Background:A recently developing pneumonia caused by SARS-CoV-2 was originated in Wuhan, China, and has quickly spread across the world. We reported the clinical characteristics of 82 death cases with COVID-19 in a single center. Methods:Clinical data on 82 death cases laboratory-confirmed as SARS-CoV-2 infection were obtained from a Wuhan local hospital's electronic medical records according to previously designed standardized data collection forms.Results: All patients were local residents of Wuhan, and the great proportion of them were diagnosed as severe illness when admitted. Most of the death cases were male (65.9%). More than half of dead patients were older than 60 years (80.5%) and the median age was 72.5 years. The bulk of death cases had comorbidity (76.8%), including hypertension (56.1%), heart disease (20.7%), diabetes (18.3%), cerebrovascular disease (12.2%), and cancer (7.3%). Respiratory failure remained the leading cause of death (69.5%), following by sepsis syndrome/MOF (28.0%), cardiac failure (14.6%), hemorrhage (6.1%), and renal failure (3.7%). Furthermore, respiratory, cardiac, hemorrhage, hepatic, and renal damage were found in 100%, 89%, 80.5%, 78.0%, and 31.7% of patients, respectively. On the admission, lymphopenia (89.2%), neutrophilia (74.3%), and thrombocytopenia (24.3%) were usually observed. Most patients had a high neutrophil-to-lymphocyte ratio of >5 (94.5%), high systemic immune-inflammation index of >500 (89.2%), increased C-reactive protein level (100%), lactate dehydrogenase (93.2%), and D-dimer (97.1%). A high level of IL-6 (>10 pg/ml) was observed in all detected patients.Median time from initial symptom to death was 15 days , and a significant association between aspartate aminotransferase (p=0.002), alanine All rights reserved. No reuse allowed without permission. author/funder, who has granted medRxiv a license to display the preprint in perpetuity. : medRxiv preprint aminotransferase (p=0.037) and time from initial symptom to death were interestingly observed. Conclusion:Older males with comorbidities are more likely to develop severe disease, even die from SARS-CoV-2 infection. Respiratory failure is the main cause of COVID-19, but either virus itself or cytokine release storm mediated damage to other organ including cardiac, renal, hepatic, and hemorrhage should be taken seriously as well.

Chemokine receptor CCR2 mediates monocyte mobilization from the bone marrow (BM) and subsequent migration into target tissues. The degree to which CCR2 is differentially expressed in leukocyte subsets, and the contribution of CCR2 to these leukocyte mobilization from the BM are poorly understood. Using red fluorescence protein CCR2 reporter mice, we found heterogeneity in CCR2 expression among leukocyte subsets in varying tissues. CCR2 was highly expressed by inflammatory monocytes, dendritic cells, plasmacytoid dendritic cells and NK cells in all tissues. Unexpectedly, more than 60% of neutrophils expressed CCR2, albeit at low levels. CCR2 expression in T cells, B cells and NK T cells was greatest in the BM compared to other tissues. Genetic CCR2 deficiency markedly sequestered all leukocyte subsets in the BM, with reciprocal reduction noted in the peripheral blood and spleen. CCR2 inhibition via treatment with CCR2 signaling inhibitor propagermanium produced similar effects. Propagermanium also mitigated lipopolysaccharide-induced BM leukocyte egress. Consistent with its functional significance, CCR2 antibody staining revealed surface CCR2 expression within a subset of BM neutrophils. These results demonstrate the central role CCR2 plays in mediating leukocyte mobilization from the BM, and suggest a role for CCR2 inhibition in managing monocytes/macrophages-mediated chronic inflammatory conditions.

There is a trend towards using the axillary artery cannulation (AXC) site for cardiopulmonary bypass surgery in patients requiring acute type A aortic dissection (AAD) repair. However, AXC has not been established as a routine procedure, because there is controversy about its clinical advantage when compared with femoral artery cannulation (FAC). This meta-analysis assesses major short-term outcomes in patients undergoing acute AAD repair with AXC or FAC using non-randomized retrospective studies dating from 1992 to 2011 comparing AXC and FAC for major outcomes. Outcomes of interest were short-term mortality, neurological dysfunction and malperfusion. The fixed-effects model was used. Sensitivity and heterogeneity were analysed. Analysis of nine non-randomized studies comprising 715 patients [AXC, 359 (50.2%) and FAC, 356 (49.8%)] showed a significantly lower incidence of short-term mortality in the AXC group [odds ratio, 0.25, 95% confidence interval (CI) (0.15, 0.42), χ(2) = 7.23, P < 0.01]. The pattern of incidence of neurological dysfunction among the AXC group [odds ratio, 0.46, 95% CI (0.29, 0.72), χ(2) = 9.01, P < 0.01] was similar. The incidence of malperfusion did not differ [odds ratio, 0.84, 95% CI (0.37, 1.90), χ(2) = 2.25, P = 0.67]. Because no study was a randomized trial, our results are more uncertain than indicated by the 95% CI. Nevertheless, AXC seems to give better short-term mortality and neurological dysfunction rates than FAC.

Macrophages are a primary immune cell involved in inflammation, and their cell plasticity allows for transition from an inflammatory to a reparative phenotype and is critical for normal tissue repair following injury. Evidence suggests that epigenetic alterations play a critical role in establishing macrophage phenotype and function during normal and pathologic wound repair. Here, we find in human and murine wound macrophages that cyclooxygenase 2/prostaglandin E 2 (COX-2/PGE 2 ) is elevated in diabetes and regulates downstream macrophage-mediated inflammation and host defense. Using single-cell RNA sequencing of human wound tissue, we identify increased NF-κB–mediated inflammation in diabetic wounds and show increased COX-2/PGE 2 in diabetic macrophages. Further, we identify that COX-2/PGE 2 production in wound macrophages requires epigenetic regulation of 2 key enzymes in the cytosolic phospholipase A 2 /COX-2/PGE 2 (cPLA 2 /COX-2/PGE 2 ) pathway. We demonstrate that TGF-β–induced miRNA29b increases COX-2/PGE 2 production via inhibition of DNA methyltransferase 3b–mediated hypermethylation of the Cox-2 promoter. Further, we find mixed-lineage leukemia 1 (MLL1) upregulates cPLA 2 expression and drives COX-2/PGE 2 . Inhibition of the COX-2/PGE 2 pathway genetically ( Cox2 fl/fl Lyz2 Cre+ ) or with a macrophage-specific nanotherapy targeting COX-2 in tissue macrophages reverses the inflammatory macrophage phenotype and improves diabetic tissue repair. Our results indicate the epigenetically regulated PGE 2 pathway controls wound macrophage function, and cell-targeted manipulation of this pathway is feasible to improve diabetic wound repair.

Background:The outbreak of coronavirus disease 2019 in Wuhan, Hubei Province, China spread worldwide, resulting in a large number of deaths.Methods: Temporary Ark hospitals (TAH) have played an important role in controlling the spread of the epidemic in the city of Wuhan. Taking one TAH with 800 beds as an example, we summarized details of the layout, setting, working mode of medical staffs, patient management, admission standards, discharge standards, and standards for transferring to another hospital, hospital operation, and so on.Results: Over the period of operation, a total of 1,124 patients were admitted for treatment. Of these, 833 patients were cured and discharged from the hospital and 291 patients were transferred to other designated hospitals owing to aggravation This article is protected by copyright. All rights reserved. Accepted Articleof their condition. The achievement is to have zero infection for medical staff, zero in-hospital deaths among admitted patients, and zero readmission for discharged patients. Conclusion:The rapid deployment of TAH provided a suitable place for treating mild/moderate or no asymptomatic COVID-19 patients and successfully helped to control the infection in Wuhan. The successful model of TAH would rapidly and effectively control the spread of COVID-19 in other cities.