Persius/hicric huggingface dataset:
Cross-cultural psychiatry

# Overview
Cross-cultural psychiatry is a branch of psychiatry concerned with the cultural and ethnic context of mental disorder and psychiatric services. It emerged as a coherent field from several strands of work, including surveys of the prevalence and form of disorders in different cultures or countries; the study of migrant populations and ethnic diversity within countries; and analysis of psychiatry itself as a cultural product. The early literature was associated with colonialism and with either sidelining or denigrating different cultures or ethnic groups. A seminal paper by Arthur Kleinman in 1977 followed by a renewed dialogue between anthropology and psychiatry, is seen as having heralded a 'new cross-cultural psychiatry'.
It is argued that a cultural perspective can help psychiatrists become aware of the hidden assumptions and limitations of current psychiatric theory and practice and can identify new approaches appropriate for treating the increasingly diverse populations seen in psychiatric services around the world
The field has, ironically, increasingly had to address the process of globalization.
It is said every city has a different culture and that the urban environment, and how people adapt or struggle to adapt to it, can play a crucial role in the onset or worsening of mental illness.
Cross-cultural psychiatry looks at whether psychiatric classifications of disorders are appropriate to different cultures or ethnic groups. It often argues that psychiatric illnesses represent social constructs as well as genuine medical conditions, and as such have social uses peculiar to the social groups in which they are created and legitimized. It studies psychiatric classifications in different cultures, whether informal (e.g category terms used in different languages) or formal (for example the World Health Organisation's ICD, the American Psychiatric Association's DSM, or the Chinese Society of Psychiatry's CCMD
Culprit artery planimetry

# Definition
A drawing and measurement method made at end diastole at each time point down the middle of the contrast filled culprit native artery. However, for grafts, the QCA should be performed at end systole and not at end diastole like for native artery segments.
The catheter should be replicated on the drawing, and the following landmarks should be noted: the catheter tip/origin of the culprit artery, the start & end of the lesion Length, the distal TIMI landmark, and the very end of the artery.
Planimetered Length to Lesion (no branches): Planimetered length from catheter tip to the start of the lesion. If the culprit artery is the circumflex, the length of the Left Main should also be measured.
Planimetered Length from Lesion to Landmark: Planimetered length from the end of the lesion to the distal TIMI landmark.
Planimetered Length from Lesion to Very End of Artery: Planimetered length from the end of the lesion to the most distal segment of artery (if visible).
Complete Assessment of Vessel Length: It should be marked if the Planimetered Length from Lesion to Very End of Artery is assessable.
Cyclin-dependent kinase 9
Cyclin-dependent kinase 9 or CDK9 is a cyclin-dependent kinase associated with P-TEFb.

# Function
The protein encoded by this gene is a member of the cyclin-dependent kinase (CDK) family. CDK family members are highly similar to the gene products of S. cerevisiae cdc28, and S. pombe cdc2, and known as important cell cycle regulators. This kinase was found to be a component of the multiprotein complex TAK/P-TEFb, which is an elongation factor for RNA polymerase II-directed transcription and functions by phosphorylating the C-terminal domain of the largest subunit of RNA polymerase II. This protein forms a complex with and is regulated by its regulatory subunit cyclin T or cyclin K. HIV-1 Tat protein was found to interact with this protein and cyclin T, which suggested a possible involvement of this protein in AIDS.
CDK9 is also known to associate with other proteins such as TRAF2, and be involved in differentiation of skeletal muscle.

# Interactions
CDK9 has been shown to interact with:
- Androgen receptor,
- CDC34 and
- CCNK,
- CCNT1,
- CCNT2,
- MYBL2,
- RELA,
- RB1,
- SKP1A,  and
- SUPT5H.
Cytokine release syndrome
Cytokine Release syndrome is a common immediate complication occurring with the use of anti-T cell antibody infusions such as ATG, OKT3 and TGN1412. Severe cases are known as  cytokine storms.
The pathogenesis is that the antibodies bind to the T cell receptor, activating the T cells before they are destroyed. The cytokines released by the activated T cells produce a type of systemic inflammatory response similar to that found in severe infection characterised by hypotension, pyrexia and rigors. The patient feels very unwell, as if in a high fever  indeed, the cytokine release syndrome is effectively a type of non-infective fever.
Deaths due to cytokine release syndrome with OKT3 have been reported, and it can cause life-threatening pulmonary oedema if the patient is fluid overloaded. However, if treated appropriately it is usually not dangerous, just extremely unpleasant for the patient.
The effect is greatly reduced by intravenous administration of an anti-histamine (such as chlorphenamine) and a corticosteroid (such as hydrocortisone) prior to starting the ATG/OKT3 infusion, with further doses of anti-histamine and steroid given during the infusion if necessary.

# Causes
- Drugs
- Blinatumomab
Dapsone adverse reactions

# Adverse Reactions
In addition to the warnings listed above, the following syndromes and serious reactions have been reported in patients on Dapsone.

## Hematologic Effects
Dose-related hemolysis is the most common adverse effect and is seen in patients with or without G6PD deficiency. Almost all patients demonstrate the inter-related changes of a loss of 1-2g of hemoglobin, an increase in the reticulocytes (2-12%), a shortened red cell life span and a rise in methemoglobin. G6PD deficient patients have greater responses.

## Nervous System Effects
Peripheral neuropathy is a definite but unusual complication of Dapsone therapy in non-leprosy patients. Motor loss is predominant. If muscle weakness appears, Dapsone should be withdrawn. Recovery on withdrawal is usually substantially complete. The mechanism of recovery is reported by axonal regeneration. Some recovered patients have tolerated retreatment at reduced dosage. In leprosy this complication may be difficult to distinguish from a leprosy reactional state.

## Body As A Whole
In addition to the warnings and adverse effects reported above, additional adverse reactions include: nausea, vomiting, abdominal pains, pancreatitis, vertigo, blurred vision, tinnitus, insomnia, fever, headache, psychosis, phototoxicity, pulmonary eosinophilia, tachycardia, albuminuria, the nephrotic syndrome, hypoalbuminemia without proteinuria, renal papillary necrosis, male infertility, drug-induced Lupus erythematosus and an infectious mononucleosis-like syndrome. In general, with the exception of the complications of severe anoxia from overdosage (retinal and optic nerve damage, etc.) these adverse reactions have regressed off drug.
Dawn-Marie Wesley suicide

# Background
Dawn-Marie Wesley, 14, from Mission, British Columbia, Canada, was a student who committed suicide on 10 November 2000, after experiencing a cycle of bullying by psychological abuse and verbal threats from three bullies.
She left behind a note to her family that referred to the bullying to which she had been subjected: "If I try to get help, it will get worse. They are always looking for a new person to beat up and they are the toughest girls. If I ratted, they would get suspended and there would be no stopping them. I love you all so much."

# Incident
At the age of 14, Dawn-Marie Wesley committed suicide after experiencing a cycle of psychological abuse and verbal threats ("bullying") from three friends. In her suicide note, Dawn-Marie named three girls, initiating a Canadian police investigation and court case where the three defendants were made to stand trial for their actions.

# Legal Proceedings
One of the defendants was acquitted, the other two were convicted.  B.C. Provincial Court Judge Jill Rounthwait's ruling stated that it was clear that one of the accused had bullied Wesley repeatedly thus giving the victim reason to fear for her life.  Rounthwaite also stated that bystanders added "to the power of the bully" by letting the harassment continue without intervention.

# See Also
- List of people who died due to bullying
- Rats & Bullies : The Dawn-Marie Wesley Story
Decay-accelerating factor
Complement decay-accelerating factor, also known as CD55 or DAF, is a protein that, in humans, is encoded by the CD55 gene.
DAF regulates the complement system on the cell surface. It recognizes C4b and C3b fragments that are created during activation of C4 (classical or lectin pathway) or C3 (alternative pathway). Interaction of DAF with cell-associated C4b of the classical and lectin pathways interferes with the conversion of C2 to C2b, thereby preventing formation of the C4b2b C3-convertase, and interaction of DAF with C3b of the alternative pathway interferes with the conversion of factor B to Bb by factor D, thereby preventing formation of the C3bBb C3 convertase of the alternative pathway. Thus, by limiting the amplification convertases of the complement
cascade, DAF indirectly blocks the formation of the membrane attack complex.
This glycoprotein is broadly distributed among hematopoietic and non-hematopoietic cells. It is a determinant for the Cromer blood group system.

# Structure
DAF is a 70 kDa membrane protein that attaches to cell membrane via a glycophosphatidylinositol (GPI) anchor.
DAF contains four complement control protein (CCP) repeats with a single N-linked glycan positioned between CCP1 and CCP2. CCP2, CCP3, CCP4 and three consecutive lysine residues in a positively charged pocket between CCP2 and CCP3 are involved in its inhibition of the alternate complement pathway. CCP2 and CCP3 alone are involved in its inhibition of the classical pathway.

# Pathology

## Paroxysmal nocturnal hemoglobinuria
Because DAF is a GPI-anchored protein, its expression is reduced in persons with mutations that reduce GPI levels such as those with paroxysmal nocturnal hemoglobinuria; in that disorder, red blood cells with very low levels of DAF and CD59 undergo complement-mediated hemolysis.

## Infectious diseases
DAF is used as a receptor by some coxsackieviruses and other enteroviruses. Recombinant soluble DAF-Fc has been tested in mice as an anti-enterovirus therapy for heart damage; however, the human enterovirus that was tested binds much more strongly to human DAF than to mouse or rat DAF. Echoviruses and coxsackie B viruses that use human decay-accelerating factor (DAF) as a receptor do not bind the rodent analogues of DAF. and DAF-Fc has yet to be tested in humans.
Deep cervical lymph nodes
The deep cervical lymph nodes are a group of cervical lymph nodes found near the internal jugular vein.
They can be divided into upper and lower groups, or superior and inferior groups.
Alternatively, they can be divided into deep anterior cervical lymph nodes and deep lateral cervical lymph nodes.
They can also be divided into three groups: "superior deep jugular", "middle deep jugular", and "inferior deep jugular".
Delayed Auditory Feedback

# Background
Delayed auditory feedback (DAF), is a device that enables a user of the device to speak into a microphone and then hears his or her voice in headphones a fraction of a second later. Some DAF devices are hardware; DAF computer software is also available.
The DAF machine is a proven technique to aid with stuttering.  When the DAF delay is short, (25 to 75 milliseconds, or about a twentieth of a second), this immediately reduces stuttering about 70%. A longer delay (75 to 200 milliseconds, or about tenth of a second) produces a greater increase in fluency, however it also causes significant reductions in rate of speech and stretched vowels. The longer delay is generally used in therapy settings. Some DAF devices have been found to produce carryover fluency, that is, to train a stutterer to no longer need the device.
DAF usage (with a 175 millisecond delay) has been proven to induce mental stress.
The DAF machine has also been claimed to be helpful with cluttering.  The DAF machine reduces the rate of a clutterer, and thus reduces the cluttering disfluencies.
Dentinogenesis imperfecta
Dentinogenesis imperfecta (hereditary Opalescent Dentin)  is a genetic disorder of tooth development. This condition causes teeth to be discolored (most often a blue-gray or yellow-brown color) and translucent. Teeth are also weaker than normal, making them prone to rapid wear, breakage, and loss. These problems can affect both primary (baby) teeth and permanent teeth. This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. Dentinogenesis imperfecta affects an estimated 1 in 6,000 to 8,000 people.
Researchers have described three types of dentinogenesis imperfecta with similar dental abnormalities.
Type I: Occurs in people who have osteogenesis imperfecta, a genetic condition in which bones are brittle and easily broken.It is usually an autosomal dominant trait with variable expressivity but can be recessive if the associated osteogenesis imperfecta is of recessive type.
Type II : Occurs in people without other inherited disorders ie Osteogenesis imperfecta.It is an autosomal dominant trait and is in fact on of the most common autosomal dominant disorders in human beings.  A few families with type II have progressive hearing loss in addition to dental abnormalities.
Type III dentinogenesis imperfecta was first identified in a population from Brandywine, Maryland. Researchers now believe that type II and type III may be the same disorder.
Mutations in the DSPP gene have been identified in people with type II and type III dentinogenesis imperfecta. Type I occurs as part of osteogenesis imperfecta, which is caused by mutations in one of several other genes. The DSPP gene provides instructions for making three proteins that are essential for normal tooth development. These proteins are involved in the formation of dentin, which is a bone-like substance that makes up the protective middle layer of each tooth. Mutations in the DSPP gene may affect the proteins made by the gene, leading to the production of abnormally soft dentin. Teeth with defective dentin are discolored, weak, and more likely to decay and break. It remains unclear how DSPP mutations lead to hearing loss in some families with dentinogenesis type II.
Clinical Features
Clinical appearance is variable.However, the teeth usually involved and more severely affected are deciduous teeth in type 1; whereas in type 2 both the dentitions are equally affected.
The teeth may be gray to yellowish brown. They exhibit transluscent or opalescent hue.Enamel is usually lost early due to loss of scalloping at DEJ. The teeth however are not more susceptible to dental caries than normal ones.
Radiographic Features'
Type 1 and 2 show total obliteration of dentin and pulp chamber.
Type 3 shows thin dentin and extremely enormous pulp chamber.These teeth are usually known as Shell Teeth.
Histology
Dentinal tubules are irregular and are bigger in diameter. Areasof uncalcified matrix are seen.Sometimes odontoblasts are seen in dentin.
This article incorporates public domain text from The U.S. National Library of Medicine
hu:Dentinogenesis imperfecta
Dermatophilus congolensis
Dermatophilus congolensis is a gram positive bacterium and is the etiologic agent of a disease called Dermatophilosis (sometimes called Mud fever) in animals and humans, a dermatologic condition that manifests itself with the formation of crusty scabs that contain the microorganism. Some people erroneously call it mycotic dermatitis.

# Morphology
D.  congolensis is facultative anaerobic actinomycete bacteria. It has two morphologic forms: filamentous hyphae and motile zoospores. The hyphae are characterized by branching filaments (1-5 m in diameter) that ultimately fragment by both transverse and longitudinal septation into packets of coccoid cells. The coccoid cells mature into flagellated ovoid zoospores (0.6-1 m in diameter).With the microscope one can observe the characteristic "tramcar line"-like D. congolensis colonies together with gram positive thin filaments and coccoid forms.

# Cultivation
D. congolensis is a carboxiphylic germ, so they need carbon dioxide to properly grow on laboratory mediums. The germ grows well on sheep-blood enriched agarose mediums; the mediums must then be incubated at a 37 degrees Celsius temperature and a 5-10% CO2 atmosphere. The bacteriae colonies become visible in 24-48 hours. Initially they are small, with a ~1mm diameter and with a grey-yellow colour. After 3-4 days the isolated bacterial colonies can reach a 3mm diameter, they have a rough surface and a yellow-golden pigmentation. Around the colonies circular hemolysis zones can be seen.

# Pathogenesis
D. congolensis causes severe skin infections in animals and humans. More frequently cattle, horses, sheep and goats are affected. Humans can also get this skin disease if elementary hygene measures are not respected after dealing with infected animals. This dermatologic condition is known by many names: streptotrichosis, "rain-scald", "lampy wool", "strawberry foot rot".
The pathogenic factors are very diverse, but the most important ones are the ones of enzymatic nature (adenase and lecitinase).
Desert hedgehog (protein)
Desert hedgehog, also Desert hedgehog homolog or Dhh, is a protein encoded by the DHH gene, and is a member of the hedgehog signaling pathway. The human homolog (DHH) is on chromosome band 12q13.1.  The protein encoded by this gene is involved in cell signaling. The several mammalian variants of the Drosophila hedgehog gene (which was the first named) have been named after the various species of hedgehog; the desert hedgehog is honored by this one. The gene is not specific to desert hedgehogs.

# Function
This gene encodes a member of the hedgehog family. The hedgehog gene family encodes signaling molecules that play an important role in regulating morphogenesis. This protein is predicted to be made as a precursor that is autocatalytically cleaved; the N-terminal portion is soluble and contains the signalling activity while the C-terminal portion is involved in precursor processing. More importantly, the C-terminal product covalently attaches a cholesterol moiety to the N-terminal product, restricting the N-terminal product to the cell surface and preventing it from freely diffusing throughout the organism. Defects in this protein have been associated with partial gonadal dysgenesis (PGD) accompanied by minifascicular polyneuropathy. This protein may be involved in both male gonadal differentiation and perineurial development.

# Clinical Significance
Defects in this protein have been associated with partial gonadal dysgenesis (PGD) accompanied by minifascicular polyneuropathy. This protein may be involved in both male gonadal differentiation and perineurial development.
Diabetes and testosterone
In a recent study, it was found that diabetic men over 45 have more than twice the risk of having hypogonadism (in men, reduced or absent secretion of testosterone).
The study included 474 diabetic men from a screening of over 2,000. This is the largest study to date. Previous studies in this area have been much smaller, with 19, 163, 227 subjects.
Over half the diabetic men in the study with low testosterone reported a decreased ability to perform sexually. It should be noted that testosterone is important to general health and not only related to sexual drive or ability.
Dr. Sherwyn Schwartz, director of the Diabetes & Glandular Disease Clinic in San Antonio, Texas, and diabetes investigator is quoted as saying "Too many times people with diabetes have gotten the short end of the deal."

# External resources
- Reuters: Diabetic men at risk of low testosterone - study
- Long-Term Pharmacokinetics of Transdermal Testosterone Gel in Hypogonadal Men
- Long-Term Testosterone Gel (AndroGel) Treatment Maintains Beneficial Effects on Sexual Function and Mood, Lean and Fat Mass, and Bone Mineral Density in Hypogonadal Men
Diabetes mellitus surgery

# Overview
Type 2 diabetes can be cured by one type of gastric bypass surgery in 80-100% of severely obese patients. The effect is not due to weight loss because it usually occurs within days of surgery, which is before significant weight loss occurs. The pattern of secretion of gastrointestinal hormones is changed by the bypass and removal of the duodenum and proximal jejunum, which together form the upper (proximal) part of the small intestine. One hypothesis is that the proximal small intestine is dysfunctional in type 2 diabetes; its removal eliminates the source of an unknown hormone that contributes to insulin resistance. This surgery has been widely performed on morbidly obese patients and has the benefit of reducing the death rate from all causes by up to 40%. A small number of normal to moderately obese patients with type 2 diabetes have successfully undergone similar operations.

# Type 1 Diabetes Through the Life Span: A Position Statement of the American Diabetes Association 2014 recommendations of Beta cell replacement therapy
- Consider solid organ pancreas transplantation simultaneously with kidney transplantation in patients with type 1 diabetes who have an indication for kidney transplantation and are poorly controlled with large glycemic excursions. (B)
- Consider solid organ pancreas transplantation after kidney transplantation in adult patients with type 1 diabetes who have already received a kidney transplant. (C)
- Judiciously consider solid organ pancreas transplantation alone in adults with type 1 diabetes, unstable glucose control, hypoglycemia unawareness, and an increased risk of diabetes-related mortality, who have attempted all of the more traditional approaches to glycemic control and have remained unsuccessful, yet are judged responsible enough to manage the antirejection medication regimen, risks, and follow-up required with an organ transplant. (C)
- Consider referral to research centers for protocolized islet cell transplantation in patients with type 1 diabetes and debilitating complications of diabetes who are interested in research possibilities and fit the criteria for the research protocol. (E)

# 2013 American Diabetes Association Standards of Medical Care in Diabetes (DO NOT EDIT)

## Bariatric Surgery