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Valentine BA de Lahunta A Divers TJ Ducharme NG Orcutt RS 《Journal of the American Veterinary Medical Association》1999,215(11):1661-5, 1621
Two Belgian geldings, 4 and 14 years old, respectively, with muscle atrophy, weakness, and abnormal gait characteristic of severe advanced shivers were examined clinically and on necropsy. Neurologic examination revealed no evidence of ataxia, and the clinical diagnosis was neuromuscular weakness and shivers. Necropsies of both horses, including examination of pituitary, brain, spinal cord, spinal roots and ganglia, and peripheral nerves, revealed no gross or histologic abnormalities. Examination of multiple skeletal muscle specimens revealed chronic myopathic changes and periodic acid-Schiff positive, amylase-resistant inclusions within muscle fibers, characteristic of equine polysaccharide storage myopathy. It is suggested that underlying metabolic myopathy may be the cause of muscle weakness and cramping in horses with shivers. 相似文献
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Polysaccharide storage myopathy is an equine neuromuscular disorder characterized by accumulation of glycogen-related polysaccharide inclusions within skeletal muscle fibers. The pathologic criteria for diagnosis of this disorder are somewhat controversial; however, periodic acid-Schiff-positive, amylase-resistant inclusions are considered pathognomonic. Although these inclusions are most often found in affected horses related to the Quarter Horse, draft horse, and Warmblood breeds, this report describes these characteristic inclusions in muscle of five horses from nonrelated breeds (two Morgans, one Arabian, one Arabian x Thoroughbred, and one Standardbred) and two Welsh cross ponies. Affected horses had histories of recurrent exertional rhabdomyolysis, and one developed progressive weakness leading to increased recumbency. The affected ponies were part of an unrelated research project and had no apparent clinical signs. 相似文献
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利用RT-PCR方法扩增了猪ERK6基因编码区的序列,将扩增产物与pMD18-T载体连接,构建了重组质粒;重组质粒经PCR、酶切鉴定后进行测序;采用Northern杂交和半定量RT-PCR方法在猪不同部位骨骼肌中分析了ERK6基因转录本的个数、大小及组织表达谱。结果显示,所克隆的猪ERK6基因片段长1113bp,含有1个1104bp的开放阅读框(ORF),该ORF编码367个氨基酸;该基因与已报道的人ERK6基因核苷酸序列相似性为90%;猪ERK6基因在肌肉组织中只有一个转录本,大小约1.5kb。此基因在骨骼肌中的表达量最高,心、子宫次之,卵巢最低;而在脂肪、胃、肝、脾、肺、肾、十二指肠和胰腺中未见表达。结果表明,猪ERK6基因与已报道的小鼠和人ERK6基因一样,主要在骨骼中特异表达。 相似文献
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Beth A Valentine Wilson K Rumbeiha Terry S Hensley Richard R Halse 《Journal of veterinary diagnostic investigation》2007,19(2):212-215
Over a 12-day period, 13 animals in a herd of 110 beef cattle developed ataxia with profound muscle fasciculations progressing to recumbency. Twelve animals (5 adults and 7 calves from 8-10 months of age) died, and 1 cow was euthanized. Hemorrhagic diarrhea occurred in some, but not all, animals. The onset of clinical signs was at least 12 hours after the cattle had gained access to contents of old buildings used for storage, and the majority of deaths occurred within 24 to 48 hours after the onset of clinical signs. Approximately 9 kg of unidentified pellets were found strewn in the barn area where the cattle had been. Autolysis considered more severe than expected for the postmortem interval, suggestive of high body temperature before death, and congestion of body tissues were the only significant findings detected in the cow that was euthanized and submitted for necropsy examination. The clinical history and lack of postmortem lesions were most consistent with toxicity. A toxic level of arsenic (6.18 ppm) was detected in the kidney, and metaldehyde was detected in the liver. The pellets were analyzed and found to contain both arsenic and metaldehyde, consistent with a discontinued molluscicidal product. 相似文献
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A Syndrome Resembling Idiopathic Noncirrhotic Portal Hypertension in 4 Young Doberman Pinschers 总被引:1,自引:0,他引:1
JoAnn DeMarco Sharon A. Center Nathan Dykes Amy E. Yeager Bruce Kornreich Ed Gschrey Kelly A. Credille Magali Guffroy Fabio del Piero Beth A. Valentine 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》1998,12(3):147-156
We describe 4 young male Doberman Pinschers (3 littermates and 1 unrelated dog) with a syndrome resembling idiopathic or noncirrhotic portal hypertension of humans. Each dog was evaluated for a hepatopathy resulting in portal hypertension, development of portosystemic collateral vessels, and hepatic encephalopathy. These dogs differ from previous reports of young dogs with hepatic insufficiency associated with portal hypertension and acquired portal systemic shunting by their lack of intrahepatic arteriovenous fistulae, portal vein atresia, or intrahepatic fibrosis. Clinicopathologic features included erythrocyte microcytosis, normal to mildly increased liver enzyme activities, increased concentrations of serum bile acids, reduced plasma indocyanine green clearance, and normal total bilirubin concentration. Abdominal ultrasonography disclosed a small liver and portosystemic collateral vessels. Radiographic imaging studies confirmed hepatofugal portal circulation and discounted hepatic arteriovenous fistulae. Histopathologic features in liver tissue from each dog were similar and consistent in all sections examined. Common findings included increased cross-sectional views of hepatic arterioles; hepatic lobular atrophy; scanty increase in connective tissue around some large portal triads; and absence of inflammation, disturbed lobular architecture, bile duct proliferation, or intrahepatic cholestasis. 相似文献