Persius/hicric huggingface dataset:
Lymphocytic choriomeningitis

# Overview
Lymphocytic choriomeningitis (LCM), is a rodent-borne viral infectious disease that presents as aseptic meningitis, encephalitis or meningoencephalitis. Its causative agent is the Lymphocytic Choriomeningitis Virus (LCMV), a member of the family Arenaviridae.

# Alternative Names
- Benign lymphocytic meningitis
- Lymphocytic meningoencephalitis
- Serous lymphocytic meningitis

# Virus biology
The first arenavirus, lymphocytic choriomeningitis virus (LCMV), was isolated in 1933 during a study of an epidemic of  St. Louis encephalitis. Although not the cause of the outbreak, LCMV was found to be a cause of nonbacterial or aseptic meningitis. LCMV is a reverse strand single stranded RNA virus.

# Infection
LCMV is naturally spread by the common house mouse, Mus musculus. Once infected, these mice can become chronically infected by maintaining virus in their blood and/or persistently shedding virus in their urine.
Chronically infected female mice usually transmit infection to their offspring, which in turn become chronically infected. About five per cent of mice, hamsters and rodents are thought to carry the disease. Pet rodents can contract the virus after exposure to infected mice.
The virus seems to be relatively resistant to drying and therefore humans can become infected by inhaling infectious aerosolized particles of rodent urine, feces, or saliva, by ingesting food contaminated with virus, by contamination of mucus membranes with infected body fluids, or by directly exposing cuts or other open wounds to virus-infected blood.  The only documented cases of transmission from animals, have occurred between humans and mice or hamsters.  However, humans rarely become infected from pet rodents.
Seroprevalence is approximately 5% of the US population. It tends to be more common among lower socio-economic groupings, probably reflecting more frequent and direct contacts with mice.
The virus normally has little effect on healthy people but can be deadly for people whose immune system has been weakened.  Person-to-person transmission does not usually occur, with the exception of vertical transmission from an infected mother to fetus.  In May 2005, reports of the deaths of at least six organ transplant patients in the US were linked to the virus.
Loin pain hematuria syndrome
Synonyms and keywords: LPHS

# Overview
Loin pain hematuria syndrome is the combination of unilateral or bilateral flank pain and microscopic or macroscopic amounts of blood in the urine that is otherwise unexplained.

# Causes
The cause of LPHS is currently not known.  One theory proposes that it is caused by a thin glomerular basement membrane and red blood cell (RBC) renal tubular congestion that leads to swelling of the kidney and distension of the renal fascia resulting in pain..  Loin pain hematuria syndrome is considered a diagnosis of exclusion.

# Differentiating Loin Pain Hematuria Syndrome from other Diseases
- Kidney stones
- Nutcracker syndrome
- IgA nephropathy
- Cancer of the genitourinary tract - classically not associated with pain
- Chronic pelvic pain
- Endometriosis

# Epidemiology and Demographics
The condition is very rare and predominately affects females.  Worldwide, only several hundred cases have been reported.

# Natural History, Complications and Prognosis
At this time no cure has been found for this disease.  LPHS is a debilitating disease due to chronic pain and the inability to know how to control the glomerular aspect. The pain of LPHS can be worsened by acts as simple as riding in the car and undertaking daily activities.  Many people with this disease are unable to maintain employment due to the debilitating pain.

# Diagnosis

## History and Symptoms
The syndrome presents with hematuria (blood in the urine) and flank (a region of the lower back beneath the ribs and above the ilium) pain which can result from a number of causes.  It has considerable overlap with chronic pelvic pain syndrome.

## Laboratory Findings
A thin glomerular basement membrane, as in thin basement membrane disease, is proposed to be the characteristic finding on renal biopsy, but not part of the syndrome definition.

# Treatment
The treatment of LPHS varies considerably from centre to centre.  As the condition is rare and poorly understood, a widely adopted standard of care is not existent.

## Medical Therapy
Pain management with opiate and non-opiate analgesia is common.  Angiotensin converting enzyme inhibitors are thought to be beneficial, as they reduce intraglomerular pressure and, presumably, reduce renal tubular congestion with RBCs.

## Surgery
Surgery (autotransplantation) is thought by some to be of benefit in selected individuals and advocated in some centres, but usually considered the last resort.
Many physicians discourage surgery, as LPHS symptoms often re-occur after autotransplantation.
Leri-Weill dyschondrosteosis
Leri-Weill dyschondrosteosis or LWD is a rare genetic disorder which results in dwarfism with short forearms and legs (mesomelic dwarfism) and a particular deformity of the forearms (Madelung's deformity).

# Causes
It is often caused by mutations in the SHOX gene found in the pseudoautosomal region PAR1 of the X and Y chromosomes.

# History
LWD was first described in 1929 by Andre Leri and Jean A. Weill.
Laboratory findings template
To go to the main page, click here.

# Introduction to the Laboratory Findings Page
- The page name should be "(Disease name) laboratory findings", with only the first letter of the title capitalized.
- Goal: to detail the important laboratory tests and findings for the disease you are describing.
- Remember this is not the section to describe imaging or other diagnostic modalities.
- As with all microchapter pages linking to the main page, at the top of the edit box put {{CMG}}, your name template, and the microchapter navigation template you created at the beginning.
- Remember to create links within Wikidoc by placing ] around key words which you want to link to other pages. Make sure you makes your links as specific as possible. For example if a sentence contained the phrase anterior spinal artery syndrome, the link should be to anterior spinal artery syndrome not anterior or artery or syndrome.  For more information on how to create links click here.
- Remember to follow the same format and capitalization of letters  as outlined in the template below.
- You should include the name of the disease in the first sentence of every subsection.

# Overview
- The overview section should include the disease name in the first sentence.
- The goal is to summarize the laboratory findings page in several sentences. This section can be the same as the laboratory findings segment on the overview page.
- To see an example of an overview section on a laboratory findings page, click here.

## Template
- First Sentence:
- Examples:
- Additional Sentences:
- Examples:

# Preferred Template Statements
IF there are diagnostic laboratory findings associated with the disease:
- An elevated/reduced concentration of serum/blood/urinary/CSF/other  is diagnostic of .
- Laboratory findings consistent with the diagnosis of  include , , and .
-  is usually normal among patients with .
- Some patients with  may have elevated/reduced concentration of , which is usually suggestive of .
IF there are no diagnostic laboratory findings:
- There are no diagnostic laboratory findings associated with .==Laboratory Findings==
- Outline or list the pertintent laboratory tests that you should obtain for the disease you are describing.
- Make sure you also indicate what the laborotory finding would be.
- For an example of a laboratory findings section on a laboratory findings page, click here.
- You can include subheadings to describe special types of laboratory tests.
Lamina of the vertebral arch

# Overview
The lamin are two broad plates directed backward and medially from the pedicles.
They fuse in the middle line posteriorly, and so complete the posterior boundary of the vertebral foramen.
Their upper borders and the lower parts of their anterior surfaces are rough for the attachment of the ligamenta flava.
The name derives from the Latin word "lamina," which refers to a thin plate, sheet, or layer.

# Additional images
- Median sagittal section of two lumbar vertebr and their ligaments.
- Vertebral arches of three thoracic vertebr viewed from the front.
- Costotransverse articulation. Seen from above.
Lamivudine drug interactions

# Drug Interactions
Lamivudine is predominantly eliminated in the urine by active organic cationic secretion. The possibility of interactions with other drugs administered concurrently should be considered, particularly when their main route of elimination is active renal secretion via the organic cationic transport system (e.g., trimethoprim). No data are available regarding interactions with other drugs that have renal clearance mechanisms similar to that of lamivudine.

## Interferon- and Ribavirin-Based Regimens
Although no evidence of a pharmacokinetic or pharmacodynamic interaction (e.g., loss of HIV-1/HCV virologic suppression) was seen when ribavirin was coadministered with lamivudine in HIV-1/HCV co-infected patients, hepatic decompensation (some fatal) has occurred in HIV-1/HCV co-infected patients receiving combination antiretroviral therapy for HIV-1 and interferon alfa with or without ribavirin .

## Zalcitabine
Lamivudine and zalcitabine may inhibit the intracellular phosphorylation of one another. Therefore, use of lamivudine in combination with zalcitabine is not recommended.

## Trimethoprim/Sulfamethoxazole (TMP/SMX)
No change in dose of either drug is recommended. There is no information regarding the effect on lamivudine pharmacokinetics of higher doses of TMP/SMX such as those used to treat PCP.

## Drugs with No Observed Interactions With EPIVIR
A drug interaction trial showed no clinically significant interaction between EPIVIR and zidovudine.
Periventricular leukomalacia
Periventricular leukomalacia (PVL) is characterized by the death of the white matter near the cerebral ventricles due to softening of the brain tissue. It can affect fetuses or newborns; premature babies are at the greatest risk of the disorder.

# Causes
PVL is caused by a lack of oxygen or blood flow to the periventricular area of the brain, which results in the death or loss of brain tissue. The periventricular area (the area around the spaces in the brain called ventricles) contains nerve fibers that carry messages within the brain.

# Presentation
Although babies with PVL generally have no outward signs or symptoms of the disorder, they are at risk for motor disorders (especially of the lower limbs), delayed mental development, coordination problems, and vision and hearing impairments. Children with PVL have higher levels of nystagmus, strabismus, optic nerve hypoplasia and  refractive error.  PVL may be accompanied by a hemorrhage or bleeding in the periventricular-intraventricular area (the area around and inside the ventricles), and can lead to cerebral palsy.

# Diagnosis
The disorder can be diagnosed by ultrasound, but magnetic resonance imaging of the head is diagnostically more accurate.

# Treatment
There is no specific treatment for PVL. Treatment is symptomatic and supportive. Children with PVL should receive regular medical screenings to determine appropriate interventions.

# Prognosis
The prognosis for individuals with PVL depends upon the severity of the brain damage. Some children exhibit fairly mild symptoms, while others have significant deficits and disabilities.
de:Periventrikulare Leukomalazie
Lincomycin adverse reactions

# ADVERSE REACTIONS
The following reactions have been reported with the use of lincomycin:

## Gastrointestinal
Glossitis, stomatitis, nausea, vomiting, antibiotic-associated diarrhea and colitis, and pruritus ani. Onset of pseudomembranous colitis symptoms may occur during or after antibiotic treatment (see WARNINGS).

## Hematopoietic
Neutropenia, leukopenia, agranulocytosis and thrombocytopenic purpura have been reported. There have been rare reports of aplastic anemia and pancytopenia in which LINCOCIN could not be ruled out as the causative agent.

## Hypersensitivity Reactions
Hypersensitivity reactions such as angioneurotic edema, serum sickness and anaphylaxis have been reported. Rare instances of erythema multiforme, some resembling Stevens-Johnson syndrome, have been associated with LINCOCIN. If an allergic reaction to LINCOCIN occurs, discontinue the drug. Serious acute hypersensitivity reactions may require treatment with epinephrine and other emergency measures, including oxygen, intravenous fluids, intravenous antihistamines,corticosteroids, pressor amines, and airway management, as clinically indicated.

## Skin and Mucous Membranes
Skin rashes, urticaria and vaginitis and rare instances of exfoliative and vesiculobullous dermatitis have been reported.

## Liver
Although no direct relationship of LINCOCIN to liver dysfunction has been established, jaundice and abnormal liver function tests (particularly elevations of serum transaminase) have been observed.

## Renal
Although no direct relationship of lincomycin to renal damage has been established, renal dysfunction as evidenced by azotemia, oliguria, and/or proteinuria has been observed in rare instances.

## Cardiovascular
After too rapid intravenous administration, rare instances of cardiopulmonary arrest and hypotension have been reported. (See DOSAGE AND ADMINISTRATION.)

## Special Senses
Tinnitus and vertigo have been reported occasionally.

## Local Reactions
Patients have demonstrated excellent local tolerance to intramuscularly administered LINCOCIN. Reports of pain following injection have been infrequent. Intravenous administration of LINCOCIN in 250 to 500 mL of 5% dextrose injection or 0.9% sodium chloride injection produced no local irritation or phlebitis.
Lyme resident survival guide

# Overview
This section provides a short and straight to the point overview of the disease or symptom.  The first sentence of the overview must contain the name of the disease.

# Causes

## Life Threatening Causes
Life-threatening causes include conditions that may result in death or permanent disability within 24 hours if left untreated.
- Life threatening cause 1
- Life threatening cause 2
- Life threatening cause 3

## Common Causes
- Common cause 1
- Common cause 2
- Common cause 3
- Common cause 4
- Common cause 5

# Diagnosis
Shown below is an algorithm summarizing the diagnosis of ] according the the  guidelines.

# Treatment
Shown below is an algorithm summarizing the treatment of ] according the the  guidelines.

# Do's
- The content in this section is in bullet points.

# Don'ts
- The content in this section is in bullet points.
MADS-box gene transcriptions
"The MADS-box encodes a novel type of DNA-binding domain found so far in a diverse group of transcription factors from yeast, animals, and seed plants."
"The MADS-box comprises 180 nucleotides, encoding 60 amino acids  MADS is an acronym for the four DNA-binding proteins MCM1 , AGAMOUS , DEFICIENS , and SRF ."
The " SQUA is a member of a family of transcription factors which contain the MADS-box, a conserved DNA binding domain."
The "MADS-box is  AGAGGGAAAGTACAACTGAAGAGGATAGAGAACAAGATCAATAGACAGGTGACTTT CTCAAAGAGGAGAGGTGGATTGTTGAAAAAAGCTCATGAGCTCTCTGTGCTTTGTG ATGCTGAAGTGGCTCTTATTGTCTTCTCTAATAAGGGGAAGCTATTTGAGTATTCT ACTGAT", which has 174 nucleotides (nts) and begins with the nucleotides for the amino acids RGK. The six nucleotides following the MADS box are "TCTTGC" which may be the additional six needed to get to 180 nts.
"RIN  binds to DNA sequences known as the CA/T-rich-G (CArG) box, which is the general target of MADS box proteins (Ito et al., 2008)."

# Peaches
"An AGC box (AGCCGCC) was found  between 886 and 892 bp upstream of the translation start site which has been shown in other ethylene-responsive PR genes to be a binding site for ethylene-responsive binding factor proteins (ERF proteins) (Ohme-Takagi and Shinshi, 1995; Sato et al., 1996; Jia and Martin, 1999; Fujimoto et al., 2000)."
"The peach ACO1 does have an AGC box that has been found to bind ethylene responsive elements in response to pathogen infections (Ohme-Takagi et al., 2000; Rushton et al., 2002). Only the apple ACO1 also contains this sequence. In addition, both PpACO1 and the apple ACO1 have a MADS box transcription factor binding site (CarG) (Tilly et al., 1998), but none of the other ACO genes do. "

# Acknowledgements
The content on this page was first contributed by: Henry A. Hoff.
Initial content for this page in some instances came from Wikiversity.
Medical laboratory assistant

# Overview
Medical Laboratory Assistants (MLAs) prepare, and in some cases process samples within a pathology laboratory. They also utilise pre-analytical systems in order for biomedical scientists (BMS) or Medical Laboratory Scientific Officers to process the biochemical tests requested on the sample. The majority of an MLA's time is spent in processing specimens. As such, the MLA has to have excellent knowledge of their particular sample acceptance policy, whilst obeying the data protection act, patient confidentiality, COSHH and the Caldicott rules.
A typical method of sample acceptance (in a clinical chemistry lab) is as follows:
- Sample is received.
- Sample is checked (to ensure that the sample is sent in the correct container for the specimen).
- Patient's details checked and matched on both form and sample (non-matching samples and/or forms rejected).
- Sample and form labelled with unique identifying number (UIN).
- Tests requested on form receipted onto UIN on computer system.
- Samples placed either on pre-analytical system by MLA or analysed immediately by BMS (dependent on test requested).
- UIN attached to patient using patient identifying details on form.
MLA's also deal with all sample queries and give low level advice to clinical staff on sample acceptance and correct sampling method. They may also do minor upkeep on the pre-analytical systems as well as further upkeep on some point of care analysers  depending on the laboratory in which they are based.
Mendelian Inheritance in Man

# Overview
The Mendelian Inheritance in Man project is a database that catalogues all the known diseases with a genetic component, and - when possible - links them to the relevant genes in the human genome and provides references for further research and tools for genomic analysis of a catalogued gene.

# Versions
It is available as a book named after the project, and it is currently in its 12th edition. The online version is called Online Mendelian Inheritance in ManTM (OMIMTM), which can be accessed with the Entrez database searcher of the National Library of Medicine and is part of the NCBI project Education.

# Collection process
The information in this database is collected and processed under the leadership of Dr. Victor A. McKusick at Johns Hopkins University, assisted by a team of science writers and editors. Relevant articles are identified, discussed and written up in the relevant entries in the MIM database

# The MIM code
Every disease and gene is assigned a six digit number of which the first number classifies the method of inheritance.
If the initial digit is 1, the trait is deemed autosomal dominant; if 2, autosomal recessive; if 3, X-linked. Wherever a trait defined in this dictionary has a MIM number, the number from the 12th edition of MIM, is given in square brackets with or without an asterisk (asterisks indicate that the mode of inheritance is known; a number symbol (#) before an entry number means that the phenotype can be caused by mutation in any of 2 or more genes) as appropriate e.g., Pelizaeus-Merzbacher disease  is a well-established, autosomal, dominant, mendelian disorder.
Micafungin drug interactions

# Drug Interactions
A total of 14 clinical drug-drug interaction studies were conducted in healthy volunteers to evaluate the potential for interaction between Mycamine and amphotericin B, mycophenolate mofetil, cyclosporine, tacrolimus, prednisolone, sirolimus, nifedipine, fluconazole, itraconazole, voriconazole, ritonavir, and rifampin. In these studies, no interaction that altered the pharmacokinetics of Mycamine was observed.
There was no effect of a single dose or multiple doses of Mycamine on mycophenolate mofetil, cyclosporine, tacrolimus, prednisolone, fluconazole, and voriconazole pharmacokinetics.
Sirolimus AUC was increased by 21% with no effect on Cmax in the presence of steady-state Mycamine compared with sirolimus alone. Nifedipine AUC and Cmax were increased by 18% and 42%, respectively, in the presence of steady-state Mycamine compared with nifedipine alone. Itraconazole AUC and Cmax were increased by 22% and 11%, respectively.
Patients receiving sirolimus, nifedipine or itraconazole in combination with Mycamine should be monitored for sirolimus, nifedipine or itraconazole toxicity and the sirolimus, nifedipine or itraconazole dosage should be reduced if necessary.
Micafungin is neither a substrate nor an inhibitor of P-glycoprotein and, therefore, would not be expected to alter P-glycoprotein-mediated drug transport activity.
Miconazole adverse reactions

# Adverse Reactions
The following serious adverse drug reactions are discussed in detail in other sections of labeling:
- Hypersensitivity reactions

# Clinical Trial Experience
Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in clinical practice.
The overall safety of ORAVIG was assessed in 480 adult subjects: 315 HIV-infected subjects, 147 subjects with head and neck cancer, and 18 healthy subjects.

### HIV Infected Patients
Two trials were conducted in immunocompromised HIV infected patients: one randomized, double-blind, double-dummy, active-controlled design (N = 290 ORAVIG, 287 control) and one non-comparative trial (N = 25).
In the randomized, double blind trial (Study 1), 290 HIV infected subjects used ORAVIG once daily for 14 days, and 287 subjects used 10 mg clotrimazole troches five times daily for 14 days. Adverse reactions occurring in  2% of patients in either treatment are presented in Table 1.
Overall local adverse reactions, including oral discomfort, oral burning, oral pain, gingival pain, gingival swelling, gingival pruritis, tongue ulceration, mouth ulceration, glossodynia, dry mouth, application site pain or discomfort, toothache, loss of taste, and altered taste, were reported by 35 (12.1%) patients who received miconazole buccal tablet compared to 27 (9.4%) patients who received clotrimazole troches.

### Head and Neck Cancer Patients
In the randomized, open-label comparative trial of oropharyngeal candidiasis in patients with head and neck cancer who had received radiation therapy (Study 2), 147 patients used ORAVIG once daily for 14 days and 147 patients used 125 mg of miconazole oral gel four times daily for 14 days. Adverse reactions occurring in 2% of patients in either arm are listed in Table 2.
Overall local adverse reactions, including oral discomfort, oral pain, dry mouth, glossodynia, loss of taste, altered taste, tongue ulceration, mouth ulceration, tooth disorder, and application site discomfort or pain, were experienced by 14 (9.5%) patients who used ORAVIG compared to 16 (10.9%) patients who used miconazole gel.
Overall ORAVIG Safety Experience In Patients and Healthy Subjects
Adverse reactions reported in the overall safety database of 480 subjects who received miconazole buccal tablet is listed in Table 3.
Discontinuation of ORAVIG due to adverse drug reactions occurred in 0.6% overall.