Differential regulation on C5 expression in goose versus mammals by glucose/palmitate provides a potential protection for goose fatty liver

Goose fatty liver is a specific type of nonalcoholic fatty liver that is protected from harmful effects associated with severe steatosis. Our previous findings suggest that suppression of the complement C5 may be relevant, but the mechanism is unclear. Therefore, in this study, we first verified the expression pattern of complement genes (including C5) during goose fatty liver formation and then determined the liver fat content and fatty acid composition by high-performance liquid chromatography (HPLC), followed by selecting the differential metabolites to treat HepG2, goose and mouse primary hepatocytes, aiming to explore the mechanism of C5 and inflammation suppression in goose fatty liver. The data confirmed the suppression of complement genes (including C5) in goose fatty livers. Moreover, fat content was significantly higher in fatty liver versus normal ones, with oleic acid and palmitic acid dominantly accounting for the difference. In line with this, high concentration of palmitate led to down regulation of C5 expression in goose primary hepatocytes whereas upregulation in mouse primary hepatocytes and HepG2 cells. In conclusion, regulation on C5 expression by fatty liver related factors including high level of palmitic acid may contribute to the protection of goose liver from severe hepatic steatosis.     

Effect of chlorogenic acid on intestinal inflammation,antioxidant status,and microbial community of young hens challenged with acute heat stress

Heat stress in poultry is deleterious to productive performance. Chlorogenic acid (CGA) exerts antibacterial, anti-inflammatory, and antioxidant properties. This study was conducted to evaluate the effects of dietary supplemental CGA on the intestinal health and cecal microbiota composition of young hens challenged with acute heat stress. 100-day-old Hy-line brown pullets were randomly divided into four groups. The control group (C) and heat stress group (HS) received a basal diet. HS + CGA₃₀₀ group and HS + CGA₆₀₀ group received a basal diet supplemented with 300- and 600-mg/kg CGA, respectively, for 2 weeks before heat stress exposure. Pullets of HS, HS + CGA₃₀₀, and HS + CGA₆₀₀ group were exposed to 38°C for 4 h while the control group was maintained at 25°C. In this study, dietary CGA supplementation had effect on mitigate the decreased T-AOC and T-SOD activities and the increasing of IL-1β and TNFα induced by acute heat stress. Dietary supplementation with 600 mg/kg CGA had better effect on increasing the relative abundance of beneficial bacterial genera, such as Rikenellaceae RC9_gut_group, Ruminococcaceae UCG-005, and Christensenellaceae R-7_group, and deceasing bacteria genera involved in inflammation, such as Sutterella species. Therefore, CGA can ameliorate acute heat stress damage through suppressing inflammation and improved antioxidant capacity and cecal microbiota composition.     

腐蚀管道剩余寿命的性能衰减模型研究

管道在长期的运行过程中，由于介质和土壤的腐蚀性，管材的微塑性变形、结构转变和渗氢等。不仅会使管道出现各种腐蚀损伤，而且还存在着老化效应和氢化作用，导致管材的脆变并改变材料的塑性，使机械性质参数发生衰退，从管材性能衰减和腐蚀损伤角度研究了管道的剩余寿命，提出了根据结构承载能力的极限值确定塑性变形时工作寿命的方法，为了确定剩余使用寿命，对剪切损伤率和屈服性能比等概念进行定义，在掌握管材金属剪切损害率和屈服性能比的时间特性基础上，建立了剩余寿命计算模型。并给出了算例。     

铜对生长猪肝中IGF—Ⅰ基因mRNA表达的影响

采用生长试验、免疫放射分析和定量PCR方法，观察了生长猪血液中类胰岛素生长因子（IGF—Ⅰ）及其结合蛋白（IGFBP3）数量的变化和IGF—Ⅰ基因在肝中表达量的变化。结果显示，每1kg饲料中添加125-250mg铜，能够上调IGF-Ⅰ基因的表达量，显著提高猪的平均日增重，促进生长猪循环血液中IGF—Ⅰ浓度的增加。试验结果证实，铜是通过促进生长激素一胰岛素样生长因子轴相关因子的合成和分泌来发挥促生长作用的。     

钢筋混凝土结构锈蚀损伤定位

对钢筋混凝土结构锈蚀损伤定位进行了研究,以频率变化平方比作为锈蚀损伤参数,从理论上证明该参数是锈蚀损伤位置的函数。锈蚀钢筋混凝土结构试验结果表明预测的损伤位置和实际的损伤位置较一致,模态参数用于检测混凝土结构构件中的损伤,为大型结构的鉴定和评估提供了新的途径。     

药物防治蝇害的研究进展

蝇害已经成为危害规模化畜禽养殖的重要问题。文章回顾了防治蝇害的三代杀虫剂的发展过程和存在的问题 ;展望了作为新一代环境友好防治蝇害药物的昆虫生长调节剂的开发前景。     

The effects of experimentally induced fever on the estimated blood flow to and oxygen utilization by the liver and the viscera drained by the portal vein in sheep

Intrajugular injection of a purified E. coli lipopolysaccharide induced a biphasic fever in sheep after a latent period of 12 to 20 min. The changes in the blood flow from the liver and from the viscera drained by the portal vein were: (a) in the latent period, decreases in total hepatic blood flow (THF) due to decreased portal venous blood flow (PVF); (b) during the first febrile phase, increases in THF due to increased hepatic arterial blood flow and, (c) in the second febrile phase, increases in THF due to decreased PVF. Although there were large variations in the oxygen supply to the viscera drained by the portal vein and to the liver, there were relatively small or no changes in their oxygen consumption.     

Histopathology of Experimental Schistosoma bovis Infection in Goats

The inflammatory host response to Schistosoma bovis in young goats was studied at necropsy by light microscopy 34 weeks after primary exposure to 3,000 cercariae (group B, n=6), 34 weeks after primary exposure to 3,000 cercariae followed by challenge with 2,500 cercariae at week 17 (group C, n=5), and 17 weeks after primary exposure to 2,500 cercariae, given on week 17 of the experiment (group D, n=6). Three goats served as uninfected controls. The faecal egg output had been minimal for 17 weeks prior to necropsy in groups B and C and only for the last 2 weeks in group D.Histological studies were carried out on the small intestine, liver, lung and spleen, and tissue egg counts were performed. In sections of the small intestine and liver, a panel of histopathological variables were quantitated to characterize the host response and differences between groups of animals were evaluated with one way analysis of variance. The mean tissue egg count in the small intestine was slightly but not significantly higher in group C than group B and about twice as high in group D (D vs B or C p<0.01). Group means of numbers of inflammatory foci per section of gut wall corresponded well with those of tissue egg counts, suggesting that the rate of inflammatory destruction of eggs did not differ markedly between the groups. Egg material was less commonly seen in granulomas of the small intestine in group B than in group D (p<0.01), suggesting lower passage of eggs through the gut wall during the later than during the earlier phase of patent primary infection. The frequency of eosinophil-rich hepatic inflammatory foci was much higher in group D than in the other groups (D vs B p<0.05, D vs C p< 0.01), and coincided with a high degree of blood eosinophilia in this group at the time of sacrifice. Challenged goats showed a significantly higher frequency of markedly fibrotic inflammatory foci in the liver and of liver granulomas with a marked giant cell component than goats of the other groups. Hepatic portal fibrosis was least prominent in animals with 17- week- old primary infections, implying a possible relation between this change and duration of infection.     

Purification and characterization of hepatic triacylglycerol lipase isolated from rainbow trout,Oncorhynchus mykiss

Trialcylglycerol (TG) lipase was isolated and partially purified from rainbow trout liver. Triacylglycerol lipase activity was assayed by measuring¹⁴C-oleic acid release from¹⁴C-triolein.¹⁴C-oleic acid release was linear for up to two hours. Optimal activity occurred at pH 7.0 and 15°C. Most of the lipase activity was recovered in the cytosolic fraction. A 27,000-fold purification was achieved after Sepharose (Bio-gel A 0.5 M, 200–400 mesh) chromatography of a resuspended 20% ammonium sulfate fraction. The molecular weight of the trout hepatic lipase as determined by size-exclusion chromatography and by SDS-polyacrylamide gel electrophoresis was 40–43 kD. Lipase-mediated hydrolysis of TG resulted in the production of diacylglycerols, monoacylglycerols, and fatty acids. Kinetic analysis indicated that V_max=0.016 nmol/h/mg protein and that K_m=0.28 mM triolein. Lipolytic activity was enhanced in the presence of cAMP/ATP-Mg²⁺. These results suggest that the liver of trout possesses a neutral TG lipase that is responsible for mobilizing stored TG and is catalytically activated by phosphorylation.A part of this work was presented at the Annual Meeting of the American Society of Zoologists, December 26–30, 1990, San Antonio, TX.     

Application of Airway Pressure Therapy in Veterinary Critical Care: Part I: Respiratory Mechanics and Hypoxemia

Over the past several decades, recognition of acute respiratory failure as the cause of death in patients suffering from various clinical conditions has prompted aggressiv investigation into the area of respiratory physiology and supportive respiratory care. With the evolution of emergency medicine and critical care services in both human and veterinary medicine, many patients previously considered unsalvageable due to the severity of their underlying disease are now being resuscitated and successfully supported, creating a new population of critically ill patients. Where only a decade ago these patients would have succumbed to their underlying disease, they now survive long enough to manifest the complications of shock and tissue injury in the form of acute respiratory failure. Investigation into the pathophysiology and treatment of this acute respiratory distress syndrom (ARDS) has facilitated increased clinical application of respiratory theerapy and machanical ventilation.¹ The purpose of this paper is to provide a basic review of respiratory mechanics and the pathophysiology of hypoxemia as they relate to airway pressure therapy in veterinary patients and to review the use of airway pressure therapy in veterinary patients This paper is divided into two parts; part I reviews respiratory mechanics and hypoxemia as they apply to respiratory therapy, while part II deals specifically with airway pressure therapy andits use in clinical cases.