Persius/hicric huggingface dataset:
Rebound headache
Synonyms and keywords: Medication overuse headaches

# Overview
Rebound headaches occur when pain medications (analgesics) are taken too frequently to relieve a headache.

# Causes
Rebound headaches can be caused by any painkiller or migraine abortive medication such as triptans as well as NSAIDs, antihistamines, and decongestants. Over-the-counter agents such as Excedrin, Tylenol and Advil can cause a rebound headache.  Prescription medications such as Fioricet, Fiorinal, Imitrex and Vicodin can cause a rebound headache.

## Most common causes
The medications most likely to cause rebound appear to be the combination analgesics such as Fioricet, Fiorinal, and Excedrin, as well as narcotic medications.  Rebound headaches frequently occur daily and can be very painful.  They are a common cause of chronic daily headache.  They typically occur in patients with an underlying headache disorder such as migraine, that "transforms" over time from an episodic condition to chronic daily headache due to more and more frequent analgesic use.  Rebound headache was first described by Dr. Lee Kudrow.

# Treatment
Rebound headache is common and can be treated. The overused medications must be stopped in order for the patient's headaches to resolve. This is usually done under the care of a neurologist. Often patients are started on preventive medications to ease their transition off the medications that induced the medication overuse / rebound cycle. It is important that the patient's physician be consulted before abruptly discontinuing medications as abruptly discontinuing some medications has the potential for creating another issue. Abrubtly discontinuing butalbital, for example, can actually induce seizures in some patients.

# Prevention
In general, any patient who has frequent headaches or migraine attacks should be considered as a potential candidate for preventive medications instead of being encouraged to take more and more painkillers or other rebound-causing medications.  Preventive medications are taken on a daily basis.  Some patients may require preventive medications for many years; others may require them for only a relatively short period of time such as six months.  Effective preventive medications have been found to come from many classes of medications including neuronal stabilizing agents (aka anticonvulsants), antidepressants, antihypertensives, and antihistamines. Some effective preventive medications include Elavil (amitriptyline), Depakote (valproate), Topamax (topiramate), and Inderal (propranolol).

# Related Chapters
- Rebound effect
- Headache
- Migraine
- Tension headache
- Cluster headache
Melvyn Rubenfire
Melvyn Rubenfire is a renowned cardiologist in the University of Michigan Health System, as well as a professor in the department of internal medicine. He is also director of the Preventive Cardiology department.

# Clinical interests
Rubenfire's clinical and research interests include: Atherosclerosis detection, preventive cardiology, lipid management, pulmonary hypertension, coronary risk factors, and vascular reactivity.

# Degrees and Professional Organizational Fellowships
Rubenfire earned a Doctor of Medicine degree from Wayne State University in Detroit, Michigan in 1965.

# Residency and Certifications
Rubenfire served his residency at Sinai Hospital in Detroit, Michigan, from 1965-1968, and received a fellowship in Cardiovascular disease at the Henry Ford Hospital in Detroit,Michigan in 1970. His certifications include: Internal Medicine in 1965, Cardiovascular Disease in 1973, and Medical Examiner in 1965. He also received a qualification in Lipid Management in 2005.  Rubenfire obtained the following fellowships: Fellow of the American College of Physicians (Internal Medicine), Fellow of the American College of Cardiology, and Fellow of the American College of Chest Physicians.

# Places of work
Rubenfire works at the outpatient facility at Domino's Farms Office Park in Ann Arbor, Michigan, and the Alfred Taubman Health Care Center.  At Domino's Farms, he practices Preventive Cardiology, Cardiac Rehabilitation, and the Cardiovascular Executive Health Program. He practices Pulmonary Hypertension at the Alfred Taubman Health Care Center.

# Footnotes

# External link
Med.umich.edu/healthcenters profile
Meridian Shiatsu
Meridian Shiatsu is a derivative form of the Japanese therapy Shiatsu. It uses the Meridian theory of Traditional Chinese Medicine that was introduced into Japan from China. Meridian Shiatsu contrasts with Tsubo Shiatsu where the tsubos or acupuncture points are determined from an anatomical and physiological perspective. However, the clinical results of Tsubo Shiatsu and Meridian Shiatsu are comparable because the location of meridian points and Tsubos are identical or very close.  Only the underlying theories differ.
In 1964, a book called "Anpuku and Shiatsu Therapy", edited by the Vice-Principal of the Japan Shiatsu College, Tadashi Izawa, introduced Meridian Shiatsu, comparing Anma, which uses meridian theory, with Shiatsu therapy for the first time.  Other styles of Shiatsu incorporating meridian theory were developed by Iwajiro Sato, the author of "Shiatsu Therapy and Syoatsu Therapy" and Shizuto Masunaga, the founder of Zen Shiatsu.  All proponents of Shiatsu using Meridian theory follow Tadashi Izawas original tenets.
Meridian Shiatsu practitioners use their entire bodies in a graceful art form to catalyze change in the patient. "Diagnosis and Therapy Combined" is a common mantra of this practice.
Setsu Shin in Japanese means "touching diagnosis" and also "cutting diagnosis" (cutting as with a knife). Meridian Shiatsu practitioners cut through the outer layers to touch the living essence within. Simply by laying hands on a recipient, meridian shiatsu practitioners seek to effect profound transformation. Touching the innermost being of a receiver equates to treatment. As the inner experience of an individual is acknowledged by their kinsmen, the internal paradoxes are reconciled and healing is possible.
Merlin (protein)
Merlin (also called Neurofibromin 2 or schwannomin) is a cytoskeletal protein. In humans, it is a tumor suppressor protein involved in Neurofibromatosis type II. Sequence data reveal its similarity to the ERM protein family.
The name "merlin" is an acronym for "Moesin-Ezrin-Radixin-Like Protein".

# Gene
Human merlin is coded by the gene NF2 in Chromosome 22. Mouse merlin gene is located on chromosome 11 and rat merlin gene on chromosome 17. Fruit fly merlin gene (symbol Mer) is located on chromosome 1 and shares 58% similarity to its human homologue.
Other merlin-like genes are known from a wide range of animals, and the derivation of merlin is thought to be in early metazoa. Merlin is a member of the ERM family of proteins including ezrin, moesin, and radixin, which are in the protein 4.1 superfamily of proteins.  Merlin is also known as schwannomin, a name derived from the most common type of tumor in the NF2 patient phenotype, the schwannoma.

# Structure
Vertebrate merlin is a 70-kDa protein. There are 10 known isoforms of human merlin molecule (the full molecule being 595 amino acids in length). The two most common of these are also found in the mouse and are called type 1 and type 2, differing by the absence or presence of exon 16 or 17, respectively). All the known varieties have a conserved N-terminal part, which contains a FERM domain (a domain found in most cytoskeletal-membrane organizing proteins). The FERM domain is followed by an alpha-helical domain and a hydrophilic tail. Merlin can dimerize with itself and heterodimerize with other ERM family proteins.

# Function
Merlin is a membrane-cytoskeleton scaffolding protein, i.e. linking actin filaments to cell membrane or membrane glycoproteins. Human merlin is predominantly found in nervous tissue, but also in several other fetal tissues, and is mainly located in adherens junctions. Its tumor suppressor properties are  probably associated with contact-mediated growth inhibition. Drosophila merlin is expressed in embryonic hindgut, salivary glands, and imaginal discs, and has apparently a slightly different role than in vertebrates.
The phosphorylation of serine 518 is known to alter the functional state of merlin. The signaling pathway of merlin is proposed to include several salient cell growth controlling molecules, including eIF3c, CD44, protein kinase A, and p21 activated kinases.
Work in Drosophila identified Merlin as an upstream regulator of the Hippo tumor suppressor pathway, a function that is conserved in mammals. The Hippo pathway is a well conserved signalling pathway that coordinately regulates cell proliferation and apoptosis.
Mutations of the NF2 gene cause a human autosomal dominant disease called neurofibromatosis type 2. It is characterized by the development of tumors of the nervous system, most commonly of bilateral vestibular schwannomas (also called acoustic neuromas). NF2 belongs to the tumor suppressor group of genes.

# Interactions
Merlin (protein) has been shown to interact with:
- CUL4A,
- DDB1,
- EZR,
- HGS,
- MED28,
- RIT1,
- SDCBP,
- SPTBN1,  and
- VPRBP.
Mesomeric effect
The mesomeric effect or resonance effect in chemistry is a property of substituents or functional groups in a chemical compound. The effect is used in a qualitative way and describes the electron withdrawing or releasing properties of substituents based on relevant resonance structures and is symbolized by the letter M. The mesomeric effect is negative (-M) when the substituent is an electron-withdrawing group and the effect is positive (+M) when based on resonance the substituent is an electron releasing group.
- Examples of -M substituents: acetyl (IUPAC ethanoyl) - nitrile - nitro
- Examples of +M substituents: alcohol - amine
The net electron flow from or to the substituent is determined also by the inductive effect. It's important to note that the mesomeric effect as a result of p - orbital overlap (resonance) has absolutely no effect on this inductive effect, as the inductive effect is purely to do with the electronegativity of the atoms and their structural chemistry (which atoms are connected to which).
The concepts of mesomeric effect, mesomerism and mesomer were introduced by Ingold in 1938 as an alternative to the Pauling's synonymous concept of resonance . Mesomerism is in this context is often encountered in German and French literature but in English literature the term resonance dominates.
Methylecgonidine
Methylecgonidine (anhydromethylecgonine; anhydroecgonine methyl ester) is a chemical intermediate derived from ecgonine or cocaine.
Methylecgonidine is a pyrolysis product formed when crack cocaine is smoked, making this substance a useful biomarker to specifically test for use of crack cocaine, as opposed to powder cocaine which does not form methylecgonidine as a metabolite. Methylecgonidine has a relatively short half-life of 18-21 minutes, after which it is metabolised to ecgonidine, meaning that the relative concentrations of the two compounds can be used to estimate how recently crack cocaine has been smoked. Methylecgonidine has been shown to be specifically more harmful to the body than other byproducts of cocaine; for example to the heart,  lungs  &  liver. 
It is also used in scientific research for the manufacture of phenyltropane analogues such as Troparil, Lometopane and CFT. Methylecgonidine could also theoretically be used to produce cocaine and so may be a controlled substance in some countries.
When methylecgonidine is made synthetically for research purposes, it is usually produced by reacting cocaine or ecgonine with hydrochloric acid, yielding ecgonidine (anhydroecgonine), followed by methylation to yield methylecgonidine. Alternatively it can be made in a two step reaction by reacting 2,4,6-cycloheptatriene-7-carboxylic acid with first a mixture of methylamine and sodium hydroxide, followed by reaction with a mixture of methanol and sulfuric acid.
Methylnaltrexone

# Overview
Methylnaltrexone (MTNX) is one of the newer agents of peripherally-acting -opioid antagonists that act to reverse some of the side effects of opioid drugs such as constipation without affecting analgesia or precipitating withdrawals. Because it contains a permanently charged tetravalent nitrogen atom, it cannot cross the blood-brain barrier, and so has antagonist effects throughout the body, counteracting effects such as itching and constipation, but without affecting opioid effects in the brain such as analgesia.

# Development
In December of 2005, Wyeth and Progenics entered into an exclusive, worldwide agreement for the joint development and commercialization of methylnaltrexone for the treatment of opioid-induced side effects, including constipation and post-operative ileus (POI), a prolonged dysfunction of the gastrointestinal (GI) tract following surgery. Under the terms of the agreement, the companies are collaborating on worldwide development. Wyeth received worldwide rights to commercialize methylnaltrexone, and Progenics retained an option to co-promote the product in the United States. Wyeth will pay Progenics royalties on worldwide sales and co-promotion fees within the United States.
Methylnaltrexone is being developed in subcutaneous and oral forms to treat opioid induced constipation (OIC) and an intravenous form for POI.
Progenics and Wyeth are conducting two global phase 3 clinical trials in POI, targeting an NDA submission in this indication in early 2008. An oral formulation for OIC in patients with chronic pain currently is under development with an anticipated NDA submission in late 2009 or early 2010.
Methylthiouracil
Methylthiouracil is an antithyroid preparation. It is a thioamide, closely related to propylthiouracil.
Methylthiouracil is not used clinically in the United States, it has a similar mechanism of action and side effect to that of propylthiouricil.
The drug acts to decrease the formation of stored thyroid hormone, as thyroglobulin in the thyroid gland.
The clinical effects of the drug to treat the hyperthyroid state can have a lag peroid of up to two weeks, depending on the stores of thyroglobulin and other factors.
Like with any drug a wide variety of side effects can occur, but four topics should be kept in mind and the patient informed:
Agranulocytosis - develops rapidly, soar throat and fever are hallmark symptoms. Can be fatal if drug is not discontinued promptly.
Allergic Skin reactions the most dangerous of which is Exfoliative Dermatitis, it rapidly can get out of control, notify the physician should a skin eruption occur.
Hepatitis - yellowing of the skin, nausea, yellowing of the whites of the eyes, flu like symptoms.
Thombocytopenia - unusual brusing or bleeding.
Source: Goodman and Gillman's Pharmacological Basis of Therapeutics, 6th edition, and Facts and Comparisons.
see link on discussion of Hyperthyrodism: #S12_CH152_T002
Metre per second
Metre per second (U.S. spelling: meter per second) is an SI derived unit of both speed (scalar) and velocity (vector quantity which specifies both magnitude and a specific direction), defined by distance in metres divided by time in seconds.
The official SI symbolic abbreviation is ms1, or equivalently, m/s; although the abbreviation mps is sometimes used colloquially. Where metres per second are several orders of magnitude too slow to be convenient, such as in astronomical measurements, velocities may be given in terms of kilometres per second, where 1 km/s is equivalent to 1,000 metres per second; in popular, non-science literature kps is occasionally used instead of km/s.
One metre per second is roughly the speed of an average person walking.

# Conversions
1 metre per second is equivalent to:
1 foot per second = 0.3048 ms1 (exactly)
1 mile per hour  0.4471 ms1 (approximately)
1 kmh-1  0.2778 ms1 (approximately)
1 kilometre per second is equivalent to:

# Remark
Although ms1 is an SI derived unit, it could be viewed as more fundamental than the metre, since the latter is derived from the speed of light in a vacuum, which is defined as exactly 299 792 458 ms1. It follows that one metre is the length of the path travelled by light in a vacuum during a time interval of 1/299 792 458 of one second.
Microalbuminuria

# Overview
Microalbuminuria occurs when the kidney leaks small amounts of albumin into the urine, in other words,  when there is an abnormally high permeability for albumin in the renal glomerulus.

# Diagnosis
The level of albumin protein produced by microalbuminuria cannot be detected by urine dipstick methods. A microalbumin urine test determines the presence of the albumin in urine. In a properly functioning body, albumin is not normally present in urine because it is retained in the bloodstream by the kidneys.
Microalbuminuria is diagnosed either from a 24-hour urine collection (between 30-300 mg/24 hours) or, more commonly, from elevated concentrations in a spot sample (30 to 300 mg/L). Both must be measured on at least two of three measurements over a two- to three-month period.. An albumin level above these values is called "macroalbuminuria", or sometimes just albuminuria.
To compensate for variations in urine concentration in spot-check samples, it is more typical in the United Kingdom to compare the amount of albumin in the sample against its concentration of creatinine. This is termed the albumin/creatinine ratio (ACR) and microalbuminuria is defined as ACR 3.5 mg/mmol (female) or 2.5 mg/mmol(male), or, with both substances measured by mass, as an ACR between 30 and 300 g albumin/mg creatinine.

# Significance
- Microalbuminuria is an indicator of subclinical cardiovascular disease
- Microalbuminuria is a marker of vascular endothelial dysfunction
- Microalbuminuria is an important prognostic marker for kidney disease particularly in
diabetes mellitus
hypertension
- diabetes mellitus
- hypertension
- Increasing microalbuminuria during the first 48 hours after admission to an intensive care unit is associated with an elevated risk for acute respiratory failure, multiple organ failure, and overall mortality
- Microalbuminuria is a risk factor for venous thromboembolism
Microstimulation

# Overview
Microstimulation is a technique that stimulates a group of nerve cells by zapping them with a small electrical current.

# Applications
Microstimulation is used in neuroanatomical research to identify the functional significance of a group of neurons.  For example, Vidal-Gonzalez et al. (2006)  applied microstimulation to the rat prelimbic and infralimbic subregions of the medial prefrontal cortex while testing the subjects in a fear-inducing low-footshock condition for various behavioral indicators of fear (such as freezing).  This test allowed them to compare the relative fear behavior of rats under microstimulation in either subregion to normal rats in the same condition.  The researchers concluded that the prelimbic subregion excites fear behavior while the infralimbic subregion inhibits fear behavior.  In this instance, the correlation between stimulation and behavior helped identify the function of these two subregions in the process of fear.
-  Vidal-Gonzalez, I., Vidal-Gonzalez, B., Rauch, S. L., & Quirk, G. J. (2006). Microstimulation reveals opposing influences of prelimbic and infralimbic cortex on the expression of conditioned fear. Learning & Memory, 13, 728-733.
Mitchella repens
Mitchella repens , or Partridge Berry, is the best known plant in the genus Mitchella. It is a herbaceous woody shrub, occurring in North America and Japan, and belonging to the madder family (Rubiaceae).
This evergreen plant is a creeping, but not climbing, vine, 15-30 cm long. The evergeen dark-green leaves are opposite, ovate to cordate, with a pale yellow midrib. The petioles are short. Roots may grow at the internodes, forming loose mats. It is part of the undergrowh vegetation in many forests.
It has dimorphous, twin white tubular flowers (grown from one  calyx) with four petals, covered with fine hairs. They grow axillary at the end of a branchlet. Each flower has one pistil and four stamens. While in one twin flower this pistil is short,in the other it is long. With a short pistil come long stamens, or vice versa. This dimorphy prevents self-fertilization by one flower.
The scarlet berries are edible but tasteless. Each berry is produced by the each of twin flowers, after pollination by insects. This happens through fusion of the ovaries. The two bright red spots on each berry reveal this process. Each berry contains eight seeds. The fruit ripens between July and October. These berries are part of the diets of several birds, such as Ruffed Grouse, Sharp-tailed Grouse, Northern Bobwhite, and Prairie Chicken. The Red Fox, raccoons and White-tailed Deer seem to like it as well.
The most common method of reproduction is vegetative, through division of the roots. Information of propagation by seed is scant.
Common names for Mitchella repens include partridge berry (or partridgeberry), squaw berry (or squaw berry), two-eyed berry, running fox, and Noon kie oo nah yeah (in the Mohawk language).
The species is dispersed throughout eastern North America.
Mixed inhibition
Mixed inhibition refers to a combination of two different types of reversible enzyme inhibition  competitive inhibition and uncompetitive inhibition.  The term 'mixed' is used when the inhibitor can bind to either the free enzyme or the enzyme-substrate complex.  In mixed inhibition, the inhibitor binds to a site different from the active site where the substrate binds.  Mixed inhibition results in an decrease in the apparent affinity of the enzyme for the substrate (K_m^{app} > K_m) and a decrease in the apparent maximum enzyme reaction rate (V_{max}^{app} > V_{max}).
Mathematically, mixed inhibition occurs when the factors  and  (introduced into the Michaelis-Menten equation to account for competitive and uncompetitive inhibition, respectively) are both greater than 1.
In the special case where  = , noncompetitive inhibition occurs, in which case V_{max}^{app} is reduced but K_m is unaffected.  This is very unusual in practice
Mondor's disease

# Overview
Mondor's disease is a rare condition which involves thrombophlebitis of the superficial veins of the breast and anterior chest wall. It sometimes occurs in the arm or penis.

# Historical Perspective
It is named after Henri Mondor (1885-1962), a surgeon in Paris, France who first described the disease in 1939.

# Differentiating Mondor's Disease from other Diseases
Mondor's disease must be differentiated from other diseases that cause breast pain and swelling.
ABBREVIATIONSLAP=Lymphadenopathy, HRT=Hormonal replacement therapy, FNA=Fine needle aspiration, DCIS=Ductal carcinoma in-situ
Mononitrotoluene

# Overview
Mononitrotoluene, or methylnitrobenzene or nitrotoluene (MNT or NT), is an organic compound, a nitro compound derivate of toluene (or alternatively a methyl derivate of nitrobenzene). Its chemical formula is C6H4(CH3)(NO2).
Mononitrotoluene comes in three isomers, differing by the relative position of the methyl and nitro groups:
- ortho-nitrotoluene (ONT), o-nitrotoluene, or 2-nitrotoluene, CAS number Template:CASREF. It is a pale yellow liquid with a subtle, characteristic smell. It is non-hygroscopic and noncorrosive. Its melting point is -9.3 C and its boiling point is 222 C. It is toxic.
- meta-nitrotoluene (MNT), m-nitrotoluene, or 3-nitrotoluene, CAS number Template:CASREF. It is a yellowish-greenish to yellow liquid with weak fragrance. Its melting point is 16.1 C.
- para-nitrotoluene (PNT), p-nitrotoluene, or 4-nitrotoluene, CAS number Template:CASREF. It is a pale yellow material forming rhombic crystals. Its melting point is 51.7 C and its boiling point is 238.3 C. It is almost insoluble in water.
Typical use of nitrotoluene is in production of pigments, antioxidants, agricultural chemicals, and photographic chemicals.
-rtho-Mononitrotoluene and para-mononitrotoluene can be also used as detection taggants for explosive detection.