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81.
Susumu Yoshikawa Jitsuo Kiji Junji Furukawa 《Macromolecular chemistry and physics.》1977,178(4):1077-1087
The dimerization of 1-alkynes by rhodium(I) complexes in the presence of phosphorus ligands is described. The products are linear and branched dimers, the ratio of which is correlated with the electronic parameters, vCO of Ni(CO)3L, of the ligands L, but no simple correlation is apparent between their steric parameter and the selectivity. Electron-donating ligands promote the formation of the linear dimer. The substituents of the 1-alkynes also affect the distribution of linear and branched dimers. Electron-donating substituents prefer linear isomer to branched one. The reactivity of the substituted 1-alkynes (R? C?C? H) increased with substituent R in the order 相似文献
82.
83.
T Furukawa 《Rinsho byori. The Japanese journal of clinical pathology》1991,39(10):1044-1048
The medical advancements, during the 20th century symbolize the industrialization of medical technologies, i.e., many clinical tests are carried out by the highly advanced automated machines. Also, the concept of intelligent processing of clinical diagnosis seems to have been established in the practice. However, it may be an illusion caused from the term artificial intelligence (AI) which attracts the attention of not only specialists of computer science but also clinicians. The essential nature of AI, especially of expert consultation systems is the same as the existing theories, such as Bayes' theorem, Boolean algebra, multivariate statistical analysis, and Fussy theorem, i.e., the evaluation of a weighted sum of multiple parameters. The weak point of these theories is the lack of time parameter. Therefore, the models using a time parameter including physiological simulation, dynamics model, Weibull model and Markov process are important to realize the revolution of clinical diagnosis from the standpoint of intelligent science and technology. 相似文献
84.
Human muscle sympathetic neural and haemodynamic responses to tilt following spaceflight 总被引:6,自引:5,他引:6
Benjamin D. Levine James A. Pawelczyk rew C. Ertl James F. Cox Julie H. Zuckerman ré Diedrich Italo Biaggioni Chester A. Ray Michael L. Smith Satoshi Iwase Mitsuru Saito Yoshiki Sugiyama Tadaaki Mano Rong Zhang Kenichi Iwasaki Lynda D. Lane Jay C. Buckey Jr William H. Cooke Friedhelm J. Baisch David Robertson Dwain L. Eckberg C. Gunnar Blomqvist 《The Journal of physiology》2002,538(1):331-340
85.
Yoshino H Futakuchi M Cho YM Ogawa K Takeshita F Imai N Tamano S Shirai T 《Clinical & experimental metastasis》2005,22(5):441-447
Previously, we established the in vivo lung metastasis model of rat HCC induced by two hepatocarcinogens, diethylnitrosamine (DEN) and N-nitrosomorpholine (NMOR)
at a dose of 120 ppm. This model allows us to investigate modifying factors leading to the inhibition of metastasis formation.
However, low survival rates made the evaluation of metastasis formation difficult. The current experiments were conducted
to modify the experimental protocol to improve survival and to establish a better animal metastasis model. Lower doses of
NMOR (80 or 40 ppm in drinking water) were given to F344 rats for 14 weeks after DEN treatment. Survival rates in the 80 ppm
group and in the 40 ppm group were 57% and 81%, respectively and these values were significantly higher than that in 120 ppm.
Incidences of lung metastasis in the 40 ppm group steadily increased up to 67% by week 36 while that in the 80 ppm increased
sharply up to 86% by week 24. Severity of lung metastases in the 40 ppm group at week 36 was mild compared with the 80 ppm
group at week 24. In the second experiment, in order to characterize HCC development and lung metastasis in the 40 ppm group,
rats given DEN and then followed with 40 ppm NMOR were killed sequentially. Development of HCC was observed at week 14 and
reached 100% incidence at week 20. First lung metastatic lesions were evident at week 22, and incidence of lung metastasis
reached 100%. Tumor cells were identified in the blood at week 20 by RT-PCR. The current study revealed that 40 ppm NMOR for
14 weeks after DEN treatment developed HCC without lung metastases at week 22, then HCC with a frequent lung metastasis at
week 40. Thus, it can be said that this system is a more appropriate model for elucidation of mechanisms of metastasis and
also for analysis of factors to inhibit natural metastasis. 相似文献
86.
Toru Furukawa Rumi Fujisaki Yoshitaro Yoshida Naomi Kanai Makoto Sunamura Tadayoshi Abe Kazunori Takeda Seiki Matsuno Akira Horii 《Modern pathology》2005,18(8):1034-1042
DUSP6/MKP-3 is identified as a candidate tumor suppressor gene for pancreatic cancer. The aim of this study was to elucidate the roles of DUSP6 in the pancreatic carcinogenesis through the pancreatic intraepithelial neoplasia and/or intraductal papillary-mucinous neoplasms, both of which are considered to be precursor lesions of invasive carcinoma of the pancreas, by comparing with involvements of other major tumor suppressive pathways. Expressions of DUSP6, CDKN2A, TP53, and SMAD4 were investigated by immunohistochemistry in a total of 206 lesions of dysplastic ductal precursors and carcinomas retrieved from 52 pancreata with invasive ductal carcinomas and 51 of those with intraductal papillary-mucinous neoplasms. The intensity of staining was evaluated in lesions at different atypical grades and statistically compared among them. Mutations of KRAS2 were analyzed by methods of the allele-specific oligonucleotide hybridization and nucleotide sequencing. In pancreata with invasive ductal carcinomas, expressions of DUSP6 were abrogated exclusively in the invasive carcinoma cells in contrast to its fairly preserved expressions in pancreatic intraepithelial neoplasia. In pancreata with intraductal papillary-mucinous neoplasms, abrogated expressions of DUSP6 were observed in a relatively small fraction of intraductal adenoma/borderlines and intraductal carcinomas. Most of the intraductal adenoma/borderline lesions with abrogation of DUSP6 harbored mutations of KRAS2. None of the molecules was associated with each other in any grade of lesions. Morphological variations of papillae of the intraductal papillary-mucinous neoplasms were evaluated and analyzed for their associations with abrogations of the molecules, which resulted in finding of no significant associations. Our results suggest that the abrogation of DUSP6 is associated exclusively with progression from pancreatic intraepithelial neoplasia to the invasive ductal carcinoma while it is potentially associated with initiation of intraductal papillary-mucinous neoplasms with mutated KRAS2, which is independent of other major tumor suppressive pathways in both types of neoplasms. 相似文献
87.
Takashi Kojima Toshinobu Yamamoto Mengdong Lan Masaki Murata Ken-ichi Takano Mitsuru Go Shingo Ichimiya Hideki Chiba Norimasa Sawada 《Medical Electron Microscopy》2004,37(2):101-113
The signal transduction pathways and activation of the MAP kinase or PI3 kinase signaling cascade regulate a variety of cellular processes, including proliferation and differentiation in hepatocytes. To elucidate the mechanisms of signal transmission required for the regulation of gap and tight junctions during DNA synthesis in rat hepatocytes, we determined changes of expression and function of gap and tight junctions of cells grown in primary culture, using inhibitors of signaling pathways for MAP kinase (PD98059) and PI3 kinase (LY294002). During the stimulation of DNA synthesis induced by epidermal growth factor (EGF), immunoreactivity and mRNAs of gap junction protein Cx32 and of tight junction protein claudin-1 markedly decreased with reduction of gap junctional intercellular communication (GJIC) and the fence function of tight junctions. In Western blots, whole-cell lysate of claudin-1 protein decreased and phosphorylated Cx32 protein in the insoluble fraction of Triton X-100 increased during the stimulation of DNA synthesis. During reinhibition of DNA synthesis, the changes of Cx32 and claudin-1 returned to control levels, as did both functions. In treatment with the inhibitors before DNA synthesis, PD98059 inhibited the changes of expression and function of Cx32, but not claudin-1, without inhibition of cell growth, whereas LY294002 completely inhibited cell growth. These findings indicate that the PI3 kinase pathway rather than the MAP kinase pathway plays an important role for EGF-induced proliferation of rat hepatocytes, and that changes of Cx32 in hepatocytes during the stimulation of DNA synthesis may be in part controlled through MAP kinase. Furthermore, Cx32, but not claudin-1, protein may be a target of activated MAP kinase in hepatocytes. 相似文献
88.
89.
Pseudotype hepatitis C virus enters immature myeloid dendritic cells through the interaction with lectin 总被引:3,自引:0,他引:3
Kaimori A Kanto T Kwang Limn C Komoda Y Oki C Inoue M Miyatake H Itose I Sakakibara M Yakushijin T Takehara T Matsuura Y Hayashi N 《Virology》2004,324(1):74-83
Dendritic cells (DC) are the most potent antigen-presenting cells that regulate immune responses. One of the mechanisms for hepatitis C virus (HCV) persistence is the ability of HCV to suppress DC function. Direct HCV infection to blood DC has been implicated for DC dysfunction. To clarify the susceptibility of each DC subset to HCV, we used pseudotype vesicular stomatitis virus (VSV) coated with chimeric HCV envelope glycoproteins (E1 and E2). We demonstrate that pseudotype VSV enters myeloid DC (MDC) but not plasmacytoid DC (PDC). The highest efficiency of pseudotype VSV entry to MDC was observed when MDC were cultured with GM-CSF. Such efficiency decreased when MDC are matured with the treatment of IL-4, CpG oligodeoxynucleotide, or CD40 ligand. Mannan inhibited pseudotype VSV entry to MDC, but Ca(2+) chelators failed to do so. These results show that pseudotype VSV possessing HCV-E1 and E2 enters immature MDC through the interaction with lectins in a Ca(2+)-independent manner. 相似文献
90.
Comparison of the inhibitory effects of glucocorticoids on the expression of eotaxin in airway epithelial cell line BEAS-2B] 总被引:2,自引:0,他引:2
Koushi Ieki Satoshi Matsukura Fumio Kokubu Masatsugu Kurokawa Mio Kawaguchi Hideki Kuga Shin Watanabe Shintaro Suzuki Miho Odaka Hiroko Takeuchi Robert P Schleimer Mitsuru Adachi 《Arerugī》2004,53(4):423-429
OBJECTIVE: Inhaled corticosteroids play a pivotal role in the treatment of asthma. To observe the mechanisms of glucocorticoids, we focused our study on the comparison of several glucocorticoids' effects on eotaxin expression in the airway epithelial cells. METHODS: Airway epithelial cell line BEAS-2B was cultured in vitro. Cells were preincubated with or without glucocorticoids (becromethasone dipropionate; BDP, budesonide; BUD, fluticasone propionate; FP) and stimulated with TNFalpha and/or IL-4. Protein levels of eotaxin in the supernatants of the cultured cells were determined by ELISA. RESULTS AND CONCLUSIONS: TNFalpha and IL-4 increased the levels of eotaxin in BEAS-2B cells. Combination of these cytokines synergistically upregulated the eotaxin expression as reported previously. Each glucocorticoid significantly inhibited the expression of eotaxin protein induced with TNFalpha and IL-4 and the compared efficacy was in order of FP>BUD>BDP. FP seemed most potent and the inhibitory effect was also observed with relatively low concentration such as 10 (-10)M. Taken together, the comparison of the potency of each glucocorticoid using airway epithelial cells may reflect the efficacy of these drugs in asthmatics. 相似文献