Traditional analyses (e.g., Schnabel 1938 or Chapman 1954 of sequential mark-recapture experiments (Petersen and Schnabel type) yield population estimates with substantial negative bias and overly large confidence intervals if the combination of the number of animals marked and examined falls too low. To address these problems, sequential mark-recapture experiments are cast into a Bayesian framework using a "noninformative" discrete uniform improper prior (a priori theoretical) distribution. Some properties of the posterior distribution (probability of each population size given the data) are briefly and informally discussed (inference, convergence, mean, mode, median, and treatment of nuisance parameters). A sequential Bayes computational algorithm, suitable for microcomputers, is given. Several examples are presented as a practical guide to computing estimates.For relatively small sample sizes, the Bayesian approach yields larger mean abundance estimates than traditional methods. There is little difference in these estimates for larger sampling efforts. Advantages of the approach include the following: the probability of observing the data at all feasible population sizes is calculated exactly; the method works for all cases regardless of sample size or sampling procedure; a plot of successive posterior distributions can be used as a visual diagnostic of conformity with basic assumptions; and finally, inferences can be made directly, since the end product completely describes the uncertainty of the population size given the data.
A computer simulation model was used to examine growth and survival of all major British Columbia salmon stocks during their first 6 mo of ocean life. Factors included in the calculations were the space–time distribution of zooplankton production, timing of salmon ocean arrival and migration especially as regards overlaps between stocks, feeding and growth in relation to food availability, and mortality rates in relation to body size. It is concluded that ocean limitation of production is unlikely unless only a small fraction of total zooplankton production is available to the salmon. The model emphasizes several critical uncertainties about the marine biology of salmon: rates of replenishment of near surface zooplankton stocks (where most salmon feeding occurs) from deeper water have not been adequately measured, and the functional response of salmon to prey density is not understood. There is inadequate data on the relationship between body size and mortality rate, and migration patterns of juvenile fish have not been documented precisely enough. Hopefully some of these uncertainties will be resolved through the salmon enhancement programs. Key words: salmon, population limitation, juvenile marine production, simulation model
Suicide accounts for >800,000 deaths annually worldwide; prevention is an urgent public health issue. Identification of risk factors remains challenging due to complexity and heterogeneity. The study of suicide deaths with increased extended familial risk provides an avenue to reduce etiological heterogeneity and explore traits associated with increased genetic liability. Using extensive genealogical records, we identified high-risk families where distant relatedness of suicides implicates genetic risk.We compared phenotypic and polygenic risk score (PRS) data between suicides in high-risk extended families (high familial risk (HFR), n = 1,634), suicides linked to genealogical data not in any high-risk families (low familial risk (LFR), n = 147), and suicides not linked to genealogical data with unknown familial risk (UFR, n = 1,865).HFR suicides were associated with lower age at death (mean = 39.34 years), more suicide attempts, and more PTSD and trauma diagnoses. For PRS tests, we included only suicides with >90% European ancestry and adjusted for residual ancestry effects. HFR suicides showed markedly higher PRS of suicide death (calculated using cross-validation), supporting specific elevation of genetic risk of suicide in this subgroup, and also showed increased PRS of PTSD, suicide attempt, and risk taking. LFR suicides were substantially older at death (mean = 49.10 years), had fewer psychiatric diagnoses of depression and pain, and significantly lower PRS of depression.Results suggest extended familiality and trauma/PTSD may provide specificity in identifying individuals at genetic risk for suicide death, especially among younger ages, and that LFR of suicide warrants further study regarding the contribution of demographic and medical risks.
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