小尾寒羊传染性胸膜肺炎的诊断与综合防治措施

近年来,小尾寒羊规模养殖场、户日益递增,由传统的河滩、山坡地放牧方式转变为圈养舍饲,由于饲养管理不善、羊群群体较大、密集拥挤、圈舍潮湿、运输应激、引种带菌、未定期消毒,尤其是羊群体质差、防疫意识不强、技术力量薄弱、天气骤然变冷、多风的秋冬气候差异等等这些因素,都是引发小尾寒羊传染性胸膜肺炎的诱因。小尾寒羊传染性胸膜肺炎又称＂烂肺病＂,是由肺炎支原体引起的一种高度接触性传染病,其临床特征为高热、咳嗽、肺和胸膜发生浆液性和纤维蛋白性炎症,

山羊传染性胸膜肺炎及其综合防控措施

山羊传染性胸膜肺炎又称＂烂肺病＂,是由丝状霉形体引起的高度接触性传染病。在自然条件下,此病仅感染山羊。感染后的典型临床症状为发热、咳嗽、肺和胸膜发生浆液性和纤维蛋白性炎症。本病常呈地方性流行,主要通过空气飞沫经呼吸道传染,接触传染性强。阴雨连绵、寒冷潮湿、营养缺乏、羊群密集、拥挤等不良因素易诱发本病。此病病死率较高,是严重危害山羊群养殖的病患之一。尤其在山羊养殖向规模化、产业化发展的情况下,此病大有增加之势,带来严重的经济损失。

猪传染性胃肠炎的防治

猪传染性胃肠炎是由猪传染性胃肠炎病毒引起的一种高度接触性肠道传染病。病原体是滤过性冠状病毒，主要感染猪。近二年来，郾城各地均有此病发生。一、发病情况本病各种年龄、性别、品种猪都可感染，以哺乳及刚断奶的仔猪发病、死亡为多，架子猪、成猪发病一般为良性经过...

奶牛乳房炎的中西医疗法

乳房炎是奶牛养殖中常见的一种多发病,主要是由多种病原微生物侵入所引起的,严重威胁着奶牛业的健康发展,也是造成经济损失最严重的一种疾病。因此做好奶牛乳房炎的防治工作十分重要。1病因奶牛乳房炎属多因素性疾病,通常是由微生物、饲养管理及奶牛自身等因素综合作用的结果。1.1微生物因素奶牛乳房炎发生主要是因为病原微生物的入侵,使乳房内的微生物种类增多而导致的。

Fibrinogen deficiency suppresses the development of early and delayed radiation enteropathy

To determine the mechanistic role of fibrinogen, a key regulator of inflammation and fibrosis, in early and delayed radiation enteropathy. METHODSFibrinogen wild-type (Fib+/+), fibrinogen heterozygous (Fib+/-), and fibrinogen knockout (Fib-/-) mice were exposed to localized intestinal irradiation and assessed for early and delayed structural changes in the intestinal tissue. A 5-cm segment of ileum of mice was exteriorized and exposed to 18.5 Gy of x-irradiation. Intestinal tissue injury was assessed by quantitative histology, morphometry, and immunohistochemistry at 2 wk and 26 wk after radiation. Plasma fibrinogen level was measured by enzyme-linked immunosorbent assay. RESULTSThere was no difference between sham-irradiated Fib+/+ and Fib+/- mice in terms of fibrinogen concentration in plasma and intestinal tissue, intestinal histology, morphometry, intestinal smooth muscle cell proliferation, and neutrophil infiltration. Therefore, Fib+/- mice were used as littermate controls. Unlike sham-irradiated Fib+/+ and Fib+/- mice, no fibrinogen was detected in the plasma and intestinal tissue of sham-irradiated Fib-/- mice. Moreover, fibrinogen level was not elevated after irradiation in the intestinal tissue of Fib-/- mice, while significant increase in intestinal fibrinogen level was noticed in irradiated Fib+/+ and Fib+/- mice. Importantly, irradiated Fib-/- mice exhibited substantially less overall intestinal structural injury (RIS, P = 0.000002), intestinal wall thickness (P = 0.003), intestinal serosal thickness (P = 0.009), collagen deposition (P = 0.01), TGF-β immunoreactivity (P = 0.03), intestinal smooth muscle proliferation (P = 0.046), neutrophil infiltration (P = 0.01), and intestinal mucosal injury (P = 0.0003), compared to irradiated Fib+/+ and Fib+/- mice at both 2 wk and 26 wk. CONCLUSIONThese data demonstrate that fibrinogen deficiency directly attenuates development of early and delayed radiation enteropathy. Fibrinogen could be a novel target in treating intestinal damage.

Plasma biomarker screening for liver fibrosis with the N-terminal isotope tagging strategy

A non-invasive diagnostic approach is crucial for the evaluation of severity of liver disease,treatment decisions,and assessing drug efficacy.This study evaluated plasma proteomic profiling via an N-terminal isotope tagging strategy coupled with liquid chromatography/Fourier transform ion cyclotron resonance mass spectrometry measurement to detect liver fibrosis staging.Pooled plasma from different liver fibrosis stages,which were assessed in advance by the current gold-standard of liver biopsy,was quantitatively analyzed.A total of 72 plasma proteins were found to be dysregulated during the fibrogenesis process,and this finding constituted a valuable candidate plasma biomarker bank for follow-up analysis.Validation results of fibronectin by Western blotting reconfirmed the mass-based data.Ingenuity Pathways Analysis showed four types of metabolic networks for the functional effect of liver fibrosis disease in chronic hepatitis B patients.Consequently,quantitative proteomics via the N-terminal acetyl isotope labeling technique provides an effective and useful tool for screening plasma candidate biomarkers for liver fibrosis.We quantitatively monitored the fibrogenesis process in CHB patients.We discovered many new valuable candidate biomarkers for the diagnosis of liver fibrosis and also partly identified the mechanism involved in liver fibrosis disease.These results provide a clearer understanding of liver fibrosis pathophysiology and will also hopefully lead to improvement of clinical diagnosis and treatment.