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Cardiovascular reflex responses have been studied in 9 newborn preterm infants with apnoeic episodes and in 2 preterm infants with periodic breathing. Respiration, blood pressure, heart rate, and peripheral blood flow were simultaneously recorded. Peripheral blood flow was measured in the leg by venous occlusion plethysmography. During apnoea, bradycardia and peripheral vasoconstriction occur. There is little change in blood pressure though pulse pressure increases. No cardiovascular changes were seen before the onset of apnoea. Periodic breathing had little effect on peripheral blood flow. Preterm infants with gestations as low as 27 weeks apparently have well developed chemoreceptor reflexes which would tend to preserve blood supply to the brain during conditions of hypoxia.  相似文献   
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S-carboxymethyl-L-cysteine (carbocysteine) improves the visco-elastic properties of bronchial mucus in vivo, possibly as a result of an increase in the relative proportions of sialomucins in bronchial mucus. Carbocysteine was therefore studied in vitro and ex vivo in both normal and bronchitic rats on pulmonary sialyl transferase, responsible for the addition of sialic acid to mucus glycoproteins. Bronchitis was induced in male Sprague-Dawley rats by repeated exposure to sulphur dioxide for two weeks. During this time they received either 500 mg kg-1 day-1 carbocysteine or its vehicle by the oral route. Rats not being exposed to SO2 received the same treatment. The animals were then killed, and subcellular fractions prepared by differential centrifugation of lung homogenates. Sialyl transferase was assayed using CMP-14C sialic acid as substrate and desialysed fetuin as exogenous acceptor. Enzyme activity was located in both the (Golgi-containing) 10,000 g and 100,000 g pellets with minor activity in the cytosolic supernatants. When tested in vitro between 10(-6) and 10(-3) M, carbocysteine had no effect on sialyl transferase activity in microsomes taken from healthy or bronchitis rats. Repeated administration of carbocysteine was without effect on the sialyl transferase activity in 10,000 g pellets taken from healthy rats. However, in bronchitic rats there was a small but statistically significant (P less than 0.05) increase in enzymic activity in the treated group compared to the animals receiving the vehicle. There was no difference in the activity of the microsomal enzyme compared to vehicle-treated controls in either healthy or bronchitic rats. We conclude that it is possible that an increase in sialyl transferase activity in a Golgi-containing fraction of bronchitic lungs could explain the relative increase in sialomucins in bronchitic subjects.  相似文献   
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为考察4′-去甲表鬼臼毒素C4位上联结含卤素原子的酯化侧链时对化合物抗肿瘤活性的影响,设计并采用选择性酯化方法合成了9个新的4′-去甲基表鬼臼毒素酯化产物。其中标题化合物在L1210白血病肿瘤细胞与KB细胞的体外生长抑制试验中普遍表现出显著的抑制活性,大部分化合物活性超过依托泊甙。而普通脂酸酯的活性较弱。  相似文献   
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Autostimulation of growth by human myelogenous leukemia cells (HL-60)   总被引:3,自引:0,他引:3  
We have studied the effects of medium conditioned by the human progranulocytic leukemia cell line, HL-60, on the subsequent growth of new inocula of HL-60 cells. When HL-60 cells were cultured at high cell density, optimal growth rate occurred in liquid suspension and confluent colony growth was observed in viscous medium without the addition of conditioned medium. However, when cells were cultured at lower cell density, growth rate was reduced and colony growth was nil unless conditioned medium from HL-60 culture was added. All HL-60 populations studied, including the earliest available passage, 9, both elaborated and responded to HL-60 CM. HL-60 CM did not stimulate normal human or mouse granulocyte-monocyte colony-forming cell (CFU-GM) growth. Conditioned media from other human cell lines varied in the ability to stimulate HL-60 cell and CFU-GM proliferation. Some, such as GCT CM, stimulated both HL-60 cells and normal CFU-GM, whereas others, like HL-60 CM, stimulated only HL-60 growth. The majority of cell line CMs tested did not stimulate either HL-60 or CFU-GM. Chromatography of HL-60 CM on Ultrogel AcA54 showed a single peak of HL-60 stimulating activity of apparent molecular weight 13,000. The ability of HL-60 cells to elaborate this activity provides a possible explanation for their proliferation at higher cell densities. Autostimulation may prove to be important in the high growth potential of other cell populations that undergo unrepressed proliferation.  相似文献   
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Fifty four children were studied 1-14 (mean 5.6) years after fabrications of illness had been identified. Thirty of the 54 children were living in families with their biological mothers and 24 were with other family members or in substitute families. Further fabrications were identified for 10 children who had been living with their mothers and there were 'other concerns' for a further eight children. Thirteen children residing with mother and 14 not residing with mother at follow up had a range of disorders including conduct and emotional disorders, and problems related to school, including difficulties in attention and concentration and non-attendance. Overall, 20 children (49% of those successfully followed up) had outcomes that were considered to be unacceptable.  相似文献   
60.

Background

Previous work has suggested that in the liver, adenosine preconditioning is mediated by nitric oxide. Whether the endothelial isoform of nitric oxide synthase plays a part in this mechanism has however not yet been investigated.

Methods

Wistar rats were used (6 in each group) – Groups: (1) sham, (2) ischemia-reperfusion, (3) adenosine + ischemia-reperfusion, (4) endothelial isoform inhibitor + adenosine + ischemia-reperfusion.

Results

Using immunohistochemistry, this study has revealed a decrease in the expression of endothelial nitric oxide synthase following hepatic ischemia-reperfusion. This was prevented by adenosine pre-treatment. When an inhibitor of endothelial nitric oxide synthase was administered prior to adenosine pre-treatment, pre-conditioning did not occur despite normal expression of endothelial nitric oxide synthase.

Conclusions

These findings suggest that adenosine attenuates hepatic injury by preventing the downregulation of endothelial nitric oxide synthase that occurs during ischemia-reperfusion.  相似文献   
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