Persius/hicric huggingface dataset:
Central giant cell granuloma

# Overview
Central giant cell granuloma (CGCG) is a benign condition of the jaws.  It is twice as likely to affect women and is more likely to occur 20 - 40 year old people.  Central giant cell granulomas are more common in the mandible and often crosses the midline.
CGCG is a benign intraosseous lesion found in the anterior of the maxilla and the mandible in younger  people (before age 20). It is characterized by large lesions that expand the cortical plate and can reabsorb roots and move teeth. It is composed of mulitnucleated giant cells. It has a slight predilection for females.
Radiographically it appears as multilocular radiolucencies of bone.
There are two types of CGCG's, Non-aggressive and aggressive. The former has a slow rate of growth and thus less likely to absorb roots and perforate the cortical plate. The aggressive form has rapid growth and thus is much more likely to absorb roots and perforate the cortical plate. It also has a high rate for recurrence and can be painful and cause paresthesia.
Differential diagnosis to include: OKC, ameloblastoma, odontogentic myxoma, hemangioma, central odontogenic fibroma, hyperparathyroid tumor, and cherubism.

# Histology
The histology of CGCG is one that is composed of many multinucleated giant cells.  There is evidence that these giant cells represent osteoclasts,(bone-eating cells), others suggest more like macrophages.  The giant cells may be diffusely located throughout the lesion, or focally aggregate in the lesion. The giant cells are large and round or small and irregular, they vary greatly in size and shape.

# Treatment
The treatment for CGCG is thorough curettage.  A referral is made to oral surgeon.  Reoccurance ranges from 15%-20%. In aggressive tumors, three alternatives to surgery are undergoing investigation.  
. corticosteroids
. calcitonin (salmon calcitonin)
. interferon -2a.  
These therapeutic approaches provide positive possible alternatives for large lesions.  
The long term prognosis of giant cell granulomas is good and metastases do not develop.
Cephalexin adverse reactions

# Gastrointestinal
Onset of pseudomembranous colitis may occur during or after antibacterial treatment (see WARNINGS). Nausea and vomiting have been reported rarely. The most frequent side effect has been diarrhea. It was very rarely severe enough to warrant cessation of therapy. Dyspepsia, gastritis, and abdominal pain have also occurred. As with some penicillins and some other cephalosporins, transient hepatitis and cholestatic jaundice have been reported rarely.

# Hypersensitivity
AlIergic reactions in the form of rash, urticaria, angioedema, and, rarely, erythema multiforme, Stevens-Johnson syndrome, or toxic epidermal necrolysis have been observed. These reactions usually subsided upon discontinuation of the drug. In some of these reactions, supportive therapy may be necessary. Anaphylaxis has also been reported.
Other reactions have included genital and anal pruritus, genital moniliasis, vaginitis and vaginal discharge, dizziness, fatigue, headache, agitation, confusion, hallucinations, arthralgia, arthritis, and joint disorder. Reversible interstitial nephritis has been reported rarely. Eosinophilia, neutropenia, thrombocytopenia, hemolytic anemia, and slight elevations in AST and ALT have been reported.
In addition to the adverse reactions listed above that have been observed in patients treated with cephalexin, the following adverse reactions and altered laboratory tests have been reported for cephalosporin class antibiotics:

# Adverse Reactions
Fever, colitis, aplastic anemia, hemorrhage, renal dysfunction, and toxic nephropathy.
Several cephalosporins have been implicated in triggering seizures, particularly in patients 
with renal impairment when the dosage was not reduced (see INDICATIONS AND USAGE
and PRECAUTIONS, General). If seizures associated with drug therapy should occur, the
drug should be discontinued. Anticonvulsant therapy can be given if clinically indicated.

# Altered Laboratory Tests
Prolonged prothrombin time, increased BUN, increased creatinine, elevated alkaline
phosphatase, elevated bilirubin, elevated LDH, pancytopenia, leukopenia, and agranulocytosis.
To report SUSPECTED ADVERSE EVENTS, contact FDA at 1-800-FDA-1088 or www.fda.gov.
Chemical oxygen iodine laser

# Overview
Chemical oxygen iodine laser, or COIL, is an infrared chemical laser. As the beam is infrared, it cannot be seen with the naked eye. It is capable of output power scaling up to megawatts in continuous mode. Its output wavelength is 1.315 m, the wavelength of transition of atomic iodine.
The laser is fed with gaseous chlorine, molecular iodine, and an aqueous mixture of hydrogen peroxide and potassium hydroxide. The aqueous peroxide solution undergoes chemical reaction with chlorine, producing heat, potassium chloride, and oxygen in excited state, with spontaneous lifetime of about 45 minutes. This singlet delta oxygen transfers its energy to the iodine molecules injected to the gas stream; they are nearly resonant with the singlet oxygen, so the energy transfer during the collision of the particles is rapid. The excited iodine then undergoes stimulated emission and lases at 1.315 m in the optical resonator region of the laser.
The laser operates at relatively low gas pressures, but the gas flow has to be nearing the speed of sound at the reaction time; even supersonic flow designs are described. The low pressure and fast flow make removal of heat from the lasing medium easy, in comparison with high-power solid-state lasers. The reaction products are potassium salt, water, and oxygen. Traces of chlorine and iodine are removed from the exhaust gases by a halogen scrubber.
COIL laser was developed by the US Air Force in 1977, for military purposes. However, its properties make it useful for industrial processing as well; the beam is focusable and can be transferred by an optical fiber, as its wavelength is not absorbed much by fused silica but is very well absorbed by metals, making it suitable for laser cutting and drilling. Rapid cutting of stainless steel and hastelloy with a fiber-coupled COIL was demonstrated. In 1996, TRW Incorporated managed to get a continuous beam of hundreds of kilowatts of power that lasted for several seconds.
RADICL, Research Assessment, Device Improvement Chemical Laser, is a 20 kW COIL laser tested by Air Force in around 1998.
COIL is the main weapon laser for the military airborne laser and advanced tactical laser programs.
All gas-phase iodine laser (AGIL) is a similar construction using all-gas reagents, more suitable for aerospace applications.
Children's Memorial Hospital
With almost 1,100 pediatric specialists focusing on 70 specialties in multiple locations, Children's Memorial Hospital routinely provides more care to more young people than any other Chicago-area hospital or medical center. The hospital is accredited by the Joint Commission (formerly known as the Joint Commission on Accreditation of Healthcare Organizations). Licensed for 270 beds, Children's Memorial cares for the most critically ill kids. In fact, its Case Mix Index (used as a severity measure) shows that the hospital is one of the country's top five children's hospitals that consistently cares for very sick children.

# History
Children's Memorial Hospital was founded in 1882 by Julia Foster Porter as the Maurice Porter Memorial Hospital in an 8-bed cottage at the corner of Halsted and Belden streets in Chicago.  It was the first hospital in Chicago dedicated to the care of children and pediatrics.

# Education
As the primary pediatric teaching hospital of Northwestern University's Feinberg School of Medicine, the hospital offers one of the country's most sought after pediatrics residency programs. The medical school's Department of Pediatrics is currently tied for 12th place in the 2007 U.S.News and World Report rankings.

# Research
The hospital is also home to Children's Memorial Research Center, the research arm of Children's Memorial Hospital and a virtual center for pediatric research at Northwestern University's Feinberg School of Medicine. Founded in 1989, the research enterprise has grown to include more than 200 investigators and more than $25 million in external funding for research, two-thirds from NIH and other federal agencies.

# Awards
Children's Memorial Hospital is currently ranked as Illinois' the top pediatric hospital and one of the nation's best by U.S.News and World Report. The hospital's nursing department received the prestigious Magnet Award for Nursing Excellence.  Children's Memorial was also named one of the 25 best places to work by Chicago magazine and one of the best 100 companies by Working Mother magazine.

# Future
Construction is scheduled to break ground in 2008 at Children's Memorial's future site in the Streeterville area of Chicago, adjacent to the rest of the McGaw Medical Center of Northwestern University. The $850 million project is scheduled to open in 2012, and the 1.1 million square foot facility will house 275 private rooms with the ability to expand to 343 by 2017. On September 5, 2007, Chicago philanthropist Ann Lurie announced will donate a record $100 million toward the new hospital. Upon completion, the new Children's Memorial will be re-named the Ann & Robert H. Lurie Children's Hospital of Chicago. It will remain the only independent pediatric hospital in Illinois, but will build on its existing partnerships with Northwestern Memorial HealthCare and the Feinberg School of Medicine.
Chloride potassium symporter
The chloride potassium symporter is a membrane transport protein that is present in the S3-segment of the renal proximal tubule. It functions in renal chloride reabsorption to transport chloride across the basolateral membrane.
They can lower intracellular chloride concentrations below the electrochemical equilibrium potential.
They are of solute carrier family 12.

# Types
Types of chloride potassium symporter are:
- Chloride potassium symporter 4
- Chloride potassium symporter 5
Each is encoded by a separate gene.
The preceding symporters are actually other types of ion pumps. Member 3, for instance, is the sodium-chloride symporter.
Choroidal neovascularization
Choroidal neovascularization is the creation of new blood vessels in the choroid layer of the eye. This is a common symptom of the degenerative maculopathy wet AMD (age-related macular degeneration).

# Causes
CNV can occur rapidly in individuals with defects in Bruch's membrane, the innermost layer of the choroid. It is also associated with excessive amounts of Vascular Endothelial Growth Factor (VEGF). As well as in wet AMD, CNV can also occur frequently with the rare genetic disease pseudoxanthoma elasticum and rarely with the more common optic disc drusen.

# Symptoms
CNV can create a sudden deterioration of central vision, noticeable within a few weeks. Hemorrhaging of the new blood vessels can accelerate the onset of symptoms of CNV.

# Treatment
- In 'wet' (also known as 'neovascular') Age-Related Macular Degeneration, CNV is treated with photodynamic therapy coupled with a photosensitive drug such as verteporfin. The drug is injected into the eye, where it accumulates in the new blood vessels. It is then activated by a laser light. The drug destroys the new blood vessels, and prevents any new vessels forming by forming thrombi. 
- Anti-VEGF drugs, such as pegaptanib and ranibizumab, are also used to treat CNV. Anti-VEGFs bind to and inactivate Vascular Endothelial Growth Factor.
Postprandial angina pectoris

# Overview
Postprandial angina pectoris is anginal chest discomfort that occurs following meals. It is thought to be due to an increase in vascular tone or a reduction in coronary blood flow.

# Pathophysiology
- Any type of angina can occur after meals as a result of increased coronary vascular tone and a decrease in coronary blood flow. However, postprandial angina occurs during physical activity after meals because of an associated increase in myocardial oxygen demand.
- Postprandial angina is almost always associated with significant atherosclerotic coronary artery disease.

# Diagnosis

## Symptoms
Postprandial angina occurs during physical activity after meals.

# Treatment
The treatment is the same as chronic stable angina.
Walk through angina pectoris

# Overview
Walk through angina is the appearance of anginal chest discomfort early in the course of exertion which subsequently subsides despite continued exertion.

# Pathophysiology
- The precise underlying mechanism of walk though angina remains unclear.
- It has been speculated that walk through angina may be due to an initial increase in coronary vascular tone with a consequent reduction in coronary blood flow at the beginning of exercise.
- It has also been speculated that recruitment of collaterals may also play a role in the walk through angina phenomenon.

# Diagnosis

### Symptoms
In the majority of patients with obstructive coronary artery disease, the intensity of the anginal pain is proportional to the the intensity of physical activity, and the pain only subsides once physical activity ceases.  However a subset of patients have walk through angina. Although these patients experience angina early in the course of physical activity (e.g. walking, gardening, and short running) it dissapears despite continuation of physical activity.

# Treatment
The treatment is the same as in chronic stable angina.
Clinical depression overview

# Overview
Major depressive disorder a psychiatric disorder characterized by a pervasive low mood, loss of interest in usual activities, and a diminished ability to experience pleasure (anhedonia).
Although the term "depression" is commonly used to describe a temporary depressed mood (i.e., "feeling blue"), major depressive disorder is a serious and often disabling condition that can significantly affect a person's work, family, and school life; sleeping and eating habits; general health; and ability to enjoy life. The course of major depressive disorder varies widely: depression can be a once-in-a-lifetime event or have multiple recurrences, it can appear either gradually or suddenly, and it can either last for a few months or be a life-long disorder. Major depressive disorder is a major risk factor for suicide. In addition, people with depression suffer from higher mortality from other causes.
When specific treatment is indicated, it usually consists of psychotherapy and antidepressants.
The impact of depression on the quality of an individual's life is more than that of having a recent myocardial infarction but less than tha of having heart failure..

# Diagnosis

## History and Symptoms
Before a diagnosis of depression can be made, a physician should perform a complete medical exam to rule out any possible physical cause for the suspected depression. If no such cause is found, a psychological evaluation should be done by the physician or by referral to a psychiatristor psychologist. The evaluation will include a complete history of symptoms, a discussion of alcohol and drug use, and whether the patient has had or is having suicidal thoughts or thinking about death. The evaluation will also include a family medical history to see if other family members suffer from any form of depression or similar mood disorder.

# Treatment

## Medical Therapy
The treatment of depression is highly individualized to the patient, based on the patient's unique combination of biological, psychological and social health factors and the severity of their condition.  The three most conventional treatments for depression include medication, psychotherapy, and electroconvulsive therapy. New treatments and less conventional options are also available, including self help, life style changes, and vagus nerve stimulation. If there is an imminent threat of suicide or the patient is a danger to others, hospitalization is employed as an intervention method to keep at-risk individuals safe until they cease to be a danger to themselves or others. At-risk individuals may also be placed in a partial hospitalization therapy, in which the patient sleeps at home but spends most of the day in a psychiatric hospital setting. This intensive treatment usually involves group therapy, individual therapy, medication management, and is used often in the case of children and adolescents.
Collagen, type XIII, alpha 1
Collagen alpha-1(XIII) chain is a protein that in humans is encoded by the COL13A1 gene.
This gene encodes the alpha chain of one of the nonfibrillar collagens. The function of this gene product is not known, however, it has been detected at low levels in all connective tissue-producing cells so it may serve a general function in connective tissues. Unlike most of the collagens, which are secreted into the extracellular matrix, collagen XIII contains a transmembrane domain and the protein has been localized to the plasma membrane. The transcripts for this gene undergo complex and extensive splicing involving at least eight exons. Like other collagens, collagen XIII is a trimer; it is not known whether this trimer is composed of one or more than one alpha chain isomer. A number of alternatively spliced transcript variants have been described, but the full length nature of some of them has not been determined.
 Collagen XIII belongs to the transmembranous subfamily of collagens, like collagen XVII, XXIII and XXV.
Systemic autoimmune diseases
Synonyms and keywords: Collagen vascular disease; collagen-vascular disease

# Overview
In systemic autoimmune diseases, the immune system attacks many different organs, tissues, and cells of the body. Examples include: systemic lupus erythematosis, rheumatoid arthritis, systemic sclerosis, and dermatomyositis.
In contrast to systemic autoimmune diseases, organ-specific or tissue-specific autoimmune diseases such as diabetes mellitus type 1, Hashimoto's thyroiditis, multiple sclerosis and myasthenia gravis affect only one organ or tissue type. For example, diabetes mellitus affects the islet cells in the pancreas, Hashimoto's thyroiditis affects the thyroid gland, multiple sclerosis affects the brain, and myasthemia gravis affects the muscles.
The systemic autoimmune diseases are rheumatological diseases. Rheumatologists specialize in their treatment.

# Synonyms
The terms "collagen vascular disease" and "collagen-vascular disease," in use since 1962 or earlier, are synonyms for systemic autoimmune disease. The term "collagen vascular disease" is a misnomer: these diseases affect many structures in addition to vascular structures, and they affect many molecules in addition to the collagen molecule.
They are also referred to as connective tissue diseases. However, although the systemic autoimmune diseases affect connective tissue, they also affect many other tissue types, including muscle tissue and neural tissue.  In addition, many connective tissue diseases (such as scurvy and Marfan syndrome) are not autoimmune in nature.
Systemic lupus erythematosis and rheumatoid arthritis can cause vasculitis (vasculitis means "inflammation of blood vessels"). However, these diseases affect many structures other than blood vessels.
Congenital chloride diarrhea

# Overview
Congenital chloride diarrhea (CCD, also congenital chloridorrhea) is a genetic disorder due to an autosomal recessive mutation on chromosome 7.  The mutation is in downregulated-in-adenoma (DRA), a gene that encodes a membrane protein of intestinal cells.  The protein belongs to the solute carrier 26 family of membrane transport proteins.  More than 20 mutations in the gene are known to date.  A rare disease, CCD occurs in all parts of the world but is more common in some populations with genetic founder effects, most notably in Finland.

# Pathophysiology
CCD causes persistent secretory diarrhea.  In a fetus, it leads to polyhydramnios and premature birth.  Immediately after birth, it leads to dehydration, hypoelectrolytemia, hyperbilirubinemia, abdominal distention, and failure to thrive.

# Diagnosis
CCD may be detectable on prenatal ultrasound.  After birth, signs in affected babies typically are abdominal distension, visible peristalsis, and watery stools persistent from birth that show chloride loss of more than 90 mmol/l.
An important feature in this diarrhea that helps in the diagnosis, is that its the only type of diarrhea that causes metabolic alkalosis rather than metabolic acidosis.

# Treatment
Available treatments address the symptoms of CCD, not the underlying defect.  Early diagnosis and aggressive salt replacement therapy result in normal growth and development, and generally good outcomes.  Replacement of NaCl and KCl has been shown to be effective in children.
A potential treatment is butyrate.

# History
Observations leading to the characterization of the SLC26 family were based on research on rare human diseases.  Three rare recessive diseases in humans have been shown to be caused by genes of this family.  Diastrophic dysplasia, congenital chloride diarrhea, and Pendred syndrome are caused by the highly related genes SLC26A2 (first called DTDST), SLC26A3 (first called CLD or DRA), and SLC26A4 (first called PDS), respectively.  Two of these diseases, diastrophic dysplasia and congenital chloride diarrhea, are Finnish heritage diseases.
Congenital melanocytic nevus

# Overview
The congenital melanocytic nevus is a type of melanocytic nevus (or mole) found in infants at birth.  Occurring in about 1% of infants in the United States, it is located in the area of the head and neck  15% of the time.
The appearance of the congenital melanocytic nevus is similar to those of acquired ones, but are usually larger in diameter and may have excess hair, called hypertrichosis.  If large with hypertrichosis, it is called giant hairy nevus.
Microscopically, the congenital melanocytic nevus appears similar to acquired nevi with two notable exceptions.  For the congenital nevus, the neval cells are found deeper into the dermis.  Also, the deeper neval cells are found along with neurovascular bundles with both surrounding hair follicles, sebaceous glands, and subcutaneous fat.
Many are surgically removed for aesthetics, but larger ones are excised for prevention of cancer.  5 - 15% transform into melanoma.

# Physical Examination

## Skin
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