非平衡态热力学理论在证候热力学研究中的应用

引入非平衡态热力学理论,诠释中医阴阳理论.借助红外成像获得的人体体表脏腑三焦等对应区域热值数据和排序,以坐标图形式表达人体区域热值数据高低(人体热结构),确立中医证候热力学研究的思路和方法,提出健康人脏腑三焦等人体热结构符合耗散结构,不同证候出现不同人体热结构,辨证论治就是根据脏腑寒热偏离,用中医方法恢复人体正常热结构的调整.     

丛品教授治疗喉痹经验

[目的]总结丛品教授诊疗喉痹的临床经验。[方法]从喉痹的病因病机、临床辨证及治疗体会方面论述丛品教授的临证思维和诊治特色,总结其常用方药配伍及加减化裁特色,并附验案举隅。[结果]丛品教授认为本病的病因病机中,应特别重视"风、热"之邪和肝、脾、胃三脏的功能失调。辨证上以症状为主、体征为辅并重视舌诊。根据以上病因病机形成了健脾和胃、疏肝理气、疏风清热、养阴生津、理气活血、化痰散结的治则治法,并运用外治法治疗难治性喉痹。在临床上收到良好疗效。[结论]丛品教授对喉痹的病因病机、辨证论治、遣方用药及外治法有其个人认识,在临床上收效良好,值得学习和应用。     

慢性阻塞性肺疾病肺外合并症的治疗现状和研究进展

正慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是一种慢性气道炎症性疾病,以不完全可逆的气流受限为主要特征,预计到2020年,COPD将上升为全球第四大死亡原因[1-2]。GOLD指南指出COPD不是单纯的一种肺脏疾病,其还具有显著的肺外合并症,常以慢性全身性炎症为共同表现,这些肺外疾病会引发COPD患者病情加重,显著增加COPD患者的发病率,导致医疗负担加重以及治疗难度增大[3]。然而COPD的肺外合并症几乎涉及全身各个系统,包括心血管系统、神经系统、内分泌系统、运动系统、消化系统、血液系统、泌尿系统。研究显示,超过一半的COPD患者的死亡原因源于其他系统疾病,而并非呼吸系统     

Edwardsiella tarda-Induced Cytotoxicity Depends on Its Type III Secretion System and Flagellin

Many Gram-negative bacteria utilize a type III secretion system (T3SS) to translocate virulence proteins into host cells to cause diseases. In responding to infection, macrophages detect some of the translocated proteins to activate caspase-1-mediated cell death, called pyroptosis, and secretion of proinflammatory cytokines to control the infection. Edwardsiella tarda is a Gram-negative enteric pathogen that causes hemorrhagic septicemia in fish and both gastrointestinal and extraintestinal infections in humans. In this study, we report that the T3SS of E. tarda facilitates its survival and replication in murine bone marrow-derived macrophages, and E. tarda infection triggers pyroptosis of infected macrophages from mice and fish and increased secretion of the cytokine interleukin 1β in a T3SS-dependent manner. Deletion of the flagellin gene fliC of E. tarda results in decreased cytotoxicity for infected macrophages and does not attenuate its virulence in a fish model of infection, whereas upregulated expression of FliC in the fliC mutant strain reduces its virulence. We propose that the host controls E. tarda infection partially by detecting FliC translocated by the T3SS, whereas the bacteria downregulate the expression of FliC to evade innate immunity.     

Tricyclic antidepressant amitriptyline inhibits autophagic flux and prevents tube formation in vascular endothelial cells

Amitriptyline is a tricyclic antidepressant and an inhibitor of lysosomal acid sphingomyelinase (ASM). Amitriptyline is well known for its cardiovascular side effects and toxicity in psychiatric patients. However, the mechanisms underlying the cardiovascular side effects of amitriptyline remain largely undefined. This study aimed to determine the effects of amitriptyline on angiogenic capability of vascular endothelial cells in physiological settings and identify its mechanism of action. The ex vivo aortic ring angiogenesis and in vitro‐cultured endothelial cell tube formation assay were used to assess the effects of amitriptyline on endothelial angiogenic capability. It was demonstrated that amitriptyline impaired the angiogenesis of aortic rings, which was similar to that found in aortic rings with haploinsufficiency of the ASM gene. In cultured mouse microvascular endothelial cells (MVECs), amitriptyline impaired the proliferation and tube formation under basal condition, which were accompanied by attenuated angiogenic signalling pathways such as endothelial nitric oxide synthase, Akt and Erk1/2 pathways. Mechanistically, amitriptyline inhibited autophagic flux without affecting autophagosome biogenesis at basal condition. ASM gene silencing or autophagy inhibition mimics the inhibitory effects of amitriptyline on endothelial cell proliferation and tube formation. Collectively, our data suggest that amitriptyline inhibits endothelial cell proliferation and angiogenesis via blockade of ASM‐autophagic flux axis. It is implicated that the cardiovascular side effects of amitriptyline may be associated with its inhibitory action on physiological angiogenesis.     

血栓弹力图评估血液毒毒蛇咬伤严重程度的临床价值

毒蛇咬伤后,轻者可能仅存在轻微的局部症状,重症可出现严重的全身毒性反应,如严重的凝血功能障碍、骨筋膜室综合征、呼吸肌麻痹、多脏器功能衰竭及休克等,甚至死亡[1]。目前,国际上较为通用的蛇咬伤病情严重性评估方法为蛇伤严重性评分量表(snakebite severity scale,SSS)[2],这种方法从临床表现、实验室检查等方面获取信息,内容详细,客观性好,但分类项目多,内容繁琐[1]。血栓弹力图(TEG)分析血小板、凝血因子等多种因素的作用,能较全面地反映整个凝血过程,已被广泛应用于临床医疗[3]。本研究中对本院收治的血液毒毒蛇咬伤患者常规进行TEG检测,研究其与血液毒毒蛇咬伤后病情严重程度的关联性,以期提高临床医师对早期检测TEG在评估血液毒毒蛇咬伤病情严重程度中意义的认识。     

湖南省郴州市一起新型冠状病毒肺炎聚集性疫情流行病学调查

目的 通过分析郴州市一起新冠肺炎聚集性疫情相关病例发病确诊过程,探讨新冠病例早发现、早报告以及病例诊断和隔离观察解除的策略依据。 方法 对该起新冠肺炎聚集性疫情的病例和密切接触者进行现场流行病学调查,描述性分析流行病学史、临床和实验室资料。 结果 利用大数据比对监测,在转送监测对象至集中场所隔离医学观察时发现了新冠肺炎确诊病例何某华,由此发现一起新冠肺炎家庭聚集性疫情,何某的5名密切接触者中有3人发病确诊（包含1名重症病例）,其中重症病例黄某第7次新型冠状病毒核酸检测阳性进而确诊,密切接触者中胡某有流行病学史、血常规白细胞下降和肺炎影像学改变,但是5次咽拭子核酸检测阴性,未确诊。 结论 大数据比对监测对发现传染病有积极作用;早期对有流行病学史人员单独隔离医学观察对防止聚集性疫情发生有重要意义;将2次核酸检测阴性作为新冠肺炎病例的排除标准和将核酸检测阳性作为确诊新冠肺炎病例的必备条件,值得探讨,这都可能放走传染源,导致新冠肺炎传播。     

芒针透刺督脉组穴联合平衡训练治疗卒中后平衡障碍

目的:观察芒针透刺督脉组穴联合平衡训练治疗脑卒中偏瘫患者平衡障碍的临床疗效。方法:90例卒中后平衡障碍患者以就诊顺序随机分为芒针通督组、普通针刺组和平衡训练组各30例。平衡训练组给予单纯平衡训练,普通针刺组在平衡训练基础上给予毫针针刺治疗,芒针通督组在平衡训练基础上给予芒针通督组穴治疗,3组患者均治疗3个疗程。比较3组患者治疗前后步行功能(Holden步行能力分级)、平衡功能(Berg平衡量表,Fugl-Meyer量表)。结果:治疗后,3组患者平衡功能、步行运动能力均优于治疗前,差异均有统计学意义(P0.05);且芒针通督组平衡功能、步行运动能力均优于其他两组,差异均有统计学意义(P0.05)。芒针通督组有效率(96.6%)显著高于普通针刺组(83.3%)、平衡训练组(73.3%),差异均有统计学意义(P0.05)。结论:芒针透刺督脉组穴联合平衡训练治疗卒中后平衡障碍患者疗效显著,可显著提高患者平衡功能、步行运动能力。     

Characterization of ibrutinib‐sensitive and ‐resistant mantle lymphoma cells

Ibrutinib inhibits Bruton tyrosine kinase (BTK), a key component of early B‐cell receptor (BCR) signalling pathways. A multicentre phase 2 trial of ibrutinib in patients with relapsed/refractory mantle cell lymphoma (MCL) demonstrated a remarkable response rate. However, approximately one‐third of patients have primary resistance to the drug while other patients appear to lose response and develop secondary resistance. Understanding the molecular mechanisms underlying ibrutinib sensitivity is of paramount importance. In this study, we investigated cell lines and primary MCL cells that display differential sensitivity to ibrutinib. We found that the primary cells display a higher BTK activity than normal B cells and MCL cells show differential sensitivity to BTK inhibition. Genetic knockdown of BTK inhibits the growth, survival and proliferation of ibrutinib‐sensitive but not resistant MCL cell lines, suggesting that ibrutinib acts through BTK to produce its anti‐tumour activities. Interestingly, inhibition of ERK1/2 and AKT, but not BTK phosphorylation per se, correlates well with cellular response to BTK inhibition in cell lines as well as in primary tumours. Our study suggests that, to prevent primary resistance or to overcome secondary resistance to BTK inhibition, a combinatory strategy that targets multiple components or multiple pathways may represent the most effective approach.