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Kenji Hibi Masahiko Koike Hiroshi Nakayama Shinichi Fujitake Yasushi Kasai Katsuki Ito Seiji Akiyama Akimasa Nakao 《Clinical cancer research》2003,9(3):1053-1056
PURPOSE AND EXPERIMENTAL DESIGN: To date, the presence of p16 gene promoter methylation associated with loss of protein expression has been demonstrated frequently in digestive tract cancers. In this study, we tested for the methylation status of p16 promoter in normal tissue specimens using the methylation-specific PCR technique to examine whether p16 methylation already existed in the background of tumors. RESULTS: Aberrant promoter methylation of p16 gene was detected in 1 of 40 esophageal and 1 of 69 gastric and no colorectal epithelium specimens, and these 2 specimens were derived from the same patient. We also found the same methylation change in both tumor and blood cell DNA. CONCLUSION: These results suggested that the p16 gene was inactivated by methylation in normal background cells of this patient and that other additional factors may promote tumor development in his esophageal and gastric tissues. 相似文献
75.
Identification of HRK as a target of epigenetic inactivation in colorectal and gastric cancer. 总被引:3,自引:0,他引:3
76.
Shigemi Onoue Takehito Katoh Yoshihisa Shibata Yasushi Mokuno Katsushi Yoshida Satoshi Kamiya Tetsuya Abe Kiyoshi Hiramatsu Minoru Esaki Haruhiko Chigira 《International journal of clinical oncology / Japan Society of Clinical Oncology》1997,2(2):121-124
We report a case of a long-term survivor with malignant melanoma of the anus who did not undergo radical surgery. A 71-year-old
woman who presented with anal bleeding and anal tumor underwent an excisional biopsy in September 1985. The biopsy specimen
was a lobulated, polypoid, pigmented mass 2 cm in diameter, that had been located on the anterior wall of the anus. A satellite
nodule 7 mm in diameter was found on the left wall of the anus at the level of the dentate line. Both tumors were histologically
diagnosed as malignant melanoma. The primary tumor was 6 mm thick. Melanoma cells were present microscopically at the cut
end of the rectum. Because of her history of ischemic heart disease, the patient rejected our recommendation that she undergo
radical surgery, and received 10 courses of carboplatin 20 mg intramuscularly and OK-432 10 K.E. (Klinische Einheit) intradermally
every week. A single, pigmented metastatic inguinal lymph node developed and was excised in June 1987. A recurrent tumor was
detected in the rectum in October 1992, so again we recommended radical surgery. The patient rejected radical surgery again,
and received 12 courses of carboplatin 10 mg intramuscularly every 2 weeks. She died of disease at home in July 1993 after
surviving for 7 years and 10 months. An autopsy was not performed. This case shows that local excision of the primary lesion
may be appropriate to preserve the quality of life of patients with early-stage malignant melanoma of the anus. 相似文献
77.
78.
Tumor-specific Activation of Mitogen-activated Protein Kinase in Human Colorectal and Gastric Carcinoma Tissues 总被引:4,自引:0,他引:4
Yasushi Kuno Ken Kondo Hiroyuki Iwata Takeshi Senga Seiji Akiyama Katsuki Ito Hiroshi Takagi Michinari Hamaguchi 《Cancer science》1998,89(9):903-909
To search for the signaling events in colorectal carcinoma relevant to its tumorigenesis, we investigated the activity of mitogen-activated protein kinase (MAPK) in human colorectal carcinoma tissues and paired normal tissues. Of 64 cases examined, approximately 75% (48 cases) showed tumor-specific activation of MAPK by in situ kinase renaturation assay, as well as in vitro kinase assay with immunoprecipitated MAPK. In addition, tumor-specific activation of MAPK was associated with the activation of MAPK kinase in the cases we examined. However, no clear correlation of MAPK activation with lymph node involvement, metastatic rate, stage, histological classification, age or sex was observed. These results suggest that the MAPK pathway is involved in colorectal tumor development, but its activation alone is not sufficient for malignant conversion. In contrast to colorectal carcinoma, gastric carcinoma tissues showed a lower rate of MAPK activation, suggesting that the signaling pathway activated in colorectal carcinoma tissues may differ in part from that of gastric carcinoma. 相似文献
79.
Asaka Takahashi Hiroki Matsuoka Keiichi Yamada Yasushi Uda 《Food and chemical toxicology》2005,43(4):521-528
3-Allyl-5-substituted 2-thiohydantoins (ATH-amino acids) derived from allyl isothiocyanate and amino acids can inhibit the mutagenicity of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) in the Salmonella assay. In this report, we studied possible mechanisms for the inhibition using rat liver S9 in assays for ethoxyresorufin O-deethylase (EROD), a marker activity for cytochrome P450 1A (CYP1A), which activates heterocyclic amines, and the Salmonella assays with the direct-acting mutagen 2-hydroxyamino-3-methylimidazo[4,5-f]quinoline (N-hydroxy-IQ). Quantitative analysis of ATH-amino acids and IQ during incubation with rat liver S9 fraction by HPLC showed that ATH-amino acids could act as S9-inhibitors, thereby inhibiting metabolic activation of IQ. Among the tested ATH-amino acids, ATH-Phe, ATH-Trp, ATH-Leu and ATH-Val showed a dose-dependent inhibition of EROD activity. ATH-Gly, ATH-Glu, and ATH-Asp behaved as blocking agents toward N-hydroxy-IQ, but exhibited no inhibition of EROD activity. 相似文献
80.
Tetsuya Mitsudomi Takayuki Kosaka Hideki Endoh Yoshitsugu Horio Toyoaki Hida Shoichi Mori Shunzo Hatooka Masayuki Shinoda Takashi Takahashi Yasushi Yatabe 《Journal of clinical oncology》2005,23(11):2513-2520
PURPOSE: To evaluate the relationship between mutations of the epidermal growth factor receptor (EGFR) gene and the effectiveness of gefitinib treatment in patients with recurrent lung cancer after pulmonary resection. PATIENTS AND METHODS: We sequenced exons 18-21 of the EGFR gene using total RNA extracted from 59 patients with lung cancer who were treated with gefitinib for recurrent lung cancer. Gefitinib effectiveness was evaluated by both imaging studies and change in serum carcinoembryonic antigen (CEA) levels. RESULTS: EGFR mutations were found in 33 patients (56%). Of these mutations, 17 were deletions around codons 746-750 and 15 were point mutations (12 at codon 858, three at other codons), and one was an insertion. EGFR mutations were significantly more prevalent in females, adenocarcinoma, and never-smokers. Gefitinib treatment resulted in tumor shrinkage and/or CEA decrease to less than half of the baseline level in 26 patients, tumor growth and/or CEA elevation in 24 patients, and gefitinib effect was not assessable in nine patients. Female, never-smoking patients with adenocarcinoma tended to respond better to gefitinib treatment. Gefitinib was effective in 24 of 29 patients with EGFR mutations, compared with two of 21 patients without mutations (P < .0001). Of note, del746-750 might be superior to L858R mutations for prediction of gefitinib response. Patients with EGFR mutations survived for a longer period than those without the mutations after initiation of gefitinib treatment (P = .0053). CONCLUSION: EGFR mutations were a good predictor of clinical benefit of gefitinib in this setting. 相似文献