Wnt/β-catenin信号通路在肝癌发病机制中作用的研究

Wnt/β-catenin信号通路也称Wnt经典信号通路,参与调控细胞分化、癌变、凋亡及机体免疫、应激等多种病理生理过程。有研究表明Wnt信号通路与肝癌(hepatocellular carcinoma,HCC)的发生相关。深入研究Wnt/β-catenin信号通路在肝癌发病中的作用,将有助于进一步揭示肝癌的发病机制,为肝癌的防治提供新的可能途径及干预靶点。     

输血相关性急性肺损伤研究进展

输血相关性急性肺损伤（transfusion-related acute lung injury,TRALI）是输血相关性疾病中最常见的类型.其发病率及病死率高,定义基于临床和影像学参数.TRALI分为免疫介导性和非免疫介导性,患者基础情况和输血因素共同决定着TRALI的发生.TRALI的预防主要包括避免使用女性供血者血浆制品及避免输注多个供血者的混合血浆.但目前所有预防措施只能减少而不是消除TRALI的发生,且对于这种危及生命的综合征尚无明确治疗方法,因此防治TRALI的工作任重而道远.本文对TRALI的定义、发病率、发病机制、临床表现、预防及治疗作一综述.     

Epigenetic mechanisms in Alzheimer's disease: Implications for pathogenesis and therapy

The vast majority of Alzheimer's disease (AD) are late-onset forms (LOAD) likely due to the interplay of environmental influences and individual genetic susceptibility. Epigenetic mechanisms, including DNA methylation, histone modifications and non-coding RNAs, constitute dynamic intracellular processes for translating environmental stimuli into modifications in gene expression. Over the past decade it has become increasingly clear that epigenetic mechanisms play a pivotal role in aging the pathogenesis of AD. Here, we provide a review of the major mechanisms for epigenetic modification and how they are reportedly altered in aging and AD. Moreover, we also consider how aberrant epigenetic modifications may lead to AD pathogenesis, and we review the therapeutic potential of epigenetic treatments for AD.     

The role of neuropeptide Y and aquaporin 4 in the pathogenesis of intestinal dysfunction caused by traumatic brain injury

Background

Although the exact incidence is unknown, traumatic brain injury (TBI) can lead to intestinal dysfunction. It has important influence on the early nutrition and prognosis of TBI patients. Experiments were designed to study the roles of neuropeptide Y (NPY) and aquaporin 4 (AQP4) in the pathogenesis of intestinal dysfunction caused by TBI and to find some new solutions for the treatment of intestinal dysfunction after TBI.

Methods

Forty adult male Wistar rats were randomly divided into control, mild trauma, moderate trauma, and severe trauma groups. TBI was induced by Feeney's impact method. Control animals were sham operated but not subjected to the impact test. All rats were killed 24 h after surgery. Blood samples were obtained from the abdominal aorta for enzyme-linked immunosorbent assay measurement of NPY concentrations. Jejunum segments 15 cm distal to the Treitz ligament were taken for analysis of NPY and AQP4 expression by polymerase chain reaction, Western blot, and immunohistochemistry. Pathologic changes in intestinal cell structure and ultrastructure were studied by light microscopy and transmission electron microscopy.

Results

The specimens from different groups showed different degrees of structural changes, ranging from swelling and degeneration of villous epithelial cells to extensive denudation and collapse of the villi. The more severe the trauma, the more serious the degree of intestinal mucosal injury. Intestinal smooth muscle also showed varying degrees of edema and structural disorder. Electron microscopy showed that intestinal mitochondria had varying degrees of swelling and the structure of mitochondrial crista was disordered and even fractured. Plasma concentrations of NPY and jejunal gene and protein expressions of NPY and AQP4 increased significantly following TBI (P < 0.05), with greater increases at higher levels of injury. Moreover, there were positive correlations between NPY and AQP4 (P < 0.05).

Conclusions

Increasing grades of TBI caused increasing degrees of intestinal ischemia and edema, and thus caused increasingly severe intestinal dysfunction. AQP4 and NPY may be involved in the pathogenesis of intestinal dysfunction after TBI. Increased NPY levels may be responsible for intestinal ischemia and hypoxia, and AQP4 may play an important role in intestinal edema. Increased NPY levels may be one of the main causes for the increase in AQP4 after TBI.     

炎症性肠病发病机制的研究进展

炎症性肠病(inflammatory bowel disease,IBD)主要包括克罗恩病(crohn’s disease,CD)和溃疡性结肠炎(ulcerative colitis,UC),是一组以持续性肠道炎症为特征的疾病。其确切的发病机制尚不十分明确,一般认为是环境因素作用于遗传易感的个体,使其免疫系统发生过度的免疫反应,最终导致肠道炎症。     

慢性心力衰竭不同原发病与中医证型特点分析

目的分析不同原发病所致慢性心力衰竭(CHF)的中医证型特点和规律,为CHF病机探索和认识提供参考。方法对117例CHF患者进行回顾性分析,根据不同原发病和心功能分级情况进行证型归纳和统计分析,分析中医证型与原发病、心功能分级的相关性。结果原发病中冠心病占31.6%,高血压占30.8%,肺心病占13.7%,风心病占11.1%,心肌病占6.8%,老年性心脏瓣膜病占4.3%;冠心病组中气虚血瘀证、心脾肾阳虚水泛兼血瘀证最多,高血压病组气虚血瘀证比例最大,风心病心脾肾阳虚水泛兼血瘀证最多,肺心病组心肺气虚证为多,心肌病以心脾阳虚兼血瘀水停证为多,老年瓣膜病以气虚血瘀证为多;心功能Ⅱ级中以心肺气虚证为主,心功能Ⅲ级中以气虚血瘀和心脾阳虚兼血瘀水停证居多,心功能IV级中以心脾肾阳虚水泛兼血瘀证居多,心功能等级以心肺气虚、心气阴虚兼血瘀,气虚血瘀,心脾阳虚兼血瘀水停,心脾肾阳虚水泛兼血瘀逐级递增(r=0.508,P<0.001);血浆脑钠肽(BNP水平)按心肺气虚、心气阴虚兼血瘀,气虚血瘀,心脾阳虚兼血瘀水停,心脾肾阳虚水泛兼血瘀逐级递增(r=0.773,P<0.001);结论引起CHF最常见的原发病是冠心病,其中气虚血瘀证和心脾肾阳虚水泛兼血瘀证常见,说明气虚、阳虚、血瘀是CHF的最突出的病理改变。     

围术期输血相关急性肺损伤的预防策略

背景 输血相关急性肺损伤(transfusion-related acute lung injury,TRALI)作为输血最常见的并发症之一,而备受输血医学、血液病学与重症医学界关注.因起病急、病情重、目前仍缺乏特效的治疗靶点,已成为输血相关病死率升高的头号致病因素;不幸的是,围术期临床工作人员却少有认识. 目的 提高对TRALI的重视,采取积极预防措施,降低TRALI发生率及死亡率. 内容 参考近期较新文献,就TRALI的定义、发病机制、预防举措等进行综述. 趋向 研究TRALI的确切发病机理,并创新有效防治手段对于治疗TRALI至关重要.     

发作性睡病病因的中西医学研究进展

发作性睡病是一种慢性睡眠障碍,是一种白天过度嗜睡的重要原因,往往伴有猝倒发作、睡眠瘫痪、睡眠幻觉等其他症状,合称为发作性睡病四联症。该文综述近年来中西医在发作性睡病病因方面的研究进展,为本病发病机制的研究提供进一步的方向。目前,西医主要认为发作性睡病的发病机制与食欲素和HLA-DQB1基因?0602亚型密切相关,此外,近年来西欧某些国家(英国、芬兰、瑞典)研究还发现, H1 N1流感疫苗的使用导致了发作性睡病发病率明显上升。中医主要认为,阴阳偏盛和营卫运行失常易引起睡眠障碍,同时儿童发作性睡病的病因与脏腑的关系也相当密切。     

Cornelia de Lange 综合征研究进展

Cornelia de Lange 综合征是一种1933年首次报道的罕见的先天性疾病。Cornelia de Lange综合征常涉及多器官的发育异常。临床表现为严重的生长迟缓、认知障碍、具有特征性的面容和上肢缺陷。随着医学科学特别是遗传学、分子生物学的迅猛发展,对 Cornelia de Lange 综合征的病因、发病机制等已有更深入的研究,该文就近年来的研究进展进行综述。     

血清IL-33水平与老年COPD患者病程分期的相关性研究

目的研究老年慢性阻塞性肺病（COPD）患者血清IL-33水平与其病程分期的相关性。方法选择60例老年COPD患者作为观察组,按病程分期分为稳定期组和急性加重组,另选择15例非COPD老年患者作为对照组;分别检测血清IL-33水平。结果各组组间比较结果显示,AECOPD组和COPD稳定期组的血清IL-33水平均高于对照组（P＜0.05）,其中,AECOPD 组的比 COPD 稳定期组的更高（P＜0.05）。结论血清 IL-33水平在老年COPD患者中增高,急性加重期更明显,提示IL-33在老年人COPD发生、发展中可能起重要作用。