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Background Many healthcare workers were infected by coronavirus disease 2019 (COVID-19) early in the epidemic posing a big challenge for epidemic control. Hence, this study aims to explore perceived infection routes, influencing factors, psychosocial changes, and management procedures for COVID-19 infected healthcare workers. Methods This is a cross-sectional, single hospital-based study. We recruited all 105 confirmed COVID-19 healthcare workers in the Zhongnan Hospital of Wuhan University from February 15 to 29, 2020. All participants completed a validated questionnaire. Electronic consent was obtained from all participants. Perceived causes of infection, infection prevention, control knowledge and behaviour, psychological changes, symptoms and treatment were measured. Results Finally, 103 professional staff with COVID-19 finished the questionnaire and was included (response rate: 98.1%). Of them, 87 cases (84.5%) thought they were infected in working environment in hospital, one (1.0%) thought their infection was due to the laboratory environment, and 5 (4.9%) thought they were infected in daily life or community environment. Swab of throat collection and physical examination were the procedures perceived as most likely causing their infection by nurses and doctors respectively. Forty-three (41.8%) thought their infection was related to protective equipment, utilization of common equipment (masks and gloves). The top three first symptoms displayed before diagnosis were fever (41.8%), lethargy (33.0%) and muscle aches (30.1%). After diagnosis, 88.3% staff experienced psychological stress or emotional changes during their isolation period, only 11.7% had almost no emotional changes. Arbidol (Umifenovir; an anti-influza drug; 69.2%) was the drug most commonly used to target infection in mild and moderate symptoms. Conclusion The main perceived mode of transmission was not maintaining protection when working at a close distance and having intimate contact with infected cases. Positive psychological intervention is necessary.

In March 2020, China had periodically controlled the coronavirus disease-19 (COVID-19) epidemic. We reported the results of health screening for COVID-19 among returned staff of a hospital and conducted a summary analysis to provide valuable experience for curbing the COVID-19 epidemic and rebound. In total, 4729 returned staff from Zhongnan Hospital of Wuhan University, Wuhan, China were examined for COVID-19, and the basic information, radiology and laboratory test results were obtained and systematically analysed. Among the 4729 employees, medical staff (62.93%) and rear-service personnel (30.73%) were the majority. The results of the first physical examination showed that 4557 (96.36%) were normal, 172 (3.64%) had abnormal radiological or laboratory test results. After reexamination and evaluation, four were at high risk (asymptomatic infections) and were scheduled to transfer to a designated hospital, and three were at low risk (infectivity could not be determined) and were scheduled for home isolation observation. Close contacts were tracked and managed by the Center for Disease Control and Prevention (CDC) in China. Asymptomatic infections are a major risk factor for returning to work. Extensive health screening combined with multiple detection methods helps to identify asymptomatic infections early, which is an important guarantee in the process of returning to work.

Increasing evidence indicates the important roles of M(3) muscarinic acetylcholine receptors (M(3) mAChR) in the regulation and maintenance of cardiac function and heart disease. In the present study, we investigated whether the M(3) mAChR mediates the cardioprotection against ischaemia-induced arrhythmias and the mechanisms involved. Myocardial ischaemia was established in Wistar rats by occlusion of the left anterior descending coronary artery. Rats were treated with choline chloride (an M(3) mAChR agonist; 10 mg/kg, i.v.) 10 min before occlusion. In addition, 4-diphenylacetoxy-N-methylpiperidine-methiodide (4-DAMP; 0.12 μg/kg, i.v.) was administered 5 min before choline in the 4-DAMP-treated group. Ischaemia-induced arrhythmias were evaluated in each group for a period of 1 h after occlusion. After 24 h occlusion, protein and mRNA levels of L-type Ca(2+) channels and the Na(+) /Ca(2+) exchanger (NCX) were determined. Ischaemia-induced arrhythmias following coronary artery occlusion were diminished by choline and this effect was reversed in the 4-DAMP-treated group. In vitro, the effects of myocardial ischaemia were simulated by incubating isolated ventricular cardiomyocytes with Tyrode's solution (pH 6.8). Intracellular Ca(2+) overload was confirmed and this was decreased by choline. Furthermore, choline reduced the L-type Ca(2+) current (I(C) (a,) (L) ) compared with cardiomyocytes incubated in Tyrode's solution (pH 6.8) alone. Choline reduced the 'ischaemia'-induced upregulated expression of L-type Ca(2+) channels and NCX at both the protein and mRNA level. Based on these results, choline has an obvious protective effect against ischaemia-induced arrhythmias that is mediated via activation of cardiac M(3) mAChR, which reduces Ca(2+) overload mediated by L-type Ca(2+) channels and the NCX.

This study was designed to evaluate the effects of pilocarpine and explore the underlying ionic mechanism, using both aconitine-induced rat and ouabain-induced guinea pig arrhythmia models. Confocal microscopy was used to measure intracellular free-calcium concentrations ([Ca2+]i) in isolated myocytes. The current data showed that pilocarpine significantly delayed onset of arrhythmias, decreased the time course of ventricular tachycardia and fibrillation, reduced arrhythmia score, and increased the survival time of arrhythmic rats and guinea pigs. [Ca2+]i overload induced by aconitine or ouabain was reduced in isolated myocytes pretreated with pilocarpine. Moreover, M3-muscarinic acetylcholine receptor (mAChR) antagonist 4-DAMP (4-diphenylacetoxy-N-methylpiperidine-methiodide) partially abolished the beneficial effects of pilocarpine. These data suggest that pilocarpine produced antiarrhythmic actions on arrhythmic rat and guinea pig models induced by aconitine or ouabain via stimulating the cardiac M3-mAChR. The mechanism may be related to the improvement of Ca2+ handling.

The M(3) subtype of muscarinic acetylcholine receptors (M(3)-mAChR) plays a protective role in myocardial ischemia and microRNAs (miRNAs) participate in many cardiac pathophysiological processes, including ischemia-induced cardiac injury. However, the role of miRNAs in M(3)-mAChR mediated cardioprotection remains unexplored. The present study was designed to identify miRNAs that are involved in cardioprotective effects of M(3)-mAChR against myocardial ischemia and elucidate the underlying mechanisms. We established rat model of myocardial ischemia and performed miRNA microarray analysis to identify miRNAs involved in the cardioprotection of M(3)-mAChR. In H9c2 cells, the viability, intracellular free Ca(2+) concentration ([Ca(2+)]i), intracellular reactive oxygen species (ROS), miR-376b-5p expression level, brain derived neurophic factor (BDNF) and nuclear factor kappa-B (NF-κB) levels were measured. Our results demonstrated that M(3)-mAChR protected myocardial ischemia injury. Microarray analysis and qRT-PCR revealed that miR-376b-5p was significantly up-regulated in ischemic heart tissue and the M(3)-mAChRs agonist choline reversed its up-regulation. In vitro, miR-376b-5p promoted H(2)O(2)-induced H9c2 cell injuries measured by cells viability, [Ca(2+)]i and ROS. Western blot and luciferase assay identified BDNF as a direct target of miR-376b-5p. M(3)-mAChR activated NF-κB and thereby inhibited miR-376b-5p expression. Our data show that a novel M(3)-mAChR/NF-κB/miR-376b-5p/BDNF axis plays an important role in modulating cardioprotection. MiR-376b-5p promotes myocardial ischemia injury possibly by inhibiting BDNF expression and M(3)-mAChR provides cardioprotection at least partially mediated by the downregulation of miR-376b-5p through NF-κB. These findings provide new insight into the potential mechanism by which M(3)-mAChR provides cardioprotection against myocardial ischemia injury.

To investigate the myocardial protective effects of puerarin on streptozotocin (STZ)-induced diabetic rats and the possible mechanism were involved. 45 Sprague-Dawley male rats were randomly divided into 3 groups as diabetic group (intraperitoneally injected STZ 65 mg/kg), puerarin treatment group (intraperitoneally injected STZ 65 mg/kg, and intraperitoneally injected puerarin 100 mg/kg/day for 4 weeks), and control group (intraperitoneally injected saline 6 ml/kg). Four weeks after the model induction, the myocardial changes were observed by H-E stain and Transmission electron microscopy, the alteration of thrombospondin-1 (TSP-1) protein and mRNA expression in the myocardium were also assessed by immunohistochemistry and real-time PCR. The heart function of three groups' rats was tested by Langendorff isolated in vivo heart perfusion. The differences in the data of weight and blood sugar of diabetic between puerarin treatment and normal groups were significant after 4 weeks (P0.01). Our results demonstrated that diabetic myocardial ultrastructural changes included myofibrillar disarrangements and mitochondria disruption. These damages were significantly less severe in the puerarin treatment group compared with the diabetic group. A significant decrease of TSP-1 expression was observed in the puerarin treated rats' myocardium compared to the diabetic rats (P0.01). Left ventricular systolic end pressure (LVSEP) and left ventricular developed pressure (LVDP) of puerarin treatment group were also significantly increased compared to diabetic group (P0.01). Altogether puerarin could improve the left ventricular function of diabetic rats and showed protective effects of myocardium by decreasing the TSP-1 expression in myocardium of diabetic rats.

To quantitatively evaluate the hemodynamic status in animal models of steroid-induced avascular osteonecrosis of femoral head (SANFH) by multislice CT (MSCT) perfusion imaging, and estimate the therapeutic efficacy on early intervention of hyperbaric oxygen (HBO) to improve the region blood flow (rBF) of ischemic femoral head.Forty-eight New Zealand male rabbits were injected with Escherichia coli endotoxin and methyl-prednisolone to establish SANFH models and then divided into 3 subgroups to undergo MSCT to measure the rBF, regional blood volume (rBV), and mean transit time (MTT) to obtain perfusion maps at the femoral head epiphysis, metaphysic, and neck of femur, and then were killed to undergo histological examination of the bilateral femoral heads 2, 4, and 6 weeks later respectively (Groups M(2), M(4), and M(6)). Twenty-four rabbits underwent HOB treatment after the second injection of E. c. endotoxin for 1-3 courses respectively (Groups H(1), H(2), and H(3)), and then underwent MSCT and pathological examination as described above. Eight rabbits were used as controls (Group N).(1) The rBF values of Groups M(2), M(4), and M(6) were all significantly lower than that of Group N (P0.001,0.001, and0.002). The rBF value of femoral head epiphysis of Group M(2) was remarkably lower than that of Group N, decreased to the lowest in Group M(4), and re-increased in Group M(6). The rBV value demonstrated similar change pattern in femoral head epiphysis. The MTT values of Groups M(2) and M(4) were longer than that of Group N, and then re-decreased in Group M(6). (2) It did differ significantly between the perfusion data of different femoral head anatomic regions in Groups M(2), M(4), M(6) and N (rBF: F = 52.190, P0.001; rBV: F = 42.677, P0.001; MTT: F = 3.09, P = 0.048). The changes of the perfusion data in femoral head epiphysis were more significant than those in other anatomic regions. (3) There were no statistically significant differences in the rBF value of the femoral head epiphysis and metaphysis (F = 2.081, P = 0.115; F = 1.142, P = 0.341), in the rBV value of the femoral metaphysis and neck of femur (F = 2.642, P = 0.059; F = 1.568, P = 0.209), and the MTT value of all the anatomic regions (F = 1.111, P = 0.347) among Groups H(1), H(2), H(3), and N. The rBF values of Groups H(1), H(2), and H(3) were statistically higher than those of the corresponding phase model groups (all P0.05).Able to detect hemodynamic status of femoral head, MSCT perfusion imaging technique may be used in the early detection of SANFH. Early intervention of HBO therapy can improve the blood perfusion of femoral head.

To observe the relationship between the level of catecholamine in plasma with bispectral index during endotracheal intubation with propofol anesthesia in order to investigate the mechanism of the preventing of endotracheal intubation response with esmolol.Thirty patients were randomly allocated into two groups: control group (n=15) and esmolol group (n=15). The patients received esmolol 1amg/kg followed by 250 microg/(kgdmin) in esmolol group and saline in control group. Two minutes later, the patients received propofol 2amg/kg for induction. Bispectral index (BIS), systolic pressure (SP), diostolic pressure (DP), and heart rate (HR) were measured before endotracheal intubation and 3amin after intubation, at the same time 8a mL arteral blood was taken for the measurement of the concentrations of norephinephrine(NE) and ephinephrine(E) in plasma.The level of BIS(63.53+/-3.11), NE(2.016+/-0.681)and E(0.578+/-0.072)in control group 3 min after endotracheal intubation were increased significantly than those before intubation (P0.05), but there were no significant change in the level of BIS, NE and E in esmolol group 3amin after endotracheal intubation . There were significant differences in the concentrations of NE(2.016+/-0.681)and E(0.578+/-0.072) in plasma 3 min after intubation between the two groups (P0.05) and there were also significant differences in BIS(63.53+/-3.11) and DeltaBIS(20.93+/-4.57)3 min after intubation between the two groups(P0.01). SP( 148+/-20)and HR(89+/-180) in control group were increased after intubation than those before intubation (P0.05) . There were no significant differences in SP, DP and HR in esmolol group after intubation than those before intubation.Esmolol can reduce the plasma concentrations of NE and E through preventing periopheal sympathetic nerve response to intubation and can reduce BIS arousal reactions after endotracheal intubation.