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Tetsuji Terazawa Takeshi Kato Masahiro Goto Katsuya Ohta Shingo Noura Hironaga Satake Yoshinori Kagawa Hisato Kawakami Hiroko Hasegawa Kazuhiro Yanagihara Tatsushi Shingai Ken Nakata Masahito Kotaka Masayuki Hiraki Ken Konishi Shiro Nakae Daisuke Sakai Yukinori Kurokawa Toshio Shimokawa Taroh Satoh 《The oncologist》2021,26(1):17-e47
Lessons Learned
- Panitumumab monotherapy showed favorable efficacy and feasibility in the treatment of frail or elderly patients with RAS wild‐type unresectable colorectal cancer.
- It is especially effective for left‐sided tumors; therefore, panitumumab as first‐line treatment could be an additional therapeutic option for frail elderly patients, particularly in those who are unsuitable for upfront oxaliplatin‐based or irinotecan‐based combination regimens.
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Yu Akazawa Yuki Saito Toshiaki Yoshikawa Keigo Saito Kazuto Nosaka Manami Shimomura Shoichi Mizuno Yasunari Nakamoto Tetsuya Nakatsura 《Cancer science》2020,111(8):2736-2746
Lung cancer is the leading cause of cancer‐related deaths worldwide. Epidermal growth factor receptor‐tyrosine kinase inhibitors (EGFR‐TKI) often have good clinical activity against non–small cell lung cancer (NSCLC) with activating EGFR mutations. Osimertinib, which is a third‐generation EGFR‐TKI, has a clinical effect even on NSCLC harboring the threonine to methionine change at codon 790 of EGFR (EGFR T790M) mutation that causes TKI resistance. However, most NSCLC patients develop acquired resistance to osimertinib within approximately 1 year, and 40% of these patients have the EGFR T790M and cysteine to serine change at codon 797 (C797S) mutations. Therefore, there is an urgent need for the development of novel treatment strategies for NSCLC patients with the EGFR T790M/C797S mutation. In this study, we identified the EGFR T790M/C797S mutation‐derived peptide (790‐799) (MQLMPFGSLL) that binds the human leukocyte antigen (HLA)‐A*02:01, and successfully established EGFR T790M/C797S‐peptide‐specific CTL clones from human PBMC of HLA‐A2 healthy donors. One established CTL clone demonstrated adequate cytotoxicity against T2 cells pulsed with the EGFR T790M/C797S peptide. This CTL clone also had high reactivity against cancer cells that expressed an endogenous EGFR T790M/C797S peptide using an interferon‐γ (IFN‐γ) enzyme‐linked immunospot (ELISPOT) assay. In addition, we demonstrated using a mouse model that EGFR T790M/C797S peptide‐specific CTL were induced by EGFR T790M/C797S peptide vaccine in vivo. These findings suggest that an immunotherapy targeting a neoantigen derived from EGFR T790M/C797S mutation could be a useful novel therapeutic strategy for NSCLC patients with EGFR‐TKI resistance, especially those resistant to osimertinib. 相似文献
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Kiyotaka Nemoto Tetsuya Shimokawa Masaki Fukunaga Fumio Yamashita Masashi Tamura Hidenaga Yamamori Yuka Yasuda Hirotsugu Azechi Noriko Kudo Yoshiyuki Watanabe Mikio Kido Tsutomu Takahashi Shinsuke Koike Naohiro Okada Yoji Hirano Toshiaki Onitsuka Hidenori Yamasue Michio Suzuki Kiyoto Kasai Ryota Hashimoto Tetsuaki Arai 《Psychiatry and clinical neurosciences》2020,74(1):56-63
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Shinji Naganawa Rintaro Ito Hisashi Kawai Toshiaki Taoka Tadao Yoshida Michihiko Sone 《Magnetic resonance in medical sciences》2020,19(4):375
Purpose:It has been reported previously that intravenously administered gadolinium-based contrast agent (GBCA) leaks into the subarachnoid space around the cortical veins at 4 h after injection in all old people over 37 years, but not in younger people up to 37 years of age in 3D-real IR images. The purpose of this study was to investigate whether there was a strict threshold of 37 years of age for the leakage of the GBCA into the subarachnoid space.Methods:The subjects included 190 patients, that were scanned for 3D-real IR images at 4 hours after intravenous injection of GBCA as a diagnostic test for endolymphatic hydrops. The patient’s age ranged from 14 to 81 years. Two experienced neuroradiologists evaluated the images to determine whether the GBCA leakage around the cortical veins was positive or negative. Any discrepancies between the two observers were discussed and a consensus was obtained.A Mann–Whitney U test and receiver operating characteristic (ROC) curve analysis were used to compare the positive and the negative group and to set the age cut-off value for the prediction of GBCA leakage.Results:The GBCA leakage around the cortical veins was negative in 35 patients and positive in 155 patients. The average age was 33 ± 11 years in the negative group, and 55 ± 12 years in the positive group (P < 0.01). In the ROC analysis for the age and leakage of the GBCA, an area under the curve was 0.905 and the cut-off age was 37.317 years (sensitivity of 0.942 and specificity of 0.771).Conclusion:Intravenously administered GBCA leaks into the subarachnoid space around the cortical veins in most patients over 37 years of age. However, it should be noted that it can be found occasionally in patients under 37 years of age. 相似文献
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Tatsuaki Takeda Hiromasa Yamamoto Ken Suzawa Shuta Tomida Shunsaku Miyauchi Kota Araki Kentaro Nakata Akihiro Miura Kei Namba Kazuhiko Shien Junichi Soh Tadahiko Shien Yoshihisa Kitamura Toshiaki Sendo Shinichi Toyooka 《Cancer science》2020,111(3):849-856
Molecular‐targeted therapies directed against human epidermal growth factor receptor 2 (HER2) are evolving for various cancers. Neratinib is an irreversible pan‐HER tyrosine kinase inhibitor and has been approved by the FDA as an effective drug for HER2‐positive breast cancer. However, acquired resistance of various cancers to molecular‐targeted drugs is an issue of clinical concern, and emergence of resistance to neratinib is also considered inevitable. In this study, we established various types of neratinib‐resistant cell lines from HER2‐amplified breast and lung cancer cell lines using several drug exposure conditions. We analyzed the mechanisms of emergence of the resistance in these cell lines and explored effective strategies to overcome the resistance. Our results revealed that amplification of YES1, which is a member of the SRC family, was amplified in two neratinib‐resistant breast cancer cell lines and one lung cancer cell line. Knockdown of YES1 by siRNA and pharmacological inhibition of YES1 by dasatinib restored the sensitivity of the YES1‐amplified cell lines to neratinib in vitro. Combined treatment with dasatinib and neratinib inhibited tumor growth in vivo. This combination also induced downregulation of signaling molecules such as HER2, AKT and MAPK. Our current results indicate that YES1 plays an important role in the emergence of resistance to HER2‐targeted drugs, and that dasatinib enables such acquired resistance to neratinib to be overcome. 相似文献
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Tetsuji Terazawa Jin Matsuyama Masahiro Goto Ryohei Kawabata Shunji Endo Motohiro Imano Shoichiro Fujita Yusuke Akamaru Hirokazu Taniguchi Mitsutoshi Tatsumi Sang-Woong Lee Yoshitaka Kurisu Hisato Kawakami Yukinori Kurokawa Toshio Shimokawa Daisuke Sakai Takeshi Kato Kazumasa Fujitani Taroh Satoh 《The oncologist》2020,25(2):119-e208