Persius/hicric huggingface dataset:
Mirtazapine overdose

# Overdosage topics
Human experience
Management

## Human experience
There is very limited experience with Mirtazapine overdose. In premarketing clinical studies, there were eight reports of Mirtazapine overdose alone or in combination with other pharmacological agents. The only drug overdose death reported while taking Mirtazapine was in combination with amitriptyline and chlorprothixene in a non-U.S. clinical study. Based on plasma levels, the Mirtazapine dose taken was 30 mg to 45 mg, while plasma levels of amitriptyline and chlorprothixene were found to be at toxic levels. All other pre-marketing overdose cases resulted in full recovery. Signs and symptoms reported in association with overdose included disorientation, drowsiness, impaired memory, and tachycardia. There were no reports of ECG abnormalities, coma or convulsions following overdose with Mirtazapine alone. Return to top

## Management
Treatment should consist of those general measures employed in the management of overdose with any drug effective in the treatment of major depressive disorder.
Ensure an adequate airway, oxygenation, and ventilation. Monitor cardiac rhythm and vital signs. General supportive and symptomatic measures are also recommended. Induction of emesis is not recommended. Gastric lavage with a large-bore orogastric tube with appropriate airway protection, if needed, may be indicated if performed soon after ingestion, or in symptomatic patients.
Activated charcoal should be administered. There is no experience with the use of forced diuresis, dialysis, hemoperfusion or exchange transfusion in the treatment of Mirtazapine overdosage. No specific antidotes for Mirtazapine are known.
In managing overdosage, consider the possibility of multiple-drug involvement. The physician should consider contacting a poison control center for additional information on the treatment of any overdose. Telephone numbers for certified poison control centers are listed in the Physicians' Desk Reference (PDR). Return to top
Adapted from the FDA Package Insert.
Miscarriage overview

# Overview
Miscarriage is the natural or spontaneous end of a pregnancy at a stage where the embryo or the fetus is incapable of surviving, generally defined in humans at a gestation of prior to 20 weeks. Miscarriage is the most common complication of early pregnancy. The medical term "spontaneous abortion" is used in reference to miscarriages because the medical term "abortion" refers to any terminated pregnancy, deliberately induced or spontaneous, although in common parlance it refers specifically to active termination of pregnancy.

# Pathophysiology
When looking for gross or microscopic pathologic symptoms of miscarriage, one looks for the products ofconception. Microscopically, these include villi, trophoblast, fetal parts, and background gestational changes in the endometrium.  Genetic tests may also be performed to look for abnormal chromosome arrangements.

# History and symptoms
The most common symptom of a miscarriage is bleeding; bleeding during pregnancy may be referred to as a threatened abortion. Of women who seek clinical treatment for bleeding during pregnancy, about half will go on to have a miscarriage. Symptoms other than bleeding are not statistically related to miscarriage.

# Treatment

## Surgery
Surgical treatment (most commonly vacuum aspiration, sometimes referred to as a D&C or D&E) is the fastest way to complete the miscarriage. It also shortens the duration and heaviness of bleeding, and is the best treatment for physical pain associated with the miscarriage. In cases of repeated miscarriage or later-term pregnancy loss, D&C is also the best way to obtain tissue samples for pathology examination.
Monomelic amyotrophy
Monomelic amyotrophy (also known as MMA, Hirayama's disease, Sobue disease or Juvenile nonprogressive amyotrophy) is an untreatable, focal, lower motor neuron disease that primarily affects young (15 - 25 year-old) males in India and Japan.  MMA is marked by insidious onset of muscular atrophy, which stabilizes at a plateau after two to five years from which it neither improves nor worsens.  There is no pain or sensory loss associated with MMA.  Unlike other lower motor neuron diseases, MMA is not believed to be hereditary and fasciculations (involuntary muscle twitches) are rare.
EMG tests reveal loss of the nerve supply, or denervation, in the affected limb without conduction block (nerve blockage restricted to a small segment of the nerve).  Increased sweating, coldness and cyanosis have been reported for a few patients, indicating involvement of the sympathetic nervous system.
While MMA will cause weakness and/or wasting in only one limb, EMG and NCV tests often show signs of reinnervation in the unaffected limbs.

# Treatment
There is no cure for MMA. Treatment consists of muscle strengthening exercises and training in hand coordination.

# Prognosis
The symptoms of MMA usually progress slowly for one to two years before reaching a plateau, and then remain stable for many years. Disability is generally slight. Rarely, the weakness progresses to the opposite limb. There is also a slowly progressive variant of MMA known as O'Sullivan-McLeod syndrome, which only affects the small muscles of the hand and forearm and has a slowly progressive course.

# Epidemiology
MMA occurs in males between the ages of 15 and 25. Onset and progression are slow. MMA is seen most frequently in Asia, particularly in Japan and India; it is much less common in North America.
Montelukast overdose

# Overdosage topics
Mortality
Treatment
Post-marketing experience/clinical studies
Peritoneal dialysis/hemodialysis

## Mortality
No mortality occurred following single oral doses of montelukast up to 5000 mg/kg in mice (estimated exposure was approximately 335 and 210 times the AUC for adults and children, respectively, at the maximum recommended daily oral dose) and rats (estimated exposure was approximately 230 and 145 times the AUC for adults and children, respectively, at the maximum recommended daily oral dose).  Return to top

## Treatment
No specific information is available on the treatment of overdosage with Montelukast. In chronic asthma studies, montelukast has been administered at doses up to 200 mg/day to adult patients for 22 weeks and, in short-term studies, up to 900 mg/day to patients for approximately a week without clinically important adverse experiences. In the event of overdose, it is reasonable to employ the usual supportive measures; e.g., remove unabsorbed material from the gastrointestinal tract, employ clinical monitoring, and institute supportive therapy, if required. Return to top

## Post-marketing experience/clinical studies
There have been reports of acute overdosage in post-marketing experience and clinical studies with Montelukast. These include reports in adults and children with a dose as high as 1000 mg. The clinical and laboratory findings observed were consistent with the safety profile in adults and pediatric patients. There were no adverse experiences in the majority of overdosage reports. The most frequently occurring adverse experiences were consistent with the safety profile of Montelukast and included abdominal pain, somnolence, thirst, headache, vomiting and psychomotor hyperactivity. Return to top

## Peritoneal dialysis/hemodialysis
It is not known whether montelukast is removed by peritoneal dialysis or hemodialysis. Return to top
Adapted from the FDA Package Insert.
Mullerian dysgenesis
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Synonyms and keywords: Mullerian congenital uterine anomalies; Mullerian anomalies; mullerian duct anomalies;female reproductive tract developmental abnormalities; paramesonephric developmental abnormalities; Mullerian agenesis

# Overview
Mullerian duct anomalies are an infrequent cause of infertility that is often treatable.

# Natural History, Complications and Prognosis

## Complications
Mullerian duct anomalies are associated with:
- Higher incidence of infertility
- Repeated first trimester spontaneous abortions
- Fetal intrauterine growth retardation
- Fetal malposition
- Preterm labor
- Retained placenta

# Acknowledgements
The content on this page was first contributed by: C. Michael Gibson, M.S., M.D.
Multihospital system
In Health services administration, Multihospital system is defined as "Institutional systems consisting of more than one health facility which have cooperative administrative arrangements through merger, affiliation, shared services, or other collective ventures."
According to the American Hospital Association, a system is defined as "either a multihospital or a diversified single hospital system. A multihospital system is two or more hospitals owned, leased, sponsored, or contract managed by a central organization. Single, freestanding hospitals may be categorized as a system by bringing into membership three or more, and at least 25 percent, of their owned or leased non-hospital preacute or postacute health care organizations. System affiliation does not preclude network participation." 

# List of multihospital systems

## United States
- Adventist Health System
- Ascension Health
- Carolinas Healthcare System
- Catholic Healthcare West
- Child Health Corporation of America 
- Hospital Corporation of America
- Kaiser Permanente
- Los Angeles County Department of Health Services
- McGaw Medical Center of Northwestern University is a consortium of hospitals
- NewYork-Presbyterian Healthcare System
- ProMedica Health System
- Providence Health & Services
- Shriners Hospitals for Children
- SSM Health Care
- Sutter Health
- Tenet Healthcare
- University of Pittsburgh Medical Center
- Wheaton Franciscan Healthcare
Multileaf collimator

# Overview
A multileaf collimator (MLC) is a device made up of individual 'leaves' of a high atomic numbered material, usually tungsten, that can move independently in and out of the path of a particle beam in order to block it.
MLCs are used on linear accelerators to provide conformal shaping of radiotherapy treatment beams. Specifically, conformal radiotherapy and Intensity Modulated Radiation Therapy (IMRT) can be delivered using MLCs.
The MLC has improved rapidly since its inception and the first use of leaves to shape structures in 1965 (Takahashi 1965) to modern day operation and use. MLCs are now widely used and have become an integral part of any radiotherapy department. MLCs were primarily used for conformal radiotherapy, and have allowed the cost effective implementation of conformal treatment with significant time saving (Brewster et al 1995, Helyer and Heisig 1995), and also have been adapted for use for IMRT treatments. For conformal radiotherapy the MLC allows conformal shaping of the linear accelerator (LINAC) beam to match the borders of the target tumour. For intensity modulated treatments the leaves of a MLC can be moved across the field to create IMRT distributions (it should be noted here that MLCs really provide a fluence modulation rather than intensity modulation).
The MLC is an important tool for radiation therapy dose delivery. It was originally used as a surrogate for alloy block field shaping and is now widely used for IMRT. As with any tool used in radiotherapy the MLC must undergo commissioning and quality assurance. Additional commissioning measurements are completed to model a MLC for treatment planning. Various MLCs are provided by different vendors and they all have unique design features as determined by specifications of design (Galvin 1993), and these differences are quite significant.
References:
Brewster L	Mohan R Mageras G Burman C Leibel S and Fuks Z Three dimensional conformal treatment planning with multileaf collimators Int. J. Rad. Onc. Biol. Phys. 33 (1995) 10819
Helyer S J	and Heisig S Multileaf collimation versus conventional shielding blocks: a time and motion study of beam shaping in radiotherapy Rad. Onc. 37 (1995) 614
Galvin J M	Smith A R and Lally B Characterization of a multi-leaf collimator system Int. J. Rad. Onc. Biol. Phys. 25 (1993) 18192
Takahashi S	Conformation radiotherapy: rotation techniques as applied to radiography and radiotherapy of cancer Acta Radiol. Suppl. 242 (1965) 1142
Multiprotein complex
A multiprotein complex (or protein complex) is a group of two or more proteins.  Protein complexes are a form of quaternary structure.  Proteins in a protein complex are linked by non-covalent protein-protein interactions, and different protein complexes have different degrees of stability over time.  Protein complex formation often serves to activate or inhibit one or more of the complex members.  In this way protein complex formation can be similar to phosphorylation.  A method that is commonly used for identifying the members of protein complexes is immunoprecipitation.
Understanding the functional interactions of proteins is an important research focus in biochemistry and cell biology.  Protein complex formation often serves to activate or inhibit one or more of the complex members and in this way, protein complex formation can be similar to phosphorylation.   These complexes are a cornerstone of many (if not most) biological processes and together they form various types of molecular machinery that perform a vast array of biological functions.  Individual proteins can participate in the formation of a variety of different protein complexes.  Different complexes perform different functions, and the same complex can perform very different functions that depend on a variety of factors.  Some of these factors are:
- Which cellular compartment the complex exists in
- Which stage in the cell cycle the complexes are present
- The nutritional status of the cell
- Others
Many protein complexes are well understood, particularly in the model organism Saccharomyces cerevisiae (a strain of yeast).  For this relatively simple organism, the study of protein complexes is now being performed genome wide and the elucidation of most protein complexes of the yeast is undergoing.
The molecular structure of protein complexes can be determined by experimental techniques such as X-ray crystallography or nuclear magnetic resonance. Increasingly the theoretical option of protein-protein docking is also becoming available.

# Homomultmeric and heteromultimeric proteins
The subunits of a multimeric protein may be identical as in a homomultimeric protein or different as in a heteromultimeric protein.
The voltage-gated potassium channels in the plasma membrane of a neuron are heteromultimeric proteins composed of four of forty known alpha subunits. Subunits must be of the same subfamily to form the multimeric protein channel. The tertiary structure of the channel allows ions to flow through the hydrophobic plasma membrane. Connexons are an example of a homomultimeric protein composed of six identical connexins. A cluster of connexons forms the gap-junction in two neurons that transmit signals through an electrical synapse .
Mycobacterium brumae
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Mycobacterium brumae is a rapidly growing environmental mycobacterial species identified in 1993.  Aside from one 2004 report of a catheter related bloodstream infection no other infections by this organism have been reported.  It was first isolated from water, soil and one human sputum sample in Spain.

# Description
Microscopy
- Gram-positive, nonmotile, mostly strongly acid-fast rods, 2.0-2.5m long and 0.3 to 0.5m wide.
Colony characteristics
- Flat, rough, and undulated yellow, nonphotochromogenic colonies
Physiology
- Rapid growth occurs within 5 days at 25C, 30C and 37C, but not at 45C on Lowenstein-Jensen medium and Middlebrook 7H10 agar.
- Production of thermostable catalase.
- Positive for -glucosidase, nitrate reductase, penicillinase, trehalase, urease and iron uptake.
- Tween 80 hydrolysis after 10 days.
- No accumulation of niacin, no degradation of salicylate to catechol.
- No growth on MacConkey agar without crystal violet.

# Pathogenesis
- In 2004 a patient with breast cancer was reported to have a catheter related bloodstream infection.

# Type Strain
- First isolated from water, soil and human sputum samples in Barcelona, Spain.
- Strain CR-270 = ATCC 51384 = CCUG 37586 = CIP 103465 = DSM 44177 = JCM 12273.
Mycobacterium caprae
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Mycobacterium caprae
Type strain: strain spc-1 = gM-1 = ATCC BAA-824 = CIP 105776.
Basonym:  Mycobacterium tuberculosis subsp. caprae Aranaz et al. 1999.
Other synonym:  Mycobacterium bovis subsp. caprae 
(Aranaz et al. 1999) Niemann et al. 2002.
Mycobacterium chitae
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Mycobacterium chitae
Type strain: strain ATCC 19627 = CCUG 39504 = CIP 105383 = DSM 44633 = JCM 12403 = NCTC 10485.
Mycobacterium cookii
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Mycobacterium cookii

# Description
Gram-positive, nonmotile and polymorphic acid-fast rods (0.8m x 1.4m  1.9m). Forms clumps, but not cords or cross bands. Does not form spores, capsules and aerial hyphae.
Colony characteristics
- Colonies are smooth and glistening with yellow-orange pigmentation (0.51.0 mm diameter, scotochromogenic).
Physiology
- Slow growth on Lowenstein-Jensen medium or Middlebrook 7H10 agar at 31C (optimal temperature). No growth at 37C, 42C or 45C.
- Most of the strains are susceptible to ethambutol, isoniazid, streptomycin, and rifampin.
Differential characteristics
- Phylogenetic position between the slowly growing pathogenic species and the saprophytic rapidly growing species by partial 16S rDNA sequencing.

# Pathogenesis
- Not pathogenic for humans, mice, guinea pigs and rabbits.  Biosafety level 1.
- Provokes a non-specific hypersensitivity reaction to bovine tuberculin.

# Type Strain
Strain NZ2 = ATCC 49103 = CIP 105396 = DSM 43922 = JCM 12404.
Mycobacterium fallax
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Mycobacterium fallax

# Description
Gram-positive, nonmotile and acid-fast rods (0.5  1m long) except for a small number (less than 20%) of cyanophil forms.
Colony characteristics
- Large, eugonic, buff coloured and rough colonies (Lowenstein-Jensen medium at 30C).
- Cauliflower-like morphology, resembling M. tuberculosis colonies. Cord formation at the edges of colonies (Middlebrook 7H10 agar at 30C).
Physiology
- Rapid growth on Lowenstein-Jensen or Middlebrook 7H10 media.
- Susceptible to ethambutol, rifampin and kanamycin.
- Resistant to isoniazid, pyrazinamide and streptomycin.
Differential characteristics
- Similarities to M. tuberculosis include colony morphology, thermolabile catalase, positive nitrate reductase; differences are negative reactions for niacin production and rapid growth at 30C.

# Pathogenesis
- Not known.  Biosafety level 1.

# Type Strain
- Isolated from environmental sources in France and the former Czechoslovakia.  Strain ATCC 35219 = CCUG 37584 = CIP 81.39 = DSM 44179 = JCM 6405.
Mycobacterium gadium
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Mycobacterium gadium

# Description
Short gram-positive, nonmotile and acid-fast rods.
Colony characteristics
- Yellow-orange, scotochromogenic colonies, but the pigmentation deepens with exposure to light. Older cultures are more dry and rough.
Physiology
- Rapid growth on Lowenstein-Jensen medium at 28C and 37C, but not at 45C.

# Pathogenesis
- Pathogenicity in humans is not known. Production of a local regressing infection but no death in mice.
- Biosafety level 1

# Type Strain
First isolated from known tuberculous patient from Cadiz, Spain.
Strain ATCC 27726 = CCUG 37515 = CIP 105388 = DSM 44077 = HAMBI 2274 = JCM 12688 = NCTC 10942.
Mycobacterium gastri
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Mycobacterium gastri

# Description
Moderately long to long, Gram-positive, nonmotile and acid-fast rods.
Colony characteristics
- Nonchromogenic, smooth to rough, white colonies on Lowenstein-Jensen medium and smooth or somewhat granular on Middlebrook 7H10 agar.
Physiology
- Growth on Lowenstein-Jensen medium or on Middlebrook 7H10 agar at 37C, (temperature range 25C-40C), within 7 or more days.
- Does not grow in the presence of ethambutol or isoniazid.
Differential characteristics
- Closely related to M. kansasii
- M. gastri and M. kansasii share an identical 16S rDNA sequence. Species differentiation is possible by differences in the ITS and hsp65 sequences.
- M. kansasii produces a photochromogenic yellow pigment.
- AccuProbes for M. kansasii are negative.

# Pathogenesis
- Casual resident of human stomachs, but not considered an etiologic agent of disease.
- Biosafety level 1

# Type Strain
- First isolated from human gastric specimen.  Also found in soil.
Strain ATCC 15754 = CCUG 20995 = CIP 104530 = DSM 43505 = JCM 12407.