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In December 2019, a new type viral pneumonia cases occurred in Wuhan, Hubei Province; and then named “2019 novel coronavirus (2019-nCoV)” by the World Health Organization (WHO) on 12 January 2020. For it is a never been experienced respiratory disease before and with infection ability widely and quickly, it attracted the world’s attention but without treatment and control manual. For the request from frontline clinicians and public health professionals of 2019-nCoV infected pneumonia management, an evidence-based guideline urgently needs to be developed. Therefore, we drafted this guideline according to the rapid advice guidelines methodology and general rules of WHO guideline development; we also added the first-hand management data of Zhongnan Hospital of Wuhan University. This guideline includes the guideline methodology, epidemiological characteristics, disease screening and population prevention, diagnosis, treatment and control (including traditional Chinese Medicine), nosocomial infection prevention and control, and disease nursing of the 2019-nCoV. Moreover, we also provide a whole process of a successful treatment case of the severe 2019-nCoV infected pneumonia and experience and lessons of hospital rescue for 2019-nCoV infections. This rapid advice guideline is suitable for the first frontline doctors and nurses, managers of hospitals and healthcare sections, community residents, public health persons, relevant researchers, and all person who are interested in the 2019-nCoV.

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.

BackgroundTo the best of our knowledge, muscle soreness is a common manifestation for the coronavirus disease-19 (COVID-19) patients, but the mechanism of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) injury to skeletal muscle remains unclear, there has been no publication focused on muscle involvement in COVID-19 patients.Case presentationWe present the case of two Chinese men with COVID-19, whose common symptoms were fatigue and muscle soreness. They went through different treatments, patient 1, 81-year-old, eventually died of multi-organ failure, and patient 2, 53-year-old, underwent amputation of the mid-lower section of left thigh. Laboratory tests in both patients showed abnormal biochemical parameters associated with skeletal muscle injury. We obtained skeletal muscle samples from these two patients, one from postmortem biopsy of gastrocnemius muscle and the other from a resected left lower limb due to thrombosis. The pathological findings in patient 1 were mainly scattered atrophic muscles, while fiber necrosis and minor inflammation were identified in patient 2, and the mild infiltrations were confirmed by CD68 and LCA staining to be predominantly macrophages and lymphocytes.ConclusionsWe report the clinical and laboratory features together with histopathological findings in skeletal muscle tissues from two COVID-19 cases and speculate that the SARS-CoV-2 may cause skeletal muscle injury. Due to the particularity of individual differences in case reports, the background of chronic neuromuscular disease in patient 1 and a minimal compartment syndrome caused by thrombosis in patient 2 need to be excluded prior to the conclusion that the skeletal muscles have been involved in COVID-19.

Shi-yin Xiao,1 Ji Zhang,2,* Zheng-quan Zhu,3,* You-ping Li,4,* Wei-ying Zhong,5 Jian-bin Chen,6 Zhen-yu Pan,7 Hai-chen Xia3 1Department of Neurosurgery, Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, China; 2Department of Neurosurgery, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China; 3Department of Neurosurgery, Tumor Hospital Affiliated of Xinjiang Medical University, Xinshi District, Urumqi, Xinjiang 830011, China; 4Department of Neurosurgery, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330046, China; 5Department of Neurosurgery, Qilu Hospital, Shandong University, Jinan 250012, China; 6Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China; 7Department of Radiation-Oncology, First Hospital of Jilin University, Changchun 130021, China *These authors contributed equally to this work Objective: Surgical resection serves an important role in the multidisciplinary treatment of cerebral metastases (CMs). Conventional white-light, microsurgical, and circumferential stripping of CMs is standard neurosurgical procedure, but is associated with a high recurrence rate. Based on this outcome, there is an urgent need for a new surgical strategy, such as fluorescence-guided resection, for CMs, in order to achieve total removal. Methods: A retrospective study was carried out in 38 patients clinically and pathologically diagnosed with breast cancer brain metastasis at three medical centers from May 2012 to June 2016. The study comprised group 1 (fluorescein-guided surgery) and group 2 (standard microsurgery). In group 1, 5 mg/kg of fluorescein sodium was injected intravenously after an allergy test and before general anesthesia for 17 patients. A yellow 560 filter was employed for microsurgical tumor resection. Group 2 consisted of 21 patients for whom fluorescein was not administered. Results: Surgical outcomes were assessed concerning the extent of resection and Karnofsky performance status. Gross total resection was achieved in these patients, with high fluorescence markedly enhancing tumor visibility. The extent of resection had a powerful influence on performance status. Overall survival after CM was 24.1 months in patients given fluorescein and was 22.8 months in the nonfluorescein group. Conclusion: Fluorescein-guided surgery is a simple, safe, and practical method to resect breast cancer brain metastasis, and leads to a higher proportion of resection compared to common microsurgery. This offers a tremendous advantage when navigating a tiny tumor, and improves the quality of life of patients with CM. Keywords: fluorescein sodium, breast cancer brain metastasis, fluorescence-guided surgery, extent of resection, KPS

This article reviews particular subgroup of B-cell lymphoma, called "double-hit" lymphoma (DHL) because of its distinct aberrations-related genes influencing various processes such as apoptosis, differentiation, and proliferation. Recent studies indicate that tumorigenesis is a complex process involving multiple genes, genetic abnormalities, including gene mutations, deletions, and chromosomal alterations. Chromosomal aberrations are not affecting only basic cellular life preserving activities such as cell proliferation, differentiation, apoptosis, and signal transduction, but are also indispensible for evaluation of lymphoma occurrence, progression, and prognosis as well differential diagnosis and other aspects assessment. DHL is group accompanied by IGH-BCL2 and MYC rearrangement, behaving highly aggressively, with a complex and distinct karyotype which can not be extrapolated solely by morphological pathological assessment, since it has not been entirely characteristic. Therefore, we are reviewing possible effects of multiple genetic rearrangements, particular genes mutations, and developing hypothesis due which pathophysiology mechanisms DHL accomplish synergistic malignant potential.

The aim of the present study was to investigate the association between glucocorticoid receptors and steroid‑induced avascular necrosis of the femoral head (SANFH). Healthy New Zealand rabbits were randomly divided into 3 groups (n=16/group); the normal (no treatment), control (horse serum injections) and treatment (horse serum and methylprednisolone injections) groups. Methylprednisolone and horse serum injections were used to establish a SANFH model in rabbits; magnetic resonance imaging (MRI) and histopathological analysis were used to evaluate the SANFH rabbit model. Total cholesterol and triglyceride contents in the blood of SANFH rabbits were determined. The protein expression levels of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) and type 2 (11β-HSD2) were determined using western blotting. The total cholesterol and triglyceride levels in the blood of methylprednisolone‑treated rabbits were significantly increased compared with the control and normal groups, which provides evidence in support of the metabolic disorder theory. Based on the results obtained from western blotting, the expression levels of 11β-HSD1 protein were increased, whereas the expression levels of 11β-HSD2 protein were decreased following injection. The results of the present study indicate that 11β-HSDs are important in the development of SANFH. Furthermore, 11β-HSDs may be important targets for preventing the development of ANFH in patients treated with steroids, which has a significant reference value for the use of steroids in clinical practice.

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.