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151.
一种多路D/A转换器,它主要由Intel 8279芯片、一路基本D/A转换电路、一个模拟开关和相应的采样保持器组成,与其它的多路D/A电路相比,其不同之处在于它用8279中的显示RAM和扫描线实现转换数据的存放和对各路D/A的循环扫描,从而减轻了CPU的负担,而且电路简单,成本低.经过研究表明,这种电路不仅能实现8路8位的D/A转换,而且还能实现16路8位和8路16位的多路D/A转换。 相似文献
152.
应用增殖抑制方法发现,无生长抑制作用的0.5mg ·L~(-1)的蝙蝠葛碱(Dau)使博莱霉素A_5单独对小鼠肉瘤S-180V细胞作用的I_(C50)值从2.1mg·L~(-1)降低到1.3mg·L~(-1),无抑制作用的1 mg·L~(-1) Dau使博莱霉素A_5单独对人喉癌HEP2细胞作用的I_(C50) 值从0.33 mg·L~(-1)降低到0.1 mg·L~(-1).克隆形成法证明:无细胞毒性的10 mg·L~(-1)的Dau明显增强博莱霉素A_5对HEP2细胞毒性.TFP法证实,有一定生长抑制作用的Dau对HEP2细胞内活化钙调素有影响.结果表明:蝙蝠葛碱有一定的增强博莱霉素A_5对肿瘤细胞的毒性. 相似文献
153.
根据因次分析与气固流动压力损失提出了快速循环流化床中压力沿床高分布的计算式,由此公式来计算轴向固体容积率.本文使用此式对从众多作者不同条件下取得的数据进行拟合,表明该式能与不同系统的实验数据很好地符合,为快速床设计计算提供了依据 相似文献
154.
A population of ventral neural tube cells has recently been shown to migrate out of the hind brain neural tube via the vagus
nerve and contribute to the developing gastrointestinal tract. Since liver is also innervated by the vagus nerve, we sought
to determine if these cells also migrate into the liver. Ventral neural tube cells in the caudal hindbrain of chick embryos
were tagged with a replication-deficient retroviral vector containing the LacZ gene on embryonic day 2. Embryos were processed
for detection of labeled cells on embryonic day 5 and 11. Labeled cells were seen in the liver on both days and identified
as hepatocytes. Previously, it was believed that all hepatocytes develop from the gut endoderm. Results of the present study
show an additional source for the formation of liver cells.
Received 25 August 1998; received after revision 5 November 1998; accepted 5 November 1998 相似文献
155.
LIUShiyong ZHANGZhiyuan SONGYechun QIUKejun ZHANGKecheng ANNing ZHOUZheng CAIWenqin YANGHui 《科学通报(英文版)》2004,49(11):1126-1136
The neural stem cells in the anterior subventricular zone (SVZa) mainly generate the progenitors that will differentiate into neurons, and along a highly circumscribed migratory access Rostral migratory stream (RMS), they migrate to the olfactory bulbs (OB). To understand the effects of BMPs on SVZa neural stem cells, in this study BMP4 at various concentrations was used to induce SVZa neural stem cells, and the living cell labeling using BMP4 promotor conjugated with red fluorescence protein showed the expression of BMP4 dynamically. The results demonstrated that low BMP4 doses (1-5 ng/mL) promoted while high doses (10-100 ng/mL) inhibited the proliferation of SVZa neural stem cells, and BMP4 promotedneuron differentiation in the early stage (1-3 d), howeverm, it inhibited the neuron commitment after 4 d. Noggin, the antagonist of BMP4, blocked the physiological effects of BMP4. In OB, BMP4 is mainly to accelerate the progenitors to withdraw from the cell cycle and trigger the differentiation, and in RMS, it promotes the proliferation of committed progenitors and not differentiation, further in SVZa, BMP4 enhances astrocyte commitment. 相似文献
156.
Lethal toxin (LT) is a major virulence factor secreted by anthrax bacteria. It is composed of two proteins, PA (protective antigen) and LF (lethal factor). PA transports the LF inside the cell, where LF, a zinc-dependent metalloprotease cleaves the mitogen activated protein kinase kinase (MAPKK) enzymes of the mitogen activated protein kinase (MAPK) signaling pathway, thereby impairing their function. This disruption of the MAPK pathway, which serves essential functions such as proliferation, survival and inflammation in all cell types, results in multisystem dysfunction in the host. The inactivation of the MAPK pathway in both macrophages and dendritic cells leads to inhibition of proinflammatory cytokine secretion, downregulation of costimulatory molecules such as CD80 and CD86, and ineffective T cell priming. The net result is an impaired innate and adaptive immune response. Endothelial cells of the vascular system undergo apoptosis upon LT exposure, also likely due to inactivation of the MAPK pathway. The activity of various hormone receptors such as glucocorticoids, progesterone and estrogen is also blocked, due to inhibition of p38 MAPK phosphorylation, thus affecting the bodys response to stress. The present review summarizes the various disarming effects of Bacillus anthracis through the use of a single weapon, the lethal toxin.Received 12 June 2004; received after revision 13 July 2004; accepted 28 July 2004 相似文献
157.
Our understanding of how immune responses are generated and regulated drives the design of possible immunotherapies for cancer
patients. For that reason, we first describe briefly the actual immunological theories and their common perspectives about
cancer vaccine development. Second, we describe cancer vaccines that are able to induce tumor-specific immune responses in
cancer patients. However, these responses are not always followed by tumor rejection. At the end of the review, we discuss
two possible reasons that might explain this dichotomy of cancer immunology. First, the immune response generated, although
detectable, may not be quantitatively sufficient to reject the tumor. Second, the tumor microenvironment may modulate tumor
cell susceptibility to the systemic immune response induced by the immunization. Finally, we discuss what, in our opinion,
might be the best way to improve cancer vaccine strategies and how the relationship between the tumor and its surroundings
might be studied in more details.
Received 21 June 2001; received after revision 15 August 2001; accepted 15 August 2001 相似文献
158.
Exposure to estrogens is a risk factor for breast and other human cancers. Initiation of breast, prostate and other cancers
has been hypothesized to result from reaction of specific estrogen metabolites, catechol estrogen-3,4-quinones, with DNA to
form depurinating adducts at the N-7 of guanine and N-3 of adenine by 1,4-Michael addition. The catechol of the carcinogenic
synthetic estrogen hexestrol, a hydrogenated derivative of diethylstilbestrol, is metabolized to its quinone, which reacts
with DNA to form depurinating adducts at the N-7 of guanine and N-3 of adenine. The catecholamine dopamine and the metabolite
catechol (1,2-dihydroxybenzene) of the leukemogen benzene can also be oxidized to their quinones, which react with DNA to
form predominantly analogous depurinating adducts. Apurinic sites formed by depurinating adducts are converted into tumor-initiating
mutations by error-prone repair. These mutations could initiate cancer by estrogens and benzene, and Parkinson's disease by
the neurotransmitter dopamine. These data suggest a unifying molecular mechanism of initiation for many cancers and neurodegenerative
diseases and lay the groundwork for designing strategies to assess risk and prevent these diseases.
Received 4 September 2001; received after revision 28 November 2001; accepted 2 December 2001 相似文献
159.
Joyce S 《Cellular and molecular life sciences : CMLS》2001,58(3):442-469
Cellular and humoral immune mechanisms recruited to defend the host from infectious agents depend upon the early immune events
triggered by antigen. The cytokine milieu within which the immune response matures is the most important of many factors that
govern the nature of the immune response. Natural T cells, whose function is controlled by CD1d molecules, are an early source
of cytokines that can bestow type 1 or type 2 differentiative potential upon helper T lymphocytes. This review attempts to
illuminate the glycolipid antigen presentation properties of CD1d, how CD1d controls the function of natural T cells and how
CD1d and natural T cells interact to jump start the immune system. CD1d is postulated to function as a sensor, sensing alterations
in cellular lipid content by virtue of its affinity for such ligands. The presentation of a neo-self glycolipid, presumably
by infectious assault of antigen-presenting cells, activates natural T cells, which promptly release pro-inflammatory and
anti-inflammatory cytokines and jumpstart the immune system.
Received 10 July 2000; received after revision 16 October 2000, accepted 16 November 2000 相似文献
160.