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1.
A six-year-old arabian stallion was admitted to The Ohio State University Veterinary Hospital for evaluation and repair of a comminuted fracture of the second phalanx. The horse developed impaired arterial oxygenation during surgey and pulmonary edema post-operatively. We postulate that impaired arterial oxygenation resulted from atelectasis of the dependent lung during annesthesia, and the pulmonary edema occurred following re-expansion of the atelectatic of the initiating cause of the edema, removal of excess lung water from the alveoli, and restoration of normal arterial oxygenation. The horse was fully recovered within 12 hours of initiation of clinical signs of respiratory compromise. The horse was fully recovered within 12 hours of initiation of clinical signs of respiratory compromise. This report describes re-expansion pulmonary edema due to reperfusion injury in a horse, treatment of the condition, and a possible explanation of the pathogenesis of this pulmonary pathology.  相似文献   
2.
A 3-year-old neutered female mixed breed dog was examined because of severe, generalized seizure activity, tetraparesis, and encephalopathic signs. Cerebrospinal fluid (CSF) evaluation was unremarkable except for a mild increase in protein. Serum and CSF titers for infectious diseases were negative. Magnetic resonance (MR) imaging examination of the brain was performed and lesions were found within the cerebral gray matter of the temporal and parietal lobes. The lesions had increased signal intensity on T1, T2, and proton density-weighted images. There was mild inhomogeneous enhancement following intravenous contrast medium administration. Neurologic status improved and the seizures were well controlled, but the dog never regained normal mentation and euthanasia was performed 10 weeks after initial evaluation. At necropsy, severe cerebral cortical necrosis was found in the regions corresponding to the lesions seen on MR imaging examination. Large numbers of fat-containing macrophages (gitter cells) were found within these areas, and are thought to be responsible for the characteristic hyperintensity seen on the MR images.  相似文献   
3.
猪大肠杆菌水肿毒素SLT-IIeA基因的克隆和序列分析   总被引:2,自引:0,他引:2  
研究以本地猪水肿病大肠杆分离物ED1株为材料 ,利用 PCR克隆了含猪水肿病大肠杆菌 (VTEC) slt-IIe A基因 987bp的片段 ,并测定了含该克隆片段的 Bam HI、Hind 酶切片段的核苷酸序列。结果表明 ,slt-IIe A基因的编码区全长 960 bp,编码 3 1 9个氨基酸的蛋白质 ,序列与国外报导的 S1 1 79株进行比较发现其核苷酸同源性为 98.9%。经推导的氨基酸序列的同源性为 99.7%。这为进一步研究 slt-IIe A的生物学特性、水肿病的分子诊断及其防制打下基础  相似文献   
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目的探讨血浆D-二聚体(D-dimer,D-D)及超敏C反应蛋白(high-sensitivity C-reactive protein,hs-CRP)水平与急性脑梗死(acute cerebral infarct,ACI)的关系。方法采用免疫透射比浊法检测102例ACI患者和50例正常对照者血浆D-D和hs-CRP水平。根据梗死灶大小102例ACI患者分为大梗死灶组、中梗死灶组和小梗死灶组,并进行相关统计分析。结果 ACI组患者血浆D-D和hs-CRP水平显著高于正常对照组(P0.01);大梗死灶组D-D和hs-CRP水平明显高于中、小梗死灶,而中梗死灶组D-D和hs-CRP水平高于小梗死灶组。结论监测血浆D-D和hs-CRP能为ACI的临床诊断、病情判断提供重要的参考依据。  相似文献   
6.
Glutamate induces neuronal damage by generating oxidative stress and neurotoxicities. The neurological damage caused by glutamate is more severe during brain development in newborns than in adults. Resveratrol is naturally present in a variety of fruits and medicinal plants and exerts a neuroprotective effect against brain damage. The goal of this study was to evaluate the neuroprotective effects of resveratrol and to identify changed proteins in response to resveratrol treatment during glutamate-induced neonatal cortical damage. Sprague-Dawley rat pups (7 days old) were randomly divided into vehicle, resveratrol, glutamate, and glutamate and resveratrol groups. The animals were intraperitoneally injected with glutamate (10 mg/kg) and/or resveratrol (20 mg/kg) and their brain tissue was collected 4 hr after drug administration. Glutamate exposure caused severe histopathological changes, while resveratrol attenuated this damage. We identified regulated proteins by resveratrol in glutamate-induced cortical damaged tissue using two-dimensional gel electrophoresis and mass spectrometry. Among identified proteins, we focused on eukaryotic initiation factor 4A2, γ-enolase, protein phosphatase 2A subunit B, and isocitrate dehydrogenase. These proteins decreased in the glutamate-treated group, whereas the combination treatment of glutamate and resveratrol attenuated these protein reductions. These proteins are anti-oxidant proteins and anti-apoptotic proteins. These results suggest that glutamate induces brain cortical damage in newborns; resveratrol exerts a neuroprotective effect by controlling expression of various proteins with anti-oxidant and anti-apoptotic functions.  相似文献   
7.
王昱  秦序  何九军 《中国畜牧兽医》2021,48(10):3864-3871
试验旨在探讨白肉灵芝水提物(Ganoderma leucocontextum aqueous extracts,GLAE)对脑缺血后海马神经元的保护作用及机制。将50只健康大鼠分为对照组、模型组、GLAE低(0.05 mg/(g·BW))、中(0.1 mg/(g·BW))、高(0.2 mg/(g·BW))剂量组。利用双侧颈总动脉夹闭法建立大鼠脑缺血模型,GLAE组灌胃不同剂量的GLAE干预,对照组和模型组灌胃同体积的生理盐水,连续2周。用跳台试验方法检测记忆获得、记忆巩固和记忆再现障碍大鼠的学习记忆能力,HE染色观察大鼠海马组织的病理形态的变化,比色法检测海马组织一氧化氮合酶(nitric oxide synthase,NOS)活性和一氧化氮(nitric oxide,NO)含量,Western blotting和实时荧光定量PCR法分别检测海马组织生长相关蛋白-43(growth associated protein-43,GAP-43)和脑源性神经生长因子(brain derived neurotrophic factor,BDNF)的水平。结果显示,与对照组相比,模型组大鼠跳台试验的逃避潜伏期显著缩短、电击次数显著增加(P<0.05);海马神经元细胞出现明显核固缩、排列松散紊乱等退行性改变,细胞数量显著减少(P<0.05);海马组织NOS活性和NO含量均显著降低(P<0.05);大鼠海马组织GAP-43蛋白表达量显著升高(P<0.05);海马组织BDNF mRNA表达量显著下调(P<0.05)。与模型组相比,GLAE干预后,大鼠逃避潜伏期均显著延长、电击次数均显著减少(P<0.05);GLAE高剂量组大鼠CA1区和齿状回锥体神经元细胞形态明显改善,神经元数量显著增加(P<0.05);GLAE低剂量组对NOS活性影响不明显(P>0.05),显著增加NO含量(P<0.05),GLAE中、高剂量组NOS活性和NO含量均显著升高(P<0.05);GLAE低、中、高剂量组海马组织GAP-43蛋白表达量均显著增加(P<0.05);GLAE低、中、高剂量组海马组织BDNF mRNA表达量均显著增加(P<0.05)。以上结果表明,GLAE可通过提高NOS活性和NO水平、促进海马神经发生和功能恢复对脑缺血后海马神经元损伤有一定的保护作用,从而改善大鼠认知功能,0.2 mg/g GLAE效果最好。  相似文献   
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9.
A new method is introduced to measure the conductivity of brain. This method uses magnetic excitation to induce eddy currents inside the brain matter and measures the magnetic field caused by the induced eddy current. The theoretical basis of this method is analyzed and the measurement system is introduced. The aufhors do the experiment and draw a conclusion that the method provided is feasible.  相似文献   
10.
Objective: To review the clinical and pathophysiologic aspects of acute respiratory distress syndrome (ARDS) in dogs and cats. Data sources: Data from human and veterinary literature were reviewed through Medline and CAB as well as manual search of references listed in articles pertaining to acute lung injury (ALI)/ARDS. Human data synthesis: Since the term ARDS was first coined in 1967, there has been a abundance of literature pertaining to this devastating syndrome in human medicine. More complete understanding of the complex interactions between inflammatory cells, soluble mediators (e.g., tumor necrosis factor, interleukin (IL)‐6, IL‐8, platelet activating factor) and the clinical patient has provided for timely recognition and mechanistically based protective strategies decreasing morbidity and mortality in human patients with ARDS. Veterinary data synthesis: Although little is known, ARDS is becoming a more commonly recognized sequela in small animals. Initial case reports and retrospective studies have provided basic clinical characterization of ARDS in dogs and cats. Additionally, information from experimental models has expanded our understanding of the inflammatory mechanisms involved. It appears that the inflammatory processes and pathologic changes associated with ARDS are similar in dogs, cats, and humans. Conclusions: Unfortunately, current mortality rates for ARDS in small animals are close to 100%. As our capability to treat patients with advanced life‐threatening disease increases, it is vital that we develop a familiarity with the pathogenesis of ARDS. Understanding the complex inflammatory interactions is essential for determining effective preventative and management strategies as well as designing novel therapies for veterinary patients.  相似文献   
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