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排序方式: 共有1896条查询结果,搜索用时 15 毫秒
91.
Rintaro Noro Kazufumi Honda Kengo Nagashima Noriko Motoi Shinobu Kunugi Jun Matsubayashi Susumu Takeuchi Hideaki Shiraishi Tetsuya Okano Ayumi Kashiro Xue Meng Yukihiro Yoshida Shunichi Watanabe Jitsuo Usuda Tatsuya Inoue Huang Wilber Norihiko Ikeda Masahiro Seike Akihiko Gemma Kaoru Kubota 《Cancer science》2022,113(3):1002
Although adjuvant tegafur/uracil (UFT) is recommended for patients with completely resected stage I non‐small‐cell lung cancer (NSCLC) in Japan, only one‐third of cases has received adjuvant chemotherapy (ADJ) according to real‐world data. Therefore, robust predictive biomarkers for selecting ADJ or observation (OBS) without ADJ are needed. Patients who underwent complete resection of stage I lung adenocarcinoma with or without adjuvant UFT were enrolled. The status of ACTN4 gene amplification was analyzed by FISH. Statistical analyses to determine whether the status of ACTN4 gene amplification affected recurrence‐free survival (RFS) were carried out. Formalin‐fixed, paraffin‐embedded samples from 1136 lung adenocarcinomas were submitted for analysis of ACTN4 gene amplification. Ninety‐nine (8.9%) of 1114 cases were positive for ACTN4 gene amplification. In the subgroup analysis of patients aged 65 years or older, the ADJ group had better RFS than the OBS group in the ACTN4‐positive cohort (hazard ratio [HR], 0.084, 95% confidence interval [CI], 0.009‐0.806; P = .032). The difference in RFS between the ADJ group and the OBS group was not significant in ACTN4‐negative cases (all ages: HR, 1.214; 95% CI, 0.848‐1.738; P = .289). Analyses of ACTN4 gene amplification contributed to the decision regarding postoperative ADJ for stage I lung adenocarcinomas, preventing recurrence, improving the quality of medical care, preventing the unnecessary side‐effects of ADJ, and saving medical costs. 相似文献
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93.
Kiyoto Ashizawa Misa Imaizumi Toshiro Usa Tan Tominaga Nobuko Sera Ayumi Hida Eri Ejima Kazuo Neriishi Midori Soda Shinichiro Ichimaru Eiji Nakashima Saeko Fujiwara Renju Maeda Shigenobu Nagataki Katsumi Eguchi Masazumi Akahoshi 《Clinical endocrinology》2010,72(5):689-695
Objective A possible association between subclinical hypothyroidism and cardiovascular disease (CVD) has been reported. Monitoring of atomic‐bomb survivors for late effects of radiation exposure at the Radiation Effects Research Foundation has provided the opportunity to examine associations between subclinical hypothyroidism and metabolic CVD risk factors. The objective of the study was to evaluate associations between subclinical hypothyroidism and metabolic CVD risk factors, and a cluster of these factors. Design and participants This was a cross‐sectional study of 3549 subjects (mean age 70 years; 1221 men and 2328 women) between 2000 and 2003 comprising 306 subjects with subclinical hypothyroidism and 3243 control euthyroid subjects in Japan. Measurements We investigated associations between subclinical hypothyroidism and metabolic CVD risk factors such as hypertension, diabetes mellitus, dyslipidaemia and hyperuricaemia, and a cluster of these factors. Results Subclinical hypothyroidism was not significantly associated with either hypertension, diabetes mellitus or hyperuricaemia defined by taking into account the use of medications in both men and women, but in men it was associated with dyslipidaemia (P = 0·02). We observed a significantly increased odds ratio (OR) for the presence of three or more metabolic CVD risk factors in men with subclinical hypothyroidism after adjusting for age, body mass index (BMI), and smoking status [OR: 1·83, 95% confidence interval (CI): 1·13–2·94, P = 0·01]. The significant associations remained after an additional adjustment for atomic‐bomb radiation dose. Conclusions There appears to be a significant increase in a cluster of metabolic CVD risk factors among people with subclinical hypothyroidism. 相似文献
94.
Thaiz Ferraz Borin Ayumi Aurea Miyakawa Leandro Cardoso Luciano de Figueiredo Borges Giovana Aparecida Gonçalves Jose Eduardo Krieger 《International journal of experimental pathology》2009,90(3):328-337
Neo-intima development and atherosclerosis limit long-term vein graft use for revascularization of ischaemic tissues. Using a rat model, which is technically less challenging than smaller rodents, we provide evidence that the temporal morphological, cellular, and key molecular events during vein arterialization resemble the human vein graft adaptation. Right jugular vein was surgically connected to carotid artery and observed up to 90 days. Morphometry demonstrated gradual thickening of the medial layer and important formation of neo-intima with deposition of smooth muscle cells (SMC) in the subendothelial layer from day 7 onwards. Transmission electron microscopy showed that SMCs switch from the contractile to synthetic phenotype on day 3 and new elastic lamellae formation occurs from day 7 onwards. Apoptosis markedly increased on day 1, while α-actin immunostaining for SMC almost disappeared by day 3. On day 7, cell proliferation reached the highest level and cellular density gradually increased until day 90. The relative magnitude of cellular changes was higher in the intima vs . the media layer (100 vs . 2 times respectively). Cyclin-dependent kinase inhibitors (CDKIs) p27Kip1 and p16INKA remained unchanged, whereas p21Cip1 was gradually downregulated, reaching the lowest levels by day 7 until day 90. Taken together, these data indicate for the first time that p21Cip1 is the main CDKI protein modulated during the arterialization process the rat model of vein arterialization that may be useful to identify and validate new targets and interventions to improve the long-term patency of vein grafts. 相似文献
95.
96.
Serum H‐ficolin levels: Clinical association with interstitial lung disease in patients with systemic sclerosis 下载免费PDF全文
Takuya Miyagawa Yoshihide Asano Yuka de Mestier Ryosuke Saigusa Takashi Taniguchi Takashi Yamashita Kouki Nakamura Megumi Hirabayashi Shunsuke Miura Yohei Ichimura Takehiro Takahashi Ayumi Yoshizaki Tomomitsu Miyagaki Makoto Sugaya Shinichi Sato 《The Journal of dermatology》2017,44(10):1168-1171
Ficolins, a group of oligomeric lectins consisting of three isoforms (H‐, L‐ and M‐ficolin), contribute to innate immunity via activating the complement pathway and/or acting directly as opsonins against pathogens and apoptotic cells. Because apoptotic cells likely drive the development of systemic sclerosis (SSc) partly through innate immunity, we assessed the clinical association of serum H‐ficolin levels in SSc patients. Despite no difference in serum H‐ficolin levels between SSc and control subjects, SSc patients with decreased serum H‐ficolin levels tended to have a higher prevalence of interstitial lung disease (ILD). More importantly, serum H‐ficolin levels inversely correlated with ground‐glass opacity score on chest computed tomography in SSc‐ILD patients. Therefore, H‐ficolin‐related innate immunity may be involved in SSc‐ILD development. 相似文献
97.
Denda Ayumi; Tang Qing; Endoh Takehiro; Tsujiuchi Toshifumi; Horiguchi Kohsuke; Noguchi Osamu; Mizumoto Yasushi; Nakae Dai; Konishi Yoichi 《Carcinogenesis》1994,15(6):1279-1283
Effects of acetylsailcylic acid (ASA) (aspirin) on the pathogenesisof fatty liver, cirrhosis and hepatocarcinogenesis caused bya choline-deficient L-amino acid-defined (CDAA) diet were examinedin male Fischer 344 rats fed a CDAA diet supplemented with 0,0.1, 0.2, 0.4 or 0.8% ASA for 30 weeks. ASA at concentrationsof >0.2% prevented the development of both cirrhosis andpreneoplastic and neoplastic nodules, but without any directlyassociated prevention of fatty changes. ASA also prevented hepatocyteproliferation and the generation of thiobarbituric acid-reactivesubstances and 8-hydroxydeoxyguanosine caused by feeding theCDAA diet, analyzed, respectively, after 1, 12 and 12 weeks.The results clearly indicate that the anti-inflammatory drugASA, which is not a lipotropic factor, can prevent the pathogenesisof cirrhosis and hepatocarcinogenesis caused by a CDAA diet,which is possibly partly associated with the prevention of reactiveoxygen species production. 相似文献
98.
Dai Nakae Yasushi Mizumoto Hitoshi Yoshiji Nobuaki Andoh Kohsuke Horiguchi Kazumi Shiraiwa Eisaku Kobayashi Takehiro Endoh Naoshi Shimoji Kazutoshi Tamura Toshifumi Tsujiuchi Ayumi Denda Yoichi Konishi 《Cancer science》1994,85(5):499-505
The present study was performed to assess the roles of hepatocellular oxidative damage to DNA and constituents other than DNA in rat liver carcinogenesis caused by a choline-deficient, l -amino acid-defined (CDAA) diet by examining the effects of the antioxidant N, N' -diphenyl- p -phenylenediamine (DPPD). The parameters used for cellular oxidative damage were the level of 8-hydroxyguanine (8-OHGua) for DNA and that of 2-thiobarbituric acid-reacting substance (TBARS) for constituents other than DNA. A total of 40 male Fischer 344 rats, 6 weeks old, were fed the CDAA diet for 12 weeks with or without DPPD (0.05, 0.10 or 0.20%) or butylated hydroxytoluene (BHT, 0.25%). In the livers of the rats, the numbers and sizes of glutathione S -transferasc (EC 2.5.1.18) placental form (GSTP)- and/or γ-glutamyltransferase (GGT, EC 2.3.2.2)-positive lesions and levels of 8-OHGua and TBARS were determined. The GSTP-positive lesions of 0.08 mm2 or larger were all stained positively for GGT as well in cross-sectional area, whereas the smaller lesions were generally negative for GGT. DPPD and BHT reduced the size of the GSTP-positive lesions without affecting their total numbers. At the same time, they reduced TBARS generation without affecting 8-OHGua formation in DNA. The present results indicate that oxidative DNA damage (represented by 8-OHGua formation) and damage to constituents other than DNA (represented by TBARS generation) may play different roles in rat liver carcinogenesis caused by the CDAA diet; the former appears to be involved in the induction of phenotypically altered hepatocyte populations while the latter may be related to the growth of such populations. 相似文献
99.
Yamamoto Kazuhiko; Tsutsumi Masahiro; Kobayashi Eisaku; Endoh Takehiro; Noguchi Osamu; Okajima Eijiro; Denda Ayumi; Mori Yukio; Konishi Yoichi 《Carcinogenesis》1995,16(11):2633-2636
Initiation activities of endogenously formed N-nitrosobis(2-hydroxypropyl)amine(NBHPA), N-nitrosodiethanolamine (NDELA) and N-nitroso-2,6-dimethylmorpholine(NDMM) were investigated in a modified short-term assay forrat hepatocarcinogenesis. Male Wistar rats were fed 1 % bis(2-hydroxypropyl)amine,0.5% diethanolamine or 0.25% 2,6-dimethylmorpholine in the dietplus 0.3% sodium nitrite in the drinking water. Two weeks afterstarting the experimental regimen they underwent 2/3 partialhepatectomy and were then maintained on the respective dietsfor a further week. Following a 2 week recovery period on basaldiet the rats were subjected to a resistant hepatocyte regimenconsisting of 0.02% 2-acetylaminofluorene in the diet for 2weeks and 1 mg carbon tetrachloride/kg body wt by gavage atthe midpoint. Initiation activity was assayed by measuring hepaticfoci positive for 相似文献
100.
Toshifumi Tsujiuchi Eisaku Kobayashi Dai Nakae Yasushi Mizumoto Nobuaki Andoh Hiromichi Kitada Kazuo Ohashi Tomokazu Fukuda Akira Kido Masahiro Tsutsumi Ayumi Denda Yoichi Konishi 《Cancer science》1995,86(12):1136-1142
The effects of methionine on hepatocarcinogenesis induced by Coadministration of a choline-deflcient L-amino acid-defined (CDAA) diet and ethionine were examined. F344 male rats were divided into 4 experimental groups. Groups 1 and 2 received the CDAA diet and a choline-supplemented L-amino acid-defined (CSAA) diet, respectively. Group 3 received the CDAA diet containing 0.05% ethionine, and group 4 the CDAA diet containing 0.05% ethionine and 0.47% methionine. Animals were killed after 12 weeks of treatment. Histologically, the CDAA diet induced intracellular fat accumulation and foci. In contrast, ethionine caused not only foci, but also hyperplastic nodules, cholangiofibrosis and the proliferation of oval cells without such fat accumulation. Methionine abolished the development of all of the liver lesions induced by Coadministration of the CDAA diet and ethionine. To investigate the effects of methionine on induction of c- myc and c-Ha- ras expression, as well as generation of 8-hydroxyguanine (8-OHGua) and 2-thiobarbituric acid-reacting substances (TBARS), by Coadministration of the CDAA diet and ethionine, subgroups of 3 to 5 animals were killed at 2, 4, 8 or 11 days after the beginning of the experiment. Coadministration of the CDAA diet and ethionine markedly enhanced the level of expression of c- myc and c-Ha- ras , 8-OHGua formation and TBARS generation as compared with the CDAA or CSAA diet within 11 days, and methionine blocked these actions. These results indicate that addition of methionine prevents the induction of c- myc and c-Ha- ras expression, 8-OHGua formation and TBARS generation, as well as hepatocellular lesions, by Coadministration of the CDAA diet and ethionine in rats, and suggest a possible involvement of oxidative stress and gene expression in hepatocarcinogenesis by these agents. 相似文献