Studying neurosurgical implants for Parkinson disease: a question of design.

North American researchers' perspectives on designing neurosurgical implant studies for Parkinson disease (PD) challenged the custom of holding surgical trials to less stringent evidentiary standards than other clinical studies. Researchers supported placebo surgery-controlled trials. The framework they used to design and evaluate studies both of deep brain stimulation and cellular implants for PD may be applicable to a broad range of surgical implants for other disorders.

Age-specific survival after Hodgkin's disease in a population-based cohort (United States).

OBJECTIVE: To examine risk factors for disease-specific survival in young and older adults diagnosed with Hodgkin's disease (HD) in a representative case series of adequate size for detecting effect modification by age group. METHODS: For 5630 young adults (ages 15-44) and 2424 older adults (ages 45 and older) diagnosed with HD and reported to the population-based Surveillance, Epidemiology, and End Results program of the National Cancer Institute between 1983 and 1995, Kaplan-Meier survival curves were constructed and Cox proportional hazards regression used to evaluate the influences of age, sex, race/ethnicity, histologic subtype, Ann Arbor stage at diagnosis, and calendar year on hazard of disease-specific death. RESULTS: The effects of most previously studied risk factors for HD death were different for young and older adults. Age was not associated with disease-specific survival in young adults, but in older adults, 1-year increases in age elevated the relative hazard of HD death by 4 6%. Male sex was related to outcome in young but not older adults, and Ann Arbor stage and B-symptom status exhibited markedly different relationships to survival by age. Older adult patients with and without B-symptoms had different hazards of mortality and had to be assessed separately. CONCLUSIONS: Factors associated with disease-specific survival were different for young and older adults with HD. These findings provide further support for two etiologically and clinically distinct disease entities.

Epstein-Barr virus and survival after Hodgkin disease in a population-based series of women.

BACKGROUND: Epstein-Barr virus (EBV) positive Hodgkin disease (HD), as defined by the presence of EBV genes or gene products in the malignant cells, differs epidemiologically from EBV negative HD. However, survival patterns for EBV-defined HD have not been well studied. To determine if EBV status influenced survival time after HD, the authors investigated a large, population-based series of female patients. METHODS: For 311 female patients living in the Greater San Francisco Bay Area who were aged 19-79 years with HD diagnosed between mid-1988 and 1994, histopathologically rereviewed archived biopsy specimens were assayed for EBV with immunohistochemistry and in situ hybridization. The 53 subjects with EBV positive and the 258 with EBV negative HD were observed for vital status through 1998; overall survival was analyzed with Kaplan-Meier and Cox proportional hazards regression methods. RESULTS: Epstein-Barr virus positive HD patients were older, received diagnosis at a later stage, and were less likely to have nodular sclerosis histology than EBV negative patients. Deaths were reported for 21 (40%) EBV positive and 37 (14%) EBV negative patients. No survival differences were observed between EBV positive and negative women aged 19-44 years, but survival was significantly poorer in women aged 45-79 years with EBV positive HD. Regression analysis confirmed this strong negative effect of EBV positive status on survival (hazard ratio for death, 3.0; 95% confidence interval, 1.5-6.2) as unrelated to age, stage at diagnosis, or tumor histology. CONCLUSIONS: This study found a marked survival disadvantage for EBV positive HD in older but not young adult women. These findings suggest influences of both EBV status and age on HD survival, as well as pathogenesis.

Evaluating local differences in breast cancer incidence rates: a census-based methodology (United States).

OBJECTIVES: We used readily accessible, existing data to assess whether or not geographic variation in breast cancer incidence rates in the San Francisco Bay Area was related to the unequal distribution of known breast cancer risk factors. METHODS: Cancer registry and 1990 census block-group data were used to look at the associations between breast cancer incidence and known risk factors (including parity, urban/rural status, and socioeconomic indicators) in 25 California counties. Average annual age-adjusted invasive breast cancer incidence rates were calculated for the period 1988-1992, and adjusted morbidity ratios were computed. RESULTS: While breast cancer incidence in Marin County was 9 percent higher than that of the other 24 counties combined (relative risk = 1.09, 95 percent confidence interval = 1.01-1.18), this increase appeared to be due to the unequal distribution of known risk factors. Block-groups that had a high level of any risk factor had higher incidence rates, regardless of geographic location. After multivariate adjustment, breast cancer incidence no longer differed between Marin and the other counties (adjusted morbidity ratio = 1.02). CONCLUSIONS: The results suggest that the unequal distribution of known risk factors was responsible for Marin County's high breast cancer incidence rate.

Passive and active maternal smoking as measured by serum cotinine: the effect on birthweight.

To determine how maternal exposure to environmental tobacco smoke affects birthweight, maternal sera obtained from 3529 pregnant women around 27 weeks gestation were analyzed for cotinine, a metabolite of nicotine. Based on cotinine levels, nonsmokers were divided into those exposed to environmental tobacco smoke (2-10 ng/mL) and those unexposed (< 2 ng/mL), and smokers were divided into tertiles. Compared with unexposed nonsmokers' infants, infants of exposed nonsmokers averaged 45 g less (P = .28) after adjustment for confounders, and smokers' infants averaged 78, 191, and 233 g less for the first, second, and third cotinine tertiles, respectively. Birthweight decreased 1 g for every nanogram per milliliter of cotinine increase (P < .001).