杜长海名老中医应用药对治疗功能性便秘的临床经验探析

功能性便秘的发生严重困扰着现代人群,进而影响人们的生活质量。杜长海名老中医认为功能性便秘究其内因为大肠传导失常,外因乃现代人的生活方式、紧张的生活氛围等等,因此杜老结合自己数十年的临床经验,根据中医辨证总结出临床常用药对,对有效治疗功能性便秘进行了经验总结。     

基于“证治代谢组学”假说探讨中药（单体/复方）药效物质基础的研究思路与实践＊

中药(单体/复方)药效物质基础研究是中医药现代研究的关键问题之一。然而,目前运用的生化和分子生物学方法很难诠释其多靶点、整体性和动态性的整合调节作用。课题组提出的"证治代谢组学"假说理论指出,不同的证候存在"证相关代谢谱群"和"证相关生物标志物",这可能是中药药效物质基础所在,辨证论治后偏离的代谢网络功能呈现回归趋势。基于"证治代谢组学"假说开展中药(单体/复方)药效物质基础研究,这将为阐释中药(单体/复方)防病治病和养生保健的科学内涵及其对疾病个体的整合调节作用提供新的思路。本文以冠心病为研究载体、气阴虚血瘀证为切入点、活血保心丸为干预措施,就该研究思路的内涵与总体模式、提出的背景与依据、实践的方式与可行性、创新与特色及其研究意义等进行了简要介绍。     

基于网络药理学和分子对接探讨钩藤-全蝎药对治疗支气管哮喘的作用机制＊

目的通过网络药理学和分子对接探究钩藤-全蝎药对治疗支气管哮喘的药理作用机制。方法通过TCMSP、TCMIP数据库搜集钩藤、全蝎的活性成分及其作用靶点,并使用Cytoscape软件进行可视化分析成分-靶点网。通过OMIM、GeneCards数据库搜集支气管哮喘的疾病靶点,整合钩藤-全蝎药对与支气管哮喘的共有靶点。利用String平台构建对共有靶点互作PPI网络,并进行GO和KEGG富集分析,通过Cytoscape软件构建成分-靶点-通路网络模型。最后通过Autodock分子对接进行验证。结果经过筛选发现钩藤-全蝎药对37个活性化合物和234个药物靶点,与哮喘6010个靶点取交集得到35个共有靶点。钩藤-全蝎包含槲皮素、山奈酚、育亨宾碱、β-谷甾醇等重要活性成分;根据PPI网络分析,核心网络连接度高的潜在治疗靶点有IL6、CASP3、ECFR、ESR1、MAPK8等;根据KEGG富集分析结果显示,钩藤-全蝎药对主要通过PI3 K-Akt信号通路、TNF信号通路,HIF-1信号通路、M APK信号通路、NF-κB信号通路等来治疗哮喘;钩藤-全蝎药对活性成分与核心靶点的分子对接结果均显示出较好的结合活性。结论钩藤-全蝎药对治疗哮喘呈现出多成分、多靶点、多通路的特点,其核心成分槲皮素、山奈酚、育亨宾碱、β-谷甾醇等可能通过CASP3、MAPK8、ESR1、IL6、ECFR等靶点调节多条通路发挥抗炎、调节免疫、抗氧化应激、改善气道重塑等作用,从而对哮喘达到有效的治疗。     

基于文献分析多囊卵巢综合征的中医证型分布及用药规律

目的:通过文献探析中医治疗多囊卵巢综合征(PCOS)的证型分布及临床用药规律。方法:检索2003年至2018年1月1日中国期刊全文数据库(CNKI)、万方、维普3个中文数据库中相关中医治疗PCOS的临床研究文献,建立中医治疗PCOS的整体证型及临床用药数据库,并对数据进行处理、分析。结果:①共纳入符合标准的文献252篇,方剂284首;②涉及证型共37种,其中常见证型为肾虚血瘀证、痰湿证、肾虚痰瘀证,共占43.31%;③涉及病位要素以肾为主,其次为肝、脾;涉及病性要素以血瘀、痰、湿为主;④涉及药物193味,按功效共分为16类,补虚药占41.44%,活血化瘀药占16.20%,化痰祛湿药占14.90%;⑤中医治疗PCOS药性以温、平为主,药味以甘为主,辛、苦次之。结论:PCOS病因病机复杂,以肾虚为本,血瘀、痰湿为标,治疗以补肾活血、化湿祛痰为主。     

自拟清热解毒、活血化瘀方联合华蟾素治疗湿热瘀毒型宫颈癌临床观察

目的:分析自拟清热解毒、活血化瘀方联合华蟾素治疗湿热瘀毒型宫颈癌临床疗效及其安全性。方法:68例湿热瘀毒型患者随机分为对照组和观察组各34例,2组均采用放化疗治疗及手术治疗。观察组加用清热解毒、活血化瘀类中药联合华蟾素治疗,观察2组临床疗效及不良反应情况。结果:总有效率观察组85.2%,对照组70.5%,2组比较差异无统计学意义(P0.05).观察组恶心呕吐、肝肾损伤、脱发、神经毒性及电解质紊乱等不良反应发生率更低,与对照组比较差异具有统计学意义(P0.05)。结论:清热解毒、活血化瘀类中药联合华蟾素治疗湿热瘀毒型宫颈癌临床疗效满意度高,不良反应少。     

Memory scrutinized through electrical brain stimulation: A review of 80 years of experiential phenomena

Electrical brain stimulations (EBS) sometimes induce reminiscences, but it is largely unknown what type of memories they can trigger. We reviewed 80 years of literature on reminiscences induced by EBS and added our own database. We classified them according to modern conceptions of memory.We observed a surprisingly large variety of reminiscences covering all aspects of declarative memory. However, most were poorly detailed and only a few were episodic. This result does not support theories of a highly stable and detailed memory, as initially postulated, and still widely believed as true by the general public.Moreover, memory networks could only be activated by some of their nodes: 94.1% of EBS were temporal, although the parietal and frontal lobes, also involved in memory networks, were stimulated. The qualitative nature of memories largely depended on the site of stimulation: EBS to rhinal cortex mostly induced personal semantic reminiscences, while only hippocampal EBS induced episodic memories. This result supports the view that EBS can activate memory in predictable ways in humans.     

Exposure and response prevention therapy with cognitive defusion exercises to reduce repetitive and restrictive behaviors displayed by children with autism spectrum disorder

Repetitive and restrictive behaviors are disruptive in children with autism spectrum disorder. Exposure is an evidence-based approach to these problems and is hypothesized to work in part by enabling rule testing that undermines rule control. The present study undermined rule control more directly through cognitive defusion exercises. Experiment 1 used a multiple baseline across participants design to assess the effects of a cognitive defusion exercise in the form of word repetition and exposure on problem behavior associated with repetitive and restrictive behaviors observed in children with autism spectrum disorder. All 3 participants demonstrated a decrease in the percentage of problem behavior following the implementation of treatment which remained at near zero during a 3-month follow-up. Experiment 2 used an alternating treatments design to compare a cognitive defusion exercise and exposure to a control exercise and exposure. All except 1 of the participants displayed larger and quicker decreases in problem behavior during the cognitive defusion exercise condition compared to the control exercise condition. The results suggest that cognitive defusion exercises can enhance the treatment effects of exposure to decrease problem behavior associated with repetitive and restrictive behaviors.     

Destruction of the hepatocyte junction by intercellular invasion of Leptospira causes jaundice in a hamster model of Weil's disease

Weil's disease, the most severe form of leptospirosis, is characterized by jaundice, haemorrhage and renal failure. The mechanisms of jaundice caused by pathogenic Leptospira remain unclear. We therefore aimed to elucidate the mechanisms by integrating histopathological changes with serum biochemical abnormalities during the development of jaundice in a hamster model of Weil's disease. In this work, we obtained three‐dimensional images of infected hamster livers using scanning electron microscope together with freeze‐cracking and cross‐cutting methods for sample preparation. The images displayed the corkscrew‐shaped bacteria, which infiltrated the Disse's space, migrated between hepatocytes, detached the intercellular junctions and disrupted the bile canaliculi. Destruction of bile canaliculi coincided with the elevation of conjugated bilirubin, aspartate transaminase and alkaline phosphatase levels in serum, whereas serum alanine transaminase and γ‐glutamyl transpeptidase levels increased slightly, but not significantly. We also found in ex vivo experiments that pathogenic, but not non‐pathogenic leptospires, tend to adhere to the perijunctional region of hepatocyte couplets isolated from hamsters and initiate invasion of the intercellular junction within 1 h after co‐incubation. Our results suggest that pathogenic leptospires invade the intercellular junctions of host hepatocytes, and this invasion contributes in the disruption of the junction. Subsequently, bile leaks from bile canaliculi and jaundice occurs immediately. Our findings revealed not only a novel pathogenicity of leptospires, but also a novel mechanism of jaundice induced by bacterial infection.     

麻黄-甘草药对抑制过敏性哮喘的效应及机制初探

目的 研究麻黄-甘草药对对过敏性哮喘的影响,并初步探讨其作用机制。方法 建立屋尘螨（HDM）诱导的过敏性哮喘模型,造模同时给予麻黄-甘草药对提取物（MG）。使用无创肺功能仪检测小鼠气道反应性,HE染色观察小鼠肺组织病理学变化,Masson染色观察小鼠肺组织的胶原沉积情况,进行血液嗜酸性粒细胞（EOS）计数,ELISA法检测支气管肺泡灌洗液（BALF）及肺组织IL-4、IL-5、IL-13、TGF-β1及血清IgE的表达,免疫组化检测肺组织E-cadherin、N-cadherin、Vimentin、α-SMA和TGF-β1蛋白表达情况。结果 MG可显著降低气道高反应性,抑制BALF及肺组织IL-4、IL-5和IL-13的表达,降低血液EOS及血清IgE的表达,并且减轻肺组织的炎症浸润及胶原沉积。进一步结果表明MG可抑制肺组织TGF-β1的表达,上调E-cadherin以及下调N-cadherin、Vimentin、α-SMA的表达。结论 MG能够通过抑制支气管上皮间质转化,从而缓解气道的炎症状态以及改善哮喘的气道重塑,进而发挥对过敏性哮喘的治疗作用。