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Biomedical subjects

J B Swartz

Publications and source records attributed to J B Swartz.

7 recordsLinked to original sources
PubMed2000

Hormone replacement therapy use in urban older women attending meal sites: associations with sociodemographic and health characteristics and use of preventive services.

OBJECTIVE: To examine sociodemographic, health and preventive health practices associated with hormone replacement therapy (HRT) use in urban community-dwelling older women. DESIGN: Survey. SETTING: Community-based meal sites throughout the city of Los Angeles. PARTICIPANTS: A convenience sample of 705 community-dwelling women older than age 60 who completed questionnaires for the Prevention for Elderly Persons Program. MEASUREMENTS: Demographic and life style characteristics, functional status, preventive practices, and current and past use of HRT. RESULTS: Among the 705 women surveyed, 13% reported current use and 17% reported past use of HRT. Current users were more likely to be younger and more likely to report a history of osteoporosis, hysterectomy, and calcium use than never users. White women were more likely to be current users than black women. CONCLUSIONS: Only a small proportion of the older urban women studied are currently using HRT. In particular, efforts to increase the use of these preventive services need to focus on black women and women who do not have a prior history of osteoporosis.

Aged↗
PubMed1999

Comparison of the entropy technique with two other techniques for detecting disease clustering using data from children with high blood lead levels.

The entropy technique was compared with two other case-control techniques for detecting disease clustering using data on blood lead levels of children who were patients at the King/Drew Medical Center in South-Central Los Angeles in 1991 to 1994. The other two methods are the nearest neighbor technique (NNT) and Moran's IPOP technique, a variation of Moran's I test, in which rates are adjusted for population size. Four different blood lead levels (15 microg/dl, 20 microg/dl, 30 microg/dl, 35 microg/dl) were used as cutoff levels to designate cases. Persons with blood lead levels greater than or equal to the cutoff level were designated as cases. The authors found significant clustering for all four cutoff levels using the entropy method, and for the first three cutoff levels using the NNT. They found significant clustering with Moran's IPOP for some scales for two of the cutoff levels. While performance of the entropy technique and the NNT were independent of scale, that of Moran's IPOP was highly scale-dependent.

Adolescent↗
PubMed1998

An entropy-based algorithm for detecting clusters of cases and controls and its comparison with a method using nearest neighbours.

A new method for detecting disease clustering based on entropy is presented. For this method cases and controls are plotted on a map. The map is divided into regions. The entropy of the space is calculated as the log of the number of possible ways of placing the cases and controls in the various regions given the total number of cases and controls and the number of cases and controls in each region. The power of the entropy technique is tested against the power of the nearest neighbour technique (NNT). The entropy method is shown to be substantially more powerful than the NNT when there is more than one cluster in the space or when the clusters are near the boundary of the space.

Algorithms↗
PubMed1992

Use of a multistage model to predict time trends in smoking induced lung cancer.

STUDY OBJECTIVE: The aims were to use a mathematical model to predict the time course of smoking induced lung cancer, and to investigate to what extent the most recent increases in lung cancer mortality are due to cigarette smoking. DESIGN: A mathematical model was developed and solved by simulation to construct detailed smoking histories of the US white male population given available prevalence data by age and cohort. A multistage carcinogenesis model was used to predict the time course of smoking induced lung cancer given the detailed smoking histories. SOURCE OF DATA AND MODEL PARAMETERS: The smoking prevalence figures were taken from work by Harris who calculated them using data collected in the Health Interview Survey. The parameters of the multistage model were taken from Whittemore who fitted the model to several sets of smoking and lung cancer data. MAIN RESULTS: The smoking model was used to construct detailed smoking histories of the US white male population from 1900 to 1985. In turn the multistage model was used to predict age and cohort specific smoking induced lung cancer mortality rates over this period. These results were compiled to predict the overall age adjusted trend in smoking induced lung cancer from 1970 to 1985. The model predicts a 12% decline in smoking induced lung cancer for this group over the 15 year period. CONCLUSIONS: The model calculations predict a 12% decline in smoking induced lung cancer for this group, during a period when the actual total rate of lung cancer increased by 26%. Taken together with the decline in average tar content in cigarettes over this period, and the relatively constant dose rate among smokers, these results strongly suggest that the recent increase in lung cancer among white males in the USA is due entirely or in large part to factors other than cigarette smoking.

Cohort Studies↗
PubMed1982

Analyses of carcinogenesis dose-response relations with dichotomous data: implications for carcinogenic risk assessment.

Dose-response data from experimental and epidemiologic carcinogenicity studies were analyzed in attempts to resolve basic questions in extrapolating from high to low doses and assessing human risk. Four models (Weibull, Mantel-Bryan, Marshall-Groer, and Mancuso-Stewart) were fit to 46 sets of experimental and 4 sets of epidemiologic data by maximizing the likelihood function with a Rosenbrock hill-climbing algorithm. The models were compared as to their adequacy in describing the data and analyzed to determine the effect of carcinogen and breeding category, species, and spontaneous tumor incidence. The shapes of the dose-response curves were analyzed, and errors in risk estimation from linear extrapolation through the origin were calculated. All models were shown to fit the data and to be comparable in accuracy. The dose-response curves were generally "stretched out," particularly for outbred strains, with one or two orders of magnitude of dose increase required to increase the proportion of tumor responders from 10% to 70%. Linear extrapolation through the origin generally underestimated the response at low doses, frequently by several orders of magnitude. The power dependence of tumor incidence on dose was generally found to be of the order of unity, substantially less than assumed in most mathematical models.

Carcinogens↗