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1.
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。  相似文献   
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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.  相似文献   
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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), P22phox and P47phox 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 P22phox and P47phox 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.  相似文献   
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Objective: To describe diagnostics, therapy, and sequelae of acute carbon monoxide (CO) toxicity because of a motor vehicle generator in 4 dogs and 2 cats. Series summary: Four dogs and 2 cats presented for recumbency, disorientation, dyspnea, and stiffness after an estimated 6–8 hour exposure to exhaust from a generator. Diagnostics included a serum carboxyhemoglobin levels evaluation, arterial blood gas analysis, pulse oximetry readings, and blood pressure measurements. Initial therapy included oxygen (O2) administration, intravenous bronchodilators, fluids, and a hemoglobin‐based O2 carrying (HBOC) molecule. Following administration of the HBOC, 4 of the 6 animals showed dramatic clinical improvement. Two weeks after hospital discharge, the owner reported potential hearing deficits in all animals. Brain auditory evoked response (BAER) tests were conducted in all surviving animals and some degree of hearing impairment was documented in all cases, with complete clinical resolution noted 6 weeks later. Unique information provided: This report describes the therapeutic use of an HBOC in acute isolated CO toxicity (i.e. without the complications of smoke inhalation). In addition, delayed nervous system dysfunction was documented in all surviving animals.  相似文献   
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Ventricular relaxation is altered in a number of cardiac disorders affecting domestic animals. Clinical determination of the ventricular relaxation rate can provide useful information regarding disease severity and response to therapy. We believe that the current gold standard for assessing left ventricular relaxation requires measurement of ventricular luminal pressure at end-expiration using a high-fidelity catheter. Ventricular pressure should be digitized at ≥200 Hz for the period of pressure fall between the minimum rate of change of ventricular pressure and 10 mm Hg above left ventricular end-diastolic pressure of the preceding beat. The rate of relaxation then should be determined from the digitized data by Marquardt nonlinear least squares parameter estimation using an exponential decay model with nonzero asymptote. The major disadvantage in using an invasive method for evaluating left ventricular relaxation is that it requires general anesthesia in animals that frequently are categorized as high-risk anesthetic patients. Noninvasive estimates of ventricular relaxation using echocardiographic parameters such as isovolumic relaxation time, peak early filling rate, and time from end-systole to peak filling rate provide a crude and nonspecific assessment of ventricular relaxation that can be obtained from conscious animals. Determinations of these echocardiographic indices are of limited usefulness in assessing changes in ventricular relaxation associated with disease progression or therapeutic intervention, unless concurrent estimates of left atrial pressure, mitral valve characteristics, and left ventricular compliance are available.  相似文献   
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