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Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 infection has spread rapidly across the world and become an international public health emergency. Both SARS-CoV-2 and SARS-CoV belong to subfamily Coronavirinae in the family Coronaviridae of the order Nidovirales and they are classified as the SARS-like species while belong to different cluster. Besides, viral structure, epidemiology characteristics and pathological characteristics are also different. We present a comprehensive survey of the latest coronavirus—SARS-CoV-2—from investigating its origin and evolution alongside SARS-CoV. Meanwhile, pathogenesis, cardiovascular disease in COVID-19 patients, myocardial injury and venous thromboembolism induced by SARS-CoV-2 as well as the treatment methods are summarized in this review.

IntroductionThere are approximately 19 million new cases of sepsis worldwide each year. Among them, more than one quarter of patients die. We aimed to assess the effects of heparin on short-term mortality in adult patients with sepsis and severe sepsis.MethodsWe searched electronic databases (Medline, Embase, and Cochrane Library databases; the Cochrane Controlled Trials Register) and conference proceedings (Web of Knowledge (Conference Proceedings Citation Index - Science, Conference Proceedings Citation Index - Social Sciences & Humanities)) from inception to July 2014, expert contacts and relevant websites. Controlled trials of heparin versus placebo in sepsis or severe sepsis were identified. In total two reviewers independently assessed eligibility, and four authors independently extracted data; consensus was reached by conference. We used the chi-square test and I2 to assess statistical heterogeneity (P <0.05). The primary analysis was based on the fixed-effect model to produce pooled odds ratios with 95% confidence intervals.ResultsA total of nine publications were included in the meta-analysis. Heparin decreased 28-day mortality (n = 3,482, OR = 0.656, 95% CI = 0.562 to 0.765, P <0.0001). According to the meta-analysis of 28-day mortality, heterogeneity was not found among the eight randomized clinical trials (RCTs) (I2 = 0.0%). Heparin had no effect on bleeding events in sepsis (seven RCTs, n = 2,726; OR = 1.063; 95% CI = 0.834 to 1.355; P = 0.623; and I2 = 20.9%). Subgroup analysis demonstrated that the sample size may be a source of heterogeneity, but experimental design was not.ConclusionsHeparin may reduce 28-day mortality in patients with severe sepsis, at the same time, there was no increase in the risk of bleeding in the heparin group. We recommend the use of heparin for sepsis and severe sepsis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-014-0563-4) contains supplementary material, which is available to authorized users.

This study investigated the contribution of survivin and its upstream regulators, AKT and hypoxia-inducible factor 1a , to the resistance of gastric cancer cells to cisplatin (CDDP). We found that over-expression of survivin increased the resistance of SGC7901 and BGC823 gastric cancer cells to CDDP. Its over-expression abrogated CDDP-induced inhibition of cell proliferation and CDDP-induced cell apoptosis. In contrast, down-regulation of survivin expression using small hairpin RNA (shRNA) vectors and the small-molecule inhibitor YM155, or inhibition of survivin function using a recombinant cell-permeable dominant-negative survivin protein (dNSur9), promoted CDDP-induced apoptosis. CDDP-resistant sub-lines generated from the parental SGC7901 and BGC823 cells by exposure to increasing concentrations of CDDP expressed higher levels of HIF-1a and survivin in response to hypoxia, and higher levels of phosphorylated AKT (pAKT). Specific inhibition of AKT reduced the expression of HIF-1a and survivin, whereas specific inhibition or depletion of HIF-1a reduced survivin expression but had no effect on the expression of phosphorylated AKT. The expression levels of survivin affected the therapeutic efficacy of CDDP in treating gastric tumors in mice. Specific inhibition of survivin, AKT and HIF-1a enhanced the sensitivity of CDDP-resistant cells to CDDP. Specific inhibition of survivin, AKT and HIF-1a synergized with CDDP to suppress the growth of gastric tumors that had been engineered to overexpress survivin. In summary, the results provide evidence that up-regulation of survivin by AKT and HIF-1a contributes to CDDP resistance, indicating that inhibition of these pathways may be a potential strategy for overcoming CDDP resistance in the treatment of gastric cancer.Gastric cancer is the third most frequent cause of cancer death in men worldwide [1]. Despite advances in diagnostic technology, most cases are already clinically advanced at the time of diagnosis, and hence chemotherapy is essential for treatment [2]. Cisplatin (CDDP) is the most commonly used chemotherapeutic agent for the treatment of gastric cancer [3]. The combination of CDDP and the 5-fluorouracil-related drug S-1 was established as the first-line chemotherapy for advanced gastric cancer based on a phase III trial in Abbreviations CDDP, cisplatin; dNSur9, recombinant cell-permeable dominant-negative survivin protein; HIF, hypoxia-inducible factor; 2ME2, 2-methoxyestradiol; pAKT, phosphorylated AKT; shRNA, small hairpin RNA; TCN, triciribine.

BackgroundGlioblastomas (GBM) are comprised of a heterogeneous population of tumor cells, immune cells, and extracellular matrix. Interactions among these different cell types and pro-/anti-inflammatory cytokines may promote tumor development and progression.AimsThe objective of this study was to develop a cytokine-related gene signature to improve outcome prediction for patients with primary GBM.MethodsHere, we used Cox regression and risk-score analysis to develop a cytokine-related gene signature in primary GBMs from the whole transcriptome sequencing profile of the Chinese Glioma Genome Atlas (CGGA) database (n=105). We also examined differences in immune cell phenotype and immune factor expression between the high-risk and low-risk groups.ResultsCytokine-related genes were ranked based on their ability to predict survival in the CGGA database. The six genes showing the strongest predictive value were CXCL10, IL17R, CCR2, IL17B, IL10RB, and CCL2. Patients with a high-risk score had poor overall survival and progression-free survival. Additionally, the high-risk group was characterized by increased mRNA expression of M2 microglia/macrophage markers and elevated levels of IL10 and TGFβ1.ConclusionThe six cytokine-related gene signature is sufficient to predict survival and to identify a subgroup of primary GBM exhibiting the M2 cell phenotype.

A number of epidemiological studies have suggested that obesity is associated, albeit inconsistently, with the incidence of prostate cancer (PCa). In order to provide a quantitative assessment of this association, the present study examined the correlation between obesity and the incidence and associated mortalities of PCa in an updated meta-analysis of cohort studies. The cohort studies were identified by searching the EMBASE and MEDLINE databases on January 1, 2014. The summary relative risks (RRs) with 95% confidence intervals (CIs) were calculated using random-effects models. In total, 17 studies, which included 3,569,926 individuals overall, were selected according to predefined inclusion criteria. Based upon the results of the random-effects models, obesity was not significantly correlated with the incidence of PCa (RR, 1.00; 95% CI, 0.95–1.06). However, further analysis revealed that obesity was significantly correlated with an increased risk of aggressive PCa (RR, 1.14; 95% CI, 1.04–1.25). Furthermore, an increased risk of PCa-associated mortality was significantly associated with obesity (RR, 1.24; 95% CI, 1.15–2.33), without any heterogeneity between the studies (I2=0.0%; P=0.847). The present study provides preliminary evidence to demonstrate that obesity is a significant risk factor for aggressive PCa and PCa-specific mortality. The low survival rates observed among obese males with PCa may be a likely explanation for this association.

The association between cancer and volatile organic metabolites in exhaled breaths has attracted increasing attention from researchers. The present study reports on a systematic study of gas profiles of metabolites in human exhaled breath by pattern recognition methods. Exhaled breath was collected from 85 patients with histologically confirmed breast disease (including 39 individuals with infiltrating ductal carcinoma, 25 individuals with cyclomastopathy and from 21 individuals with mammary gland fibroma) and 45 healthy volunteers. Principal component analysis and partial least squares discriminant analysis were used to process the final data. The volatile organic metabolites exhibited significant differences between breast cancer and normal controls, breast cancer and cyclomastopathy, and breast cancer and mammary gland fibroma; 21, 6, and 8 characteristic metabolites played decisive roles in sample classification, respectively (P < 0.05). Three volatile organic metabolites in the exhaled air, 2,5,6-trimethyloctane, 1,4-dimethoxy-2,3-butanediol, and cyclohexanone, distinguished breast cancer patients from healthy individuals, mammary gland fibroma patients, and patients with cyclomastopathy (P < 0.05). The identified three volatile organic metabolites associated with breast cancer may serve as novel diagnostic biomarkers.

The published literature relating to damage to planar solid oxide fuel cells caused by thermally induced stresses and thermal cycling is reviewed. This covers reported studies of thermal cycling performance and stresses induced by temperature gradients and differences in thermal expansion coefficients in typical planar SOFC configurations, namely electrolyte supported; anode supported and inert substrate supported cells. Generally good agreement is found between electrolyte residual stresses measured by X-ray diffraction or cell curvature and stresses calculated from simple thermo-elastic analysis. Finite element modelling of temperature distributions in cells and stacks in steady state operation are well advanced and capable of being extended to compute stress distributions. Failure criteria are then discussed for laminated cell structures based on critical energy release rate fracture mechanics models developed originally for coatings. However, in most cases the data required to apply the models quantitatively (such as elastic moduli of actual laminated material and fracture energies of materials and interfaces) are not available. Where data are available there are inconsistencies that require resolution. Seals are critical components in many planar solid oxide fuel cell configurations, but again there are discrepancies in experimental mechanical properties and the role of internal stresses in their fracture. In addition, there is as yet no firm evidence that thermal cycling damage involves any true materials fatigue process. Effect of thermal cycling on SOFC integrityTaniguchi et al. 7 investigated the thermal cycling performance of electrolyte supported planar SOFCs