牦牛转铁蛋白对小鼠巨噬细胞释放一氧化氮的影响

用从牦牛血清中分离纯化的转铁蛋白和Sigma公司提供的牛转铁蛋白对小鼠腹腔巨噬细胞释放一氧化氮的影响进行研究.一氧化氮以伊利康生物技术有限公司提供的试剂盒测定.结果:脂多糖终浓度为20 μg/ml、培养时间12 h时,巨噬细胞释放一氧化氮的量显著增加,且满足实验需要,当两种转铁蛋白的浓度在25 μg/ml时能显著抑制小鼠腹腔巨噬细胞一氧化氮释放.这表明转铁蛋白对巨噬细胞的生长及免疫功能的影响与其抑制一氧化氮的释放有关.抑制一氧化氮生成,可能是转铁蛋白抑制细菌及病毒生长等的作用机制之一.     

串珠镰刀菌素的培养提取及对鸡的免疫病理损伤

从广东某饲料厂所用玉米上分离到串珠镰刀菌,并将该菌株接种玉米面,在25℃培养10d,转4℃培养7d,再转25℃培养10d的条件下,进行产毒培养。培养物灭菌干燥后采用乙腈-水(95∶5)提取串珠镰刀菌素(MON),并用薄层色谱验证和高效液相色谱测定提取物MON含量;将提取的MON按照23mg/kg加入试验组雏鸡饲料中,进行毒性试验,测定试验鸡免疫器官胸腺、法氏囊、脾脏指数及血清中一氧化氮的含量。结果表明:试验组比对照组鸡的胸腺、法氏囊及胸腺指数显著降低(P<0.05),血清中NO含量极显著升高(P<0.01)。     

纳米ZnO/PEG/PET复合材料的原位聚合制备及其性能

通过原位聚合制备了纳米氧化锌颗粒增强不同添加量和分子量的聚乙二醇（PEG）与聚对苯二甲酸乙二醇酯（PET）共聚物的复合材料。研究了纳米粒子在基体里的分散，以及纳米粒子和PEG对复合材料结晶行为的影响。结果显示，纳米粒子在基体中以纳米尺度分散起晶核作用。PEG的加入使得纳米粒子分散更加均匀，PEG分子链段改善了PET分子链的柔性，由此导致复合材料的冷结晶温度降低，结晶速率提高。研究发现，当添加10％分子量为4000的PEG时，复合材料的结晶速率快速提高。复合材料的力学性能结果说明，纳米粒子对PET基体有增强增韧作用，但PEG会弱化该作用。     

Effects of dietary caffeine on growth,body composition,somatic indexes,and cerebral distribution of acetyl‐cholinesterase and nitric oxide synthase in gilthead sea bream (Sparus aurata), reared in winter temperature

This study aims at examining the effect of caffeine administration on growth, feed efficiency, and consumption of sea bream (Sparus aurata), reared in winter temperatures. Moreover, it is questioned whether caffeine has a central action in the brain and its effects are partly mediated via central brain mechanisms. For this, we studied the influences of caffeine treatment on the cerebral pattern of the cholinergic neurotransmission and the novel neuromodulator nitric oxide (NO), by means of acetyl‐cholinesterase (AchE) and nitric oxide synthase (NOS) histochemistry. Five different diets containing 0.0, 0.1, 1.0, 2.0 and 5.0 g caffeine kg^?1 of diet were administrated to five groups of fish. Caffeine adversely affected sea‐bream growth at a concentration higher than 1 g kg^?1 diet and increased feed conversion ratio in the treatments of 2 and 5 g kg^?1 (P < 0.05). The daily consumption of feeds was similar to all groups, indicating that caffeine did not influence diet palatability. AChE‐ and NADPH‐diaphorase histochemistry showed densely labeled cells and fibers mainly in dorsal telencephalon, preoptic, pretectal, hypothalamic areas, optic tectum, reticular formation, cerebellum and motor nuclei. When compared with matched caffeine‐treated animals, no differences in the histochemical pattern and cell densities of cerebral AChE and NADPH‐diaphorase were found.     

N2O-Freisetzung auf gemähtem Dauergrünland in Abhängigkeit von Standort und N-Düngung

N₂O Emissions from True Meadows Dependent on Location and N Fertilization Agricultural production is thought to be a main anthropogenic emitter of nitrous oxide (N₂O), which contributes to global warming and the destruction of the ozone layer. There is still considerable uncertainty about the amount of N₂O emission, and the site‐specific parameters that affect N₂O emission. From October 1995 until March 1998 experiments were conducted at established field plots (true meadows) at three different sites, i.e. low mountain range (Eifel), lowland (Niederrhein), and moist meadows (Münsterland). Plots were fertilized with calcium ammonium nitrate (CAN) at nitrogen equivalents ranging from 0 to 360 kg N ha^–1. N₂O fluxes were measured throughout the whole year using the closed‐chamber method. In addition, data on temperature, water‐filled pore space and precipitation were collected. N₂O emission rates (mg N₂O‐N ha^–1 h^–1) were highest either after fertilizer application or in winter during frost, depending on the experimental site and N dosage. The annual amount of N losses due to N₂O emission was dependent on the experimental site and the type and dosage of fertilizer. Disregarding the 360 kg N ha^–1 level of the CAN treatments, the N losses in this experiment were less than 1.5 kg N₂O‐N ha^–1 yr^–1. At low fertilizer dosage there was no reliable correlation between the amount of N that was applied and the amount of N₂O that was emitted. However, with high fertilizer levels the N₂O emissions increased gradually. Finally, N₂O emissions were more influenced by the amount of CAN than by the site.     

诱导型一氧化氮合酶与动物疾病

一氧化氮（nitric oxide,NO)是近年来引起人们特别注意的无机气体自由基，有独特的理化性质和生物学活性，几乎对全身各个系统都有影响，其中诱导型一氧化氮合酶及其催化产生的NO在动物疾病的发生、发展过程中都起着重要的作用。     

一氧化氮和内皮素在窒息新生大鼠胃黏膜损伤中的作用

本研究旨在探讨围产期窒息时内皮素( ET)和一氧化氮 ( NO)的变化与急性胃黏膜损伤的关系及 NO的前体 L-精氨酸 ( L-Arg)和NO合成酶抑制剂 L-硝基 -精氨酸甲酯 ( L-NAME)在胃黏膜损伤中的作用。结果显示窒息组血浆 ET和胃壁 NO水平显著高于正常对照组 ( p<0 .0 1 ) ,胃黏膜损伤明显 ;L -Arg组血浆ET水平较窒息组显著下降 ( p <0 .0 1 ) ,血浆和胃壁 NO含量则显著升高 ( p <0 .0 1 ) ,胃黏膜损伤减轻 ;L-NAME组血浆 ET水平和 L I显著高于正常对照组和 L -Arg组 ( p <0 .0 1 ) ,血浆和胃壁 NO含量较 L-Arg组显著下降 ( p <0 .0 1 ) ,表明围产期窒息时 NO和 ET的变化与胃黏膜损伤的程度密切相关。NO在围产期窒息时有保护胃黏膜的作用 ,而 ET则作用相反。L -Arg的保护作用和 L -NAME的损伤作用均是通过 NO的变化来实现的。     

Astragalus polysaccharides protects against free fatty acid-induced human vascular endothelial cell dysfunction via AMPK-eNOS pathway

AIM: To study the protective effect of Astragalus polysaccharides (APS) on free fatty acid-induced injury in human umbilical vein endothelial cells (HUVECs). METHODS: Cultured HUVECs were divided into control group, APS group [APS (200 mg/L) treated for 24 h], free fatty acid group [free fatty acid (0.25 mmol/L) treated for 24 h], free fatty acid plus APS group [free fatty acid (0.25 mmol/L) and APS (200 mg/L) treated for 24 h], and compound C group [free fatty acid (0.25 mmol/L) and APS (200 mg/L) and AMPK inhibitor compound C (10 μmol/L) treated for 24 h]. The cell viability was detected by MTT assay. Nitric oxide (NO) content in the medium was determined by nitrate reductase assay. The protein levels of total adenosine monophosphate-activated protein kinase (AMPK), phosphorylated adenosine monophosphate-activated protein kinase (p-AMPK), endothelial nitric oxide synthase (eNOS) and phosphorylated endothelial nitric oxide synthase (p-eNOS) were measured by Western blot. RESULTS: No significant difference of all indexes between APS group and control group was observed. The cell viability in free fatty acid group decreased significantly compared with control group. The cell viability in free fatty acid plus APS group was significantly improved as compared with free fatty acid group. The cell viability in compound C group was almost the same as that in free fatty acid group. The No content and protein levels of p-AMPK and p-eNOS in free fatty acid group decreased obviously as compared with control group, while the NO content and protein levels of p-AMPK and p-eNOS in free fatty acid plus APS group increased obviously compared with free fatty acid group. No significant difference of the p-AMPK and p-eNOS protein levels between free fatty acid plus APS group and free fatty acid group was observed. No significant difference of the AMPK and eNOS protein levels in all groups was found. CONCLUSION: APS attenuates the free fatty acid-induced injury, and its mechanism is related to the AMPK-eNOS signal pathway.     

Sphingosine-1-phosphate receptor-2 attenuates lipopolysaccharide-induced acute lung injury

AIM: To investigate the effects and mechanisms of sphingosine-1-phosphate receptor-2 (S1P2R)on lipopolysaccharide (LPS)-induced acute lung injury (ALI). METHODS: ALI model was induced by intratracheal administration of LPS in both wild-type mice and S1P2R -deficient mice. The pathological changes in the lung tissues were observed, and the protein concentration, total cell number, neutrophil ratio, TNF-α level and IL-6 level were determined in the bronchoalveolar lavage fluid (BALF) 24 h after LPS injection. In order to investigate the mechanisms of S1P2R in LPS-induced ALI, 10 min before LPS injection, both wild-type mice and S1P2R -deficient mice were injected with nitric oxide synthase inhibitor by tail vein injection, the pathological changes of the lung tissues were observed, and the protein concentration and total cell number in BALF were determined 12 h after LPS injection. RESULTS: Compared with wild-type mice, S1P2R -deficient mice showed more severe LPS-induced ALI, and the protein concentration, neutrophils and inflammatory cytokines in BALF were significantly increased in S1P2R -deficient mice. Administration of nitric oxide synthase inhibitor N^ω-L-nitro-arginine methyl ester protected S1P2R -deficient mice from aggravation of ALI. CONCLUSION: S1P2R mediates the protection from LPS-induced ALI possibly through inhibiting nitric oxide synthase.