2012年玉米大斑病重发原因和控制对策

玉米大斑病是由真菌引起的世界性玉米病害,常给生产造成严重损失。2012年玉米大斑病在东北、华北地区大流行,本文归纳了玉米大斑病全国发生概况、区域分布和各地病情。总结了2012年玉米大斑病发病时间早,流行速度快,品种间和地区间发病程度差异大等发生特点,分析了适宜天气条件、主栽品种不抗病、栽培管理措施不合理是导致大斑病重发的主要原因。并针对性地提出了重视玉米病害的预测预报、推荐种植抗病品种、加强病害综合防治的对策建议,旨在对今后进一步做好玉米大斑病测报工作,指导玉米病害防治、有效控制其危害、保障玉米生产有所裨益。     

儿茶素的药理作用研究综述

目的研究表儿茶素(EC)对小鼠急性肺损伤(ALI)炎症反应的调节作用。方法采用吸入式气管滴注法在BALB/c小鼠中建立ALI模型,H8LE染色观察肺组织病理学变化,并结合基于超高效液相色谱与四极杆—飞行时间质谱联用技术(HILIC UHPLC-Q-TOF MS)的非靶向代谢组学方法对小鼠肺组织进行研究。结果对比空白对照组,LPS处理后的小鼠肺组织发生严重的炎症变化,而EC预处理组炎症现象比LPS组轻。经肺组织代谢轮廓分析发现：二十羟基花生四烯酸、色氨酸、苯丙氨酸、酪氨酸、ATP、磷酸胆碱、二十碳四烯酸、磷酸、烯醇和二磷酸葡萄糖等差异物与小鼠急性肺损伤内源性代谢密切相关,且涉及甘油酯代谢、糖酵解、甘油磷脂代谢、苯丙氨酸、酪氨酸和色氨酸生物合成、抗坏血酸代谢和胆碱代谢等6条代谢路径。结论运用代谢组学方法探讨了EC干预小鼠ALI的差异代谢物变化情况,为表儿茶素抗炎特性的研究提供了理论依据。     

Ameliorative Effects of Oyster Protein Hydrolysates on Cadmium-Induced Hepatic Injury in Mice

Cadmium (Cd) is a widespread environmental toxicant that can cause severe hepatic injury. Oyster protein hydrolysates (OPs) have potential effects on preventing liver disease. In this study, thirty mice were randomly divided into five groups: the control, Cd, Cd + ethylenediaminetetraacetic acid (EDTA, 100 mg/kg), and low/high dose of OPs-treatment groups (100 mg/kg or 300 mg/kg). After continuous administration for 7 days, the ameliorative effect of OPs on Cd-induced acute hepatic injury in Cd-exposed mice was assessed. The results showed that OPs significantly improved the liver function profiles (serum ALT, AST, LDH, and ALP) in Cd-exposed mice. Histopathological analysis showed that OPs decreased apoptotic bodies, hemorrhage, lymphocyte accumulation, and inflammatory cell infiltration around central veins. OPs significantly retained the activities of SOD, CAT, and GSH-Px, and decreased the elevated hepatic MDA content in Cd-exposed mice. In addition, OPs exhibited a reductive effect on the inflammatory responses (IL-1β, IL-6, and TNF-α) and inhibitory effects on the expression of inflammation-related proteins (MIP-2 and COX-2) and the ERK/NF-κB signaling pathway. OPs suppressed the development of hepatocyte apoptosis (Bax, caspase-3, and Blc-2) and the activation of the PI3K/AKT signaling pathway in Cd-exposed mice. In conclusion, OPs ameliorated the Cd-induced hepatic injury by inhibiting oxidative damage and inflammatory responses, as well as the development of hepatocyte apoptosis via regulating the ERK/NF-κB and PI3K/AKT-related signaling pathways.     

补中益气丸对糖尿病大鼠胃组织MUC1、COX、NOS表达变化及相互作用

观察补中益气丸对糖尿病大鼠胃组织MuC1、COX-1、COX-2、cNOS、iNOS不同病程表达变化及其相互作用的影响、大鼠随机分为正常组。模型组和中药组,采用STZ腹腔注射结合乙醇灌胃的方法建立糖尿病大鼠胃黏膜损伤模型．检测胃组织NO、PGE2、6-ketoPC-F1d、MuCl、COX-1、cOX2、cNOS和iNOs随病程的表达变化及其相互作用。结果显示,糖尿病大鼠出现胃黏膜损伤和胃肠功能紊乱,胃组织MUC1、COX2、iNOS发生显著变化．MUC1随病程进展逐渐降低,iNOs和COX-2表现为早期活性降低,晚期活性升高,PGE2、6-keto—PGF1d和NO随病程显著升高,相关分析发现．COX1与cNOS呈显著正相关,与iNOS呈著负相关。补中益气丸能调节MUC1、COX-2、iNOS的表达及其相互作用,阻止胃黏膜损伤。结果表明,STZ腹腔注射结合乙醇灌胃的方法可成功诱导糖尿病大鼠胃黏膜损伤模型,iNOS与COX2可能为相互协作和相互介导的关系,在糖尿病胃黏膜损伤方面起重要作用,补中益气丸通过升高MUC1、降低iNOS和COX-2的表达及其相互作用,阻止胃黏膜损伤和糖尿病的发展。     

赤峰地区敖汉苜蓿冻害及其防御技术

敖汉苜蓿在赤峰地区受冻害程度有4种类型;全株未受冻;根颈上端受冻受黑,下端仍能再生新芽;全部根颈和根的部分受冻变黑,已不能再生新芽;全株受冻死亡。引起冻害的主要原因是播种期偏晚,在播种当年生长期短,根颈入土浅。结果表明,越冬前苜蓿必须具有2个以上分枝,根颈入土深>5cm以上,根颈膨大,直径>0.3cm以上者方能减轻或避免受冻。适时早播,施种肥,延长生长期促进幼苗生长,在封冻前对平作进行浅耕覆土或深开沟磨平等措施,均能增加根颈保温层,有效提高苜蓿越冬率。     

灵芝组方保肝的研究

按照国家保健食品审批标准，对灵芝组方后提取有效部份，进行保肝实验，研究结果表明．以0.67、2．00、6．00g／kgBw剂量的灵芝益甘粉灌胃给予小鼠30d，并以四氯化碳造成急性肝损伤模型．灵芝益甘粉067、6．00g／kgBW剂量组的AST，6．00g／kgBW剂量组肝细胞坏死病变程度均低于模型对照组．差异有显著性（P〈0．05）．灵芝益甘粉对化学性损伤有保护功能．     

农业产业化主体的困惑——个人理性与团体理性的冲突

龙头企业、中介服务机构和农户构成农业产业链条不可缺少的组成部分。任何一方对个人理性的盲目追求，会损害团体理性。因此，有必要对个人理性作适当的调整，以利于团体理性的发挥。     

Observations on calf scours in New Zealand

Extract

Scouring syndromes constitute a major disease group in dairy calves in New Zealand.     

Injury Induces a Change in the Functional Characteristics of Cells Recovered from Equine Tendon

Injury initiates a repair process characterized by influx of fibroblasts and the rapid formation of fibrous scar tissue and subsequent tissue contraction. The response to injury and behavior of the different tendon fibroblast populations, however, has been poorly characterized. We hypothesized that the fibroblasts recovered from tendon with acute injury would exhibit different cell properties relating to adhesion, migration and tensegrity. To test this hypothesis we evaluated the ability of fibroblasts recovered from normal and injured equine superficial digital flexor tendons (SDFTs). The injured tendon-derived cells showed greater contraction of the collagen gel but poorer adhesion to pepsin-digested collagen, and migration over extracellular matrix proteins compared to normal SDFT-derived fibroblasts. Thus, the cells present within the tendon after injury display different behavior related to wound healing.