非平行直纹面的电解磨削

为解决整体叶轮扭曲叶片型面的精加工难题,本文进行了五轴联动数控展成电解磨削的基础研究.在分析平行直纹展成电解磨削整体叶轮扭曲叶片的过切误差、得到过切误差计算公式的基础上,提出用圆锥磨轮和组合式五轴联动数控方案来消除过切误差的方法.文中还介绍了数控展成电解磨床的结构与运动、经济型多轴数控系统及其联动控制方法,并建立了电解磨削非平行直纹展成曲面的数学模型,开发了五轴联动数控展成电解磨削自动数控编程系统,对航空发动机整体叶轮的叶片型面进行电解磨削.结果表明,加工效率比手工修磨、抛光提高了12倍以上.     

略论西北地区渔业发展现状及对策

通过对西北地区渔业现状的分析，从中挖掘出西北地区渔业落后的社会经济原因，并结合当前的社会经济状况和渔业发展形势，总结了西北地区渔业发展的优势所在，以此为基础提出了加强市场宣传和资源开发、引进资金和技术以及政策引导等发展西北渔业的几点建议。     

特优175高产结构分析和配套栽培技术探讨

特优175分蘖力中强、穗大粒重、株型理想、高产稳产.经调查分析,其高产结构中,以每穗结实粒数的变异(cv=17.20%)最大,与产量相关最密切(r=0.591 1**,对产量的通径(p=1.035 6)和净贡献率(pr=0.612 1)最大;其次为有效穗(cv=10.40%,p=0.709 5,r=0.184 4,pr=0.130 8);千粒重是品种的稳定性状,对产量的贡献有限.每公顷产量7 500 kg左右的适宜产量结构为:每公顷250万穗,每穗结实120粒、千粒重28 g左右.在保持一定的穗数下,较高的每穗结实粒数是高产栽培的主攻重点.配套栽培技术是:(1)适时播种,培育壮秧;(2)适时移栽,合理密植(每公顷基本苗150～180万);(3)合理调控水肥,每公顷施纯氮150～180 kg,氧化钾120～160 kg,五氧化二磷60～80 kg;(4)综合防治病虫害.     

不同放牧强度对三峡地区灌丛草地灌木重要值变化的影响

对三峡地区灌丛草地灌木植被在山羊放牧条件下的数量特征进行了定量研究。结果表明，不同放牧强度处理区内灌木种间平均重要值的大小均存在着显著差异(P＜0.05)，各区内平均重要值最大者均为白栎，对照、轻牧和重牧区内其平均重要值分别为57.1%、51.3%和39.7%。放牧(轻牧和重牧，5月、7月和9月)期间白栎的重要值为上升趋势(除9月重牧之外)，美丽胡枝子的重要值为下降趋势(除5月轻牧之外)，水锦树的重要值为上升趋势(除9月轻牧之外)。轻牧能使白栎、麻栎、盐肤木、柳杉、美丽胡枝子、马桑和小果蔷薇的重要值增加，这说明轻牧在一定程度上能促进它们的再生，增加植冠盖度，从而提高它们在灌木群落中的优势地位。而对于某些粗蛋白质含量较高的灌木种，如宜昌木兰和黄檀等，放牧会影响其再生，故应严格控制其放牧强度才不致使其从灌木群落中衰减甚至消失。     

通过病毒分离鉴定和基因检测首次发现虎流感

应用F81猫肾传代细胞，从高热、拒食和间有神经症状的死亡率病科中分离获得1株病毒，经形态学、理化学、生物学和血清学系统鉴定，证明为流感病毒。采用流感病毒核蛋白基因引物，对分离病毒及该虎病科进行RT－PCR扩增和序列分析，结果从分离病毒和虎病科中均扩增出与理论值大小相符的464bp基因片段；其序列与A、B、C3型流感病毒相比较，同源性分别为84．9％、35．0％、24．8％。由此说明，所分离病毒为A型流感病毒，命名为/蘧／哈尔滨（中国）／01／2002。用此分离病毒静脉接种于3月龄家猫3号，均出现与病虎相似的临床症状，其中1号耐过，2只死亡。死亡猫剖检变化与死虎相似，主要是呈肺炎病变，并可从病科中回收到所接种病毒。从此分离病毒为HA抗原，进行虎与猫血清的HI抗体检测，结果康复虎血清比其病初血清、康复猫血清比其接种前血清HI抗体均增高4倍以上，表明该病毒具有致病性，是引起该虎与试验猫发病甚至死亡的病原。     

银杏幼苗叶片转化酶活性及其动力学

采用波钦诺克XH法研究了田间和室内栽培的银杏幼苗叶片转化酶的活性及其动力学性质。结果表明:银杏幼苗叶片转化酶在pH值5.0、温度55℃时活性最强;该酶的米氏常数为3.7×10-2mol·L-1;室内盆栽的银杏幼苗叶片转化酶的活性显著高于田间栽培的同龄银杏幼苗叶片转化酶的活性。     

高寒牧区牧鸡鸭治蝗效果试验

在青海湖北岸高寒牧区利用人工饲养的鸡鸭进行放牧防治草原蝗虫。结果表明,在60d的防治期内,牧鸡鸭平均灭治效果达91.4%,为人工利用天敌治虫技术在高寒牧区的应用提供了依据。     

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AIM: To investigate the contribution of angiotensin-converting enzyme inhibitor (ACEI) to the regulation of calpain system in infarcted myocardium. METHODS: Rat myocardial infarction (MI) model was established by permanent ligation of the left coronary artery. The treatment with the ACEI inhibitor rampril (1 mg·kg-1·d-1) was started 7 days prior to surgery. On day 1, 3, 7 and 14 after MI, protein levels of calpainⅠ, Ⅱ and calpastatin were determined in left ventricular free wall (LVFW), interventricular septum (IS) and right ventricule. RESULTS: CalpainⅠprotein level was increased in IS 14 d post MI, whereas the protein level of calpainⅡ was maximally increased in LVFW 3 d post MI. Rampril decreased protein up-regulation of calpainⅠ and Ⅱ, and reduced infarct size and interstitial fibrosis. Calpastatin protein expression was not affected by ACEI. CONCLUSIONS: CalpainⅠ is involved in cardiac remodelling in the late and calpainⅡ contributes to cardiac tissue damage in the early phase of MI. The heart protective effect of ACEI may be related to the inhibition of calpain system in the pathogenesis of myocardial infarction.     

农田沙漠化演变中土壤质量的生物学特性变化

通过研究处于沙漠化过程中的科尔沁沙地旱作农田土壤酶活性与基础土壤呼吸活性，分析了土壤质量生物学特性的沙漠化演变。结果表明，土壤酶活性与基础土壤呼吸对沙漠过程中环境的变化反应敏感，随着沙漠化程度增加，与土壤物理化学肥力因素有关的过氧化氢酶、脲酶和碱性磷酸酶的活性和土壤呼吸活性随之下降。土壤酶活性和呼吸活性与土壤有机质和养分有极显著的相关，在一定程度上可以用酶活性和呼吸强度表征有机质和养分的状况及其数量的变异，因此，可以作为农田沙漠化演变中土壤质量特征变化的重要辅助指标。     

Establishment of chronic obstructive pulmonary disease rat models by passive cigarette smoking and intratracheal instillation of lipopolysaccharide

AIM:To establish rat chronic obstructive pulmonary disease(COPD) models by passive cigarette smoking plus intratracheal instillation of lipopolysacchride(LPS) or passive cigarette smoking only, which would be similar to the pathogenesis of human COPD. METHODS:48 Wistar rats were randomly divided into 4 groups.(1) Healthy control I group(n=12), rats were bred 4 weeks;healthy control II group(n=12), rats were bred for 3months. (2) Model group I (n=12), 200μg lipopolysaccharide(LPS) was instilled intratracheally once for every two weeks and the rats were exposured to 5% of cigarette smoke, 0.5 h/d for 4 weeks.(3) Model group II(n=12),rats were exposed to 5% of cigarette smoke, 0.5 h/d for 3 months. The pathologic changes of airways and lung tissues, pulmonary function and blood gas analysis were determined. The airway wall lymphocytes and alveolar macrophages were counted. The cross areas of epithelial layer, smooth muscle layer and lamina propria of bronchi were measured. The hydroxyproline of lung tissue homogenates was determined by biochemistry method.RESULTS:The pathologic changes of airways and lung tissue of two models were similar to but milder than those of COPD patients(biopsy data). The collagen deposition and the cross areas of epithelial layer and smooth muscle layer in airway walls of two model groups were significantly increased than those of control groups(P＜0.01,P＜0.05).FEV_0.3/FVC% of two model groups, PaO₂ and SaO₂ of model I group were significantly decreased, while R_i and R_e in model I group were significantly increased than that of control I group(P＜0.05). The PaCO₂ and the counts of lymphocytes and alveolar macrophages of both model groups were significantly increased than those of the control groups (P＜0.01). Lots of alveolar macrophages had phagocyted smoke granules. The amounts of hydroxyproline of two model groups were significantly increased than those of control group((P＜0.05) and were negatively related to the FEV_0.3/FVC%, respectively (P＜0.01,P＜0.01) and positively related to airway resistance of model I group(P＜0.01). CONCLUSIONS:COPD rat models were successfully established by passive cigarette smoking plus intratracheal instillation of LPS and cigarette smoking only. The pathologic changes were similar but milder than those of COPD patients. The airway obstruction of model I group was more severe than that of model II group, but they have no significant difference.