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TMPRSS2/ERG promotes epithelial to mesenchymal transition through the ZEB1/ZEB2 axis in a prostate cancer model 总被引:1,自引:0,他引:1
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Diana E. Moedano Maria E. Irigoyen Aida Borges‐Yez Ismael Flores‐Snchez Ricardo C. Rotter 《Gerodontology》2011,28(1):19-27
doi: 10.1111/j.1741‐2358.2009.00342.x Osteoporosis, the risk of vertebral fracture, and periodontal disease in an elderly group in Mexico City Objectives: The aims of this study were to identify the possible association of osteoporosis, fracture risk and periodontitis, and consider the role of pharmacological treatment of osteoporosis and the periodontal condition. Methods: Patients aged 60 and older from the Mexican National Medical Science and Nutrition Institute Salvador Zubirán participated in the study. DXA was used to assess osteoporosis and risk of vertebral fracture. A modified version of the extent and severity index (ESI) was applied to evaluate periodontitis (cut‐off point for attachment loss ≥ 4 mm) and all teeth were examined. Results: One hundred and sixty‐six patients were examined, 88.6% were females, 47.0% had osteoporosis and 38.6% showed a high risk of fracture. The modified ESI was 5.13 mm (SD 1.4), 57.8% (SD 29.7). The model for periodontitis severity showed an association with oral hygiene (OR = 1.85) and use of osteoporosis medication (OR = 0.43). The model for the extent of periodontitis identified an association with smoking (OR = 2.37), osteoporosis (OR = 1.82) and osteoporosis medication (OR = 0.36). The model for tooth loss detected an association with fracture risk (OR = 3.02) and osteoporosis medication (OR = 0.33). Conclusion: Periodontitis extent was associated with osteoporosis, and tooth loss with fracture risk. 相似文献
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Li Huang Junjie Han Danya Ben-Hail Luwei He Baowei Li Ziheng Chen Yueying Wang Yanlei Yang Lei Liu Yushan Zhu Varda Shoshan-Barmatz Hongwei Liu Quan Chen 《The Journal of biological chemistry》2015,290(39):23563-23578
The pro-apoptotic Bax and Bak proteins are considered central to apoptosis, yet apoptosis occurs in their absence. Here, we asked whether the mitochondrial protein VDAC1 mediates apoptosis independently of Bax/Bak. Upon screening a fungal secondary metabolite library for compounds inducing apoptosis in Bax/Bak-deficient mouse embryonic fibroblasts, we identified cyathin-R, a new cyathane diterpenoid compound able to activate apoptosis in the absence of Bax/Bak via promotion of the VDAC1 oligomerization that mediates cytochrome c release. Diphenylamine-2-carboxilic acid, an inhibitor of VDAC1 conductance and oligomerization, inhibited cyathin-R-induced VDAC1 oligomerization and apoptosis. Similarly, Bcl-2 overexpression conferred resistance to cyathin-R-induced apoptosis and VDAC1 oligomerization. Silencing of VDAC1 expression prevented cyathin-R-induced apoptosis. Finally, cyathin-R effectively attenuated tumor growth and induced apoptosis in Bax/Bak-deficient cells implanted into a xenograft mouse model. Hence, this study identified a new compound promoting VDAC1-dependent apoptosis as a potential therapeutic option for cancerous cells lacking or presenting inactivated Bax/Bak. 相似文献
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Fumin Chang Christopher A. Lemmon Voraphoj Nilaratanakul Varda Rotter Lewis Romer 《The journal of histochemistry and cytochemistry》2014,62(11):774-790
Biologically relevant, three-dimensional extracellular matrix is an essential component of in vitro vasculogenesis models. WI-38 fibroblasts assemble a 3D matrix that induces endothelial tubulogenesis, but this model is challenged by fibroblast senescence and the inability to distinguish endothelial cell-derived matrix from matrix made by WI-38 fibroblasts. Matrices produced by hTERT-immortalized WI-38 recapitulated those produced by wild type fibroblasts. ECM fibrils were heavily populated by tenascin-C, fibronectin, and type VI collagen. Nearly half of the total type I collagen, but only a small fraction of the type IV collagen, were incorporated into ECM. Stable hTERT-WI-38 transfectants expressing TagRFP-fibronectin incorporated TagRFP into ~90% of the fibronectin in 3D matrices. TagRFP-fibronectin colocalized with tenascin-C and with type I collagen in a pattern that was similar to that seen in matrices from wild type WI-38. Human Umbilical Vein Endothelial Cells (HUVEC) formed 3D adhesions and tubes on WI38-hTERT-TagRFP-FN-derived matrices, and the TagRFP-fibronectin component of this new 3D human fibroblast matrix model facilitated the demonstration of concentrated membrane type 1 metalloprotease and new HUVEC FN and collagen type IV fibrils during EC tubulogenesis. These findings indicate that WI-38-hTERT- and WI-38-hTERT-TagRFP-FN-derived matrices provide platforms for the definition of new matrix assembly and remodeling events during vasculogenesis. 相似文献
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Shira Weisthal Nurit Keinan Danya Ben-Hail Tasleem Arif Varda Shoshan-Barmatz 《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》2014
VDAC1, an outer mitochondrial membrane (OMM) protein, is crucial for regulating mitochondrial metabolic and energetic functions and acts as a convergence point for various cell survival and death signals. VDAC1 is also a key player in apoptosis, involved in cytochrome c (Cyto c) release and interactions with anti-apoptotic proteins. Recently, we demonstrated that various pro-apoptotic agents induce VDAC1 oligomerization and proposed that a channel formed by VDAC1 oligomers mediates cytochrome c release. As VDAC1 transports Ca2 + across the OMM and because Ca2 + has been implicated in apoptosis induction, we addressed the relationship between cytosolic Ca2 + levels ([Ca2 +]i), VDAC1 oligomerization and apoptosis induction. We demonstrate that different apoptosis inducers elevate cytosolic Ca2 + and induce VDAC1 over-expression. Direct elevation of [Ca2 +]i by the Ca2 +-mobilizing agents A23187, ionomycin and thapsigargin also resulted in VDAC1 over-expression, VDAC1 oligomerization and apoptosis. In contrast, decreasing [Ca2 +]i using the cell-permeable Ca2 +-chelating reagent BAPTA-AM inhibited VDAC1 over-expression, VDAC1 oligomerization and apoptosis. Correlation between the increase in VDAC1 levels and oligomerization, [Ca2 +]i levels and apoptosis induction, as induced by H2O2 or As2O3, was also obtained. On the other hand, cells transfected to overexpress VDAC1 presented Ca2 +-independent VDAC1 oligomerization, cytochrome c release and apoptosis, suggesting that [Ca2 +]i elevation is not a pre-requisite for apoptosis induction when VDAC1 is over-expressed. The results suggest that Ca2 + promotes VDAC1 over-expression by an as yet unknown signaling pathway, leading to VDAC1 oligomerization, ultimately resulting in apoptosis. These findings provide a new insight into the mechanism of action of existing anti-cancer drugs involving induction of VDAC1 over-expression as a mechanism for inducing apoptosis. This article is part of a Special Issue entitled: Calcium Signaling in Health and Disease. Guest Editors: Geert Bultynck, Jacques Haiech, Claus W. Heizmann, Joachim Krebs, and Marc Moreau 相似文献
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