子痫前期发病机制的研究进展

子痫前期是妊娠特有的疾病,由于该病对母儿的危害极大,其发病机制一直是产科研究的焦点。随着研究的不断深入,目前认为该病主要与遗传、血管内皮受损、免疫失衡及炎症反应等因素相关,其中遗传因素是内因,血管内皮损伤因子水平异常升高、血管内皮保护因子水平降低是该病发生、发展的关键环节,而免疫失衡及炎症反应进一步加重血管内皮的损伤,多种机制相互作用导致子痫前期的发生。     

Deep vein thrombosis and pulmonary embolism in cirrhotic patients:Systematic review

Patients with liver cirrhosis were traditionally believed to be protected against development of blood clots.Lately,studies have shown that these patients may probably be at an increased risk of venous thrombotic complications.Although the hemostatic changes in the chronic liver disease patients and the factors that may predict bleeding vs thrombotic complications remains an area of active research,it is believed that the coagulation cascade is delicately balanced in these patients because of parallel reduced hepatic synthesis of pro and anticoagulant factors.Thrombotic state in cirrhotic patients is responsible for not only portal or non-portal thrombosis[deep vein thrombosis(DVT)and pulmonary embolism(PE)];it has also been associated with progression of liver fibrosis.The use of anticoagulants in cirrhosis patients is a challenging,and often a scary situation.This review summarizes the current literature on the prevalence of venous thrombosis(DVT and PE),risk factors and safety of prophylactic and therapeutic anticoagulation in patients with chronic liver disease.     

可逆性后部白质脑病综合征的发病机制及研究进展

可逆性后部白质脑病综合征(RPLS)是多种病因引起的神经系统受损临床综合征,目前关于其发病机制主要有以下两种学说:脑过度灌注理论和血管痉挛理论,前者主要包括血管机制、血管内皮损伤机制及免疫机制。该病主要临床表现为头痛、抽搐发作、视觉障碍、意识改变及精神行为异常等;典型的神经影像学改变是大脑半球后部白质水肿,以双侧顶枕叶受累最为多见,具有可逆性。     

Non-alcoholic fatty liver disease: What has changed in the treatment since the beginning?

Non-alcoholic fatty liver disease(NAFLD) is an umbrella term to describe the entire spectrum of this common liver disease. In patients with NAFLD, especially those with non-alcoholic steatohepatitis(NASH), most often have one or more components of the metabolic syndrome, but this is not universal. Although most patients with NAFLD share many clinical features, only a subset of patients develops significant liver inflammation and progressive fibrosis. On the other hand, not all patients with NASH exhibit insulin resistance. NASH can be seen in patients who are lean and have no identifiable risk factors. Many clinical studies have tried numerous drugs and alternative medicine, however, investigators have failed to identify a safe and effective therapy for patients with NASH. As summarized, the heterogeneity of pathogenic pathways in individual patients with NASH may warrant the development of an individualized treatment according to the underlying pathogenic pathway. The differentiation of pathogenetic targets may require the development of diagnostic and prognostic biomarkers, and the identification of genetic susceptibilities. At present, evidence-based medicine provides only a few options including life-style modifications targeting weight loss, pioglitazone and vitamin E in non-diabetic patients with biopsy-proven NASH.     

Clinical approaches to non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease(NAFLD)ranges from simple steatosis to nonalcoholic steatohepatitis(NASH),leading to fibrosis and potentially cirrhosis,and it is one of the most common causes of liver disease worldwide.NAFLD is associated with other medical conditions such as metabolic syndrome,obesity,cardiovascular disease and diabetes.NASH can only be diagnosed through liver biopsy,but noninvasive techniques have been developed to identify patients who are most likely to have NASH or fibrosis,reducing the need for liver biopsy and risk to patients.Disease progression varies between individuals and is linked to a number of risk factors.Mechanisms involved in the pathogenesis are associated with diet and lifestyle,influx of free fatty acids to the liver from adipose tissue due to insulin resistance,hepatic oxidative stress,cytokines production,reduced very low-density lipoprotein secretion and intestinal microbiome.Weight loss through improved diet and increased physical activity has been the cornerstone therapy of NAFLD.Recent therapies such as pioglitazone and vitamin E have been shown to be beneficial.Omega 3 polyunsaturated fatty acids and statins may offer additional benefits.Bariatric surgery should be considered in morbidly obese patients.More research is needed to assess the impact of these treatments on a long-term basis.The objective of this article is to briefly review the diagnosis,management and treatment of this disease in order to aid clinicians in managing these patients.     

无症状性脑梗死与睡眠障碍共病的研究进展

无症状性脑梗死（SBI）是指常无明确的卒中史、典型的临床症状及神经系统阳性体征,需通过颅脑影像学或尸检发现的脑梗死。随着研究的深入,SBI已被证实并非完全无症状,部分患者可能存在头晕、头痛、睡眠障碍、记忆力下降等非特异性神经功能损害表现。同时,大量临床报道显示,睡眠障碍是脑卒中后常见的并发症,并常会对患者的预后和生活质量产生不利影响。SBI作为脑梗死类型中的一种,与睡眠障碍也存在一定的联系,但由于SBI的临床特征,本身常被临床医生忽视,睡眠问题便更不受关注,国内外也缺乏相关研究报道。因此,本文对SBI与睡眠障碍共病的可能发生机制以及可能伴发的负面影响进行了综述,以便提高临床医生对其的关注度,做到早期诊治。     

血管性痴呆发病机制的研究进展

血管性痴呆(VaD)是因脑缺血后缺血组织缺氧和出血性脑损害所导致的智能及认知功能障碍的临床综合征。VaD目前已经成为致我国人民精神和躯体残疾的主要因素之一。随着人口老龄化,其发病率日益增高。VaD患者生活水平下降,给社会、家庭带来沉重的负担,而其发病机制不明确。VaD是老年期痴呆中有希望预防和治疗的痴呆,因此各方面研究日益受重视,探索其发病机制尤为重要。     

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。     

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.