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91.
92.
Hitoshi Kotanagi Toshiaki Yoshioka Osamu Muto Hiroshi Kon Ryuichi Yanagida Masanao Ito Toshiki Kikuchi Kenji Koyama 《International journal of clinical oncology / Japan Society of Clinical Oncology》1997,2(3):133-137
Background Japanese surgeons have to macroscopically assess nodal metastasis from colon cancer according to the general rules established
in Japan. Adjuvant therapy is sometimes started after macroscopic assessment of nodal metastasis. Macroscopic assessment,
however, is difficult in many cases.
Methods We evaluated the reliability of macroscopic assessment of nodal metastasis in colon cancer by (1) comparing the number of
nodes picked up macroscopically with that of nodes recognized microscopically, and (2) by comparing the number of metastatic
nodes found between macroscopic and microscopic examination.
Results The number of nodes found during macroscopic examination was equal to that found in microscopic examination in only 52 of
206 cases (25%). Although 120 of 206 cases (58%) were judged macroscopically to have metastatic nodes, 61 had no metastatic
nodes found microscopically. Sensitivity and specificity for the recognition of cases with nodal metastasis was 85.5% and
55.5%, respectively. The number of metastatic nodes in macroscopic examination was equal to that in microscopic examination
in 90 cases (44%).
Conclusion Because macroscopic assessment of nodal metastasis is not reliable, physicians should not rely on macroscopic assessment to
indicate the need for further therapy, such as adjuvant chemotherapy. The recommendation for macroscopic assessment of nodal
metastasis should be eliminated from the general rules in Japan. 相似文献
93.
Homotypic Adhesion through Carcinoembryonic Antigen Plays a Role in Hepatic Metastasis Development 总被引:2,自引:0,他引:2
Toshiaki Yoshioka Takashi Masuko Hitoshi Kotanagi Osamu Aizawa Yuri Saito Hiroshi Nakazato Kenji Koyama Yoshiyuki Hashimoto 《Cancer science》1998,89(2):177-185
We established a cell line with high metastatic potential to the liver (LS-LM4) after four successive repetitions of splenic injection of liver-metastatic cells in SCID mice. This cell line strongly expressed CEA and showed increased homotypic adhesion as compared with the parent cell line (LS174T). To examine the role of CEA in the increased homotypic adhesion, LS-LM4 cells were treated with anti-CEA antibody and subjected to an in vitro adhesion and aggregation assay. Further, to study the role of CEA in the hepatic metastasis of cells with high metastatic potential, LS-LM4 cells were treated with anti-CEA antibody, and the inhibition of hepatic metastasis after splenic injection in vivo was examined. There was a 62% decrease in the homotypic adhesion of anti-CEA antibody-treated (100 μg/ml) LS-LM4 cells under a Ca2+ -free condition as compared with the control ( P <0.01). Anti-CEA antibody (100 μg/ml) inhibited cell aggregation under a Ca2+ -free condition ( P <0.05). Treatment with anti-E-cadherin antibody (60 μ/ml) plus anti-CEA antibody (100 μg/ml) inhibited cell aggregation more potently than anti-E-cadherin antibody treatment alone in the presence of Ca2+ . In vivo , there was a 75% decrease in the number of hepatic metastatic nodules in the G125 anti-CEA antibody-treated group as compared with the control group ( P <0.01). Similarly, there was a 40% decrease in the diameter of metastatic nodules and there was a 90% decrease in total tumor volume of hepatic metastasis in the G125 anti-CEA antibody-treated group as compared with the control ( P <0.01). These results suggest that increased metastatic potential to the liver is at least partly due to increased homotypic binding mediated by CEA. 相似文献
94.
Absence of p53 Overexpression and Favorable Response to Cisplatin-based Neoadjuvant Chemotherapy in Urothelial Carcinomas 总被引:3,自引:0,他引:3
Yoshiyuki Kakehi Enver Özdemir Tomonori Habuchi Hirohiko Yamabe Takayuki Hashimura Yoshitaka Katsura Osamu Yoshida 《Cancer science》1998,89(2):214-220
It has been controversial whether cancer cells harboring loss or inactivation of the tumor suppressor p53 are resistant or sensitive to DNA-damaging agents including cisplatin and doxorubicin. Overexpression of mdm2 oncoprotein, a negative regulator of p53, is assumed to be an alternative to p53 dysfunction. Archival urothelial carcinoma specimens obtained from 60 patients prior to cisplatin-based chemotherapy were immunohistochemically studied for overexpression of p53 and mdm2. Thirty-two patients (group I) were treated with chemotherapy in the neoadjuvant setting, while 28 patients (group II) underwent chemotherapy for distant metastases or inoperable locoregional tumors. In group I, the responsiveness was correlated with staining status of p53 ( P =0.0225) and the combination of p53 and mdm2 ( P =0.0497). Negative staining of p53 and negative for both p53 and mdm2 could have predicted favorable response to chemotherapy in 16 of 18 (88.9%) and in 12 of 13 (92.3%) tumors, respectively. On the other hand, p53-positive and p53 and/or mdm2-positive staining could have predicted poor response only in 7 of 14 (50.0%) and 8 of 19 (42.1%) tumors, respectively. Disease-specific survival of the p53-negative group was significantly superior to that of the p53-positive group ( P =0.0086). Difference in survival did not become more significant when overexpression of mdm2 was taken into consideration ( P =0.0456). In contrast, in group II, there was no correlation of responsiveness to chemotherapy or survival with p53- or p53/mdm2-staining status. The patients with urothelial carcinomas negative for overexpression of p53 will benefit from neoadjuvant chemotherapy. From clinical viewpoint, however, p53 status alone or the combination of p53 and mdm2 status is not enough to identify those patients who will not benefit from the treatment. 相似文献
95.
Osamu Miyamoto Takehiro Nakamura Shin-ich Yamagami Tetsuro Negi Masaaki Tokuda Hideki Matsui Toshifumi Itano 《Brain research》2000,873(1):418
To investigate the mechanism of chronic cell death following postischemic hypothermia, the change of N-methyl-
-aspartate receptor (NMDAR) were examined by immunohistochemistry of NMDAR1 and long-term potentiation (LTP) in the CA1 subfield of the gerbil hippocampus. At 1 week following postischemic hypothermia (32°C×4 h), all CA1 neurons survived; however, immunoreactivity of NMDAR1 increased in neuronal perikarya whereas decreased in dendrites in the CA1 neurons. The abnormality was still observed in remaining CA1 neurons at 1 month after hypothermia. LTP was also significantly depressed at 1 week after hypothermia. These results suggest that some abnormalities in the glutamate receptor may be caused by ischemia; such abnormality would persist in spite of hypothermia treatment, resulting in the depression of LTP. 相似文献
96.
97.
Wang L Kuroiwa Y Kamitani T Li M Takahashi T Suzuki Y Shimamura M Hasegawa O 《Journal of neurology》2000,247(5):356-363
To determine whether there are characteristic changes in event-related potentials (ERPs) in parkinsonian syndromes we studied
8 patients with progressive supranuclear palsy (PSP), 10 patients with corticobasal degeneration (CBD), 9 patients with striatonigral
degeneration (SND), and 16 patients with idiopathic Parkinson's disease (PD) with a mean duration of illness shorter than
5 years in each group. A visual oddball paradigm was employed to elicit P300. P300 to the rare target and rare nontarget stimuli
and reaction time (RT) to rare target stimuli in each group were compared with those in the corresponding age-matched normal
control group and to each other after age correction. The correlation of P300 and RT to motor disability score was also studied.
In PSP P300 amplitude was markedly reduced while in CBD P300 latency was prolonged. P300 amplitude to rare nontargets in SND
and PD was attenuated. The mean RT in the PSP and the CBD group was significantly longer than in the other two groups. The
mean RT in PD and P300 amplitude to rare nontargets in both CBD and PD showed significant correlation with the severity of
motor disability. Simultaneous measurement of P300 and RT may yield useful supplementary information in facilitating diagnosis
of parkinsonian syndromes in addition to clinical criteria.
Received: 6 April 1999, Received in revised form: 5 August 1999, Accepted: 12 January 2000 相似文献
98.
Takeo Shimo Naoki Ashizawa Koji Matsumoto Takashi Nakazawa Osamu Nagata 《Toxicological sciences》2005,87(1):267-276
The possible mechanism of the underlying nephropathy found in the rat toxicity study of FYX-051, a xanthine oxidoreductase inhibitor, was investigated. Rats received oral treatment of either 1 or 3 mg/kg of FYX-051, with and without citrate for four weeks to elucidate whether nephropathy could be caused by materials deposited in the kidney. Furthermore, analysis of the renal deposits in rats was also performed. Consequently, interstitial nephritis comprising interstitial inflammatory cell infiltration, dilatation, basophilia and epithelial necrosis of renal tubules and collecting ducts, deposits in renal tubules and collecting ducts, and so forth was seen in six of the eight rats and in all eight rats in the 1 and 3 mg/kg FYX-051 alone groups, respectively, with the intensity in the 3 mg/kg group being moderate to severe. In the simultaneous treatment with citrate group, however, no alterations were observed in the kidney, except for minimal interstitial nephritis in one instance in the 3 mg/kg FYX-051 + citrate group along with an increased urinary pH, leading to an increase in xanthine solubility. Analysis of intrarenal deposits showed that the entity would be composed of xanthine crystals. The present study, therefore, showed that nephropathy in rats occurring after the administration of FYX-051 was a secondary change caused by xanthine crystals being deposited in the kidney, and no other causes could be implicated in this kidney lesion. 相似文献
99.
Colocalization of the tetraspanins, CO-029 and CD151, with integrins in human pancreatic adenocarcinoma: impact on cell motility. 总被引:6,自引:0,他引:6
Sabine Gesierich Claudia Paret Dagmar Hildebrand Jürgen Weitz Kaspar Zgraggen Friedrich H Schmitz-Winnenthal Vaclav Horejsi Osamu Yoshie Dorothee Herlyn Leonie K Ashman Margot Z?ller 《Clinical cancer research》2005,11(8):2840-2852
PURPOSE: Patients with pancreatic adenocarcinoma have a poor prognosis due to the extraordinary high invasive capacity of this tumor. Altered integrin and tetraspanin expression is suggested to be an important factor. We recently reported that after protein kinase C activation, colocalization of alpha6beta4 with the tetraspanin CO-029 strongly supports migration of a rat pancreatic adenocarcinoma. The finding led us to explore whether and which integrin-tetraspanin complexes influence the motility of human pancreatic tumors. EXPERIMENTAL DESIGN: Integrin and tetraspanin expression of pancreatic and colorectal adenocarcinoma was evaluated with emphasis on colocalization and the impact of integrin-tetraspanin associations on tumor cell motility. RESULTS: The majority of pancreatic and colorectal tumors expressed the alpha2, alpha3, alpha6, beta1, and beta4 integrins and the tetraspanins CD9, CD63, CD81, CD151, and CO-029. Expression of alpha6beta4 and CO-029 was restricted to tumor cells, whereas alpha1, alpha2, alpha3, alpha6, beta1, and CD9, CD81, CD151 were also expressed by the surrounding stroma. CD63, CD81, and beta1 expression was observed at comparably high levels in healthy pancreatic tissue. alpha3beta1 frequently colocalized and coimmunoprecipitated with CD9, CD81, and CD151, whereas alpha6beta4 colocalized and coimmunoprecipitated mostly with CD151 and CO-029. Notably, protein kinase C activation strengthened only the colocalization of CD151 and CO-029 with beta4 and was accompanied by internalization of the integrin-tetraspanin complex, decreased laminin 5 adhesion, and increased cell migration. CONCLUSION: alpha6beta4 is selectively up-regulated in pancreatic and colorectal cancer. The association of alpha6beta4 with CD151 and CO-029 correlates with increased tumor cell motility. 相似文献
100.