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941.
Jessica Erriquez Silvia Bernascone Monica Ciarletta Nicoletta Filigheddu Andrea Graziani Carla Distasi 《Cell calcium》2009,46(3):197-208
Ghrelin is a hormone regulating energy homeostasis via interaction with its receptor, GHSR-1a. Ghrelin activities in dorsal root ganglia (DRG) cells are unknown. Herein we show that ghrelin induces a change of cytosolic calcium concentration in both glia and neurons of embryonic chick DRG. Both RT-PCR and binding studies performed with fluorescent ghrelin in the presence of either unlabeled ghrelin or GHSR-1a antagonist D-Lys3-GHRP-6, indicate that DRG cells express GHSR-1a. In glial cells the response is characterized by a rapid transient rise in [Ca2+]i followed by a long lasting rise. The calcium elevation is dependent on calcium release from thapsigargin-sensitive intracellular stores and on activation of two distinct Ca2+ entry pathways, a receptor activated calcium entry and a store operated calcium entry. Surprisingly, D-Lys3-GHRP-6 exerts several activities in the absence of exogenous ghrelin: (i) it activates calcium release from thapsigargin-sensitive intracellular stores and calcium entry via voltage-operated channels in non-neuronal cells; (ii) it inhibits calcium oscillations in non-neuronal cells exhibiting spontaneous Ca2+ activity and iii) it promotes apoptosis of DRG cells, both neurons and glia. In summary, we provide the first evidence for ghrelin activity in DRG, and we also demonstrate that the widely used D-Lys3-GHRP-6 ghrelin antagonist features ghrelin independent activities. 相似文献
942.
In the cochlea, cell damage triggers intercellular Ca2+ waves that propagate through the glial-like supporting cells that surround receptor hair cells. These Ca2+ waves are thought to convey information about sensory hair cell-damage to the surrounding supporting cells within the cochlear epithelium. Mitochondria are key regulators of cytoplasmic Ca2+ concentration ([Ca2+]cyt), and yet little is known about their role during the propagation of such intercellular Ca2+ signalling. Using neonatal rat cochlear explants and fluorescence imaging techniques, we explore how mitochondria modulate supporting cell [Ca2+]cyt signals that are triggered by ATP or by hair cell damage. ATP application (0.1–50 μM) caused a dose dependent increase in [Ca2+]cyt which was accompanied by an increase in mitochondrial calcium. Blocking mitochondrial Ca2+ uptake by dissipating the mitochondrial membrane potential using CCCP and oligomycin or using Ru360, an inhibitor of the mitochondrial Ca2+ uniporter, enhanced the peak amplitude and duration of ATP-induced [Ca2+]cyt transients. In the presence of Ru360, the mean propagation velocity, amplitude and extent of spread of damage-induced intercellular Ca2+ waves was significantly increased. Thus, mitochondria function as spatial Ca2+ buffers during agonist-evoked [Ca2+]cyt signalling in cochlear supporting cells and play a significant role in regulating the spatio-temporal properties of intercellular Ca2+ waves. 相似文献
943.
Carina Klein Anja Grahnert Aliaa Abdelrahman Christa E. Müller Sunna Hauschildt 《Cell calcium》2009,46(4):263-272
Extracellular nicotinamide adenine dinucleotide (NAD+) is known to increase the intracellular calcium concentration [Ca2+]i in different cell types and by various mechanisms. Here we show that NAD+ triggers a transient rise in [Ca2+]i in human monocytes activated with lipopolysaccharide (LPS), which is caused by a release of Ca2+ from IP3-responsive intracellular stores and an influx of extracellular Ca2+. By the use of P2 receptor-selective agonists and antagonists we demonstrate that P2 receptors play a role in the NAD+-induced calcium response in activated monocytes. Of the two subclasses of P2 receptors (P2X and P2Y) the P2Y receptors were considered the most likely candidates, since they share calcium signaling properties with NAD+. The identification of P2Y1 and P2Y11 as receptor subtypes responsible for the NAD+-triggered increase in [Ca2+]i was supported by several lines of evidence. First, specific P2Y1 and P2Y11 receptor antagonists inhibited the NAD+-induced increase in [Ca2+]i. Second, NAD+ was shown to potently induce calcium signals in cells transfected with either subtype, whereas untransfected cells were unresponsive. Third, NAD+ caused an increase in [cAMP]i, prevented by the P2Y11 receptor-specific antagonist NF157. 相似文献
944.
Panzavolta S Torricelli P Bracci B Fini M Bigi A 《Journal of inorganic biochemistry》2009,103(1):101-106
We have investigated the effect of Alendronate and Pamidronate, two bisphosphonates widely employed for the treatment of pathologies related to bone loss, on the setting properties and in vitro bioactivity of a calcium phosphate bone cement. The cement composition includes α-tricalcium phosphate (α-TCP) (90 wt%), nanocrystalline hydroxyapatite (5 wt%) and CaHPO4 · 2H2O (5 wt%). Disodium Alendronate and disodium Pamidronate were added to the liquid phase (bidistilled water) at two different concentrations: 0.4 and 1 mM (AL0.4, AL1.0, PAM0.4, PAM1.0). Both the initial and the final setting times of the bisphosphonate-containing cements increase with respect to the control cement. X-ray diffraction analysis, mechanical tests, and SEM investigations were carried out on the cements after different times of soaking in physiological solution. The rate of transformation of α-TCP into calcium deficient hydroxyapatite, as well as the microstructure of the cements, is not affected by the presence of Alendronate and Pamidronate. At variance, the bisphosphonates provoke a modest worsening of the mechanical properties. MG63 osteoblasts grown on the cements show a normal morphology and biological tests demonstrate very good rate of proliferation and viability in every experimental time. In particular, both Alendronate and Pamidronate promote osteoblast proliferation and differentiation, whereas they inhibit osteoclastogenesis and osteoclast function. 相似文献
945.
Involvement of Cd Bioaccumulation in Spinal Deformities Occurrence in Natural Populations of Mediterranean Killifish 总被引:1,自引:0,他引:1
The aim of this study was to investigate the possible influence of environmental exposure to cadmium (Cd) on the spinal deformities
occurrence in the Mediterranean killifish, Aphanius fasciatus (Pisces: Cyprinodontidae). For this purpose, some indicators of skeletal bone mineralization, Cd, and calcium (Ca) concentrations
in spinal column as well as bioaccumulation of Cd from the water and the sediment have been compared in normal and deformed
fish collected from polluted (S1) and nonpolluted (S2) areas in the Gulf of Gabès in Tunisia. When compared to the normal
fish, the deformed fish showed signs of spinal column demineralization such as significant decrease in the ash weight/dry
weight ratio, percentage of nonorganic components content, and Ca concentration. Cd concentrations in spinal column and liver
were significantly higher in deformed fish than in normal fish. A highly significant negative correlation (r = −0.915, p < 0.01) between Cd and Ca concentrations was noted in spinal column of deformed fish. Bioaccumulation factors of Cd in the
liver from the water and the sediment in deformed fish were also significantly higher (p < 0.0001) than in normal fish from S1 and S2. These findings suggest that the ability to accumulate large amount of Cd may
represent a potential risk to induce spinal deformities in natural populations of Mediterranean killifish. 相似文献
946.
The present study was performed to investigate the effects of strenuous exercise and calcium supplementation on cortisol and
adrenocorticotropic hormone levels in athletes at rest and exhaustion. Thirty male athletes, ages 17–21 years, were enrolled
in the 4-week study. They were divided into three groups as follows: group 1 (n = 10): training without supplementation; group 2 (n = 10): training and calcium supplemented, and group 3 (n = 10): calcium supplemented without training. Venous blood samples were obtained for determination of the hormones. One-month
supplementation with calcium does not influence the cortisol and adrenocorticotropic hormone in athletes, but strenuous exercise
results in a significant increase in their levels with or without supplementation (p < 0.05). 相似文献
947.
D. Brian Foster Jennifer E. Van Eyk Eduardo Marbán Brian O’Rourke 《Journal of bioenergetics and biomembranes》2009,41(2):159-168
As we learn more about the factors that govern cardiac mitochondrial bioenergetics, fission and fusion, as well as the triggers
of apoptotic and necrotic cell death, there is growing appreciation that these dynamic processes are finely-tuned by equally
dynamic post-translational modification of proteins in and around the mitochondrion. In this minireview, we discuss the evidence
that S-nitrosylation, glutathionylation and phosphorylation of mitochondrial proteins have important bioenergetic consequences.
A full accounting of these targets, and the functional impact of their modifications, will be necessary to determine the extent
to which these processes underlie ischemia/reperfusion injury, cardioprotection by pre/post-conditioning, and the pathogenesis
of heart failure. 相似文献
948.
949.
Activity-Dependent Bulk Synaptic Vesicle Endocytosis—A Fast,High Capacity Membrane Retrieval Mechanism 总被引:1,自引:0,他引:1
M. A. Cousin 《Molecular neurobiology》2009,39(3):185-189
Central nerve terminals are placed under considerable stress during intense stimulation due to large numbers of synaptic vesicles
(SVs) fusing with the plasma membrane. Classical clathrin-dependent SV endocytosis cannot correct for the large increase in
nerve terminal surface area in the short term, due to its slow kinetics and low capacity. During such intense stimulation,
an additional SV retrieval pathway is recruited called bulk endocytosis. Recent studies have shown that bulk endocytosis fulfils
all of the physiological requirements to remedy the acute changes in nerve terminal surface area to allow the nerve terminal
to continue to function. This review will summarise the recent developments in the field that characterise the physiology
of bulk endocytosis which show that it is a fast, activity-dependent and high capacity mechanism that is essential for the
function of central nerve terminals. 相似文献
950.
Qin B Polansky MM Sato Y Adeli K Anderson RA 《The Journal of nutritional biochemistry》2009,20(11):901-908
We have reported previously that a cinnamon extract (CE), high in type A polyphenols, prevents fructose feeding-induced decreases in insulin sensitivity and suggested that improvements of insulin sensitivity by CE were attributable, in part, to enhanced insulin signaling. In this study, we examined the effects of CE on postprandial apolipoprotein (apo) B-48 increase in fructose-fed rats, and the secretion of apoB48 in freshly isolated intestinal enterocytes of fructose-fed hamsters. In an olive oil loading study, a water-soluble CE (Cinnulin PF, 50 mg/kg body weight, orally) decreased serum triglyceride (TG) levels and the over production of total- and TG-rich lipoprotein-apoB48. In ex vivo 35S labeling study, significant decreases were also observed in apoB48 secretion into the media in enterocytes isolated from fructose-fed hamsters. We also investigated the molecular mechanisms of the effects of CE on the expression of genes of the insulin signaling pathway [insulin receptor (IR), IR substrate (IRS)1, IRS2 and Akt1], and lipoprotein metabolism [microsomal TG transfer protein (MTP), sterol regulatory element-binding protein (SREBP1c) in isolated primary enterocytes of fructose-fed hamsters, using quantitative real-time polymerase chain reaction. The CE reversed the expression of the impaired IR, IRS1, IRS2 and Akt1 mRNA levels and inhibited the overexpression of MTP and SREBP1c mRNA levels of enterocytes. Taken together, our data suggest that the postprandial hypertriglycerides and the overproduction of apoB48 can be acutely inhibited by a CE by a mechanism involving improvements of insulin sensitivity of intestinal enterocytes and regulation of MTP and SREBP1c levels. We present both in vivo and ex vivo evidence that a CE improves the postprandial overproduction of intestinal apoB48-containing lipoproteins by ameliorating intestinal insulin resistance and may be beneficial in the control of lipid metabolism. 相似文献