxin tablet/use in specific populations

# Pregnancy

## Teratogenic Effects
Pregnancy Category C. Animal reproduction studies have not been conducted with digoxin. It is also not known whether digoxin can cause fetal harm when administered to a pregnant woman or can affect reproductive capacity. Digoxin should be given to a pregnant woman only if clearly needed.

# Nursing Mothers
Studies have shown that digoxin concentrations in the mothers serum and milk are similar. However, the estimated exposure of a nursing infant to digoxin via breastfeeding will be far below the usual infant maintenance dose. Therefore, this amount should have no pharmacologic effect upon the infant. Nevertheless, caution should be exercised when digoxin is administered to a nursing woman.

# Pediatric Use
Newborn infants display considerable variability in their tolerance to digoxin. Premature and immature infants are particularly sensitive to the effects of digoxin, and the dosage of the drug must not only be reduced but must be individualized according to their degree of maturity. Digitalis glycosides can cause poisoning in children due to accidental ingestion.

# Geriatric Use
The majority of clinical experience gained with digoxin has been in the elderly population. This experience has not identified differences in response or adverse effects between the elderly and younger patients. However, this drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, which should be based on renal function, and it may be useful to monitor renal function (see DOSAGE AND ADMINISTRATION).
Light-harvesting complexes of green plants
The light-harvesting (or antenna) complex of plants is an array of protein and chlorophyll molecules embedded in the thylakoid membrane which transfer light energy to one chlorophyll a molecule at the reaction center of a photosystem.
The antenna pigments are predominantly chlorophyll a, chlorophyll b and carotenoids. Their absorption spectra are non-overlapping in order to broaden the range of light that can be absorbed in photosynthesis. The carotenoids have another role as an antioxidant to prevent photo-oxidative damage of chlorophyll molecules. Each antenna complex has between 250 and 400 pigment molecules and the energy they absorb is shuttled by resonance energy transfer to a specialized chlorophyll-protein complex known as the reaction center of each photosystem. The reaction center initiates a complex series of chemical reactions that capture energy in the form of chemical bonds.
For photosystem II, when either of the two chorophyll a molecules at the reaction center absorb energy, an electron is excited and transferred to an electron acceptor molecule, phaeophytin, leaving the chlorophyll a in an oxidized state. The oxidised chlorophyll a replaces the electrons by photolysis that involves the reduction of water molecules to oxygen, protons and electrons.
Under changing light conditions, the reversible phosphorylation of light harvesting chlorophyll a/b binding proteins (LHCII) represents a system for balancing the excitation energy between the two photosystems.
The N-terminus of the chlorophyll A-B binding protein extends into the stroma where it is involved with adhesion of granal membranes and photo-regulated by reversible phosphorylation of its threonine residues. Both these processes are believed to mediate the distribution of excitation energy between photosystems I and II.
This family also includes the photosystem II protein PsbS, which plays a role in energy-dependent quenching that increases thermal dissipation of excess absorbed light energy in the photosystem.
Lower respiratory tract infection overview

# Overview
While often used as a synonym for pneumonia, the rubric of lower respiratory tract infection can also be applied to other types of infection including lung abscess, acute bronchitis, and emphysema.

# Epidemiology and Demographics
Lower respiratory tract infection is commonly known as the most prolific cause of death amongst all infectious diseases. Bronchitis affects over 40 adults per 1000 each year. Since 1993 there has been a slight reduction in the total number of deaths from lower respiratory tract infection. However in 2002 they were still the leading cause of deaths among all infectious diseases accounting for 3.9 million deaths worldwide and 6.9% of all deaths that year.

# Treatment

## Medical Therapy
There are a number of acute and chronic infections that can affect the lower respiratory tract. Antibiotics are often thought to be the first line treatment in lower respiratory tract infections however these are not indicated in viral infections. It is important to use appropriate antibiotic selection based on the infecting organism and to ensure this therapy changes with the evolving nature of these infections and the emerging resistance to conventional therapies.

# Cost-Effectiveness of Therapy
Lower respiratory tract infections place a considerable strain on the health budget and are generally more serious than upper respiratory infections.
Lymphangiomyomatosis (patient information)
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# Overview
Symptoms of lymphangiomyomatosis  may include constipation, dyspnea, and cough. Lymphangiomyomatosis may be diagnosed using CT,Xray, and immunohistochemistry. The mainstay of therapy for lymphangiomyomatosisis include sirolimus, medroxyprogesterone, gonadotropin-releasing hormone agonists, and tamoxifen. Common complications of  lymphangiomyomatosis include ascitis, chylous pleural effusion, pneumothorax, hemoptysis, chyloptysis, chyluria, hematuria, pericardial effusion, pneumoperitoneum, lymphedema, respiratory failure, osteoporosis, and meningioma.

# What are the symptoms of Lymphangiomatosis?
Symptoms of lymphangiomyomatosis  may include constipation, difficulty breathing, and cough.

# Diagnosis
Lymphangiomyomatosis may be diagnosed using CT,Xray, and immunohistochemistry.

# Treatment options
The mainstay of therapy for lymphangiomyomatosisis include sirolimus, medroxyprogesterone, gonadotropin-releasing hormone agonists, and tamoxifen.

# Possible complications
Common complications of  lymphangiomyomatosis include ascitis, chylous pleural effusion, pneumothorax, hemoptysis, chyloptysis, chyluria, hematuria, pericardial effusion, pneumoperitoneum, lymphedema, respiratory failure, osteoporosis, and meningioma.

# Sources
Medical University of the Americas - Nevis
Medical University of the Americas - Nevis (MUA) is located on the island of Nevis. It is a four-year medical school, which grants the degree of Doctor of Medicine (MD).  Instruction is divided into ten trimesters: the first five semesters are didatic and held on the island on Nevis in the Federation of St. Christopher and Nevis, and the remaining five semesters are clinical, and training is held in hospitals throughout the United States.

# Accreditation
MUA-Nevis is listed in the FAIMER International Medical Education Directory  as being recognized as a medical school by the appropriate local government agency.
MUA-Nevis is approved by the State of New York Department of Education for students to do more than 12 weeks of Clinical Clerkships in that state .
Megaloblastic anemia (patient information)
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# Overview
Megaloblastic anemia is a blood disorder in which there is anemia with larger-than-normal red blood cells.
Anemia is a condition in which the body does not have enough healthy red blood cells. Red blood cells provide oxygen to body tissues.

# What are the symptoms of Megaloblastic anemia?
- People with mild anemia may have no symptoms, or symptoms may be very mild.
- More typical symptoms of vitamin B12 deficiency anemia include:
- Diarrhea or constipation
- Fatigue, lack of energy, or light-headedness when standing up or with exertion
- Loss of appetite
- Pale skin
- Problems concentrating
- Shortness of breath, mostly during exercise
- Swollen, red tongue or bleeding gums

# What causes Megaloblastic anemia?
- Megaloblastic anemia is usually caused by a deficiency of folic acid or vitamin B12.
- Other less common causes are:
- Alcohol abuse
- Certain inherited disorders
- Drugs that affect DNA, such as chemotherapy drugs
- Leukemia
- Myelodysplastic syndrome
- Myelofibrosis
- The anticonvulsant drug dilantin

# Who is at highest risk?
Risk factors relate to the causes.

# When to seek urgent medical care?
Call your health care provider if you have any of the symptoms of anemia.

# Diagnosis
- A physical exam may show problems with reflexes or a positive Babinski reflex.
- The following tests may be done:
- Complete blood count
- Reticulocyte count
- Schilling test (if pernicious anemia is suspected)
- Serum LDH
- Serum vitamin B12 level and serum folate levels
- Esophagogastroduodenoscopy (EGD) to examine the stomach, or enteroscopy to examine the small intestine may be done.
- Bone marrow biopsy is done only when the diagnosis is not clear.

# Treatment options
Treatment depends on the cause of B12 and folate deficiencies.

# Where to find medical care for Megaloblastic anemia?
Directions to Hospitals Treating Megaloblastic anemia

# What to expect (Outlook/Prognosis)?
Anemia usually responds well to treatment within 2 months.

# Sources
No observable adverse effect level (NOAEL)
NOAEL (No observable adverse effect level) denotes the level of exposure of an organism, found by experiment or observation, at which there is no biologically or statistically significant (e.g. alteration of morphology, functional capacity, growth, development or life span) increase in the frequency or severity of any adverse effects in the exposed population when compared to its appropriate control.
In toxicology it is specifically the highest tested dose or concentration of a substance (i.e. a chemical) or agent (e.g. radiation), at which no such adverse effect is found in exposed test organisms where higher doses or concentrations resulted in an adverse effect.
This level may be used in the process of establishing a dose-response relationship, a fundamental step in most risk assessment methodologies.