Confidence Intervals for the Expectation of a Poisson Variable

Crow, Edwin L.; Gardner, Robert S.

doi:10.2307/2333541

Cited by 45 publications

(50 citation statements)

References 5 publications

(6 reference statements)

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“…To investigate the effects of sex, age at diagnosis, race, and year at diagnosis (1965-1969, 1970 -1974, and 1975-1979), Cox proportional hazard model was used. The 95% CIs were determined based on the Poisson distribution (16). Statistical analyses were conducted with SAS software (17).…”

Section: Discussionmentioning

confidence: 99%

Mortality Trends in Type 1 Diabetes

Nishimura

LaPorte²,

Dorman³

et al. 2001

Diabetes Care

140

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OBJECTIVES -To investigate long-term mortality and its temporal trends as of 1 January 1999 among the 1,075 patients with type 1 diabetes (onset age Ͻ18 years, diagnosed between 1965 and 1979) who comprise the Allegheny County population-based registry.RESEARCH DESIGN AND METHODS -Overall, sex-and race-specific mortality rates per person-year of follow-up were determined. Standardized mortality ratios were also calculated. Survival analyses and Cox proportional hazard model were also used. Temporal trends were examined by dividing the cohort into three groups by year of diagnosis (1965-1969, 1970 -1974, and 1975-1979).RESULTS -Living status of 972 cases was ascertained as of January 1, 1999 (ascertainment rate 90.4%). The mean duration of diabetes was 25.2 Ϯ 5.8 (SD) years. Overall, 170 deaths were observed. The crude mortality rate was 627 per 100,000 person-years (95% CI 532-728) and standardized mortality ratio was 519 (440 -602). Life-table analyses by the Kaplan-Meier method indicated cumulative survival rates of 98.0% at 10 years, 92.1% at 20 years, and 79.6% at 30 years duration of diabetes. There was a significant improvement in the survival rate between the cohort diagnosed during 1965-1969 and that diagnosed during 1975-1979 by the log-rank test (P ϭ 0.03). Mortality was higher in African-Americans than in Caucasians, but there were no differences seen by sex. The improvement in recent years was seen in both ethnic groups and sexes.

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Section: Discussionmentioning

confidence: 99%

Mortality Trends in Type 1 Diabetes

Nishimura

LaPorte²,

Dorman³

et al. 2001

Diabetes Care

140

View full text Add to dashboard Cite

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“…In some intervals, recovery of only one recombinant class was possible and in these instances, R equals 2X (one recombinant class) divided by the total progeny number. The 95% confidence intervals were estimated by using previously published statistics (11).…”

Section: Methodsmentioning

confidence: 99%

Multiple Genetic Pathways Involving the Caenorhabditis elegans Bloom's Syndrome Genes him-6, rad-51, and top-3 Are Needed To Maintain Genome Stability in the Germ Line

Wicky

Alpi

Passannante

et al. 2004

Molecular and Cellular Biology

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Bloom's syndrome (BS) is an autosomal-recessive human disorder caused by mutations in the BS RecQ helicase and is associated with loss of genomic integrity and an increased incidence of cancer. We analyzed the mitotic and the meiotic roles of Caenorhabditis elegans him-6, which we show to encode the ortholog of the human BS gene. Mutations in him-6 result in an enhanced irradiation sensitivity, a partially defective S-phase checkpoint, and in reduced levels of DNA-damage induced apoptosis. Furthermore, him-6 mutants exhibit a decreased frequency of meiotic recombination that is probably due to a defect in the progression of crossover recombination. In mitotically proliferating germ cells, our genetic interaction studies, as well as the assessment of the number of double-strand breaks via RAD-51 foci, reveal a complex regulatory network that is different from the situation in yeast. Although the number of double-strand breaks in him-6 and top-3 single mutants is elevated, the combined depletion of him-6 and top-3 leads to mitotic catastrophe concomitant with a massive increase in the level of double-strand breaks, a phenotype that is completely suppressed by rad-51. him-6 and top-3 are thus needed to maintain low levels of double-strand breaks in normally proliferating germ cells, and both act in partial redundant pathways downstream of rad-51 to prevent mitotic catastrophy. Finally, we show that topoisomerase III␣ acts independently during a late stage of meiotic recombination.

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“…Significances of other differences were calculated by chi-square. Confidence limits were derived from the tables of Crow and Gardner [18].…”

Section: Statistical Analysesmentioning

confidence: 99%

Comparison of the genetic effects of equimolar doses of ENU and MNU: While the chemicals differ dramatically in their mutagenicity in stem-cell spermatogonia, both elicit very high mutation rates in differentiating spermatogonia

Russell

Hunsicker

Russell

2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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Mutagenic, reproductive, and toxicity effects of two closely related chemicals, ethylnitrosourea (ENU) and methylnitrosourea (MNU), were compared at equimolar and near-equimolar doses in the mouse specific-locus test in a screen of all stages of spermatogenesis and spermiogenesis. In stemcell spermatogonia (SG), ENU is more than an order of magnitude more mutagenic than MNU. During post-SG stages, both chemicals exhibit high peaks in mutation yield when differentiating spermatogonia (DG) and preleptotene spermatocytes are exposed. The mutation frequency induced by 75 mg MNU/kg during this peak interval is, to date, the highest induced by any single-exposure mutagenic treatment -chemical or radiation -that allows survival of the exposed animal and its germ cells, producing an estimated 10 new mutations per genome. There is thus a vast difference between stem cell and differentiating spermatogonia in their sensitivity to MNU, but little difference between these stages in their sensitivity to ENU.During stages following meiotic metaphase, the highest mutation yield is obtained from exposed spermatids, but for both chemicals, that yield is less than one-quarter that obtained from the peak interval. Large-lesion (LL) mutations were induced only in spermatids. Although only a few of the remaining mutations were analyzed molecularly, there is considerable evidence from recent molecular characterizations of the marker genes and their flanking chromosomal regions that most, if not all, mutations induced during the peak-sensitive period did not involve lesions outside the marked loci. Both ENU and MNU treatments of post-SG stages yielded significant numbers of mutants that were recovered as mosaics, with the proportion being higher for ENU than for MNU.Comparing the chemicals for the endpoints studied and additional ones (e.g., chromosome aberrations, toxicity to germ cells and to animals, teratogenicity) revealed that while MNU is generally more effective, the opposite is true when the target cells are SG.

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Confidence Intervals for the Expectation of a Poisson Variable

Cited by 45 publications

References 5 publications

Mortality Trends in Type 1 Diabetes

Mortality Trends in Type 1 Diabetes

Multiple Genetic Pathways Involving the Caenorhabditis elegans Bloom's Syndrome Genes him-6, rad-51, and top-3 Are Needed To Maintain Genome Stability in the Germ Line

Comparison of the genetic effects of equimolar doses of ENU and MNU: While the chemicals differ dramatically in their mutagenicity in stem-cell spermatogonia, both elicit very high mutation rates in differentiating spermatogonia

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