Two-body Ds+ decays to eta pi +, eta ' pi +, eta rho +, eta ' rho +, and phi rho +
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Biomedical subjects
Publications and source records attributed to R Ehrlich.
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Chest radiographs were read from a sub-cohort of 386 factory workers with short term exposure to amosite asbestos (median exposure six months) and long follow up (median 25 years). Prevalence of abnormality was determined independently by two readers from the first film available after 20 years from first employment. Serial films were obtainable for 238 men (median interval from first to last film: nine years). Progression was classified with a direct progression scoring scale. Individual dust exposure estimates were derived from dust counts from two similar plants. With as little as one month or less of employment, about 20% of the films showed parenchymal abnormality and about a third showed pleural abnormality. Those in the lowest cumulative exposure stratum (less than 5 fibre-years/ml) were similarly found to have high rates of abnormality. Dose-response relations were present in the data of both readers. Smokers had higher rates of parenchymal abnormality. On multivariate analysis, cumulative exposure was the exposure variable most closely related to parenchymal abnormality, and time from first employment was the variable most closely related to pleural abnormality. Progression (including first attacks) 20 or more years after ceasing employment occurred and was more common for pleural than for parenchymal abnormality. It is concluded that with exposure to high concentrations to amosite such as existed in this factory and with follow up for at least 20 years, (1) exposure for as little as a month was sufficient to produce radiological signs of parenchymal and pleural fibrosis, (2) no cumulative exposure threshold for parenchymal and pleural fibrosis was detectable, and (3) parenchymal and pleural progression were still detectable >/= 20 years after the end of exposure.
To assess the relationship between passive smoking and asthma, we investigated (1) whether passive smoking was more prevalent among asthmatic than control children and (2) whether exposure to tobacco smoke was higher in acute asthma than in nonacute asthma. Three groups were recruited into a case-control study: 72 acute asthmatic children from the emergency room (ER), 35 nonacute asthmatic children from the asthma clinic, and 121 control children from the ER. Both questionnaire and urinary cotinine/creatinine ratio (CCR) were used to assess passive smoking. Levels of CCR greater than or equal to 30 ng/mg were used to identify children exposed at home. Mean CCR was also computed. Acute and nonacute asthmatic children had similar prevalences of passive smoking at home. Acute cases showed a higher mean CCR than nonacute cases, but this was not significant. In comparing all asthmatic to control children, smoking by the maternal caregiver was more prevalent among asthmatic children (odds ratio OR = 2.0, 95% CI 1.1, 3.4). This was confirmed by CCR greater than or equal to 30 ng/mg (OR = 1.9, 95% CI 1.04, 3.35) and by the difference in mean CCR (43.6 versus 25.8 ng/mg, p = 0.06). We conclude that smoking by the maternal caregiver is associated with clinically significant asthma in children. We could not show that it is a trigger of acute asthma attacks.
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The clinical, cardiac, and echocardiographic test results of 20 children with marfanoid features are reviewed. Fifteen were diagnosed as having Marfan syndrome, two had "possible" Marfan syndrome, and three had other diagnoses. On first evaluation, eight patients with Marfan syndrome (53%) had mitral regurgitation and none had aortic regurgitation. Echocardiography showed aortic root enlargement in 12 (80%) of 15 patients and mitral valve prolapse in 12 (80%) of 15. None had a normal echocardiogram. At follow-up examination, one patient had developed aortic root enlargement, and one patient, mitral valve prolapse. Thus, although aortic root enlargement is usually present in early childhood in patients with Marfan syndrome, it is not considered specific because in this study it also occurred in one child with Alport's syndrome and in one with marfanoid features. Four patients with aortic root enlargement were treated with propranolol and their echocardiograms showed no further increase in the aortic root diameter for several years. We recommend echocardiography in the diagnosis and routine management of children in whom Marfan syndrome is suspected.
To elucidate its potential role in the framework of bone marrow transplantation, we studied the toxicologic and pharmacologic properties of high doses of the triepoxide derivate 1,2,4-triglycidylurazol (TGU) in a preclinical dog model. Dose-dependent and dose-limiting gastrointestinal toxicity occurred in a dose range between 40 and 75 mg/kg, with the lethal dose for 50% of animals (LD50) being estimated at 60 mg/kg. Severe and life-threatening hematologic toxicity developed at all dose levels examined but was generally reversible. The combination of TGU and total-body irradiation produced synergistic gastrointestinal toxicity, necessitating reductions of the TGU dose by 50% as compared with the single-agent dose. In contrast, the combination of TGU and high-dose busulfan resulted in no apparent nonhematologic synergistic toxicities. The immunosuppressive properties of TGU given in this combination enabled sustained histocompatible allogeneic marrow engraftment in three of four animals. The pharmacokinetics of TGU were not influenced by prior total-body irradiation or high-dose busulfan. We conclude that the myelotoxic, pharmacologic and immunosuppressive properties of high-dose TGU observed in this preclinical model seem to render the drug particularly suitable for use in regimens preparatory to bone marrow transplantation.
Transformation of rodent cells by human adenoviruses is a well-established model system for studying the expression, regulation, and function of class I antigens. In this report, we demonstrate that the highly oncogenic adenovirus type 12 operates at the transcriptional and posttranscriptional levels in regulating the activity of major histocompatibility complex class I genes and products in transformed cells. Adenovirus type 12 suppresses the cell surface expression of class I antigens in most cell lines. Nevertheless, in a number of cell lines suppression is the result of reduction in the amount of stable specific mRNA, while in another group of cell lines suppression involves interference with processing of a posttranscriptional product. The two mechanisms operate both for the endogenous H-2 genes and for a miniature swine class I transgene that is expressed in the cells.
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