Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We tried the new method of urinary diversion via a continent ileal reservoir, reported by Kock in 1982, and now being accepted with great enthusiasm and satisfaction not only by doctors, but also by patients in Europe and in the United States. With this method, continency with storage of urine under low pressure is well maintained so that no external appliances are necessary. Ileorenal reflux is also prevented with this nipple valve forming technique, minimizing impairment of renal function. We report for the first time in Japan 13 cases, in which this method of innovative urinary diversion was used, with special attention paid to its demanding surgical technique and early results with its complications. From November, 1984 to August, 1985, we performed urinary diversion via the Kock pouch in 13 cases: 10 males and 3 females, from 35 to 67 years old (mean age 49 years), 11 bladder cancer patients, and 2 rectal cancer patients. The 2 patients with rectal cancer died from cancer and 1 bladder cancer patient with psychosis died from mental crisis 4 months after the operation. Of the 10 cases followed up long enough, 7 cases were in excellent condition with complete continence, 2 cases were in good condition with minor leak due to intermittent prolapse of the nipple valve, and in one case with failure, due to the postoperative ileus and eversion of the nipple valve, which made it difficult to catheterize into the pouch. Excision of the pouch and conversion to the standard ileal conduit was performed by reoperation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Urinary diversion with the Kock continent ileal reservoir: report of 13 cases]. 391 15

An animal model for studying the actions of hallucinogenic drugs using primate social colonies is presented. Although hallucinogens induce a number of behavioral changes in this paradigm, one emergent behavior, limb jerks, appears to be selectively induced by three classes of hallucinogens in doses which correlate with those reported to be hallucinogenic in humans. Several non-hallucinogenic congeners of hallucinogens failed to significantly elicit this response. Other behavioral changes induced by hallucinogens in monkeys such as ptosis and social withdrawal may be useful in studying aspects of hallucinogen intoxication other than hallucinations, or psychosis in general. Upon daily administration, tolerance developed to all hallucinogens tested except two, as is seen in humans. Moreover, cross-tolerance between hallucinogens could be demonstrated. Further experiments with the hallucinogen 5-methoxy N,N-dimethyltryptamine revealed that although certain individual behaviors could be antagonized by serotonin antagonists, dopamine antagonists, and physostigmine, no drug completely reversed the behavioral abnormalities induced by this hallucinogen. It is suggested that this paradigm, which offers an hallucinogen-induced behavior which correlates well with the human hallucinogen response and permits observation of a wide variety of other potentially relevant behaviors in primates, may be useful in developing and testing theories of hallucinogenic drug action. It may be especially valuable in view of the present difficulties of conducting hallucinogen research in humans.
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PMID:A primate model for the study of hallucinogens. 395 28

We report a 20-year-old man with intractable myasthenia gravis successfully treated with total lymphoid irradiation (TLI). An encapsulated thymoma in the anterior mediastinum was resected as extended thymectomy by video-assisted thoracoscopic surgery at 2 months after the onset of ptosis and muscle weakness. Following treatments, such as ambenonium hydrochloride, an immunosuppression therapy (prednisolone and azatioprine), 5 courses of immunoadsorption therapy, and a high dose of cyclophosphamide and methylprednisolone, did not make persistent improvement of myasthenic symptoms. Ageusia occurred twice prior to myasthenic crises and subsided with other myasthenic symptoms after treatments. Steroid psychosis and secondary Cushing's syndrome made us to reduce the dose of prednisolone. Post-operative residual, recurrent, or metastatic thymus was not unveiled, then we added the low dose fractionated irradiation (1.5 Gy x 12 = 18 Gy) to the mediastinum. Three months after the irradiation, however, a crisis occurred and the titer of anti-acetylcholine receptor antibody increased up to 100 nmol/l. Therefore, we performed TLI (Mantle; 1.5 Gy x 9 = 13.5 Gy, paraaortic and inverted-Y; 1.5 Gy x 14 = 21 Gy), which brought about persistent improvement of myasthenic symptoms with decrease in the titer of anti-acetylcholine receptor antibody.
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PMID:[A patient with intractable myasthenia gravis successfully treated with total lymphoid irradiation]. 1054 16

We report 10 children (7 male, 3 female), 3 homozygous for c.319C>T mutation and 7 heterozygous for c.319C>T on one allele and c.625G>A variant on the other in the short-chain acyl-CoA dehydrogenase (SCAD) gene (ACADS). All were of Ashkenazi Jewish origin in which group we found a c.319C>T heterozygote frequency of 1:15 suggesting the presence of a founder mutation or selective advantage. Phenotype was variable with onset from birth to early childhood. Features included hypotonia (8/10), developmental delay (8/10), myopathy (4/10) with multicore changes in two and lipid storage in one, facial weakness (3/10), lethargy (5/10), feeding difficulties (4/10) and congenital abnormalities (3/7). One female with multiminicore myopathy had progressive external ophthalmoplegia, ptosis and cardiomyopathy with pneumonia and respiratory failure. Two brothers presented with psychosis, pyramidal signs, and multifocal white matter abnormalities on MRI brain suggesting additional genetic factors. Two other infants also had white matter changes. Elevated butyrylcarnitine (4/8), ethylmalonic aciduria (9/9), methylsuccinic aciduria (6/7), decreased butyrate oxidation in lymphoblasts (2/4) and decreased SCAD activity in fibroblasts or muscle (3/3) were shown. Expression studies of c.319C>T in mouse liver mitochondria showed it to be inactivating. c.625G>A is a common variant in ACADS that may confer disease susceptibility. Five healthy parents were heterozygous for c.319C>T and c.625G>A, suggesting reduced penetrance or broad clinical spectrum. We conclude that the c.319C>T mutation can lead to wide clinical and biochemical phenotypic variability, suggesting a complex multifactorial/polygenic condition. This should be screened for in individuals with multicore myopathy, particularly among the Ashkenazim.
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PMID:Short-chain acyl-CoA dehydrogenase gene mutation (c.319C>T) presents with clinical heterogeneity and is candidate founder mutation in individuals of Ashkenazi Jewish origin. 1805 10