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1.
The Na+–Ca2+ exchange (NCX) system plays a pivotal role in regulating intracellular Ca2+ concentration in cardiomyocytes, neuronal cells, kidney and a variety of other cells. It performs a particularly important function in regulating cardiac contractility and electrical activity. One of the leading NCX inhibitors is KB‐R9743 (KBR) that appears to exhibit selectivity for Ca2+‐influx‐mode NCX activity (reverse mode of NCX). In this article we reviewed pharmacology of KBR and provide a brief summary of studies with other NCX inhibitors, such as SEA0400 (SEA) and SN‐6 (SN). Potential clinical usefulness of KBR and other NCX inhibitors is still controversial but the reviewed findings may be helpful in designing more selective and clinically useful NCX inhibitors for the treatment of cardiac, neuronal and kidney diseases. 相似文献
2.
目的 研究环维黄杨星D对分离的大鼠心室肌细胞内向整流钾电流 (IK1 )、瞬时外向钾电流 (Ito)、L 型钙电流(ICa L)和动作电位时程 (APD)的影响。方法 采用全细胞膜片钳技术记录大鼠心室肌细胞IK1 、Ito、ICa L 和APD。结果 1和10 μmol·L- 1 环维黄杨星D明显延长分离大鼠心室肌细胞APD50 和APD90 ,10 μmol·L- 1 可明显降低静息膜电位 (RP)。环维黄杨星D对IK1 内向电流和外向电流均有明显抑制作用 ,当指令电压为 - 10 0mV时 ,1和 10 μmol·L- 1 环维黄杨星D分别使IK1 电流密度从给药前的 ( - 8.0± 1.1)pA pF降至 ( - 4 .1± 0 .7)pA pF和 ( - 3.4± 0 .8)pA pF ;当指令电压 - 30mV时 ,分别使IK1 电流密度从 ( 1.10± 0 .2 4 )pA pF降至 ( 0 .6 1± 0 .18)pA pF和 ( 0 .36± 0 .11)pA pF ;在钳制电位从 0到 + 6 0mV之间 ,环维黄杨星D明显抑制Ito,当指令电压 4 0mV时 ,1和 10 μmol·L- 1 环维黄杨星D分别使Ito电流密度从给药前的 ( 8.9± 2 .0 )pA pF降至 ( 5 .5± 1.2 )pA pF和 ( 4 .9± 0 .9)pA pF。环维黄杨星D浓度依赖性抑制ICa L,在指令电压为 10mV时 ,1和 10 μmol·L- 1 分别使ICa L电流密度从给药前的 ( - 9.9± 1.8)pA pF降至 ( - 6 .4± 1.4 )pA pF和 ( - 4 .2± 0 .6 )pA pF。结论 环 相似文献
3.
《Clinical neurophysiology》2021,132(9):2152-2162
ObjectiveChildren diagnosed with auditory processing disorder (APD) show deficits in processing complex sounds that are associated with difficulties in higher-order language, learning, cognitive, and communicative functions. Amblyaudia (AMB) is a subcategory of APD characterized by abnormally large ear asymmetries in dichotic listening tasks.MethodsHere, we examined frequency-specific neural oscillations and functional connectivity via high-density electroencephalography (EEG) in children with and without AMB during passive listening of nonspeech stimuli.ResultsTime-frequency maps of these “brain rhythms” revealed stronger phase-locked beta-gamma (~35 Hz) oscillations in AMB participants within bilateral auditory cortex for sounds presented to the right ear, suggesting a hypersynchronization and imbalance of auditory neural activity. Brain-behavior correlations revealed neural asymmetries in cortical responses predicted the larger than normal right-ear advantage seen in participants with AMB. Additionally, we found weaker functional connectivity in the AMB group from right to left auditory cortex, despite their stronger neural responses overall.ConclusionOur results reveal abnormally large auditory sensory encoding and an imbalance in communication between cerebral hemispheres (ipsi- to -contralateral signaling) in AMB.SignificanceThese neurophysiological changes might lead to the functionally poorer behavioral capacity to integrate information between the two ears in children with AMB. 相似文献
4.
以含不同浓度 Zn~(2+)的实验液分别灌流豚鼠心室乳头肌标本,用玻璃微电极引导细胞内的电信号,输入紫金Ⅱ微机系统;对所记录图形用博士851程序进行采样、分析和存储,并将图形和分析结果打印。实验结果表明,低浓度 Zn~(2+)灌流可使心肌细胞复极化过程延长,特别是APD_(50)延长尤为明显。Zn 可使 Ca~(2+)内流受阻,对抗由于细胞内 Ca~(2+)超负荷所引起的心肌细胞损伤。随着 Zn~(2+)浓度的增大,Ca~(2+)内流严重受阻,心肌细胞不能维持必要的 Ca~(2+)内流使 APD 逐渐缩短,特别是 APD_(50)缩短更为显著。 相似文献
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6.
Tone Stokkereit Mattsson Ola Lind Turid Follestad Kjell Grøndahl Wayne Wilson Ståle Nordgård 《International journal of audiology》2019,58(5):301-310
Objective: The suppression of evoked otoacoustic emissions (EOAE) may serve as a clinical tool to evaluate the medial olivocochlear (MOC) reflex, which is thought to aid speech discrimination (particularly in noise) by selectively inhibiting cochlear amplification. The present study aimed to determine if contralateral transient evoked otoacoustic emission (TEOAE) suppression was present in a clinical sample of children with listening difficulties with and without auditory processing disorder (APD).Design: A three-group, repeated measure design was used.Study sample: Forty three children aged 8–14?years underwent an auditory processing assessment and were divided into three groups: children with reported listening difficulties with APD, children with reported listening difficulties without APD, and children with normal hearing. APD was defined as per British Society of Audiology.Results: TEOAE suppression was present in all three participant groups. No significant group, age or ear effects were observed for TEOAE suppression in dB or as a normalised index.Conclusion: Contralateral TEOAE suppression method could not be used as a clinical tool to identify APD in this study’s participating children and did not support the hypothesised link between reduced MOC function and general listening difficulties in background noise in children with or without APD. 相似文献
7.
ZHONG CHEN M.B.B.S ROCIO CABRERA‐LOZOYA Ph.D. JATIN RELAN Ph.D. MANAV SOHAL M.B.B.S ANOOP SHETTY M.D. RASHED KARIM Ph.D. HERVE DELINGETTE Ph.D. JASWINDER GILL M.D. KAWAL RHODE Ph.D. NICHOLAS AYACHE Ph.D. PETER TAGGART D.Sc. CHRISTOPHER ALDO RINALDI M.D. MAXIME SERMESANT Ph.D. REZA RAZAVI M.D. 《Journal of cardiovascular electrophysiology》2016,27(7):851-860
8.
Pasdois P Beauvoit B Costa AD Vinassa B Tariosse L Bonoron-Adèle S Garlid KD Dos Santos P 《Journal of molecular and cellular cardiology》2007,42(3):631-642
The aim of this study was to investigate the effects of HMR1098, a selective blocker of sarcolemmal ATP-sensitive potassium channel (sarcK(ATP)), in Langendorff-perfused rat hearts submitted to ischemia and reperfusion. The recovery of heart hemodynamic and mitochondrial function, studied on skinned fibers, was analyzed after 30-min global ischemia followed by 20-min reperfusion. Infarct size was quantified on a regional ischemia model after 2-h reperfusion. We report that the perfusion of 10 microM HMR1098 before ischemia, delays the onset of ischemic contracture, improves recovery of cardiac function upon reperfusion, preserves the mitochondrial architecture, and finally decreases infarct size. This HMR1098-induced cardioprotection is prevented by 1 mM 2-mercaptopropionylglycine, an antioxidant, and by 100 nM nifedipine, an L-type calcium channel blocker. Concomitantly, it is shown that HMR1098 perfusion induces (i) a transient and specific inhibition of the respiratory chain complex I and, (ii) an increase in the averaged intracellular calcium concentration probed by the in situ measurement of indo-1 fluorescence. Finally, all the beneficial effects of HMR1098 were strongly inhibited by 5-hydroxydecanoate and abolished by glibenclamide, two mitoK(ATP) blockers. This study demonstrates that the HMR1098-induced cardioprotection occurs indirectly through extracellular calcium influx, respiratory chain complex inhibition, reactive oxygen species production and mitoK(ATP) opening. Taken together, these data suggest that a functional interaction between sarcK(ATP) and mitoK(ATP) exists in isolated rat heart ischemia model, which is mediated by extracellular calcium influx. 相似文献
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10.
Cooper GD Harrold JA Halford JC Goudie AJ 《Progress in neuro-psychopharmacology & biological psychiatry》2008,32(2):428-436
The ability of clozapine to induce weight gain in female rats was investigated in three studies with progressively lowered doses of clozapine. In an initial preliminary high dose study, clozapine at 6 and 12 mg/kg (i.p., b.i.d.) was found to induce weight loss. In a subsequent intermediate dose study, we obtained no evidence for clozapine-induced weight gain despite using identical procedures and doses of clozapine (1-4 mg/kg, i.p., b.i.d.) with which we have observed olanzapine-induced weight gain, hyperphagia, enhanced adiposity and metabolic changes [Cooper G, Pickavance L, Wilding J, Halford J, Goudie A (2005). A parametric analysis of olanzapine-induced weight gain in female rats. Psychopharmacology; 181: 80-89.]. Instead, clozapine induced weight loss without alteration in food intake and muscle mass or changes in levels of glucose, insulin, leptin and prolactin. However, these intermediate doses of clozapine enhanced visceral adiposity and elevated levels of adiponectin. In a final study, low doses of clozapine (0.25-0.5 mg/kg, i.p, b.i.d.) induced weight loss. These data demonstrate that clozapine-induced weight gain can be much more difficult to observe in female rats than olanzapine-induced weight gain. Moreover, these findings contrast with clinical findings with clozapine, which induces substantial weight gain in humans. Clozapine-induced enhanced adiposity appears to be easier to observe in rats than weight gain. These findings, along with other preclinical studies, suggest that enhanced adiposity can be observed in the absence of antipsychotic-induced weight gain and hyperphagia, possibly reflecting a direct drug effect on adipocyte function independent of drug-induced hyperphagia [e.g. Minet-Ringuet J, Even P, Valet P, Carpene C, Visentin V, Prevot D, Daviaud D, Quignard-Boulange A, Tome D, de Beaurepaire R (2007). Alterations of lipid metabolism and gene expression in rat adipocytes during chronic olanzapine treatment. Molecular Psychiatry; 12: 562-571.]. These and other findings which show that the results of studies of antipsychotic treatment in animals do not always mimic clinical findings have important implications for the use of animal models of antipsychotic-induced weight gain. With regard to weight gain the results obtained appear to depend critically on the experimental procedures used and the specific drugs studied. Thus such models are not without limitations. However, they do consistently demonstrate the ability of various antipsychotics to enhance adiposity. 相似文献