国内外安宁疗护准入标准的研究进展

安宁疗护可提高患者在生命终末阶段的生活质量，减轻患者和家属的身心痛苦。科学合理的安宁疗护准入标准可帮助医护人员识别出需要安宁疗护服务的患者，使其及时获得安宁疗护服务，因此明确安宁疗护的准入标准是推进安宁疗护发展的基础。本文就国内外安宁疗护准入标准的制定方法、具体内容及优缺点进行综述，以期为我国安宁疗护准入标准的构建提供参考。     

心脏瓣膜置换术后患者的出院准备度现状及其影响因素分析

目的:调查心脏瓣膜置换术后患者的出院准备度现状,并分析其影响因素。方法:于2018年9月至2019年3月用一般资料、出院准备度量表、出院指导质量量表对139例瓣膜置换术后患者进行调查。结果:心脏瓣膜置换术后患者的出院准备度总分为(89.51±8.53)分,与出院指导质量呈正相关;多元回归分析显示,主要照顾者、婚姻状况、工作状态、服药种类、出院指导质量为出院准备度影响因素。结论:心脏瓣膜置换术后患者的出院准备度有待提高,患者感知的个人状态得分不理想;护士应鼓励患者配合进行早期康复,强化出院指导,采取有效措施提供康复信息,满足患者及其家属需求,提高出院准备度。     

Lysophosphatidylcholine‐induced cytotoxicity and protection by heparin in mouse brain bEND.3 endothelial cells

A pathological feature in atherosclerosis is the dysfunction and death of vascular endothelial cells (EC). Oxidized low‐density lipoprotein (LDL), known to accumulate in the atherosclerotic arterial walls, impairs endothelium‐dependent relaxation and causes EC apoptosis. A major bioactive ingredient of the oxidized LDL is lysophosphatidylcholine (LPC), which at higher concentrations causes apoptosis and necrosis in various EC. There is hitherto no report on LPC‐induced cytotoxicity in brain EC. In this work, we found that LPC caused cytosolic Ca²⁺ overload, mitochondrial membrane potential decrease, p38 activation, caspase 3 activation and eventually apoptotic death in mouse cerebral bEND.3 EC. In contrast to reported reactive oxygen species (ROS) generation by LPC in other EC, LPC did not trigger ROS formation in bEND.3 cells. Pharmacological inhibition of p38 alleviated LPC‐inflicted cell death. We examined whether heparin could be cytoprotective: although it could not suppress LPC‐triggered Ca²⁺ signal, p38 activation and mitochondrial membrane potential drop, it did suppress LPC‐induced caspase 3 activation and alleviate LPC‐inflicted cytotoxicity. Our data suggest LPC apoptotic death mechanisms in bEND.3 might involve mitochondrial membrane potential decrease and p38 activation. Heparin is protective against LPC cytotoxicity and might intervene steps between mitochondrial membrane potential drop/p38 activation and caspase 3 activation.     

Liguzinediol对阿霉素诱导的慢性心衰大鼠心功能的影响

目的 通过阿霉素（Dox）复制大鼠慢性心力衰竭（CHF）模型，观察Liguzinediol对CHF大鼠心功能的影响。方法 通过血流动力学观察Liguzinediol对Dox（腹腔注射，2 mg/kg）诱导的CHF大鼠左心室内压最大上升/下降速率(±dp/dt_max)、左心室内压(LVSP)、动脉收缩压(ASP)、动脉舒张压(ADP)和心率(HR)的变化；观察Liguzinediol对血清一氧化氮（NO）、一氧化氮合成酶（NOS）、超氧化物歧化酶（SOD）、肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）以及血浆中丙二醛（MDA）的影响。结果 Liguzinediol能增加LVSP、+dp/dt_max、ASP、ADP、AP、HR，降低-dp/dt_max(P<0.05~0.01)；降低NO、iNOS以及MDA的浓度，同时增强了SOD的活性(P<0.05~0.01)；抑制IL-6和TNF-α的生成(P<0.05~0.01)。结论 Liguzinediol可明显改善Dox诱导的CHF大鼠血流动力学指标，减少模型大鼠炎症因子的释放以及抑制氧自由基的生成。      

HBV患者血清YKL-40、CA19-9、GP73水平与其病情相关性

目的 分析HBV患者YKL-40、CA19-9、GP73水平差异及与患者病情轻重程度的相关性,探讨HBV患者病情的判定指标。方法 选取2015年5月—2018年5月收治的100例HBV患者,其中慢性HBV感染组40例、慢性乙型肝炎组36例、HBV相关肝硬化组24例,同期选择我院健康体检的健康者50例作为健康对照组;检测患者血中YKL-40、CA19-9、GP73水平;分析HBV感染患者血清YKL-40、CA19-9、GP73水平与病情轻重程度的相关性。结果 慢性HBV感染、慢性乙型肝炎及HBV相关肝硬化患者血中YKL-40水平分别为（36.38±4.19）ng/mL 、（49.02±4.32）ng/mL、（65.14±5.21）ng/mL ,CA19-9分别为（12.03±1.03）KU/L、（13.84±0.98）KU/L、（16.94±0.81）KU/L,GP73分别为（47.22±5.38）ng/mL 、（98.53±10.24）ng/mL 、（229.85±12.19）ng/mL,均明显高于对照组的（28.19±3.27）ng/mL 、（7.34±0.92）KU/L 、（30.93±3.89）ng/mL,均P=0.000 0。随着慢性HBV感染者、慢性乙型肝炎患者和不同HBV相关肝硬化患者肝脏炎症及纤维化程度加重,患者血中YKL-40、CA19-9和GP73也随之显著增加,均P=0.000 0;YKL-40、CA19-9和GP73均是影响HBV感染患者体内炎症坏死及肝脏纤维化的独立性影响因素,差异有统计学意义（P<0.05）。结论 HBV感染患者血清中YKL-40、CA19-9、GP73水平是HBV感染患者病情轻重程度的独立性影响因素。     

Cardiac Denervation for Arrhythmia Treatment with Transesophageal Ultrasonic Strategy in Canine Models

Stellate ganglion (SG) modification has been investigated for arrhythmia treatment. In this study, transesophageal SG imaging and intervention were explored using a homemade 30F integrated focused ultrasonic catheter in healthy mongrel canines in vivo. Anatomic details of SGs were ultrasonically imaged and evaluated. SG had a heterogeneous echoic structure and characteristic profiles sketched by hyper-echoic outlines in an ultrasonogram. Left SGs in the experimental group were successfully ablated through the esophagus under ultrasonic guidance provided by the catheter itself. Two weeks after the ablation, the QT and QTc of the experimental group decreased compared with those of the sham group and at baseline (both p values < 0.001). Histologic examination revealed that left SGs were destroyed. No major complications were observed. This approach may be further explored as a method for ganglia remodeling evaluation and as a strategy of ganglia modification for arrhythmia and for other diseases.