硫横苯丁锡混合悬浮剂中苯丁锡含量的测定

本文介绍样品用二氯甲烷提取后，经薄层分离去除干扰，用硫酸 硝酸 过氧化氢消化，使苯丁锡转化成四价锡，以邻苯二酚紫-N-溴代十六烷基吡啶作显色剂，在波长660nm处进行比色测定，其标准偏差为0.04445，变异系数为0.87%，重现性好，方法平均回收率为99.61%。     

The Distribution of Soluble Copper- and Zinc-Binding Proteins in Liver and Kidney of Chronic Copper-Poisoned Goats

The distribution of copper and zinc among the soluble proteins in the liver and kidney from chronic copper-poisoned goats was examined after gel filtration of the proteins. The concentrations of copper in the liver and kidney cortex from five experimentally copper-poisoned goats were: 550–810 µg/g liver and 190–420 µg/g kidney cortex (wet weight). In general the copper-binding proteins from, both the liver and kidney samples were separated into two different fractions with approximate molecular weights (m.w.) of > 65,000 and 10,000, respectively. From the liver samples, varying amounts of copper were eluted in a fourth fraction with m.w. < 2,000. In the majority of kidney samples the dominating copper-binding protein fraction was the high molecular weight fraction. Absolute amounts of copper recovered in the metallothionein-like protein fraction were nearly the samt for all samples investigated. The distribution of zinc-binding proteins in both liver and kidney samples was nearly the same. The high molecular weight fraction dominated, and no zinc was bound to metallothionein-like proteins.     

Serum nitrate and nitrite in dogs with spontaneous cardiac disease

The purpose of this study was to determine whether nitric oxide (NO) concentrations are high in dogs with chronic valvular disease (CVD) and dilated cardiomyopathy (DCM) compared to healthy controls and to determine whether NO concentrations are correlated with type of cardiac disease, disease severity, medical therapy, or serum tumor necrosis factor (TNF) and interleukin-1 (IL-1). Blood was collected from 32 dogs with DCM, from 10 dogs with CVD, and from 10 healthy controls. Indirect determination of NO concentrations was performed by a commercial photoabsorbance assay that uses a Greiss reagent to measure the concentration of nitrite and nitrate (NN), end products of NO metabolism. TNF and IL-1 activities were measured by bioassay. Mean NN concentrations were significantly higher in dogs with heart disease (median, 4.57 microM; range, 0.00-31.05 microM) than in controls (median, 0.00 microM; range, 0.00-6.16 microM; P = .04). NN concentrations in dogs with cardiac disease were not correlated with type or severity of cardiac disease, medication type, or TNF and IL-1 concentrations. NN concentrations were inversely correlated with fractional shortening. The results of this study suggest that metabolites of NO are increased in some dogs with cardiac disease, but these increases appear to be independent of disease severity, TNF and IL-1 concentrations, and type of pharmacologic intervention.     

二乙基己烯雌酚对成年仓鼠睾丸一氧化氮生成和生精细胞凋亡的影响

探讨了在二乙基己烯雌酚（DES）诱发成年动物生精细胞凋亡过程中睾丸一氧化氮（NO）生成和生精细胞一氧化氮合酶（eNOS和iNOs）表达的变化，以期为阐明DES诱发生精细胞凋亡机理的研究提供基础资料。成年雄性仓鼠皮下注射不同剂量DES（分别为0．01、0．1和1mg／kg体重），连续注射7d后取其睾丸，进行NO含量的测定和eNOS、iNOS免疫组化染色。电镜观察生精细胞超微结构的变化，并用TUNEL法检测睾丸中生精细胞凋亡的变化，苏丹Ⅲ染色法检测睾丸生精小管内脂滴分布的变化。结果显示：NO的生成与DES呈剂量依赖性。DES处理后，在1mg／kg体重剂量组，大量生精细胞表达eNOS和iNOS，并出现大量凋亡，退化的生精细胞胞浆内有大量髓样结构，并有大量脂滴分布于生精细胞内和细胞间。eNOS和iNOS阳性生精细胞与凋亡的生精细胞数量和类型基本一致，主要为精母细胞和圆形精子细胞。     

高铜对雏鸡器官组织病理损害的研究

将420只1日龄艾维菌健雏，随机分为7组，分别饲以含铜量11mg／kg的基础日粮和含铜量分别为100、200、300、400、500和600mg／kg的6种高铜日粮6周，研究高铜对雏鸡的病理损害。结果显示，日粮含铜100和200mg／kg对雏鸡有促生长作用。日粮铜水平达300mg／kg以上时，对雏鸡器官组织造成不同程度的病理损伤，表现为肌胃角质层增厚呈黄褐色；肝呈浅黄色或深褐色，肝细胞脂肪变性；消化道上皮细胞变性坏死；免疫器官和肾、心脏、胰腺、大脑等器官的实质细胞肿胀；淋巴免疫器官体积缩小，淋巴细胞数量减少。超微结构观察发现，肝细胞胞浆和胞核内见有数量不等、大小不一的高电子密度的沉积物；凋亡的淋巴细胞染色质呈花瓣样、半月形或环形，聚集在核膜下。表明，肝、消化道和免疫器官是高铜损害的主要靶器官。     

铜在奶牛生产中的应用及存在问题

本文就铜的生物学效应和生理功能,奶牛对铜的需要量、耐受量和中毒量等进行阐述。     

铜的来源和水平对生长猪生长性能禾粪铜排出量的影响

选用平均体重29．6kg的三元杂（杜×大×长）生长猪144头，按随机区组设计分为6个处理。饲粮中分别添加0、100、200mg／kg硫酸铜、200mg／kg碱式氯化铜、100mg／kg小肽铜、100mg／kg复合氨基酸螯合铜（以铜含量计）。结果表明：100mg／kg小肽铜和100mg／kg复合氨基酸螯合铜均能有效提高生长猪日增重和日采食量，其促生长效果与200mg／kg硫酸铜无显著（P〉0．05）差异，而粪中铜含量分别下降了36．8％和48．4％（P〈0．05）。     

Preliminary experiments on mechanical stretch-induced activation of skeletal muscle satellite cells in vivo

We have shown in vitro that mechanical stretch triggers activation of quiescent satellite cells of skeletal muscle to enter the cell cycle through an intracellular cascade of events including nitric oxide (NO) synthesis that results in the release of hepatocyte growth factor (HGF) from its extracellular association and its subsequent presentation to signaling receptors. In order to explore the activation mechanism in vivo, stretch experiments were conducted in the living animal using our suspension model developed. This system used the weight of the hind portion of rats to stretch the inside muscles of the left hind limb suspended for a period of 0.5–2.0 h. At the end of the stretch period, the rats received an intraperitoneal injection of bromodeoxyuridine followed by immunocytochemistry for its incorporation as an index of satellite cell activation in vivo. Depending on the period of stretch, bromodeoxyuridine labeling was increased significantly over the contralateral unstretched leg or control muscle from untreated rats. A stretched muscle extract prepared from the 2 h stretched tissue by incubating it in PBS, showed the active form of HGF as revealed by immunoblotting and it could stimulate the activation of unstretched satellite cells. Also, administering NO synthase inhibitor L‐NAME prior to muscle stretch abolished the stretch activation of satellite cells. Therefore, the results from these experiments demonstrate that stretching muscle triggers NO synthesis and HGF release, which could activate satellite cells in vivo.