Persius/hicric huggingface dataset:
Feature integration theory
The feature integration theory, developed by Treisman and Gelade since the early 1980s has been one of the most influential psychological models of human visual attention. According to Treisman, in a first step to visual processing, several primary visual features are processed and represented with separate feature maps that are later integrated in a saliency map that can be accessed in order to direct attention to the most conspicuous areas.
Treisman distinguishes two kinds of visual search tasks, feature search and conjunction search. Feature search can be performed fast and pre-attentively for targets defined by primitive features. Conjunction search is the serial search for targets defined by a conjunction of primitive features. It is much slower and requires conscious attention. She concluded from many experiments that color, orientation, and intensity are primitive features, for which feature search can be performed.
It was widely speculated that the saliency map could be located in early visual cortical areas, e.g. the Primary Visual Cortex (V1), though this is controversial. Wolfe's popular Guided Search Model has many similarities to the feature integration theory.

# Research literature
- Treisman, A., Features and objects: the fourteenth Bartlett Memorial Lecture. Quarterly Journal of Experimental Psychology, 40A, 201-236, 1988
- Treisman, A. M.  and Gelade, G., A feature-integration theory of attention, Cognitive Psychology, Vol. 12, No. 1, pp. 97-136, 1980
- Treisman, Anne M., and Nancy G.Kanwisher, "Perceiving visually presented objects: recognition, awareness, and modularity," Current Opinion in Neurobiology, 8 (1998), pp 218-226
Ferric subsulfate solution
Ferric subsulfate solution is a styptic or haemostatic agent used after superficial skin biopsies. Ferric subsulfate solution is also known as Basic Ferric Sulfate Solution or Monsel's Solution. It has a recognised formula published in United States Pharmacopeia 29.

# Active ingredients
Ferric subsulfate solution is prepared from ferrous sulfate, sulfuric acid and nitric acid.
It contains, in each 100 mL, basic ferric sulfate equivalent to not less than 20g and not more than 22g of iron.

# Storage
Ferric subsulfate solution should be stored in airtight containers at a temperature above 22 degrees Celsius. Crystallisation may occur at temperatures below 22 degrees. Warming the solution may redissolve the crystals. The solution should be protected from light.

# Brandnames
AstrinGyn by CooperSurgical is a thickened and specially modified gel formulation.
Fimbria of the hippocampus

# Overview
With regard to the brain, the fimbria  is a prominent band of white matter along the medial edge of the hippocampus.

# Structure
The fimbria is an accumulation of myelinated axons (mostly efferent) that first collect on the ventricular surface of the hippocampus as the alveus (a thin layer resembling an inverted trough).

# Relations
Near the splenium the fimbria separates from the hippocampus as the crus of the fornix.

# Additional images
- Diagram of hippocampus
- Section of brain showing upper surface of temporal lobe.
- Scheme of rhinencephalon.
- Posterior and inferior cornua of left lateral ventricle exposed from the side.
- Inferior and posterior cornua, viewed from above.
- Diagram of the fornix.
- The fornix and corpus callosum from below.
Flexor retinaculum of foot

# Overview
The laciniate ligament (internal annular ligament, flexor retinaculum of foot) is a strong fibrous band, extending from the tibial malleolus above to the margin of the calcaneus below, converting a series of bony grooves in this situation into canals for the passage of the tendons of the Flexor muscles and the posterior tibial vessels and tibial nerve into the sole of the foot.
It is continuous by its upper border with the deep fascia of the leg, and by its lower border with the plantar aponeurosis and the fibers of origin of the Abductor hallucis muscle.
Enumerated from the medial side, the four canals which it forms transmit the tendon of the Tibialis posterior; the tendon of the Flexor digitorum longus; the posterior tibial vessels and tibial nerve, which run through a broad space beneath the ligament; and lastly, in a canal formed partly by the talus, the tendon of the Flexor hallucis longus.
Flunitrazepam side effects

# Overview
flunitrazepam/Rohypnol is a prescription drug - the only sedative that has been used in many date rapes in the US. Rohypnol's medical use is a preoperation anesthetic or strong sleeping pill, but stronger doses can bring on amnesia. It takes effect very quickly - sometimes as quick as 10 minutes after taken - and reaches its peak eight hours later when it can render a patient totally unconscious. 
Rohypnol comes as a pill that can diissolve in liquids. Some are round , small and white. Newer pills are oval and green-grey in colour. When slipped into a drink , a dye in these new pills makes clear liquids turn blue and the dark drinks turn cloudy. But this colour change might br hard to see in a dark drink, or in a dark room.Also the pills with no dye are available. these pills may be grounded up into a powder.

# Adverse effects
The effects of rohypnol can be felt within 30 minutes of being drugged and can last for several hours. If an individual is drugged he/she might look and act like someone who is drunk. There can be trouble in standing. The person's speech might be slurred. These effects can be short term or long term.
- Short term effects
- Relaxation or sedation of the body.
- Vomiting and headache
- Difficulty in breathing
- Nausea
- Rapid mood swings, outburst of temper
- Stomach problems
- Breathing and heart rate slow down to dangerous levels
- Memory loss,dizziness and sleepiness
- Coma and seizures
- Death
- Long term effects
- Uses it more frequently
- Need more and ,more to get the same effect
- Become preoccupied by using it
- Spend more money than needed on the drug
- Miss classes,fail to complete assignments or miss other obligations
- Make new friends who do it and neglect old friends
- Find it hard to be happy and relaxed without it
- Have headache and trouble sleeping without it
Free fatty acid receptor 2
Free fatty acid receptor 2 (FFAR2) is a G-protein coupled receptor encoded by the FFAR2 gene.

# Expression
FFAR2 mRNA is expressed in adipose tissue, pancreas, spleen, lymph nodes, bone marrow, and peripheral blood mononuclear cells. FFAR2 transcription is regulated by the XBP1 transcription factor which binds to the core promoter.

# Function
Mouse studies utilizing Ffar2 gene deletions have implicated the receptor in the regulation of energy metabolism and immune responses. Short Chain Fatty Acids (SCFA's) generated in the processing of fiber by intestinal microbiota act as ligands for the receptor and can affect neutrophil chemotaxis.  However, discrepancies between the pathways activated by FFAR2 agonists in human cells and the equivalent murine counterparts have been observed.

# Heteromerization
FFAR2 may interact with FFAR3 to form a FFAR2-FFAR3 receptor heteromer with signalling that is distinct from the parent homomers.
Free fatty acid receptor 3
Free fatty acid receptor 3 (FFA3) is a G-protein coupled receptor that in humans is encoded by the FFAR3 gene.

# Animal studies
Knockout mouse studies have implicated FFAR3 in diabetes, coilitis, hypertension and asthma. However, discrepancies between the pathways activated by FFAR3 agonists in human cells and the equivalent murine counterparts have been observed.

# Heteromerization
FFAR3 may interact with FFAR2 to form a FFAR2-FFAR3 receptor heteromer with signalling that is distinct from the parent homomers.
Gallbladder polyp overview

# Overview
Gallbladder polyps are a common clinical findings occurring in 5% of patients who often have cross-sectional imaging for non-specific abdominal symptoms.

# Historical Perspective

# Classification

# Pathophysiology
In patients with gallbladder polyps, it is important to note what type of polyp is described. While true polyps are adenomatous, gallbladder polyps are often non-epithelial growths and, in fact, about 70% of polyps are cholesterol polyps that have no malignant potential. Adenomas are uncommon and constitute approximately 8% of all gallbladder polyps. Less common polypoid lesions include gallbladder adenocarcinomas, inflammatory polyps, gallstones masquerading as polyps and heterotopic tissue.

# Causes

# Differentiating Gallbladder polyp overview from Other Diseases

# Epidemiology and Demographics
The incidence of gallbladder polyps is higher among men than women.  The overall prevalence among men of Chinese ancestry is 9.5%, higher than other ethnic types.  Polypoid lesions of the gallbladder affect approximately 5% of the adult population.  The causes are uncertain, but there is a definite correlation with increasing age and the presence of gallstones (cholelithiasis). Most affected individuals do not have symptoms. The gallbladder polyps are detected during abdominal ultrasonography performed for other reasons.

# Risk Factors

# Screening

# Natural History, Complications, and Prognosis

## Natural History
After considering the type of polyps, the risk of development of cancer should be determined. Most demographic data suggest that men and women have an equal propensity to develop adenomatous polyps, however, one study found that men had an increased risk of polyp development. In addition, several studies have noted that patients with primary sclerosing cholangitis (PSC) that have polyps are more likely to develop adenocarcinoma. Finally, patients with advancing age may be predisposed to have cancer because some data suggests that gallbladder polyps, like colonic polyps, have an adenoma-to-carcinoma sequence and, therefore, advancing age would permit malignant transformation.

## Complications

## Prognosis

# Diagnosis

## Diagnostic Criteria

## History and Symptoms
Most polyps do not cause noticeable symptoms.  Gallbladder polyps are usually found incidentally when examining the abdomen  by ultrasound for other conditions, usually abdominal pain.

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy

## Surgery

## Prevention
Gamma-glutamyl carboxylase
Gamma-glutamyl carboxylase is an enzyme that in humans is encoded by the GGCX gene, located on chromosome 2 at 2p12.

# Function
Gamma-glutamyl carboxylase is an enzyme that catalyzes the posttranslational modification of vitamin K-dependent proteins. Many of these vitamin K-dependent proteins are involved in coagulation so the function of the encoded enzyme is essential for hemostasis.  Most gla domain-containing proteins depend on this carboxylation reaction for posttranslational modification.  In humans, the gamma-glutamyl carboxylase enzyme is most highly expressed in the liver.

# Catalytic reaction
Gamma-glutamyl carboxylase oxidizes Vitamin K hydroquinone to Vitamin K 2,3 epoxide, while simultaneously adding CO2 to protein-bound glutamic acid (abbreviation = Glu) to form gamma-carboxyglutamic acid (also called gamma-carboxyglutamate, abbreviation = Gla). The carboxylation reaction will only proceed if the carboxylase enzyme is able to oxidize vitamin K hydroquinone to vitamin K epoxide at the same time; the carboxylation and epoxidation reactions are said to be coupled reactions.

# Clinical significance
Mutations in this gene are associated with vitamin K-dependent coagulation defect and PXE-like disorder with multiple coagulation factor deficiency.
Germinal matrix hemorrhage

# Overview
Germinal matrix hemorrhage is a bleeding into the subependymal germinal matrix with or without subsequent rupture into the lateral ventricle. The microcirculation in this particular area is extremely sensitive to hypoxia and changes in perfusion pressure. It is most frequent before 35 weeks gestation and is typically seen in low birth-weight (<1500g) premature infants.
Germinal matrix hemorrhage (GMH) and intraventricular hemorrhage (IVH) are the most common neurologic injuries in preterm neonates. The brain of a premature infant lacks the ability to autoregulate cerebral blood pressure. Fluctuations in cerebral blood pressure and flow can rupture the primitive germinal matrix vessels or lead to infarction of the metabolically active germinal matrix. The damage can extend into the periventricular white matter, resulting in significant neurologic sequelae, including cerebral palsy, mental retardation, and seizures. A common lesion that characterizes the neuropathology of GMH/IVH is bleeding into the subependymal germinal matrix, with or without subsequent rupture into the lateral ventricle. Sequelae of GMH/IVH include germinal matrix destruction, periventricular hemorrhagic infarction with subsequent encephalomalacia], and posthemorrhagic hydrocephalus. Because maturation of the germinal matrix vasculature occurs in the perinatal period for premature infants, most cases of GMH/IVH occur in the first week of life for these infants. Approximately 50% of cases of GMH/IVH occur in the first day of life. The major risk factors for GMH include a young gestational age, low birth weight, acute amnionitis, and exposure to antenatal steroids for less than 48 hours.
- Grade 1: Hemorrhage that is confined to the germinal matrix
- Grade 2: Extension of the hemorrhage into the lateral ventricles without hydrocephalus
- Grade 3: Ventricular hemorrhage with the presence of associated hydrocephalus
- Grade 4: Parenchymal hemorrhage

## Ultrasound
- US is the primary modality for both screening and follow-up of GMH/IVH in neonates.
- Acute subependymal hemorrhage appears as a homogeneous echogenic mass, often in the caudothalamic groove. The hematoma becomes less echogenic over time, beginning with the central portion. Subsequent to eventual clot retraction, a subependymal cyst may develop, or a linear echo may result.
- Acutely, IVH also appears echogenic. Cerebrospinal fluid (CSF)blood fluid levels may be observed. When large, the clot forms a cast of the ventricle.
Glossopharyngeal neuralgia
Synonyms and keywords: Cranial mononeuropathy IX

# Overview
Glossopharyngeal neuralgia is a condition marked by repeated episodes of severe pain in the tongue, throat, ear, and tonsils, which can last from a few seconds to a few minutes.

# Epidemiology and Demographics
Symptoms usually begin in people over 40 years of age.

# Pathophysiology
Glossopharyngeal neuralgia is believed to be caused by irritation of the ninth cranial nerve.
In most cases, the source of irritation is never discovered. Nevertheless, tumors or infections of the throat and mouth, compression of the glossopharyngeal nerve by neighboring blood vessels, and other lesions at the base of the skull can sometimes cause this type of neuralgia (nerve pain).

# Diagnosis

## Symptoms
Symptoms include severe pain in the areas connected to the ninth cranial nerves. This includes the throat, tonsillar region, posterior third of the tongue, nasopharynx (back of nose and throat), larynx, and ear. The pain is episodic and may be severe. It can sometimes be triggered by swallowing, chewing, speaking, laughing, or coughing.

## Laboratory Tests
Occasionally, certain blood tests may be needed when the diagnosis is not clear, to rule out other causes of peripheral nerve problems (peripheral neuropathy), such as hyperglycemia.

## Imaging Studies
Tests will be done to identify an abnormality at the base of the skull, particularly tumors. These may include x-rays, CAT scan of the head, and head MRI. Sometimes the MRI may show evidence of inflammation of the glossopharyngeal nerve.
To determine whether a blood vessel is compressing the nerve, pictures of the brain arteries may be obtained using magnetic resonance angiography (MRA) or conventional angiography (x-rays of the arteries with a dye).

# Treatment
Treatment is aimed at controlling pain. Unfortunately, over-the-counter pain killers such as aspirin and acetaminophen are not very effective for the relief of neuralgia. The most effective drugs are actually anti-seizure medications, like carbamazepine, gabapentin, and phenytoin. Some anti-depressants like amitriptyline are sometimes tried with variable degrees of success.
In severe cases, when pain is difficult to treat, surgery aiming at decompressing the glossopharyngeal nerve may be required.

# Prognosis
Prognosis depends on the underlying cause and the effectiveness of initial treatment. Surgery is considered effective for cases that do not benefit from medications.

# Complications
Decreased pulse and fainting may occur when pain is severe. Side-effects of medications may complicate treatment.
Glycerol phosphate shuttle
The glycerol-3-phosphate shuttle is a mechanism that regenerates NAD+ from NADH, a by-product of glycolysis.  Its importance in transporting reducing equivalents is secondary to the malate-aspartate shuttle.

# Reaction
In this shuttle, the enzyme called cytoplasmic glycerol-3-phosphate dehydrogenase converts dihydroxyacetone phosphate to glycerol 3-phosphate by oxidizing one molecule of NADH to NAD+ as in the following reaction:

# Reverse path
Glycerol-3-phosphate gets converted back to dihydroxyacetone phosphate by a membrane-bound mitochondrial glycerophosphate dehydrogenase, this time reducing one molecule of enzyme-bound flavin adenine dinucleotide (FAD) to FADH2.  FADH2 then reduces coenzyme Q (ubiquinone to ubiquinol) which enters into oxidative phosphorylation. This reaction is irreversible.

# Function
The glycerol-3-phosphate shuttle allows the NADH synthesized in the cytosol by glycolysis to contribute to the oxidative phosphorylation pathway in the mitochondria to generate ATP. It has been found in animals, fungi, and plants.
Thoracic splanchnic nerves
Thoracic splanchnic nerves arise from the sympathetic trunk in the thorax and travel inferiorly to provide sympathetic innervation to the abdomen.  The nerves contain preganglionic sympathetic and visceral afferent fibers.
There are three main thoracic splanchnic nerves:
The nerve's origins can be remembered by the "4-3-2 rule", accounting for the number of ganglia giving rise to each nerve. However, different sources define the nerves in different ways, so this rule may not always be reliable.

# Additional images
- Diagram of efferent sympathetic nervous system.
- Plan of right sympathetic cord and splanchnic nerves.
- Thoracic portion of the sympathetic trunk.
- The celiac ganglia with the sympathetic plexuses of the abdominal viscera radiating from the ganglia.
- Lower half of right sympathetic cord.
- The relations of the viscera and large vessels of the abdomen. Seen from behind, the last thoracic vertebra being well raised.
Hashimoto's encephalopathy
Synonyms and keywords: steroid-responsive encephalopathy associated with autoimmune thyroiditis, SREAT

# Overview
Hashimoto's Encephalopathy is a very rare condition associated with Hashimoto's thyroiditis.  Hashimoto's Encephalopathy is a neuroendocrine disorder. Much like the antibodies in Hashimoto's thyroiditis attack the thyroid, in Hashimoto's encephalopathy, antibodies attack neurons of the brain.

# Differentiating Hashimoto's encephalopathy from other disease
- Stroke - associated symptoms of paresis
- Alzheimer's disease- seen in old age and dementia is the most prominent symptom

# Pathophysiology
A few theories are proposed for Hashimoto encephalopathy.
- Neuronal injury due to antibody mediated destruction.
- Immmune complex mediated vasculitis
- Toxic effect of increased thyroid stimulating hormone.

# Diagnosis

## Symptoms
- Headache
- Disorientation
- Psychosis
- Tremors
- Concentration and memory problems

## Physical examination
- Jerks in the muscles
- Lack of coordination
- Partial paralysis
- Speech problems

## Laboratory Findings

### Blood and Biomarker Studies
- Blood TSH, T3, T4 levels
- Anti thyroid peroxidase levels
- CSF analysis - increased protein concentration, lymphocytic pleocytosis

### Electroencephalogram
- Generalized slowing of activity

### CT and MRI
- Non specific and show normal results
- In few patients atrophy may be seen

# Treatment
Steroids or immunosuppressant treatment, this condition is now also referred to as "steroid-responsive" encephalopathy.
Hepatocyte nuclear factors
Hepatocyte nuclear factors (HNFs) are a group of phylogenetically unrelated transcription factors that regulate the transcription of a diverse group of genes into proteins.  These proteins include blood clotting factors and in addition, enzymes and transporters involved with glucose, cholesterol, and fatty acid transport and metabolism.

# Function
As the name suggests, hepatocyte nuclear factors are expressed predominately in the liver.  However HNFs are also expressed and play important roles in a number of other tissues so that the name hepatocyte nuclear factor is somewhat misleading.  Nevertheless, the liver is the only tissue in which a significant number of different HNFs are expressed at the same time.  In addition, there are a number of genes which contain multiple promoter and enhancer regions each regulated by a different HNF.  Furthermore, efficient expression of these genes require synergistic activation by multiple HNFs.  Hence hepatocyte nuclear factors function to ensure liver specific expression of certain genes.
As is the case with many transcription factors, HNFs regulate the expression of a wide variety of target genes and therefore functions.  These functions (and especially functions involving the liver) include development and metabolic homeostasis of the organism.  For example, HNFs  influence expression of the insulin gene as well as genes involved in glucose transport and metabolism.  In embryo development, HNF4 is thought to have an important role in the development of the liver, kidney, and intestines.

# Disease implication
Variants of the  genes can cause several relatively rare forms of MODY, an inherited, early onset form of diabetes.   Mutations in the HNF4, HNF1, or HNF1 genes are linked to MODY1, MODY3, and MODY5 respectively. Mutations in HNF genes are also associated with a number of others diseases including hepatic adenomas and renal cysts.

# Members
The following is a list of  human hepatocyte nuclear factors (see also boxes to the right for additional information about these proteins):

## HNF1
Members of the HNF1 subfamily contain a POU-homeodomain and bind to DNA as homodimers.
- HNF1/TCF1/MODY3 (TCF1)
- HNF1/TCF2/MODY5 (TCF2)

## HNF3
The HNF3 subfamily members contain a winged helix DNA-binding domain and bind to DNA as monomers.
- HNF3/FOXA1 (forkhead box A1)
- HNF3/FOXA2 (forkhead box A2)
- HNF3/FOXA3 (forkhead box A3)

## HNF4
Members of the HNF4 subfamily are nuclear receptors and bind to DNA either as homodimers or RXR heterodimers.
- HNF4/TCF14/MODY1 (HNF4a)
- HNF4 (HNF4g)

## HNF6
The HNF6 subfamily members contain a cut-homeodomain (ONECUT) bind to DNA as monomers.
- HNF6/OC-1/ONECUT1  (ONECUT1)
- HNF6/OC-2/ONECUT2  (ONECUT2)
Herpesvirus entry mediator
Herpesvirus entry mediator (HVEM), also known as tumor necrosis factor receptor superfamily member 14 (TNFRSF14), is a human cell surface receptor of the TNF-receptor superfamily.

# Nomenclature
This protein was originally known as herpesvirus entry mediator A (HveA); HveB and HveC are structurally unrelated proteins of the immunoglobulin superfamily. It is also known as CD270 in the cluster of differentiation classification. Moreover, it is also referred to as ATAR (another TRAF-associated receptor).

# Function
The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor was identified as a cellular mediator of herpes simplex virus (HSV) entry. Binding of HSV viral envelope glycoprotein D (gD) to this receptor protein has been shown to be part of the viral entry mechanism. The cytoplasmic region of this receptor was found to bind to several TRAF family members, which may mediate the signal transduction pathways that activate the immune response.
In melanocytic cells TNFRSF14 gene expression may be regulated by MITF.

# Interactions
TNFRSF14 has been shown to interact with TRAF2, TNFSF14 and TRAF5.

# Clinical relevance
Mutations in this gene have been recurrently been associated to cases of diffuse large B-cell lymphoma.