炎性细胞因子与脑梗死的研究进展

脑梗死的病理生理过程中存在着炎症反应和免疫调节，而多种炎性细胞因子参与了再灌注损伤和炎症反应，其中白细胞介素（IL-1β、IL-6、IL-18等）、肿瘤坏死因子（TNF-α）、超敏C反应蛋白（hs-CRP）、基质金属蛋白酶-9（MMP-9）、细胞间黏附分子（ICAM-1）等与炎症反应密切相关。随着分子生物学技术的进展，炎性细胞因子在脑梗死发病机制中的作用更加受到重视。研究炎性细胞因子及炎症反应对缺血性脑损伤的机制可能为脑梗死的防治带来收益。本文就部分炎性细胞因子的生物学活性、理化性质及其在脑缺血损伤中的作用进行了综述。     

Th17/Treg细胞及其相关细胞因子在溃疡性结肠炎发病中的作用及其研究进展

溃疡性结肠炎(UC)是一种慢性非特异性肠道炎性疾病,发病机制尚不明确。目前研究认为,Th17/Treg细胞失衡与UC的发生发展密切相关。本文就Th17/Treg细胞及其相关细胞因子在UC发病中的作用及其研究进展进行综述,发现:无论是Th17细胞的增加还是Treg细胞的减少均可导致UC的发生。Th17细胞在UC的发病中发挥着双重作用,既可以通过维持免疫微环境的平衡对肠道黏膜起保护作用,又可以加重肠道炎症反应,但以促炎作用为主。而Treg细胞主要通过调节IL-10、TGF-β的分泌来抑制肠道炎症级联和放大反应。     

骨桥蛋白与支气管哮喘的关系研究进展

骨桥蛋白(Osteopontin,OPN)是一种多功能的磷酸化糖蛋白,最初作为一种细胞外基质蛋白发现于骨组织中,后来研究发现它还作为一种细胞因子存在于免疫系统的多种细胞中。OPN参与了组织重塑、纤维化、炎症反应、免疫调节及肿瘤转移等多种过程,近年来,越来越多的证据表明OPN可能通过促进炎性细胞向气道的迁移,参与气道炎症以及气道重塑等过程,进而影响支气管哮喘的发生、发展。本文就骨桥蛋白的结构、生物学功能及其在支气管哮喘中的作用研究进展作一综述,以期指导今后进一步研究。     

国产无机三氧化物聚合物的免疫相容性研究

目的 以细胞因子（肿瘤坏死因子α和白细胞介素1β）为研究对象,对国产无机三氧化物聚合物（MTA）介导的炎症反应进行相关的免疫学评价.方法 运用双抗夹心ELISA检测新材料国产MTA引起体外小鼠的单核巨噬细胞系RAW264.7细胞TNF-a和IL-1β的变化.结果 未经脂多糖诱导的RAW264.7细胞与阳性材料接触后,TNF-α和IL-1β的表达均高于阴性材料,差异均有显著性意义（P〈0.05）;国产MTA组和进口MTA组TNF-α和lL-1β的表达与阴性材料比较差异无显著性意义（P〉0.05）;经脂多糖诱导的RAW264.7细胞与阳性材料、国产MTA、进口MTA接触后,TNF-a和IL-1β的表达均高于阴性材料,差异均有显著性差异（P〈0.01）.结论 国产MTA具有良好的生物相容性.     

HMGB1在急性胰腺炎中作用的研究进展

早期合并的器官功能障碍是导致急性胰腺炎患者死亡的主要原因,全身炎症反应综合征是诱发其发生的关键环节,但其具体发病机制仍不清楚。本文对近年来国内外有关急性胰腺炎后全身炎症反应综合征导致器官功能障碍的研究进行了梳理,综述了非经典晚期炎症介质-高迁移族率蛋白B1(HMGB1)的功能,及病理情况下胞外的HMGB1在急性胰腺炎后全身炎症反应综合征乃至器官功能障碍发生中的作用,总结了三者之间的关系,并提出抑制细胞外的HMGB1有望成为急性胰腺炎的一种新的治疗策略。     

热性惊厥儿童血液IL-6、IL-10和MMP-9表达的研究

目的 热性惊厥是儿童痫性发作最常见的形式.炎性细胞因子可能导致热性惊厥的发展.本研究探讨白介素-6(IL-6)、白介素-10(IL-100和金属蛋白酶-9(MMP-9)等炎性细胞因子在小儿热性惊厥中是否被激活以及其表达与原发性癫痫中的不同.方法 回顾性研究自2010年12月到2012年11月入院的相关病人资料.分热性惊厥组(N=43)、高热对照组(N=40)、原发性癫痫组(N=32)及正常儿童组(N=15).在惊厥发生的24h内收集病人血液.酶联免疫吸附试验(ELISA)进行IL-6、IL-10和MMP-9等细胞因子水平测定.结果 IL-6、IL-10和MMP-9在热性惊厥组的表达均高于原发性癫痫组(p＜0.05)和正常组(p＜0.05).IL-6与MMP-9在热性惊厥组的表达高于高热对照组,IL-10的表达在热性惊厥组与高热对照组之间无明显差异(P＞0.05).结论 IL-6、IL-10和MMP-9在热性惊厥儿童表达明显升高;炎性因子可能参与热性惊厥的病理过程,且其参与机制可能不同于其在原发性癫痫病理过程中的作用.     

反应动力学参数变化对MOVPE生长GaN的反应路径模拟的影响

在金属有机化学气相外延(MOVPE)生长GaN薄膜的反应-输运过程数值模拟中,反应动力学参数(活化能和指前因子)的选取存在很大的不确定性,从而导致不同的气相反应路径和生长速率.本文对前人采用的反应动力学参数的偏差做了归纳总结,讨论了偏差的来源.在此基础上,本文对垂直转盘式MOVPE反应器生长GaN的反应-输运过程进行数值模拟研究.模拟改变不同的反应动力学参数组合,包括加合物的生成和可逆分解的指前因子、加合物不可逆分解生成氨基物的活化能和指前因子以及三聚物生成的指前因子.通过分析主要含Ga物质的摩尔浓度和对应的生长速率的变化,研究上述反应动力学参数变化对GaN生长反应路径的模拟结果的影响.研究的主要结论如下:(1)不同的指前因子和活化能导致不同的反应路径和生长速率的差异,而热解路径比起加合路径能够更有效地提高生长速率.(2)在不考虑三聚物反应时,预测的生长速率值都与实验值接近.原因在于,输运限制的生长速率取决于含Ga粒子的输运速率,不同的反应路径对含Ga粒子的影响此消彼长,但到达衬底的含Ga粒子的总量变化不大,这也很好地解释了不同文献采用不同的动力学参数模拟都与实验基本吻合的原因.(3)改变三聚物反应的指前因子发现,由于热泳力对大分子的排斥作用,三聚物对生长的贡献很小,生成的三聚物越多,与实验的误差越大.模拟结果澄清了前人在模拟MOVPE生长GaN的反应-输运过程中存在的一些问题,并加深了对GaN生长机理的了解.     

低地球轨道环境中原子氧在航天器表面防护材料上的反应-扩散模型

基于过热原子氧撞击硅表面,在超薄氧化区产生低扩散垒与反应垒的部分阴性原子氧离子及其相应的电场和映像势致扩散增加等特点,通过变扩散系数及变反应率常数途径,完善Almeida-Goncalves-Baumvol（AGB）模型.据此,模拟了硅氧化膜的演化,与Tagawa等人的结果拟合显示,理论曲线与实验数据吻合;并浅析了扩散系数、反应率常数、衰减长度及调节参数等与原子氧的平动能、通量、温度以及切向通量等的相关性.模拟结果初步证实,本文构架的反应-扩散理论模型合理,可为LEO环境中抗原子氧防护膜厚度提供评估手段.     

黄芪多糖对帕金森大鼠模型的治疗作用及机制探讨

目的观察黄芪提取物黄芪多糖(APS)治疗帕金森病(PD)的效果,探索APS治疗PD的作用机制。方法建立PD大鼠模型,采用行为学、ELISA等检查方法,观察模型成功后黄芪多糖组(APS组)治疗1天、7天、14天的大鼠旋转行为及第14天的黑质病理变化、脑组织中炎性细胞因子含量变化,并与对照组(PD组)比较。结果 APS组旋转圈数较PD组减少,与阳性对照组相当,酪氨酸羟化酶含量显著高于PD组,黑质b FGF蛋白表达均较PD组减少,脑组织中炎性细胞因子含量亦明显减少。结论黄芪多糖可能通过免疫调节作用治疗帕金森大鼠模型。     

有序化与调幅分解共存现象的理论研究

从经典固溶体理论得出的最基本结论是：有序化与调幅分解／丛聚是相反的两种溶体失稳方式。但是，从大量合金中发现的有序化和调幅分解的共存现象对上述理论提出了重大挑战。对发生共存反应合金进行统计，发现了一个重要的规律：共存反应与合金大的原子尺寸因子密切联系。     

Knowledge translation: airway epithelial cell migration and respiratory diseases

Airway epithelial cell migration is essential for lung development and growth, as well as the maintenance of respiratory tissue integrity. This vital cellular process is also important for the repair and regeneration of damaged airway epithelium. More importantly, several lung diseases characterized by aberrant tissue remodeling result from the improper repair of damaged respiratory tissue. Epithelial cell migration relies upon extracellular matrix molecules and is further regulated by numerous local, neuronal, and hormonal factors. Under inflammatory conditions, cell migration can also be stimulated by certain cytokines and chemokines. Many well-known environmental factors involved in the pathogenesis of chronic lung diseases (e.g., cigarette smoking, air pollution, alcohol intake, inflammation, viral and bacterial infections) can inhibit airway epithelial cell migration. Further investigation of cellular and molecular mechanisms of cell migration with advanced techniques may provide knowledge that is relevant to physiological and pathological conditions. These studies may eventually lead to the development of therapeutic interventions to improve lung repair and regeneration and to prevent aberrant remodeling in the lung.     

Quality control of homologous recombination

Exogenous and endogenous genotoxic agents, such as ionizing radiation and numerous chemical agents, cause DNA double-strand breaks (DSBs), which are highly toxic and lead to genomic instability or tumorigenesis if not repaired accurately and efficiently. Cells have over evolutionary time developed certain repair mechanisms in response to DSBs to maintain genomic integrity. Major DSB repair mechanisms include non-homologous end joining and homologous recombination (HR). Using sister homologues as templates, HR is a high-fidelity repair pathway that can rejoin DSBs without introducing mutations. However, HR execution without appropriate guarding may lead to more severe gross genome rearrangements. Here we review current knowledge regarding the factors and mechanisms required for accomplishment of accurate HR.     

Astrocytes in multiple sclerosis: A product of their environment

It has long been thought that astrocytes, like other glial cells, simply provide a support mechanism for neuronal function in the healthy and inflamed central nervous system (CNS). However, recent evidence suggests that astrocytes play an active and dual role in CNS inflammatory diseases such as multiple sclerosis (MS). Astrocytes not only have the ability to enhance immune responses and inhibit myelin repair, but they can also be protective and limit CNS inflammation while supporting oligodendrocyte and axonal regeneration. The particular impact of these cells on the pathogenesis and repair of an inflammatory demyelinating process is dependent upon a number of factors, including the stage of the disease, the type and microenvironment of the lesion, and the interactions with other cell types and factors that influence their activation. In this review, we summarize recent data supporting the idea that astrocytes play a complex role in the regulation of CNS autoimmunity.     

Regulation of intestinal epithelial permeability by tight junctions

The gastrointestinal epithelium forms the boundary between the body and external environment. It effectively provides a selective permeable barrier that limits the permeation of luminal noxious molecules, such as pathogens, toxins, and antigens, while allowing the appropriate absorption of nutrients and water. This selective permeable barrier is achieved by intercellular tight junction (TJ) structures, which regulate paracellular permeability. Disruption of the intestinal TJ barrier, followed by permeation of luminal noxious molecules, induces a perturbation of the mucosal immune system and inflammation, and can act as a trigger for the development of intestinal and systemic diseases. In this context, much effort has been taken to understand the roles of extracellular factors, including cytokines, pathogens, and food factors, for the regulation of the intestinal TJ barrier. Here, I discuss the regulation of the intestinal TJ barrier together with its implications for the pathogenesis of diseases.     

B Lymphocytes in obesity-related adipose tissue inflammation and insulin resistance

Obesity-related insulin resistance is a chronic inflammatory condition that often gives rise to type 2 diabetes (T2D). Much evidence supports a role for pro-inflammatory T cells and macrophages in promoting local inflammation in tissues such as visceral adipose tissue (VAT) leading to insulin resistance. More recently, B cells have emerged as an additional critical player in orchestrating these processes. B cells infiltrate VAT and display functional and phenotypic changes in response to diet-induced obesity. B cells contribute to insulin resistance by presenting antigens to T cells, secreting inflammatory cytokines, and producing pathogenic antibodies. B cell manipulation represents a novel approach to the treatment of obesity-related insulin resistance and potentially to the prevention of T2D. This review summarizes the roles of B cells in governing VAT inflammation and the mechanisms by which these cells contribute to altered glucose homeostasis in insulin resistance.     

Cytokine-mediated proteolysis in tissue remodelling

Summary Proteolytic enzymes play a key role in a variety of physiological processes in which the degradation of macromolecules is essential: angiogenesis, embryogenesis, bone and tissue remodelling, blood hemostasis and cell migration. The action of these enzymes is also crucial in the development of many pathological conditions such as wound healing, neoplasia, inflammation and arthritic disorders.the activity of proteases is negatively affected by specific protease-inhibitors. Various growth factors and other cytokines modulate the synthesis and secretion of both proteases and protease-inhibitors. The study of this regulation results in a better insight into (patho)physiology at the molecular level and promises to result in alternative treatment strategies.