Persius/hicric huggingface dataset:
Winchester syndrome
Synonyms and keywords: Torg-Winchester syndrome, Nodulosis-arthropathy-osteolysis syndrome, NAO syndrome, Torg syndrome

# Overview
Winchester syndrome in a rare congenital connective tissue disease.

# Historical perspective
It was first described in 1969.

# Pathophysiology
Winchester syndrome is an autosomal recessive connective tissue disorder caused by mutations in the matrix metalloproteinase 2 (MMP2) gene.  A 2006 study showed other mutations in the same gene, and observed that Winchester syndrome is probably part of a continuum that also includes Torg syndrome and nodulosis-arthropathy-osteolysis syndrome (NAO).

# Differentiating from other diseases
Winchester syndrome should be differentiated from rheumatoid arthritis.

# Diagnosis

## Symptoms
- Multiple, painless, subcutaneous nodules
- Pain due to fractures
- Vision problems
- Joint pains

## Physical examination

### Appearance of the patient
The characteristic features include short stature with coarse facial features.

### Head
Coarse face

### Eye
Opacities in the cornea

### Extremities
Marked contractures of joints

## Lab tests
Increased uronic acid was demonstrated in cultured fibroblasts from the skin and to a lesser degree in both parents. Despite initial tests not showing increased mucopolysaccharide excretion, the disease was regarded as a mucopolysaccharidosis.

## Imaging

### X-ray
- Dissolution of the carpal and tarsal bones (in the hands and feet respectively)
- Characteristic widening of the metacarpal and metatarsal bones
- Osteoporosis and bone thinning
Nabumetone overdose

# Overdose topics
Manifestations
Treatment
Long term effects

## Manifestations
Symptoms following acute NSAIDs overdoses are usually limited to lethargy, drowsiness,
nausea, vomiting, and epigastric pain, which are generally reversible with supportive care.
Gastrointestinal bleeding can occur. Hypertension, acute renal failure, respiratory depression, and
coma may occur, but are rare. Anaphylactoid reactions have been reported with therapeutic ingestion
-f NSAIDs, and may occur following an overdose. Return to top

## Treatment
Patients should be managed by symptomatic and supportive care following a NSAIDs
-verdose. There are no specific antidotes. Emesis and/or activated charcoal (60 to 100 grams in adults,
1 to 2 g/kg in children), and/or osmotic cathartic may be indicated in patients seen within 4 hours of
ingestion with symptoms or following a large overdose (5 to 10 times the usual dose). Forced diuresis,
alkalinization of urine, hemodialysis, or hemoperfusion may not be useful due to high protein binding. Return to top

## Long term effects
There have been overdoses of up to 25 grams of RELAFEN reported with no long-term
sequelae following standard emergency treatment (i.e., activated charcoal, gastric lavage, IV
H2-blockers, etc.). Return to top
Adapted from the FDA Package Insert.
Nefazodone overdose

# Overdosage topics
Human experience
- Pre-marketing clinical studies
- Post-marketing experience
Overdose management
- Monitoring patient
- Treatment
- Other considerations

## Human experience

### Pre-marketing clinical studies
In premarketing clinical studies, there were seven reports of Nefazodone overdose alone or in combination with other pharmacological agents. The amount of Nefazodone ingested ranged from 1000 mg to 11,200 mg. Commonly reported symptoms from overdose of Nefazodone included nausea, vomiting, and somnolence. One nonstudy participant took 2000 to 3000 mg of Nefazodone with methocarbamol and alcohol; this person reportedly experienced a convulsion (type not documented). None of these patients died. Return to top

### Post-marketing experience
In postmarketing experience, overdose with Nefazodone alone and in combination with alcohol and/or other substances has been reported. Commonly reported symptoms were similar to those reported from overdose in premarketing experience. While there have been rare reports of fatalities in patients taking overdoses of Nefazodone, predominantly in combination with alcohol and/or other substances, no causal relationship to Nefazodone has been established. Return to top

## Overdose management
Treatment should consist of those general measures employed in the management of overdosage with any antidepressant. Return to top

### Monitoring patient
Ensure an adequate airway, oxygenation, and ventilation. Monitor cardiac rhythm and vital signs. General supportive and symptomatic measures are also recommended. Induction of emesis is not recommended. Gastric lavage with a large-bore orogastric tube with appropriate airway protection, if needed, may be indicated if performed soon after ingestion, or in symptomatic patients. Return to top

### Treatment
Activated charcoal should be administered. Due to the wide distribution of Nefazodone in body tissues, forced diuresis, dialysis, hemoperfusion, and exchange transfusion are unlikely to be of benefit. No specific antidotes for Nefazodone are known. Return to top

### Other considerations
In managing overdosage, consider the possibility of multiple drug involvement. The physician should consider contacting a poison control center for additional information on the treatment of any overdose. Telephone numbers for certified poison control centers are listed in the Physicians Desk Reference (PDR). Return to top
Adapted from the FDA Package Insert.
Neoadjuvant therapy

# Overview
Neoadjuvant therapy is the administration of therapeutic agents before a main treatment. One example is neoadjuvant hormone therapy prior to radical radiotherapy for adenocarcinoma of the prostate. Neoadjuvant therapy aims to reduce the size or extent of the cancer before using radical treatment intervention, thus making procedures easier and more likely to succeed, and reducing the consequences of a more extensive treatment technique that would be required if the tumor wasn't reduced in size or extent.
Another related concept is that neoadjuvant therapy acts on micrometastatic disease. The downstaging is then a surrogate marker of efficacy on undetected dissemination, resulting in improved longtime survival compared to the surgery-alone strategy.
This systemic therapy (chemotherapy, immunotherapy or hormone therapy) or radiation therapy is commonly used in cancers that are locally advanced - where clinicians plan an operation at a later stage. The use of such therapy can effectively reduce the difficulty and morbidity of more extensive procedures.
The use of therapy can turn a tumour from untreatable to treatable by shrinking the volume down. Often it can be unclear which surrounding structures are directly involved in the disease and which are just showing signs of inflammation. By administering therapy a distinction can often be made. Some doctors give the therapy in the hope that a response will be seen so that they can then decide what is the best course of action. Unfortunately, not everyone is suitable for therapy in this way because it can be extremely toxic. Some patients react so severely that further treatments, especially surgery, are precluded because the patient is rendered unfit for anesthetic.

# See Also
- Adjuvant chemotherapy
Nepenthes boschiana
Nepenthes boschiana (after Johannes van den Bosch) is highland species of pitcher plant from Borneo. It is most closely related to N. faizaliana. N. borneensis is considered a synonym of this species.
N. boschiana has no known natural hybrids. No valid forms or varieties have been described.
B. H. Danser, in his 1928 monograph The Nepenthaceae of the Netherlands Indies, wrote the following:
Korthals states the natives who accompanied him on Mt. Sakoembang gathered the not yet opened pitchers, as the water which they contained was a medicament against inflammation of the eyes, whereas others cut the opened pitchers as playthings for their children. He describes the habitat as sterile, open and stony. The vernacular name 'daoen sompitan' is translated by him as blow-pipe-leaf; according to dictionaries this is right.
- Original illustration of N. boschiana from 1839 by Pieter Willem Korthals.
Original illustration of N. boschiana from 1839 by Pieter Willem Korthals.

# Infraspecific taxa
- Nepenthes boschiana var. lowii Hook.f. (1873) 
- Nepenthes boschiana var. sumatrana Miq. (1858)
Neural tube defects

# Overview
Normally, in human embryos, the closure of the neural tube occurs around the 30th day after fertilization. However, if something interferes and the tube fails to close properly, a neural tube defect will occur.
The incidence of neural tube defects is 2.6 in 1,000 worldwide.

# Causes
Pregnant women taking medication for epilepsy have a higher chance of having a child with a neural tube defect. Research has shown that women with folic acid deficiencies also have a higher chance of having a child with a neural tube defect, but this is only one factor. Taking folic acid does not completely negate the risk of neural tube problems, but it does significantly reduce the risk.

# Prevention
In Canada, mandatory fortification of selected foods with folic acid has been shown to reduce the incidence of neural tube defects by 46%.
Women who are or could become pregnant are advised to take daily supplements of folic acid, unless their dietary intake of this nutrient is normally high.

# Detection
Neural tube defects may be detected by a variety of methods, including some prenatal screening tests and medical imaging.  Often, these defects are apparent at birth, but occult defects may be not diagnosed until much later in life.

# Types of neural tube defects
- Anencephaly
- Encephalocele
- Spina bifida including myelomeningocele and others
Tachykinin peptides
Tachykinin peptides are one of the largest family of neuropeptides, found from amphibians to mammals.  They were so named due to their ability to rapidly induce contraction of gut tissue.  The tachykinin family is characterized by a common C-terminal sequence, Phe-X-Gly-Leu-Met-NH2, where X is either an Aromatic or an Aliphatic amino acid.  The genes that produce tachykinins encode precursor proteins called preprotachykinins, which are chopped apart into smaller peptides by posttranslational proteolytic processing.   The genes also code for multiple splice forms which are made up of different sets of peptides.
Tachykinins excite neurons, evoke behavioral responses, are potent vasodilators and contract (directly or indirectly) many smooth muscles. Tachykinins are from ten to twelve residues long.
The two human tachykinin genes are called TAC1 and TAC3 for historical reasons, and are equivalent to Tac1 and Tac2 of the mouse, respectively.
TAC1 encodes neurokinin A (formerly known as substance K), neuropeptide K (which has also been called neurokinin K), neuropeptide gamma, and substance P.  Alpha, beta, and gamma splice forms are produced; the alpha form lacks exon 6 and the gamma form lacks exon 4.  All three splice forms of TAC1 produce substance P, but only the beta and gamma forms produce the other three peptides.  Neuropeptide K and neuropeptide gamma are N-terminally longer versions of neurokinin A which appear to be final peptide products in some tissues.
TAC3 encodes neurokinin B.
The most notable tachykinin is Substance P.

# Receptors
There are three known mammalian tachykinin receptors termed NK1, NK2 and NK3. All are members of the 7 transmembrane g protein-coupled family of receptors and induce the activation of phospholipase C, producing inositol triphosphate. NK1, NK2 and NK3 selectively bind to substance P, neurokinin A and neurokinin B, respectively.  Whilst the receptors are not specific to any individual tachykinin, they do have differing affinity for the tachykinins:
- NK1: SP>NKA>NKB;
- NK2: NKA>NKB>SP;
- NK3: NKB>NKA>SP.
Antagonists of neurokinin-1 (NK1) receptors (NK1 receptor antagonists), through which substance P acts, have been proposed to belong to a new class of antidepressants,
 while NK2 antagonists have been proposed as anxiolytics and NK3 antagonists have been proposed as antipsychotics.
Tachykinin peptides are also involved in inflammation, and tachykinin receptor antagonists have been researched for use in treating inflammatory conditions such as asthma and irritable bowel syndrome.
 The main use for which these drugs have been applied so far however is as antiemetics, in both human and veterinary medicine.
Examples of tachykinin antagonists include;
- Aprepitant
- Casopitant
- Fosaprepitant
- Maropitant
- Nepadutant
- Osanetant
- Saredutant
- Talnetant

# Subfamilies
- Tachykinin InterPro: IPR008215
Neurorehabilitation
Neurorehabilitation is a complex medical process which aims to aid recovery from a nervous system injury, and to minimize and/or compensate for any functional alterations resulting from it.
In case of a serious disability, such as one caused by a severe spinal injury or brain damage, the patient and his/her families' abilities, life style and projects are suddenly shattered. In order to cope with this situation, the person and his/her family must establish and negotiate a "new way of living", both with their changed body and as a changed individual within a wider community.
Thus, neurorehabilitation works with the skills and attitudes of the disabled person and his/her family and friends. It promotes his/her skills to work at the highest level of independence possible for him/her. It also encourages him/her to rebuild self-esteem and a positive mood. Thus, he/she can adapt to the new situation and become empowered for successful and committed community reintegration.
Effective and high quality neurorehabilitation must be:
- Holistic It should cater for the physical, cognitive, psychological, social and cultural dimensions of the personality, stage of progress and lifestyle of both the patient and his/her family.
- Patient-focused Customized health care strategies should be developed, focused on the patient and his/her family.
- Inclusive Care plans should be designed and implemented by multidisciplinary teams made up of motivated practitioners being highly qualified and trained in multidisciplinary work.
- Participatory The patient and his/her family's active cooperation is a must. The patient and family must be well-informed, and must have a trusting relationship with the multidisciplinary team.
- Sparing Treatment must aim at empowering the patient to maximise independence, and to reduce physical impairment and reliance on mobility aids.
- Lifelong The patient's various needs throughout his/her life must be catered for, by ensuring continuity of care all the way through from injury onset to the highest possible level of recovery of function. This may include addressing medical complications of the injury or illness later in life.
- Resolving Treatment has to include adequate human and material resources for efficiently resolving each patient's problems as they arise.
- Community-focused. It is necessary to look for the solutions best adapted to the specific characteristics of the community and to further the creation of community resources favouring the best possible community reintegration of the disabled person.
Nevus depigmentosus
Synonyms and keywords: Nevus achromicus

# Overview
Nevus depigmentosus or nevus achromicus is a depigmentation problem in skin which can be easily differentiated from vitiligo. Although age factor has not much involvement in the nevus depigmentosus but in about 19% of the cases these are noted at birth. Their size may however grow in proportion to growth of the body. The distribution is also fairly stable and are nonprogressive hypopigmented patches. Those with nevus depigmentosus may be prone to sunburn due to the lack of pigment, and the patient should use good sun protection.
Sunscreen should be applied to all exposed skin, since reduced tanning of normal skin will decrease the contrast with hypopigmented skin. Most patients with nevus depigmentosus do not pursue treatment for their lesion. There is no way to repigment  the skin. If, however, the lesion is of cosmetic concern, camouflage makeup is effective. If the lesion is small one could also consider excision.

# Causes
- The exact cause of nevus depigmentosus is still not clearly understood. A sporadic defect in the embryonic development has been suggested to be a causative factor.
- It has been described as "localised albinism", though this is incorrect.

# Pathophysiology
- The hypopigmented spots in this disease result from abnormalities in the function of melanocytes which produce little pigment thereby resulting in white spots in skin.

# Differential Diagnosis
- Nevus depigmentosus must be differentiated from vitiligo.

# Physical Examination
- These are localized white spots on skin which may affect any area of the body, but these white spots are quite stable lesions. In the majority of patients, the lesions are not completely achromic, but are hypopigmented and resemble splashed paint.
- If there is hair in an affected area, it is usually colourless or white.
- The individual lesions found in nevus depigmentosus are permanent.

# Treatment
- There are no effective therapies for re-pigmenting this nevus.
- Different therapeutic modalities have been attempted to repigment the lesions of nevus depigmentosus such as PUVA (psoralen + UVA treatment), excimer laser, and different grafting techniques.
- PUVA therapy has not been shown to be beneficial.
- Successful repigmentation was reported in a single case with 14 sessions of excimer laser treatment.- Though the repigmentation of nevus depigmentosus is possible by grafting techniques, the results are inconsistent and recurrence is possible. In consideration of the experience of other authors and us, the quality and retention of pigment are unpredictable.
- These factors need to be considered while consulting and offering any treatment to the patient of nevus depigmentosus.

# Gallery
Image obtained from Dermatology Atlas
Nicotine stomatitis

# Overview
Nicotine stomatitis is an oral pathologic condition that appears in the hard palate of the mouth as a white lesion.  It is not considered to be premalignant and results from tobacco smoking (especially pipes or cigars) or long-term drinking of very hot beverages.  Nicotine stomatitis should not be confused with reverse smoker's palate, which is a severe form of palatal keratosis and caused from smoking a cigarette with the lit end inside the mouth.
The cause of nicotine stomatitis is from the palate being exposed to very hot conditions.  Pipe smoking produces more heat on the palate than any other form of smoking.  The frequency of this condition depends on a society's use of consuming hot beverages and of smoking in its various forms.  More commonly found in men over 45 years of age, it is characterized as a "fissured" or "dried mud" appearance from excess keratin production by cells.  The palate may appear gray or white and contain many papules that are slightly elevated with red in their center.  Furthermore, the teeth may be stained brown or black from tobacco smoke.
Microscopically, epithelial cells of the palate exhibit signs of hyperkeratosis and acanthosis.  There may be metaplasia of excretory ducts, which results in the visible papules if the ducts become hyperplastic.
There is usually no treatment since there is no increased risk of cancer.  Immediate cessation of smoking may be advised in order to monitor lesion.  Nicotine stomatitis should completely resolve on its own after 1 -2 weeks upon termination of smoking.  If the lesion persists, a biopsy may be done to confirm diagnosis.
Nin Jiom Pei Pa Koa
King-to Nin Jiom Pei Pa Koa () or more commonly, Nin Jiom Pei Pa Koa or simply Pei Pa Koa is a Traditional Chinese natural herbal remedy used for the relief of sore throat, coughs, hoarseness, and loss of voice. It is a throat demulcent and expectorant.  Today, it is manufactured and sold by Nin Jiom Medicine Manufactory Limited, a Hong Kong corporation.  It is available worldwide.
In the name of the company, "King-to" means "capital", referring to Beijing, and "Nin Jiom" means "in memory of my mother".  "Pei Pa Koa" means "Loquat syrup".

# History
The formula for Pei Pa Koa was originally created by Doctor Ip Tin-See, a physician for the Qing Dynasty .  Yang Xiao-Lian, a provincial commander, asked Doctor Ip to treat his mother's persistent cough.  They were so impressed that they created a factory to mass-produce it.  Later, the Yang family sold the business to Tse Sui-Bong, a medicine practitioner.  Nin Jiom Medicine Manufacturing was incorporated in 1962 to expand the business.
Today, Pei Pa Koa has annual sales of 45 million USD .

# Effectiveness
A study at the China Academy of Traditional Chinese Medicine published in a 1994 article, "Pharmacological studies of nin jion pei pa koa", indicated that Pei Pa Koa had significant effect on relieving coughs, removing sputum, relieving asthma in vivo and in vitro.

# Composition
Pei Pa Koa is made up of a blend of herbal ingredients including the fritillary bulb(chuan bei mu), loquat leaf(pi pa ye), ladybell root(nan sha shen), poria cocos(fu ling), pomelo peel(mao ju hong),chinese bellflower root(jie geng), pinellia rhizome(ban xia), schisandra chinensis seed(wu wei zi), trichosanthes seed(gua lou zi), coltsfoot flower (guan dong hua), thinleaf milkwort root(yuan zhi), bitter apricot kernel(ku xing ren), fresh ginger (shen jiang), licorice root(gan cao) in a syrup and honey base.
Ninein-like protein
Ninein-like protein is a protein that in humans is encoded by the NINL gene. It is part of the centrosome.

# Model organisms
Model organisms have been used in the study of NINL function. A conditional knockout mouse line, called Ninltm1a(EUCOMM)Wtsi was generated as part of the International Knockout Mouse Consortium program  a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists  at the Wellcome Trust Sanger Institute. Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.
Twenty five tests were carried out on mutant mice, however no significant abnormalities were observed.
Niobium(V) chloride
Niobium(V) chloride, also known as niobium pentachloride, is a yellow crystalline solid often used as a starting material in niobium chemistry. It is prepared by heating niobium metal in chlorine. It is often contaminated with small amounts of niobium(V) oxychloride, NbOCl3, formed by hydrolysis or from traces of oxygen during the preparation. NbCl5 may be purified by sublimation.

# Structure and properties
Niobium(V) chloride forms chloro-bridged dimers in the solid state (see figure). Each niobium centre is six-coordinate, but the octahedral coordination is significantly distorted. The niobiumchlorine bond lengths are 225 pm (terminal) and 256 pm (bridging), while the NbClNb angle at the bridge is 101.3. The NbNb distance is 395.1 pm, too long for any metal-metal interaction. NbBr5, TaCl5 and TaBr5 are isostructural with NbCl5, but NbI5 and TaI5 have different structures.

# Uses
Niobium(V) chloride is used in organic chemistry as a Lewis acid in activating alkenes for the carbonyl-ene reaction and the Diels-Alder reaction. Niobium chloride can also generate N-acyliminium compounds from certain pyrrolidines which are substrates for nucleophiles such as allyltrimethylsilane, indole, or the silyl enol ether of benzophenone.