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1.
Active production of anti-human T-lymphotropic virus type I (HTLV-I) IgM antibody in HTLV-I-associated myelopathy 总被引:2,自引:0,他引:2
Kunihiko Nagasato Tatsufumi Nakamura Ohishi Kiyosumi Kohji Shibayama Masakatsu Motomura Ichinose Katsuhiro Mitsuhiro Tsujihata Shigenobu Nagataki 《Journal of neuroimmunology》1991,32(2):105-109
We investigated the presence of anti-human T-lymphotropic virus type I (HTLV-I) IgM in sera and cerebrospinal fluid from patients with HTLV-I-associated myelopathy (HAM) by Western blot analysis. Analyses of 36 serum samples revealed that most patients (31/36; 86.1%) had anti-HTLV-I IgM, whereas only four of 23 (17.4%) HTLV-I carriers had it. In studies of cerebrospinal fluid, anti-HTLV-I IgM was detected in 24 of 36 (66.7%) HAM patients, whereas none was detected in nine HTLV-I carriers. The differences were statistically significant (p less than 0.01). These results suggest that persistent active replication of HTLV-I occurs in the central nervous system as well as in the peripheral blood of HAM patients, and may contribute to the development of HAM. 相似文献
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3.
Yoshiharu Kikawa Akio Nakai Yosuke Shigematsu Masakatsu Sudo Kimitaka Kato Shinichi Haruki 《Pediatric nephrology (Berlin, Germany)》1990,4(4):343-344
Leukotriene B4 (LTB4) production in polymorphonuclear leucocytes (PMN) was examined in ten children with steroid-responsive nephrotic syndrome (SRNS) before, during, and after steroid administration. Comparison of LTB4 production was made in 14 children with non-inflammatory disease who were not receiving steroid therapy. No significant change was noted in PMN LTB4 biosynthesis in children with SRNS throughout any phase of the disease. Furthermore, there was no significant difference in LTB4 biosynthesis in PMN between SRNS patients before steroid therapy and patients with non-inflammatory disease. These findings suggest that inhibition of LTB4 production is not involved in the mechanism underlying steroid action in SRNS. 相似文献
4.
应用Y型迷宫研究了急性与慢性东莨菪碱和吗啡对小鼠记忆能力的影响。单剂量东莨菪碱(1mg/kgip)和吗啡(10mg/kgip)均能显著损害小鼠的短时记忆(workingmemory)。重复给药后东莨菪碱的这种作用很快消失。但吗啡每天一次,连续3次给药这种作用加强,连续5次给药这种作用反而减弱。东莨菪碱不能损害小鼠长时记忆(referencememory),而吗啡对长时记忆有损害作用。结果还提示小鼠短时记忆不受自发活动能力的影响。 相似文献
5.
N Motomura K Kitaura S Shirakata K Ohga T Oka 《[Zasshi] [Journal]. Nihon Kyōbu Geka Gakkai》1992,40(11):2057-2060
The size of a thoracic aortic aneurysm (TAA) is an important factor of the operative indication. We experienced a ruptured TAA the diameter of which was only 4 cm. A 71 years old man was admitted due to the severe back pain under the shocked condition. We diagnosed him a ruptured TAA by CT scan. Because he had no progressive anemia and the hemodynamics was very stable, we followed him conservatively. Two months later, the operation was performed. We resected the aneurysm and inserted an aortic prosthetic graft. From the operative findings, the aneurysm was certified as a true aneurysm, and the maximal diameter was only 4 cm. First choice for the treatment of ruptured TAA is the emergent operation. But when the hemodynamics is extremely stable and the anemia does not progress at all, a conservative therapy can be selected. Even if the aneurysm is very small, the control of hypertension is quite important. 相似文献
6.
Gou Takeo Masakatsu Motomura Hidenori Matsuo Kiyosumi Ohishi Toshiro Yoshimura Shigenobu Nagataki Mitsuhiro Tsujihata 《Muscle & nerve》1993,16(8):840-848
We investigated the effect of the lgG from patients with myasthenia gravis (MG) on the degradation of normal rat junctional acetylcholine receptor (AChR) labeled with 125l-α-bungarotoxin (BuTx) and calculated the degradation rate (DR). The DR for the lgG from these patients was significantly higher than that from healthy volunteers and patients with other autoimmune diseases. For MG, DR was significantly correlated with the severity of the disease but not with anti-AChR antibody titer. DR was accelerated by lgG from patients with generalized MG whose antibody titers were in the normal range and by lgG from patients with ocular MG. These results indicate that measurement of the DR of junctional AChR in normal rats is more closely correlated with the severity of the disease than is measurement of anti-AChR antibody and that the former is a sensitive and confirmatory method for evaluating MG. © 1993 John Wiley & Sons, Inc. 相似文献
7.
Terashima Y Onai N Murai M Enomoto M Poonpiriya V Hamada T Motomura K Suwa M Ezaki T Haga T Kanegasaki S Matsushima K 《Nature immunology》2005,6(8):827-835
Ligation of the chemokine receptor CCR2 on monocytes and macrophages with its ligand CCL2 results in activation of the cascade consisting of phosphatidylinositol-3-OH kinase (PI(3)K), the small G protein Rac and lamellipodium protrusion. We show here that a unique clathrin heavy-chain repeat homology protein, FROUNT, directly bound activated CCR2 and formed clusters at the cell front during chemotaxis. Overexpression of FROUNT amplified the chemokine-elicited PI(3)K-Rac-lamellipodium protrusion cascade and subsequent chemotaxis. Blocking FROUNT function by using a truncated mutant or antisense strategy substantially diminished signaling via CCR2. In a mouse peritonitis model, suppression of endogenous FROUNT markedly prevented macrophage infiltration. Thus, FROUNT links activated CCR2 to the PI(3)K-Rac-lamellipodium protrusion cascade and could be a therapeutic target in chronic inflammatory immune diseases associated with macrophage infiltration. 相似文献
8.
9.
Seiichi Motomura Kohtaro Fukushima Hideo Nishitani Hajime Nawata & Takeharu Nishimoto 《Genes to cells : devoted to molecular & cellular mechanisms》1996,1(12):1101-1112
Background: We have previously isolated a series of temperature-sensitive mutants for cell-proliferation from the BHK21 cell line, derived from the golden hamster. These mutants proliferate at 33.5 °C, the permissive temperature, but not at 39.5 °C the restrictive temperature. Using DNA-mediated gene transfer, human genes complementing these ts mutants were cloned.
Results: At 39.5 °C the tsBN250 cell line, a temperature-sensitive mutant of the BHK21 cell line, had a defect in the G1 phase, but not in the S phase. The human gene complementing tsBN250 cells was found to encode histidyl-tRNA synthetase. Indeed, the tsBN250 cell line had a single base change—guanine to adenine at the second position of the 362nd codon of hamster histidyl-tRNA-synthetase, converting arginine to histidine. Following release from serum starvation, cyclin E, but not cyclin D1, was accumulated, while, at 39.5 °C, the mRNA of cyclin D1 was normally expressed in tsBN250 cells. A similar inhibition of cyclin D1 accumulation was observed in another ts mutant, tsBN269, which has a single point mutation in lysyl-tRNA synthetase. Overexpression of cyclin D1 enabled tsBN250 cells to enter the S phase.
Conclusion: tsBN250 cells have a single point mutation in histidyl tRNA synthetase that causes a loss of histidyl-tRNA synthetase activity which in turn reduces the content of cyclin D1, but not of cyclin E, thereby resulting in G1 arrest. 相似文献
Results: At 39.5 °C the tsBN250 cell line, a temperature-sensitive mutant of the BHK21 cell line, had a defect in the G1 phase, but not in the S phase. The human gene complementing tsBN250 cells was found to encode histidyl-tRNA synthetase. Indeed, the tsBN250 cell line had a single base change—guanine to adenine at the second position of the 362nd codon of hamster histidyl-tRNA-synthetase, converting arginine to histidine. Following release from serum starvation, cyclin E, but not cyclin D1, was accumulated, while, at 39.5 °C, the mRNA of cyclin D1 was normally expressed in tsBN250 cells. A similar inhibition of cyclin D1 accumulation was observed in another ts mutant, tsBN269, which has a single point mutation in lysyl-tRNA synthetase. Overexpression of cyclin D1 enabled tsBN250 cells to enter the S phase.
Conclusion: tsBN250 cells have a single point mutation in histidyl tRNA synthetase that causes a loss of histidyl-tRNA synthetase activity which in turn reduces the content of cyclin D1, but not of cyclin E, thereby resulting in G1 arrest. 相似文献
10.
Analysis of mRNA with microsomal fractionation using a SAGE-based DNA microarray system facilitates identification of the genes encoding secretory proteins 总被引:1,自引:0,他引:1 下载免费PDF全文
Toyoda N Nagai S Terashima Y Motomura K Haino M Hashimoto S Takizawa H Matsushima K 《Genome research》2003,13(7):1728-1736
In the regulation of host defense responses such as inflammation and immunity, the secretory proteins, including membrane proteins, play central roles. Although many secretory proteins have been identified by using methods such as differential display, random screening, or the signal sequence trap method, each method suffers from poor reproducibility, low sensitivity, or time-consuming or laborious work. Therefore, the strategy for facilitating the selection of the genes encoding the secretory proteins is desired. In this paper, we describe a system for isolating the genes encoding secretory proteins by analyzing mRNAs with microsomal fractionation on serial analysis of gene expression (SAGE)-based DNA microarray system. This system succeeded in discriminating the genes encoding secretory proteins from ones encoding nonsecretory proteins with 80% accuracy. We applied this system to human T lymphocytes. As a result, we were able to identify the genes that are not only encoding secretory proteins but also expressing selectively in a specific subset of T lymphocytes. The SAGE-based DNA microarray system is a promising system to identify the genes encoding specific secretory proteins. 相似文献