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191.
为进一步探究鸭肠炎病毒(duck enteritis virus,DEV)的致病机理,试验采用鸭蛋白激酶C (protein kinase C,PKC)的抑制剂星形孢菌素(staurosporine,SP)和激活剂佛波醇(phorbol-12-myristate-13-acetate,PMA)研究PKC/PKCI能否对DEV的增殖产生影响,为阐述DEV致病机理提供新的思路。用SP/PMA处理正常鸭胚成纤维细胞(duck embryo fibroblast,DEF)后,实时荧光定量PCR方法检测不同时间段PKC/PKCI基因表达;用DEV病毒液感染SP/PMA处理的DEF后,收集不同时间段培养物,以Reed-Muench法计算DEV半数组织培养感染量(TCID50)值,实时荧光定量PCR方法检测分析DEV NP基因转录水平。结果显示,SP处理对宿主细胞PKC/PKCI基因表达水平无显著影响(P>0.05);而PMA处理可极显著提高宿主细胞PKC基因表达(P<0.01),但对PKCI基因表达水平无显著影响(P>0.05);SP/PMA处理对DEV复制能力影响显著(P<0.05;P<0.01),且在感染前期可显著或极显著降低DEV NP基因的转录水平(P<0.05;P<0.01)。综上所述,SP和PMA对PKC、PKCI基因表达水平的影响效果不同,且都能有效抑制DEV增殖,本试验结果可为DEV的防控及其致病机理的研究提供基础资料。  相似文献   
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Considering market demands concerning the decreased use of growth promoters and anticoccidial drugs in feed formulations, the poultry industry has been trying to reduce or eliminate the inclusion of subtherapeutic doses of antimicrobials into feed. Formulating diets not only to meet birds’ nutrient requirements for growth but also for gastrointestinal health parameters is increasingly important. Maintenance and enhancement of intestinal integrity is essential for bird performance when antimicrobials are not included in feed, as commercial poultry face numerous enteric pathogen challenges. Necrotic enteritis has reemerged as an important disease of poultry in recent years. The reduction in the use of antimicrobials in poultry feeds has been attributed as one of the main contributing factors for the increasing incidence of necrotic enteritis (NE) in commercial poultry. Mortality due to NE is extremely high (1% daily mortality), which results in great economic losses. Economic losses due to NE are not only associated with high mortality, but also associated with decreases in bird performance and FE, particularly in subclinical cases of NE. Birds that survive NE outbreaks usually have a reduced ability to digest and absorb nutrients due to extensive damage to the mucosal lining, which ultimately results in reduced profitability.  相似文献   
194.
Necrotic enteritis is an acute gastrointestinal infectious disease with high morbidity and mortality which caused by Clostridium perfringens. The disease not only harms the livestock health and animal welfare,but also has been an emerging threat for breeding industry and human health. Antibacterial drugs played a positive role on preventing this disease,however,drug-resistant strains were increasing with irrational use of antibiotics,the incidence of necrotic enteritis has drastically increased, prevention and treatment of it faced severe challenges. The author reviewed the characteristics of necrotic enteritis include the etiology,physicochemical properties, epidemiology and clinical signs,at the same time, the control measures and common drugs were summarized,and the new development trend and direction for prevention and treatment necrotic enteritis was objective analyzed, aiming to establish a comprehensive understanding of the disease,provide references for prevention and treatment of the disease.  相似文献   
195.
为筛选出鸭肠炎病毒(DEV)gC糖蛋白胞外区的优势抗原表位,本试验通过抗原表位作图法对DEV-gC基因进行分段克隆并构建重组表达载体,表达蛋白经纯化后进行Western blot分析。结果显示,经过4轮筛选,DEV-gC糖蛋白优势抗原表位为第73-88位氨基酸。该优势表位的发现为DEV-gC糖蛋白具体功能区的研究、诊断试剂及表位疫苗的研制奠定了物质基础。  相似文献   
196.
犬肠炎型细小病毒病,是犬类第二烈性传染病,以剧烈呕吐和出血性腹泻为特征。近年来,给养犬业造成了严重的危害。2010年7月20日,一只两月龄黑色小藏犬来就诊,根据病史调查、临床症状和实验室检查确诊为犬肠炎型细小病毒病,同时并发肠道线虫病。采取了中和病毒、抗茵消炎、驱除寄生虫、止吐、止泻和止血等综合治疗方案,获得了良好的治疗效果。  相似文献   
197.
The present study revealed several previously not recognized etiological details in the development of necrotic enteritis (NE) in broilers. We provide evidence that the pathological process leading to mucosal epithelium necrosis follows morphologically distinct phases commencing at the basal domain of the mucosal epithelium and then progressively invading the entire lamina propria. Initially mucosal epithelium appears normal, but as the pathological changes progress throughout the lamina propria, the adjacent enterocytes begin to show features of necrotic cell death and the necrotic process of the epithelium progresses from being focal to locally extensive.Ultra-structural examination showed that primary changes occur at the level of basal and lateral domains of the enterocytes, whereas the apical domain of enterocytes remains intact even in the face of advanced necrotic changes. This indicates that the mucosal necrosis does not result from direct damage to the mucosal epithelium. Rather, the necrotic death of enterocytes is a consequential effect of the destruction of lamina propria, the extra-cellular matrix, and intercellular junctions.The nature of these morphological changes indicates that initiation of the pathological process leading to NE involves proteolytic factors affecting the extra-cellular matrix and cellular junctions. Further studies revealed that, indeed, the elevated activity of collagenolytic enzymes in the mucosal milieu and in intestinal tissue represents an integral component of the pathological process leading to NE. In the first instance we discovered that Clostridium perfringens strains isolated from field cases of NE secrete several potent collagenolytic enzymes. In the second instance we observed that, in comparison to controls, broilers challenged with C. perfringens isolated from field cases of NE show high levels of several collagenolytic enzymes in the intestinal tissue. A major component of the overall collagenolytic activity detected in the intestinal tissue was identified by zymography as matrix metalloproteinases (MMPs). Dominant activity was associated with MMP-2. We confirmed using immuno-histochemistry that this enzyme is expressed at high levels in mucosal tissue showing signs of NE.The high levels of collagenolytic activities, in particular associated with MMP-2, demonstrated in our studies are consistent with the nature of morphological changes observed primarily in extra-cellular matrix (ECM) at the basal domain of enterocytes, as well lateral domains of enterocytes. The lack of changes at the level of apical domain of mucosal epithelium indicates that the lipolytic aspect of alpha toxin in NE is not an essential factor in primary lesions development. Taken together, our findings indicate that the early lesions leading to NE are associated with virulence factors that induce proteolytic activity, rather than lipolytic activity.  相似文献   
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199.
人工感染鸭病毒性肠炎急性病例超微结构变化   总被引:1,自引:0,他引:1  
用鸭病毒性肠炎病毒(Duck enteritis virus,DEV)CH强毒株感染成年鸭复制鸭病毒性肠炎急性病例,分别于接种后不同时间,取心、肝、肾、脾、胸腺、十二指肠、法氏囊、脑和胰组织,制作超薄切片,电镜观察。结果表明:病变最早发生于肝和肾,而鸭死亡后以免疫器官和消化器官损伤最严重;各种细胞的变化主要表现为细胞肿胀,染色质或浓缩、碎裂或溶解,线粒体溶解成空泡样结构,其他细胞器破坏;脾、胸腺、法氏囊以及小肠固有层中的淋巴细胞在感染24h后,在出现细胞坏死的同时还出现较为明显的细胞凋亡变化;而鸭死亡后淋巴细胞主要表现为黑洞核样变化,整个细胞凝聚深染,染色质固缩,细胞浆均质深染,细胞膜模糊或不完整。  相似文献   
200.
CASE HISTORY: A retrospective study was conducted to investigate 11 outbreaks of presumptive fatal adenovirus infection diagnosed through two New Zealand diagnostic laboratories during 2014 and 2015. Outbreaks occurred in 6–12-month-old Friesian or Friesian cross cattle during autumn, winter and spring. Individual outbreaks were short in duration, with mortality rates ranging from 3/250 to 20/600 (1.2 to 3.3%).

CLINICAL AND PATHOLOGICAL FINDINGS: Clinical signs included severe diarrhoea, depression, recumbency, and death. Post-mortem examination revealed congestion and oedema of the alimentary tract and fluid to haemorrhagic intestinal contents. Histopathological lesions were characterised by congestion and haemorrhage of the alimentary tract mucosa, oedema of the submucosa, and mild interstitial inflammation in the kidneys. Large basophilic intranuclear inclusion bodies were identified in vascular endothelial cells of the alimentary tract in 11/11 cases and of the kidney in 8/9 cases.

MOLECULAR TESTING: A real-time quantitative PCR (qPCR) assay was designed to detect bovine adenovirus type 10 (BAdV-10) using hexon gene sequences available in GenBank. DNA extracted from a field case and confirmed by sequencing was used as a positive control. The qPCR had a reaction efficiency of 101% (R2=0.99) and the limit of detection was <10 DNA copies/reaction. The qPCR detected BAdV-10 in formalin-fixed paraffin-embedded (FFPE) tissue from 10/11 cases. DNA sequencing of PCR products from nine of these cases showed them to be identical to BAdV-10 sequences in GenBank. For the PCR-negative case, the PCR product had a hexon sequence 99% similar to bovine adenovirus Wic isolate Ma20-1, a close relative of BadV-10.

DIAGNOSIS: Bovine adenovirus type 10 was identified in FFPE tissues from cattle with histopathological evidence of adenovirus infection.

CLINICAL RELEVANCE: Bovine adenoviruses, and especially BAdV-10, should be considered in the differential diagnosis for acute enteric disease and death in young cattle. The qPCR detected BAdV-10 from FFPE tissue of cattle with suspected adenoviral infection diagnosed by histopathology. However results should be interpreted in light of clinical and pathological findings due to the possibility of adenovirus shedding by healthy cattle and the presence of pathogenic adenoviruses other than BAdV-10.  相似文献   

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