Night sweats may happen because the sleep environment is too warm, either because the bedroom is unusually hot or because there are too many covers on the bed. [2] Night sweats have been associated with a long list of clinical conditions. [5] However, there is very little evidence that supports clinical recommendations for this condition. [5] Associated conditions [ edit ] The condition may be a sign of various disease states, including but not exclusive to the following: Cancers Lymphoma [6] [7] Leukemia [6] [7] Infections HIV/AIDS [6] [8] Tuberculosis [6] [7] Mycobacterium avium-intracellulare infection [6] Infectious mononucleosis [6] Fungal infections ( histoplasmosis , coccidioidomycosis ) [6] Lung abscess [6] Infective endocarditis [6] Brucellosis [9] Pneumocystis pneumonia (most often - in immunocompromised individuals) Endocrine disorders Menopause [10] Premature ovarian failure [6] Hyperthyroidism [6] Diabetes mellitus ( nocturnal hypoglycemia ) [6] Endocrine tumors ( pheochromocytoma , carcinoid ) [6] Orchiectomy [6] Rheumatic disorders Takayasu's arteritis [6] Temporal arteritis [6] Other Obstructive sleep apnea [6] Gastroesophageal reflux disease [6] Chronic fatigue syndrome [6] Fibromyalgia Granulomatous disease [6] Chronic eosinophilic pneumonia [6] Lymphoid hyperplasia [6] Diabetes insipidus [6] Prinzmetal's angina [6] Anxiety [6] Pregnancy [6] Drugs Antipyretics ( salicylates , acetaminophen ) [6] Antihypertensives [6] Anabolic–androgenic steroids , in particular trenbolone , and the nandrolones [6] Dinitrophenol - a common side effect Phenothiazines [6] Drug withdrawal: ethanol , benzodiazepines , heroin (and other opioids ), Over- bundling [6] Autonomic over-activity [6] Inflammatory bowel disease (IBD) - Crohn's disease / ulcerative colitis References [ edit ] ^ "Hyperhidrosis - MeSH - NCBI" . www.ncbi.nlm.nih.gov . ... Journal of Mid-Life Health . 10 (1): 6–13. doi : 10.4103/jmh.JMH_7_19 . ISSN 0976-7800 . ... Journal of the American Board of Family Medicine: JABFM . 25 (6): 878–893. doi : 10.3122/jabfm.2012.06.120033 . ... In a page: Pediatric signs & symptoms . Lippincott Williams & Wilkins. p. 6. ISBN 978-1-4051-0427-2 . ^ Tao Le; Vikas Bhushan (2006). ... Archives of Women's Mental Health . 10 (6): 247–257. doi : 10.1007/s00737-007-0209-5 .

Since the first isolation of human herpesvirus-6 (HHV-6) by Salahuddin et al. (1986), widespread infection by this virus has become apparent. As with other herpesviruses, HHV-6 remains latent in the host after primary infection. Transmission of HHV-6 via the saliva from mother to infant is thought to be the most common route. ... Bandobashi et al. (1997) reported the case of a woman with HHV-6-infected Burkitt lymphoma (113970). ... The patient's asymptomatic husband also carried HHV-6 DNA integrated at 1q44. To assess the possibility of chromosomal transmission of HHV-6 DNA, Daibata et al. (1999) looked for HHV-6 DNA in the peripheral blood of the couple's daughter.

Retrieved 2019-12-02 . ^ a b Stover, Patrick J; Field, Martha S (2015). "Vitamin B-6" . Advances in Nutrition . 6 (1): 132–133. doi : 10.3945/an.113.005207 . ... "Dispelling the Myths of Vitamin B 6 " (PDF) . Nutrition Bytes . 1 (1). ... Journal of Applied Toxicology . 24 (6): 497–500. doi : 10.1002/jat.1007 . ... J.; Bast, A.; Haenen GRMM (2017). "The vitamin B 6 paradox: Supplementation with high concentrations of pyridoxine leads to decreased vitamin B 6 function". ... European Food Safety Authority (EFSA). 2006. pp. 29–44. ISBN 978-92-9199-014-6 . Archived from the original (PDF) on 2019-04-12. ^ "Vitamin B 6 " .

[6] [8] Causes Ciliopathic or chromosomal genetic conditions, often not identified [5] Diagnostic method MRI , prenatal ultrasound or CT [6] Differential diagnosis Blake's pouch cyst (BPC), [3] [8] mega cisterna magna(?) ... However, later studies found that these foramina are usually open in DWM. [6] Hydrocephalus is also usually (80% of the time) not present at birth in those with DWM. [6] The impairment to CSF flow may lie beyond the outlets of the fourth ventricle. ... American Journal of Roentgenology . 153 (6): 1289–1300. doi : 10.2214/ajr.153.6.1289 . ... American Journal of Diseases of Children . VIII (6): 406–482. doi : 10.1001/archpedi.1914.02180010416002 . ... European Journal of Pediatric Surgery . 12 (6): 366–374. doi : 10.1055/s-2002-36849 .

6-phosphogluconate dehydrogenase deficiency Crystallographic structure of sheep 6-phosphogluconate dehydrogenase complexed with adenosine 2'-monophosphate [1] 6-phosphogluconate dehydrogenase Identifiers Symbol 6PGD Pfam PF00393 Pfam clan CL0106 InterPro IPR006114 PROSITE PDOC00390 SCOP2 2pgd / SCOPe / SUPFAM Available protein structures: Pfam structures / ECOD PDB RCSB PDB ; PDBe ; PDBj PDBsum structure summary 6-Phosphogluconate dehydrogenase deficiency ( 6PGD deficiency ), or partial deficiency, is an autosomal hereditary disease characterized by abnormally low levels of 6-phosphogluconate dehydrogenase (6PGD), a metabolic enzyme involved in the Pentose phosphate pathway . ... Pathophysiology [ edit ] Pentose phosphate pathway with a breakdown in the conversion of 6-phosphogluconate dehydrogenase to ribulose-5-phosphate due to a deficiency of 6-phosphogluconate dehydrogenase enzyme Reaction mechanism [ edit ] 6-Phosphogluconate dehydrogenase (6PGD) is an enzyme in the pentose phosphate pathway (see image). 6PGD catalyzes the reaction of 6-phosphogluconate to an unstable form of 3-keto-6-phosphogluconate, and yields a co-enzyme nicotinamide adenine dinucleotide phosphate (NADPH) as a byproduct. ... The reaction is the second NADPH releasing reaction in the pentose phosphate pathway, the first being catalyzed by glucose-6-phosphate dehydrogenase. 3-keto-6-phosphogluconate then rapidly (in an irreversible reaction) decarboxylates to CO 2 and ribulose-5-phosphate , which is the precursor to many vital metabolic processes. ... Structure . 2 (7): 651–68. doi : 10.1016/s0969-2126(00)00066-6 . PMID 7922042 . ^ Monga A, Makkar RP, Arora A, Mukhopadhyay S, Gupta AK (July 2003). "Case report: Acute hepatitis E infection with coexistent glucose-6-phosphate dehydrogenase deficiency" .

Dystonia 6 can appear at any age from childhood through adulthood; the average age of onset is 18. ... Involvement of one or more limbs is common, and in some cases occurs before the head and neck problems. Dystonia 6 gradually gets worse, and it may eventually involve most of the body. Frequency The prevalence of dystonia 6 is unknown. Studies indicate that it likely accounts for between 1 and 3 percent of all cases of dystonia. For reasons that are unclear, the disorder appears to be slightly more prevalent in females than in males. Causes Dystonia 6 is caused by mutations in the THAP1 gene. ... Problems with DNA binding likely disrupt the proper regulation of gene activity, leading to the signs and symptoms of dystonia 6. A particular THAP1 gene mutation is specific to a Mennonite population in the Midwestern United States in which dystonia 6 was first described.

INHERITANCE - Autosomal recessive HEAD & NECK Head - Microcephaly (in 1 of 6 patients) ABDOMEN Gastrointestinal - Anal atresia (in 1 of 6 patients) - Duplicated appendix and distal colon (in 1 of 6 patients) GENITOURINARY External Genitalia (Male) - Bifid phallus (in 1 of 6 patients) - Bifid scrotum (in 1 of 6 patients) Kidneys - Pelvicalyceal dilatation (in 1 of 6 patients) Ureters - Ureteric dilatation (in 1 of 6 patients) Bladder - Bladder exstrophy (in 1 of 6 patients) SKELETAL Spine - Scoliosis (in 1 of 6 patients) NEUROLOGIC Central Nervous System - Hypotonia, neonatal - Delayed psychomotor development, severe (in 2 of 6 patients) - Mental retardation (in 2 of 6 patients) - Normal development (in 2 of 6 patients) - Seizures (in 2 of 6 patients) - Dystonic movements (in 1 of 6 patients) - Speech disorder (in 1 of 6 patients) - EEG shows hypsarrhythmia (in 1 of 6 patients) - Status epilepticus (in 1 of 6 patients) - MRI shows delayed myelination (1 of 6 patients) LABORATORY ABNORMALITIES - Increased urinary dihydropyrimidines - Increased urinary, plasma, and CSF N-carbamyl-beta-alanine - Increased urinary, plasma, and CSF N-carbamyl-beta-aminoisobutyric acid - Increased urinary, plasma, and CSF dihydrouracil - Increased urinary, plasma, and CSF dihydrothymine - Absence of beta-ureidopropionase activity and protein in liver biopsy MISCELLANEOUS - Onset in infancy - Six genetically confirmed patients have been reported (as of December 2009) - Inborn error of the pyrimidine degradation pathway MOLECULAR BASIS - Caused by mutation in the beta-ureidopropionase gene (UPB1, 606673.0001 ) ▲ Close

HHV-6 encephalitis refers to inflammation of the brain due to an infection with human herpesvirus 6. People who have undergone allogeneic hematopoietic cell transplantation are at an increased risk for developing HHV-6 encephalitis, particularly when umbilical cord blood stem cells are used. ... EEG's may also be recommended when seizures are suspected. HHV-6 encephalitis is treated with an antiviral agent with activity against HHV-6.

Glucose-6-phosphate dehydrogenase deficiency is a genetic disorder that occurs almost exclusively in males. ... In affected individuals, a defect in an enzyme called glucose-6-phosphate dehydrogenase causes red blood cells to break down prematurely. ... Frequency An estimated 400 million people worldwide have glucose-6-phosphate dehydrogenase deficiency. ... Glucose-6-phosphate dehydrogenase deficiency occurs most frequently in areas of the world where malaria is common. Learn more about the gene associated with Glucose-6-phosphate dehydrogenase deficiency G6PD Inheritance Pattern Glucose-6-phosphate dehydrogenase is inherited in an X-linked pattern.

The most significant manifestation is bilateral, diffuse uveitis , which affects the eyes. [2] [3] VKH may variably also involve the inner ear , with effects on hearing, the skin and the meninges of the central nervous system . [2] [3] [4] [5] [6] Contents 1 Signs and symptoms 1.1 Overview 1.2 Phases 2 Cause 3 Risk factors 4 Diagnosis 4.1 Types 5 Management 6 Outcomes 7 Eponym 8 References 9 External links Signs and symptoms [ edit ] Overview [ edit ] Uveitis with poliosis of the eyelashes The disease is characterised by bilateral diffuse uveitis , with pain, redness and blurring of vision . The eye symptoms may be accompanied by a varying constellation of systemic symptoms, such as auditory ( tinnitus , [6] vertigo , [6] and hypoacusis ), neurological ( meningismus , with malaise, fever, headache, nausea, abdominal pain, stiffness of the neck and back, or a combination of these factors; [6] meningitis , [4] CSF pleocytosis , cranial nerve palsies , hemiparesis , transverse myelitis and ciliary ganglionitis [6] ), and cutaneous manifestations, including poliosis , vitiligo , and alopecia . [4] [5] [6] The vitiligo often is found at the sacral region . [6] Phases [ edit ] The sequence of clinical events in VKH is divided into four phases: prodromal, acute uveitic, convalescent, and chronic recurrent. [2] [5] [6] The prodromal phase may have no symptoms, or may mimic a non-specific viral infection, marked by flu-like symptoms that typically last for a few days. [6] There may be fever, headache, nausea, meningismus , dysacusia (discomfort caused by loud noises or a distortion in the quality of the sounds being heard), tinnitus , and/or vertigo. [6] [7] Eye symptoms can include orbital pain, photophobia and tearing. [6] The skin and hair may be sensitive to touch. [6] [7] Cranial nerve palsies and optic neuritis are uncommon. [6] The acute uveitic phase occurs a few days later and typically lasts for several weeks. [6] This phase is heralded by bilateral panuveitis causing blurring of vision . [6] In 70% of VKH, the onset of visual blurring is bilaterally contemporaneous; if initially unilateral, the other eye is involved within several days. [6] The process can include bilateral granulomatous anterior uveitis, variable degree of vitritis, thickening of the posterior choroid with elevation of the peripapillary retinal choroidal layer, optic nerve hyperemia and papillitis , and multiple exudative bullous serous retinal detachments . [2] [5] [6] The convalescent phase is characterized by gradual tissue depigmentation of skin with vitiligo and poliosis , sometimes with nummular depigmented scars, as well as alopecia and diffuse fundus depigmentation resulting in a classic orange-red discoloration ("sunset glow fundus" [5] [8] [7] ) and retinal pigment epithelium clumping and/or migration. [2] [6] The chronic recurrent phase may be marked by repeated bouts of uveitis, but is more commonly a chronic, low-grade, often subclinical, uveitis that may lead to granulomatous anterior inflammation, cataracts , glaucoma and ocular hypertension. [2] [3] [5] [6] Full-blown recurrences are, however, rare after the acute stage is over. [8] Dysacusia may occur in this phase. [7] Cause [ edit ] Although there is sometimes a preceding viral infection, or skin or eye trauma, [6] the exact underlying initiator of VKH disease remains unknown. [4] However, VKH is attributed to aberrant T-cell -mediated immune response directed against self-antigens found on melanocytes . [3] [4] [6] Stimulated by interleukin 23 (IL-23), T helper 17 cells and cytokines such as interleukin 17 (IL-17) appear to target proteins in the melanocyte. [8] [9] Risk factors [ edit ] Affected individuals are typically 20 to 50 years old. [3] [4] The female to male ratio is 2:1. [4] [5] [6] By definition, there is no history of either surgical or accidental ocular trauma . [3] VKH is more common in Asians, Latinos, Middle Easterners, American Indians, and Mexican Mestizos; it is much less common in Caucasians and in blacks from sub-Saharan Africa. [3] [4] [5] [6] VKH is associated with a variety of genetic polymorphisms that relate to immune function. For example, VKH has been associated with human leukocyte antigens (HLA) HLA-DR4 and DRB1/DQA1, [10] copy-number variations (CNV) of complement component 4 , [10] a variant IL-23R locus [10] and with various other non-HLA genes. [10] HLA-DRB1*0405 in particular appears to play an important susceptibility role. [2] [4] [8] [6] Diagnosis [ edit ] If tested in the prodromal phase, CSF pleocytosis is found in more than 80%, [6] [7] mainly lymphocytes . [7] This pleocytosis resolves in about 8 weeks even if chronic uveitis persists. [7] Functional tests may include electroretinogram and visual field testing . [2] Diagnostic confirmation and an estimation of disease severity may involve imaging tests such as retinography , fluorescein or indocyanine green angiography , optical coherence tomography and ultrasound . [2] [5] [9] [7] For example, indocyanine green angiography may detect continuing choroidal inflammation in the eyes without clinical symptoms or signs. [5] [8] Ocular MRI may be helpful [6] and auditory symptoms should undergo audiologic testing. [6] Histopathology findings from eye and skin are discussed by Walton. [6] The diagnosis of VKH is based on the clinical presentation; the diagnostic differential is extensive, and includes (among others) sympathetic ophthalmia , sarcoidosis , primary intraocular B-cell lymphoma , posterior scleritis , uveal effusion syndrome, tuberculosis, syphilis, and multifocal choroidopathy syndromes. [3] [6] Types [ edit ] Based on the presence of extraocular findings, such as neurological, auditory and integumentary manifestations, the "revised diagnostic criteria" of 2001 [2] [11] classify the disease as complete (eyes along with both neurological and skin), incomplete (eyes along with either neurological or skin) or probable (eyes without either neurological or skin) . [1] [3] [5] [6] [11] By definition, for research homogeneity purposes, there are two exclusion criteria: previous ocular penetrating trauma or surgery, and other concomitant ocular disease similar to VKH disease. [2] [6] [11] Management [ edit ] The acute uveitis phase of VKH is usually responsive to high-dose oral corticosteroids ; parenteral administration is usually not required. [2] [3] [6] However, ocular complications may require a subtenon [6] or intra vitreous injection of corticosteroids [4] [6] or bevacizumab . [9] In refractory situations, other immunosuppressives such as cyclosporine , [2] [3] or tacrolimus , [9] antimetabolites ( azathioprine , mycophenolate mofetil or methotrexate [9] ), or biological agents such as intravenous immunoglobulins (IVIG) or infliximab may be needed. [2] [6] Outcomes [ edit ] Visual prognosis is generally good with prompt diagnosis and aggressive immunomodulatory treatment. [2] [3] [8] Inner ear symptoms usually respond to corticosteroid therapy within weeks to months; hearing usually recovers completely. [6] Chronic eye effects such as cataracts , glaucoma , and optic atrophy can occur. [6] Skin changes usually persist despite therapy. [6] Eponym [ edit ] VKH syndrome is named for ophthalmologists Alfred Vogt from Switzerland and Yoshizo Koyanagi and Einosuke Harada from Japan. [12] [13] [14] [15] Several authors, including the Arabic doctor Mohammad-al-Ghâfiqî in the 12th century as well as Jacobi, Nettelship and Tay in the 19th century, had described poliosis, neuralgias and hearing disorders. [15] This constellation was probably often due to sympathetic ophthalmia but likely included examples of VKH. [15] Koyanagi's first description of the disease was in 1914, but was preceded by Jujiro Komoto, Professor of Ophthalmology at the University of Tokyo, in 1911. [15] It was the much later article, published in 1929, that definitively associated Koyanagi with the disease. [15] Harada's 1926 paper is recognized for its comprehensive description of what is now known as Vogt–Koyanagi–Harada disease. [15] References [ edit ] ^ a b "Vogt-Koyanagi-Harada Disease" . ... "Vogt-Koyanagi-Harada disease: diagnosis and treatments update". Curr Opin Ophthalmol . 21 (6): 430–5. doi : 10.1097/ICU.0b013e32833eb78c .

Clinical Features Armfield et al. (1999) reported a family with 6 males with mental retardation in 3 generations, consistent with X-linked inheritance. Other features included short stature (6 of 6), small hands and feet (5 of 5), seizures (6 of 6), cleft palate (2 of 6), and cataracts/glaucoma (3 of 6). ... INHERITANCE - X-linked recessive GROWTH Height - Short stature HEAD & NECK Head - Prominent forehead - Midface hypoplasia (in some patients) Eyes - Cataracts (in some patients) - Glaucoma (in some patients) - Strabismus (in some patients) Mouth - Cleft palate (in some patients) SKELETAL Hands - Small hands Feet - Small feet NEUROLOGIC Central Nervous System - Mental retardation, moderate to severe - Seizures MISCELLANEOUS - One family with 6 probands described (as of September 2000) ▲ Close

Two alternative possibilities were considered: (1) a defect in the phosphodiesterase that normally uncovers the mannose 6-phosphate marker, or (2) a defect in the mannose 6-phosphate receptor. ... Mutant Chinese hamster ovary cells with altered mannose 6-phosphate receptors were studied by Robbins and Myerowitz (1981). ... Alexander et al. (1986) showed that mannose 6-phosphate receptors in the fibroblasts from a member of this family were functioning normally but the cells had only half-normal levels of phosphodiester glycosidase activity. ... Treatment of the abnormal Hex-B with exogenous placental phosphodiester glycosidase (607985) increased its binding to mannose 6-phosphate receptors 3-fold. Secretion rates of 7 lysosomal enzymes from the subject's fibroblasts were, on average, twice as great as rates measured for 2 I-cell disease heterozygote fibroblast lines. ... Lab - Elevated plasma lysosomal enzymes - Normal urinary and CSF lysosoal enzymes - Normal levels of acid phosphatase, alkaline phosphatase and beta-glucuronidase - Mannose 6-phosphate receptor recognition defect Inheritance - Autosomal dominant - homozygotes expected to have I-cell disease ▲ Close

PTPS is an intermediate in this cycle and is needed to convert 7,8 - dihydroneopterin triphosphate to 6-Pyruvoyltetrahydryobiopterin. 6-Pyruvoyltetrahydryobiopterin is converted into BH 4 (Tetrahydrobiopterin), but since it stops at 6-Pyruvoyltetrahydrobiopterin no BH 4 is made. [5] The absence of BH 4 affects the metabolism of Phenylalanine . ... "Orphanet: 6 pyruvoyl tetrahydropterin synthase deficiency" . www.orpha.net . ... "Mutations in the GTP cyclohydrolase I and 6-pyruvoyl-tetrahydropterin synthase genes". ... The EMBO Journal . 13 (6): 1255–1262. doi : 10.1002/j.1460-2075.1994.tb06377.x . ... Human Genome Variation Society . 37 (6): 508–515. doi : 10.1002/humu.22980 .

Spread of infection is reduced by also treating sexual contacts . [6] Risk factors include being sexually active men under the age of 25, having a recent new sexual partner, or having unprotected sex. [6] Contents 1 Definition and clinical features 2 Causes 3 Evaluation 4 Treatment 5 Epidemiology 6 References Definition and clinical features [ edit ] Play media This male presented discharge commonly found in an early stage of gonorrhea. This is one of the possible symptoms seen in up 90% of males with gonorrhea, usually within 2 to 5 days [4] Penile discharge is liquid from the urethra at the end of the penis that is not urine or semen. [2] The dripping of clear fluid when sexually excited is normal. [2] There may be pain or burning when passing urine, soreness inside the penis or feeling of wanting to pass urine frequently. [6] Causes [ edit ] Common causes include infections due to gonorrhea , chlamydia , or trichomoniasis . [3] Other causes include: Non-specific urethritis [2] Acute prostatitis [2] Infection under the foreskin [2] Warts at the opening of the urethra [2] Herpes simplex virus ulcer at the opening of the urethra [2] Object in the urethra [2] or recent surgical procedure. [5] A bloody discharge may be a sign of urethral cancer . [5] Evaluation [ edit ] A swab of the discharge is usually performed. [5] Other investigations may include tests for HIV, hepatitis and syphilis. [6] Men who have sex with men may also need to have throat and rectal swabs. [6] Treatment [ edit ] Treatment depends on the cause and any antibiotic prescribed depends on which infection is found. [6] Spread of infection is reduced by informing sexual partners so that they can also be treated, and not having sex (including oral or anal) until tests are completed and seven days have passed after treatment. [6] Epidemiology [ edit ] Risk factors include being sexually active men under the age of 25, having a recent new sexual partner, unprotected sex (without a condom), or having the presence of any sexually transmitted infection. [6] References [ edit ] ^ "Details - Public Health Image Library(PHIL)" . phil.cdc.gov . ... ISBN 978-0-323-59454-7 . ^ a b "Gonorrhea - CDC Fact Sheet" . cdc.gov . Retrieved 6 December 2014 . ^ a b c d e Kahan, Scott; Miller, Redonda; Smith, Ellen G. (2008). "126. ... ISBN 978-0-7817-7043-9 . ^ a b c d e f g h "Urethritis and Urethral Discharge in Men" . patient.info . Retrieved 6 December 2014 .

Hung Medien. Retrieved April 6, 2017. ^ "Ultratop.be – Peter Fox – Stadtaffe" (in Dutch). Hung Medien. Retrieved April 6, 2017. ^ "Longplay-Chartverfolgung at Musicline" (in German). ... Hung Medien. Retrieved April 6, 2017. ^ "Jahreshitparade Alben 2008" . ... GfK Entertainment Charts . Retrieved April 6, 2017 . ^ "Jahreshitparade Alben 2009" . ... GfK Entertainment Charts . Retrieved April 6, 2017 . ^ "Schweizer Jahreshitparade 2009" .

When lobsters are moribund, they may lie on their sides, and frequently lose appendages . [6] The effects of gaffkaemia are slowed by low temperatures, such that death can occur within two days of infection at 20 °C (68 °F), but can take over 60 days at 3 °C (37 °F). [6] As few as five bacteria can lead to clinical disease. When they enter the host, the bacteria colonise the heart and hepatopancreas . [6] They may be engulfed by phagocytosis into the lobster's blood cells, but continue to survive within the blood cells, feeding on the cytoplasm . The lobster's blood cell count drops, and the infection develops into septicaemia . [6] The stores of glycogen in the hepatopancreas become depleted, concentrations of glucose and lactic acid in the blood drop, and concentrations of adenosine triphosphate in muscles also fall. [6] In a severe infection, the ability of the lobster's blood pigment haemocyanin to carry oxygen may be reduced by up to 50%. [6] Diagnosis [ edit ] The classical method of diagnosis is to culture aliquots of haemolymph in phenylethyl alcohol broth. ... They include the shrimp Pandalus platyceros , and the crabs Cancer borealis , Cancer irroratus , Metacarcinus magister , Libinia emarginata , Chionoecetes opilio and Chaceon quinquedens . [6] Spiny lobsters appear to be either immune or resistant to gaffkaemia. [6] Control [ edit ] The primary method for controlling the incidence of gaffkaemia is improved hygiene. [6] Other measures include limiting damage to the exoskeleton (preventing the bacterium's entry), reducing the water temperature, and reducing the stocking density. [6] Antibiotics may be effective against the bacterium, but only tetracycline is currently approved by the U.S Food and Drug Administration for use in American lobsters. [6] Further reading [ edit ] Crustaceans portal References [ edit ] ^ Spencer J. ... Cambridge University Press . pp. 120–155. ISBN 978-0-521-87593-6 . v t e Diseases of crustaceans Bitter crab disease Crayfish plague Gaffkaemia Infectious hypodermal and haematopoietic necrosis Necrotising hepatopancreatitis Paragonimiasis Taura syndrome White spot syndrome Yellowhead disease

Locura , which translates to " madness " in Spanish, [1] [2] is a mental disorder characterized as severe chronic psychosis. [2] [3] [4] The term refers to a culture-bound syndrome , found mostly in Latin America and Latin Americans in the United States . [5] [6] [3] [7] Also referred to as ataques de locura (meaning "madness attacks"), [6] it is categorized as a more severe form of nervios [7] ataque de nervios [6] [3] with symptoms appearing similar to those of schizophrenia . [2] [3] As the term may have multiple meanings in multiple environments, research on locura is limited and conflicting. [7] The term can be used loosely in Spanish when discussing madness in other psychological meaning, specifically describing a "deviance from the norm due to mental illness." [7] Besides for the implications found in the DSM-IV, the word is not used in English. [4] Contents 1 Classification 2 Signs and symptoms 3 History 4 See also 5 References Classification [ edit ] In the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders ( DSM-IV ), locura is classified as a culture-bound syndrome. Culture-bound syndromes can be found in an appendix of the manual named, Outline for Cultural Formulation and Glossary of Culture-Bound Syndromes. [4] However, the DSM - 5 does not include locura in its equivalent appendix named, Glossary of Cultural Concepts of Distress. [8] One author chooses to describe the symptoms as correlating to a somatoform disorder of conversive type. [6] Signs and symptoms [ edit ] Locura is thought to develop during times of stress or vulnerability in one's life, as well as the accumulation of difficulties or traumas. [3] [7] [4] Another possible cause is through the manifestation of supernatural maneuvers, [7] or maleficios (meaning "curses"). [6] [9] The DSM-IV includes symptoms of incoherence, agitation, inability to follow rules of social interaction, unpredictability, and possible violence. [4] Other sources include headache, fainting, convulsive attacks, difficulty in breathing, an urge to run away, hallucinations, and visions of people, visions, or demons. [2] [6] [7] History [ edit ] Locura has been examined in an indigenous group in Colombia called Embera . [6] After four members of the Embera community began exhibiting symptoms later described as, "repetitive episodes of what resembled a dissociative fugue disorder," [6] a local shaman explained that the outbreak could be attributed to a shaman from a different region. ... The shaman's treatments reportedly reduced the frequency of the symptoms greatly in all of the patients and eliminated symptoms completely in two patients. [6] See also [ edit ] Ataques de nervios Culture-bound syndrome References [ edit ] ^ "Locura - Spanish to English Translation | Spanish Central" . www.spanishcentral.com . ... Archives of Clinical Psychiatry . 42.5-6 (6): 171–178. doi : 10.1590/0101-60830000000070 . ^ a b c d e f g h i Piñeros, Marion; Rosselli, Diego; Calderon, Claudia (1998). ... Social Science and Medicine . 46 (11): 1425–1428. doi : 10.1016/S0277-9536(97)10094-6 . PMID 9665572 . ^ a b c d e f g Garcia Briggs, Mary Jo (2012).

"Clinical features of infants with primary human herpesvirus 6 infection (exanthem subitum, roseola infantum)". ... "The spectrum of human herpesvirus 6 infection: from roseola infantum to adult disease". ... PMID 10774474 . ^ a b Strausbaugh, Larry J.; Caserta, Mary T.; Mock, David J.; Dewhurst, Stephen (2001-09-15). "Human Herpesvirus 6" . Clinical Infectious Diseases . 33 (6): 829–833. doi : 10.1086/322691 . ... Current Opinion in Virology . 9 : 91–6. doi : 10.1016/j.coviro.2014.09.013 . ... PMC 5329081 . PMID 27538995 . ^ a b "HHV-6 & Rash/Roseola | HHV-6 Foundation | HHV-6 Disease Information for Patients, Clinicians, and Researchers | Apply for a Grant" . hhv-6foundation.org .

Two phenotypic variants are recognized, B 6 -responsive homocystinuria and B 6 -non-responsive homocystinuria. ... Enzyme analysis cannot reliably distinguish B 6 -responsive from B 6 -non-responsive individuals. ... The two phenotypic variants of classic homocystinuria are B 6 -responsive and B 6 -non-responsive homocystinuria. ... Ectopia lentis usually occurs earlier in affected individuals who are B 6 non-responsive than in those who are B 6 responsive. ... IQ in individuals with homocystinuria ranges from 10 to 138. B 6 -responsive individuals are more likely than individuals with B 6 -non-responsive homocystinuria to be cognitively intact or only mildly affected; the mean IQ of untreated individuals with B 6 responsiveness is 79 versus 57 for those who are B 6 non-responsive.

Dissociative identity disorder and psychotic symptoms in schizoaffective disorder have considerable overlap, yet a different overall treatment approach. [40] DSM-5 criteria [ edit ] The most widely used criteria for diagnosing schizoaffective disorder are from the American Psychiatric Association 's Diagnostic and Statistical Manual of Mental Disorders-5 . [6] The DSM-IV schizoaffective disorder definition was plagued by problems of being inconsistently (or unreliably ) used on patients; [6] when the diagnosis is made, it doesn't stay with most patients over time; [6] and it has questionable diagnostic validity (that is, it doesn't describe a distinct disorder, nor predict any particular outcome). [6] These problems have been slightly reduced (or "modestly improved") in the DSM-5 according to Carpenter. [6] When psychotic symptoms are confined to an episode of mania or depression (with or without mixed features ), the diagnosis is that of a “ psychotic ” mood disorder , namely either psychotic bipolar disorder or psychotic major depression . ... DSM-5 requires two episodes of psychosis (whereas DSM-IV needed only one) to qualify for the schizoaffective disorder diagnosis. [6] As such, it is no longer an "episode diagnosis." [6] The new schizoaffective framework looks at the time from "the [first episode of] psychosis up to the current episode [of psychosis], rather than only defining a single episode with [co-occurring] psychotic and mood syndromes ." [6] Specifically, one of the episodes of psychosis must last a minimum of two weeks without mood disorder symptoms, but the person may be mildly to moderately depressed while psychotic. [6] The other period of psychosis "requires the overlap of mood [disorder] symptoms with psychotic symptoms to be conspicuous" and last for a greater portion of the disorder. [41] These two changes are intended by the DSM-5 workgroup to accomplish two goals: [6] Increase the diagnosis' consistency (or reliability) when it is used; Significantly decrease the overall use of the schizoaffective disorder diagnosis. ... As stated above, the DSM-IV schizoaffective disorder diagnosis is very inconsistently used or unreliable. [6] A diagnosis is unreliable when several different mental health professionals observing the same individual make different diagnoses excessively. [6] Even when a structured DSM-IV diagnostic interview and best estimate procedures were made by experts in the field that included information from family informants and prior clinical records, reliability was still poor for the DSM-IV schizoaffective diagnosis. [6] The DSM-IV schizoaffective diagnosis isn't stable over time either. [6] An initial diagnosis of schizoaffective disorder during time spent at a psychiatric inpatient facility was stable at 6-month and 24-month follow ups for only 36% of patients. [6] By comparison, diagnostic stability was 92% for schizophrenia, 83% for bipolar disorder and 74% for major depression. [6] Most patients diagnosed with DSM-IV schizoaffective disorder are later diagnosed with a different disorder, and that disorder is more stable over time than the DSM-IV schizoaffective disorder diagnosis. [6] In April 2009, Carpenter and the DSM-5 schizoaffective disorder workgroup reported that they were "developing new criteria for schizoaffective disorder to improve reliability and face validity ," and were "determining whether the dimensional assessment of mood [would] justify a recommendation to drop schizoaffective disorder as a diagnostic category." [12] Speaking to an audience at the May 2009 annual conference of the American Psychiatric Association , Carpenter said: [12] We had hoped to get rid of schizoaffective [disorder] as a diagnostic category [in the DSM-5] because we don't think it's [a] valid [scientific entity] and we don't think it's reliable. ... The American Journal of Psychiatry . 164 (12): 1900–6. doi : 10.1176/appi.ajp.2007.06010017 . ... "Cannabis use and earlier onset of psychosis: a systematic meta-analysis" . Arch. Gen. Psychiatry . 68 (6): 555–61. doi : 10.1001/archgenpsychiatry.2011.5 .