L-酪氨酸苄酯的合成及其影响因素研究

以L-酪氨酸和苯甲醇为原料合成一种新型的L-酪氨酸衍生物——L-酪氨酸苄酯。首先用苯甲醇与氯化亚砜反应生成氯化亚硫酸酯,合成物再与L-酪氨酸发生酯化反应得到L-酪氨酸苄酯,其结构经质谱(MS)分析法确证。在此基础上研究了影响该合成工艺的主要因素,即原料配比、反应温度、反应时间、pH值。结果显示合成L-酪氨酸苄酯的较佳工艺条件为:物料摩尔比mol(SOCl2)∶mol(L-酪氨酸)=1.3∶1.0,室温下反应3h,120℃下反应2h,后处理溶液pH为7.5。本工艺适宜于工业化大规模生产。     

Increased susceptibility to Toxoplasma gondii infection in SAG-1 transgenic mice

SAG-1, one of the major surface proteins of Toxoplasma gondii, has been reported to play an important role in immune and pathogenic mechanisms of the parasites but its exact function is still unclear. We investigated the time courses of T. gondii infection in B6C3F1 transgenic mice carrying the SAG-1 gene. SAG-1 transgenic mice were infected intraperitoneally with a high virulent RH strain or a low virulent Beverley strain of T. gondii. When infected with RH strain tachyzoites, no significant differences in time courses of survivals between SAG-1 transgenic and wild-type mice were observed. Both groups succumbed to an acute infection within 8 days after infection. However, a lower survival rate (20%) was observed in SAG-1 transgenic mice than in wild-type (80%), when infected with Beverley strain cysts. This result indicates that SAG-1 transgenic mice are more susceptible to T. gondii infection as compared with their wild-type counterpart. ELISA using recombinant SAG-1 protein indicates that SAG-1 transgenic mice do not produce antibodies to the SAG-1 molecule. These findings may provide a critical tool for analysing the molecular mechanisms of pathogenesis and host immune responses during toxoplasmosis.     

POMP与SuFu相互作用调控Hedgehog信号通路的活性

Hedgehog信号通路在胚胎发育、组织再生中发挥重要的作用,且与癌症发生发展密切相关. 其胞内调控组分Suppressor of Fused（SuFu）蛋白通过结合转录因子Gli(s),负调控该信号通路,但其作用的分子机制仍不甚清楚. 在本项研究中,以人SuFu作为诱饵蛋白,利用酵母双杂交技术成功地筛选到1个新的相互作用因子-蛋白酶体成熟蛋白（POMP）. 通过免疫共沉淀、体外GST pull-down和免疫细胞化学实验验证其相互作用. 为了探究POMP与SuFu的相互作用对Hedgehog信号通路的影响,构建了POMP的过表达质粒和干扰质粒（miR-RNAi）以及转录因子Gli活性检测系统,即荧光素酶报告基因法,结果显示,过表达SuFu蛋白时POMP正调控Hedgehog信号通路,而下调POMP的表达则抑制Gli的活性. 该研究结果揭示了POMP新的生物学功能,为阐明Hedgehog信号通路的具体分子机制提供了新的线索.     

基于社会-生态系统的沙漠化逆转过程脆弱性评价指标体系

土地沙漠化是当今世界最为严峻的生态环境问题之一。沙漠化逆转作为其反向转化过程,存在一定的脆弱性和不稳定性,即沙漠化逆转趋势减弱或反向发展的倾向。社会-生态系统理念是当今世界生态系统分析的新思路,从该视角界定沙漠化逆转过程的脆弱性概念,选取Driving-Pressure-Status-Impact-Response(DPSIR)分析框架,以农牧交错带典型沙漠化逆转区宁夏盐池县为案例,针对沙漠化逆转的因果联系和过程特点,构建一套涵盖气候湿润指数、生态治理指数、沙地所占比例在内的4层、5要素、41指标的评价体系,进而探讨驱动力、压力、状态、影响、响应5项要素间的逻辑因果关系及其脆弱性定量化计算方法,以期科学评估沙漠化逆转过程的脆弱性,为该类型区沙漠化问题的进一步治理和调控提供科学依据。     

化感水稻根际微生物类群及酶活性变化

以化感水稻PI312777（PI）和非化感水稻Lemont（LE）为材料,分别测定不同水稻叶龄期（3～7叶期）根际微生物区系变化及根际土壤酶活性.结果表明,化感水稻明显影响土壤根际微生物类群及相关酶活性.化感水稻PI根际细菌、放线菌、固氮菌的数量高于非化感水稻LE,增幅分别在11.2%～28.3%、40%～78.6%和111.5%～173.9%之间,而真菌数量低于非化感水稻LE,最高仅为其值的25.5％,说明化感水稻PI对绝大多数细菌、放线菌、固氮菌生长有促进作用,对一些真菌生长有抑制作用.进一步分析表明,化感水稻PI对氨化细菌、亚硝酸细菌、硝酸细菌、好气性固氮菌、好气性纤维素分解菌、硫化细菌的生长具有促进作用,其中以氨化细菌、好气性固氮菌的更为明显,最低增幅分别为53.7％和57.6％;而对反硫化细菌、反硝化细菌生长有抑制作用,其值最高分别为非化感水稻的54.2％和50.6％.此外,化感水稻PI根系分泌物对脲酶、磷酸酶、蔗糖酶的活性具有促进作用,而对过氧化氢酶则呈抑制作用.     

Alpha-lipoic acid regulates the autophagy of vascular smooth muscle cells in diabetes by elevating hydrogen sulfide level

Dysfunctional vascular smooth muscle (VSM) plays a vital role in the process of atherosclerosis in patients with type 2 diabetes mellitus (T2DM). Alpha-lipoic acid (ALA) can prevent the altered VSM induced by diabetes. However, the precise mechanism underlying the beneficial effect of ALA is not well understood. This study aimed to determine whether ALA ameliorates VSM function by elevating hydrogen sulfide (H₂S) level in diabetes and whether this effect is associated with regulation of autophagy of VSM cells (VSMCs). We found decreased serum H₂S levels in Chinese patients and rats with type 2 diabetes mellitus (T2DM). ALA treatment could increase H₂S level, which reduced the autophagy-related index and activation of the 5′-monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway, thereby protecting vascular function in rats with T2DM. Propargylglycine (PPG), a cystathionine-γ-lyase inhibitor, could weaken the ALA effect. In cultured VSMCs, high glucose level also reduced H₂S level, upregulated the autophagy-related index and activated the AMPK/mTOR pathway, which were reversed by concomitant application of sodium hydrosulfide (NaHS, an H₂S donor) or ALA. The protective effect of NaHS or ALA was attenuated by rapamycin (an autophagy activator), 5-amino-1-β-d-ribofuranosyl-imidazole-4-carboxamide (an AMPK activator) or PPG. In contrast, Compound C (an AMPK inhibitor) enhanced the effect of ALA or NaHS. ALA may have a protective effect on VSMCs in T2DM by elevating H₂S level and downregulating autophagy via the AMPK/mTOR pathway. This study provides a new target for addressing diabetic macroangiopathy.