Persius/hicric huggingface dataset:
Louisa Gross Horwitz Prize
Louisa Gross Horwitz Prize for Biology or Biochemistry is an annual prize awarded by Columbia University to a researcher or group of researchers that have made an outstanding contribution in basic research in the fields of biology or biochemistry.
The Prize was established at the bequest of S. Gross Horwitz and is named to honor his mother. The prize was first awarded in 1967.
Out of 74 Prize Recipients, 39(53%) have won Nobel Prize in Medicine(29) or Chemistry(10) subsequently. It is regarded as one of the important precursors of future Nobel Prize award.

# Recipients
- 1967 Luis Leloir
- 1968 Har Gobind Khorana, Marshall Warren Nirenberg
- 1969 Max Delbruck, Salvador E. Luria
- 1970 Albert Claude, George E. Palade, Keith R. Porter
- 1971 Hugh E. Huxley
- 1972 Stephen W. Kuffler
- 1973 Renato Dulbecco, Harry Eagle, Theodore T. Puck
- 1974 Boris Ephrussi
- 1975 K. Sune D. Bergstrom, Bengt Samuelsson
- 1976 Seymour Benzer, Charles Yanofsky
- 1977 Michael Heidelberger, Elvin A. Kabat, Henry G. Kunkel
- 1978 David Hubel, Vernon Mountcastle, Torsten Wiesel
- 1979 Walter Gilbert, Frederick Sanger
- 1980 Cesar Milstein
- 1981 Aaron Klug
- 1982 Barbara McClintock, Susumu Tonegawa
- 1983 Stanley Cohen, Viktor Hamburger, Rita Levi-Montalcini
- 1984 Michael S. Brown, Joseph L. Goldstein
- 1985 Donald D. Brown, Mark Ptashne
- 1986 Erwin Neher, Bert Sakmann
- 1987 Gunter Blobel
- 1988 Thomas R. Cech, Philip A. Sharp
- 1989 Alfred G. Gilman, Edwin G. Krebs
- 1990 Stephen Harrison, Michael G. Rossmann, Don C. Wiley
- 1991 Richard R. Ernst, Kurt Wuthrich
- 1992 Christiane Nusslein-Volhard, Edward B. Lewis
- 1993 Nicole Le Douarin, Donald Metcalf
- 1994 Philippa Marrack, John W. Kappler
- 1995 Leland H. Hartwell
- 1996 Clay M. Armstrong, Bertil Hille
- 1997 Stanley B. Prusiner
- 1998 Arnold J. Levine, Bert Vogelstein
- 1999 Pierre Chambon, Robert Roeder, Robert Tjian
- 2000 H. Robert Horvitz, Stanley J. Korsmeyer
- 2001 Avram Hershko, Alexander Varshavsky
- 2002 James E. Rothman, Randy W. Schekman
- 2003 Roderick MacKinnon
- 2004 Tony Hunter, Tony Pawson
- 2005 Ada Yonath
- 2006 Roger D. Kornberg
- 2007 Joseph G. Gall, Elizabeth H. Blackburn, Carol W. Greider

# Notes
-  As of 2006.
Lymphoepithelioma overview

# Overview
Lymphoepithelioma is a type of poorly differentiated nasopharyngeal carcinoma characterized by prominent infiltration of lymphocytes in the area involved by tumor.  Lymphoepithelioma is also known as "class III nasopharyngeal carcinoma" in the WHO classification system. Most cases are associated with Epstein-Barr virus infection.
Lymphoepithelioma may also be referred to as Schmincke-Regaud tumor, after the German pathologist Alexander Schminke and French radiologist Claude Regaud.
Lymphoepithelioma-like carcinomas are carcinomas that arise outside of the nasopharynx, but resemble a lymphoepithelioma histologically.  Lymphoepithelioma-like carcinomas may be found in almost any epithelial organ, including the lung, thymus, breast, colon, endometrium, prostate, and skin.
Reticuloendothelial system

# Overview
The reticuloendothelial system (RES), part of the immune system, consists of the phagocytic cells located in reticular connective tissue, primarily monocytes and macrophages. These cells accumulate in lymph nodes and the spleen. The Kupffer cells of the liver and tissue histiocytes are also part of the RES.
Mononuclear phagocytic system and lymphoreticular system are synonymous with RES.
The reticuloendothelial system is divided into primary and secondary lymphoid organs.

# Primary lymphoid organs
Primary (or "central") lymphoid organs - the sites where the cells of the RES are produced.  The cells of the RES are produced in the bone marrow.
The thymus is also included as it is the required site for T cell maturation.

# Secondary  lymphoid organs
Secondary (or "peripheral") lymphoid organs - the sites where the cells of the RES function.  This includes the lymph nodes, spleen, and "MALT" (mucosa-associated lymphoid tissue).
- MALT is further divided into the "GALT" (gut-associated lymphoid tissue) and the "BALT" (bronchus-associated lymphoid tissue).
- The Kupffer cells of the liver act as part of this system but are not organized into a tissue; rather, they are dispersed throughout the liver sinusoids.

## Function
The secondary lymphoid structures function to survey all entering or circulating antigen and to mobilize an immune response against foreign antigen upon its discovery.  The GALT and BALT are privy to the myriads of antigen entering the gastrointestinal and respiratory tracts, respectively.  All extracellular fluid must filter through lymph nodes as it traverses the lymphatics on its way back to the systemic circulation.  Antigen residing in the interstitium is thus swept to the lymph nodes for processing.
Finally, the spleen filters the blood in search of antigen.  Upon the discovery of foreign antigen, all of these tissues react in a similar manner to amass an appropriate and multifaceted immune response.

# Clinical significance
In patients with haemochromatosis the reticuloendothelial system is a site of iron acumulation.
Lymphoma of the reticuloendothelial system is called reticuloendotheliosis.
Mycobacterium tuberculosis
Synonyms and keywords: M. Tuberculosis

# Overview
Mycobacterium tuberculosis is the bacterium responsible for tuberculosis. M. tuberculosis is an obligate aerobe, non-encapsulated, non-motile, acid-fast bacillus. .  M. tuberculosis is one of the Mycobacterium tuberculosis complex, which also includes bacteria, such as M. bovis and M. africanum.  The bacterium has a very slow rate of replication, and its genetic variations account for the different strains and the growing drug resistance.  M. tuberculosis has tropism for different kinds of human cells, with preference for cells of the lung. The main natural reservoir for M. tuberculosis are Human beings; however, the bacteria can also infect other species.

# Taxonomy
Cellular organisms; bacteria; Actinobacteria; Actinobacteria; Actinobacteridae; Actinomycetales; Corynebacterineae; Mycobacteriaceae; Mycobacterium;  Mycobacterium tuberculosis complex; M. tuberculosis

# Biology
- Mycobacterium tuberculosis belongs to the Mycobacterium tuberculosis complex.  This complex includes M. tuberculosis, M. bovis, M. africanum, M. canetti, and M. microti.
- M. tuberculosis is an obligate aerobe, non-encapsulated, non-motile, acid-fast bacillus.
- Its shape is slender, straight or slightly curved bacillus with rounded ends.
- It can be present singly, in pairs or in small groups or clumps.
- It cannot form spores.
- It favors tissues with high oxygen levels.
- Due to the high lipid and mycolic acid content of its cell wall, It stains weakly gram-positive or does not retain the dye.
- Microscopic examination of sputum samples cannot differentiate it  from other acid-fast bacteria, such as Nocardia spp.
- M. tuberculosis divides every 15-20 hours which is considered an extremely low rate of division. This feature, in addition to its ability to remain latent for long time, are responsible for the long treatment duration needed.
- It can withstand dryness for weeks and also weak disinfectants.
- Genetic variations in the M. tuberculosis genome lead to important phenotypical changes. As a result, there are several variable strains of the bacteria, six of which have particular geographical distribution. Three strains, the Beijing family, strain W and the W-like strains, were reported to be associated with higher incidence of multi-drug resistance.

# Tropism
There is no particular tissue tropism for M. tuberculosis and it can infect almost all human tissues. However, M. tuberculosis prefers tissues with high levels of oxygen , hence, pulmonary tuberculosis has the highest rate. 

# Natural Reservoir
The main natural reservoir for M. tuberculosis are Human beings; however, the bacteria can also infect other species.
Myeloperoxidase deficiency
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# Overview
Myeloperoxidase deficiency is a common genetic disorder featuring deficiency, either in quantity or function, of myeloperoxidase, an enzyme found in certain phagocytic immune cells, especially polymorphonuclear leukocytes.
It can appear similar to chronic granulomatous disease on some screening tests.

# Presentation
Although MPO deficiency classically presents with immune deficiency (especially candida albicans infections), the majority of individuals with MPO deficiency show no signs of immunodeficiency.
The lack of severe symptoms suggest that role of myeloperoxidase in the immune response must be redundant to other mechanisms of intracellular killing of phagocytosed bacteria.
Mafenide adverse reactions

# Adverse Reactions
In the clinical setting of severe burns, it is often difficult to distinguish between an adverse reaction to Mafenide Acetate and burn sequelae. In a clinical study of pediatric patients with acute burns requiring autografts who received Mafenide Acetate,USP for  5% SOLUTION in addition to double antibiotic solution (DAB) wound therapy (neomycin sulfate 40 mg and polymyxin B 200,000 units/ liter), the incidence of rash (4.6%) and itching (2.8%) in the group which received Mafenide Acetate USP For 5% Solution was not different from that experienced with (DAB) dressings alone (5.7% and 1.3%, respectively).
From other clinical settings, a single case of bone marrow depression and a single case of an acute attack of porphyria have been reported following therapy with Mafenide Acetate. Fatal hemolytic anemia with disseminated intravascular coagulation, presumably related to a glucose-6-phosphate dehydrogenase deficiency, has been reported following therapy with mafenide acetate. The following adverse reactions have been reported with topical Mafenide Acetate therapy

## Dermatologic and Allergic
Pain or burning sensation, rash and pruritus (often localized to the area covered by the wound dressing), erythema, skin maceration from prolonged wet dressings, facial edema, swelling, hives, blisters, eosinophilia.

## Respiratory or Metabolic
Tachypnea, hyperventilation, decrease in pCO2, metabolic acidosis, increase in serum chloride.
Matrix metallopeptidase 12
Matrix metalloproteinase-12 (MMP-12) also known as macrophage metalloelastase (MME) or macrophage elastase (ME) is an enzyme that in humans is encoded by the MMP12 gene.

# Function
Proteins of the matrix metalloproteinase (MMP) family are involved in the breakdown of extracellular matrix in normal physiological processes, such as embryonic development, reproduction, and tissue remodeling, as well as in disease processes, such as arthritis and metastasis. Most MMP's are secreted as inactive proproteins. The prodomain is cleaved by extracellular proteinases when the enzyme is activated. The active enzyme is constituted by two domains, the catalytic domain resposnsible for its enzymatic activity and the hemopexin-like domain that in some MMPs plays a role in substrate recognition and can contribute to increasing catalytic efficiency. It is thought that the protein encoded by this gene is cleaved at both ends to yield the active enzyme, but this processing has not been fully described. The enzyme degrades soluble and insoluble elastin. The gene is part of a cluster of MMP genes which localize to chromosome 11q22.3.

# Clinical significance
MMP12 may play a role in aneurysm formation and studies in mice and humans suggest a role in the development of emphysema.
Mediastinal tumor overview

# Overview
Masses in the anterior portion of the mediastinum can include thymoma, lymphoma, and germ cell tumors including teratoma.  Lung cancer typically spreads to the lymph nodes in the mediastinum.
Anterior mediastinal compartment, also known as anterosuperior compartment, is anterior to the pericardium. Masses in this area is more likely to be malignant than those in other compartments Most common masses found here include thymomas, germ cell tumors, lymphomas, thyroid tissue, and parathyroid lesions.

# Anterior mediastinal tumor

### Thymoma
Most common primary anterior mediastinal tumor (20%) in adults but rarely seen in children. It can be classified as lymphocytic, epithelial, or spindle cell histologies, but this is not very significant clinically. Tonofibrils seen under electron microscopy can differentiate thymoma from other tumors such as carcinoid, Hodgkin's, and seminoma. Patients are usually asymptomatic but can present with myasthenia gravis-related symptoms, substernal pain, dyspnea, or cough. Invasive tumors can produce compression effects such as superior vena cava syndrome.
Thymomas are diagnosed with CT or MRI revealing mass in anterior mediastinum.
Therapy in stage I tumors consists of surgical resection with good prognosis.
Stage II-III requires maximal resection possible followed by radiation.
Stage IV disease requires addition of cisplatin-based chemotherapy in addition to those in stage II and III.
For those with invasive thymoma, treatment is based on induction chemotherapy, surgical resection, and post-surgical radiation.
5-year survival for invasive thymoma is between 12-54% regardless of any myasthenia gravis symptoms.

### Lymphoma
Secondary most common primary anterior mediastinal mass in adults. Most are seen in the anterior compartment and rest are seen in middle compartment. Hodgkin's usually present in 40-50's with nodular sclerosing type, and non-Hogdkin's in all age groups. Can also be primary mediastinal B cell lymphoma with exceptionally good prognosis   
Common symptoms include fever, weight loss, night sweats, and compressive symptoms such as pain, dyspnea, wheezing, SVC syndrome, pleural effusions.
Diagnosis usually by CT showing lobulated mass. Confirmation done by tissue biopsy of accompanying nodes if any, mediastinoscopy, mediastinotomy, or thoracotomy. FNA biopsy usually not adequate.
Treatment of mediastinal Hodgkin's involves chemotherapy and/or radiation. 5 year survival is now around 75%. Large-cell type may have somewhat better prognosis. Surgery is generally not performed because of invasive nature of tumor.
Of all cancers involving the same class of blood cell, 2% of cases are mediastinal large B cell lymphomas.
Melanocytic nevus overview

# Overview
A mole, technically known as a melanocytic nevus, is a small, dark spot on human skin. According to the American Academy of Dermatology, the majority of moles appear during the first two decades of a persons life while about one in every 100 babies are born with moles.  Acquired moles are a form of benign neoplasm, while congenitalmoles are considered a minor malformation, or hamartoma. A mole can be either subdermal (composed of melanin), or a pigmented growth on the skin, formed mostly of a type of cell known as melanocytes. The high concentration of the bodys pigmenting agent, melanin, is responsible for their dark color. Moles are a member of the family of skin lesions known as nevi.

# Historical Perspective
At one time in the 1950s and 60s, (and, to lesser extent, currently) a mole was known as a beauty mark when it appeared in certain spots on a womans face. Examples include Marilyn Monroe, model Cindy Crawford and singer Madonna. Madonna's facial mole -- below her right nostril -- has been surgically removed.

# Classification
Melanocytic nevus is a type of melanocytic lesion. Depending on the degree of cytologic atypia it can be classified into mild, moderate or severe.

# Pathophysiology
Melanocytic nevus is a benign growth on the skin (usually tan, brown, or flesh-colored) that contains a cluster of melanocytes and surrounding supportive tissue.

# Causes
Scientists suspect that overexposure to ultraviolet light, including excessive sunlight, may play a role in the formation of acquired moles. However, more research is needed in this area.

# Differentiating Melanocytic Nevus from Other Diseases
Melanocytic nevus must be differentiate from dysplastic nevus, melanoma and epidermal nevus.

# Epidemiology and Demographics
Darker skin shades tend to have fewer moles compared to fair complexion.

# Risk Factors
Most important risk factor for melanocytic nevus is sunlight however, genetic predisposition is an important factor as well.

# Natural History, Complications, and Prognosis
Vast majority of moles are benign. Nonetheless, the National (U.S.) Cancer Institute reported 59,940 new cases of melanoma by June, 2007, with 8,110 deaths.

# Diagnosis

## Diagnostic Study of Choice

## History and Symptoms

## Physical Examination

## Laboratory Findings

## Electrocardiogram

## X-ray

## Echocardiography and Ultrasound

## CT scan

## MRI

## Other Imaging Findings

## Other Diagnostic Studies

# Medical Therapy

# Surgery
If a mole is highly suspicious of being a melanoma, then it might need to be removed and biopsied (microscopic evaluation by a pathologist). Other reasons for removal may be cosmetic, or because a raised mole interferes with daily living (e.g. shaving).
Moles can be removed by laser, surgery or electrocautery. They leave a red mark on the site which morphs back to the patients usual skin color in about two weeks. However, there might still be a risk of spread of the melanoma, so the methods of Melanoma diagnosis, including e.g. excitional biopsy.
Metastability in molecules
Metastability is the ability of a non-equilibrium state to persist for some period of time.
Metastability in molecules is the ability of a non-equilibrium chemical state to persist for a long period of time.
Usually metastability is due to a relatively slow phase transformation.  For example, at room temperature, diamonds are metastable because the phase transformation to the stable graphite form is extremely slow.  At higher temperatures, the rate of phase transformation is increased and the diamond will transform to graphite.
Martensite  is a metastable phase used to control the hardness of most steel.  The bonds between the building blocks of polymers such as DNA, RNA and proteins are also metastable.
IUPAC recommend that the term "metastable" be avoided and "transient" be used instead because "metastable" can misleadingly associate a thermodynamic term to a kinetic property, even though most transients are thermodynamically unstable with respect to reactants or products.
Mineralocorticoid receptor
The mineralocorticoid receptor (or MR, MLR, MCR), also known as the aldosterone receptor or nuclear receptor subfamily 3, group C, member 2,  (NR3C2) is a protein that in humans is encoded by the NR3C2 gene that is located on chromosome 4q31.1-31.2.
MR is a receptor with equal affinity for mineralocorticoids and glucocorticoids. It belongs to the nuclear receptor family where the ligand diffuses into cells, interacts with the receptor and results in a signal transduction affecting specific gene expression in the nucleus.

# Function
MR is expressed in many tissues, such as the kidney, colon, heart, central nervous system (hippocampus), brown adipose tissue and sweat glands. In epithelial tissues, its activation leads to the expression of proteins regulating ionic and water transports (mainly the epithelial sodium channel or ENaC, Na+/K+ pump, serum and glucocorticoid induced kinase or SGK1) resulting in the reabsorption of sodium, and as a consequence an increase in extracellular volume, increase in blood pressure, and an excretion of potassium to maintain a normal salt concentration in the body.
The receptor is activated by mineralocorticoids such as aldosterone and its precursor deoxycorticosterone as well as glucocorticoids, like cortisol. In intact animals, the mineralocorticoid receptor is "protected" from glucocorticoids by co-localization of an enzyme, corticosteroid 11-beta-dehydrogenase isozyme 2 (a.k.a. 11-hydroxysteroid dehydrogenase 2; 11-HSD2), that converts cortisol to inactive cortisone. It also responds to some progestins. Spironolactone and eplerenone are steroidal MR antagonists of the spirolactone group.
Activation of the mineralocorticoid receptor, upon the binding of its ligand aldosterone, results in its translocation to the cell nucleus, homodimerization and binding to hormone response elements present in the promoter of some genes. This results in the complex recruitment of the transcriptional machinery and the transcription into mRNA of the DNA sequence of the activated genes.

# Interactions
Mineralocorticoid receptor has been shown to interact with:
- Glucocorticoid receptor and
- TRIM24.
Monoamine neurotransmitter
Monoamine neurotransmitters are neurotransmitters and neuromodulators that contain one amino group that is connected to an  aromatic ring by a two-carbon chain (-CH2-CH2-). All monoamines are derived from aromatic amino acids like phenylalanine, tyrosine, tryptophan, and the thyroid hormones by the action of aromatic amino acid decarboxylase enzymes.

# Examples
- Histamine
- Thyronamines, a new group of compounds derived from thyroid hormones
- Catecholamines:
Dopamine (DA)
Norepinephrine (NE) (noradrenaline, NA)
Epinephrine (Epi) (adrenaline)
- Dopamine (DA)
- Norepinephrine (NE) (noradrenaline, NA)
- Epinephrine (Epi) (adrenaline)
- Tryptamines:
Serotonin (5-HT)
Melatonin
- Serotonin (5-HT)
- Melatonin
- Trace amines:
-Phenylethylamine (PEA, -PEA)
Tyramine
Tryptamine
Octopamine
3-iodothyronamine
- -Phenylethylamine (PEA, -PEA)
- Tyramine
- Tryptamine
- Octopamine
- 3-iodothyronamine
Specific transporter proteins called monoamine transporters exist that transport monoamines in or out of a cell. These are the dopamine transporter (DAT), serotonin transporter (SERT), and the norepinephrine transporter (NET) in the outer cell membrane and the vesicular monoamine transporter (VMAT1 and VMAT2) in the membrane of intracellular  vesicles.
After release into the synaptic cleft, monoamine neurotransmitter action is ended by reuptake into the presynaptic terminal.  There, they can be repackaged into synaptic vesicles or degraded by the enzyme monoamine oxidase (MAO), which is a target of monoamine oxidase inhibitors, a class of antidepressants.
Morning glory disc anomaly

# Overview
The morning glory disc anomaly (MGDA) is a congenital deformity resulting from failure of the optic nerve to completely form in utero. The term was coined in 1970 by Kindler, noting a resemblance of the malformed optic nerve to the morning glory flower. The condition is usually unilateral.
On fundoscopic examination, there are three principal findings comprising the anomaly:
- an enlarged, funnel-shaped excavation in optic disc
- an annulus or ring of chorioretinal pigmentary changes surrounding the optic disc excavation
- a central glial tuft overlying the optic disc

# Associated conditions
Although the finding itself is rare, MGDA can be associated with midline cranial defects and abnormal carotid circulation, such as carotid stenosis/aplasia or progressive vascular obstruction with collateralization (also known as Moya moya). The vascular defects may lead to ischemia, stroke, or seizures and so a finding of MGDA should be further investigated radiographic imaging.

# Complications
Serous retinal detachment can occur in the affected eye.
See also
- Coloboma of optic nerve
- Eye wiki: Morning glory anomaly