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101.
Statistical detection of HLA and disease association 总被引:1,自引:0,他引:1
Katsuhirci Fukuda Kazuaki Sugawa Akemi Wakisaka Junko Mokiuchi Nobuo Matsuura Yoshiharu Sato 《Tissue antigens》1985,26(2):81-86
102.
Hiroshi Takahashi Nobuo Tsuda Shuichi Fujita Fumiaki Tezuka Haruo Okabe 《Pathology international》1990,40(9):655-664
Fifty-four adenoid cystic carcinomas (ACC) arising in major and minor salivary glands as well as in normal salivary glands were studied by immunohistochemistry for the presence of vimentin, neuron specific enolase (NSE), α1 -antichymotrypsin (α1 -ACT) and α1 -- antitrypsin (α1 -- AT). Five patterns of histological differentiation were found in ACC, and for the cellular components of each, it was possible to establish a special immunohistochemical profile. In ACC, vimentin-positive cells were observed in the outer tubular, cyst-lining and small angular cells. NSE was positive in the myoepithelial cells of normal salivary gland. Neoplastic cells of ACC showed NSE positivity mainly in the small angular cells and partly in the duct luminal cells. α1 -ACT was localized in the intercalated duct cells and serous acinar cells of normal salivary gland, and in the duct luminal cells of ACC. α1 -AT could not be detected in any of the epithelial cells of normal salivary gland. In ACC, eosinophilic hyaline material in the cribriform spaces was positive for α1 -AT, but no positivity was demonstrated in tumor cells. The present study showed that there are at least two populations of tumor cells in ACC: duct luminal cells that express α1 -ACT, thus indicating their ductal character, and small angular cells that express vimentin, characteristic of non-luminal cells. Moreover, our results indicate that α1 -AT is a useful marker of basement membrane-like material. 相似文献
103.
104.
Katsuro Hagiwara Noriko Momiyama Hiroyuki Taniyama Takaaki Nakaya Nobuo Tsunoda Chiaki Ishihara K. Ikuta 《Medical microbiology and immunology》1997,186(1):19-24
Sero- and molecular-epidemiological studies on Borna disease virus (BDV) infection show that BDV RNA is not always detected
in the peripheral blood mononuclear cells (PBMCs) from serum anti-BDV antibody-positive individuals such as horses, sheep,
cattle, cats, and humans. In this study we demonstrated BDV RNA signals by polymerase chain reaction only in restricted regions
of the brain from horses with locomotor disease. Four of six horses examined showed apparently positive reactions for anti-BDV
antibodies. Specific regions of the brain of these four horses were positive for BDV RNA but the internal organs, lymph nodes,
and PBMCs were negative. Histological studies of their brains revealed no apparent histological abnormalities such as inflammatory
reactions. These results suggest that BDV chronically infects certain restricted regions of brain in seropositive horses.
Received: 6 January 1997 相似文献
105.
Hirata T Iida A Shiraki-Iida T Kitazato K Kato A Nagai Y Hasegawa M 《Journal of virological methods》2002,104(2):125-133
An improved system is described to recover non-transmissible Sendai virus that lack the envelope fusion (F) gene from cloned cDNA. The system (1) used plasmids that expressed the F and the HN viral envelope proteins, as well as the plasmids that expressed the viral NP, P, and L proteins as helper plasmids for recovery, and (2) overlaid packaging cells that expressed the F protein. With this improved system, we have succeeded in recovery of F-defective Sendai virus expressing two foreign proteins, and expression vectors that do not contain the EGFP reporter gene. This system may provide the basis for constructing recombinant F-defective Sendai virus for preventing and treating human diseases in the form of vaccines and vectors for gene therapy. 相似文献
106.
107.
Muto S Aiba A Saito Y Nakao K Nakamura K Tomita K Kitamura T Kurabayashi M Nagai R Higashihara E Harris PC Katsuki M Horie S 《Human molecular genetics》2002,11(15):1731-1742
Mutations of either PKD1 or PKD2 are associated with autosomal dominant polycystic kidney disease (ADPKD). The molecular function of the gene product of PKD1, polycystin-1, in vitro has been elucidated recently, but the molecular pathological consequences of the loss of polycystin-1 in vivo have remained unclear. We have generated a mouse with a targeted deletion of exons 2-6 of Pkd1 to study the molecular defects in Pkd1 mutants. Homozygote embryos (Pkd1(-/-)) developed hydrops, cardiac conotruncal defects and renal cystogenesis. Total protein levels of beta-catenin in heart and kidney and c-MYC in heart were decreased in Pkd1(-/-) embryos. In the kidneys of Pkd1(-/-), the expression of E-cadherin and PECAM in basolateral membranes of renal tubules was attenuated, and tyrosine phosphorylation of epidermal growth factor receptor and Gab1 were constitutively enhanced when cystogenesis started on embryonic day (E) 15.5-16.5. Maternally administered pioglitazone, a thiazolidinedione compound, resolved these molecular defects of Pkd1(-/-). Treatment with pioglitazone improved survival of Pkd1(-/-) embryos and ameliorated the cardiac defects and the degree of renal cystogenesis. Long-term treatment with pioglitazone improved the endothelial function of adult Pkd1(+/-). These data indicated that molecular defects observed in Pkd1(-/-) embryos contributed to the pathogenesis of ADPKD and that thiazolidinediones had a compensatory effect on the pathway affected by the loss of polycystin-1. Pathways activated by thiazolidinediones may provide new therapeutic targets in ADPKD. 相似文献
108.
Terada Y Imoto I Nagai H Suwa K Momoi M Tajiri T Onda M Inazawa J Emi M 《American journal of medical genetics》2001,103(2):176-180
We performed molecular analysis of a germline interstitial deletion of chromosome 4 [del(4)(q21.22q23)], which had been observed in a male infant manifesting early-onset hepatoblastoma (HBL). The chromosomal anomaly in this child was associated with a unique congenital syndrome including HBL, atrial septal defect, ventricular septal defect, patent ductus arteriosus, mental retardation, and seizures. However, the patient did not exhibit a megalencephaly typical of 4q21-22 deletions. His HBL was associated with an increasing serum alpha-fetoprotein level and rapid growth. To define the chromosomal deletion at the molecular level in this child, we analyzed his lymphoblasts with fluorescence in situ hybridization, using as probes a panel of BAC/PAC genomic clones containing STS markers covering the 4q12-27 region. The analysis revealed that the affected chromosome had an 8-cM deletion within 4q21-q22, flanked by markers D4S2964 and D4S2966. This microdeletion overlaps with the commonly deleted region at 4q21-q22 that was recently defined in adult hepatocellular carcinomas. 相似文献
109.
Takehiko Ohzeki Keiichi Hanaki Nobuo Ishitani Hiroko Ohtahara Hirofumi Urashima Toshinori Tsukuda Jun-Ichi Nagaishi Kazuo Shiraki 《American journal of human biology》1995,7(2):237-240
Skinfold thicknessess (SFT) were measured at ulnar, triceps, subscapular and suprailiac sites in 730 boys and 724 girls (age 3–12 years) whose stature ranged from 100 to 150 cm and whose weight was within ±20% of the average. Means and standard deviation (SD) were calculated after logarithmic transformation of the original skinfold readings to demonstrate stature-based standards of SFT in Japanese children. The means of SFT exhibited nadirs (boys/ girls: ulnar 5.1/5.9 mm, triceps 7.9/9.5 mm, subscapular 4.9/6.1 mm, suprailiac 4.5/6.2 mm) in subjects 110–115 cm tall except for ulnar SFT in girls. SFT values increased as children increased in stature. Standard deviations of SFT at the four sites in short children (staturte < mean ?1 SD) were estimated using the stature-based standard as well as an age-based standard. Susms of the SDs assessed by the age-based standard were significantly smaller than those assessed by the stature-based standard in boys (P < 0.05) and girls (P < 0.01) with short stature, suggesting that SFT in short children was falsely understimated by the age-based standard. Thus, the stature-based standard is beneficial for the assessment of SFT, especially in children whose stature is below the mean ?-1 SD. © 1995 Wiley-Liss, Inc. 相似文献
110.