Essential-states mechanism of optical nonlinearity in pi -conjugated polymers.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S Mazumdar.
Explore the source record for details and available documents.
A program package using FORTRAN and GLIM is presented to compute lifetime risks of dying from a particular cause of death for a worker subjected to specific risk exposures using death rates adjusted for selected covariates (risk factors). Calculations of the exposure index and adjusted rates depend on several commonly used procedures. Tests of homogeneity and trend for adjusted rates are provided. Lifetime risks are calculated in two different ways: adjusting or ignoring competing causes of death.
The modeling of cohort data based on the Armitage-Doll multistage model of the carcinogenic process has gained popular acceptance as a methodology for quantitative risk assessment for estimating the dose-related relationships between different occupational and environmental carcinogenic exposures and cancer mortality. The multistage model can be used for extrapolation to low doses relevant for setting environmental standards and also provides information regarding whether more than one stage is dose-related, which assists in determining whether different carcinogens affect different stages of the cancer process. This paper summarizes recent developments in the multistage modeling of cohort data and emphasizes practical issues such as handling data arising from large epidemiologic follow-up studies, the time-dependent nature of exposures and statistical issues such as multicollinearity in time-related variables, robustness of parameter estimates, validating of the fitted models, and routine inferential procedures. Problems related to uncertainties of risk estimates are discussed also. Computer programs for fitting multistage models with one or two dose-related stages to cohort data incorporating time-dependent exposure patterns; constructing confidence regions for model parameters; and predicting lifetime risks of dying from cancer adjusting for competing causes of death are detailed. Illustrations are provided using lung cancer mortality in a cohort of nonwhite male coke oven workers exposed to coal tar pitch volatiles.
The sleep of thirty elderly patients with recurrent unipolar depression was examined at baseline (before acute treatment of the index episode) and again in a state of symptomatic remission with nortriptyline (mean steady-state level: 82.1 ng/ml). Continuation therapy with nortriptyline was associated with improvement of polysomnographic sleep maintenance (mainly in the third and fourth sleep cycles, to a level similar to that of controls), prolongation of rapid-eye-movement (REM) sleep latency (exceeding that of controls), and potentiation of slow-wave activity during the first non-REM (NREM) sleep period. Clinical improvement, as measured by the Hamilton Depression Rating Scale, was significantly associated with shift of delta activity toward sleep onset (p less than 0.002), prolongation of REM sleep latency (p less than 0.0001), and improvement in sleep maintenance (p less than 0.0002). Multiple regression analysis showed that the single best correlate of clinical change was prolongation of REM sleep latency (i.e., prolongation of first NREM period). Perceived sleep quality improved significantly during early continuation therapy with nortriptyline, but not to the level reported by a group of 30 age- and sex-matched healthy controls. The findings are consistent with the concept that anti-depressant drug efficacy may depend upon strengthening of the homeostatic regulation of sleep and upon changes in the REM-sleep regulation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Injections of Crohn's disease (CD) tissue filtrates produce lymphoma and hyperplastic lymph nodes from plasma cell hyperplasia (PCH) in athymic nude (nu/nu) mice; these lymphoid tissue contain an antigen(s) recognized by CD serum/gamma G immunoglobulin (IgG). To immortalize the "CD-reactive antigen(s)," the authors fused the lymphoid cells from a CD tissue filtrate primed nu/nu mouse with nonsecretory mouse myeloma cells. Hybrids were screened and selected based on their reactivity with CD serum IgG, but not with control serum IgG in an indirect immunofluorescence assay (IF). Two CD-positive hybridomas were examined by IF with sera from 47 CD, 38 ulcerative colitis (UC), 13 controls with other gastrointestinal diseases, 19 with autoimmune diseases, and 21 normal subjects. Sera from 16 CD patients (34%) reacted with the two hybridomas, but only one of 38 UC sera and none of the 53 other disease or normal control sera reacted. The immunoreactivity of CD sera was significantly higher than UC sera (P less than 0.01) and each of the other groups (P less than 0.007). Using immunoperoxidase techniques at light and electron microscopic levels, the authors localized CD-associated antigen(s) in the plasma membrane of the two hybridomas. Further characterization of these hybridomas and the immunoreactive protein(s) may provide an important probe(s) for the diagnosis and the understanding of the pathogenesis of CD.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Multistage modeling incorporating a time-dependent exposure pattern is applied to lung cancer mortality data obtained from a cohort of 2802 arsenic-exposed copper-smelter workers who worked 1 or more years during the period 1940-1964 at a copper smelter at Tacoma, Washington. The workers were followed for death through 1976. There were 100 deaths due to lung cancer during the follow-up period. Exposures to air arsenic levels measured in micrograms/m3 were estimated from departmental air arsenic and workers urinary arsenic measurements. Relationships of different temporal variables with excess death rates are examined to judge qualitatively the implications of the multistage cancer process. Analysis to date indicates a late stage effect of arsenic although an additional early stage effect cannot be ruled out.
A cohort analysis was performed to predict the lifetime lung cancer risk to a US or Canadian nonwhite male steelworker exposed to coke oven emissions. The procedure employed required that the lung cancer mortality (used for risk assessment) be estimated by addition of the excess to the background rates. The age-specific excess rates were obtained following selection of the proper excess risk function as implied by the multistage theory of carcinogenesis. A quantitative approach based on model fitting was used for selection of the excess risk function. The results show no evidence that coke oven emissions have a late stage carcinogenic effect. The indication that the agent acts as an initiator is moderate to weak. The number of carcinogenic stages involved was estimated to be four. Based on the assumption that exposure was set at a high concentration for 40 years with a starting age of 20 years, it was estimated that the lifetime risk through age 85+ years for a hypothetical US or Canadian nonwhite male oven worker could be as high as 0.40. This represents a 15-fold increase of the baseline risk.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The assumption that discharge diagnoses of chronic obstructive pulmonary disease and other allied conditions accurately reflect patient medical records was tested using a sample of 553 hospital discharges from the Pittsburgh, Pennsylvania area. Three validation criteria were used in reviewing patient hospital records: 1) the presence of abnormal spirometry test results; 2) reference made to a previous diagnosis of one of the conditions; and 3) reports of respiratory symptoms consistent with these conditions. The findings were that 1 per cent of the 432 cases with a primary diagnosis in this disease category and 10 per cent of the 121 cases with a primary diagnosis of heart disease and a secondary diagnosis in this disease category were not supported by any of the selected criteria.
Explore the source record for details and available documents.
Groups of guinea pigs were exposed to respirable particles of cotton dust obtained from opening and carding rooms of a textile mill. The bulk cotton dust was resuspended with a modified sonic sifter. Exposures were conducted 6 hr/day at concentrations varying between 16 and 25 mg/m3. The particle size for these exposures varied around a 3 micron aerodynamic equivalent diameter. In animals exposed for 5 days, a pulmonary effect began to develop 3 hr after the start of exposure on the first day and was maximal 18 hr postexposure. The pulmonary effect faded during the ensuing weekdays as daily exposures continued. In one group exposed for 6 weeks, 5 days/week, the pulmonary effect was apparent on each Monday and faded during the week. The pulmonary response can best be characterized as a reflex restriction of breathing from stimulation of vagal nerve endings, resulting in rapid shallow breathing. This effect was exaggerated upon challenge of the animals with air containing 10% CO2. In humans this pattern of rapid shallow breathing is associated with symptoms of shortness of breath, dyspnea, breathlessness, and fatigue upon exertion. Such symptoms are characteristic of those reported by workers exposed to cotton dust. This animal model is proposed for further evaluation of the possible relationship between the acute responses to cotton dust and the development of a chronic response.