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971.
972.
Bergami Elisa Caroselli Erik Vaccari Lisa Corsi Ilaria Semenov Alexander Macali Armando 《Coral reefs (Online)》2021,40(4):1355-1360
Coral Reefs - Larval settlement is a critical step for sessile benthic species such as corals, whose ability to thrive on diverse natural and anthropogenic substrates may lead to a competitive... 相似文献
973.
Mello Victor Galvão Escudeiro Heloisa Weckwerth Ana Carolina Villas Bôas Andrade Maria Izilda Fusaro Ana Elisa de Moraes Eloise Brasil Ruiz Luciana da Silva Baptista Ida Maria Foschiani Dias 《Mycopathologia》2021,186(1):71-80
Mycopathologia - Dermatomycoses caused by Candida spp. are increasingly common, however there are few reports in the literature regarding their epidemiology, pathogenesis and antifungal... 相似文献
974.
Fernanda G. Fleury Luísa R. F. Guimarães Elisa B. Rezende Tracy M. M. Martins Cássia R. S. Caires Fernanda C. A. dos Santos Sebastião R. Taboga Ana P. da S. Perez 《Cell biology international》2021,45(10):2074-2085
This study evaluated such as exposure to ethinylestradiol during the prenatal (18th–22nd day) and pubertal (42nd–49th day) periods acts on the male ventral prostate and female prostate of 12-month old gerbils. We performed the analysis to serum hormone levels for estradiol and testosterone. The prostates were submitted to morphometric and immunohistochemical analyses. Exposure to ethinylestradiol during these developmental periods decreased the testosterone serum levels in males and increased the estradiol serum levels in females. Morphologically, prostate intraepithelial neoplasia and disorders in the arrangement of the fibrous components were observed in the prostate glands of both sexes of gerbil exposed to ethinylestradiol during development periods. In the male prostate, the ethinylestradiol promoted decreased in the frequency of positive epithelial cell for androgen receptor (AR) and increased the frequency of positive stromal cell for estrogen receptor α. However, in the female prostate, this synthetic estrogen caused AR upregulation and increased cell proliferation. This study shows that the exposure to ethinylestradiol during development phases alters the morphology and the hormonal signaling in the male and female prostates of old gerbils, confirming the action of ethinylestradiol as endocrine disruptor. 相似文献
975.
976.
Pasquini LA Millet V Hoyos HC Giannoni JP Croci DO Marder M Liu FT Rabinovich GA Pasquini JM 《Cell death and differentiation》2011,18(11):1746-1756
Galectins control critical pathophysiological processes, including the progression and resolution of central nervous system (CNS) inflammation. In spite of considerable progress in dissecting their role within lymphoid organs, their functions within the inflamed CNS remain elusive. Here, we investigated the role of galectin-glycan interactions in the control of oligodendrocyte (OLG) differentiation, myelin integrity and function. Both galectin-1 and -3 were abundant in astrocytes and microglia. Although galectin-1 was abundant in immature but not in differentiated OLGs, galectin-3 was upregulated during OLG differentiation. Biochemical analysis revealed increased activity of metalloproteinases responsible for cleaving galectin-3 during OLG differentiation and modulating its biological activity. Exposure to galectin-3 promoted OLG differentiation in a dose- and carbohydrate-dependent fashion consistent with the 'glycosylation signature' of immature versus differentiated OLG. Accordingly, conditioned media from galectin-3-expressing, but not galectin-3-deficient (Lgals3(-/-)) microglia, successfully promoted OLG differentiation. Supporting these findings, morphometric analysis showed a significant decrease in the frequency of myelinated axons, myelin turns (lamellae) and g-ratio in the corpus callosum and striatum of Lgals3(-/-) compared with wild-type (WT) mice. Moreover, the myelin structure was loosely wrapped around the axons and less smooth in Lgals3(-/-) mice versus WT mice. Behavior analysis revealed decreased anxiety in Lgals3(-/-) mice similar to that observed during early demyelination induced by cuprizone intoxication. Finally, commitment toward the oligodendroglial fate was favored in neurospheres isolated from WT but not Lgals3(-/-) mice. Hence, glial-derived galectin-3, but not galectin-1, promotes OLG differentiation, thus contributing to myelin integrity and function with critical implications in the recovery of inflammatory demyelinating disorders. 相似文献
977.
Occupational exposure to photocopiers has been indicated as being responsible for a number of health complaints, particularly effects on the respiratory, immunological, and nervous systems. In this study, we investigated oxidative and genotoxic damage in photocopier operators by assessing catalase activity (CAT), reduced vs. oxidized glutathione ratio (GSH/GSSG), level of lipid peroxidation (TBARS), damage index by Comet assay (DICA), and buccal cells with micronuclei (BCMN). Our results reveal that the TBARS levels in operators were increased (27%; p<0.05) but that no significant alterations to GSH/GSSG or CAT activity were observed. The DICA and the number of BCMN were significantly increased (134% and 100%, respectively; p<0.05) in the exposed group. There was a significant association between the time in months spent at work and DNA damage in lymphocytes (r(s)?=?0.720; p<0.001) and buccal cell with MN (r(s)?=?0.538; p<0.001). Because laser printers and photocopiers have become increasingly used, it is important to control human exposure using reliable biomarkers. 相似文献
978.
Martino S Tiribuzi R Ciraci E Makrypidi G D'Angelo F di Girolamo I Gritti A de Angelis GM Papaccio G Sampaolesi M Berardi AC Datti A Orlacchio A 《The international journal of biochemistry & cell biology》2011,43(5):775-783
The identity of biochemical players which underpin the commitment of CD34(+) hematopoietic stem cells to immunogenic or tolerogenic dendritic cells is largely unknown. To explore this issue, we employed a previously established cell-based system amenable to shift dendritic cell differentiation from the immunogenic into the tolerogenic pathway upon supplementation with a conventional cytokine cocktail containing thrombopoietin (TPO) and IL-16. We show that stringent regulation of cathepsins S and D, two proteases involved in antigen presentation, is crucial to engage cell commitment to either route. In response to TPO+IL-16-dependent signaling, both cathepsins undergo earlier maturation and down-regulation. Additionally, cystatin C orchestrates cathepsin S expression through a tight but reversible interaction that, based on a screen of adult stem cells from disparate origins, CD14(+) cells, primary fibroblasts and the MCF7 cell line, appears unique to CD34(+) stem cells from peripheral and cord blood. As shown by CD4(+) T cell proliferation in mixed-lymphocyte reactions, cell commitment to either pathway is disrupted upon cathepsin knockdown by RNAi. Surprisingly, similar effects were also observed upon gene overexpression, which prompts atypically accelerated maturation of cathepsins S and D in cells of the immunogenic pathway, similar to the tolerogenic route. Furthermore, RNAi studies revealed that cystatin C is a proteolytic target of cathepsin D and has a direct, causal impact on cell differentiation. Together, these findings uncover a novel biochemical cluster that is subject to time-controlled and rigorously balanced expression to mediate specific stem cell commitment at the crossroads towards tolerance or immunity. 相似文献
979.
Marcuzzi A Piscianz E Girardelli M Crovella S Pontillo A 《Apoptosis : an international journal on programmed cell death》2011,16(9):882-888
The inhibition of mevalonate pathway by the aminobisphosphonate alendronate (ALD) has been previously associated with an augmented
lipopolysaccharide-induced interleukin-1beta (IL-1β) secretion in monocytes, as demonstrated in an auto-inflammatory disease
known as mevalonate kinase deficiency (MKD). In this study we investigated the effect of ALD + LPS on monocyte cell line (Raw
264.7) death. ALD strongly augmented LPS-induced programmed cell death (PCD) as well as IL-1β secretion in Raw murine monocytes,
whereas necrosis was rather unaffected. ALD + LPS induced caspase-3 activation. Inhibition of IL-1β stimulation partially
restored cell viability. These findings suggest that the inhibition of mevalonate pathway, together with a bacterial stimulus,
induce a PCD partly sustained by the caspase-3-related apoptosis and partly by caspase-1-associated pyroptosis. The involvement
of pyroptosis is a novel hit in our cell model and opens discussions about its role in inflammatory cells with chemical or
genetic inhibition of mevalonate pathway. 相似文献
980.