Biomedical subjects

K Drescher

Publications and source records attributed to K Drescher.

7 recordsLinked to original sources

PubMed1991

Smoking cessation and nonsmoking intervals: effect of different smoking patterns on lung cancer risk.

A case-control study of lung cancer was conducted in northwestern Germany in 1985-86. The study included 194 lung cancer cases and the same number of hospital controls and population controls who were matched to the cases by sex and age. Personal interviews were conducted by trained interviewers. We report here the effect of different smoking patterns--such as nonsmoking intervals, and time since quitting smoking--on lung cancer risk. Both quitting smoking and having a nonsmoking interval are seen to reduce lung cancer risk significantly. For a nonsmoking interval of three years or more, relative risk (RR) = 0.21, 95 percent confidence interval (CI) = 0.08-0.52; for quitting smoking for 10 years or more, RR = 0.23, CI = 0.11-0.48). A dose-response relationship was estimated for cigarette dose, length of nonsmoking interval, and time since stopped smoking.

Adult↗

PubMed1991

Attributable risk estimation from case-control data via logistic regression.

By fitting an unconditional logistic regression model to unmatched case-control data, an estimate of the joint population attributable risk for the factor included is obtained. This estimate and its asymptotic variance can easily be computed from the intercept parameter and its asymptotic variance. A generalization to the analysis of stratified data with large strata enables the calculation of stratum-specific attributable risks and their variances via stratum-specific intercept parameters. If sampling of cases is independent of strata, an estimate of the summary attributable risk and its asymptotic variance may be obtained as a weighted sum of the stratum-specific attributable risks.

Biometry↗

PubMed1990

The design of case-control studies: the effect of confounding on sample size requirements.

This paper considers the extent to which confounding effects of covariates, which are not controlled for by matching in the design, may influence the sample size necessary for case-control studies. The quantitative calculations are performed for an age-matched case-control study on lung cancer and air pollution, and are based on different evaluation methods. For illustrative purposes attention is confined to a dichotomous risk factor and a single dichotomous covariate. By using the numerical values of a pilot study investigating lung cancer and air pollution, it turns out that the sample size required for detecting a relative risk as close as 1.15 to 1 is only slightly influenced by the strength of the association between confounder and risk factor for reasonable variations around our empirical values. On the other hand, sample size considerably increases with increasing relative risk of a confounder even when the association remains small. The sample size required for an individually matched analysis practically equals that for an age-stratified analysis when the relative risk of the covariate is one. With a relative risk greater than one, however, the size for a matched analysis exceeds that for a stratified analysis and the ratio between them increases with increasing relative risk.

Air Pollutants↗

PubMed1990

[Results of the epidemiology of lung cancer in females].

In the context with an extensive pilot study investigating risk factors for lung cancer, aetiological and clinical questions were analysed for lung cancer mortality in women. In a first step all available data sources about the prevalence of smoking in the FRG were used to determine the correlation between the prevalence of smoking and lung cancer mortality. 88% of the variance (R2) of lung cancer mortality for women could be explained by smoking. In a second step medical records of 133 female lung cancer patients from three hospitals were analysed with regard to the histological types of lung cancer and smoking. Small cell lung cancers were more frequent among female smokers while adenocarcinoma was more prevalent among non-smokers. Survival analysis for 421 men and 97 women showed a significantly longer survival time for women as compared to men, taking into account other relevant prognostic factors. The association between smoking and lung cancer is discussed and analysed in greater detail.

Cause of Death↗

PubMed1988

Influence of antipsychotics and serotonin antagonists on presynaptic receptors modulating the release of serotonin in synaptosomes of the nucleus accumbens of rats.

In the nucleus accumbens of rats the release of [3H]serotonin (5-HT) from superfused synaptosomes stimulated by 30 mM K+ was investigated. In the presence of 40 microM of the uptake inhibitor cocaine the release of [3H]5-HT was inhibited by 5-HT in a concentration-dependent manner (IC50 = 0.45 microM). The maximum inhibitory effect of 5-HT was 54% of controls. The inhibition of K+-stimulated release of [3H]5-HT induced by 5-HT was antagonized completely by methiothepine and clozapine, respectively, whereas methysergide had only a weak antagonizing effect in a concentration of 20 microM or less, haloperidol was ineffective. Furthermore, the synaptosomal K+-stimulated release of [3H]5-HT was also inhibited by dopamine (DA) in a concentration-dependent manner (IC50 = 0.1 microM). This inhibitory effect was antagonized by antipsychotic drugs, the rank order of antagonistic potencies was sulpiride greater than haloperidol greater than clozapine; methiothepine was ineffective. The experimental system (the K+-stimulated synaptosomal release of [3H]5-HT seems to be a suitable model for differentiating dopaminergic and/or serotonergic components of antipsychotics or other drugs on presynaptic receptors.

Animals↗

PubMed1986

Influence of antipsychotics on presynaptic receptors modulating the release of dopamine in synaptosomes of the nucleus accumbens of rats.

The release of preloaded [3H]dopamine (DA) from superfused synaptosomes stimulated by 30 mM K+ was investigated in the nucleus accumbens of rats. Under conditions preventing the uptake of DA (presence of 40 microM cocaine) release of [3H]DA was inhibited by DA and apomorphine in a concentration-dependent manner (IC50s 0.65 and 0.3 microM, respectively). The maximal inhibitory effects of DA, as well as of apomorphine, were about 50% of the controls. The DA-induced inhibition was antagonized by antipsychotics completely; the rank order of antagonistic potencies was haloperidol greater than clozapine greater than sulpiride; methiothepine was ineffective. Furthermore, the K+-stimulated release of [3H]DA was inhibited by serotonin in a concentration-dependent manner (IC50 = 0.9 microM). This inhibitory effect was antagonized by methiothepine with a high efficiency, by clozapine and methysergide with moderate efficiencies; haloperidol and sulpiride were ineffective. The experimental system demonstrated appears to be suitable for characterizing the DA- and serotonin-antagonistic potencies of antipsychotics and other drugs on presynaptic autoreceptors as well as receptors modulating release of DA in the nucleus accumbens.

Animals↗

PubMed1979

Time course of clinical-chemical parameters under long-term lithium treatment.

In 40 manic-depressive patients under lithium prophylaxis the time course of the following variables has been studied over a period of 3 years (retrospective investigation): Diff. blood smear, hemoglobine, leucocytes, electrolytes in serum, electrophoresis, GPT, GOT, alcaline phosphatase, creatinine and urea in serum. Appr. 1000 blood samples were evaluated. The issue of additional psychotropic medication has been given special consideration.

Adult↗