Persius/hicric huggingface dataset:
Microtrauma
Microtrauma is the general term given to small injuries to the body.
Microtrauma can include the microtearing of muscle fibres, the sheath around the muscle and the connective tissue. It can also include stress to the tendons, and to the bones (see Wolf's Law). It is unknown whether or not the ligaments adapt like this. Increased lubrication in response to microtrauma to the bowels is a key factor to the beneficial effects of dietary fibre in increasing bowel robustness, though this is dissimilar to muscular hypertrophy. Some believe microtrauma to the skin (compression, impact, abrasion) can also cause increases in a skin's thickness, as seen in running barefoot. If it does occur, it might be increased skin cell replication at sites under stress where cells rapidly slough off or undergo compression or abrasion.
Most microtrauma cause a low level of inflammation that cannot be seen or felt. These injuries can arise in muscle, ligament, vertebrae, and discs, either singly or in combination. Repetitive microtrauma which are not allowed time to heal can result in the development of more serious conditions.
Back pain can develop gradually as a result of microtrauma brought about by repetitive activity over time. Because of the slow and progressive onset of this internal injury, the condition is often ignored until the symptoms become acute, often resulting in disabling injury. Acute back injuries can arise from stressful lifting techniques done without adequate recovery, especially when experimenting with more ballistic work, or work where the extensor spinae are stressed during spinal flexion when much of the load is commonly taken up by the slower to heal ligaments which may not adapt progressively to the stress. While the acute injury may seem to be caused by a single well-defined incident, it may have been preventable or lessened if not for the years of injury to the musculoskeletal support mechanism by repetitive microtrauma.
One possible example of beneficial microtrauma is in the form of microtears to the muscle fibres as a result of intensive exercise. This is done deliberately in weight training in order to stimulate the building of stronger muscles, ligaments, and tendons during the repair process. However, it is not known if this practice is as beneficial as originally thought. Sufficient time must be allowed for healing, to avoid overtraining.
Mithramycin
Mithramycin is an anti-neoplastic antibiotic. Its major use is as an IV infusion to reduce very high levels of plasma calcium. It inhibits RNA synthesis in osteoclasts. Typically use a dose of 
25 microgram per kilogram IV given over four to six hours. This dose can be repeated in 1 to 2 days if necessary. Ca++ levels start falling after 12 hours, with maximal reduction at 48-72 hours.
Hypercalcaemia recurs in days to several weeks. With repeated use, organotoxicity (kidney, liver, haematopoetic system) can become a problem.
Mixing test
The mixing test is a medical laboratory study used to clarify the differential diagnosis of blood clotting abnormalities. Other names for the test include mixing studies, PT mixing study, PTT mixing study, circulating anticoagulant screening test, PT, 50/50, or inhibitor screen.
The test is most often initiated when a patient has an abnormally long prothrombin time (PT)  or more usually, a prolonged partial thromboplastin time (PTT), to distinguish whether the underlying problem is a clotting factor deficiency on the one hand, or a factor inhibitor on the other hand.
The test relies on the fact that the circulating level of any coagulation factor must be reduced to a level significantly less than 50% in order to affect the PT or PTT. Thus when the patient's blood is mixed with an equal volume of blood donated by a person known to have normal clotting, the mixture (which will have at least 50% factor activity for all factors) will clot more quickly if the initial disorder was because of a deficiency, while it will not clot any faster if the initial disorder was because of a factor inhibitor.
If the PTT of the mixed blood is normal, factor deficiency is indicated, and further testing will be performed for specific factors. If the PTT of the mixed blood is still prolonged, an inhibitor is suggested, and further studies (typically starting with an assay for lupus anticoagulant) will be performed. This result, however, can also be seen if the patient is taking heparin or another anticoagulant. If the PTT of the mixed blood initially normalized, but becomes prolonged again after a two hour incubation,  the test is suggestive of a factor VIII inhibitor (because their effect requires this amount of time to become effective). When a mixing test shows this result, a factor VIII inhibitor assay will be performed.
Mohr's salt
Mohr's Salt, or ammonium iron sulfate, is a double salt of iron sulfate and ammonium sulfate, with the formula 226H2O.
Mohr's salt is preferred over iron(II) sulfate for titration purposes as it is much less affected by oxygen in the air than iron(II) sulfate, solutions of which tend to oxidise to iron(III). The oxidation of solutions of iron(II) is very pH dependent, occurring much more readily at high pH. The ammonium ions make solutions of Mohr's salt slightly acidic, which prevents this oxidation from occurring. The relevant equation for this is:
The presence of protons keeps this equilibrium to the left, the Fe(II) side.
Mohr's salt is named after the German chemist Karl Friedrich Mohr, who made many important advances in the methodology of titration in the 19th century.
ar:   
de:Ammoniumeisen(II)-sulfat
nl:Mohr's zout
Monilethrix

# Overview
Monilethrix is an autosomal dominant hair disease that results in short, fragile, broken hair that appears beaded.  It comes from the Latin word for necklace (monile) and the Greek word for hair (thrix).

# Presentation
The presentation may be of alopecia.  Individuals vary in severity of symptoms.  Nail deformities may also be present as well as hair follicle keratosis and follicular hyperkeratosis.

# Causes
The genes KRTHB1 (KRT81), KRTHB3 (KRT83), or KRTHB6 (KRT86) that are mutated in this condition code for type II hair cortex keratins.

# Physical examination

## Gallery

### Head
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Monotropism
Monotropism and polytropism are according to Murray, Lesser and Lawson different strategies in distributing attention in the human brain. Monotropism refers to an attention-tunnel (undivided attention or attention-tunnel), while polytropism refers to multiple divided attention in the brain.
The Monotropism hypothesis was developed by Murray, Lesser and Lawson, a Doctor of Philosophy, a mathematician and a social worker, and regards attention-tunnels as the central feature of autism.
Autists don't have the ability to "multi-task".
In this model of mind, mental events compete for and consume attention. In a polytropic mind, many interests have a moderate amount of  attention put into them, while in a monotropic mind, the person's attention is put into a few more specialized interests. The theory argues that when many interests are aroused, multiple complex behaviors emerge, but if only a few interests are aroused, fewerbut more intensebehaviors emerge.

# Notes
-  Murray D, Lesser M, Lawson W (2005). "Attention, monotropism and the diagnostic criteria for autism" (PDF). Autism. 9 (2): 13956. doi:10.1177/1362361305051398. PMID 15857859. Retrieved 2007-07-24.CS1 maint: Multiple names: authors list (link) .mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
Moon facies
Synonyms and keywords: moon face, Cushingoid appearance

# Overview
Moon facies refers to a round, full, puffy face due to extra fluid or fat around the sides of the face.

# Pathophysiology
Fluid and fat deposits along the sides of the face make it look rounder.  The fat deposition may be due to obesity or excess cortisol released by the adrenal glands (hyperadrenocorticalism or hypercortisolism).

# Causes
- ACTH releasing pituitary tumor or tumor in the thymus, lung or pancreas
- Adrenal gland tumors that release cortisol
- Allergies
- Cushing's syndrome
- Obesity
- Steroids such asprednisone. It is more common with oral than with injected or inhaled steroids

# Diagnosis

## Head
The face is round, full and puffy and the ears may not be visible when looking at the front of the face.
Moro reflex

# Overview
The Moro reflex, also known as the startle reflex, is one of the infantile reflexes.
It may be observed in incomplete form in premature birth after the 28th week of gestation, and is usually present in complete form by week 34 (third trimester).  It is normally present in all infants/newborns up to 4 or 5 months of age, and its absence indicates a profound disorder of the motor system. An absent or inadequate Moro response on one side is found in infants with hemiplegia, brachial plexus palsy, or a fractured clavicle. Persistence of the Moro response beyond 4 or 5 months of age is noted only in infants with severe neurological defects.  It was discovered and first described by Austrian pediatrician Ernst Moro (1874-1951).
This reflex is a response to unexpected loud noise or when the infant feels like it is falling. It is believed to be the only unlearned fear in human newborns. The little Albert study used the startle reflex in the famous classical conditioning experiment to make him fear white fuzzy things.
The primary significance of this reflex is in evaluating integration of the central nervous system (CNS), since the reflex involves 4 distinct components:
- Startle
- spreading out the arms (abduction)
- unspreading the arms (adduction)
- Crying (usually)
Absence of any component (except crying) or any asymmetry in the movements is abnormal, as is persistence of the reflex in older infants, children and adults. However, in individuals with cerebral palsy, persistence and exacerbation of this reflex is common.
In adults, the startle reflex is modulating by expressions of observers.
Motavizumab

# Overview
Motavizumab (proposed INN, trade name Numax) is a humanized monoclonal antibody. It is being investigated by MedImmune (today a subsidiary of AstraZeneca) for the prevention of respiratory syncytial virus infection in high-risk infants. As of  September 2009, it is undergoing Phase II and III clinical trials.
In June 2010, the FDA Antiviral Drugs Advisory Committee declined to endorse MedImmune's request for licensure of Motavizumab in a 14 to 3 decision. The members of that panel cited several reasons for the decision, and many were concerned that "we're not looking at a product that has evidence of superiority in terms of efficacy" when compared to the already available monoclonal antibody Palivizumab.
In December 2010, AstraZeneca in a stock market statement stated that it would be writing down $445m (286m) after discontinuing a key development programme for Motavizumab. The company stated that it would no longer develop Motavizumab for the prevention of respiratory syncytial virus (RSV), and as a result was withdrawing its licence application to the US Food and Drug Administration. It added that it would continue to develop Motavizumab for other treatments of RSV.
Motor skill
A motor skill is a skill that requires an organism to utilize their skeletal muscles effectively in a goal directed manner. Motor skills and motor control depend upon the proper functioning of the brain, skeleton, joints, and nervous system. Most motor skills are learned throughout the lifespan and can be affected by disabilities. Motor development is the development of action and coordination of one's limbs, as well as the development of strength, posture control, balance, and perceptual skills.
Motor skills are divided into two parts:
- Gross motor skills include lifting one's head, rolling over, sitting up, balancing, crawling, and walking. Gross motor development usually follows a pattern. Generally large muscles develop before smaller ones. Thus, gross motor development is the foundation for developing skills in other areas (such as fine motor skills). Development also generally moves from top to bottom. The first thing a baby usually learns is to control is it eyes.
- Fine motor skills include the ability to manipulate small objects, transfer objects from hand to hand, and various hand-eye coordination tasks.  Fine motor skills may involve the use of very precise motor movement in order to achieve an especially delicate task. Some examples of fine motor skills are using the pincer grasp (thumb and forefinger) to pick up small objects, cutting, coloring and writing, and threading beads. Fine motor development refers to the development of skills involving the smaller muscle groups.
Fine Motor Disabilities negatively impact a child's performance in school but have no bearing on their intellectual ability. It strictly speaks to an individuals struggle to control the small muscles in their hand as they write. Since communication in the form of writing is important and still heavily relied upon in our society and schools, kids with this disability face a variety of obstacles. Simply writing their name is not only time consuming, it may also end up illegible. To make their work legible, these individuals must exert a great deal of focus and energy which leaves very little left over for concentrating on what they are writing about.

# Disabilities affecting motor skills
- ADC
- Alzheimer's disease
- Catatonia
- Cerebral palsy
- Developmental Dyspraxia
- Hypotonia
- Multiple sclerosis
- Parkinson's Disease
- Syphilis
Muscle tone

# Overview
Muscle tone (aka residual muscle tension or tonus) is the continuous and passive partial contraction of the muscles. It helps maintain posture, and it declines during REM sleep. Note that muscular tone is not defined as muscular shaping or the aspect of general Human physical appearance.

# Purpose
Unconscious nerve impulses maintain the muscles in a partially contracted state. If a sudden pull or stretch occurs, the body responds by automatically increasing the muscle's tension, a reflex which helps guard against danger as well as helping to maintain balance.
The presence of near-continuous innervation makes it clear that tonus describes a "default" or "steady state" condition. There is, for the most part, no actual "rest state" insofar as activation is concerned.
In terms of skeletal muscle, both the extensor muscle and flexor muscle use the term tonus to refer to the "at rest" or normal enervation that maintains current positions of bones.
Cardiac muscle and smooth muscle, although not directly connected to the skeleton, also have tonus in the sense that although their contractions are not matched with those of antagonist muscles; their non-contractive state is characterized by (sometimes random) enervation.

# Pathological tonus
Physical disorders can result in abnormally low (hypotonia) or high (hypertonia) muscle tone. Another form of hypertonia is Paratonia, which is associated with dementia.

# Tonus in surgery
In ophthalmology, tonus may be a central consideration in eye surgery, as in the manipulation of extraocular muscles to repair strabismus. Tonicity aberrations are associated with many diseases of the eye (e.g. Adie syndrome).
Mycolactone
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Mycolactone is a polyketide-derived macrolide produced and secreted by the pathogenic mycobacteria M. ulcerans, M. liflandii, M. pseudoshottsii, and a few M. marinum isolates.
The M. ulcerans toxins comprise a family of polyketide-derived macrolides, mycolactones, which are formed through condensation of two polyketide chains. Each isolate of M. ulcerans produces a characteristic mixture of mycolactone congeners. M. ulcerans strains from different geographic areas produce distinct patterns of mycolactone congeners. The structural heterogeneity in mycolactones is due to variations in the fatty acid side chain. The structure of the core lactone is invariant.
Genes for mycolactone biosynthesis form a contiguous 110-kb cluster (Fig. 1A) on a large plasmid. The lactone core is encoded by two polyketide synthase (Pks) genes, mlsA1 and mlsA2, and a third polyketide synthase gene, mlsB, encodes the fatty acid side chain. Three accessory genes are found in the mycolactone cluster. One of these, MUP053, encodes a p450 monooxygenase that is thought to produce the hydroxyl at C-12 on the fatty acid side chain. The gene encoding a FabH-like, type III ketosynthase (KS), located upstream of mlsA1, encodes a putative joinase (MUP045), and a small type II thioesterase (TE II) gene (MUP037) is located between mlsA2 and mlsB.
Five categories have been described so far:
- Mycolactone A/B (M. ulcerans from Africa, Malaysia, ...)
- Mycolactone C (8 Australian M. ulcerans isolates)
- Mycolactone D (M. ulcerans from Asia)
- Mycolactone E (M. liflandii)
- Mycolactone F (M. pseudoshottsii and M. marinum from Israel)
Nitrosamine

# Overview
Nitrosamines are chemical compounds of the chemical structure R1N(-R2)-N=O, some of which are carcinogenic.

# Occurrence in food
Nitrosamines are produced from nitrites and secondary amines, which often occur in the form of proteins. Their formation can occur only under certain conditions, including strongly acidic conditions such as that of the human stomach. High temperatures, as in frying, can also enhance the formation of nitrosamines.
The nitrite forms nitrous acid (HNO2), which splits into the nitrosonium cation, N=O+, and the hydroxide anion, OH. The nitrosonium cation then reacts with an amine to produce nitrosamine.
Nitrosamines are found in many foodstuffs especially beer, fish, fish byproducts, and in meat and cheese products preserved with nitrite pickling salt. The US government established limits on the amount of nitrites used in meat products to decrease cancer risk in the population. There are also rules about adding ascorbic acid or related compounds to meat, because they inhibit nitrosamine formation.

# Occurrence in other consumer products
Nitrosamines can be found in tobacco smoke and latex products. A test of party balloons and condoms indicated that many of them release small amounts of nitrosamines. However, nitrosamines from condoms are not expected to be of toxicological significance.

# Cancer
Nitrosamines can cause cancers in a wide variety of animal species, a feature which suggests that they may also be carcinogenic in humans. Epidemiological data suggests that nitrosamines in preserved food cause stomach cancer.

# Uses
- Rubber products
- Pesticides
- Certain cosmetics

# Examples of nitrosamines

## Tobacco-specific nitrosamines
- N-Nitrosonornicotine (NNN)
- NNK
- NNAL
- NAT
- NAB
- iso-NNAL
- iso-NNAC

## Other nitrosamines
- NDEA
- NDMA
NACA (gene)
Nascent-polypeptide-associated complex alpha polypeptide, also known as NACA, is a protein which in humans is encoded by the NACA gene.

# Function
NACA prevents short recently synthesized (i.e., nascent) ribosome-associated polypeptides from inappropriate interactions with cytosolic proteins. NACA binds nascent-polypeptide domains emerging from ribosomes unless it contains a signal peptide which is fully exposed. Depletion of NACA from ribosomes carrying nascent polypeptides allows the signal recognition particle (SRP) to crosslink to polypeptides regardless of whether or not they contain signal peptides or not. In the absence of NACA, proteins lacking signal peptides can be mis-translocated into the endoplasmic reticulum.
The NACA protein is expressed in bone during development and acts as a transcriptional coactivator in conjunction with acidic activators.

# Interactions
NACA has been shown to interact with BTF3, FADD, C-jun, and 3 members of taxilin family.
NAD+ kinase
NAD+ kinase (EC 2.7.1.23, NADK) is an enzyme that converts nicotinamide adenine dinucleotide (NAD+) into NADP+ through phosphorylating the NAD+ coenzyme. NADP+ is an essential coenzyme that is reduced to NADPH primarily by the pentose phosphate pathway to provide reducing power in biosynthetic processes such as fatty acid biosynthesis and nucleotide synthesis. The structure of the NADK from the archaean Archaeoglobus fulgidus has been determined.
In humans, the genes NADK and MNADK encode NAD+ kinases localized in cytosol and mitochondria, respectively. Similarly, yeast have both cytosolic and mitochondrial isoforms, and the yeast mitochondrial isoform accepts both NAD+ and NADH as substrates for phosphorylation.

# Reaction
ATP + NAD+ \rightleftharpoons ADP + NADP+

# Mechanism
NADK phosphorylates NAD+ at the 2 position of the ribose ring that carries the adenine moiety. It is highly selective for its substrates, NAD and ATP, and does not tolerate modifications either to the phosphoryl acceptor, NAD, or the pyridine moiety of the phosphoryl donor, ATP. NADK also uses metal ions to coordinate the ATP in the active site. In vitro studies with various divalent metal ions have shown that zinc and manganese are preferred over magnesium, while copper and nickel are not accepted by the enzyme at all. A proposed mechanism involves the 2' alcohol oxygen acting as a nucleophile to attack the gamma-phosphoryl of ATP, releasing ADP.

# Regulation
NADK is highly regulated by the redox state of the cell. Whereas NAD is predominantly found in its oxidized state NAD+, the phosphorylated NADP is largely present in its reduced form, as NADPH. Thus, NADK can modulate responses to oxidative stress by controlling NADP synthesis. Bacterial NADK is shown to be inhibited allosterically by both NADPH and NADH. NADK is also reportedly stimulated by calcium/calmodulin binding in certain cell types, such as neutrophils. NAD kinases in plants and sea urchin eggs have also been found to bind calmodulin.

# Clinical significance
Due to the essential role of NADPH in lipid and DNA biosynthesis and the hyperproliferative nature of most cancers, NADK is an attractive target for cancer therapy. Furthermore, NADPH is required for the antioxidant activities of thioredoxin reductase and glutaredoxin. Thionicotinamide and other nicotinamide analogs are potential inhibitors of NADK, and studies show that treatment of colon cancer cells with thionicotinamide suppresses the cytosolic NADPH pool to increase oxidative stress and synergizes with chemotherapy.
While the role of NADK in increasing the NADPH pool appears to offer protection against apoptosis, there are also cases where NADK activity appears to potentiate cell death. Genetic studies done in human haploid cell lines indicate that knocking out NADK may protect from certain non-apoptotic stimuli.