野大豆(Glycine soja)叶绿体的光谱及其激子能量转移

野大豆叶绿体在低温(77K)时出现三条荧光发射谱带,它们来源于不同的色素蛋白复合体。 在纳秒脉冲激光激发下,捕光天线色素的相对荧光量子产额,随激光强度的增加有明显下降现象。用激子理论和动力学方程讨论和计算了激子扩散参量。指出激子转移是随机的,非相干的。     

Interleukin-33/ST2 signaling promotes production of interleukin-6 and interleukin-8 in systemic inflammation in cigarette smoke-induced chronic obstructive pulmonary disease mice

Interleukin-33 is a newly described member of the interleukin-1 family. Recent research suggests that IL-33 is increased in lungs and plays a critical role in chronic airway inflammation in cigarette smoke-induced chronic obstructive pulmonary disease (COPD) mice. To determine the role of IL-33 in systemic inflammation, we induced COPD mice models by passive cigarette smoking and identified the IL-33 expression in bronchial endothelial cells and peripheral blood mononuclear cells (PBMCs) of them. After isolation, PBMCs were cultured and stimulated in vitro. We measured expressions of interleukin-6 and interleukin-8 in PBMCs in different groups. The expression of IL-33 in bronchial endothelial cells and PBMCs of COPD mice were highly expressed. Stimulated by cigarette smoke extract (CSE), the expression of IL-6 and IL-8 were induced and enhanced by IL-33. PBMCs of COPD mice produced more IL-6 and IL-8 stimulated by CSE and IL-33. Expression of IL-6 and IL-8 were decreased when stimulated by IL-33 together with soluble ST2. The mRNA production of ST2 in IL-33 stimulated PBMCs was increased. Being pretreated with several kinds of MAPK inhibitors, the secretions of IL-6 and IL-8 in PBMCs did not decrease except for the p38 MAPK inhibitor. We found that IL-33 could induce and enhance the expression of IL-6 and IL-8 in PBMCs of COPD mice via p38 MAPK pathway, and it is a promoter of the IL-6 and IL-8 production in systemic inflammation in COPD mice.     

O‐GlcNAcylation of protein kinase A catalytic subunits enhances its activity: a mechanism linked to learning and memory deficits in Alzheimer's disease

Alzheimer's disease (AD) is characterized clinically by memory loss and cognitive decline. Protein kinase A (PKA)‐CREB signaling plays a critical role in learning and memory. It is known that glucose uptake and O‐GlcNAcylation are reduced in AD brain. In this study, we found that PKA catalytic subunits (PKAcs) were posttranslationally modified by O‐linked N‐acetylglucosamine (O‐GlcNAc). O‐GlcNAcylation regulated the subcellular location of PKAcα and PKAcβ and enhanced their kinase activity. Upregulation of O‐GlcNAcylation in metabolically active rat brain slices by O‐(2‐acetamido‐2‐deoxy‐d ‐glucopyranosylidenamino) N‐phenylcarbamate (PUGNAc), an inhibitor of N‐acetylglucosaminidase, increased the phosphorylation of tau at the PKA site, Ser214, but not at the non‐PKA site, Thr205. In contrast, in rat and mouse brains, downregulation of O‐GlcNAcylation caused decreases in the phosphorylation of CREB at Ser133 and of tau at Ser214, but not at Thr205. Reduction in O‐GlcNAcylation through intracerebroventricular injection of 6‐diazo‐5‐oxo‐l ‐norleucine (DON), the inhibitor of glutamine fructose‐6‐phosphate amidotransferase, suppressed PKA‐CREB signaling and impaired learning and memory in mice. These results indicate that in addition to cAMP and phosphorylation, O‐GlcNAcylation is a novel mechanism that regulates PKA‐CREB signaling. Downregulation of O‐GlcNAcylation suppresses PKA‐CREB signaling and consequently causes learning and memory deficits in AD.     

Expression of the large isoform of ribulose-1,5-bisphosphate carboxylase/oxygenase activase gene driven by rbcS promoter in Oryza sativa enhances the photosynthetic capacity

In order to investigate the effect of large isoform of ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBPCO) activase (RuBPCO-A) on photosynthesis, cDNA of the enzyme (rca) was transferred to rice cultivars (Oryza sativa f. japonica cv. Nipponbare) under the control of RuBPCO small subunit gene promoter (rbcS) via Agrobacterium tumefaciens-mediated transformation. Transgenic rice plants were identified by polymerase chain reaction (PCR) and Southern and Western blot analyses. Net photosynthetic rate (P _N) values of the T₁ transgenic lines 34 (T34) and 40 (T40) were 45.26 and 46.32 % higher than that of the control plants, respectively. At the same time, their carboxylation efficiency and RuBPCO initial activity, quantum yield of electron transport in photosystem 2 (Φ_PS2), and steady state photochemical fluorescence quenching (q_P) increased. In addition, heading time of the transgenic rice was advanced. Thus increasing the amount of large isoform of RuBPCO-A in the transgenic rice might have a stimulatory effect on both photosynthesis and plant growth.     

GABA神经元在金黄地鼠视觉中枢的分布

本文用免疫细胞化学技术研究了GABA在金黄地鼠视觉中枢的分布特征,同时用统计学方法作了定量分析,结果表明:GABA阳性神经元分布在整个视皮层和上丘中,呈不均匀分布,外膝体中GABA阳性神经元密度较低.视皮层中GABA阳性神经元密度为781mm~2,占视皮层细胞总数的19.7%,上丘中其密度为812/mm~2,占22.3%,视皮层Ⅰ层中GABA阳性神经元为52%,上丘表层(浅灰层及视觉层GABA阳性神经元为56%,GABA阳性神经元包括不同类型的细胞.在视皮层中可观察到GABA免疫疫应阳性的锥体细胞.     

猫扣带回前部内脏伤害感受神经元的膜电学特性

目的：研究猫扣带回前部内脏大神经刺激相关神经元的膜电生理特性,以便从神经元水平进一步了解大脑皮质内脏伤害感受的特性及机制,为痛觉理论“特异性学说”提供新的实验依据。方法：应用在体玻璃微电极细胞内电位记录技术及细胞内注入极化电流的方法,测量和计算神经元的膜电学参数。结果：将20只猫扣带回前部176个内脏大神经刺激相关神经元,分为内脏伤害(148个)和非伤害(28个)感受神经元。发现它们在膜电阻、时间常数、膜电容及I—V曲线等方面存在差异。注入去极化电流引发的放电幅值及频率也存在差异。结论：扣带回前部内脏伤害与非伤害感受神经元可能在细胞膜结构、细胞大小等形态学方面存有差别。     

生石膏对致热原作用下猫PO／AH温敏神经元放电的影响

目的:研究中药生石膏解热作用的中枢机制.方法:复制发热模型后,静脉注射生石膏,应用微电极细胞外记录技术记录视前区-下丘脑前部(PO/AH) 温敏神经元单位放电的变化情况.结果:给予致热原后,PO/AH 区热敏神经元放电频率显著减少(P<0.01 ),冷敏神经元放电频率明显增加(P<0.05); 静脉注射生石膏后,可反转致热原对PO/AH区温敏神经元的上述作用,与给药前相比,热敏神经元放电频率明显回升(P<0.01 ),冷敏神经元放电频率明显回降(P<0.05).结论:提示生石膏是通过影响致热原作用下PO/AH区温敏神经元的放电活动,在中枢神经元水平上发挥解热作用的.     

ITE and TCDD Differentially Regulate the Vascular Remodeling of Rat Placenta via the Activation of AhR

Vascular remodeling in the placenta is essential for normal fetal development. The previous studies have demonstrated that in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, an environmental toxicant) induces the intrauterine fetal death in many species via the activation of aryl hydrocarbon receptor (AhR). In the current study, we compared the effects of 2-(1′H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) and TCDD on the vascular remodeling of rat placentas. Pregnant rats on gestational day (GD) 15 were randomly assigned into 5 groups, and were exposed to a single dose of 1.6 and 8.0 mg/kg body weight (bw) ITE, 1.6 and 8.0 µg/kg bw TCDD, or an equivalent volume of the vehicle, respectively. The dams were sacrificed on GD20 and the placental tissues were gathered. The intrauterine fetal death was observed only in 8.0 µg/kg bw TCDD-exposed group and no significant difference was seen in either the placental weight or the fetal weight among all these groups. The immunohistochemical and histological analyses revealed that as compared with the vehicle-control, TCDD, but not ITE, suppressed the placental vascular remodeling, including reduced the ratio of the placental labyrinth zone to the basal zone thickness (at least 0.71 fold of control), inhibited the maternal sinusoids dilation and thickened the trophoblastic septa. However, no marked difference was observed in the density of fetal capillaries in the labyrinth zone among these groups, although significant differences were detected in the expression of angiogenic growth factors between ITE and TCDD-exposed groups, especially Angiopoietin-2 (Ang-2), Endoglin, Interferon-γ (IFN-γ) and placenta growth factor (PIGF). These results suggest ITE and TCDD differentially regulate the vascular remodeling of rat placentas, as well as the expression of angiogenic factors and their receptors, which in turn may alter the blood flow in the late gestation and partially resulted in intrauterine fetal death.