大鼠缺氧预处理心肌酶活性及其ATP酶的电镜细胞化学观察

本实验通过对大鼠反复４次缺氧５ｍｉｎ（常压,氧浓度１０±０．５％）的缺氧预处理与经典的缺血预处理（Ｍｕｒｙ法）的对比观察表明,两者均能明显降低心肌丙二醛含量和肌酸激酶的漏出,提高心肌超氧化物岐化酶,Ｃａ２＋Ｍｇ２＋－ＡＴＰａｓｅ、细胞色素氧化酶、琥珀酸脱氢酶活性及维持细胞超微结构的完整性,提示这种非创伤性缺氧预处理具有与缺血预处理相类似的抗心肌缺血的作用     

新疆麦田主要蚜虫的生态位

利用生态位理论,对新疆塔城、伊犁两地区麦田的麦双尾蚜Diuraphis noxia (Mordvilko)、麦二叉蚜Shizaphis graminum (Rondani)、麦长管蚜Sitobion avenae (F.)和禾谷缢管蚜Rhopalosiphum padi (L.)等4种麦蚜生态位宽度和重叠度进行了估测和分析。在塔城麦田麦双尾蚜时间生态位宽度最大,麦双尾蚜和麦二叉蚜时间生态位重叠最大,竞争激烈。伊犁麦田禾谷缢管蚜时间生态位宽度最大,麦二叉蚜在空间生态位和时 空二维生态位上均占有明显的优势,麦长管蚜和麦双尾蚜的时间生态位重叠最大,麦长管蚜和麦二叉蚜在空间生态位和时 空生态位重叠最大。     

乙酰胆碱酯酶在蚕豆保卫细胞中集中分布

动物细胞中,乙酰胆碱酯酶负责把乙酰胆碱水解为胆碱和乙酸以起到终止信号的作用。蚕豆（ＶｉｃｉａｆａｂａＬ．）保卫细胞原生质体表面具有特异的水解乙酰胆碱的酯酶,光可以激活该酶的活性。组织学定位的结果显示,酶反应产物主要分布于气孔保卫细胞内壁和腹壁的外侧及内壁和腹壁中,表明一种类似于动物突触传递的机制可能存在于气孔保卫细胞和周围细胞之间,即乙酰胆碱发挥作用后由乙酰胆碱酯酶分解以终止其作用;此外开放的气孔周围具有更高的酶活性,说明乙酰胆碱酯酶可通过水解气孔周围的乙酰胆碱而调控气孔运动     

Evaluation of Novel Human Immunodeficiency Virus Type 1 Gag DNA Vaccines for Protein Expression in Mammalian Cells and Induction of Immune Responses

Human immunodeficiency virus (HIV)-specific cytotoxic T lymphocytes (CTL) are an important parameter of host defenses that limit viral replication after infection. Induction of effective CTL against conserved viral proteins such as Gag may be essential to the development of a safe and effective HIV type 1 (HIV-1) vaccine. DNA vaccination represents a novel strategy for inducing potent CD8(+) CTL responses in vivo. However, expression of HIV-1 structural proteins by DNA vectors has been hampered by a stringent requirement for coexpression with other viral components, such as Rev and RRE. Furthermore, even with Rev and RRE present, the level of expression of HIV-1 Gag, Pol, or Env is very low in murine cells. These problems have limited our ability to address the key issue of how to generate effective CTL responses to Gag in a mouse model. To overcome this problem, we compared several novel DNA expression vectors for HIV-1 Gag protein expression in primate and mouse cells and for generating immune responses in mice after DNA vaccination. A DNA vector containing wild type HIV-1 gag coding sequences did not induce detectable Gag expression in any of the cells tested. Attempts to increase nuclear export of Gag expression RNA by adding the constitutive transport element yielded only a moderate increase in Gag expression in monkey-derived COS cells and an even lower increase in Gag expression in HeLa cells or several mouse cell lines. In contrast, silent-site mutations in the HIV-1 gag coding sequences significantly increased Gag expression levels in all cells tested. Furthermore, this construct induced both Gag-specific antibody and CTL responses in mice after DNA vaccination. Using this construct, we achieved stable expression of HIV-1 Gag in the mouse cell line p815, which can now be used as a target cell for measuring HIV-1 Gag-specific CTL responses in immunized mice. The DNA vectors described in this study should make it possible to systematically evaluate the approaches for maximizing the induction of CTL responses against HIV-1 Gag in mouse and other animal systems.     

角倍蚜冬寄主侧枝匐灯藓的生长特性研究

角倍蚜［Ｓｃｈｌｅｃｈｔｅｎｄａｌｉａｃｈｉｎｅｎｓｉｓ（Ｂｅｌ）］是致瘿形成五倍子的主要蚜虫之一,由它寄生在盐肤木（ＲｈｕｓｃｈｉｎｅｎｓｉｓＭｉｌ．）复叶的叶翅上形成的虫瘿角倍,其产量占我国五倍子总产量的７５％以上。角倍蚜完成一个生活周期,必须经...     

IL-17A injury to retinal ganglion cells is mediated by retinal Müller cells in diabetic retinopathy

Diabetic retinopathy (DR), the most common and serious ocular complication, recently has been perceived as a neurovascular inflammatory disease. However, role of adaptive immune inflammation driven by T lymphocytes in DR is not yet well elucidated. Therefore, this study aimed to clarify the role of interleukin (IL)-17A, a proinflammatory cytokine mainly produced by T lymphocytes, in retinal pathophysiology particularly in retinal neuronal death during DR process. Ins2^Akita (Akita) diabetic mice 12 weeks after the onset of diabetes were used as a DR model. IL-17A-deficient diabetic mice were obtained by hybridization of IL-17A-knockout (IL-17A-KO) mouse with Akita mouse. Primarily cultured retinal Müller cells (RMCs) and retinal ganglion cells (RGCs) were treated with IL-17A in high-glucose (HG) condition. A transwell coculture of RGCs and RMCs whose IL-17 receptor A (IL-17RA) gene had been silenced with IL-17RA-shRNA was exposed to IL-17A in HG condition and the cocultured RGCs were assessed on their survival. Diabetic mice manifested increased retinal microvascular lesions, RMC activation and dysfunction, as well as RGC apoptosis. IL-17A-KO diabetic mice showed reduced retinal microvascular impairments, RMC abnormalities, and RGC apoptosis compared with diabetic mice. RMCs expressed IL-17RA. IL-17A exacerbated HG-induced RMC activation and dysfunction in vitro and silencing IL-17RA gene in RMCs abolished the IL-17A deleterious effects. In contrast, RGCs did not express IL-17RA and IL-17A did not further alter HG-induced RGC death. Notably, IL-17A aggravated HG-induced RGC death in the presence of intact RMCs but not in the presence of RMCs in which IL-17RA gene had been knocked down. These findings establish that IL-17A is actively involved in DR pathophysiology and particularly by RMC mediation it promotes RGC death. Collectively, we propose that antagonizing IL-17RA on RMCs may prevent retinal neuronal death and thereby slow down DR progression.Subject terms: Cell death, Medical research     

Associations of the PTEN − 9C>G polymorphism with insulin sensitivity and central obesity in Chinese

Background

Phosphatase and tensin homolog on chromosome 10 gene (PTEN) is known as a tumor-suppressor gene. Previous studies demonstrated that PTEN dysfunction affects the function of insulin. However, investigations of PTEN single nucleotide polymorphisms (SNPs) and IR-related disease associations are limited. The aim of the present study was to investigate whether its polymorphism could be involved in the risk of metabolic syndrome (MetS).

Methods

The genotype frequency of PTEN − 9C>G polymorphism was determined by using a Matrix-Assisted Laser Desorption/Ionization Time of Flight Mass Spectrometry (MALDI-TOF MS) method in 530 subjects with MetS and 202 healthy control subjects of the Han Ethnic Chinese population in a case–control analysis.

Results

The PTEN − 9C>G polymorphism was not associated with MetS or its hyperglycemia, hypertension and hypertriglyceridemia components. In the control individuals aged < 60 years or ≥ 60 years, the CG genotype individuals had lower insulin sensitivity than CC individuals (P < 0.05). In the < 60-year-old MetS group and normal glucose tolerance (NGT) subgroup, the CG individuals had lower insulin sensitivity and higher waist circumference (WC) and waist-height-ratio (WHtR) than CC individuals (P < 0.05). Multiple linear regression analysis showed that the PTEN polymorphism (P = 0.001) contributed independently to 4.2% (adjusted R²) of insulin sensitivity variance (estimated by Matsuda ISI), while age (P = 0.004), gender (P = 0.000) and the PTEN polymorphism (P = 0.032) contributed independently to 5.6% (adjusted R²) of WHtR variance.

Conclusions

The CG genotype of PTEN − 9C>G polymorphism was not associated with MetS and some of its components as well. However, it may not only decrease insulin sensitivity in the healthy control and MetS in pre-elderly or NGT subjects, but may also increase the risk of central obesity among these MetS individuals.