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101.
D. Veloso 《Scandinavian journal of clinical and laboratory investigation》2013,73(4):279-286
Both elevated plasma total homocysteine and cigarette smoking are associated with an increased risk of occlusive cardiovascular disease. We examined whether smoking cessation for a mean time of 10-11 weeks lowered plasma total homocysteine concentrations in men and women with (n = 59) and without (n = 55) established cardiovascular disease. Blood tests were available for 58 quitters and 29 subjects who did not stop smoking. Compared with subjects who continued to smoke, quitters had statistically significant higher HDL cholesterol concentrations, but plasma total homocysteine concentrations did not differ between the two groups. Likewise, no differences were found between quitters and non-quitters whose baseline homocysteine concentrations were above the 75th percentile. 相似文献
102.
齐墩果酸对血小板功能的影响 总被引:1,自引:0,他引:1
本文研究了齐墩果酸对老龄小白鼠某些功能的影响。研究结果表明,老龄小白鼠灌胃给予齐墩果酸后可明显抑制胶原及ADP诱导的血小板聚集,连续给药一周,其对血小板聚集的抑制作用明显优于一次给药的作用,剂量增加,作用加强;又可使血小板电泳迁移速率加快。 相似文献
103.
血小板ADP受体及其抑制剂 总被引:1,自引:0,他引:1
1 引言 40年前人们就发现ADP这个来源于红细胞的因子,既可影响血小板粘附,也可诱导血小板聚集,作为最重要的参与止血与血栓过程的介质之一,它很快得到了认可。20年后,一种抗血小板药噻氯匹啶(ticlopidine)被发现,作为一个选择性的ADP诱导血小板聚集的抑制剂,其作用机理也被进一步阐明。 相似文献
104.
PAcouldinhibitadenosinediphosphate(ADP),arachidonicacid(AA),CaCI,,thrombin,A,,,,,andclonidine--inducedplateletaggregation[1-4),PAcouldinhibitproductionofthromboxaneB,(TXB,)inAA--inducedplateletaggregaion['J.PAalsocouldreduceplateletadhesion[SJ,andinhibitpulmonarythromboembolismandmalondialdehyde(MDA)production['j.WedidnotknowifthiseffectwasrelatedtotheinhibitionofTXB,productionalthoughitwasdemonstratedthatPAcouldinhibitADP--inducedplateletaggregation['J,andalsothishasnotbeenreport… 相似文献
105.
APNFO1341为穿心莲第三代提取物之一。本文采用血小板聚集(PAG)试验比浊法观察发现APN FO 1341在一定剂量范围内呈剂量依赖性抑制二磷酸腺苷(ADP)和血小板活化因子(PAF)诱导的人富血小板血浆(PRP)的PGA。其对虫ADP诱导第1分钟和第5分钟PAG的IC_(50)分别为2.6mg/L和1.4 mg/L;对由PAF诱导PAG的IC_(50)分别为0.58mg/L和0.38mg/L。通过血小板鲁米诺化学发光技术证明APN FO 1341 2mg/L即显著抑制静息及刺激后人洗涤血小板的化学发光,提示其尚具有清除活性氧的作用。APN FO 1341 2mg/L与PRP孵育后上清液中乳酸脱氢酶活性没有明显变化。表明APN FO 1341没有破坏血小板的作用。 相似文献
106.
M. Lahrichi Pierrette Tarallo Y. Houpert G. Siest 《Clinica chimica acta; international journal of clinical chemistry》1977,79(2):479-487
We studied the influence of substrates and glycolysis inhibitors on the release of proteins and enzymes from human leukocytes. We show the relationship between metabolic level and percentage of enzyme release.Leukocyte kept alive in a nutrient-free bicarbonate medium liberate enzymes even though their metabolic state is satisfactory. The addition of glucose to the medium significantly decreases this phenomenon without affecting the energy level. Addition of glycolysis inhibitors increases it, reduces the energy level, and interferes with other metabolic pathways.The results are discussed and compared to those obtained by other authors using various cell models. 相似文献
107.
On the Mechanism of Inhibition of KATP Channels by Glibenclamide in Rat Ventricular Myocytes 总被引:1,自引:0,他引:1
CRISTINA RIPOLL Ph .D.† W. JON LEDERER M.D. Ph.D. COLIN G. NICHOLS Ph .D. 《Journal of cardiovascular electrophysiology》1993,4(1):38-47
Glibenclamide Block of KATP Channels. Introduction: The mechanism by which glibenclamide inhibits KATP channel activity has been examined in membrane patches from isolated rat ventricular cells. Methods and Results: Inside-out patches were exposed to zero, or low, [ATP] to activate KATP channels. Glibenclamide did not affect single channel conductance, but reversibly reduced channel open probability from either side of the membrane. Internal (cytoplasmic) glibenclamide inhibited with half-maximal inhibitory [glibenclamide] = 6 μM, Hill coefficient = 0.35. Complete channel inhibition was not observed, even at 300 μM [glibenclamide]. The response to step increases of internal [glibenclamide] could be resolved into two phases of channel inhibition (t1/2, fast , < 1 sec, t1/2, slow = 10.5 ± 0.9 sec, n = 8). Step decrease of [glibenclamide] caused a single resolvable phase of reactivation (t1/2 = 20.4 ± 0.7 sec, n = 16). Channel inhibition by internal glibenclamide could be relieved by ADP, but only in the presence of Mg2+ .
Conclusion: Glibenclamide can inhibit KATP channels from either side of the membrane, with block from one side being competitive with block from the other. Internal MgADP antagonizes the blocking action of glibenclamide. Glibenclamide inhibition of cardiac KATP channels differs quantitatively and qualitatively from the inhibition of pancreatic KATP channels. 相似文献
Conclusion: Glibenclamide can inhibit K
108.
Inhibition of bovine platelet function by T-2 toxin, HT-2 toxin, diacetoxyscirpenol and deoxynivalenol 总被引:1,自引:0,他引:1
The aggregation of bovine platelets suspended in homologous plasma is inhibited in the presence of T-2 toxin, HT-2 toxin, diacetoxyscirpenol (DAS) or deoxynivalenol (DON) when either collagen or ADP is used as the stimulatory agent for aggregation. For each of the mycotoxins the degree of inhibition is dependent on the amount of trichothecene present in the platelet suspension but is not dependent on the time of exposure of the platelets to the toxin. For both ADP- and collagen-stimulated platelets, the order of potency of inhibition is T-2 toxin greater than HT-2 toxin greater than DAS greater than DON. A significant (P less than 0.01) dose-dependent decrease was also observed in the amount of the thromboxane B2 released from collagen-stimulated platelets in the presence of each of the mycotoxins. 相似文献
109.
Platelets from rats fed a diet high in linoleic acid (6%) bound increased amounts of fibrinogen on stimulation with ADP, compared to those from rats fed diets with low (2%) or no linoleic acid. However, this increased fibrinogen binding was associated with a decrease in platelet aggregation induced by ADP. Changes in the linoleic acid concentration in platelet membranes may cause changes in this relationship. 相似文献
110.
Summary ATP is as effective as inorganic pyrophosphate in retarding the rate of dissolution of calcium hydroxyapatite at pH 7, ADP
is less effective, and AMP is without effect. The inhibition is due to the adsorption of ATP and ADP units on the crystal
surface. 相似文献