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991.
Kazuki Ito Hiroki Sugihara Susumu Nishikawa Yoshihiko Adachi Shuuji Kato Akihiro Azuma Hiroaki Matsubara Shinichi Osa Masahiro Abe Hitoshi Iino Hidehito Shiobara Michihiko Morisaki Hayato Mitsuyama Manabu Fujinawa Masato Kurihara Akira Yamashina Katsuji Ikekubo Megumu Hino Hidetomi Ito Hiroyuki Ohtsuka Yasuhiko Saiki Yuuji Asano Katsumi Ishh Takao Sagiuchi Kazushige Hayakawa Kei Kikuchi Kouji Jinguuji Yukitoshi Ohta Katsumi Abe Shigeru Kosuda Shoichi Kusano Masayoshi Nagata Katsuji Ikekubo Kiyoko Kusakabe Shinichi Kanaya Naofumi Ishikawa Kunihiro Nakada Yutaka Mori 《Annals of nuclear medicine》2003,17(8):739-741
992.
993.
Simvastatin attenuates plaque inflammation: evaluation by fluorodeoxyglucose positron emission tomography. 总被引:11,自引:0,他引:11
Nobuhiro Tahara Hisashi Kai Masatoshi Ishibashi Hiroyuki Nakaura Hayato Kaida Kenkichi Baba Naofumi Hayabuchi Tsutomu Imaizumi 《Journal of the American College of Cardiology》2006,48(9):1825-1831
OBJECTIVES: We investigated whether simvastatin attenuates plaque inflammation by using 18F-fluorodeoxyglucose positron emission tomography (18FDG-PET) co-registered with computerized tomography. BACKGROUND: Inflammation plays a key role in progression and destabilization of atherosclerotic plaque. 18F-fluorodeoxyglucose PET is a promising tool for visualizing inflammation of atherosclerotic plaque. Antiinflammatory action is one of the pleiotropic effects of statins. METHODS: Forty-three consecutive subjects, who underwent 18FDG-PET for cancer screening and had 18FDG uptakes in the thoracic aorta and/or the carotid arteries, were randomized to either statin group receiving simvastatin (n = 21) or diet group receiving dietary management only (n = 22). The maximum standardized uptake values (SUVs) were measured in individual plaques, and were averaged for analysis of the subjectwise results. The responses were assessed after 3-month treatments. RESULTS: Positron emission tomography revealed 117 and 123 18FDG-positive plaques in the statin and diet groups, respectively. Simvastatin, but not diet alone, attenuated plaque (18)FDG uptakes and decreased the SUVs (p < 0.01). Simvastatin reduced low-density lipoprotein cholesterol (LDL-C) by 30% (p < 0.01) and increased high-density lipoprotein cholesterol (HDL-C) by 15% (p < 0.01), whereas LDL-C and HDL-C levels were not changed in the diet group. In the statin group, the decrease in the SUV was well correlated with the HDL-C elevation (p < 0.01) but not with the LDL-C reduction. CONCLUSIONS: 18F-fluorodeoxyglucose PET visualized plaque inflammation and simvastatin attenuated it. The LDL-C-independent effects of simvastatin may participate in the beneficial effect. 18F-fluorodeoxyglucose PET has a potential for visually monitoring plaque inflammation and the therapeutic effectiveness of statins. 相似文献
994.
S. Juki I. Ani K. Koba D. Najar-Fleger & K Matsumoto 《International endodontic journal》1997,30(3):175-180
The histological response of the dental pulp after laser irradiation was studied. After pulpotomy was performed in the premolar and molar teeth of dogs, the exposed pulp tissue at the root canal opening was lased using either a CO2 or Nd:YAG laser. The laser parameters were 2 W, 10 ms, 5 times per second for 1, 2 and 3 s for CO2 laser and 2 W, 20 pulses per second for 1, 2 and 3 s for the Nd:YAG laser. Observations were made 30 and 45 days after treatment. The results revealed that laser irradiation caused carbonization, necrosis, infiltration of inflammation cells, oedema and haemorrhage in the pulp tissue. Under the conditions of this experiment, there was little histological evidence of repair to the treated pulp with a newly formed dentine barrier, which was in contrast to the control samples treated with a calcium hydroxide-containing cement (Dycal). 相似文献
995.
Utility of KRAS mutation detection using circulating cell‐free DNA from patients with colorectal cancer
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Takeshi Yamada Takuma Iwai Goro Takahashi Hayato Kan Michihiro Koizumi Akihisa Matsuda Seiichi Shinji Aya Yamagishi Yasuyuki Yokoyama Atsushi Tatsuguchi Tatsuro Kawagoe Shiro Kitano Masato Nakayama Satoshi Matsumoto Eiji Uchida 《Cancer science》2016,107(7):936-943
In this study, we evaluated the clinical utility of detecting KRAS mutations in circulating cell‐free (ccf)DNA of metastatic colorectal cancer patients. We prospectively recruited 94 metastatic colorectal cancer patients. Circulating cell‐free DNA was extracted from plasma samples and analyzed for the presence of seven KRAS point mutations. Using the Invader Plus assay with peptide nucleic acid clamping method and digital PCR, KRAS mutations were detected in the ccfDNA in 35 of 39 patients previously determined to have primary tumors containing KRAS mutations using the Luminex method, and in 5 of 55 patients with tumors containing wild‐type KRAS. Curative resection was undertaken in 7 of 34 patients with primary and ccfDNA KRAS mutations, resulting in the disappearance of the mutation from the cell‐free DNA in five of seven patients. Three of these patients had tumor recurrence and KRAS mutations in their ccfDNA reappeared. Epidermal growth factor receptor blockade was administered to 24 of the KRAS tumor wild‐type patients. Of the 24 patients with wild‐type KRAS in their primary tumors, three patients had KRAS mutations in their ccfDNA and did not respond to treatment with epidermal growth factor receptor (EGFR) blockade. We also detected a new KRAS mutation in five patients during chemotherapy with EGFR blockade, before disease progression was detectable with imaging. The detection of KRAS mutations in ccfDNA is an attractive approach for predicting both treatment response and acquired resistance to EGFR blockade, and for detecting disease recurrence. 相似文献
996.
Calpain inhibitor calpeptin suppresses pancreatic cancer by disrupting cancer–stromal interactions in a mouse xenograft model
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Masaki Yoshida Yoshihiro Miyasaka Kenoki Ohuchida Takashi Okumura Biao Zheng Nobuhiro Torata Hayato Fujita Toshinaga Nabae Tatsuya Manabe Masaya Shimamoto Takao Ohtsuka Kazuhiro Mizumoto Masafumi Nakamura 《Cancer science》2016,107(10):1443-1452
Desmoplasia contributes to the aggressive behavior of pancreatic cancer. However, recent clinical trials testing several antifibrotic agents on pancreatic cancer have not shown clear efficacy. Therefore, further investigation of desmoplasia‐targeting antifibrotic agents by another mechanism is needed. Calpeptin, an inhibitor of calpains, suppressed fibroblast function and inhibited fibrosis. In this study, we investigated the anticancer effects of calpeptin on pancreatic cancer. We investigated whether calpeptin inhibited tumor progression using a mouse xenograft model. We used quantitative RT‐PCR to evaluate the expression of calpain‐1 and calpain‐2 mRNA in pancreatic cancer cells (PCCs) and pancreatic stellate cells (PSCs). We also undertook functional assays, including proliferation, migration, and invasion, to evaluate the inhibitory effects of calpeptin on PCCs and PSCs. Quantitative RT‐PCR indicated that PCCs and PSCs expressed calpain‐2 mRNA. Calpeptin reduced tumor volume (P = 0.0473) and tumor weight (P = 0.0471) and inhibited the tumor desmoplastic reaction (P < 0.001) in xenograft tumors in nude mice. Calpeptin also inhibited the biologic functions of PCCs and PSCs including proliferation (P = 0.017), migration (P = 0.027), and invasion (P = 0.035) in vitro. Furthermore, calpeptin reduced the migration of PCCs and PSCs by disrupting the cancer–stromal interaction (P = 0.0002). Our findings indicate that calpeptin is a promising antitumor agent for pancreatic cancer, due not only to its suppressive effect on PCCs and PSCs but also its disruption of the cancer–stromal interaction. 相似文献
997.
An in vitro system to characterize prostate cancer progression identified signaling required for self‐renewal
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998.
Ryuki Kawamura Hitoshi Saiki Hayato Tada Akihiro Hata 《Journal of clinical lipidology》2018,12(1):246-249
We report the case of acute myocardial infarction in a 25-year-old woman with sitosterolemia. She was treated using statins, but her low-density lipoprotein cholesterol (LDL-C) levels did not decrease appreciably. Genetic analysis revealed mutations in the ABCG8 gene. Ezetimibe treatment was initiated, and her LDL-C levels decreased substantially. Sitosterolemia must be considered in the differential diagnosis of familial hypercholesterolemia in case of early onset cardiovascular disease patient with high LDL-C. 相似文献
999.
1000.
Asuka Tsuchiya Hayato Yamana Takuya Kawahara Yusuke Tsutsumi Hiroki Matsui Kiyohide Fushimi Hideo Yasunaga 《Burns : journal of the International Society for Burn Injuries》2018,44(8):1954-1961