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21.
复方中药注射液对小白鼠艾氏腹水癌细胞膜表面的(Na~+-K~+)-ATP酶和微绒毛影响的电镜观察 总被引:2,自引:0,他引:2
本实验应用电镜细胞化学和扫描电镜技术,观察到小白鼠艾氏腹水癌细胞在复方中药注射液的连续作用下,膜表面(Na~+-K~+)-ATP酶活性减弱,微绒毛减退等变化,同时观察到该复方中药注射液对癌细胞增殖的抑制作用,抑瘤率可达87%,癌细胞增殖和(Na~+-K~+)-ATP酶活性及微绒毛的多少有平行关系。讨论了该复方中药抑制癌细胞增殖与膜表面(Na~+-K~+)-ATP酶活性和微绒毛变化的关系。 相似文献
22.
Schultheiss G Lán Kocks S Diener M 《Pflügers Archiv : European journal of physiology》2005,449(6):553-563
During inflammatory bowel disease, reactive oxygen metabolites are released by phagocytes reacting with intraluminal NH3 to produce monochloramine (NH2Cl). NH2Cl is assumed to play role in the pathogenesis of inflammation-associated diarrhoea, as it is able to induce intestinal secretion. The aim of the present study was to determine the action sites of NH2Cl in rat colonic epithelium with Ussing chamber and fura-2 experiments. In intact mucosa, NH2Cl (5·10–6–10–4 mol·l–1) evoked a concentration-dependent increase in short-circuit current (Isc), consistent with the induction of anion secretion, as demonstrated by anion substitution and transport blocker experiments. When the apical membrane was permeabilised by the ionophore nystatin, two basolateral action sites of NH2Cl (5·10–5 mol·l–1) could be identified, i.e. an increase in the K+ conductance and a stimulation of the Na+–K+ pump. When tissues were basolaterally depolarised by a high K+ concentration, the stimulation of an apical Cl– conductance by NH2Cl was observed. In isolated colonic crypts loaded with the Ca2+-sensitive fluorescent dye fura-2, NH2Cl (5·10–5 mol·l–1) evoked an increase in the intracellular Ca2+ concentration. This increase was independent from the presence of Ca2+ in the extracellular medium, but was inhibited by blockade of intracellular sarcoplasmatic, endoplasmatic Ca2+-ATPases with cyclopiazonic acid (10–5 mol·l–1). The NH2Cl-evoked Ca2+ release was sensitive against inhibition of ryanodine receptors with ruthenium red (5·10–5 mol·l–1) and against inhibition of inositol-1,4,5-trisphosphate (IP3) receptors with 2-aminoethoxydiphenylborate (10–4 mol·l–1). Both blockers also inhibited the NH2Cl-induced increase in Isc. These results indicate that an intracellular Ca2+ release via ryanodine and/or IP3 receptors is involved in oxidant stimulation of anion secretion in rat colon. 相似文献
23.
Neuropeptide Y (NPY) has at least three receptors (Y1, Y2 and Y3) through which it influences different mechanisms in many cell types. Previous data suggest that the Y2 receptor may be divided into prejunctional and postjunctional subgroups. We have examined the intracellular signalling pathways of the postjunctional Y2 receptor in rat renal proximal tubules. The results indicate that NPY regulates Na+,K+-ATPase through several signalling pathways: (1) In proximal tubule (PT) cells NPY increased intracellular calcium. The response was blocked by removing extracellular calcium and was also blocked by using nifedipine. This suggests that calcium was increased by influx from the extracellular space through L -type calcium channels. (2) NPY increased Na+,K+-ATPase activity in PT segments and this effect was also blocked by nifedipine. CaMKII-Ala286[281–302] a blocker of Ca2+/calmodulin-dependent protein kinase II (CaMKII) inhibited the NPY-stimulated Na+,K+-ATPase activity. This implies that increased intracellular calcium activates CaMKII which subsequently increases Na+,K+-ATPase activity. CaMKII thus appear to act similar to what has been proposed for protein phosphatase 2B. (3) Calphostin C, an inhibitor of protein kinase C (PKC), did not inhibit NPY-stimulated Na+,K+-ATPase activity. PKC is, therefore, unlikely to be involved. (4) Y2 receptors are negatively coupled to the cAMP pathway. NPY attenuated forskolin-stimulated cAMP production in renal tubules and exogenous cAMP counteracted the NPY-stimulated Na+,K+-ATPase activity. This illustrated the importance of NPY for the regulation of renal sodium handling. We also propose that the renal tubule cell is a good model for studying the function and mechanisms of postjunctional Y2 receptors. 相似文献
24.
目的观察 7-氯苄基四氢巴马汀 ( 7-chlor -BTHP)对大鼠心肌肥厚和心室肌原纤维质膜Ca2 -Mg2 -ATP酶活力的影响。方法用L -甲状腺素诱发大鼠心肌肥厚 ,然后观察 7-chlor -BTHP对大鼠心肌肥厚及左心室肌原纤维Ca2 -Mg2 -ATPase的影响 ,以普萘洛尔 (Pro)作为阳性对照。结果经过 7-chlor-BTHP治疗 3天后 ,心肌肥厚明显改善 ,Ca2 -Mg2 -ATPase活力明显降低。结论 7-chlor-BTHP能明显消退L -甲状腺素诱发的大鼠心肌肥厚 ,并能显著降低心室肌原纤维膜Ca2 -Mg2 -ATPase酶活力。 相似文献
25.
银杏内酯B对体外培养乳鼠心肌细胞氧化损伤的保护作用 总被引:4,自引:1,他引:4
目的探讨银杏内酯B对体外培养乳鼠心肌细胞氧化损伤的保护作用及其机制.方法利用低浓度过氧化氢诱导原代培养乳鼠心肌细胞氧化损伤为模型,通过电镜观察细胞超微结构,以及培养介质中LDH活力,MDA含量,心肌细胞内Na -K -ATPase,GSH-PX活力的改变,来评价银杏内酯B对心肌细胞的保护作用,并探讨其机制.结果过氧化氢对心肌细胞有显著的损伤作用.银杏内酯B可使培养介质中的LDH和MDA水平显著下降,细胞内Na -K -ATPase,GSH-PX活力显著提高,同时细胞超微结构得到改普.结论银杏内酯B对过氧化氢致心肌细胞损伤有保护作用,机理与其抑制脂质过氧化和提高细胞内钠钾泵活力的作用有关. 相似文献
26.
Hansen O 《Pflügers Archiv : European journal of physiology》1999,437(4):517-522
Purified Na+/K+-ATPase (EC 3.6.1.37) isolated from the rectal gland of Squalus acanthias was characterized in ouabain-binding studies and with respect to isoform(s) of the α peptide. To avoid enzyme inactivation
[3H]ouabain equilibrium binding was carried out at 20°C. The heterogeneity of Na+/K+-ATPase isolated from shark rectal gland was similar in [3H]ouabain binding as previously seen in hydrolytic studies. The binding isotherms were compatible with the existence of a
high-affinity (K
dis 0.69 nM) and a low-affinity (K
dis 42 nM) component of 1.46 and 0.79 nmol.(mg protein)–1, respectively. In Western blots the α peptide of the enzyme hybridized with an isoform-specific polyclonal antibody raised
to an α3-specific region of the large intracellular domain of rat Na+/K+-ATPase, but not with the supposed α3-specific monoclonal antibody MA3-915 with its epitope near the N-terminus. Semi-quantitative analysis of the reaction of
the α3-specific polyclonal antibody with the α peptide from the shark enzyme compared to the reaction with α peptide from rat brain
enzyme indicated that this region is not exactly the same in the two species. The α peptide of shark enzyme was not recognized
by α1- or α2-specific polyclonal antibodies, or by the α1-specific monoclonal antibodies 3B and F6. The large intracellular domain of Na+/K+-ATPase from shark rectal gland thus seems to be α3-like and no α isoform heterogeneity seems able to account for the heterogeneity seen in ouabain binding.
Received: 7 August 1998 / Accepted: 6 November 1998 相似文献
27.
Prasada Rao S. Kodavanti Joseph A. Cameron Prabhakara R. Yallapragada Parminder J. S. Vig Durisala Desaiah 《Archives of toxicology》1991,65(4):311-317
Organotin compounds have been shown to interfere with cardiovascular system. We have studied the in vitro and in vivo effects of tributyltin bromide (TBT), triethyltin bromide (TET) and trimethyltin chloride (TMT) on the cardiac SR Ca2+ pump, as well as on protein phosphorylation of SR proteins, in order to understand the relative potency of these tin compounds. All the three tin compounds inhibited cardiac SR45Ca uptake and Ca2+-ATPase in vitro in a concentration-dependent manner. The order of potency for Ca2+-ATPase as determined by IC50, is TBT (2 M) > TET (63 M) > TMT (280 M). For45Ca uptake, it followed the same order i.e., TBT (0.35 M) > TET (10 M) > TMT (440 M). In agreement with the in vitro results, both SR Ca2+-ATPase and45Ca uptake were significantly inhibited in rats treated with these tin compounds, indicating that these tin compounds inhibit cardiac SR Ca2+ transport. cAMP significantly elevated (70–80%) the32P-binding to SR proteins in vitro in the absence of any organotin. In the presence of organotins, cAMP-stimulated32P-binding to proteins was significantly reduced, but the decrease was concentration dependent only at lower concentrations. The order of potency is TBT > TET > TMT. In agreement with in vitro studies, cAMP-dependent32P bound to proteins was significantly reduced in rats treated with TBT, TET and TMT. SDS-polyacrylamide gel electrophoresis of the cardiac SR revealed at least 30 Coomassie blue stainable bands ranging from 9 to 120 kDa. Autoradiographs from samples incubated in the presence of cAMP indicated32P incorporation in seven bands. Of these, the band corresponding to about 24 kDa molecular weight protein decreased in its intensity with the treatment of organotins. These results suggest that triorganotins may be affecting Ca2+ pumping mechanisms through the alteration of phosphorylation of specific proteins in rat cardiac SR.This work has been presented in part at the Annual meeting of Society of Toxicology, 1990 at Miami Beach, FL. The Toxicologist 10: 35 & 108 (1990). 相似文献
28.
29.
仙芦抗癌胶囊抗肿瘤作用及对肝癌HepG2细胞内Ca2+浓度的影响 总被引:2,自引:0,他引:2
目的观察仙芦抗癌胶囊的体内外抗肿瘤作用及对人肝癌HepG2细胞内Ca2 浓度([Ca2 ]i)的影响,从而揭示仙芦抗癌胶囊的抗肿瘤作用机制。方法通过观察仙芦抗癌胶囊对S180A荷瘤小鼠瘤质量和H22小鼠生存时间的影响,观察其体内抗肿瘤作用。通过MTT法观察含药血清对肝癌HepG2细胞的细胞毒作用。通过Fluo-3/AM标记HepG2肝癌细胞,激光共聚焦扫描显微术测定肿瘤细胞[Ca2 ]i,ATP酶试剂盒测定HepG2细胞膜Ca2 ,Mg2 -ATP酶活性。结果仙芦抗癌胶囊(1.00、0.50、0.25g/kg)对S180A小鼠的瘤体生长有显著的抑制作用,对H22小鼠的生存时间有显著的延长作用。仙芦抗癌胶囊体外对HepG2细胞有细胞毒作用;对细胞[Ca2 ]i有显著升高作用,高、中剂量(1.00、0.50g/kg)能够降低HepG2肝癌细胞膜Ca2 ,Mg2 -ATP酶活性。结论仙芦抗癌胶囊有明显的体内外抗肿瘤作用,其作用机制为抑制肿瘤细胞膜Ca2 ,Mg2 -ATP酶活性,增加细胞[Ca2 ]i,从而诱导肿瘤细胞凋亡,达到抗肿瘤作用的目的。 相似文献
30.
目的 研究外伤性前部PVR睫状体Na ,K ATP酶和碳酸酐酶活性变化 ,进一步探讨外伤性前部PVR导致慢性低眼压的机制。方法 制作外伤性前部PVR导致慢性低眼压兔眼模型 ,伤后分别于 2、4、8、16周测量眼压后取眼球 ,部分睫状体做普通病理切片 ,HE染色观察 ,部分睫状体做Na ,K ATP酶活性测定和碳酸酐酶组织化学观察。结果 伤后实验组Na ,K ATP酶活性下降 ,而对照组变化不很明显 ,2组间比较有显著性差异 ;实验眼睫状体上皮碳酸酐酶组织化学显色部分区域为浓棕黑色 ,表明这部分上皮碳酸酐酶活性接近正常水平 ,而上皮破坏区域 ,酶组织化学显色比较弱 ,接近于阴性对照睫状体上皮的颜色 ,为淡黄褐色 ,表明这部分上皮碳酸酐酶活性较低。结论 外伤性前部PVR睫状体Na ,K ATP酶和碳酸酐酶活性降低 ,是导致房水分泌减少及慢性低眼压的一个重要原因。 相似文献