ObjectivesAn outbreak of the highly contagious severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has sickened thousands of people in China. The purpose of this study was to explore the early clinical characteristics of COVID-19 patients with cardiovascular disease (CVD).MethodsThis is a retrospective analysis of patients with COVID-19 from a single centre. All patients underwent real-time reverse transcription PCR for SARS-CoV-2 on admission. Demographic and clinical factors and laboratory data were reviewed and collected to evaluate for significant associations.ResultsThe study included 541 patients with COVID-19. A total of 144 (26.6%) patients had a history of CVD. The mortality of patients with CVD reached 22.2%, which was higher than that of the overall population of this study (9.8%). Patients with CVD were also more likely to develop liver function abnormality, elevated blood creatinine and lactic dehydrogenase (p<0.05). Symptoms of sputum production were more common in patients with CVD (p=0.026). Lymphocytes, haemoglobin and albumin below the normal range were pervasive in the CVD group (p<0.05). The proportion of critically ill patients in the CVD group (27.8%) was significantly higher than that in the non-CVD group (8.8%). Multivariable logistic regression analysis revealed that CVD (OR: 2.735 (95% CI 1.495 to 5.003), p=0.001) was associated with critical COVID-19 condition, while patients with coronary heart disease were less likely to reach recovery standards (OR: 0.331 (95% CI 0.125 to 0.880), p=0.027).ConclusionsConsidering the high prevalence of CVD, a thorough CVD assessment at diagnosis and early intervention are recommended in COVID-19 patients with CVD. Patients with CVD are more vulnerable to deterioration.

Purpose Coronavirus disease 2019 (COVID-19) has become a topic of concern worldwide; however, the impacts of type 2 diabetes mellitus (T2DM) on disease severity, therapeutic effect, and mortality of patients with COVID-19 are unclear. Methods All consecutive patients with COVID-19 admitted to the Renmin Hospital of Wuhan University from January 11 to February 6, 2020, were included in this study. Results A total of 663 patients with COVID-19 were included, while 67 patients with T2DM accounted for 10.1% of the total. Compared with patients with COVID-19 without T2DM, those with T2DM were older (aged 66 years vs 57 years; P &lt; 0.001) and had a male predominance (62.7% vs 37.3%; P = 0.019) and higher prevalence of cardiovascular diseases (61.2% vs 20.6%; P &lt; 0.001) and urinary diseases (9% vs 2.5%; P = 0.014). Patients with T2DM were prone to developing severe (58.2% vs 46.3%; P = 0.002) and critical COVID-19 (20.9% vs 13.4%; P = 0.002) and having poor therapeutic effect (76.1% vs 60.4%; P = 0.017). But there was no obvious difference in the mortality between patients with COVID-19 with and without T2DM (4.5% vs 3.7%; P = 0.732). Multivariate logistic regression analysis identified that T2DM was associated with poor therapeutic effect in patients with COVID-19 (odd ratio [OR] 2.99; 95% confidence interval [CI], 1.07-8.66; P = 0.04). Moreover, having a severe and critical COVID-19 condition (OR 3.27; 95% CI, 1.02-9.00; P = 0.029) and decreased lymphocytes (OR 1.59; 95% CI, 1.10-2.34; P = 0.016) were independent risk factors associated with poor therapeutic effect in patients with COVID-19 with T2DM. Conclusions T2DM influenced the disease severity and therapeutic effect and was one of the independent risk factors for poor therapeutic effect in patients with COVID-19.

Background: KIFC3, belongs to kinesin superfamily proteins (KIFs), is well known for its role in intracellular cargo movement. KIFC3 has been identified as a docetaxel resistance gene in breast cancer cells, however, the role of KIFC3 and its potential mechanism in colorectal cancer (CRC) remains elusive.Objectives: We aims to investigate the effects of KIFC3 in proliferation, migration, and invasion in CRC as well as the potential mechanism inside.Methods: We investigated the expression of KIFC3 in the Oncomine, Gene Expression Profiling Interactive Analysis databases. The KIFC3 protein expression and mRNA level in CRC cells were evaluated by western blot and qRT-PCR. Cell proliferation ability was detected by CCK-8, EdU, colony formation assay and xenograft tumor in nude mice. Flow cytometry was used to detect the cell cycle. The effect of KIFC3 on the epithelial-to-mesenchymal transition (EMT) was investigated by transwell and wound healing assay. The association of KIFC3 with EMT and PI3K/AKT/mTOR signaling pathway were measured by western blot and immunofluorescence staining.Results: The expression of KIFC3 was higher in CRC tissues than normal colorectal tissue, and was negatively correlated with the overall survival of patients with CRC. KIFC3 silencing inhibited the proliferation, migration and invasion of CRC cells. Meanwhile, it could decrease the number of cells in S phase. KIFC3 silencing inhibited the expression of proliferating cell nuclear antigen, Cyclin A2, Cyclin E1, and CDK2 and increased the expression of p21 and p53. KIFC3 overexpression promoted the G1/S phase transition. KIFC3 silencing inhibited the EMT process, which decreased the level of N-cadherin, Vimentin, SNAIL 1, TWIST, MMP-2, MMP-9 and increased E-cadherin, while KIFC3 overexpression show the opposite results. Furthermore, the knockdown of KIFC3 suppressed the EMT process by modulating the PI3K/AKT/mTOR signaling pathway. KIFC3 silencing decreased the expression of phosphorylated PI3K, AKT, mTOR, but total PI3K, AKT, mTOR have no change. Inversely, the upregulation of KIFC3 increased the expression of phosphorylated PI3K, AKT and mTOR, total PI3K, AKT, mTOR have no change. In a xenograft mouse model, the depletion of KIFC3 suppressed tumor growth. the increased expression levels of KIFC3 could enhance the proliferation, migration and invasion of CRC cells, and enhance the EMT process through the PI3K/AKT/mTOR pathway.Conclusion: Our study substantiates that KIFC3 can participate in the regulation of CRC progression by which regulates EMT via the PI3K/AKT/mTOR axis.

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