Persius/hicric huggingface dataset:
Kernicterus (patient information)
For the WikiDoc page for this topic, click here
Synonyms and Keywords: Bilirubin encephalopathy

# Overview
Kernicterus is a rare neurological condition that occurs in some newborns with severe jaundice.

# What are the symptoms of Kernicterus?
The symptoms depend on the stage of kernicterus.
- Early stage:
- Extreme jaundice
- Absent startle reflex
- Poor feeding or sucking
- Extreme sleepiness (lethargy)
- Mid stage:
- High-pitched cry
- Arched back with neck hyperextended backwards
- Bulging fontanel (soft spot)
- Seizures
- Late stage (full neurological syndrome):
- High-frequency hearing loss
- Mental retardation
- Muscle rigidity
- Speech difficulties
- Seizures
- Movement disorder

# What causes Kernicterus?
- Kernicterus is caused by very high levels of bilirubin. Bilirubin is a yellow pigment that is created in the body during the normal recycling of old red blood cells. High levels of bilirubin in the body can cause the skin to look yellow (which is called jaundice).
- In some cases when there are extremely high levels of bilirubin in the body or the baby is extremely ill, the substance will move out of the blood and collect in the brain tissue. This can lead to serious neurological complications, including brain damage and hearing loss.
- Kernicterus usually develops in the first week of life, but may be seen up until the third week. Newborns with [[Hemolytic disease of the newborn (patient information)
Rh hemolytic disease]] that may lead to hydrops fetalis are at high risk for severe jaundice that leads to this condition. However, kernicterus has been seen in apparently healthy babies.

# When to seek urgent medical care?
Seek immediate medical help if your baby has signs of this condition.

# Diagnosis
A blood test will show a high bilirubin level (greater than 20-25 mg/dL).
Note: Normal value ranges may vary slightly among different laboratories. Talk to your doctor about the meaning of your specific test results.

# Treatment options
- Treatment depends on how old the baby is (in hours) and whether the baby has any risk factors (such as prematurity).
- It may include:
- Light therapy (phototherapy)
- Exchange transfusions

# Where to find medical care for Kernicterus?
Directions to Hospitals Treating Kernicterus

# What to expect (Outlook/Prognosis)?
Kernicterus is a serious condition. The outcome is guarded. Many infants with late stage nervous system complications die.

# Possible complications
- Permanent brain damage
- Hearing loss
- Death

# Prevention
- Early diagnosis and treatment of jaundice or conditions that lead to jaundice may help prevent this complication.
- The American Academy of Pediatrics recommends that infants with the first signs of jaundice have their bilirubin level measured within 24 hours. If the level is high, the infant should be screened for diseases that involve the destruction of red blood cells (hemolysis).
- The association also recommends that all newborns have a follow-up appointment within 2 to 3 days after leaving the hospital. This is particularly important for premature or near-term babies.

# Source
Lamivudine zidovudine description

# Description
COMBIVIR: COMBIVIR Tablets are combination tablets containing lamivudine and zidovudine. Lamivudine (EPIVIR) and zidovudine (RETROVIR, azidothymidine, AZT, or ZDV) are synthetic nucleoside analogues with activity against HIV-1.
COMBIVIR Tablets are for oral administration. Each film-coated tablet contains 150 mg of lamivudine, 300 mg of zidovudine, and the inactive ingredients colloidal silicon dioxide, hypromellose, magnesium stearate, microcrystalline cellulose, polyethylene glycol, polysorbate 80, sodium starch glycolate, and titanium dioxide.
Lamivudine: The chemical name of lamivudine is (2R,cis)-4-amino-1-(2-hydroxymethyl-1,3-oxathiolan-5-yl)-(1H)-pyrimidin-2-one. Lamivudine is the (-)enantiomer of a dideoxy analogue of cytidine. Lamivudine has also been referred to as (-)2,3-dideoxy, 3-thiacytidine. It has a molecular formula of C8H11N3O3S and a molecular weight of 229.3. It has the following structural formula:
Lamivudine is a white to off-white crystalline solid with a solubility of approximately 70 mg/mL in water at 20C.
Zidovudine: The chemical name of zidovudine is 3-azido-3-deoxythymidine. It has a molecular formula of C10H13N5O4 and a molecular weight of 267.24. It has the following structural formula:
Zidovudine is a white to beige, odorless, crystalline solid with a solubility of 20.1 mg/mL in water at 25C.
Lansoprazole detailed information
Lansoprazole (lan-SOE-pra-zole, INN) is a proton pump inhibitor which prevents the stomach from producing acid. It is manufactured by a number of companies worldwide under several trade names.  It was first approved by the FDA in 1995 .

# Pharmacology
Lansoprazole is a proton pump inhibitor (PPI) in the same pharmacologic class as omeprazole.  Lansoprazole has been marketed for many years and is one of several PPI's available.
Lansoprazole's plasma elimination half-life is not proportional to the duration of the drug's effects (i.e. gastric acid suppression). The mean plasma elimination half-life is 1.5 hours, and the effects of the drug last for over 24 hours after it has been used for 1 day or more.

# Indications
Lansoprazole is indicated for:
- Treatment of ulcers of the stomach and duodenum, and NSAID-induced ulcers
- Treatment of gastroesophageal reflux disease (GERD) (also known as acid reflux disease)
- Treatment of Zollinger-Ellison Syndrome
- Adjunctive treatment of Helicobacter pylori infection, alongside antibiotics

# Drug Interactions
- PPIs reduce absorption of antifungals (itraconazole and ketoconazole) and possibly increase Digoxin in plasma
- Increases plasma concentrations of Cilostazol (risk of toxicity)
- Absorption of lansoprazole possibly reduced by:
sucralfate
ampicillin
bisacodyl
delavirdine
fluvoxamine
iron salts
theophylline
voriconazole
aminophylline and theophylline
astemizole
- sucralfate
- ampicillin
- bisacodyl
- delavirdine
- fluvoxamine
- iron salts
- theophylline
- voriconazole
- aminophylline and theophylline
- astemizole

# Side effects
- Infrequent: dry mouth, insomnia, drowsiness, blurred vision, rash, pruritus
- Rarely and very rarely: taste disturbance, liver dysfunction, peripheral oedema, hypersensitivity reactions (including bronchospasm, urinary, angioedema, anaphylaxis), photosensitivity, fever, sweating, depression, interstitial nephritis, blood disorders (including leukopenia, leukocytosis, pancytopenia, thrombocytopenia), arthralgia, myalgia, skin reactions (including Stevens-Johnson syndrome, toxic epidermal necrolysis, bullous eruption)
- Severe: Gastro-intestinal disturbances (such as nausea 1.3%, abdominal pain 2.1%, diarrhea 3.8%

# Brand names
The drug is sold under several brand names, including: 
- Aprazol (Turkey)
- Duogast (Syria)
- Lanpro (India)
- Lansox (Italy)
- Lanton (Israel)
- Lanzor (France)
- Laprazol (Greece)
- Limpidex (Italy)
- Ogast and OgastORO (France)
- Prevacid (U.S. and Canada) Prevacid is a product of TAP Pharmaceutical Products.
- Prosogan and Prosogan FD (Indonesia)
- Refluxon (Hungary)
- SOLOX (New Zealand)
- Takepron (Japan)
- Zoton (Italy, Ireland, Australia, UK)
Lansoprazole is also available as a generic drug in the UK, Belgium, France, Colombia, Italy and Mexico.
Lateral circumflex femoral artery
The lateral circumflex femoral artery (lateral femoral circumflex artery, external circumflex artery) is an artery in the upper thigh.

# Structure
The lateral femoral circumflex artery arises from the lateral side of the profunda femoris artery, passes horizontally between the divisions of the femoral nerve, and behind the sartorius and rectus femoris, and divides into ascending, transverse, and descending branches. The lateral femoral circumflex artery may occasionally arise directly from the femoral artery.

## Branches
The ascending branch passes upward, beneath the tensor fasciae latae muscle, to the lateral aspect of the hip, and anastomoses with the terminal branches of the superior gluteal artery and deep circumflex iliac artery.
The descending branch runs downward, behind the rectus femoris, upon the vastus lateralis, to which it gives offsets; one long branch descends in the muscle as far as the knee, and anastomoses with the superior lateral genicular artery. It is accompanied by the branch of the femoral nerve to the vastus lateralis muscle.
The transverse branch, the smallest, passes lateralward over the vastus intermedius, pierces the vastus lateralis, and winds around the femur, just below the greater trochanter, anastomosing on the back of the thigh with the medial femoral circumflex artery, the inferior gluteal artery, and the perforating arteries of the profunda femoris artery.
Left bundle branch block overview

# Overview
Left bundle branch block is a cardiac conduction abnormality seen on the electrocardiogram (ECG) whereby there is an impairment of transmission of the cardiac electrical impulse along the fibers of the left main bundle branch, or both the left anterior fascicle and left posterior fascicle.  This conduction disturbance is characterized by wide (greater than or equal to 0.12 seconds) QRS complexes.  In this condition, activation of the left ventricle is delayed, which results in the left ventricle contracting later than the right ventricle.

# Epidemiology and Demographics
LBBB is uncommon among patients under 50 years of age (<0.5%).  It occurs in 6% to 8% of patients over the age of 50.

# Diagnosis

## Physical Examination
On examination of the cardiovascular system, a paradoxical split of the second heart sound may be heard.

# Treatment

## Management Strategy
Asymptomatic patients with isolated left bundle branch block and no underlying heart disease require no treatment.  Routine follow-up is required in such patients. In symptomatic patients treatment is directed at the underlying cause of left bundle branch block, such as ST elevation myocardial infarction.  Patients withsyncope and LBBB may have a rhythm disturbance that requires a pacemaker.  Given the dys-ynchrony that occurs with left ventricular contractility,cardiac resynchronization therapy in heart failure patients may be of benefit.
Levofloxacin detailed information
Levofloxacin is an advanced generation fluoroquinolone antibiotic, marketed by Ortho-McNeil under the trade name Levaquin in the United States. In Europe, it is marketed by Sanofi-Aventis under the trade name Tavanic, in Chile as Gatigol by Alpes Selection, in India under the trade name Levoday marketed by Zydus_Cadila and in Asia it is marketed by Daiichi under the trade name Cravit.  Levofloxacin was launched in the Japanese market in 1993, and thus has had more than 13 years of testing in efficiency and safety globally.  Chemically, levofloxacin is the S-enantiomer (L-isomer) of ofloxacin, and has approximately twice the potency of ofloxacin, because the R+enantiomer (D-isomer) of ofloxacin is essentially inactive.  In addition, the S-enantiomer (L-isomer) of ofloxacin, has substantially less toxicity. Like other fluoroquinolines, it works by inhibiting DNA gyrase, an enzyme that negatively supercoils DNA.
Levofloxacin is effective against a number of gram-positive and gram-negative bacteria. Because of its broad spectrum of action, levofloxacin is frequently prescribed empirically for a wide range of infections (e.g. pneumonia, urinary tract infection) before the specific causal organism is known. If the causal organism is identified, levofloxacin may be discontinued and the patient may be switched to an antibiotic with a narrower spectrum of activity. Levofloxacin is currently the only respiratory fluoroquinolone approved by the U.S. FDA for the treatment of nosocomial pneumonia.

# Susceptible organisms

## Gram-positive bacteria
- Enterococcus faecalis (many strains are only moderately susceptible)
- Staphylococcus aureus (methicillin-susceptible strains)
- Staphylococcus epidermidis (methicillin-susceptible strains)
- Staphylococcus saprophyticus
- Streptococcus pneumoniae (including Multidrug-resistant strains, MDRSP)
- Streptococcus pyogenes

## Gram-negative bacteria
- Enterobacter clacae
- Klebsiella pneumoniae
- Pseudomonas aeruginosa
- Escherichia coli
- Legionella pneumophila
- Serratia marcescens
- Haemophilus influenzae
- Moraxella catarrhalis
- Haemophilus parainfluenzae
- Proteus mirabilis
- Campylobacter

## Other
- Chlamydia pneumoniae
- Mycoplasma pneumoniae
- Peptostreptococcus sp.
- More bacterial coverage is available as per prescribing information for levofloxacin in Japan (Cravit)
de:Levofloxacin
th:
Suspensory muscle of the duodenum

# Overview
The suspensory muscle of the duodenum is the proper name of what is commonly known as the ligament of Treitz (named for Vaclav Treitz), and it refers to tissue that connects the duodenum of the small intestines to the diaphragm.  It is also known as the suspensory ligament of the duodenum.

# Structure
It arises from the connective tissue around the stems of the celiac trunk and superior mesenteric artery and inserts into the third and fourth portions of the duodenum and frequently into the duodenojejunal (DJ) flexure (between the duodenum and the jejunum) as well. Composed of a slip of skeletal muscle from the right crus of the diaphragm and a fibromuscular band of smooth muscle from the third and fourth parts of the duodenum, when it contracts, it has the effect of opening the DJ flexure and permitting the flow of chyme.
While commonly referred to as a ligament, it is officially both a suspensory muscle and a suspensory ligament due to its composition and function.

# Clinical significance
This muscle/ligament is an important anatomical landmark of the duodenojejunal junction, used to divide the GI tract into an upper portion and a lower portion.
It is an especially important landmark to note when looking at the bowel for the presence of  malrotation of the gut, a syndrome often suspected in young children when they have episodes of recurrent vomiting.  Visualizing a normal location of the ligament of Treitz in radiological images is critical in ruling out malrotation of the gut in a child;  it is abnormally located when malrotation is present.
List of countries by suicide rate
The following is a List of suicide rates by country according to data from the World Health Organization in which a country's rank is determined by its total rate of suicides. Male and female suicide rates are out of total male population and total female population, respectively (e.g. total male population divided by total number of male suicides).  The total rate of suicides is based on the total number of suicides divided by the total population rather than merely the average of the male and female suicide rates, because the gender ratio in many countries is not 1:1.  Year refers to the most recent year that data was available for a particular country.
This list should be used with caution. Little data is available documenting suicide rates in Africa, and the Middle East.  Even in countries where cause-of-death data is collected systematically, differing societal attitudes toward suicide may impact the recorded figures (e.g., misreporting a suicide as an accidental death out of deference for the bereaved).

# Notes
-  Table of WHO suicide rates by gender
-  WHO country reports and charts for suicide rates
-  Template:Lt icon Lithuanian suicide rate graph as of 2005
-  Template:Lt icon Official report on death causes in Lithuania
sv:Sjalvmordsstatistik
List of elements by atomic number
A table of chemical elements ordered by atomic number and color coded according to type of element.  Given is each element's name, element symbol, group and period, Chemical series, and atomic mass (or most stable isotope).

# Notes
-  Jump up to: 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 1.30 1.31 1.32 1.33 1.34 1.35 1.36 1.37 1.38 The isotopic composition of this element varies in some geological specimens, and the variation may exceed the uncertainty stated in the table.
-  Jump up to: 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 The isotopic composition of the element can vary in commercial materials, which can cause the atomic weight to deviate significantly from the given value.
-  Jump up to: 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 The isotopic composition varies in terrestrial material such that a more precise atomic weight can not be given.
-  The atomic weight of commercial Lithium can vary between 6.939 and 6.996analysis of the specific material is necessary to find a more accurate value.
-  Jump up to: 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 5.10 5.11 5.12 5.13 5.14 5.15 5.16 5.17 5.18 5.19 5.20 5.21 5.22 5.23 5.24 5.25 5.26 5.27 5.28 5.29 5.30 5.31 5.32 5.33 5.34 5.35 The element does not have any stable nuclides, and a value in brackets, e.g. , indicates the mass number of the longest-lived isotope of the element or characteristic isotopic composition.
-  This element has not been discovered/synthesized.
Liver spots (patient information)
For the WikiDoc page for this topic, click here

# Overview
Liver spots are flat, brown-black spots that usually appear on the skin in sun-exposed areas of the body. They have nothing to do with the liver or liver function.

# What are the symptoms of Liver spots?
Skin lesion that is:
- A flat patch or area of skin color change (macule)
- Light brown to black
- On the hands, arms, or forehead
- Painless

# What causes Liver spots?
Liver spots are changes in skin color that occur in older skin. The increased color may be due to aging, exposure to the sun or other forms of ultraviolet light, or other unknown causes.
They occur most often on areas that have had the greatest sun exposure, such as the:
- Backs of the hands
- Face
- Forearms
- Forehead
- Shoulders

# Who is at highest risk?
Liver spots are very common after age 40.

# Diagnosis
A diagnosis is based on the appearance of the skin, especially if you are over 40 and have had a lot of sun exposure over the years. A liver spot that looks irregular may be biopsied to confirm that it is not skin cancer.

# When to seek urgent medical care?
Call for an appointment with your health care provider if:
- You have liver spots and want them removed
- You develop any new symptoms, especially changes in the appearance of any liver spot

# Treatment options
No treatment is needed in most cases. You can improve the appearance of your skin by using skin bleaching lotions or creams. Most bleaching lotions use hydroquinone. This can cause blisters or skin reactions in some people. See your health care provider before starting treatment if you are worried.
Freezing (cryotherapy) or laser treatment can be used to destroy the liver spots.

# Where to find medical care for Liver spots?
Directions to Hospitals Treating Liver spots

# What to expect (Outlook/Prognosis)?
Liver spots are not medically dangerous. They are permanent skin changes that may affect the cosmetic appearance of the skin.

# Possible complications
Liver spots are harmless and painless, but they may affect the appearance. This can cause emotional distress.
Occasionally, liver spots may make it difficult to diagnose skin cancers.

# Prevention of Liver spots
Protect your skin from the sun by taking the following precautions:
- Wear protective clothing such as hats, long-sleeved shirts, long skirts, or pants.
- Use sunglasses to protect your eyes.
- Try to avoid sun exposure at midday, when sunlight is most intense.
- Use high-quality sunscreens, preferably with sun protection factor (SPF) ratings of at least 30. Apply sunscreen at least a half hour before exposure, and reapply often. Use sunscreen in the winter, too.

# Sources
Long-chain-aldehyde dehydrogenase
Fatty aldehyde dehydrogenase (or Long-chain-aldehyde dehydrogenase) is an aldehyde dehydrogenase enzyme that in human is encoded in the ALDH3A2 gene on chromosome 17. 
Aldehyde dehydrogenase enzymes function to remove toxic aldehydes that are generated by the metabolism of alcohol and by lipid peroxidation.

# Structure
The ALDH3A2 belongs to the aldehyde dehydrogenase superfamily and is a membrane-associated protein typically containing 485 residues. The mature protein functions as a dimer. The structure was resolved using X-ray crystallography at 2.1 Angstrom resolution. It contains an element in the C-terminal region referred to as a "gatekeeper" helix, which is adjacent to the membrane-anchored transmembrane domain and the catalytic core. The gatekeeper helix appears to control access of molecular substrates to the catalytic core and allows efficient transit between membranes and catalytic sites.

# Function
ALDH3A2 catalyzes the oxidation of long-chain aliphatic aldehydes into fatty acids. It is known to act on a variety of both saturated and unsaturated aliphatic aldehydes between 6 and 24 carbons in length, as well as dihydrophytal, a 20-carbon branched chain aldehyde. It requires NAD+ as a co-factor. The encoded enzyme is responsible for conversion of the sphingosine 1-phosphate (S1P) degradation product hexadecenal to hexadecenoic acid. ALD3H2 is expressed in the human liver and has been found to localize the microsome fraction inside the cell.
At least two alternative splicing isoforms of ALDH3A2 are known to exist. The alternative transcript differs by an additional exon and anchors differently to the endoplasmic reticulum vs. the peroxisome 

# Clinical significance
Mutations and deletions of in the ALDH3A2 gene have been widely associated with the autosomal recessive Sjogren-Larsson syndrome, an autosomal recessive neurocutaneous disease. Multiple mutations have been found in different families, including those that molecularly disrupts the protein dimerization interface or reduces mRNA stability. Absence or insufficiency of ALDH3A2 protein products in mutant cells are known to cause abnormal metabolism of sphingosine 1-phosphate to ether-linked glycerolipids and the abnormal accumulation of lipid precursors.