Persius/hicric huggingface dataset:
Ketoconzole adverse reactions

# Adverse Reactions
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 practice.
The following adverse reactions were reported in clinical trials:
Immune System Disorders: anaphylactoid reaction
Endocrine Disorders: gynecomastia
Metabolism and Nutrition Disorders: alcohol intolerance, anorexia, hyperlipidemia, increased appetite
Psychiatric Disorders: insomnia, nervousness
Nervous System Disorders: headache, dizziness, paresthesia, somnolence
Eye Disorders: photophobia
Vascular Disorders: orthostatic hypotension
Respiratory, Thoracic and Mediastinal Disorders: epistaxis
Gastrointestinal Disorders: vomiting, diarrhea nausea, constipation, abdominal pain, abdominal pain upper, dry mouth, dysgeusia, dyspepsia, flatulence, tongue discoloration
Hepatobiliary Disorders: hepatitis, jaundice, hepatic function abnormal
Skin and Subcutaneous Tissues Disorders: erythema multiforme, rash, dermatitis, erythema, urticaria, pruritus, alopecia, xeroderma
Musculoskeletal and Connective Tissue Disorders: myalgia
Reproductive System and Breast Disorders: menstrual disorder
General Disorders and Administration Site Conditions: asthenia, fatigue, hot flush, malaise, edema peripheral, pyrexia, chills
Investigations: platelet count decreased.
Post-Marketing Experience
The following adverse reactions have been identified during postapproval use of ketoconazole tablets. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.

# Post-Marketing Experience
Blood and Lymphatic System Disorders: thrombocytopenia
Immune System Disorders: allergic conditions including anaphylactic shock, anaphylactic reaction, angioneurotic edema
Endocrine Disorders: adrenocortical insufficiency
Nervous System Disorders: reversible intracranial pressure increased (e.g. papilloedema, fontanelle bulging in infants)
Hepatobiliary Disorders: serious hepatotoxicity including hepatitis cholestatic, biopsyconfirmed hepatic necrosis, cirrhosis, hepatic failure including cases resulting in transplantation or death
Skin and Subcutaneous Tissue Disorders: acute generalized exanthematous pustulosis, photosensitivity
Musculoskeletal and Connective Tissue Disorders: arthralgia
Reproductive System and Breast Disorders: erectile dysfunction; with doses higher than the recommended therapeutic dose of 200 or 400mg daily, azoospermia.
Ketoconzole contraindications

# Contraindications

### Drug Interactions
Coadministration of a number of CYP3A4 substrates is contraindicated with ketoconazole tablets. Coadministration with ketoconazole can cause elevated plasma concentrations of these drugs and may increase or prolong both therapeutic and adverse effects. For example, increased plasma concentrations of some of these drugs can lead to QT prolongation and ventricular tachyarrhythmias including occurrences of torsades de pointes, a potentially fatal arrhythmia.

### Liver Disease
The use of ketoconazole tablets is contraindicated in patients with acute or chronic liver disease.

### Hypersensitivity
Ketoconazole tablets USP, 200 mg is contraindicated in patients who have shown hypersensitivity to the drug.
Lung volume reduction surgery

# Overview
Lung volume reduction surgery, or LVRS, can improve the quality of life for certain COPD and emphysema patients. Parts of the lung that are particularly damaged by emphysema are removed, allowing the remaining, relatively good lung to expand and work better.
Conventional LVRS involves resection of the most severely affected areas of emphysematous, non-bullous lung (aim is for 20-30%). This is a surgical option involving a mini-thoracotomy for patients suffering end stage COPD due to underlying emphysema, and can improve lung elastic recoil as well as diaphragmatic function.
The National Emphysema Treatment Trial (Fishman et al., 2003) was a large multicentre study (N = 1218) comparing LVRS with medical treatment. Results suggested that:
- There was no overall survival advantage in the LVRS group, except for mainly upper-lobe emphysema + poor exercise capacity, and
- Significant improvements were seen in exercise capacity in the LVRS group.
Possible complications (Hopkins et al., 2006):
- Mortality at 90 days of 1.8% and survival at 3 and 5 years of 91.1% and 76% respectively.
- Prolonged air leak (mean duration post surgery until all ICC's removed is 10.9 +/- 8.0 days)
Laboratory diagnosis of virus
Laboratory diagnosis of virus is the procedure confirm and investigate viral infections. In the diagnostic laboratory virus infections are confirmed by several methods that include:
- Growth of the virus in a cell culture from a specimen taken from the patient.
- Detection of virus-specific antibodies in the blood.
- Detection of virus antigens
- Detection of virus nucleic acids
- Observation of virus particles by electron microscopy.
- Hemagglutination assay

# Cell culture
When growing virus in a cell culture, the cells affected with virus will evolve morphologic changes, often specific for the type of virus involved.

# Antibody detection
When the adaptive immune system of a vertebrate encounters a virus, it produces specific antibodies which bind to the virus and render it non-infectious. This is called humoral immunity. Two types of antibodies are important. The first called IgM is highly effective at neutralizing viruses but is only produced by the cells of the immune system for a few weeks. The second, called, IgG is produced indefinitely. The presence of IgM in the blood of the host is used to test for acute infection, whereas IgG indicates an infection sometime in the past. Both types of antibodies are measured when tests for immunity are carried out.

# Antigen detection
Detection of virus antigens can be done by ELISA in tissues and fluids.
Other techniques are:
- immunofluorescence
- immunoperoxidase

# Hemagglutination assay
Many viruses attach to molecules present on the surface of red blood cells. A consequence of this is that - at certain concentrations - a viral suspension may bind together (agglutinate) the red blood cells thus preventing them from settling out of suspension. Usefully, agglutination is rarely linked to infectivity, attenuated viruses can therefore be used in assays.

# Nucleic acid detection
Detection of virus encoded DNA and RNA is done with PCR. Nucleic acid hybridization with virus-specific probes detects specific viruses.
Lateral myocardial infarction
Synonyms and keywords: Lateral MI

# Overview
A lateral myocardial infarction (MI) is a heart attack or cessation of blood flow to the heart muscle that involves the inferior side of the heart.  Inferior MI results from the total occlusion of the left circumflex artery.  Lateral MI is characterized by ST elevation on the electrocardiogram (EKG) in leads I and aVL.

# EKG Examples
Shown below is an EKG demonstrating sinus rhythm and a QRS with a rightward axis, as well as wide Q waves in leads I and aVL as well as a poor R wave progression across the anterior chest leads. There is also slight ST elevation in leads I,aVL, and T wave inversion in the lateral leads. The EKG is consistent with a lateral wall myocardial infarction.
Copyleft image obtained courtesy of, 
Shown below is an EKG demonstrating sinus rhythm. The remarkable feature is the poor R wave progression in the V1 and V2 leads and the ST elevation and T wave changes in leads V1 to V4 and I and aVL. The cardiogram suggests an anterior/ lateral MI possibly acute. There is also terminal P wave negativity in V1 suggesting a left atrial abnormality.
Copyleft image obtained courtesy of, :E209.jpg
Shown below is an EKG demonstrating acute myocardial infarction in in a patient with a pacemaker and LBBB. Concordant ST elevation in V5-V6 are clearly visible. There is discordant ST segment elevation > 5 mm in lead V3.
Copyleft image obtained courtesy of,
Shown below is an EKG demonstrating findings in the same patient as in the first example 2 months before the myocardial infarction. Normal LBBB pattern.
Copyleft image obtained courtesy of,
Shown below is an EKG showing ST elevation MI.
Copyleft image obtained courtesy of, :De-KJcasus12.jpg
Law of the iterated logarithm
In probability theory,
the law of the iterated logarithm is the name given to several theorems which describe the magnitude of the fluctuations of a random walk.
The original statement (1924) of the law of the iterated logarithm is due to A. Y. Khinchin.
Another statement was given by A.N. Kolmogorov (1929).
One of the simpler forms of the law of the iterated logarithm can be stated as follows (Theorem 3.52 in Breiman).
where Sn is the sum of n independent, identically distributed variables with mean zero and finite variance 2.
See also: Brownian motion
Leukocyte adhesion deficiency

# Overview
Leukocyte adhesion deficiency (abbreviated LAD), is a rare autosomal recessive disorder characterized by immunodeficiency resulting in recurrent infections. The disorder is often divided into two separate genotypes called type I and type II, with type II being associated with fewer infections but more developmental delay.

# Epidemiology
LAD is a rare disease; its estimated prevalence is 1 in 100,000 births. There is no described racial or ethnic predilection.

# Clinical manifestations
LAD was first recognized as a distinct clinical entity in the 1970s. The classic descriptions of LAD included recurrent bacterial infections, defects in neutrophil adhesion, and a delay in umbilical cord sloughing. The defects in adhesion result in poor neutrophil chemotaxis and phagocytosis.
Patients with LAD suffer from bacterial infections beginning in the neonatal period. Infections such as omphalitis, pneumonia, gingivitis, abscesses, and peritonitis are common and often life-threatening due to the infant's inability to properly destroy the invading pathogens.

# Molecular defect
The inherited molecular defect in patients with LAD is a deficiency of the -2 integrin subunit, also called 
CD18, of the leukocyte cell adhesion molecule, which is found on chromosome 21. This subunit is involved in making three other proteins (LFA-1, Integrin alphaXbeta2, and Mac-1/CD3) This basically means that the gene creates a non-functioning protein. This results in the lack of important molecules which help neutrophils make their way from the blood stream into the infected areas of the body (ie the lungs in pneumonia). Those neutrophils which do manage to make it to the infected areas have a difficult time phagocytosing (swallowing) the bacteria. The bacteria can then proliferate, leading to symptomatic infection. The infection can spread unimpeded and cause serious injury to important tissue.

# Diagnosis
Typically, diagnosis is made after several preliminary tests of immune function are made, including basic evaluation of the humoral immune system and the cell-mediated immune system. A WBC differential will reveal extremely elevated levels of neutrophils (on the order of 6-10x normal) because they are unable to leave the blood vessels.  Specific diagnosis is made through monoclonal antibody testing for CR3, one of the three complete proteins which fail to form properly as a result of -2 integrin subunit deficiency.

# Treatment
Once the diagnosis of LAD is made, bone marrow transplantation is the current standard of care. However, some progress has been made in gene therapy, an active area of research.
Lifestyle center (healthcare)
The term lifestyle center is used in a variety of ways.  The most common use is to refer to a clinical center where lifestyle intervention is used in the treatment of patient's lifestyle-related conditions.  Lifestyle-related conditions are those diseases which result from unhealthy lifestyle practices.  Lifestyle centers can be inpatient (residential) or outpatient.  Programs at inpatient lifestyle centers typically run for about 18 days but vary by program.
Clinical lifestyle centers often involve placing a patient on a heart-healthy, plant-based diet and starting them on a vigorous exercise program.  Other lifestyle interventions may include getting adequate water and sleep, stress management, and natural remedies.
Lifestyle centers will frequently be supervised by physicians but include a multi-disciplinary approach using nurses, therapists, exercise physiologists, preventive care specialists, counselors, and chaplains.
Linear IgA bullous dermatosis
Synonyms and keywords:

# Overview
Linear IgA bullous dermatosis (also known as "Linear IgA dermatosis") is frequently associated with medication exposure, especially vancomycin, with men and women being equally affected.:135  It was first described by Tadeusz Chorzelski in 1979. Linear IgA dermatosis is a rare immune-mediated blistering skin disease that may be divided into two types::587
- Adult linear IgA disease is an acquired, autoimmune blistering disease that may present with a clinical pattern of vesicles indistinguishable from dermatitis herpetiformis, or with vesicles and bullae in a bullous pemphigoid-like appearance. 
- Childhood linear IgA disease (also known as "Chronic bullous disease of childhood") is an acquired, self-limited bullous disease that may begin by the time the patient is age 2 to 3 and usually remits by age 13. 

# Historical Perspective

# Classification

# Pathophysiology

# Causes

# Differentiating Linear IgA bullous dermatosis from other Diseases

# Epidemiology and Demographics

## Age

## Gender

## Race

# Risk Factors

# Natural History, Complications and Prognosis

# Diagnosis

## Diagnostic Criteria

## Symptoms

## Physical Examination

### Skin
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.
- Childhood linear IgA disease. Adapted from Dermatology Atlas.

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
Linear atrophoderma of Moulin
Synonyms and keywords: Atrophodermia linearis Moulin; LAM; Moulin disease

# Overview
Linear atrophoderma of Moulin (LAM) is an acquired unilateral hyperpigmented dermatitis localized along the Blaschko's lines.

# Historical Perspective
This disease was first referred to as Atrophoderma of Moulin after Dr. Moulin who first reported it in 1992 then was renamed as linear atrophoderma of Moulin.

# Pathophysiology
LAM is a cutaneous form of mosaicism.

# Differential Diagnosis
The LAM must be distinguished from other linear dermatoses:
- Blaschkitis acuta
- Epidermal naevi
- Inflammatory linear verrucous epidermal naevus
- Lichen striatus
- Linear lupus erythematosus
- Linear scleroderma
- Reticulate hyperpigmentation of Iijima

# Epidemiology and Demographics
Only a few dozen cases of LAM have been described. LAM affects children or adolescents of both genders.

# Natural History, Complications, Prognosis

## Natural History
There is neither preceding inflammation, nor later induration or scleroderma.

## Complications
The condition can be disfiguring and lead to emotional distress.

## Prognosis
The prognosis is good.

# Diagnosis

# Physcial Examination

## Skin
- The rash generally involves the trunk and limbs.

# Laboratory Studies
The clinical diagnosis is supported by micropatholgy.

# Treatment
Intravenous penicillin G administered for 14 days in a dosage of 10 x 106 IU twice daily has been prescribed in the past.
List of neuroimaging software
Neuroimaging software is used to study the structure and function of the brain.
- 3D Slicer developed at MIT has many uses, including diffusion tensor imaging tractography.
- Analysis of Functional NeuroImages (AFNI) 
- Analyze developed by the Biomedical Imaging Resource (BIR) at Mayo Clinic. AnalyzeDirect homepage
- BrainVISA 
- BrainVoyager 
- CamBA 
- Camino Open-source toolkit for diffusion MRI. Camino homepage
- Caret  Van Essen Lab, Washington University in St. Louis
- FMRIB Software Library (FSL) 
- FreeSurfer 
- ISAS (Ictal-Interictal SPECT Analysis by SPM)
- LONI Pipeline Laboratory of Neuro Imaging, UCLA
- MNI MINC McConnell Brain Imaging Center, Montreal Neurological Institute, McGill University
- MRIcro 
- NeuroLens
- NIfTI
- Statistical parametric mapping (SPM) 
- AutoSPM: Automated SPM for Surgical Planning
Logan College of Chiropractic
Logan College of Chiropractic, a private chiropractic college founded in 1935, is located in Chesterfield, Missouri, near St. Louis.  The institution offers degrees in Chiropractic, Pre-Chiropractic, Sport Science and Rehabilitation. The university's current president is Dr. George A. Goodman, D.C., F.I.C.C.  Dr. Goodman was appointed President of Logan in 1993.

# History
Logan College of Chiropractic (known at its founding as Logan Basic College of Chiropractic) was named for its founder and first president, Hugh B. Logan, D.C. Logan College enrolled its first class of seven men and women on the first of September 1935. The college was housed in a converted residence at 4490 Lindell Boulevard, St. Louis.  The college eventually moved to a 17-acre (68,800 m2) estate in the suburb of St. Louis called Normandy.  In the summer of 1973, Logan College moved to its present location, formerly a Maryknoll Seminary. The campus is on a 112-acre (0.45 km2) wooded hilltop in Chesterfield, Missouri.

# Accreditation
In June 1978, Logan College received accreditation from the Council on Chiropractic Education (C.C.E.).  In 1987, the North Central Association granted Logan College accreditation of the academic program.  Logan has received continuous reaccreditation from both organizations since receiving accredited status.

# Education
Logan offers four degree programs: Doctor of Chiropractic, Master of Science in Sport Science and Rehabilitation and Bachelor Science degrees in Human Biology and Life Sciences.
Pre-requisites for entering the DC (Doctor of Chiropractic) program include at least 90 semester hours (135 quarter hours) of undergraduate coursework (approximately three years of collegiate coursework).  Specific entrance requirements include 6 semester hours (9 quarter hours) of Biological Sciences, Inorganic (General) Chemistry, Organic Chemistry and Physics (with appropriate labs).  Additional requirements include 6 semester hour (9 quarter hours) of English/Language Skills, 3 semester hours (4.5 quarter hours) of Psychology and 15 semester hours (22.5 quarter hours) of Humanities/Social Sciences.  The Doctor of Chiropractic program is 10 trimesters in length (313 years).
Prerequisites for the Master of Science in Sports Science and Rehabilitation include a bachelors degree and some science requirements.  The Master of Science in Sports Science program is offered as a combined degree (M.S./D.C.) and as an independent graduate degree (M.S.).  The Master of Science program is 5 trimester in length.

# Presidents

# Affiliate Colleges
Logan College merged with Carver Chiropractic College in Oklahoma City in 1958 and with Missouri College of Chiropractic in 1964.
Luliconazole clinical studies

# Clinical Studies

## Interdigital Tinea Pedis
The safety and efficacy of LUZU (luliconazole) Cream, 1% was evaluated in two randomized, double-blind, vehicle-controlled, multi-center clinical trials in 423 subjects with a clinical and culture-confirmed diagnosis of interdigital tinea pedis. Subjects were randomized to receive LUZU Cream, 1% or vehicle. Subjects applied either LUZU Cream, 1% or vehicle cream to the entire area of the forefeet including all interdigital web spaces and approximately 2.5 cm (1 in) of the surrounding area of the foot once daily for 14 days.
The mean age of the study population was 41 years; 82% were male; 53% were White and 40% were Black or African American. Signs and symptoms of tinea pedis (erythema, scaling, and pruritus), KOH exam and dermatophyte culture were assessed at baseline, end-of-treatment (Day 14), 2 and 4 weeks post-treatment.
Overall treatment success was defined as complete clearance (clinical cure and mycological cure) at 4 weeks post-treatment. LUZU Cream, 1% demonstrated completed clearance in subjects with interdigital tinea pedis. Treatment outcomes at 4 weeks post-treatment are summarized in Table 1.

## Tinea Cruris
The safety and efficacy of LUZU (luliconazole) Cream, 1% was evaluated in a randomized, double-blind, vehicle-controlled, multi-center clinical trial in 256 subjects with a clinical and culture confirmed diagnosis of tinea cruris. Subjects were randomized to receive LUZU Cream, 1% or vehicle. Subjects applied either LUZU Cream, 1% or vehicle cream to the affected area and approximately 2.5 cm (1 in) of the surrounding area once daily for 7 days.
The mean age of the study population was 40 years; 83% were male; 58% were White and 34% were Black or African American. Signs and symptoms of tinea cruris (erythema, scaling, and pruritus), positive KOH exam and dermatophyte culture were assessed at baseline, end-of-treatment (Day 7), 2 and 3 weeks post-treatment.
Overall treatment success was defined as complete clearance (clinical cure and mycological cure) at 3 weeks post-treatment. LUZU Cream, 1% demonstrated completed clearance in subjects with tinea cruris. Treatment outcomes at 3 weeks post treatment are summarized in Table 2.