Persius/hicric huggingface dataset:
Mini mental state examination

# Overview
The mini-mental state examination (MMSE) or Folstein test is a brief 30-point questionnaire test that is used to assess cognition. It is commonly used in medicine to screen for dementia. In the time span of about 10 minutes, it samples various functions, including arithmetic, memory and orientation. It was introduced by Folstein et al in 1975, and is widely used with small modifications. Various other tests are also used, such as the Hodkinson abbreviated mental test score (1972, geriatrics) and longer formal tests for deeper analysis of specific deficits. This test is not the same thing as a mental status examination.

# The Test
The MMSE test includes simple questions and problems in a number of areas: the time and place of the test, repeating lists of words, arithmetic, language use and comprehension, and copying a drawing.

# Interpretation
Any score over 27 (out of 30) is effectively normal. Below this, 20-26 indicates mild dementia; 10-19 moderate dementia, and below 10 severe dementia. The normal value is also corrected for degree of schooling and age. Low to very low scores correlate closely with the presence of dementia, although other mental disorders can also lead to abnormal findings on MMSE testing. The presence of purely physical problems can also interfere with interpretation if not properly noted; for example, a patient may be physically unable to hear or read instructions properly, or may have a motor deficit that affects writing and drawing skills.

# MMSE Copyright
With the significant popularity of the test, the current copyright owner (Psychological Assessment Resources (PAR)) decided, after many years, to start enforcing the copyright and set-up a website to sell official versions of the test. The enforcement of the copyright on the MMSE has been compared to stealth patents, where a patent holder waits until an invention gains widespread popularity until commencing enforcement.
This has led to removal of the Sweet 16 from the Internet at the request of PAR
Copies of their MMSE can be purchased (). A copy of the Mini-mental state examination can be found in the appendix of the original publication.

# Related Chapters
- Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE)
- Mental status examination
Macular degeneration overview

# Overview
Macular degeneration is a medical condition predominantly found in elderly adults in which the center of the inner lining of the eye, known as the macula area of the retina, suffers thinning, atrophy, and in some cases bleeding. This can result in loss of central vision, which entails inability to see fine details, to read, or to recognize faces. According to the American Academy of Ophthalmology, it is the leading cause of central vision loss (blindness) in the United States today for those over the age of fifty years. Although some macular dystrophies that affect younger individuals are sometimes referred to as macular degeneration, the term generally refers to age-related macular degeneration (AMD or ARMD).

# Differentiating Macular Degeneration from other Diseases
Macular degeneration should be differentiated from other causes of distorted vision with a very different etiology and different treatment such as epiretinal membrane or macular pucker or leaking blood vessels in the eye.

# Natural History, Complications and Prognosis
Macular degeneration, in its advanced forms, can result in legal blindness, resulting in a loss of driving privileges and an inability to read all but very large type. Perhaps the most grievous loss is the inability to see faces clearly or at all. Some of these losses can be offset by the use of adaptive devices.  A closed-circuit television reader can make reading possible, and specialized screen-reading computer software, e.g., JAWS for Windows, can give the blind person access to word processing, spreadsheet, financial, and e-mail access.

# Diagnosis

## Other Diagnostic Studies
Fluorescein angiography allows for the identification and localization of abnormal vascular processes. Optical coherence tomography is now used by most ophthalmologists in the diagnosis and the followup evaluation of the response to treatment by using either Avastin or Lucentis which are injected into the vitreous of the eye at various intervals.
Magnetic resonance microscopy
Magnetic Resonance Microscopy (MRM, MRI) is Magnetic Resonance Imaging (MRI) at a microscopic level. A strict definition is MRI having voxel resolutions of better than 100m3 .

# Differences between MRI and MRM
- Resolution: Typical medical MRI resolution is about 1 mm3; the desired resolution of MRM is 100 m3 or smaller.
- Specimen size: Medical MRI mechines are designed to fit into a patient. MRM chambers are usually small, typically less than 1 cm3.

# Current status of MRM
Although MRI is very common for medical applications, MRM is still developed in laboratories. The major barriers for practical MRM include:
- Magnetic field gradient: High gradient focus the magnetic resonance in a smaller volume (smaller point spread function), results in a better spatial resolution. The gradients for MRM are typically 50 to 100 times those of clinical systems. However, the construction of radio frequency (RF) coil used in MRM does not allow ultrahigh gradient.
- Sensitivity: Because the voxels for MRM can be 100,000 times smaller than those in MRI, the signal will be 100,000 times weaker .

# Alternative MRM
Magnetic Resonance Force Microscopy (MRFM) is claimed to have nm3-scale resolutions. It improves the sensitivity issue by introducing microfabricated cantilever to measure tiny signals. The magnetic gradient is generated by a micrometre-scale magnetic tip, yielding a typical gradient 10 million times larger than those of clinical systems. This technique is still in the beginning stage. Because the specimen need to be in high vacuum at cryogenic temperatures, MRFM can be only used for solid state matters.
Mandibular advancement splint

# Background
A mandibular splint or mandibular advancement splint is a small plastic device worn in the mouth that may be used for correcting jaw and tooth problems, or for improving the quality of sleep by reducing some types of snoring or sleep apnea.
If the snoring is caused by the base of the tongue, the splint will advance the mandible (lower jaw) forward, helping keep the tongue clear of the pharynx (the back of the throat). This is an alternative treatment to a positive pressure mask, known as nCPAP (nasal continuous positive airway pressure).
Significant TMJ dysfunction (pain/clicking/limited opening/lateral deviation on protrusion) may preclude treatment with a mandibular advancement splint.
Mandibular advancement splints are widely used in the United States and are beginning to be used in Britain and Israel. Where appropriate, they are considered a good therapy choice as they are non-invasive, easily reversible, quiet and generally well accepted by the patient. The focus of improvement in appliance design is in reducing bulk, permitting free jaw movement (I.E. for yawning, speaking, drinking), permitting you to breathe through your mouth (early 'welded gum shield' type devices prevented oral breathing) and providing a robust and adjustable (in terms of advancement) device.
Some countries allow "DIY" devices to be sold to the public, whereas other countries (notably USA) prohibit them.  Countries which allow DIY devices include Australia, Britain and South Africa.
This type of oral appliance is sometimes known as a mandibular advancement device or mandibular repositioning device, mandibular advancers, or any of these names with "jaw" in place of the word "mandibular."

# Notes
-  Mandibular Advancement Splints for Snoring (Commercial website, citing only for common terminology). Retrieved on 2008-08-19.
Mandibular decubitus syndrome

# Overview
The Mandibular Decubitus Syndrome is a group of disorders of the masticatory apparatus 
such as the loss of balance of the jaw and the facial asymmetry due to the constant use, during sleep, of positions that can represent an obstacle to the natural movements of the jaw.
In these incorrect positions the jaw is displaced in a forced, unbalanced, lateral occlusion  with static load lying on the three components of the stomatognathic system: neuromuscular, osteoarticular and dentoperiodontal. For this reason the natural meccanism of the deglutition (performed normally every four minutes) become cause of teeth chafing which, obviously, damages all the dental structures. Evident consequences of the mandibular decubitus are malocclusions of teeth, nocturnal bruxism and periodontitis.
Mannan-binding lectin pathway
The Mannan-binding lectin pathway is homologous to the classical complement pathway. This pathway uses a protein similar to C1q of the classical complement pathway, which binds to mannose residues and other sugars in a pattern that allows binding on multiple pathogens. Mannan-binding lectin (MBL; also called mannose-binding lectin) is a protein belonging to the collectin family that is produced by the liver and can initiate the complement cascade by binding to pathogen surfaces.
MBL is a 2-6 headed molecule that forms a complex with MASP-I (Mannan-binding lectin Associated Serine Protease) and MASP-II, two protease zymogens. MASP-I and MASP-II are very similar to C1r and C1s molecules of the classical complement pathway and are thought to have a common evolutionary ancestor. When the carbohydrate-recognising heads of MBL bind to specifically arranged mannose residues on the phospholipid bilayer of a pathogen, MASP-I and MASP-II are activated to cleave complement components C4 and C2 into C4a, C4b, C2a, and C2b. C4b and C2b combine on the surface of the pathogen to form C3 convertase (C4b2b), while C4a and C2a act as chemoattractants.

# Clinical significance
It has been found that people deficient in MBL experience a substantial increase in infections during the early years of childhood.
Medial cutaneous nerve of arm

# Overview
The medial brachial cutaneous nerve (lesser internal cutaneous nerve; nerve of Wrisberg, medial cutaneous nerve of arm) is distributed to the skin on the medial brachial side of the arm.
It is the smallest branch of the brachial plexus, and arising from the medial cord receives its fibers from the eighth cervical and first thoracic nerves. It passes through the axilla, at first lying behind, and then medial to the axillary vein, and communicates with the intercostobrachial nerve.
It descends along the medial side of the brachial artery to the middle of the arm, where it pierces the deep fascia, and is distributed to the skin of the back of the lower third of the arm, extending as far as the elbow, where some filaments are lost in the skin in front of the medial epicondyle, and others over the olecranon.
It communicates with the ulnar branch of the medial antebrachial cutaneous nerve.
Medullary laminae of thalamus
Medullary laminae of thalamus are layers of myelinated fibres that appear on cross sections of the thalamus.  They also are commonly referred to as laminae medullares thalami or medullary layers of thalamus.  The specific layers are:
- Lamina medullaris lateralis (external medullary lamina) - separates ventral and lateral thalamus from the subthalamus and thalamic reticular nucleus
- Lamina medullaris medialis (internal medullary lamina) - positioned between the dorsomedial and ventral nuclei of thalamus, encloses the intralaminar nuclei (centromedian nucleus, paracentral, and central lateral)
Melasma (patient information)
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# Overview
Melasma is a dark skin discoloration that appears on sun-exposed areas of the face.

# What are the symptoms of Melasma?
Melasma doesn't cause any other symptoms besides skin discoloration but may be of great cosmetic concern.
A uniform brown color is usually seen over the cheeks, forehead, nose, or upper lip. It is most often symmetrical (matching on both sides of the face).

# What causes Melasma?
Melasma is a very common skin disorder.

# Who is at highest risk?
Though it can affect anyone, young women with brownish skin tones are at greatest risk.
Melasma is often associated with the female hormones estrogen and progesterone. It is especially common in pregnant women, women who are taking birth control pills (oral contraceptives) and women taking hormone replacement therapy (HRT) during menopause.
Sun exposure is also a strong risk factor for melasma. The condition is particularly common in tropical climates

# Diagnosis
Your health care provider can usually diagnose melasma based upon the appearance of your skin. A closer examination using a Wood's lamp may help guide your treatment.

# When to seek urgent medical care?
Call your health care provider if you have persistent darkening of your face.

# Treatment options
Treatments may include:
- Creams containing a combination of tretinoin, kojic acid, and azelaic acid have been shown to improve the appearance of melasma.
- Your doctor may recommend chemical peels or topical steroid creams.
- In severe cases, laser treatments can be used to remove the dark pigment.
Avoiding the sun and using sunscreen are key to preventing melasma.

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

# What to expect (Outlook/Prognosis)?
Melasma often fades over several months after stopping birth control pills or HRT, or after delivering a child. It may return with additional pregnancies or use of these medications.

# Prevention of Melasma
Daily sunscreen use not only helps prevent melasma but is crucial in the prevention of skin cancer and wrinkles.

# Sources
Melkersson-Rosenthal syndrome

# Overview
Melkersson-Rosenthal syndrome is a rare neurological disorder characterized by recurring facial paralysis, swelling of the face and lips (usually the upper lip), and the development of folds and furrows in the tongue. Onset is in childhood or early adolescence. After recurrent attacks (ranging from days to years in between), swelling may persist and increase, eventually becoming permanent. The lip may become hard, cracked, and fissured with a reddish-brown discoloration. The cause of Melkersson-Rosenthal syndrome is unknown, but there may be a genetic predisposition. It can be symptomatic of Crohn's disease or sarcoidosis.

# Treatment
Treatment is symptomatic and may include medication therapies with nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids to reduce swelling, as well as antibiotics and immunosuppressants. Surgery may be recommended to relieve pressure on the facial nerves and to reduce swollen tissue, but its effectiveness has not been established. Massage and electrical stimulation may also be prescribed.

# Prognosis
Melkersson-Rosenthal syndrome may recur intermittently after its first appearance. It can become a chronic disorder. Follow-up care should exclude the development of Crohn's disease or sarcoidosis.

# Eponym
It is named for Ernst Melkersson and Curt Rosenthal.

# Physical examination

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Microvillus inclusion disease
Microvillus inclusion disease, also known as Davidson's disease, congenital microvillus atrophy and, less specifically, microvillus atrophy (note: microvillus is often misspelled as microvillous), is a rare genetic disorder of the small intestine that is inherited in an autosomal recessive pattern.

# Presentation
It is characterized by chronic, intractable diarrhea in new-born infants, starting in the first few days of life.
This results in metabolic acidosis and severe dehydration. Pregnancy and birth are usually normal.

# Prognosis
It is nearly always fatal unless, like short bowel syndrome patients, treated with parenteral nutrition or an intestinal transplant. The patient is often classified as being in "intestinal failure" and treated with the cohort of patients known as "short bowel syndrome" patients.

# Pathophysiology
It is caused by a congenital lack of apical microvilli in the epithelial cells of the small intestine.

# Diagnosis
Prenatal  screening in utero is currently offered by several medical centers since the gene(s) involved in the disease were  recently discovered to be MYO5B; Diagnosis is typically made by biopsy of the small intestine.

## Biopsy
The appearance of microvillous inclusion disease on light microscopy is similar to celiac sprue; however, it usually lacks the intraepithelial lymphocytic infiltration characteristic of celiac sprue and stains positive for carcinoembryonic antigen (CEA).  
The definitive diagnosis is dependent on electron microscopy.

## Differential diagnosis
The differential diagnosis of chronic and intractable diarrhea is:
- Intestinal epithelial dysplasia
- Syndromatic diarrhea
- Immunoinflammatory enteropathy

# Genetic prevalence
File:Autorecessive.svg
Microvillus inclusion disease is thought to be extremely rare; only approximately 200 cases have been identified in children in Europe.
One patient, a teenage female living in Arizona, suddenly began to grow microvilli after thirteen years of TPN (Total Parenteral Nutrition) and Lipid dependency. She now enjoys a typical teenage diet and is seen regularly by her Gastroenterologist.
One patient from the UK was documented to achieve nutritional independence at age 3.
On 26 June 2009 a six-year-old girl diagnosed with microvillus inclusion disease became the third person in the UK to die of swine flu.

# History
Microvillus inclusion disease was first described in 1978 by Davidson et al.  It was originally described as familial enteropathy.
Miliary tuberculosis overview
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# Overview
Miliary tuberculosis is a form of tuberculosis that is characterized by a wide dissemination into the human body and by the tiny size of the lesions (1-5 mm). Its name comes from a distinctive pattern seen on a chest X-ray of many tiny spots distributed throughout the lung fields with the appearance similar to millet seeds, thus the term "miliary" tuberculosis.  Miliary TB may infect any number of organs including the lungs, liver, and spleen.  It is a complication of 1-3% of all TB cases.

# Pathophysiology
Tuberculosis (TB) infection can develop after inhaling droplets sprayed into the air from a cough or sneeze by someone infected with the Mycobacterium tuberculosis bacteria. Small areas of infection, called granulomas (granular tumors), develop in the lungs.

# Causes
Disseminated TB develops in the small number of infected people whose immune systems do not successfully contain the primary infection. It can occur within weeks of the primary infection. Sometimes, it does not occur until years after you become infected. Chances of having miliary tuberculosis is high if the immune system is weakened due to disease (such as AIDS) or certain medications. Infants and the elderly are also at higher risk.

# Diagnosis

## Symptoms
A patient with miliary tuberculosis will tend to present with non-specific signs such as low grade fever, cough, and generalized lymphadenopathy. Miliary tuberculosis can also present with hepatomegaly (40% of cases), splenomegaly (15%), pancreatitis (<5%), and multiorgan dysfunction with adrenal insufficiency.

# Treatment

## Secondary Prevention
TB is a preventable disease, even in those who have been exposed to an infected person. Skin testing for TB is used in high risk populations or in people who may have been exposed to TB, such as health care workers.
Monocarboxylate transporter 1
Monocarboxylate transporter 1 is a protein that in humans is encoded by the SLC16A1 gene (also known as MCT1). It is a proton coupled monocarboxylate transporter.

# Biochemistry
Detailed kinetic analysis of monocarboxylate transport in erythrocytes revealed that MCT1 operates through an ordered mechanism. MCT1 has a substrate binding site open to the extracellular matrix which binds a proton first followed by the lactate anion. The protein then undergoes a conformational change to a new closed conformation that exposes both the proton and lactate to the opposite surface of the membrane where they are released, lactate first and then the proton. For net transport of lactic acid, the rate-limiting step is the return of MCT1 without bound substrate to the open conformation. For this reason, exchange of one monocarboxylate inside the cell with another outside is considerably faster than net transport of a monocarboxylate across the membrane.

# Animal studies
Overexpression of MCT1 has been shown to increase the efficacy of an anti-cancer drug currently undergoing clinical trials called 3-bromopyruvate in breast cancer cells.

# Clinical significance
Most cases of alveolar soft part sarcoma show PAS(+), diastase-resistant (PAS-D (+)) intracytoplasmic crystals which contain CD147 and monocarboxylate transporter 1 (MCT1). Overexpression of MCT1 in pancreatic beta cells leads to hyperinsulinism during exercise.
Monocarboxylate transporter 2
Monocarboxylate transporter 2 (MCT2) also known as solute carrier family 16 member 7 (SLC16A7) is a protein that in humans is encoded by the SLC16A7 gene. MCT2 is a proton-coupled monocarboxylate transporter. It catalyzes the rapid transport across the plasma membrane of many monocarboxylates such as lactate, pyruvate, branched-chain oxo acids derived from leucine, valine and isoleucine, and the ketone bodies acetoacetate, beta-hydroxybutyrate and acetate. It also functions as high-affinity pyruvate transporter.
Both Northern blot analysis and inspection of the human expressed sequence tag (EST) database suggest relatively little expression of MCT2 in human tissues. As well, the sequence of MCT2 is far less conserved across species than that of MCT1 or MCT4 and there also appear to be considerable species differences in the tissue expression profile of this isoform.
Of the four known mammalian lactate transporters (MCTs 1-4), MCT2 harbors the highest affinity for lactate.  In parallel, MCT2 gene transcription has been demonstrated to respond with high-sensitivity to hypoxia, intracellular pH, and, to lactate.