Statistics in Biosciences最新文献

To confine the spread of an infectious disease, setting a sensible quarantine time is crucial. To this end, it is imperative to well understand the distribution of incubation times of the disease. Regarding the ongoing COVID-19 pandemic, 14-days is commonly taken as a quarantine time to curb the virus spread in balancing the impacts of COVID-19 on diverse aspects of the society, including public health, economy, and humanity perspectives, etc. However, setting a sensible quarantine time is not trivial and it depends on various underlying factors. In this article, we take an angle of examining the distribution of the COVID-19 incubation time using likelihood-based methods. Our study is carried out on a dataset of 178 COVID-19 cases dated from January 20, 2020 to February 29, 2020, with the information of exposure periods and dates of symptom onset collected. To gain a good understanding of possible scenarios, we employ different models to describe incubation times of COVID-19. Our findings suggest that statistically, the 14-day quarantine time may not be long enough to control the probability of an early release of infected individuals to be small. While the size of the study data is not large enough to offer us a definitely acceptable quarantine time, and further in practice, the decision-makers may take account of other factors related to social and economic concerns to set up a practically acceptable quarantine time, our study demonstrates useful methods to determine a reasonable quarantine time from a statistical standpoint. Further, it reveals some associated complexity for fully understanding the COVID-19 incubation time distribution.

Supplementary information: The online version contains supplementary material available at 10.1007/s12561-021-09320-8.

Leveraging external data is a topic that have recently received much attention. The propensity score-integrated approaches are a methodological innovation for this purpose. In this paper we adapt these approaches, originally introduced to augment single-arm studies with external data, for the augmentation of both arms of a randomized controlled trial (RCT) with external data. After recapitulating the basic ideas, we provide a step-by-step tutorial of how to implement the propensity score-integrated approaches, from study design to outcome analysis, in the RCT setting in such a way that the study integrity and objectively are maintained. Both the Bayesian (power prior) approach and the frequentist (composite likelihood) approach are included. Some extensions and variations of these approaches are also outlined at the end of this paper.

Gene expression data are often collected from tissue samples that are composed of multiple cell types. Studies of cell type composition based on gene expression data from tissue samples have recently attracted increasing research interest and led to new method development for cell type composition estimation. This new information on cell type composition can be associated with individual characteristics (e.g., genetic variants) or clinical outcomes (e.g., survival time). Such association analysis can be conducted for each cell type separately followed by multiple testing correction. An alternative approach is to evaluate this association using the composition of all the cell types, thus aggregating association signals across cell types. A key challenge of this approach is to account for the dependence across cell types. We propose a new method to quantify the distances between cell types while accounting for their dependencies, and use this information for association analysis. We demonstrate our method in two applied examples: to assess the association between immune cell type composition in tumor samples of colorectal cancer patients versus survival time and SNP genotypes. We found immune cell composition has prognostic value, and our distance metric leads to more accurate survival time prediction than other distance metrics that ignore cell type dependencies. In addition, survival time-associated SNPs are enriched among the SNPs associated with immune cell composition.

Growing evidence supports a positive association between childhood obesity and chronic diseases in later life. It is also suggested that childhood obesity is more prevalent for children born from pregnancies complicated by metabolic disorders such as gestational diabetes, and can be related to maternal dietary factors during gestation. Extending conventional analyses that report only the marginal associations within non-causal mediation frameworks, we present mediation analysis in the case of multiple exposures and multiple mediators using a regularized two-stage approach. By placing shrinkage priors on each parameter relating to direct and indirect effects, a parsimonious model can be obtained, and consequently, the most relevant pathways will be selected to inform the development of efficient prevention programs. We apply this method to data from the Danish site of the Diabetes & Women's Health Study, Danish National Birth Cohort (DNBC), and find 6 significant maternal risk factors either directly or indirectly affecting childhood body mass index $z$ score at age 7. Simulations with data-generating mechanisms similar to the DNBC data demonstrate good performance of the proposed model.