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581.
Background
Pseudomonas fluorescens has long been considered as a psychrotrophic microorganism. Recently, we have shown that clinical strains of P. fluorescens (biovar 1) are able to adapt at a growth temperature of 37°C or above and induce a specific inflammatory response. Interestingly, a highly specific antigen of P. fluorescens, I2, is detected in the serum of patients with Crohn's disease but the possible role of this bacterium in the disease has not yet been explored. In the present study, we examined the ability of a psychrotrophic and a clinical strain of P. fluorescens to modulate the permeability of a Caco-2/TC7 intestinal epithelial model, reorganize the actin cytoskeleton, invade the target cells and translocate across the epithelium. The behaviour of these two strains was compared to that of the well known opportunistic pathogen P. aeruginosa PAO1.Results
Both strains of P. fluorescens were found to decrease the transepithelial resistance (TER) of Caco-2/TC7 differentiated monolayers. This was associated with an increase in paracellular permeability and F-actin microfilaments rearrangements. Moreover, the invasion and translocation tests demonstrated that the two strains used in this study can invade and translocate across the differentiated Caco-2/TC7 cell monolayers.Conclusions
The present work shows for the first time, that P. fluorescens is able to alter the intestinal epithelial barrier function by disorganizing the F-actin microfilament network. Moreover, we reveal that independently of their origins, the two P. fluorescens strains can translocate across differentiated Caco-2/TC7 cell monolayers by using the transcellular pathway. These findings could, at least in part, explain the presence of the P. fluorescens specific I2 antigen in the serum of patients with Crohn's disease. 相似文献582.
Background and purpose:
Carisbamate is being developed for adjuvant treatment of partial onset epilepsy. Carisbamate produces anticonvulsant effects in primary generalized, complex partial and absence-type seizure models, and exhibits neuroprotective and antiepileptogenic properties in rodent epilepsy models. Phase IIb clinical trials of carisbamate demonstrated efficacy against partial onset seizures; however, its mechanisms of action remain unknown. Here, we report the effects of carisbamate on membrane properties, evoked and spontaneous synaptic transmission and induced epileptiform discharges in layer II-III neurones in piriform cortical brain slices.Experimental approach:
Effects of carisbamate were investigated in rat piriform cortical neurones by using intracellular electrophysiological recordings.Key results:
Carisbamate (50–400 µmol·L−1) reversibly decreased amplitude, duration and rise-time of evoked action potentials and inhibited repetitive firing, consistent with use-dependent Na+ channel block; 150–400 µmol·L−1 carisbamate reduced neuronal input resistance, without altering membrane potential. After microelectrode intracellular Cl− loading, carisbamate depolarized cells, an effect reversed by picrotoxin. Carisbamate (100–400 µmol·L−1) also selectively depressed lateral olfactory tract-afferent evoked excitatory synaptic transmission (opposed by picrotoxin), consistent with activation of a presynaptic Cl− conductance. Lidocaine (40–320 µmol·L−1) mimicked carisbamate, implying similar modes of action. Carisbamate (300–600 µmol·L−1) had no effect on spontaneous GABAA miniature inhibitory postsynaptic currents and at lower concentrations (50–200 µmol·L−1) inhibited Mg2+-free or 4-aminopyridine-induced seizure-like discharges.Conclusions and implications:
Carisbamate blocked evoked action potentials use-dependently, consistent with a primary action on Na+ channels and increased Cl− conductances presynaptically and, under certain conditions, postsynaptically to selectively depress excitatory neurotransmission in piriform cortical layer Ia-afferent terminals. 相似文献583.
盐酸普鲁卡因经皮离子导入的研究 总被引:2,自引:2,他引:2
目的:考察盐酸普鲁卡因的离子导入与电流强度、药物浓度的关系。方法:测定不同的电流强度、不同的药物浓度的离子导入增渗倍数(ER)。结果:固定药物浓度,电流强度为0.1,0.2和0.3mA时的ER值分别为68.99和127。固定电流强度0.2mA,药物浓度为0.0151,0.0304和0.0605g/100ml时的ER值分别为95,99和98,结论:离子导入可以显著提高药物渗透速率,增渗倍数(ER)随 相似文献
584.
585.
目的中性粒细胞粘附在缺血再灌注损伤中有非常重要的作用.本文用SD大鼠趾长屈肌缺血再灌注损伤模型,观察L-粘附素单抗LAM1-116在缺血再灌注损伤中的作用.方法30只SD大鼠被均分为2组LAM1-116组和生理盐水对照组.每只大鼠的一侧趾长屈肌作为正常对照,另外一侧进行3 h缺血4 h再灌注.结果LAM1-116组实验侧的髓过氧化物酶为正常的2倍(2.3±2.2),生理盐水对照组则为正常的28倍(27.5±11.7)(P<0.001);LAM1-116组的湿重比(1.10±0.10)、疲劳肌力(77.1%±12.1%)与对照组相比(分别为1.23±0.10和49.7%±9.3%)明显改善(P<0.05);组织学上,LAM 1-116组的中性粒细胞局部浸润显著减少,水肿减轻.结论通过L-粘附索单克隆抗体LAM1-116阻断L-粘附素的功能,可以有效地降低中性粒细胞在再灌注肌肉中的浸润,防止组织水肿,从而改善肌肉的功能. 相似文献