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991.
AIM:To observe the influence of transection of the cervical sympathetic track (TCST) on the content of NO and the expression of eNOS mRNA and iNOS mRNA in placenta of the rats with pregnancy-induced hypertension syndrome (PIH).METHODS: Pregnant Wistar rats were randomly divided into 5 groups: control group (C): saline was injected subcutaneously from 14th day to 20th day of gestation;PIH group 1 (H1) and group 2 (H2): L-NAME was respectively injected with 125 mg/kg and 62.5 mg/kg,respectively,then the other procedures were the same as group C;Operation group (O): TCST was operated on 14th day of the gestation,then the other procedures were the same as group H1;sham operation group (S): the cervical sympathetic trunk was only separated and exposed on 14th day of the gestation,then the other procedures were the same as group H1.RESULTS: (1) Except the base value of the BP and protein in urine of the pregnant rats,all the parameters observed in group H1 and H2 were higher than those in group C significantly (P<0.01),and in group H2 were lower than those in group B1 markedly (P<0.01).(2) In comparison with those in group C,the size and body weigh of fetus in group H1,H2 decreased markedly (P<0.01).The above indexes in group H1 were lower than those in group H2 markedly (P<0.01,P<0.05).The changes of the rate of embryo absorption and fetal death,and deformity rate of the fetal rats were contrary to the above indexes.(3) The content of NO and the expression of eNOS mRNA and iNOS mRNA in placenta in group H1 and H2 were lower than those in group C markedly (P<0.01).Those in group H1 were lower than those in group H2 obviously (P<0.01,P<0.05).Those in group O were higher than those in group H1 markedly (P<0.01).CONCLUSION: TCST protects pregnant rats against PIH,and it was related to the mRNA expression of eNOS and iNOS and the content of NO in placenta tissue. 相似文献
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以网状内皮增生症病毒(REV)和禽白血病病毒J亚群(ALV-J)单一感染和共感染1日龄商品代AA肉鸡后不同时间,采用3H-TdR掺入法测定血液和脾脏的淋巴细胞对ConA的增殖反应能力。结果表明,血液淋巴细胞对ConA增殖反应能力在REV和ALV-J共感染后7 d均下降,REV单一感染组在感染后17、37 d均极显著低于对照组(P〈0.01),ALV-J单一感染组也呈现下降趋势。在脾淋巴细胞反应中,REV感染组在感染后37 d极显著降低(P〈0.01),ALV-J组显著降低(P〈0.05)。REV和ALV-J共感染抑制淋巴细胞对ConA增殖反应较单一感染强,效应期也较长,在感染后37 d,共感染对血液和脾淋巴细胞反应的抑制作用均大于REV和ALV-J的单一感染(P〈0.05)。在感染后273、7 d检测NDV抗体,单一感染组降低显著(P〈0.05),而共感染组下降极显著(P〈0.01),且显著低于单一感染组(P〈0.05)。本研究表明REV、ALV-J感染不仅能抑制体液免疫反应,也能抑制细胞免疫反应,且共感染比单一感染的抑制作用更强。 相似文献
996.
绿色荧光蛋白(green fluorescent protein,GFP)是源于海洋生物多管水母(aequoia victoria)的一种发光蛋白,能够自身催化形成生色团并在蓝光激发下发出绿色荧光,能在活细胞内稳定表达,本试验首先从含有GFP的大肠杆菌中提取质粒,并利用胶回收试剂盒纯化质粒,采用氯化钙法将工程菌DH5a制成感受态细胞,然后将纯化后的质粒转入已制备好的感受态细胞中,使得工程菌DH5a转化成具有抗氨苄青霉素的大肠杆菌,并表达绿色荧光蛋白,接种于加氨苄青霉素的LB培养基上,筛选阳性克隆。 相似文献
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998.
AIM: To study the protective effects of bone marrow-derived mesenchymal stem cells on damaged dopaminergic neurons induced by 1-methyl-4-phenylpytidinium(MPP+).METHODS: The parkinson disease(PD) models were established in newborn rats. Bone marrow mesenchymal stem cells(MSCs) obtained from adult bone marrow were cultured, isolated and purified. MSCs were co-cultured with brain slice and the immunohistochemical technique, electron microscopy, propidium iodide staining were used to observe the changes of neurons. RESULTS: In the MPP+ treatment group, the neurites grew slowly and sparsely, dead cells were found in all regions. In the co-culture group, the neuritis grew densely, only a few cells were dead, the number of tyrosine hydroxylase(TH)-stained neurons increased and the structure of organellae was normal. CONCLUSION: MSCs may protect dopaminergic neurons against damage induced by MPP+. These results provide some data for cell transplantation therapy to Parkinsons disease. 相似文献
999.
AIM:To investigate the effect of 17β-estradiol (E2) on myocardial hypertrophy induced by endothelin-1(ET-1) and the related mechanism. METHODS:Myocardial cells from neonate rats were cultured in vitro and myocardial hypertrophy model was established with ET-1.The effects of 17β-estradiol on myocardial hypertrophy were observed. The role of ERK1/2 in the effects of 17β-estradiol was also detected. RESULTS:Compared with control group,ET-1 increased cell protein content,cell surface area and [3H]-Leucine [3H]-Leu) incorporation. Pretreatment with E2 for 24 h could inhibit the increase in cell protein content,cell surface area and [3H]-Leu incorporation induced by ET-1.ET-1 significantly stimulated ERK1/2 activity,which was prevented by pretreatment with E2.Tamoxifen,estradiol receptor antagonist,partially inhibited the effect of E2. The ability of ET-1 to stimulate [3H]-Leu incorporation was significantly blocked by PD98059,which could enhance the inhibitory effect of E2 on the increase of [3H]-Leu incorporation in cardiomyocytes induced by ET-1.CONCLUSION:E2 can inhibit cardiomyocyte hypertrophy induced by ET-1. This effect is mediated by estrogen receptor. ERK1/2 signal pathway is closely correlated with the inhibitory effect of E2 on cardiomyocyte hypertrophy induced by ET-1. 相似文献
1000.
青藏高原草地退化原因述评 总被引:23,自引:11,他引:23
导致青藏高原草地退化的因子很多,主要有气候、野生动物和人类活动等。在气候因素中以气温和降水的影响为主,短期内气候的变化不会成为草地退化的主导因素,从长期来看,气候变化与草地退化之间的相互作用可引起草地生态系统的退化;野生动物因素中主要以植食性小哺乳动物的影响为主,其危害程度取决于其种群数量的高低,同时大型野生草食动物对草地退化的影响也不容忽视;人类活动因素中主要以家畜过度放牧为主,在一定程度上,家畜放牧强度的高低直接决定草地的退化程度;草地退化是多种因素综合作用的结果。不同地区导致草地退化的主要因素不尽相同,导致青藏高原草地退化最主要的因子是过度放牧和植食性小哺乳动物种群爆发。针对退化的原因,提出了青藏高原退化草地恢复与管理过程中应注意的事项。 相似文献