奶牛难产激发应激性急性肾上腺皮质功能不全——心衰、水电解质严重失调辩析

应激性急性肾上腺皮质功能不全症的病理机制十分复杂,目前人医的各类文献中大都以“垂体—肾上腺轴”功能不全、功能衰竭、或发生广泛性出血坏死性病演作解释。本病在奶牛分娩难产过程中并不少见,病牛的症状表现以心衰和失钠性低血症为主征。但在兽医临床上由于认识不足,曾有不少中外学者将奶牛产后卧地不起的各类疾病,含糊地统称为“母牛睡倒爬不起来综合征”;更由于救治不当,病牛常以淘汰或死亡告终。本文通过对一具体典型病例辨析,着重讨论了本病的基本病理反应和确立诊断依据,强调对本病救护施治时应遵循的基本原则,供同道们在分析和解决这一实际问题时参考。     

Equine pituitary pars intermedia dysfunction: current understanding and recommendations from the Australian and New Zealand Equine Endocrine Group

The purpose of this article is to provide a review of the current knowledge and opinions about the epidemiology, clinical findings (including sequelae), diagnosis, treatment and monitoring of equine pituitary pars intermedia dysfunction, particularly in the Australian context. This information and the recommendations provided will assist practitioners in making informed decisions regarding the diagnosis and management of this disorder.     

Describing Human–Wildlife Interaction from a European Perspective

European researchers from both the natural and social sciences show growing interest in studying interactions between society and wildlife. A wealth of theoretical frameworks, concepts, and methods are used, but an integration of perspectives is lacking. This research note summarizes results from two workshops that included 63 delegates from 25 European countries, as well as a follow-up survey of 41 respondents. Two main theoretical approaches to the study of human–wildlife interactions were identified. One approach focuses on the collective societal level relying on theories of governance, social representation, deliberative procedures, and commons theory. The other approach targets individuals or groups, and is based on theories such as the cognitive hierarchy, theory of reasoned action, and theory of planned behavior. Interdisciplinary collaboration is needed to identify the best options for wildlife conservation and management in a more politically integrated Europe.     

Role of chlorogenic acid in endothelial dysfunction in db/db mice

AIM: To explore the effects of chlorogenic acid (CGA) on endothelial dysfunction in db/db mice and the possible mechanism. METHODS: Male db/db mice (n=12) were divided into control group and CGA group, with 6 mice in each group. The mice in CGA group were treated with diet containing 0.02% CGA, while the mice in control group were given normal diet only. The observation period was 12 weeks. Fasting blood glucose level, tail blood pressure and the body weight were analyzed each week. At the end of the 12th week, the mice were anesthetized and blood was taken from carotid artery. The plasma levels of heme oxygenase-1 (HO-1), catalase (CAT), NAD(P)H dehydrogenase quinone 1 (NQO1) and glutathione peroxidase-1 (GPx-1) were measured by ELISA. The mouse aortas were isolated, and the superoxide anion and nitric oxide (NO) levels were measured by DHE and DAF-2 DA staining, respectively. Wire Myograph System was used to detect the vasorelaxation of db/db mouse aorta. The protein levels of peroxisome proliferator-activated receptor α (PPARα), nuclear factor E2-related factor 2 (Nrf2), phosphorylated AMP-activated protein kinase (p-AMPK), phosphorylated endothelial NO synthase (p-eNOS), P22^phox and P47^phox were determined by Western blot. RESULTS: Dietary CGA decreased fasting blood glucose and body weight in db/db mice as compared with control group (P<0.01 or P<0.05). The plasma levels of HO-1, CAT, NQO1 and GPx-1 in CGA group were higher than those in control group (P<0.01 or P<0.05). Administration of CGA for 12 weeks attenuated superoxide anion level, increased NO level in the mouse endothelium and improved endothelium-dependent relaxation of the db/db mouse aorta. CGA also increased the protein levels of PPARα, Nrf2, p-AMPK and p-eNOS, and decreased P22^phox and P47^phox levels (P<0.01). CONCLUSION: Dietary CGA improves db/db mouse endothelium-dependent relaxation. This effect may be related to the increases in the levels of antioxidant molecules PPARα, Nrf2 and p-AMPK, and the up-regulation of antioxidant capacity, thus decreasing the oxidative stress, promoting eNOS phosphorylation, and increasing NO level.