非侵入物理疗法——红光照射改善脂多糖诱发小鼠抑郁样行为

目的 抑郁的发生机制不清及药物的临床疗效不佳,导致其成为世界难题。已有研究发现甲醛的气态暴露或液态腹腔注射都可直接诱发小鼠抑郁样行为,而内源甲醛是否参与抑郁的发生尚不清楚。本研究探索脂多糖（lipopolysaccharide,LPS）是否通过刺激内源甲醛产生而诱发小鼠抑郁的分子机制;并观察非侵入物理疗法——630 nm红光照射是否能激活甲醛脱氢酶而降解甲醛,从而改善小鼠抑郁样行为。方法 雄性成年C57BL/6J小鼠随机分组：a.对照组,腹腔注射磷酸缓冲液（phosphate buffer solution,PBS）;b.抑郁模型组,按浓度梯度腹腔注射LPS;c.红光干预组,按浓度梯度腹腔注射LPS后并定时进行630 nm全身红光照射。采用旷场实验（open field test,OFT）、糖水偏爱（suorose preference test,SPT）、悬尾实验（tail suspension test,TST）、强迫游泳（forced swimming test,FST）等方法,评估小鼠的抑郁样行为;用甲醛荧光（Na-FA,特异甲醛荧光探针）定量法及整脑甲醛荧光成像法,检测小鼠脑...     

广西北部湾海岸带、海岛的外来入侵植物

为保护广西北部湾海岸带、海岛的植物多样性和生态系统多样性,通过样方、样带法野外实地调查并结合文献资料,对其外来入侵植物的物种组成、原产地、生活型、入侵途径和危害状况等进行了分析。结果表明,广西北部湾海岸带、海岛共有入侵植物64种,隶属28科55属,其中菊科(Asteraceae)最多(15种)。草本植物最多,有48种(75.00%)。原产地来自美洲的植物最多,有49种。入侵风险等级可划分为5个等级,其中Ⅰ级严重危害的有8种(12.50%)。与广西、广东、海南及华南地区的外来入侵植物在物种组成、生活型和原产地等方面呈现出较强的相似性;北部湾与广西中越边境内陆地区来自美洲的入侵植物都超过60%。因此推测广西外来入侵植物有两条可能的入侵线路：一是从海南登录,二是从中越边境跨入。广西北部湾海岸带、海岛的外来入侵植物总数(相对整个广西)虽较少,但其8种Ⅰ级严重危害植物的防治,仍需引起重视。     

固相萃取与气相色谱⁃质谱法联用测定食用植物油和含脂肪食品中氯丙醇酯的方法验证研究

氯丙醇酯是国际上广泛关注的食品加工过程污染物,其水解产物氯丙醇对人体（特别是婴幼儿）危害风险较大。采用固相萃取与气相色谱-质谱（gas chromatography-mass spectrometry,GC-MS）联用技术,对食用植物油和含脂食品中的氯丙醇酯[3-氯-1,2-丙二醇脂肪酸酯（简称3-MCPD酯）和2-氯-1,3-丙二醇脂肪酸酯（简称2-MCPD酯）]进行检测。该方法准确度高（3-MCPD酯和2-MCPD酯的平均回收率分别为98.9%和96.5%)、灵敏度高(3-MCPD酯和2-MCPD酯的检出限分别为0.042 mg·kg^-1和0.058 mg·kg^-1)、重现性好(相对标准偏差均低于5%)。76批次监测样品中,3-MCPD酯和2-MCPD酯的含量分别为0.042~4.865 mg·kg^-1(平均值为0.773 mg·kg^-1)和0.058~2.592 mg·kg^-1(平均值为0.469 mg·kg^-1)。经机构间的协同验证和英国FAPAS样的能力验证,2种氯丙醇酯在0.200~3.000 mg·kg^-1范围内线性良好,为进一步研究奠定了基础,同时也为食品加工企业严格控制生产过程建立了一种可行的检测方法。     

人体β-珠蛋白基因5’旁侧调控元件与不同发育时期调控因子的相互作用

人β-珠蛋白基因主要在成年期的骨髓中表达,在胎儿肝,成年肝和K 562细胞中则处于关闭状态。凝胶电泳阻抑法分析发现,在人胎儿肝,成年肝及K 562细胞的核蛋白抽提物中存在着不同的与β-珠蛋白基因5'旁侧调控元件(-372到-194 bp)相结合的红系组织特异性的调控因子。竟争试验的结果表明,成年肝和K 562细胞中的调控因子与β-珠蛋白基因5'旁侧调控元件相互作用的方式具有一定的相似性,这两种细胞的调控因子既结合于负调控区(NCR 2)也结合于正调控区,说明两种细胞中β-珠蛋白基因的关闭机制可能是相似的。胎儿肝的核蛋白因子只结合于负调控区,推测在胎儿期存在独特的关闭机制。     

多元方差分析中的单一自由度独立比较

本文根据一元方差分析的单一自由度比较原理提出了多元方差分析中的单一自由度比较方法,以用于各种平衡试验设计中具多个变量的处理间多重比较．     

In Situ Microdialysis for Monitoring of Extracellular Glutathione Levels in Normal, Ischemic and Post-Ischemic Skeletal Muscle

Microdialysis probes were inserted into the tibialis anterior muscle and into the femoral vein of anaesthetised Sprague-Dawley rats for monitoring of reduced (GSH) and oxidized (GSSG) extracellular glutathione. The dialysates were analysed using HPLC. The levels of GSH and GSSG were high immediately after implantation in the skeletal muscle and declined to steady state levels after 90 minutes into the same range as that found in the venous dialysate. Total ischemia was induced two hours after implantation of the dialysis probe after steady state levels had been reached. The extracellular levels of GSH increased during total ischemia and had doubled at the end of the ischemic period compared to preischemic values. During the following initial 30 minutes of reperfusion the levels increased further to four-fold the preischemic levels. The levels of GSSG also increased (100%) during the initial 30 minutes of reperfusion. The extracellular GSH levels remained elevated for 1 hour of reperfusion, but the GSSG levels returned to preischemic levels. The results indicate that intermittent hypoxia or anoxia in muscle tissue through hypoperfusion or ischemia decreases intracellular GSH stores by leakage, reducing the intracellular antioxidative capacity and increasing the risk for oxidative reperfusion injury upon final normalization of tissue blood supply.     

龙血树真菌群及其对血竭形成的影响

从柬埔寨龙血树（Ｄｒａｃａｅｎａｃｏｃｈｉｎｃｈｉｎｅｎｓｉｓ）茎杆中分离到３０３株真菌,其中镰刀菌属（Ｆｕｓａｒｉｕｍ）菌株占总分离频率的５２％,其次是短梗霉（Ａｕｒｅｏｂａｓｉｄｉｕｍ）和枝孢霉（Ｃｌａｄｏｓｐｏｒｉｕｍ）。通过活体接种对血竭产生的影响试验表明,对血竭形成起重要作用的真菌主要是禾谷镰刀菌龙血树变种（Ｆ．ｇｒａｍｉｎｕｍｖａｒ．ｄｒａｃａｅｎａ）等４株红色镰刀菌,可使血竭形成量提高６６％－１２０％。     

Trypsin complexed with α1-proteinase inhibitor has an increased structural flexibility

Mutant rat trypsin Asp¹⁸⁹Ser was prepared and complexed with highly purified human α₁-proteinase inhibitor. The complex formed was purified to homogeneity and studied by N-terminal amino acid sequence analysis and limited proteolysis with bovine trypsin. As compared to uncomplexed mutant trypsin, the mutant enzyme complexed with α₁-proteinase inhibitor showed a highly increased susceptibility to enzymatic digestion. The peptide bond selectively attacked by bovine trypsin was identified as the Arg¹¹⁷-Val¹¹⁸ one of trypsin. The structural and mechanistic relevance of this observation to serine proteinase-substrate and serine proteinase-serpin reactions are discussed.     

Trypsin and forskolin decrease the sensitivity of L-type calcium current to inhibition by cytoplasmic free calcium in guinea pig heart muscle cells.

A key feature of trypsin action on ionic membrane currents including L-type Ca2+ current (ICa) is the removal of inactivation upon intracellular application. Here we report that trypsin also occludes the resting cytoplasmic free Ca2+ ([Ca2+]i)-induced inhibition of peak ICa in isolated guinea pig ventricular cardiomyocytes, using the whole-cell patch clamp in combination with the Fura-2 ratio-fluorescence technique. The effectiveness of trypsin to guard ICa against [Ca2+]i-induced inhibition was compared with that of forskolin, as cAMP-dependent phosphorylation had been suggested to confer protection against [Ca2+]i-induced inactivation. Intracellular dialysis of trypsin (1 mg/ml) augmented ICa by 7.2-fold, significantly larger than the threefold increase induced by forskolin (3 microM). Forskolin application after trypsin dialysis did not further enhance ICa. An increase in [Ca2+]i from resting levels (varied by 0.2, 10, and 40 mM EGTA dialysis) to submicromolar concentrations after replacement of external Na+ (Na(o)+) with tetraethylammonium (TEA+) resulted in monotonic inhibition of control ICa, elicited from a holding potential of -40 mV at 22 degrees C. AFter trypsin dialysis, however, ICa became less sensitive to submicromolar [Ca2+]i; the [Ca2+]i of half-maximal inhibition (K0.5, normally around 60 nM) increased by approximately 20-fold. Forskolin also increased the K0.5 by approximately threefold. These and accompanying kinetic data on ICa decay are compatible with a model in which it is assumed that Ca2+ channels can exist in two modes (a high open probability "willing" and a low open probability "reluctant" mode) that are in equilibrium with one another. An increase in [Ca2+]i places a larger fraction of channels in the reluctant mode. This interconversion is hindered by cAMP-dependent phosphorylation and becomes nearly impossible after tryptic digestion.