生物信息学技术在生殖领域中的研究进展

生物信息学（bioinformatics）在生殖系统的研究中被广泛应用于各个技术层面,包括基因组、转录组、蛋白组和代谢组。通过数据的系统化采集和可视化处理,生殖过程中各种关键分子的作用机制正逐步被发现并阐明。生物信息学技术在生殖系统研究中的应用,既在保障严谨性和科学性的基础上有效地推动了生殖系统研究的发展与创新,如从基因组、转录组、蛋白组和代谢组等不同层次水平上分析生殖系统中不同器官的正常功能或其异常病理现象;同时也促进了生殖系统相关疾病临床诊断和治疗的进展,如在对疾病诊治中,新的临床疾病标志物及药物靶点的发现等。综述近年生殖医学前沿研究的最新生物信息学技术并总结现有生殖医学相关生物信息学研究的主要进展,这也为后续的各类研究提供了重要的方向和思路。     

松针提取液对实验性高脂血症及脂质过氧化作用的影响

经 8周高脂乳剂饲养后 ,选高脂血症造模成功的家兔 1 5只 ,随机分为对照组、松针提取液小剂量治疗组 (实验Ⅰ组 )、松针提取液大剂量治疗组 (实验Ⅱ组 )。取血测TG、TC、MDA含量和SOD活性及总抗氧化活力。结果动物经松针提取液治疗后 ,血TC及MDA含量降低 ,SOD活性及总抗氧化活力升高 ,与对照组比较 ,治疗Ⅱ组的降脂作用和抗氧化能力更显著。结论 :松针提取液对高脂血症有较强的降脂和抗氧化作用。     

急性后颅窝血肿的微创穿刺术治疗

目的：探讨应用IL－2型特种针进行微创穿刺术治疗后颅窝血肿的可行性及临床应用。材料及方法：回顾性分析我们自1995年9月至1999年9月对28例后颅窝高血压性或外伤性脑内血肿及硬膜外血肿进行微创穿刺引流治疗的病例。结果：28例病例中除1例于穿刺成功后死于脑干功能衰竭外,其余病例均获成功,病人无后遗症,痊愈出院,其中1例伴发再出血,经血肿腔内止血药冲洗引流治疗再出血停止,结论：此穿刺针特点为针钻一体,解决了针在颅骨上固定问题,也解决了立体定向不能留置针管问题,微创穿刺方法治疗后颅窝血肿可避免传统后颅窝开颅手术,安全性高,疗效良好,操做简便,费用较低,易于在各级医院普遍开展,具有较大推广使用价值。     

肝豆状核变性分子生物学研究

【目的】探讨中国人肝豆状核变性(WD)的分子发病机制和基因诊断的方法。【方法】应用基因工程技术对WD进行了10年的分子生物学研究。【结果】①WD的基因定位研究通过RFLP及微卫星多态性分析,应用两位点及多位点连锁软件,建立了中国人WD基因在D     

Pancreatic solid pseudopapillary neoplasm

Pancreatic solid pseudopapillary neoplasm (SPN) is a rare low grade malignant tumour. Distinguishing this entity from other pancreatic neoplasms is critical for therapeutic decision making and prognostication. It predominantly affects young female patients <40 years of age, with excellent clinical outcome following surgical removal. The gold standard diagnostic test is cytopathological or histopathological assessment of fine needle aspirate. There are two main difficulties with this. First, SPN can present with morphological and immunohistochemical appearances that can closely mimic other pancreatic tumours, in particular, pancreatic neuroendocrine tumour (NET). Second, the amount of diagnostic material from fine needle aspiration can be limited. Here, we present a cytopathological case with both challenges during the pre-operative investigation of SPN. The case exemplifies the importance of combining morphological features with a targeted panel of immunohistochemistry to arrive at the diagnosis.     

Impact of donor extracellular vesicle release on recipient cell “cross-dressing” following clinical liver and kidney transplantation

In several murine models of transplantation, the “cross-dressing” of recipient antigen presenting cells (APCs) with intact donor major histocompatibility complex (MHC) derived from allograft-released small extracellular vesicles (sEVs) has been recently described as a key mechanism in eliciting and sustaining alloimmune responses. Investigation of these processes in clinical organ transplantation has, however, been hampered by the lack of sensitivity of conventional instruments and assays. We have employed advanced imaging flow cytometry (iFCM) to explore the kinetics of allograft sEV release and the extent to which donor sEVs might induce cross-dressing following liver and kidney transplantation. We report for the first time that recipient APC cross-dressing can be transiently detected in the circulation shortly after liver, but not kidney, transplantation in association with the release of HLA-bearing allograft-derived sEVs. In liver transplant recipients the majority of circulating cells exhibiting donor HLA are indeed cross-dressed cells and not passenger leukocytes. In keeping with experimental animal data, the downstream functional consequences of the transfer of circulating sEVs harvested from human transplant recipients varies depending on the type of transplant and time posttransplant. sEVs released shortly after liver, but not kidney, transplantation exhibit immunoinhibitory effects that could influence liver allograft immunogenicity.     

Increased risk of neonatal complications and infections in children of kidney-transplanted women: A nationwide controlled cohort study

Information related to short- and long-term risks of children born to kidney-transplanted women remains limited. With the aim of investigating the risk of neonatal complications, and the short- and long-term risk of infections in offspring of kidney-transplanted women, all children born to kidney-transplanted women in Denmark from 1964 to 2016 were identified in a nationwide retrospective matched cohort study. A total of 124 children of kidney-transplanted women were identified and matched on gender, birth year, and number of siblings at birth 1:10 with children born to nontransplanted women identified in the Danish general population. Prevalence of low birth weight (37.9%, risk ratio [RR] = 12.61; 95% confidence interval [CI], 8.5-18.5), premature birth (46.0%, RR = 11.32; 95% CI, 8.1-15.7) and malformations (11.3%, RR = 1.98; 95% CI, 1.2-3.4) was increased in children of kidney-transplanted women compared with controls. Similarly, prevalence of hospitalization due to infection was increased during the first year of life (21.0%, RR = 1.94; 95% CI, 1.3-2.8), from age 1 to 5 (34.2%, RR = 1.89; 95% CI, 1.4-2.5), and overall (41.9%, RR = 1.67; 95% CI, 1.3-2.1). The risk of infection was also higher in children of kidney-transplanted mothers born preterm or with low birth weight compared with similar controls. In conclusion, risk of neonatal complications, malformations, and both early and late infection were increased in children born to kidney-transplanted women.     

Platelet glycoprotein VI-dependent thrombus stabilization is essential for the intraportal engraftment of pancreatic islets

Platelet activation and thrombus formation have been implicated to be detrimental for intraportal pancreatic islet transplants. The platelet-specific collagen receptor glycoprotein VI (GPVI) plays a key role in thrombosis through cellular activation and the subsequent release of secondary mediators. In aggregometry and in a microfluidic dynamic assay system modeling flow in the portal vein, pancreatic islets promoted platelet aggregation and triggered thrombus formation, respectively. While platelet GPVI deficiency did not affect the initiation of these events, it was found to destabilize platelet aggregates and thrombi in this process. Interestingly, while no major difference was detected in early thrombus formation after intraportal islet transplantation, genetic GPVI deficiency or acute anti-GPVI treatment led to an inferior graft survival and function in both syngeneic mouse islet transplantation and xenogeneic human islet transplantation models. These results demonstrate that platelet GPVI signaling is indispensable in stable thrombus formation induced by pancreatic islets. GPVI deficiency resulted in thrombus destabilization and inferior islet engraftment indicating that thrombus formation is necessary for a successful intraportal islet transplantation in which platelets are active modulators.