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AIM:To investigate the effect of the heat shock response on the reperfusion arrhythmias(RAs) and the possible mechanism involved. METHODS:Fifty-five Sprague Dawley rats were randomly divided into 2 groups: the heat shock group (group H,n=29) and the control group (group C,n=26). The rats in group H were preconditioned with heat shock 24 hours before, and that in group C were not. The hearts of 16 rats in group H and 16 in group C were exercised and mounted on a non-circulating Langendorff perfusion apparatus and perfused retrogradely with modified K-H buffer and mimic ischemia/reperfusion was applied. Additionally, conventional intracellular microelectrode techniques were used for recording such electrophysiological parameters as resting potential(RP), action potential amplitude(APA), over shot(OS), maximum depolarization velocity(Vmax) of the hearts of other 13 rats in group H and 10 in group C. RESULTS:①Prior heat stress significantly decreased reperfusion arrhythmia. ②The amount of CK release in the effluent in group H was much less than that in group C. ③Myocardial HSP70 content was elevated significantly in group H. ④Heat stress significantly increased myocardial anti-oxydases activity and decreased lipid peroxydative products. Additionally, heat stress significantly reduced the Vmax of action potential. It indicated that rapid Na+ channel of papillary muscles may be inhibited by heat shock. The degree of change of Vmax after ischemia in H group was significantly less than that in group C. And the time of reperfusoin with Tyrode's solution till the action potential appeared as large as that before perfusion with mimic ischemic solution is shorter in group H than in group C. CONCLUSION:Heat shock pretreatment markedly reduces ischemia/reperfusion-induced injury of heart and ventricular arrhythmias in rats and this effect may be associated with the inhibition of rapid Na+ channel of papillary muscles by heat shock and the increase in myocardial HSP70 and anti-oxydase activity. 相似文献
33.
CHEN Xiao-yin ZHANG Qun YANG Qin-he XIE Qiu-ling SHEN Qiang XU Yun-sheng 《园艺学报》2002,18(12):1529-1531
AIM: To examine the effect of traditional chinese medicine recipe, Taoren Honghua(semen persicae-flos carthami) decoction, on hyperlipidemia without symptom. METHODS: The plasma TC, TG, LDL, HDL, apolipoprotein(Apo) A, Apo Bof the patients with hyperlipidemia without symptom were measured using automatic analyzer (shimadiu CL-7200), the production of nitric oxide(NO) was detected by Greiss reaction, and SODactivity and MDAformation were examined using o-trihydroxy benzene and barbituric methotheds, respectively. RESULTS: After oral administration of Taoren Honghua decoction, the plasma levels of TC, TG, LDL, and MDAof the patients were markedly decreased, however, the plasma levels of ApoA, HDL, SODand NOwere significantly increased and almost no change was detected in the plasma level of Apo B. In control group, it was found that although the plasma level of TC, TG and LDL were decreased ( P<0.05 ) and ApoAas well as HDLwere increased, ApoB, SOD, MDA and NO production were all unchanged. CONCLUSION: The traditional chinese medicine recipe, Taoren Honghua decoction,has a significant therapeutic effect on patients with hyperlipidemia by removing blood stasis, promoting qi circulation and in turn reducing blood lipid level. 相似文献
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引进丹麦先进仪器FAT—O—MEAT’ER(肉脂仪)对中国鲁梅克斯食品总公司名山县屠宰场中5821头猪进行了现场测定,测量性状为最后一根肋骨处离背中线4~5cm处的膘厚(P2)和倒数第三、四根肋骨之间,离背中线4—5cm处的膘厚(RF)以及眼肌厚度(RM),并估测出瘦肉率。对所测胴体各性状的均数和相关性分析,表明本地商品肉猪胴体质量低于国外水平。 相似文献
36.
雾培法根际CO2对马铃薯生长和光合作用的影响 总被引:13,自引:0,他引:13
通过汽雾栽培方式对马铃薯根际连续 35d的CO2 处理表明 :温室大气处理 (CO2 380~ 92 0 μL·L-1 O2 2 1% )和室外大气处理 (CO2 380 μL·L-1 O2 2 1% )马铃薯植株的形态特征非常接近 ,其株高、叶面积、根系质量、匍匐茎数量、块茎产量以及生物量均比根际高CO2 处理 (CO2 36 0 0 μL·L-1 O2 2 1% )明显提高 ,叶片的气孔导度和胞间CO2 浓度增加 ,光呼吸速率与CO2 补偿点降低 ,叶片光系统Ⅱ功能改善 ,光合速率提高 ,植株生长发育旺盛 ,块茎产量增加 ,说明合适的根际CO2 浓度 (CO2 380~ 92 0 μL·L-1 O22 1% )可能是汽雾栽培马铃薯植株生长旺盛的重要原因 相似文献
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AIM: To investigate the role of nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC) and protein kinase C (PKC) signaling in tumor necrosis factor-α (TNF-α)-induced cardioprotection against hypoxia/reoxygenation (H/R) injury. METHODS: Neonatal rat ventricular myocytes were pretreated with TNF-α or sodium nitroprusside (SNP) or L-arginine (L-Arg), respectively, for 12 h and then subjected to continuous hypoxia for 12 h, followed by reoxygenation for 6 h. The manganese superoxide dismutase (Mn-SOD) activity of the cells was measured after H/R. Myocyte injury was determined by the release of lactic dehydrogenase (LDH). RESULTS: TNF-α (105 U/L) significantly increased the Mn-SOD activity and decreased release of LDH from ventricular myocytes. The cardioprotection against H/R injury was induced by the pretreatment with SNP (5 μmol/L) or L-Arg (5 mmol/L), which was blocked by ODQ (10 μmol/L), the specific sGC inhibitor, and Chel (5 μmol/L), the specific PKC inhibitor. Pretreatment with L-NAME (100 μmol/L), ODQ, Chel, antoxidant 2-MPG (400 μmol/L) or tyrosine kinase inhibitor genistein (50 μmol/L) attenuated the increased Mn-SOD activity and reduced LDH level induced by TNF-α. CONCLUSION: The results suggest that NO may play a role in TNF-α-induced cardioprotection, which is mediated by sGC and PKC. 相似文献
39.
LIU Nian NIU Hui-yan LI Yang ZHANG Cun-tai ZHOU Qiang RUAN Yan-fei PU Jun LU Zai-ying 《园艺学报》2004,20(12):2227-2231
AIM: To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), and to investigate the changes of action potential duration (APD),transient outward potassium current (Ito), delayed rectifier potassium current (IK) and inward rectifier potassium current (IK1) of left ventricular myocytes in noninfarcted zone of HMI. METHODS: 12 rabbits were randomly assigned in two groups: HMI group (thoracotomy and ligation of the circumflex coronary); sham-operated group (thoracotomy but no conorary ligation). 3 months after operation, whole cell patch clamp technique was used to record APD, Ito, IK and IK1 of ventricular myocytes in non-infarcted zone. RESULTS: Membrane capacitance was larger in HMI group than that in sham-operated group. Action potential duration was lengthened significantly in HMI group and early after depolarization (EAD) appeared in HMI group. The densities of Ito, IK,tail and IK1 were reduced significantly in HMI group (P<0.01), from (6.72±0.42) pA/pF, (1.54±0.13) pA/pF and (25.6±2.6) pA/pF in Sham-operated group to (4.03±0.33) pA/pF, (1.14±0.11) pA/pF and (17.6±2.3) pA/pF, respectively. CONCLUSION: The reduced densities of Ito, IK,tail and IK1 in ventricular myocytes of non-infarcted zone in HMI are responsible for the prolongation of APD and the presentation of EAD, which play important roles in the malignant arrhythmia of HMI. 相似文献
40.