Future research should focus on expanding our preliminary findings to include a larger examination of articles to show evidence for or against the relationship between higher Altmetric scores and higher citation scores.
 Altmetric scores may offer a viable and relatively rapid metric of the likely uptake and impact of manuscripts. Ultimately, these findings represent preliminary evidence of the benefits of widespread dissemination of eating disorder research beyond traditional academic methods. Future research should focus on expanding our preliminary findings to include a larger examination of articles to show evidence for or against the relationship between higher Altmetric scores and higher citation scores.Degradation and collapse of stalled replication forks are main sources of genomic instability, yet the molecular mechanisms for protecting forks from degradation/collapse are not well understood. Here, we report that human CST (CTC1-STN1-TEN1) proteins, which form a single-stranded DNA-binding complex, localize at stalled forks and protect stalled forks from degradation by the MRE11 nuclease. CST deficiency increases MRE11 binding to stalled forks, leading to nascent-strand degradation at reversed forks and ssDNA accumulation. In addition, purified CST complex binds to 5' DNA overhangs and directly blocks MRE11 degradation in vitro, and the DNA-binding ability of CST is required for blocking MRE11-mediated nascent-strand degradation. Our results suggest that CST inhibits MRE11 binding to reversed forks, thus antagonizing excessive nascent-strand degradation. Finally, we uncover that CST complex inactivation exacerbates genome instability in BRCA2 deficient cells. Collectively, our findings identify the CST complex as an important fork protector that preserves genome integrity under replication perturbation.
  Coeliac disease is an immune-mediated intestinal disease characterised by lifelong intolerance to dietary gluten in genetically predisposed individuals. Microbial factors including infections or bacterial microbiota have long been suspected to be involved in the aetiology, but the scientific literature on the topic is scattered and heterogeneous.
 
  To review human observational studies on microbes and coeliac disease METHODS We identified 135 publications judged relevant. Most studies were cross-sectional, and prone to reverse causation and other biases. Only a few were prospective. Cohort studies and longitudinal studies that have sampled biological specimens before disease onset are emphasised in the review.
 
  Infections during early childhood were associated with an increased risk of subsequent coeliac disease in nine studies , whereas maternal infections during pregnancy did not show a clear association. For the most frequently studied microbial factors, some evidence for an association was found, including Helicobacter pylori (four out of 16 studies), adenovirus (two out of nine studies) and enterovirus (two out of six studies). Rotavirus infections have been associated with disease development, and rotavirus vaccination may reduce the risk. Among the many studies of gut microbiota, most were cross-sectional and, therefore, potentially influenced by reverse causation. Only two smaller prospective case-control studies with sampling before disease onset were identified; they reported inconsistent findings regarding the faecal microbiome.
 
  Several microbes are potentially linked to coeliac disease. As microbial factors are amenable to interventions, larger prospective studies are still warranted.
 Several microbes are potentially linked to coeliac disease. As microbial factors are amenable to interventions, larger prospective studies are still warranted.For a continuous time-to-event outcome and an expensive-to-measure exposure, we develop a pooling design and propose a likelihood-based approach to estimate the hazard ratios (HRs) of a Cox proportional hazards (PH) model. Our proposed approach fits a PH model based on pooled exposures with individually observed time-to-event outcomes. The design and estimation exploits the equivalence of the conditional logistic likelihood functions arising from a matched case-control study and the partial likelihood function of a riskset-matched, nested case-control (NCC) subset of a cohort study. To create the pools, we first focus on an NCC subcohort. Pools are formed at random while keeping the matching intact. Pool-level exposure and confounders are then evaluated and used in the likelihood to estimate the HR and the standard error of the estimates. The estimators are MLEs, provide consistent estimates of the individual-level HRs, and are asymptotically normal. Our simulation results indicate that the pooled estimates are comparable to the estimates obtained from the NCC subcohort. The units of analysis for the pooled design are the pools and not the individual participants. Hence the effective sample size is reduced. Therefore, the variance of the HR estimate increases with increasing poolsize. However, this variance inflation in small samples can be offset by including more matched controls per case within the NCC subcohort. An application is demonstrated with the Second Manifestations of ARTerial disease (SMART) study.Transmissible cancers are elusive and understudied parasitic life forms caused by malignant clonal cells (nine lineages are known so far). They emerge by completing sequential steps that include breaking cell cooperation, evade anti-cancer defences and shedding cells to infect new hosts.  https://www.selleckchem.com/products/YM155.html  Transmissible cancers impair host fitness, and their importance as selective force is likely largely underestimated. It is, therefore, crucial to determine how common they might be in the wild. Here, we draw a parallel between the steps required for a transmissible cancer to emerge and the steps required for an intelligent civilisation to emerge in the Milky Way using a modified Drake equation. Using numerical analyses, we estimate the potential number of extant marine and bivalve species in which transmissible cancers might exist. Our results suggest that transmissible cancers are more common than expected, and that new lineages can be found by screening a large number of species.