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981.
S Miscia A Cataldi A Ognibene A M Martelli L Manzoli A M Billi C De Marchis L Cocco 《Cell biology international reports》1988,12(5):347-354
Since phospholipids have been suggested to play some role in the molecular organisation of the nuclear matrix, the effect of their removal by means of phospholipase C has been investigated in regenerating rat liver nuclear matrix. The matrix-bound DNA polymerase alpha shows an almost complete loss of activity following the digestion with phospholipase C. Since the polymerase activity is restored by adding exogenous DNA, we suggest that the effect is due to the removal of matrix residual DNA, which is in some way linked to the nuclear matrix by means of hydrophobic interactions. 相似文献
982.
Ultrastructural studies of Ascidia malaca blood reveal particular cell types, which are characterized by a polymorphism in the organization of the electron dense cytoplasmic material. A new pathway of morula cell differentiation is suggested. X-ray microanalysis shows that vanadium is localized in vacuolated, granular and morular cells. Iron, which is accumulated by this species to a lesser degree than vanadium, is found in vacuolated amebocytes and, together with vanadium, in granular cells. Our results are discussed in the light of the relations between selective metal absorption in blood cells and their specialization and differentiation. 相似文献
983.
Lucio Cocco Matilde Y. Follo Irene Faenza Alberto Bavelloni Anna Maria Billi Alberto M. Martelli Lucia Manzoli 《Advances in enzyme regulation》2007,47(1):2-9
Location impinges on function of some of the main players of nuclear inositol lipid cycle. Here we have discussed the behavior of PI-PLCβ1 in myelodysplastic and cultured leukemia cells.The presence of a cryptic deletion of PI-PLCβ1 gene in high-risk MDS patients is accompanied by altered expression of its mRNA in that the overall decrease of mRNA is characterized by a dramatic decrease of the splicing variant 1a, which is cytosolic and partially nuclear, whilst the splicing variant 1b is still highly represented. This suggests that altered expression of nuclear PI-PLCβ1 could be involved in a disregulation of the cell cycle and have also important effects on cell apoptotic pathways.Moreover, in cultured leukemia cells (Felc) it has been reported by means of a proteomic approach that the splicing factor SRp20 interacts with nuclear PI-PLCβ1 and its expression is modulated by this signaling molecule.All in all, it appears more and more evident that nuclear signaling elicited by PI-PLCβ1 is a key event in the control of cell cycle progression. 相似文献
984.
Coral García-Pastor Rafael Blázquez-Serra Ricardo J. Bosch Francisco J. Lucio Cazaña Ana B. Fernández-Martínez 《生物化学与生物物理学报:疾病的分子基础》2019,1865(9):2504-2515
The therapeutic efficacy of the antineoplastic drug cisplatin is limited by its nephrotoxicity, which affects particularly to proximal tubular cells (PTC). Cisplatin-induced cytotoxicity appears to be multifactorial and involves inflammation, oxidative stress as well as apoptosis. We have recently shown that the cyclo-oxygenase-2 (COX-2)/intracellular prostaglandin E2 (iPGE2)/EP receptor pathway mediates the apoptotic effect of cisplatin on human proximal tubular HK-2 cells. Here, we studied the effects on HK-2 cells of apoptotic bodies (ABs) generated after treatment of HK-2 cells with cisplatin. We found that ABs inhibited cell growth, induced apoptosis and increased COX-2 expression and iPGE2 in ABs-recipient HK-2 cells. Inhibition of the COX-2/iPGE2/EP receptor pathway in these cells prevented the effects of ABs without interfering with their internalization. Interestingly, 2nd generation ABs (i.e. ABs released by cells undergoing apoptosis upon treatment with ABs) did not trigger apoptosis in naïve HK-2 cells, and stimulated cell proliferation through the COX-2/iPGE2/EP receptor pathway. These results suggest that ABs, through iPGE2-dependent mechanisms, might have a relevant role in the natural history of cisplatin-induced acute kidney failure because they contribute first to the propagation of the noxious effects of cisplatin to non-injured PTC and then to the promotion of the proliferative tubular response required for proximal tubule repair. Since iPGE2 also mediates both cisplatin-induced HK-2 cell apoptosis, intervention in the COX-2/iPGE2/EP receptor pathway might provide us with new therapeutic avenues in patients with cisplatin-induced acute kidney injury. 相似文献
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