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91.
Murakami Y Iwata H Kitano E Kitamura H Ikada Y 《Journal of biomaterials science. Polymer edition》2005,16(3):381-395
Bioartificial pancreas, in which the islets of Langerhans are enclosed in artificial membrane to be protected from the host immune system, is expected to be a promising medical device to treat patients who suffer from insulin-dependent diabetes. Our strategy for preparation of a bioartificial pancreas involves utilizing a membrane including polymeric materials that can inhibit the complement reaction. In this study, we examined the effects of poly(styrene sulfonic acid) (PSSa) on the alternative pathway of the serum complement system to identify the mechanism(s) involved. PSSa was dissolved in pooled normal human serum (NHS), and the mixtures were incubated at 37 degrees C for 30 min. Complement activities in sera were determined by hemolytic assays. Amounts of complement activation products released were determined by ELISA. Interactions of PSSa with complement components and fragments were examined with electrophoresis and immunoblotting. From these examinations, it appeared that the manner of PSSa effects on the alternative pathway (AP) highly depends on its concentration. PSSa seemingly acted as an activator when its concentration was 0.005 g/dl to 0.05 g/dl, while it acted as an inhibitor when its concentration was more than 0.1 g/dl. In terms of activation or inhibition of the AP, forming complex of PSSa with factor H induced activation, and that with factor D induced inhibition. 相似文献
92.
IL-6-STAT3 controls intracellular MHC class II alphabeta dimer level through cathepsin S activity in dendritic cells 总被引:1,自引:0,他引:1
Kitamura H Kamon H Sawa S Park SJ Katunuma N Ishihara K Murakami M Hirano T 《Immunity》2005,23(5):491-502
We found IL-6-STAT3 pathway suppresses MHC class II (MHCII) expression on dendritic cells (DCs) and attenuates T cell activation. Here, we showed that IL-6-STAT3 signaling reduced intracellular MHCII alphabeta dimmer, Ii, and H2-DM levels in DCs. IL-6-mediated STAT3 activation decreased cystatin C level, an endogenous inhibitor of cathepsins, and enhanced cathepsin activities. Importantly, cathepsin S inhibitors blocked reduction of MHCII alphabeta dimer, Ii, and H2-DM in the IL-6-treated DCs. Overexpression of cystatin C suppressed IL-6-STAT3-mediated increase of cathepsin S activity and reduction of MHCII alphabeta dimer, Ii, and H2-DM levels in DCs. Cathepsin S overexpression in DCs decreased intracellular MHCII alphabeta dimer, Ii, and H2-DM levels, LPS-mediated surface expression of MHCII and suppressed CD4(+) T cell activation. IL-6-gp130-STAT3 signaling in vivo decreased cystatin C expression and MHCII alphabeta dimer level in DCs. Thus, IL-6-STAT3-mediated increase of cathepsin S activity reduces the MHCII alphabeta dimer, Ii, and H2-DM levels in DCs, and suppresses CD4(+) T cell-mediated immune responses. 相似文献
93.
Three novel mutations of the fibrillin-1 gene and ten single nucleotide polymorphisms of the fibrillin-3 gene in Marfan syndrome patients 总被引:8,自引:0,他引:8
Uyeda T Takahashi T Eto S Sato T Xu G Kanezaki R Toki T Yonesaka S Ito E 《Journal of human genetics》2004,49(8):404-407
Marfan syndrome (MFS) is an autosomal dominant disorder of the extracellular matrix. Allelic variations in the gene for fibrillin-1 (FBN1) have been shown to cause MFS. To date, over 550 mutations have been identified in patients with MFS and related connective tissue diseases. However, about a half of MFS cases do not possess mutations in the FBN1 gene. These findings raise the possibility that variants located in other genes cause or modify MFS. To explore this possibility, firstly we analyzed FBN1 allelic variants in 12 Japanese patients with MFS, and secondly we analyzed fibrillin-3 gene (FBN3) in patients without FBN1 mutations using conformation sensitive gel electrophoresis (CSGE) and direct sequencing analysis. We identified three novel FBN1 mutations and ten FBN3 single nucleotide polymorphisms (SNPs). In this report, we could not detect a responsible mutation of the FBN3 gene for MFS. Although the number of the cases in this report is small, at least these results suggest that disease-causing mutations in exon regions of the FBN3 gene are very rare in MFS.Nucleotide sequence data reported are available in the DDBJ/EMBL/GenBank databases under the accession numbers: AB177797, AB177798, AB177799, AB177800, AB177801, AB177802, AB177803 相似文献
94.
Tocopherol-associated protein (TAP) was expressed in mouse mast cells. TAP was predominantly localized in the cytoplasm, and the subcellular localization was not changed by alpha-tocopherol. The results suggest that the physiological role of TAP in mast cells is not regulation of tocopherol function but an as-yet-unidentified activity. 相似文献
95.
A consistent region of deletion on 1p36 in meningiomas: identification and relation to malignant progression 总被引:5,自引:0,他引:5
Murakami M Hashimoto N Takahashi Y Hosokawa Y Inazawa J Mineura K 《Cancer Genetics and Cytogenetics》2003,140(2):99-106
We analyzed the genetic aberrations on chromosome arms 1p, 10q, and 14q, which are thought to be loci that include putative tumor suppressor genes in meningiomas. We initially conducted molecular genetic testing on a total of 72 tumors including 15 atypical and 8 anaplastic meningiomas using double-target fluorescence in situ hybridization. An incidence of deletion of 1p was observed in 16.3% of histologically benign, 86.7% of atypical, and 87.5% of anaplastic meningiomas. Microsatellite analysis for loss of heterozygosity on 1p, 10q, and 14q was performed in 15 tumors (6 benign, 6 atypical, and 3 anaplastic meningiomas). We detected a limited deleted region on 1p36 in two tumors and suggest a new consistent region of deletion at 1p36.21p23 distal to D1S507 and proximal to D1S214, which spans 8.21 megabases. In addition, loss of 10q was detected in two of three secondary atypical meningiomas, and loss of 14q in two of three primary anaplastic meningiomas. We suggest that one of the putative suppressor genes is located at 1p36.21p23, and that 10q loss may contribute to the malignant progression from benign to atypical meningiomas. 相似文献
96.
Kandori A Hosono T Chiba Y Shinto M Miyashita S Murakami M Miyashita T Ogata K Tsukada K 《Medical & biological engineering & computing》2003,41(1):33-39
The paper presents an evaluation of the possibility of using fetal magnetocardiogram (FMCG) signals to estimate and classify
the accessory pathway in fetal Wolff-Parkinson-White (WPW) syndrome. The FMCG signals of two fetuses with WPW syndrome (type
A) were detected using a 64-channel superconducting quantum-interference device system. An average across the cycles of these
signals was taken to obtain clear WPW signals. To determine the direction and position of the accessory pathway in a fetal
heart accurately, the accessory pathway and activated pathway at the peak of the QRS complex thus obtained were estimated
for each fetus, using a single-dipole model. The phase angle (about 90o) between the equivalent current dipoles (ECDs) was the same for both fetuses. This angle suggested that the accessory pathway
is in the left side of the heart, i.e. that the pathway exists in the position of the accessory pathway in a fetus with WPW
syndrome from the angle between the ECD of the accessory pathway and the ECD of the peak in the QRS complex was thus demonstrated. 相似文献
97.
Doi A Okano M Akagi H Nishizaki K Taguchi T Murakami T Ohtsuka A 《Anatomical science international / Japanese Association of Anatomists》2003,78(1):62-67
The musk shrew, Suncus murinus, is one of the primitive mammals and has a pair of palatine tonsils. In the present study,
we investigated the blood microvascular architecture of the tonsil in this animal by scanning electron microscopy of corrosion
casts. The paranodular arterioles entered the lymph nodule to form a coarse capillary plexus within the nodule. Some of the
arterioles reached the dome region to give rise to a fine meshwork of dome subepithelial capillaries. This dome subepithelial
capillary network did not show any hairpin or switch-back patterns, as seen in human and rabbit tonsils. Both of the nodular
and dome capillaries were drained into the postcapillary venules in the periphery of the nodular or the paranodular region.
On the surface of these cast venules, oval-shaped indentations were seen corresponding to the luminal surface of the high
endothelial venules. These venules were collected into the large vein at the bottom of the tonsil. The blood vascular architecture
of the musk shrew tonsil is basically the same as those of other mucosa-associated lymphoid tissues in mammals. 相似文献
98.
Hirata I Hioki Y Toda M Kitazawa T Murakami Y Kitano E Kitamura H Ikada Y Iwata H 《Journal of biomedical materials research. Part A》2003,66(3):669-676
Since complement activation is recognized as a common response of the host defense system when an artificial medical device is applied to a patient, great effort has been devoted to studies on the interaction of the complement system with artificial materials. However, some uncertainties remain, partially because of the lack of well characterized surfaces and suitable analytic methods for study of the surface phenomena that occur on artificial materials under physiologic conditions. In this study, we employed self-assembled monolayers (SAMs) and the surface plasmon resonance (SPR) technique to study interactions of the serum complement with well characterized surfaces. Self-assembled monolayers carrying various concentrations of hydroxyl groups were prepared using 11-mercapto-1-undecanol (C11-OH) and one of n-nonanethiol, n-dodecanethiol, and n-hexadecanethiol. The amount of NHS deposition on the SAMs increased with increasing C11-OH content of the SAMs, and the amount of anti-C3b antibody immobilization formed on the NHS deposition layers increased with increasing C11-OH content of the SAMs. These results clearly demonstrate that a large amount of C3b, produced through the activation of the complement system, binds covalently to and is adsorbed by hydroxyl-group-rich surfaces. The combination of SAMs and the SPR technique is suitable for studying the interaction of the complement system with solid surfaces, and the results should give basic information needed for a rational design of biocompatible surfaces on synthetic materials. 相似文献
99.
Neonatal treatment of female rats with androgen decreases the nuclear volume of the anteroventral periventricular nucleus of the preoptic area (AVPv-POA). In order to examine the effect of androgen on the neural substrates in the developing AVPv-POA which show a sexual dimorphism in nuclear volume, the cell death pattern in the AVPv-POA was compared between normal females and androgenized females. Wistar female rats were treated with 50 micrograms of testosterone propionate (TP) for 5 days from the day of birth. Degenerating cells (pyenotic cells) and normal cells were counted in every third section from days 1 to 13 of life. The rate of pycnotic cells to 1000 cells in TP-treated females sacrificed at days 7 and 10 was significantly higher than that in normal females. These results may suggest that neonatal androgen regulates neuronal death in the AVPv-POA, decreasing the number of neurons in the nucleus. 相似文献
100.