全文获取类型
收费全文 | 1869篇 |
免费 | 115篇 |
国内免费 | 31篇 |
专业分类
耳鼻咽喉 | 17篇 |
儿科学 | 45篇 |
妇产科学 | 32篇 |
基础医学 | 192篇 |
口腔科学 | 24篇 |
临床医学 | 92篇 |
内科学 | 609篇 |
皮肤病学 | 30篇 |
神经病学 | 121篇 |
特种医学 | 67篇 |
外科学 | 422篇 |
综合类 | 2篇 |
预防医学 | 28篇 |
眼科学 | 38篇 |
药学 | 77篇 |
中国医学 | 2篇 |
肿瘤学 | 217篇 |
出版年
2024年 | 3篇 |
2023年 | 25篇 |
2022年 | 24篇 |
2021年 | 77篇 |
2020年 | 58篇 |
2019年 | 78篇 |
2018年 | 70篇 |
2017年 | 47篇 |
2016年 | 71篇 |
2015年 | 62篇 |
2014年 | 90篇 |
2013年 | 87篇 |
2012年 | 114篇 |
2011年 | 134篇 |
2010年 | 73篇 |
2009年 | 68篇 |
2008年 | 113篇 |
2007年 | 92篇 |
2006年 | 104篇 |
2005年 | 116篇 |
2004年 | 102篇 |
2003年 | 83篇 |
2002年 | 85篇 |
2001年 | 21篇 |
2000年 | 19篇 |
1999年 | 19篇 |
1998年 | 19篇 |
1997年 | 14篇 |
1996年 | 15篇 |
1995年 | 18篇 |
1994年 | 12篇 |
1993年 | 7篇 |
1992年 | 3篇 |
1991年 | 9篇 |
1990年 | 6篇 |
1989年 | 5篇 |
1988年 | 5篇 |
1987年 | 5篇 |
1986年 | 6篇 |
1985年 | 3篇 |
1984年 | 7篇 |
1983年 | 6篇 |
1982年 | 9篇 |
1981年 | 10篇 |
1980年 | 3篇 |
1978年 | 2篇 |
1976年 | 2篇 |
1975年 | 5篇 |
1972年 | 2篇 |
1971年 | 3篇 |
排序方式: 共有2015条查询结果,搜索用时 78 毫秒
21.
22.
Jun Yoshida Masaaki Mizuno Itaru Inoue Toshihiko Wakabayasi Kenichiro Sugita Hisao Seo Kazumi Chiba 《Journal of neuro-oncology》1990,8(3):221-229
Summary Monoclonal antibody (MCA) G-22 is directed against a human glioma-associated surface antigen. Its availability for the radioimmunodetection of human glioma was analyzed by utilizing the xenografts in athymic mice. Nude mice with subcutaneous grafts of U251-MG or U251-SP glioma received intravenous administration of 123I or 131I labeled F(ab)2 fragment or whole immunoglobulin. Results of radioimaging revealed that 123I-labeled antibody was better than the 131I-labeled. It was also noted that administration of 123I-labeled F(ab)2 fragment of G-22 MCA enabled the imaging of human glioma xenografts weighing 80–650 mg after 48 hours. When biodistribution of 123I MCA was compared between G-22 and control antibodies, the percentages of dose/g in tumors were 5.228–1.799 at 30 hours and 4.112–1.132 at 48 hours with G-22 and they were 4.164–1.248 and 0.314–0.142 with control. The tumor/blood ratio until 72 hours after injection was constantly above 1 with G-22 and less than 1 with control antibody. These results indicate the potential usefulness of G-22 MCA for the radioimmunodetection of human gliomas. 相似文献
23.
Role of Ca2+-activated K+ channels in acetylcholine-induced dilatation of the basilar artery in vivo 下载免费PDF全文
Takanari Kitazono Setsuro Ibayashi Tetsuhiko Nagao Kenichiro Fujii Masatoshi Fujishima 《British journal of pharmacology》1996,120(1):102-106
- We tested the hypothesis that activation of large conductance calcium-activated potassium channels is involved in dilator responses of the basilar artery to acetylcholine in vivo. Using a cranial window in anaesthetized rats, we examined responses of the basilar artery to acetylcholine.
- Topical application of acetylcholine (10−6 and 10−5 M) increased diameter of the basilar artery from 238±7 μm to 268±7 and 288±7 μm, respectively (P<0.05 vs. baseline diameter). Iberiotoxin (10−8 M), an inhibitor of large conductance calcium-activated potassium channels, did not affect baseline diameter of the basilar artery. In the presence of 10−8 M iberiotoxin, 10−6 and 10−5 M acetylcholine increased diameter of the basilar artery from 239±7 μm to 246±7 and 261±7 μm, respectively. Thus, iberiotoxin attenuated acetylcholine-induced dilatation of the basilar artery (P<0.05).
- Sodium nitroprusside (10−7 and 10−6 M) increased diameter of the basilar artery from 242±9 μm to 310±12 and 374±13 μm, respectively (P<0.05 vs. baseline diameter). In the presence of iberiotoxin (10−8 M), sodium nitroprusside (10−7 and 10−6 M) increased diameter of the basilar artery from 243±6 μm to 259±9 and 311±12 μm, respectively. Thus, iberiotoxin attenuated dilator responses of the basilar artery to sodium nitroprusside (P<0.05).
- Iberiotoxin partly inhibited dilator responses of the basilar artery to forskolin, a direct activator of adenylate cyclase, but did not affect vasodilatation produced by levcromakalim, a potassium channel opener.
- These results suggest that dilator responses of the basilar artery to acetylcholine and sodium nitroprusside are mediated, in part, by activation of large conductance calcium-activated potassium channels. Because both acetylcholine and sodium nitroprusside have been shown to activate guanylate cyclase via nitric oxide, activation of large conductance calcium-activated potassium channels may be one of the major mechanisms by which cyclic GMP causes dilatation of the basilar artery in vivo.
24.
The objective of the present study was to assess the relationship between the amount of lactate accumulated during complete ischaemia and the ensuing changes in extra- and intracellular pH (pHe and pHi, respectively). The preischaemic plasma glucose concentration of anaesthetized rats was varied by administration of glucose or insulin, pHe was determined in neocortex with ion-sensitive microelectrodes, and tissue lactate and CO2 contents were measured, tissue CO2 tension being known from separate experiments. The experiments were carried out in both normocapnic [arterial CO2 tension (PaCO2) approximately 40 mm Hg] and hypercapnic (PaCO2 approximately 80 mm Hg) animals. Irrespective of the preischaemic CO2 tension, DeltapHe was linearly related to tissue lactate content. Depending on the preischaemic glucose concentration, DeltapHe varied from <0.4 to >1.4 units. The results thus fail to confirm previous results that the changes in pHe describe two plateau functions (DeltapHe approximately 0.5 and 1.1, respectively), with a transition zone at tissue lactate contents of 17 - 20 mmol kg-1. Changes in pHi given in this study are based on the assumption of a uniform intracellular space. The pHi changed from a normal value of approximately 7.0 to 6.5, 6.1 and 5.8 at tissue lactate contents of 10, 20 and 30 mmol kg-1. The intrinsic (non-bicarbonate) buffer capacity, derived from these figures, was 23 mmol kg-1 pH-1. Some differences in pH and in HCO3- concentration between extra- and intracellular fluids persisted in the ischaemic tissue. These differences were probably caused by a persisting membrane potential in the ischaemic cells. 相似文献
25.
Sung Yeon Kim Y R Santosh Laxmi Naomi Suzuki Kenichiro Ogura Tadashi Watabe Michael W Duffel Shinya Shibutani 《Drug metabolism and disposition》2005,33(11):1673-1678
Tamoxifen (TAM) is used as the standard endocrine therapy for breast cancer patients and as a chemopreventive agent for women at high risk for this disease. Unfortunately, treatment of TAM increases the incidence of endometrial cancer; this may be due to the genotoxic damage induced by TAM metabolites. Formation of TAM-DNA adducts in rat liver correlates with the development of hepatocarcinoma. TAM-DNA adducts are proposed to be formed through O-sulfonation and/or O-acetylation of alpha-hydroxylated TAM and its metabolites. However, the role of O-sulfonation and O-acetylation in the formation of TAM-DNA adducts has not been extensively investigated. Rat or human hydroxysteroid sulfotransferases (HST), acetyltransferases, and liver cytosol were incubated with calf thymus DNA, alpha-OHTAM, and either 3'-phosphoadenosine 5'-phosphosulfate (PAPS) or acetyl coenzyme A (acetyl-CoA) as a cofactor and analyzed for TAM-DNA adduct formation, using 32P postlableling/polyacrylamide gel electrophoresis analysis. TAM-DNA adduct was formed when PAPS, not acetyl-CoA, was used. No TAM-DNA adducts were produced using human N-acetyltransferase I and II. HST antibody inhibited approximately 90% of TAM-DNA adduct formation generated by the cytosol or HST, suggesting that HST is primarily involved in the formation of TAM-DNA adducts. The formation of TAM-DNA adducts with rat liver cytosol and HST was much higher than that of human liver cytosol and HST. Our results indicate that TAM-DNA adducts are formed via O-sulfonation, not O-acetylation, of alpha-hydroxylated TAM and its metabolites. 相似文献
26.
Dihydropyrimidine dehydrogenase activity in 150 healthy Japanese volunteers and identification of novel mutations. 总被引:4,自引:0,他引:4
27.
Takashi Yamaguchi Min Gi Shotarou Yamano Masaki Fujioka Kumiko Tatsumi Satoko Kawachi Naomi Ishii Kenichiro Doi Anna Kakehashi Hideki Wanibuchi 《Experimental and toxicologic pathology》2017,69(1):1-7
Diphenylarsinic acid (DPAA), a chemical warfare-related neurotoxic organic arsenical, is present in the groundwater and soil in some regions of Japan due to illegal dumping after World War II. The purpose of the present study was to evaluate the potential toxicity of DPAA when administered to rats in their drinking water for 52 weeks. DPAA was administered to groups 1–4 at concentrations of 0, 5, 10, and 20 ppm in their drinking water for 52 weeks. There were no significant differences in the final body weights between the control groups and the treatment groups in male or female rats. In serum biochemistry, in females 20 ppm DPAA significantly increased alkaline phosphatase and γ-glitamyl transferase compared to controls, and 10 and 20 ppm DPAA significantly increased total cholesterol compared to controls. Absolute and relative liver weights were significantly increased in females treated with 20 ppm DPAA compared to the control group. Dilation of the common bile duct outside the papilla of Vater and stenosis of the papilla of Vater was observed in all male and female rats administered 20 ppm DPAA. The incidence of intrahepatic bile duct hyperplasia was significantly increased in male and female rats treated with 20 ppm DPAA compared to the control groups. These results suggest that DPAA is toxic to the bile duct epithelium in rats. The no-observed adverse effect levels of DPAA were estimated to be 10 ppm (0.48 mg/kg b.w./day) for males and 5 ppm (0.35 mg/kg b.w./day) for females under the conditions of this study. 相似文献
28.
29.
Endoscopic features associated with development of metachronous gastric cancer in patients who underwent endoscopic resection followed by Helicobacter pylori eradication 下载免费PDF全文
30.
Aki Masuzawa Chikako Kiyotani Tomoo Osumi Yoko Shioda Kazutoshi Iijima Osamu Tomita Kazuhiko Nakabayashi Keisuke Oboki Kazuki Yasuda Hiromi Sakamoto Hitoshi Ichikawa Kenichiro Hata Teruhiko Yoshida Kenji Matsumoto Nobutaka Kiyokawa Tetsuya Mori 《European journal of haematology》2014,92(3):263-267
In addition to BCR, various rare fusion partners for the ABL1 gene have been reported in leukemia. We have identified the fusion gene SNX2‐ABL1 in a pediatric case of acute lymphoblastic leukemia (ALL), which has only once previously been reported in an adult patient. Cytogenetic analysis detected this fusion gene arising from a t(5;9)(q22;q34) translocation. ALL cells carrying a SNX2‐ABL1 fusion exhibited a BCR‐ABL1+ ALL‐like gene expression profile. The patient poorly responded to dasatinib but partially responded to imatinib. Treatment using tyrosine kinase inhibitors requires further investigation to optimize the genotype‐based treatment stratification for patients with SNX2‐ABL1 fusion. 相似文献