Persius/hicric huggingface dataset:
Exosome (vesicle)
Exosomes are 50-90 nm vesicles secreted by a wide range of mammalian cell types. First discovered in maturing mammalian reticulocytes, they were shown to be a mechanism for selective removal of many plasma membrane proteins. These proteins are lost or reduced in amount, without concomitant degradation, during the maturation to the erythrocyte. Although the exosomal protein composition varies with the cell of origin, most exosomes contain the soluble protein Hsc 70. Certain immune cells, such as dendritic cells and B cells, secrete exosomes that many scientists believe play a functional role in mediating adaptive immune responses to pathogens and tumors.
An exosome is created intracellularly when a segment of the cell membrane spontaneously invaginates and is endocytosed. The internalized segment is broken into smaller vesicles that are subsequently expelled from the cell. The latter stage occurs when the late endosome, containing many small vesicles, fuses with the cell membrane, triggering the release of the vesicles from the cell. The vesicles (once released are called exosomes) consist of a lipid raft embedded with ligands common to the original cell membrane.
Exosomes from red cells contain the transferrin receptor which is absent in mature erythrocytes. Dendritic cell-derived exosomes express MHC I, MHC II, and costimulatory molecules. Exosomes derived from dendritic cells have proven to be able to induce and enhance antigen-specific T cell responses in vivo. In addition, the first exosome-based cancer vaccination platforms are being explored in early clinical trials.. Exosomes can also contain both functional mRNA and microRNA, which can be shuttled from one cell to another, affecting the recipient cell's protein production. This RNA is called "exosomal shuttle RNA" (esRNA; Valadi et al., Nat Cell Biol 2007 Jun;9(6):654-9).
Eye pain overview

# Overview
Pain in the may be described as a burning, throbbing or stabbing sensation in or around the eye. It can result from within the eye or from the structures around it. It can even be due to some other systemic problem or drugs used for other condition.
Severe pain in the eye may be an alarming symptom to seek medical help. The goal of the primary care physician in case of eye pain will be to assess whether it is an emergency or benign condition.
Pain can be due surface problems causing pain with every blink. It can even be due to the deep structures in the globe causing retrobulbar pain with movements of the eye.

## Pathophysiology
Eye pain is caused by the inflammation of layers of eye. It is carried to the brain by different nerves of eye and face. Incresaed intra ocular pressure also causes pain in the eye.

## Epidemiology and Demographics
There is no significant difference in occurrence of eye pain the population. It depends on the occurrence of different diseases in that population.

## Risk Factors
There are no specific risk factors for eye pain. Several conditions cause inflammation and infection of eye causing eye pain.

## Causes
There are multiple conditions which lead to eye pain. It is commonly confused with other symptoms like headache, sinus pain.
Common causes include: Blepharitis , Corneal abrasion, Conjunctivitis , Stye, Foreign bodies, Glaucoma , Uveitis, Optic neuritis and Sinusitis.

## Natural History, Prognosis and Complications
Progression of eye pain depends largely on the cause of the pain. Every cause has its own prognosis. The role of physician is to identify the cause and do the needful.

# Diagnosis

## History
There are certain important clues that can be obtained from history of the patients. Enquiry of patient certain things will help in accaurate diagnosis and treatment.

## Physical Examination
There are number of features we will observe in a painful eye depending upon the cause. various tests are performed to evaluate eye pain.Physical examination is very important in evaluation of cause and determining the prognosis. Several tests including opthalmoscopy, slit lamp examination, tonometry are done.

## Laboratory Tests
There are only few tests which help in prognosis of eye pain.

## Chest X Ray
This is a non specific test for eye pain. It is done only if associated respiratory symptoms are present.
Eyespot apparatus
The eyespot apparatus (or stigma) is a photoreceptive organelle found in the flagellate (motile) cells of green algae and other unicellular photosynthetic organisms such as euglenids. It allows the cells to sense light direction and intensity and respond to it by swimming either towards the light (phototaxis) or away from the light ("photoshock" or photophobic response). This helps the cells in finding an environment with optimal light conditions for photosynthesis. Eyespots are the simplest and most common "eyes" found in nature, composed of photoreceptors and a signal transduction system generating a phototactic response.

# Microscopic structure
Under the light microscope, eyespots appear as dark, often reddish, spots or stigmata. They get their color from the chromoproteins they contain, such as chlamyopsin, volvoxopsin or other photopigments.
The eyespot apparatus of Euglena comprises the paraflagellar body connecting the eyespot to the flagellum. In electron microscopy, the eyespot apparatus appears as a highly ordered lamellar structure formed by membranous rods in a helical arrangement.
In Chlamydomonas, the eyespot is part of the chloroplast and takes on the appearance of a membranous sandwich structure. It is assembled from chloroplast membranes (outer, inner, and thylakoid membranes) and carotenoid-filled granules overlaid by plasma membrane. It disassembles during cell division and reforms in the daughter cells in an asymmetric fashion in relation to the cytoskeleton.

# Eyespot proteins
The predominant eyespot proteins are the photoreceptor proteins that sense light. The photoreceptors found in unicellular organisms fall into two main groups: flavoproteins and retinylidene proteins (rhodopsins). Flavoproteins are characterized by containing flavin molecules as chromophores, whereas retinylidene proteins contain retinal. The photoreceptor protein in Euglena is likely a flavoprotein. In contrast, Chlamydomonas phototaxis is mediated by archaeal-type rhodopsins.
Besides photoreceptor proteins, eyespots contain a large number of structural, metabolic and signaling proteins. The eyespot proteome of Chlamydomonas cells consists of roughly 200 different proteins.

# Photoreception and signal transduction
The Euglena photoreceptor was identified as a blue-light-activated adenylyl cyclase. Excitation of this receptor protein results in the formation of cyclic adenosine monophosphate (cAMP) as a second messenger. Chemical signal transduction ultimately triggers changes in flagellar beat patterns and cell movement.
The archaeal-type rhodopsins of Chlamydomonas contain an all-trans retinylidene chromatophore which undergoes photoisomerization to a 13-cis isomer. This activates a photoreceptor channel, leading to a change in membrane potential and cellular calcium ion concentration. Photoelectric signal transduction ultimately triggers changes in flagellar strokes and thus cell movement.
Faidherbia albida
Faidherbia albida (syn. Acacia albida Delile) is a species of Faidherbia native to Africa and the Middle East, formerly widely included in the genus Acacia. It has also been introduced to India and Pakistan. Common names for it include Apple-ring Acacia, Ana Tree and Winter Thorn.
It is a thorny tree growing up to 630 m tall and 2 m in trunk diameter. Its deep-penetrating tap root makes it highly resistant to drought. The bark is grey, and fissured when old. There are 11000 seeds/kg. Faidherbia albida is not listed as being a threatened species.
It grows in areas with 250-600mm/yr. of rain.
Faiderbia albida is known in the Bambara language as "balanzan", and is the official tree of the city of Segou, on the Niger River in central Mali. According to legend, Segou is home to 4,444 "balanzan" trees, plus one mysterious "missing tree" the location of which cannot be identified.

# Cultivation and uses
Faidherbia albida is important for raising bees, since its flowers provide bee forage at the close of the rainy season, when most plants in the Sahel do not.
The seed pods are very important for raising livestock and are used as camel fodder in Nigeria.
Its wood is used for canoes, pestles, and for firewood. The wood has a density of about 560 kg/m3 at a water content of 12%. The energy value of the wood as fuel is 19.741 kJ/kg.
It is also used for nitrogen fixation, erosion control for crops, for food, drink and medicine. Unlike most other trees, it sheds its leaves in the rainy season; for this reason, it is highly valued in agroforestry as it can grow among field crops without shading them. It contains the psychoactive chemical compound dimethyltryptamine in its leaves.

## Medicinal uses
The tree has medicinal value for the treatment of infections such as those of the respiratory kind, also for malaria and fevers. It is useful in treating problems of the digestive system. The bark is employed in dental hygiene and its extract is employed in the treatment of toothache. The extract is also used to treat ocular infections in farm animals.
Fastigial nucleus
The nucleus fastigius is located in the cerebellum. It is made up of the nucleus dentatus, nucleus emboliformis, nucleus globosus, and nucleus fastigii, and is grey matter embedded in the white matter of the cerebellum.
The fastigial nucleus or nucleus fastigii refers specifically to the concentration of gray matter nearest to the middle line at the anterior end of the superior vermis, and immediately over the roof of the fourth ventricle, from which it is separated by a thin layer of white matter.  It is smaller than the nucleus dentatus, but somewhat larger than the nucleus emboliformis and nucleus globosus, the other two independent centers of gray matter in the cerebellum.
The fastigial nucleus receives its afferent input from the flocculonodular lobe and the vermis. Most of its efferent connections travel via the inferior cerebellar peduncle to the vestibular nuclei, which is located at the junction of the pons and medulla.
The fastigial nucleus deals with antigravity muscle groups and other synergies involved with standing and walking.
Fechtner syndrome
Fechtner syndrome, like the May-Hegglin anomaly (155100) and the Sebastian syndrome (605249) (2 giant-platelet disorders) are caused by allelic mutations in the gene encoding nonmuscle myosin heavy chain-9 (MYH9; 160775) on chromosome 22q.
The name of the syndrome is derived from teh surname of a family in which 8 members of 4 generations developed nephritis, deafness, congenital cataracts, macrothrombocytopenia, and leukocyte inclusions in various combinations.  The family differed from others reported, such as families with Epstein syndrome, in that their hematologic abnormalities included not only macrothrombocytopenia but also small, pale blue cytoplasmic inclusions in the neutrophils and eosinophils.  Deafness was high-tone sensorineural. Renal disease ranged from microscopic hematuria to end-stage renal failure necessitating dialysis and kidney transplantation. All affected adults had cataracts.
A second family was reported on by Gershoni-Baruch et al. in 1988 in which 16 members were affected.

# Diagnosis
The blood smear can show giant platelets which are the size of granulocytes. By light microscopy, there is the appearance of the inclusions that resemble that of toxic Dohle bodies and inclusions of May-Hegglin anomaly, but their ultrastructural appearance is unique.  In some patients, there is impaired liver function and hypercholesterolemia.

# Differentiation from Sebastian Syndrome
Sebastian platelet syndrome as an autosomal dominant disorder characterized by the same hematologic changes as those in the Fechtner syndrome but without the manifestations of Alport syndrome.
Because of the phenotypic similarities between May-Hegglin anomaly and Fechtner syndrome and the demonstration that the 2 disease loci are mapped to overlapping regions on chromosome 22, the May-Hegglin/Fechtner Syndrome Consortium (2000) suggested that they, as well as Sebastian syndrome, might be allelic. MYH9 was a strong candidate gene because it is located within that region of chromosome 22, is expressed in platelets, and is upregulated during granulocyte differentiation. The May-Hegglin/Fechtner Syndrome Consortium (2000) identified 6 MYH9 mutations (1 nonsense and 5 missense) in 7 unrelated probands from families with one or another of these 3 syndromes.
Feingold syndrome
Feingold syndrome (also called oculodigitoesophagoduodenal syndrome) is a rare autosomal dominant hereditary disorder. It is named after Murray Feingold, an American physician who first described the syndrome in 1975. Until 2003, at least 79 patients have been reported worldwide 

# Characteristics
Feingold syndrome is marked by various combinations of microcephaly, limb malformations, esophageal and duodenal atresias, and sometimes learning disability or mental retardation.

# Diagnosis and treatment
The diagnosis is based on the following clinical findings:
- microcephaly
- clinodactyly and shortness of index and little fingers
- syndactyly of 2nd & 3rd and 4th & 5th toe
- short palpebral fissures
- esophageal and/or duodenal atresia

# Genetic etiology
Feingold syndrome is caused by mutations in the neuroblastoma-derived V-myc avian myelocytomatosis viral-related oncogene (MYCN; OMIM 164840 ) which is located on the short arm of chromosome 2 (2p24.1).
Fetal fibronectin

# Overview
Fetal fibronectin (fFN) is a protein produced by fetal cells and a type of fibronectin. fFN is found at the interface of the chorion and the decidua (between the fetal sack and the uterine lining).
It can be thought of as an adhesive or "biological glue" that binds the fetal sack to the uterine lining.  It is an excellent biological marker of premature (preterm) delivery; a delivery before 37 weeks of gestation.
Fetal fibronectin "leaks" into the vagina if a preterm delivery is likely to occur and can be measured in a diagnostic test.  When the fFN test is considered positive, delivery is likely to occur soon.  When the fFN test is negative, it means that there is little if any danger of preterm labour for 7-10 days.  The test is easily performed.  A specimen is collected from the patient using a vaginal swab.  The swab is placed in a transport tube and sent to the lab for testing.  The lab can easily produce a test result in less than one hour.
A systematic review of the medical literature found that fetal fibronectin is a good predictor of spontaneous preterm birth before cervical dilation. The test may be run on patients between 22 and 35 weeks gestation.
Fetal malposition
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# Overview
Related Key Words and Synonyms:

# Epidemiology and Demographics

# Risk Factors

# Screening

# Pathophysiology & Etiology

# Molecular Biology

# Genetics

# Natural History

# Diagnosis

## Differential Diagnosis

## History and Symptoms

## Physical Examination

### Appearance of the Patient

### Vital Signs

### Skin

### Eyes

### Ear Nose and Throat

### Heart

### Lungs

### Abdomen

### Extremities

### Neurologic

### Other

## Laboratory Findings

### Electrolyte and Biomarker Studies

### Electrocardiogram

### Chest X Ray

### MRI and CT

### Echocardiography or Ultrasound

### Other Imaging Findings

## Other Diagnostic Studies

# Risk Stratification and Prognosis

# Treatment

## Pharmacotherapy

### Acute Pharmacotherapies

### Chronic Pharmacotherapies

## Surgery and Device Based Therapy

### Indications for Surgery

### Pre-Operative Assessment

### Post-Operative Management

### Transplantation

## Primary Prevention

## Secondary Prevention

## Cost-Effectiveness of Therapy

## Future or Investigational Therapies

# "The Way I Like To Do It ..." Tips and Tricks From Clinicians Around The World

## Suggested Revisions to the Current Guidelines
Fiber diffraction

# Overview
Fiber diffraction is a scattering technique in which molecular structure is determined from scattering data (usually of X-rays or electrons) from filaments composed of a regular array of molecules distinguished by a single direction (the fiber axis).
The resulting diffraction patterns show layer lines, each with Bessel function intensities.

# Historical role
Fiber diffraction data led to several important advances in the development of structural biology, e.g., the original models of the -helix and the Watson-Crick model of double-stranded DNA.
Thrombolytic drug

# Overview
Thrombolytic drugs are used in medicine to dissolve blood clots in a procedure termed thrombolysis. They limit the damage caused by the blockage of the blood vessel.

# Uses
Thrombolysis is used in for myocardial infarction (heart attack), ischemic strokes, deep vein thrombosis and pulmonary embolism to clear a blocked artery and avoid permanent damage to the perfused tissue (e.g. myocardium, brain, leg) and death. A less frequent use is to clear blocked catheters that are used in long-term medical therapy.
It should be noted that thrombolytic therapy in hemorrhagic strokes is contraindicated, as its use in that situation would prolong bleeding into the intracranial space and cause further damage.

# Members
The thrombolytic drugs include:
- t-PA (alteplase Activase)
- reteplase (Retavase)
- tenecteplase (TNKase)
- anistreplase (Eminase)
- streptokinase (Kabikinase, Streptase)
- urokinase (Abbokinase)
These drugs are most effective if administered immediately after it has been determined they are clinically appropriate. The advantage of administration is highest within the first ninety minutes, but may extend up to six hours after the start of symptoms.
The drugs are often given in combination with intravenous heparin, or low molecular weight heparin, which are anticoagulant drugs.

# Side-effects
Hemorrhagic stroke is a rare but serious complication of thrombolytic therapy. If a patient has had thrombolysis before, an allergy against the thrombolytic drug may have developed (especially after streptokinase). If the symptoms are mild, the infusion is stopped and the patient is commenced on an antihistamine before infusion is recommenced. Anaphylaxis generally requires immediate cessation of thrombolysis.
First pass effect
The first-pass effect (or first-pass metabolism) is a phenomenon of drug metabolism whereby the concentration of a drug is greatly reduced before it reaches the systemic circulation.
After a drug is swallowed, it is absorbed by the digestive system and enters the hepatic portal system. It is carried through the portal vein into the liver before it reaches the rest of the body. The liver metabolizes many drugs, sometimes to such an extent that only a small amount of active drug emerges from the liver to the rest of the circulatory system. This first pass through the liver thus greatly reduces the bioavailability of the drug. Alternative routes of administration like intravenous, intramuscular, and sublingual avoid the first-pass effect because they allow drugs to be absorbed directly into the systemic circulation.
The four primary systems that affect the first pass effect of a drug are the enzymes of the gastrointestinal lumen, gut wall enzymes, bacterial enzymes, and hepatic enzymes.
Flaccid paralysis
Flaccid paralysis is a clinical manifestation characterized by weakness or paralysis and reduced muscle tone without other obvious cause (e.g., trauma).

# Causes

## Polio
The term acute flaccid paralysis (AFP) is often used to describe a sudden onset, as might be found with polio.
AFP is the most common sign of acute polio, and used for surveillance during polio outbreaks. AFP is also associated with a number of other pathogenic agents including enteroviruses, echoviruses, and adenoviruses, among others.

## Botulism
The Clostridium botulinum bacteria are the cause of botulism.  Vegetative cells of C. botulinum may be injested. Introduction of the bacteria may also occur via endospores in a wound.  When the bacteria is in vivo they induce flaccid paralysis.  This happens because C. botulinum produces a toxin which blocks the release of acetylcholine.  When this occurs, the muscles are unable to contract.

## Other
Flaccid paralysis can be associated with a lower motor neuron lesion. This is in contrast to a upper motor neuron lesion, which often presents with spastic paralysis.
Included in AFP,s list are Poliomyelitis, Transverse myelitis, Guillain-Barre syndrome, enteroviral encephalopathy , traumatic neuritis etc.
An AFP Surveillance program is conducted to increase case yield of poliomyelitis. This includes collection of  2 stool samples within 14 days of onset of paralysis and identification of virus. and control of the outbreak and strengthening immunization in that area.

# Differential diagnosis
Flap endonuclease
Flap endonucleases (FENs, also known as 5' nucleases in older references) are a class of nucleolytic enzymes that act as both 5'-3' exonucleases and structure specific endonucleases on specialised DNA structures that occur during the biological processes of DNA replication, DNA repair and DNA recombination. Flap endonucleases have been identified in eukaryotes, prokaryotes, archaea and some viruses. Organisms can have more than one FEN homologue, this redundancy may give an indication of the importance of these enzymes. In prokaryotes, the FEN enzyme is found as an N-terminal domain of DNA polymerase I, but some prokaryotes appear to encode a second homologue. 
The endonuclease activity of FENs was initially identifed as acting on a DNA duplex which has a single stranded 5' overhang on one of the strands (termed a "5' flap", hence the name flap endonuclease). FENs catalyse hydrolytic cleavage of the phosphodiester bond at the junction of single and double stranded DNA. FENs can also act as 5'-3' exonucleases on the 5' terminus of the the flap strand and on 'nicked' DNA substrates.
Protein structure models based on X-ray crystallography data suggest that FENs have a flexible arch created by two -helices through which the single 5' strand of the 5' flap structure can thread .
Flap endonucleases have been used in biotechnology, for example the Taqman PCR assay  and the Invader single nucleotide polymorphism (SNP) assay .
For a more detailed reviews of FENs see  
-   Sayers (1994) J Theor Biol, 170, 415
-   Harrington and Lieber (1994) EMBO J., 13, 1235-1246
-   Ceska et al., (1996) Nature, 382, 90-93
-   Olivier (2005) Mutat. Res. 573, 103-110
-   Liu et al., (2004) Annu. Rev. Biochem., 73, 589-615
-   Ceska and Sayers, (1998) Trends Biochem. Sci., 23, 331-336