The sequence of the mouse genome is a key informational tool for understanding the contents of the human genome and a key experimental tool for biomedical research. Here, we report the results of an international collaboration to produce a high-quality draft sequence of the mouse genome. We also present an initial comparative analysis of the mouse and human genomes, describing some of the insights that can be gleaned from the two sequences. We discuss topics including the analysis of the evolutionary forces shaping the size, structure and sequence of the genomes; the conservation of large-scale synteny across most of the genomes; the much lower extent of sequence orthology covering less than half of the genomes; the proportions of the genomes under selection; the number of protein-coding genes; the expansion of gene families related to reproduction and immunity; the evolution of proteins; and the identification of intraspecies polymorphism.

Measuring gene expression in individual cells is crucial for understanding the gene regulatory network controlling human embryonic development. Here we apply single-cell RNA sequencing (RNA-Seq) analysis to 124 individual cells from human preimplantation embryos and human embryonic stem cells (hESCs) at different passages. The number of maternally expressed genes detected in our data set is 22,687, including 8,701 long noncoding RNAs (lncRNAs), which represents a significant increase from 9,735 maternal genes detected previously by cDNA microarray. We discovered 2,733 novel lncRNAs, many of which are expressed in specific developmental stages. To address the long-standing question whether gene expression signatures of human epiblast (EPI) and in vitro hESCs are the same, we found that EPI cells and primary hESC outgrowth have dramatically different transcriptomes, with 1,498 genes showing differential expression between them. This work provides a comprehensive framework of the transcriptome landscapes of human early embryos and hESCs.

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@ERSpublications These data showed that age ⩾65 years, pre-existing concurrent cardiovascular or cerebrovascular diseases, CD3 + CD8 + T-cells ⩽75 cells·μL −1 and cardiac troponin I ⩾0.05 ng·mL −1 were four risk factors predicting high mortality of COVID-19 pneumonia patients https://bit.ly/2Rh6NqvABSTRACT The aim of this study was to identify factors associated with the death of patients with COVID-19 pneumonia caused by the novel coronavirus SARS-CoV-2.All clinical and laboratory parameters were collected prospectively from a cohort of patients with COVID-19 pneumonia who were hospitalised to Wuhan Pulmonary Hospital (Wuhan City, Hubei Province, China) between 25 December 2019 and 7 February 2020. Univariate and multivariate logistic regression was performed to investigate the relationship between each variable and the risk of death of COVID-19 pneumonia patients.In total, 179 patients with COVID-19 pneumonia (97 male and 82 female) were included in the present prospective study, of whom 21 died. Univariate and multivariate logistic regression analysis revealed that age ⩾65 years (OR 3.765, 95% CI 1.146-17.394; p=0.023), pre-existing concurrent cardiovascular or cerebrovascular diseases (OR 2.464, 95% CI 0.755-8.044; p=0.007), CD3 + CD8 + T-cells ⩽75 cells·μL −1 (OR 3.982, 95% CI 1.132-14.006; p<0.001) and cardiac troponin I ⩾0.05 ng·mL −1 (OR 4.077, 95% CI 1.166-14.253; p<0.001) were associated with an increase in risk of mortality from COVID-19 pneumonia. In a sex-, age-and comorbid illness-matched case-control study, CD3 + CD8 + T-cells ⩽75 cells·μL −1 and cardiac troponin I ⩾0.05 ng·mL −1 remained as predictors for high mortality from COVID-19 pneumonia.We identified four risk factors: age ⩾65 years, pre-existing concurrent cardiovascular or cerebrovascular diseases, CD3 + CD8 + T-cells ⩽75 cells·μL −1 and cardiac troponin I ⩾0.05 ng·mL −1 . The latter two factors, especially, were predictors for mortality of COVID-19 pneumonia patients.

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