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941.
《Chronobiology international》2013,30(5):309-320
Chronopathology of cardiovascular disease is now well documented. Silent myocardial ischaemia involves the same pathophysiological changes as conventional ischaemia. Early morning peaks in angina and myocardial ischaemia call for adequate timing of medication. β-blockers abolish the morning peak, and aspirin reduces morning infarctions. The effects of other antianginals on these phenomena are presently unknown. 相似文献
942.
Ion antagonism in phytochrome-mediated calcium-dependent germination of turions of Spirodela polyrhiza (L.) Schleiden 总被引:1,自引:0,他引:1
The light-dependent germination response of turions (resting fronds) is mediated by phytochrome and requires the presence
of Ca2+ in the medium (K.-J. Appenroth and H. Augsten, 1990, Photochem. Photobiol. 52: 61–65). The Ca2+ requirement of germination is apparent only in the presence of exogenous Mg2+. A competitive ion antagonism was demonstrated between Ca2+ and Mg2+ in this physiological response; Mg2+ could also be replaced by Ba2+ or Sr2+. Without exog-enous Mg2+, a Ca2+ concentration as low as 0.9 μM fulfilled the Ca2+ requirement. This type of ion antagonism resembled the competitive Ca/Mg interaction reported previously for calcium-binding
proteins. The physiological response was blocked by inhibitors of Ca2+ uptake (verapamil, La3+). It was concluded that uptake of Ca2+ from the external medium is an essential step in the phytochrome-mediated germination of turions. The results are in agreement
with the assumption that the uptake of Ca2+ is blocked at the side of entry by other alkaline earth ions. Treatment of turions with Mg2+ (1 mM) for 24 h at varying times after the red light pulse in otherwise virtually Ca2+-free KNO3 solution resulted in a response similar to a Ca2+ step-down treatment. This is in agreement with the assumption that the Ca2+- and the Mg2+-sensitive periods coincide. The ion interaction described here represents the first photophysiological example in plants
of an antagonistic effect between Ca2+ and Mg2+ similar to that which occurs in vitro with calmodulin.
Received: 12 June 1998 / Accepted: 28 December 1998 相似文献
943.
Vlado Buljan Karen M Cullen 《Biochemical and biophysical research communications》2009,381(2):224-228
Here we show a new effect of Ca2+ on microtubule morphology: Ca2+ can cause smooth curving of microtubules in the presence of microtubule-associated proteins (MAPs). In vitro, microtubules self-organize, forming complex dissipative structures. Such structures may be strongly affected by relatively weak external factors. A factor such as Ca2+ potentially influences spatiotemporal patterns of microtubule assembly, but the dynamics are unclear. We tested Ca2+ effects on microtuble formation. Using EM, microtubule length, curvature, and alignment and were measured in two systems: 2 mg/ml microtubule protein containing MAPs and 1 mM EGTA with and without 1 mM Ca2+. The two systems were then tested using light scattering. In low Ca2+, a birefringent microtubular pattern is seen, increasing with polymerization. When 1 mM Ca2+ is added to the solution. anisotropic phase is prevented without microtubule disruption. This demonstrates an additional mechanism by which Ca2+ can alter the dynamics and morphology of microtules. 相似文献
944.
Dee Van Riper Nicholas Latchana Amber N. Mitchell Dana R. Crawford 《Archives of biochemistry and biophysics》2008,472(1):43-50
RCAN1 (Adapt78) functions mainly, if not exclusively, as a regulator of calcineurin, a phosphatase that mediates many cellular responses to calcium. Identification of this regulatory activity has led to a surge of interest in RCAN1, since calcineurin is involved in many cellular and tissue functions, and its abnormal expression is associated with multiple pathologies. Recent studies have implicated RCAN1 as a regulator of angiogenesis. To more fully investigate the role of RCAN1 in vascular function, we first extended previous studies by assessing RCAN1 response in cultured endothelial cells to various vascular agonists. Strong induction of isoform 4 but not isoform 1 was observed in human umbilical vein- and bovine pulmonary aortic-endothelial cells in response to VEGF, thrombin, and ATP but not other agonists. Inductions were both calcium and calcineurin dependent, with the relative effect of each agonist cell-type dependent. Ectopic RCAN1 expression also inhibited calcineurin signaling in the HUVEC cells. Based on these strong RCAN1 responses and a lack of RCAN1-associated vascular studies beyond angiogenesis, we investigated the potential role of RCAN1 in vascular tone using whole mounted mesenteric artery. RCAN1 knockout mice exhibited an attenuated mesenteric vasoconstriction to phenylephrine as compared with wild-type. Overall contractility was unaffected, suggesting that this component of smooth muscle action is similar in the two mouse strains. Constriction in the knockout artery appeared to be potentiated by the addition of the nitric oxide synthase (NOS) inhibitor l-NAME, suggesting that elevated nitric oxide (NO) production occurs in the knockout vasculature and contributes to the weakened vasoconstriction. Our results reveal a newly identified vascular role for RCAN1, and a potential new target for treating vascular- and calcineurin-related disorders. 相似文献
945.
Soon-Jae Kwon 《Biochemical and biophysical research communications》2009,390(4):1389-1394
Junctate is a newly identified sarcoplasmic reticulum (SR) Ca2+ binding protein, but its function in cardiac muscle has remained unclear. Our previous study showed that chronic over-expression of junctate in transgenic mice led to altered SR functions and development of severe hypertrophy. In this study, we identified the interaction of junctate with SERCA2a by co-immunoprecipitation and GST-pull-down assay. This interaction was inhibited by higher Ca2+ concentration. Immunolocalization assays also showed that junctate and SERCA2a were co-localized in the SR of cardiomyocytes. Direct binding of the C-terminal region of junctate (amino acids 79-270) and luminal domain of SERCA2a (amino acids 70-89) was observed by deletion mutation experiments. Adenovirus-mediated transient over-expression of junctate in cardiomyocytes showed a reduced decay time of Ca2+ transients and increased oxalate-supported SERCA2 Ca2+ uptake, suggesting an increased activity of SERCA2a. Taken together, according to our data, junctate may play an important role in the regulation of SR Ca2+ cycling through the interaction with SERCA2a in the murine heart. 相似文献
946.
Conclusion In this review, we have described the functional properties and regulation of the InsP3R. Not all aspects of InsP3R function and regulation were covered, the main focus was on the most recent and physiologically important data. Information about the structure, heterogeneity, functional properties, and regulation of the InsP3R is useful for understanding the spatiotemporal aspects of Ca signaling. The combination of biochemical, biophysical and molecular biological techniques has revealed the intricacies of the InsP3R over the past decade. However, questions about the functional differences between various isoforms and splice variants of the InsP3R, the structural determinants responsible for regulation of InsP3R by Ca and ATP, the functional effects of InsP3R phosphorylation and many others remain to be elucidated. Future investigations can be expected to provide answers to these important questions.We thank S. Bezprozvannaya for expert technical assistance. This work was supported by National Institutes of Health grants HL 33026 and GM 39029, and a Grant-in-Aid from the Patrick and Catherine Weldon Donaghue Medical Research Foundation. 相似文献
947.
Limor Cohen Hila Asraf Israel Sekler Michal Hershfinkel 《The Journal of biological chemistry》2012,287(40):33339-33350
Zinc activates a specific Zn2+-sensing receptor, ZnR/GPR39, and thereby triggers cellular signaling leading to epithelial cell proliferation and survival. Epithelial cells that express ZnR, particularly colonocytes, face frequent changes in extracellular pH that are of physiological and pathological implication. Here we show that the ZnR/GPR39-dependent Ca2+ responses in HT29 colonocytes were maximal at pH 7.4 but were reduced by about 50% at pH 7.7 and by about 62% at pH 7.1 and were completely abolished at pH 6.5. Intracellular acidification did not attenuate ZnR/GPR39 activity, indicating that the pH sensor of this protein is located on an extracellular domain. ZnR/GPR39-dependent activation of extracellular-regulated kinase (ERK)1/2 or AKT pathways was abolished at acidic extracellular pH of 6.5. A similar inhibitory effect was monitored for the ZnR/GPR39-dependent up-regulation of Na+/H+ exchange activity at pH 6.5. Focusing on residues putatively facing the extracellular domain, we sought to identify the pH sensor of ZnR/GPR39. Replacing the histidine residues forming the Zn2+ binding site, His17 or His19, or other extracellular-facing histidines to alanine residues did not abolish the pH dependence of ZnR/GPR39. In contrast, replacing Asp313 with alanine resulted in similar Ca2+ responses triggered by ZnR/GPR39 at pH 7.4 or 6.5. This mutant also showed similar activation of ERK1/2 and AKT pathways, and ZnR-dependent up-regulation of Na+/H+ exchange at pH 7.4 and pH 6.5. Substitution of Asp313 to His or Glu residues restored pH sensitivity of the receptor. This indicates that Asp313, which was shown to modulate Zn2+ binding, is an essential residue of the pH sensor of GPR39. In conclusion, ZnR/GPR39 is tuned to sense physiologically relevant changes in extracellular pH that thus regulate ZnR-dependent signaling and ion transport activity. 相似文献
948.
Yoshito Mizoguchi Takahiro A. Kato Yoshihiro Seki Masahiro Ohgidani Noriaki Sagata Hideki Horikawa Yusuke Yamauchi Mina Sato-Kasai Kohei Hayakawa Ryuji Inoue Shigenobu Kanba Akira Monji 《The Journal of biological chemistry》2014,289(26):18549-18555
Microglia are immune cells that release factors, including proinflammatory cytokines, nitric oxide (NO), and neurotrophins, following activation after disturbance in the brain. Elevation of intracellular Ca2+ concentration ([Ca2+]i) is important for microglial functions such as the release of cytokines and NO from activated microglia. There is increasing evidence suggesting that pathophysiology of neuropsychiatric disorders is related to the inflammatory responses mediated by microglia. Brain-derived neurotrophic factor (BDNF) is a neurotrophin well known for its roles in the activation of microglia as well as in pathophysiology and/or treatment of neuropsychiatric disorders. In this study, we sought to examine the underlying mechanism of BDNF-induced sustained increase in [Ca2+]i in rodent microglial cells. We observed that canonical transient receptor potential 3 (TRPC3) channels contribute to the maintenance of BDNF-induced sustained intracellular Ca2+ elevation. Immunocytochemical technique and flow cytometry also revealed that BDNF rapidly up-regulated the surface expression of TRPC3 channels in rodent microglial cells. In addition, pretreatment with BDNF suppressed the production of NO induced by tumor necrosis factor α (TNFα), which was prevented by co-adiministration of a selective TRPC3 inhibitor. These suggest that BDNF induces sustained intracellular Ca2+ elevation through the up-regulation of surface TRPC3 channels and TRPC3 channels could be important for the BDNF-induced suppression of the NO production in activated microglia. We show that TRPC3 channels could also play important roles in microglial functions, which might be important for the regulation of inflammatory responses and may also be involved in the pathophysiology and/or the treatment of neuropsychiatric disorders. 相似文献
949.
Seedling roots of corn were treated with different concentrations of mannitol-containing solution for 1 to 1.5 hr, and net
fluxes of Ca2+ and H+ were measured in the elongation region. H+ fluxes were much more sensitive to osmotic pressure than were Ca2+ fluxes. Oscillations of 7-min period in H+ flux, normally observed in the control, were almost fully suppressed at high osmotic concentrations. Net H+ flux was shifted from average efflux of 25 ± 3 nmol m−2 sec−1 to average influx of 10 ± 5 nmol m−2 sec−1 after the incubation in 100 mm mannitol. The larger the osmotic concentration, the larger was the H+ influx. This flux caused the unbuffered solution of pH 4.85 to change to pH 5.3 after mannitol application. It appears that
the osmoticum suppresses oscillatory H+ extrusion at the plasma membrane. Discrete Fourier Transforms of the H+ flux data showed that, apart from suppression of the 7-min oscillations in H+ flux, mannitol also promoted the appearance of faster 2-min oscillations. Ca2+ influx slightly increased after mannitol treatment. In addition the 7-min oscillatory component of Ca2+ flux remained apparent thereby showing independence of H+ flux.
Received: 25 April 1997/Revised: 11 August 1997 相似文献
950.
A. Toledo R. Rodriguez J. Sabriá J. Rodriguez I. Blanco 《Journal of neurochemistry》1991,56(2):380-384
In a previous work we have shown that histidine decarboxylase (HD) activity is found in a soluble and a membrane-bound form. A major part (82%) of the membrane-bound HD activity in the crude mitochondrial fraction (P2) was present in the synaptic plasma membrane-containing subfraction. Physiological concentrations of Ca2+ had no direct effect on HD activity but caused a solubilization of approximately 50% of membrane-bound HD in the P2 fraction. Mg2+ had similar but lower effects (20% solubilization) than Ca2+. Incubation with depolarizing concentrations of K+ in the presence of 1 mM CaCl2 caused a significant (30%) solubilization of HD. 相似文献