Persius/hicric huggingface dataset:
Male oral contraceptive
A male oral contraceptive is not medically available to the public, although several forms are in various stages of research and development.

# Botanical compounds
- In 1980, a test was successfully performed on male rats using leaves from the neem tree.
- In 1995, researchers isolated compounds from a Chinese plant called Tripterygium wilfordii.
- In 2002, researchers fed extracts from the seeds of papaya fruits (Carica papaya) to monkeys.  Subsequently, the monkeys had no sperm in their ejaculate. 
- In 2002, tests were performed on male rats using oleanolic acid, extracted from Eugenia jambolana, a tree in the southern part of Africa.  The tests demonstrated that the chemical was found to reversibly lower the rats' sperm motility without affecting the sperm count.
- Pills made from gossypol, a compound found in cotton seeds, have been abandoned as a potential male contraceptive because the compound was proven to cause permanent infertility.

# Pharmaceutical tests
- Calcium channel blockers such as nifedipine may cause reversible infertility by altering the lipid metabolism of sperm so that they are not able to fertilize an egg.

# Research on sperm
- Dr. George Witman has performed research on sperm tail proteins required for motility.
- Dr. David Claphamhas performed research on sperm-specific ion exchange channels needed for hyperactivation.
- Dr. Joseph Hall performed research on sperm head enzymes needed to recognize an egg.
Mammalian embryogenesis

# Overview
Mammalian embryogenesis is the process of cell division and cellular differentiation during early prenatal development which leads to the development of a mammalian embryo.

# Difference from human embryogenesis
Most mammals develop similarly to homo sapiens; during the earliest stages of development, the embryo is largely indistinguishable from another mammal.
However, there are phenomenons found in human being not found in all other mammals, as well as phenomenons occurring in other mammals, but not in humans.

## Humans but not all mammals
Mammals don't necessarily have the same human chorionic gonadotropin released from the embryo.

## Mammals but not humans
The anatomy of the area surrounding an embryo or fetus, however, is different in litter-bearing animals compared to humans: each unborn animal is surrounded by placental tissue and is lodged along one of two long uterine horns rather than in the center of the pear-shaped uterus found in a human female.
Mandibular second molar
The mandibular second molar is the tooth located distally (away from the midline of the face) from both the mandibular first molars of the mouth but mesial (toward the midline of the face) from both mandibular third molars.  This is true only in permanent teeth.  In deciduous (baby) teeth, the mandibular second molar is the last tooth in the mouth and does not have a third molar behind it.  The function of this molar is similar to that of all molars in regard to grinding being the principle action during mastication, commonly known as chewing.  Though there is more variation between individuals to that of the first mandibular molar, there are usually four cusps on mandibular second molars: two on the buccal (side nearest the cheek) and two palatal (side nearest the palate).  There are great differences between the deciduous (baby) mandibular molars and those of the permanent mandibular molars, even though their function are similar.  It is important to note that the permanent mandibular molars are not considered to have any teeth that precede it.  Despite being named molars, the deciduous molars are followed by permanent premolars.
In the universal system of notation, the deciduous mandibular second molars are designated by a letter written in uppercase. The right deciduous mandibular second molar is known as "T", and the left one is known as "K". The international notation has a different system of notation. Thus, the right deciduous mandibular second molar is known as "85", and the left one is known as "75".
In the universal system of notation, the permanent mandibular second molars are designated by a number.  The right permanent mandibular second molar is known as "31", and the left one is known as "18".  In the Palmer notation, a number is used in conjunction with a symbol deknown as "47", and the left one is known as "37".and Stanley J. Nelson, 2003. Wheelers Dental Anatomy, Physiology, and Occlusion. 8th edition.
nl:Tweede molaar
Mefloquine microbiology

# Microbiology

## Mechanism of Action
Mefloquine is an antimalarial agent which acts as a blood schizonticide. Its exact mechanism of action is not known.

## Activity In Vitro and In Vivo
Mefloquine is active against the erythrocytic stages of Plasmodium species (see Indications And Usage). However, the drug has no effect against the exoerythrocytic (hepatic) stages of the parasite. Mefloquine is effective against malaria parasites resistant to chloroquine (see Indications And Usage).

## Drug Resistance
Strains of P. falciparum with decreased susceptibility to mefloquine can be selected in vitro or in vivo. Resistance of P. falciparum to mefloquine has been reported in areas of multi-drug resistance in South East Asia. Increased incidences of resistance have also been reported in other parts of the world.

## Cross-Resistance
Cross-resistance between mefloquine and halofantrine and cross-resistance between mefloquine and quinine have been observed in some regions.
Melanocortin 3 receptor
Melanocortin receptor 3 is a protein that in humans is encoded by the MC3R gene.

# Function
This gene encodes MC3, a G-protein coupled receptor for melanocyte-stimulating hormone and adrenocorticotropic hormone that is expressed in tissues other than the adrenal cortex and melanocytes. This gene maps to the same region as the locus for benign neonatal epilepsy. Mice deficient for this gene have increased fat mass despite decreased food intake suggesting a role for this gene product in the regulation of energy homeostasis.

# Research
Studies performed by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), found that two specific polymorphisms in the MC3R gene may be associated with pediatric obesity and greater body mass because of greater energy intake. Children who were homozygous for C17A + G241A consumed approximately 38% more than those who did not contain aforementioned polymorphisms. The study concluded that these genetic variants did not affect energy expenditure.
Melanocortin 5 receptor
Melanocortin receptor 5 is a protein that in humans is encoded by the MC5R gene. It is located on the chromosome 18 in the human genome. When the melanocortin 5 receptor was disrupted in transgenic mice, it induced disruption of their exocrine glands and resulted in decreased production of sebum.

# Physiology
MC5R is necessary for normal sebum production. Stimulation of MC5R promotes fatty acid oxidation in skeletal muscle and lypolysis in adipocytes. MC5R is essential for erythrocyte differentiation. MC5R is involved in inflammation. MC5R helps maintain thermal homeostasis.
MC5R is expressed in the brain at different levels depending on physical activity.

## Pheromones
MC5R is heavily expressed in the preputial gland in mice (a modified sebaceous gland involved in pheromone production). MC5R deficiency in male mice decreases aggressive behavior, promotes defensive behavior and encourages other male mice to attack MC5R-deficient males through pheremonal signals.

## MRAP
Melanocortin 2 Receptor accessory protein (MRAP) traps MC5R protein inside cells.
Mendelian randomization
In epidemiology, Mendelian randomization is "the use of the genetic variation of known functions or phenotypes to correlate the causal effects of those functions or phenotypes with a disease outcome". Mendelian randomization controlls for extraneous influences when a true controlled experiment, or a sequence of randomized clinical trials, cannot be carried out. The method takes its name from Gregor Mendel, the father of modern genetics.

# Background
An important focus of observational epidemiology is the identification of modifiable causes of common diseases that are of public health interest.  In order to have firm evidence that a recommended public health intervention will have the desired beneficial effect, the observed association between the particular risk factor and disease must imply that the risk factor actually causes the disease.
Well-known successes include the identified causal links between smoking and lung cancer, and between blood pressure and stroke.  However, there have also been notable failures when identified exposures were later shown by randomised controlled trials (RCTs) to be non-causal. For instance, it has now been shown that hormone replacement therapy will not prevent cardiovascular disease, as was previously thought, and may have other adverse health effects. The reason for such spurious findings in observational epidemiology is most likely to be confounding social, behavioural or physiological factors which are difficult to control for and particularly difficult to measure accurately.  Moreover, many findings cannot be replicated by RCTs for ethical reasons.

# Implementing Mendelian randomization
Mendelian randomization is a method that allows one to test for, or in certain cases to estimate, a causal effect from observational data in the presence of confounding factors. It uses common genetic polymorphisms with well-understood effects on exposure patterns (e.g., propensity to drink alcohol) or effects that mimic those produced by modifiable exposures (e.g., raised blood cholesterol). Importantly, the genotype must only affect the disease status indirectly via its effect on the exposure of interest. Because genotypes are assigned randomly when passed from parents to offspring during meiosis, the population genotype distribution should be unrelated to the confounders that typically plague observational epidemiology studies. In this regard, Mendelian randomization can be thought of as a natural RCT. The method relies on getting good estimates from genetic association studies. Misleading conclusions can also be drawn in the presence of linkage disequilibrium, genetic heterogeneity, pleiotropy, or population stratification.
Methysergide overdosage

# Overdosage
Few cases of acute Sansert (methysergide maleate) intoxication have been reported. The possible symptom complex is therefore not fully known. The following symptoms are based on these few case reports. Euphoria, hyperactivity, tachycardia, dilated pupils, and dizziness have been reported in a child with a dose of 20-24 mg of Sansert (methysergide maleate). In adults, peripheral vasospasm, with diminished or absent pulses, coldness, mottling and cyanosis, has been observed at a dose of 200 mg. Ischemic tissue damage has not been reported in acute overdosage with Sansert (methysergide maleate).
Treatment consists of removal of the offending drug by induction of emesis, or gastric lavage in the case of very recent intake, repeat dose administration of activated charcoal and catharsis. There is no evidence that forced diuresis accelerates the elimination of Sansert(methysergide maleate). However, I.V. fluids may be given as a general supportive measure.
Treatment of peripheral vasospasm should consist of warmth, but not heat, and protection of the ischemic limbs. In reported cases of Sansert (methysergide maleate) overdosage, the use of vasodilators has not been necessary. However, if vasospasm is persistent, severe, or if there is evidence of impending ischemic tissue damage, these agents may be beneficial. Careful nursing care is recommended in order to prevent tissue damage.
Up-to-date information about the treatment of overdose can often be obtained from a certified Regional Poison Control Center. Telephone numbers of certified Regional Poison Control Centers are listed in the Physicians Desk Reference.
Miconazole how supplied

# How Supplied/Storage And Handling
ORAVIG 50 mg buccal tablets are supplied as off-white tablets containing 50 mg of miconazole. 
ORAVIG tablets have a rounded side and a flat side. ORAVIG tablets are packaged in bottles of 14 tablets (NDC 43288-250-14).
ORAVIG should be stored at 20 to 25C (68 to 77 F) ; excursions between 15 and 30C permitted at room temperature. Protect from moisture, and keep out of reach of children.
Miconazole microbiology

# Microbiology

## Mechanism of Action
Miconazole inhibits the enzyme cytochrome P450 14-demethylase which leads to inhibition of ergosterol synthesis, an essential component of the fungal cell membrane. Miconazole also affects the synthesis of triglycerides and fatty acids and inhibits oxidative and peroxidative enzymes, increasing the amount of reactive oxygen species within the cell.

## Activity in vitro and in vivo
Miconazole is active against Candida albicans, C. parapsilosis, and C. tropicalis. Correlation between minimum inhibitory concentration (MIC) results in vitro and clinical outcome has yet to be established.

## Drug Resistance
In vitro studies have shown that some Candida strains that demonstrate reduced susceptibility to one antifungal azole may also exhibit reduced susceptibility to other azoles suggesting cross-resistance.
Clinically relevant resistance to systemically utilized triazoles may occur in Candida species. Resistance may occur by multiple mechanisms such as changes in amino acids and/or in the regulation of the target enzyme and of a variety of efflux pump proteins. Multiple mechanisms may co-exist in the same isolate. Resistance breakpoints, correlating in vitroactivity with clinical efficacy, have not been established for miconazole.

# Clinical Studies

## Study in HIV Infected Patients
The efficacy and safety of ORAVIG in the treatment of OPC was evaluated in a randomized, double-blind, double-dummy, multicenter trial comparing ORAVIG 50 mg once daily for 14 consecutive days (n = 290) with clotrimazole troches 10 mg 5 times per day for 14 days (n = 287) in HIV-positive patients with OPC. Seventy-five percent of patients were not receiving highly active antiretroviral treatment, 5% had CD4+ cell count < 50 cells/mm 3, and 17% had a history of previous OPC. The mean viral load was 117,000 copies/mL. Patients were required to have symptoms and microbiological documentation of OPC for study entry. Most of the infections were caused by C. albicans (85%), followed by C. tropicalis (9%), and C. parapsilosis (3%). About 2% of the subjects were infected with more than one Candidaspecies.
Clinical cure , and clinical relapse by days 35-38 (21-24 days after end of therapy) are presented in Table 5. Mycological cure  at the TOC visit (days 17-22) is also reported in the table.
Study in Head and Neck Cancer Patients
The efficacy and safety of ORAVIG 50 mg was evaluated in an open-label, randomized, multicenter trial comparing ORAVIG 50 mg once daily for 14 days to miconazole oral gel 125 mg four times daily for 14 days in head and neck cancer patients who had received radiation therapy. Most of the infections were caused by C. albicans (71%), andC. tropicalis (8%). About 7% of the subjects were infected with more than one Candida species. Success rates of treatment at day 14  are shown in Table 6. Also reported in Table 6 are relapse rate at day 30, and mycologic cure assessed at day 14.
Migrating motor complex

# Overview
Migrating motor complexes (or migrating myoelectric complex) are waves of activity which sweep through the intestines in a regular cycle during fasting state.
These motor complexes help trigger peristaltic waves which facilitate transportation of indigestible substances such as bone, fiber and foreign bodies from the stomach, through the small intestine past the ileocecal sphincter into the colon.
The MMC originates in the stomach roughly every 75-90 minutes during the interdigestive phase (between meals) and is responsible for the rumbling experienced when hungry.
It also serves to transport bacteria from the small intestine to the large, and to inhibit the migration of colonic bacteria into the terminal ileum.
The MMC is thought to be partially regulated by motilin which is initiated in the stomach as a response to vagal stimulation, and does not depend on extrinsic nerves directly.

# Reference
Septomarginal trabecula
The septomarginal trabecula (or moderator band) is a muscular band of heart tissue found in the right ventricle. It is well-marked in sheep and some other animals, and frequently extends from the base of the anterior papillary muscle to the ventricular septum.
From its attachments it was thought to prevent overdistension of the ventricle, and was named the "moderator band".
However, more recent research has indicated that it is more properly considered part of the electrical conduction system of the heart, and in that capacity it is called the "septomarginal trabecula". The TA name is "trabecula  septomarginalis".
The moderator band is often used by radiologists to more easily identify the right ventricle in prenatal ultrasound.
Monoacylglycerol lipase
Monoacylglycerol lipase, also known as MAG lipase, MAGL, MGL or MGLL is a protein that, in humans, is encoded by the MGLL gene. MAGL is a 33-kDa, membrane-associated member of the serine hydrolase superfamily and contains the classical GXSXG consensus sequence common to most serine hydrolases. The catalytic triad has been identified as Ser122, His269, and Asp239.

# Function
Monoacylglycerol lipase functions together with hormone-sensitive lipase (LIPE) to hydrolyze intracellular triglyceride stores in adipocytes and other cells to fatty acids and glycerol. MGLL may also complement lipoprotein lipase (LPL) in completing hydrolysis of monoglycerides resulting from degradation of lipoprotein triglycerides.
Monoacylglycerol lipase is a key enzyme in the hydrolysis of the endocannabinoid 2-arachidonoylglycerol (2-AG).  It converts monoacylglycerols to the free fatty acid and glycerol. The contribution of MAGL to total brain 2-AG hydrolysis activity has been estimated to be ~85% (ABHD6 and ABHD12 are responsible for ~4% and ~9%, respectively, of the remainder), and this in vitro estimate has been confirmed in vivo by the selective MAGL inhibitor JZL184. Chronic inactivation of MAGL results in massive (>10-fold) elevations of brain 2-AG in mice, along with marked compensatory downregulation of CB1 receptors in selective brain areas.

# Inhibitors
MAGL enzyme inhibitors (URB602, URB754, JZL184) produce cannabinoid behavioral effects in mice.
Further examples include:
- KML-29
- JZL195
- JNJ-42165279
- JW 642
Trigeminal nerve nuclei

# Overview
The sensory trigeminal nerve nucleus is the largest of the cranial nerve nuclei, and extends through the whole of the brainstem, midbrain to medulla.
The nucleus is divided into three parts, from rostral to caudal (top to bottom in humans):
- The mesencephalic nucleus
- The chief sensory nucleus (or "pontine nucleus")
- The spinal trigeminal nucleus
There is also a distinct trigeminal motor nucleus that is medial to the chief sensory nucleus.
Mycobacterium africanum
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Mycobacterium africanum

# Epidemiology
M.africanum is most commonly found in West African countries, causing up to a quarter of cases of tuberculosis in countries such as the Gambia. It is an infection of humans only and is spread by an airbourne route from individuals with open cases of disease.
It has a similar degree of infectivity to the regular m.tuberculosis organism but is less likely to progress to clinical disease in an immunocompetent individual.
M.africanum is more likely to progress from infection to causing disease in an HIV positive patient, hence in countries where m.africanum is endemic, it represents an important opportunistic infection of the later stages of HIV disease.

# Pathogenesis
It is not fully understood how the genetic differences between m.africanum and m.tuberculosis give rise to the lower pathogenicity of the former.

# Treatment
M.africanum tuberculosis is treated with an identical regime to tuberculosis caused by m.tuberculosis. The overall rate of cure is similar, but as more m.africanum patients are likely to be HIV positive, they may have higher mortality from other HIV-related disease

# Type Strain
ATCC 25420 = CIP 105147
Mycobacterium aichiense
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Mycobacterium aichiense is a yellow-orange scotochromogenic, rapidly growing mycobacterium first isolated from soil and human sputum in Japan.  It has not been formally associated with disease in humans.

# Description
Microscopy
- Gram-positive, nonmotile and acid-fast rods less than 2m. Acid-fast in young cultures but may lose acid-fastness on prolonged culture.
Colony characteristics
- Yellow-orange scotochromogenic colonies.
Physiology
- Grows at 25-37C, not at 45C, in 3-4 days or less
- Acid phosphatase and arylsulfatase (3 days) is positive.
- Negative for nitrate reduction, isonicotinamidase, and citrate utilisation.
- Does not grow in the presence of hydroxylamine HCl (500mg/l) and does not degrade PAS.

# Pathogenesis
- Not associated with disease.

# Type Strain
- First isolated in Japan from soil and human sputum.
- Strain 49005 (previously, strain 5545) = ATCC 27280 = CIP 106808 = DSM 44147 = JCM 6376 = LMG 19259 = NCTC 10820.
Mycobacterium asiaticum
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Mycobacterium asiaticum is a slowly growing photochromogenic mycobacterium first isolated from monkeys in 1965.  M. asiaticum can, but rarely, causes human pulmonary disease.

# Description
Microscopy
- Gram-positive, nonmotile, acid-fast, coccoid rods.
Colony characteristics
- Dysgonic and yellow photochromogenic (pigment not produced in the dark) colonies.
Physiology
- Slow growth on Lowenstein-Jensen medium at 37C after 15-21 days.
Differential characteristics
- Unique 16S rRNA sequence.
- Biochemically M. asiaticum (photochromogenic) and Mycobacterium gordonae (scotochromogenic) can only by the mode of pigmentation.

# Pathogenesis
- Rarely causes human pulmonary disease.

# Type Strain
- First isolated from monkeys in 1965.
- Strain ATCC 25276 = CCUG 29115 = CIP 106809 = DSM 44297 = JCM 6409.