what is oligoteratoasthenozoospe syndrome?
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James L. Schaller, MD, MAR, PA, DABPN, DABFM\n\nClinical and Research Psychiatry and Medicine\nAdult Psychiatry and Psychotherapy Services\nSubspecialty Child & Adolescent Psychiatry\nHormonal & Nutraceutical Consultation\nAnti-Aging & Obesity Consultation\n\nwww.personalconsult.com\nOchratoxins and Ochratoxicosis\nBy Jack Dwayne Thrasher, Ph.D.\ntoxicology@drthrasher.org\n\nIntroduction\n\nOchratoxins are metabolites of Aspergillus, Fusarium, and Penicillium species. The most commonly implicated species are A. ochraceus and ostianus, P. viridicatum, griseofulvum and possibly solitum.1 Recent evidence shows that these mycotoxins are present in a variety of foods (cereals, pork, poultry, coffee, beer, wine, grape juice and milk. Analyses of these food products demonstrated that ochratoxins are also produced by P. vercucosum and A. niger and carbonarius.2,3\n\nThere are three generally recognized ochratoxins, designated A, B and C. Ochratoxin A (OTA) is chlorinated and is the most toxic, followed by OTB and OTC. Chemically they are described as 3,4-dihydro-methylisocoumarin derivative linked with an amide bond to the amino group of L-b-phenylalanine (Fig. 1).4\n\nFigure 1. Chemical Structure of Ochratoxin A (OTA); Adapted from Hussein et al, 2001, ref. 4\n\nThe role and risk assessment of OTA in animal and human disease has been reviewed. The tolerable dosage in humans was estimated at 0.2 to 4.2 ng/kg body weight based upon NTP carcinogenicity study in rats. OTA is mutagenic, immunosuppressive and teratogenic in several species of animals. Its target organs are the kidneys (nephropathy) and the developing nervous system.5,6 Following intravenous administration OTA is eliminated with a half-life from body in Vervet monkeys in 19-21 days.7 There is no reason to suspect that the elimination half-life would be significantly different in humans. OTA has been detected in human blood and milk. Other than nephropathy and urinary tumors, the evidence for human toxicology is scant. The toxicology of OTA will be briefly reviewed.\n\nCarcinogenesis\n\nThere is inadequate evidence that OTA is carcinogenic in humans. There is sufficient evidence in experimental animals. Overall OTA is possibly carcinogenic to humans and is a Group 2B carcinogen.\n\nResearch Animals: Oral administration of OTA produced tubular cell carcinomas of the kidneys in male and female rats, and fibroadenomas of the mammary gland in the females.1\n\nAdministration of OTA in the diet of ddy mice produced tumors of kidneys: solid renal tumors and cystic adenomas. Also, hepatic-tumors and hyperplastic liver nodules were found and unspecified lung tumors. In addition, solid renal-cell tumors occurred in ddd mice fed OTA in their diet.1\n\nMale and Female Fischer rats given oral doses of OTA had does related increased in kidney tumors: renal-cell adenomas, and renal-cell adeno-carcinomas. Metastasis of the renal cell tumors occurred in 17 males and one female.1\n\nHumans: Balkan endemic neuropathy (BEN) associated with OTA occurs in Europe (Bulgaria, Croatia, Turkey, Egypt, and Yugoslovia) where OTA is relatively high in the diet. Individuals with BEN were surveyed for the presence of urinary tract tumors. The incidence of tumors in the urinary system was elevated in both men and women. Furthermore, the observations suggested that individuals with urinary tract tumors had elevated levels of OTA in the blood and urine. Approximately one-third of patients dying from BEN have papillomas and/or carcinomas of the renal pelvis, ureter or bladder.1,8 -12\n\nRecently, it has been suggested that OTA can cause testicular cancer in humans.13 The hypothesis that consumption of foods contaminated with OTA causes testicular cancer was tested. The incidence of rates of testicular cancer in 20 countries were significantly correlated with the per-capita consumption of coffee and pigmeat. Scwhartz concluded: "Thus, OTA is a biologically plausible cause of testicular cancer. Future epide
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What kind of syndrome... I found this Velocardiofacial (Spritzen) syndrome, but I don't know if that's right.\n\nI know I am not helping much but all I can find is "SPRITZEN syndrome" but I haven't found an answer to your question
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From your question, I'm guessing you already know that Barth Syndrome is an x-linked recessive disorder, which means it's caused by a mutation on the x-chromosome that shows up if you've got either two x-chromosomes with the mutation, or one x with the mutation, and one y chromosome.\n\nBarth Syndrome is caused by a mutation in the G4.5 tafazzn (TAZ) gene, which is located at Xq28 (which if you don't already know, specifies a paricular location on the x-chromosome).  The predicted protein sequence for the gene is 292 amino acids long, and has strong homology with (i.e. very similar to) a superclass of acyltransferases (a type of enzyme used in various cellular functions) that are highly conserved among different species.  There are over 50 different mutations of the TAZ gene that are associated with Barth Syndrom, of which 60% completely disrupt the function of the proteins, and another 30% change the charge of the protein.
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Not sure that there is such a thing. I think you might mean Raynaud's disease. It is a circulation disorder where your peripheral circulation (to fingers and toes) is impaired and these parts feel cold and numb in response to cold and stress.\n\n During a Raynaud's attack, these arteries narrow, limiting blood circulation to affected areas.\n\nYou can have Raynaud's without any underlying disease associated with it, in which case it's called Raynaud's disease or primary Raynaud's. Or it can be part of another disease, in which case doctors may refer to it as Raynaud's phenomenon or secondary Raynaud's.\n\nRaynaud's disease affects a small percentage of Americans. Women are more likely than men are to have the disorder. It's more common in people who live in colder climates.\n\nHere are some very good sites for information:
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It's spelled Guillain Barre Syndrome. Just google it and you'll get plenty of info.
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Well, the commonest cause of this is intoxication with certain medications. In cases where it doesn't go away in a few weeks, it could be "Horner's Syndrome", or it could be "Myasthenia Gravis".\n\nA Dr. would have to help you with this determination.  If it continues more than 6 weeks. It could be a sign of nerve damage, or a neurological disease.\n\nHORNER'S SYNDROME:\n\nHorner syndrome is a relatively rare disorder characterized by a constricted pupil (miosis), drooping of the upper eyelid (ptosis), absence of sweating of the face (anhidrosis), and sinking of the eyeball into the bony cavity that protects the eye (enophthalmos). These are the four classic signs of the disorder. \n\nThe congenital, and more rare, form of Horner syndrome is present at birth but the cause is not known. Most often, Horner syndrome is acquired as a result of some kind of interference with the sympathetic nerves serving the eyes. The underlying causes can vary enormously, from a snake or insect bite to a neck trauma made by a blunt instrument.\n\nMYASTHENIA GRAVIS:\n\nWeakness in specific muscles, problems with the nerves that move the eyes, drooping eyelid, or double vision, are the beginning symptoms of Myasthenia Gravis in two-thirds of patients. The severity of weakness fluctuates during the day, usually being least severe in the morning and worse as the day progresses, especially after prolonged use.
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I know some one who had suffered from this problem, his was also due to M.S.. His eyes made small involuntary movements, but the condition seems to have disappeared. He is taking a virtually unknown prescription drug that is working miracles in people with M.S.and other autoimmune disorders, it is known as Low Dose Naltrexone. Doctor Bernard Bihari of New York City has been working with this drug since the 80's. and it is just now starting to get some attention. The second annual Low Dose Naltrexone Conference was held in Washington this year, you can hear the lectures off the web site. Because the monthly treatment cost is only $38 u.s. per patient don't expect any drug company involvement any time soon. A few private clinical trails have commenced world wide and the preliminary results are all quite promising. If you have not heard of this little know treatment yet. try clicking on the link below and start your research, it might be a viable option for you.\n\nAnother very important avenue you should explore when treating M.S. is neurotoxin damage both dietary and environmental. Things like monosodium glutamate, aspartame, heavy metals,food additives, preservatives, fungal and bacterial mycotoxins maybe causing or exacerbating your condition. Many M.S. sufferers have made their symptoms disappear by eliminating the above mentioned poisons from their body.\n\nBecause most packaged foods have M.S.G. (under a disguised category such as modified corn starch, spices, yeast extract, hydrolyzed vegetable protein etc.) I would stick to fresh organically raised foods, stay away from anything packaged . Drink clean distilled or R.O. water only.\n\nGet checked for heavy metal contamination, have both Hair analysis and Urinalysis through Calcium EDTA provocation. There is a possibility that you have mercury poisoning, from either vaccination, or through food consumption. If you are positive for heavy metals, then chelation therapy should be explored. Dr Gary Gordon of Tempe Arizona is the expert here. He also works with Dr Amy Yasko that specializes in patients with neurological disorders.\n\nTo check for biotoxin exposure I would recommend Dr.Shoemaker’s website listed below. On his site there is information on doing a VCS (visual contrast sensitivity) test. This doctor specializes on treating people with biotoxin-induced illness.\n\nSome final recommendations I have for you is to look into: enzyme therapy such as Wobenzym N, (it is very popular in Europe especially Germany), Vitamin D therapy and Histamine therapy \n\nAlthough the doctors mentioned below are available for phone consultations, Dr Bihari will be extremely difficult to speak with, instead I would call one of the compounding pharmacies listed on the web site and ask for names of doctors in your area that might be sending prescriptions to them.\n\nI have confidence that you can beat this thing, or put it into remission, all the best to you!
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It is a constellation of symptoms and risk factors. Including but not limited to Abdominal Obesity, High triglycerides, low HDL, cholesterol and LDL chol high. These can bring about worsening of plague build ups in artery walls. Elevated Blood Pressure, Insulin Resistance or glucose intolerance. Also Proinflammatory state. Most people diagnosed with the syndrome are at increased risk for coronary heart disease, stroke and peripheral vascular disease, and type 2 diabetes. \nSome of the other things that go along with it are physical inactivity, hormonal imbalance and aging as well as genetic predisposition. \nAs for treatment the goal is to manage the symptoms and factors and reduce the risk for complications. Such things as weight loss, increase physical if able to at least 30 minutes 4x a week, even walking can help. Better eating habits to control diabetes if diagnosed and also to regulate blood sugars and lower cholesterol.  Cut out the salt if you use it a lot.\nMy mom was diagnosed with  it and was able to signiificantly lower her risk factors by the changes mentioned. ( I did however check the American Heart Association web site to be sure I was giving the correct information in regards to the list of factors.) My mom's doctor told her it's not so much an illness as it is a group of symptoms and several diseases and or disorders than when all together can be very  troublesome. Try the American Heart Association site. The info they have is pretty straighforward and also helpful I found. Good Luck and I hope I helped.
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Sequence Tagged Microsatellite Site(STMS) is a special short repeat in the DNA sequence. It is also known as Microsattelite, Simple Sequence Repeat(SSR), Simple Sequence Repeat Polymorphism(SSRP).
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It is a rare congenital condition called Hypertrichosis. It is the condition that afflicts the "wolf boys" that were in the news a few years ago.
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Prader-Willi syndrome is a genetic disorder characterized in infancy by diminished muscle tone, feeding difficulties, and failure to grow and gain weight.  You can read more here\nhttp://www.med.umich.edu/1libr/yourchild/praders.htm
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If you are talking about pneumonoultramicroscopicsilicovolcanoconiosis, it's a pnuemoconiosis caused by the inhallatation of very fine silicate or quartz dust.  In other words, a black lung disease
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check here for extensive info:\n\n\nhttp://rarediseases.org/search/rdbdetail_abstract.html?disname=Angelman%20Syndrome
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Mononucleosis is what my boyfriend gave me for Christmas, but it could have been worse: he could have given me clamydia.\n\nOkay, that was grosser than I intended.
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There are some genetically related disorders including: \nHypochondroplasia \nFGFR-related craniosynostosis \nThanatophoric dysplasia \nSADDAN dysplasia=Severe achondroplasia
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Cushing's is a very specific syndrome but there is a variety of causes.\n\nTreatment varies from medication to control the secretion of cortisol to surgical removal of the adrenal glands and lifelong steroid therapy.
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Menetrier Disease \nMeniere's Disease\nMeniere's Syndrome \nMeningeal Plague\nMeningioma\nMeningiomas, Multiple\nMeningiomatosis\nMeningitis, Bacterial\nMeningitis, Viral\nMenkes Kinky Hair Syndrome\nMenkes Syndrome\nMenopause\nMenstruation Disorders \nMenstruation Disturbances\nMenstruation, Retrograde\nMental Disorders\nMental Retardation