Wilsonnorth6338

Shock is one of the major complications and causes of death in the early stage of burns. Although burn shock is an old problem, its clinical treatment is often not timely nor standardized, resulting in the shock to pass unsteadily or even be difficult to correct, leading to early infection and organ complications. To standardize the prevention and treatment of burn shock, the expert group developed this consensus through discussions on major pathophysiology, clinical manifestations and diagnosis, prophylaxis and treatment, monitoring as well as matters of concern and safety precautions. This consensus can be used as a reference for the prevention and treatment of burn shock, with the specific application being determined according to the actual situation of patients.Objective To investigate the effect of mild hypothermia therapy on liver after cardiopulmonary resuscitation. Methods Thirty-three inbred Chinese Wuzhishan (WZS) minipigs, weighted (28±2) kg, were used to establish a ventricular fibrillation model. And 30 animals survived after cardiopulmonary resuscitation reached basic life support. The surviving animals were randomly divided into two groups mild hypothermia group (group M, n=15) and conventional treatment group (group C, n=15). All the animals were observed for 24 hours. Blood samples were extracted at baseline, 0.5, 1, 2, 4, 6, 12 and 24 h after successful resuscitation. The concentrations of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were detected at the time points. The enzyme-linked immunosorbent assay (ELISA) was used to detect the concentrations of interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α). The data were compared between the two groups, LSD test was used when the variance was homogeneous, and Tamhane T2 ter ischemia reperfusion injury. After successful resuscitation, the liver undergoes ischemia-reperfusion injury, which may be related to the release of inflammatory mediators such as TNF-α and IL-6. MLN7243 Mild hypothermia therapy can prevent the release of TNF-α, IL-6 to reduce the degree of liver damage after resuscitation.Objectives To investigated whether berberine could ameliorate septic cardiomyopathy in a rat model of sepsis and it's mechanisms. Methods SD rats were divided into 3 groups sepsis group (LPS group), rats were intraperitoneal injected of LPS (10 mg/kg); Berberine intervention group (Ber group), Ber (50 mg/kg, one time per day) was gavage fed 3 days before intraperitoneally injection of lipopolysaccharides (LPS); control group (Con group), rats were gavage fed with double distilled water (2 ml/100 g, one time per day) 3 days before intraperitoneal injection of normal saline (1 ml/100 g). LPS group and the Ber group was further divided into 3 subgroups (n=6), and the follow-up experiments were conducted at 6 h, 24 h and 48 h after LPS injection (of which 48 h subgroup rats were gavage fed with Ber/saline at 24 h). Left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), and the maximum rate of change of left ventricular pressure (±dp/dtmax) were monitored, the level of cardiac t 6 hours, severe at 24 hours, and become more serious at 48 hours after LPS injection. Further, TLR4 and NF-κB p65 subunits, which were the two key factors of the TLR4/NF-κB signaling, were upregulated in the LPS group and attenuated in the Ber group. Consistently, the expression levels of the downstream cytokines TNF-α and IL-1β were lower in the Ber group than those in the LPS group (all P less then 0.05). Myocardial injury markers were positively correlated with the markers of TLR4/NF-κB signals and the downstream host inflammatory factors (all P less then 0.05). Conclusions Berberine can improve myocardial injury and cardiac function in sepsis rats, the mechanism is considered to be related to that it can inhibit the activation of TLR4/NF-κB signaling pathway induced by LPS and further reducing the production of TNF-α and IL-1β.Objective To investigate the effect and mechanism of Polyphyllin Ⅱ on the proliferation, invasion and chemosensitivity of glioma cells. Method CCK-8 cell proliferation assays and Transwell assays were employed to determine the effect of Polyphyllin Ⅱ on the proliferation and invasion of glioma cells (T98G and LN18), respectively. The expression of E-cadherin, Snail and O6-methylguanine DNA methyltranferase (MGMT) were quantified by Western blot analysis. Results Polyphyllin Ⅱ could inhibit the proliferation of glioma cells in a time- and does-dependent manner. The half maximal inhibitory concentration (IC(50)) of T98G at 24 h, 48 h and 72 h were (5.82±0.32), (3.57±0.07) and (1.48±0.35) µmol/L, respectively. The IC(50) of LN18 at 24 h, 48 h and 72 h were (6.83±0.11), (4.28±0.29), (2.66±0.22) µmol/L, respectively. After being treated with 2 µmol/L, 4 µmol/L and 6 µmol/L Polyphyllin Ⅱ for 24 h, the percentage of invasive cell area in the chamber area was lower than those in T98G and LN18 control groups (P less then 0.05). Western blot analysis showed that compared with glioma cells without Polyphyllin Ⅱ treatment, the expression of E-cadherin in T98G and LN18 was higher (F=85.56, P less then 0.05; F=60.80, P less then 0.05), but the expression of snail was lower (F=25.34, P less then 0.05; F=48.28, P less then 0.05). When temozolomide was used in combination with Polyphyllin Ⅱ at different concentrations, the coefficient of drug interaction (CDI) was less than 1. Western blot showed that MGMT expressions in T98G and LN18 were inhibited compared with glioma cells without Polyphyllin Ⅱ treatment (F=40.38, P less then 0.05; F=48.44, P less then 0.05). Conclusion Polyphyllin Ⅱ can inhibit the proliferation and invasion of glioma cells, and improve its sensitivity to Temozolomide.Objective To evaluate the clinical impact of percutaneous coronary intervention (PCI) on left ventricular myocardial remodeling and main adverse cardiovascular and cerebrovascular events (MACE) in ischemic cardiomyopathy patients with different left ventricular ejection fraction and SYNTAX score≤22. Methods A total of 191 ischemic cardiomyopathy patients who underwent PCI in Department of Cardiology from May 2017 to October 2018 were enrolled in this study, and they were divided into three groups according to preoperative left ventricular ejection fraction (≥50% group, 36%~49% group and ≤35% group). The main outcomes and left ventricular ejection fraction, left ventricular end-diastolic volume were analyzed at 12 months follow-up. The main outcomes were the recurrence of acute left ventricular failure, recurrent angina, restenosis, revascularization, non-fatal myocardial infarction, cardiovascular death and non-cardiovascular death. Results The incidence of MACE was 32.6% (15 cases) in ≥50% group, 32.0% (31 cases) in 36%-49% group, 45.