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1.
B. A. Reikhardt L. M. Belyavtseva O. G. Kulikova 《Bulletin of experimental biology and medicine》1992,113(5):682-684
Academician S. V. Anichkov Department of Pharmacology, Research Institute of Experimental Medicine, Academy of Medical Sciences, St. Petersburg. (Presented by Academician of the Academy of Medical Sciences A. N. Klimov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 113, No. 5, pp. 506–508, May, 1992. 相似文献
2.
The presence of diadenosine polyphosphates (ApxA), diadenosine tetraphosphate (Ap4A), diadenosine pentaphosphate (Ap6A), and diadenosine hexaphosphate (Ap6A), has been described in secretory granules of chromaffin cells, Torpedo synaptic vesicles, and rat brain synaptosomes. The release of these compounds by the action of secretagogues and depolarizing agents, in the presence of calcium, increases their importance as active neurotransmitters. Two high affinity receptors have been described in the three neural models, with Kd values ranging from 0.08 to 0.40 nM for the first binding site and from 5.6 to 18nM for the second lower affinity binding site. Both binding sites exhibit a P2y-like profile in chromaffin cells and Torpedo synaptic terminals and a different pattern in rat brain synaptosomes, suggesting the presence of a novel P2-purinoceptor tentatively named P2d. Studies about the second messenger linked to this receptor, in chromaffin cells, demonstrate the mobilization of calcium from internal stores. ApxA receptors at the extracellular milieu are responsible for the inhibition of catecholamine release stimulated by secretagogues. Finally, all diadenosine polyphosphates are destroyed by the action of an ecto-phosphodiesterase which, in chromaffin cells, shows Km values ranging from 1 to 4 μM. © 1993 Wiley-Liss, Inc. 相似文献
3.
锌离子对大鼠海马突触体Ca^2+—Mg^2+ATP酶活性及蛋白合成的影响 总被引:5,自引:0,他引:5
行为实验己经证明,锌过多或缺锌均可影响脑功能。锌作为体内重要的微量元素,影响多种酶的活性及蛋白质和核酸的台成。本实验通过体外分离大鼠脑海马突触体,观察不同浓度锌离子对Ca2 -Mg2 ATP酶的活性和3H-Leu掺入突触蛋白合成的影响.结果表明:1.锌离子浓度在25μmol/L时增加该酶的活性(<0.01),并促进3H-Leur掺入蛋白质的合成(<0.05)。2.锌离子在50,100,200μmol/L的较高浓度时对Co2 -M2 ATP酶的活性有显著的抑制作用(分别为:P<0.05.P<0.01,P<0.01),仅200μmol/L对3H—Leu掺入突触蛋白合成有抑制作用。本研究提示:适量的锌对突触体功能的维持是必要的,但剂量过高则起相反作用。 相似文献
4.
The effect of verapamil on resting and depolarization-induced monoamine release was investigated in rat hippocampal synaptosomes prelabeled with [3H]-5-hydroxytryptamine (HT) or [3H]-norepinephrine (NE) and rat striatal synaptosomes prelabeled with [3H]-dopamine (DA). Verapamil (50 μM) completely abolishes high K+-induced [3H]-NE release, but paradoxically facilitates high K+-induced [3H]-5-HT and [3H]-DA release. All these high K+-evoked responses were Ca2+ dependent. Verapamil does not modify [3H]-NE baseline release, but increases dose dependently [3H]-5-HT and [3H]-DA baseline release. Verapamil (10 μM, for 5 min) increases endogenous DA release (70%) and endogenous 5-HT release (40%) independently on the presence of external Ca2+. The total amount of these monoamines (released plus retained by the preparation) and their metabolites (DOPAC and 5-HIAA) was similar in control and verapamil-treated synaptosomes. Verapamil displaces [3H]-spiroperidol specific binding (Ki of 2.4 × 10?6M) and [3H]-SCH-23390 specific binding (Ki of 9 × 10?6M) from striatal synaptosomal membranes, and [3H]-5-HT specific binding (Ki of 3 × 10?5M) from hippocampal synaptosomal membranes. It is concluded that in addition to the Ca2+ antagonistic properties of verapamil on the Ca2+-dependent, depolarization-induced release of some neurotransmitters [gamma aminobutyric acid (GABA and NE)], another mechanism probably mediated by presynaptic receptors underlies the effects of verapamil on DA and 5-HT release from discrete brain regions. © 1995 Wiley-Liss, Inc. 相似文献
5.
J. Blasi G. Egea M. J. Castiella M. Arribas C. Solsona P. J. Richardson J. Marsal 《Journal of neural transmission (Vienna, Austria : 1996)》1992,90(2):87-102
Summary Torpedo electric organ has been used to study the binding of botulinum neurotoxin type A to pure cholinergic synaptosomes and presynaptic plasma membrane.125I-labeled botulinum neurotoxin type A exhibits specific binding to cholinergic fractions. Two binding sites have been determined according to data analysis: a high affinity binding site (synaptosomes: Kd=0.11±0.03 nM, Bmax=50±10 fmol · mg prot–1; presynaptic plasma membrane: Kd=0.2±0.05 nM, Bmax=150±15 fmol · mg prot–1) and a low affinity binding site (synaptosomes: Kd 26 nM, Bmax 7.5 pmol · mg prot–1; presynaptic plasma membrane: Kd 30 nM, Bmax 52 pmol · mg prot–1). The binding of125I-botulinum neurotoxin type A is decreased by previous treatment of synaptosomes by neuraminidase and trypsin, and by a preincubation with bovine brain gangliosides or antiserum raised against Torpedo presynaptic plasma membrane. When presynaptic plasma membranes are blotted to nitrocellulose sheet, either125I-botulinum neurotoxin or botulinum toxin-gold complexes bind to a Mr 140,000 protein. Botulinum toxin-gold complexes have also been used to study the toxin internalization process into Torpedo synaptosomes. The images fit the three step sequence model in the pathway of botulinum neurotoxin poisoning. 相似文献
6.
Use of post-mortem human synaptosomes for studies of metabolism and transmitter amino acid release 总被引:2,自引:0,他引:2
J A Hardy P R Dodd A E Oakley A M Kidd R H Perry J A Edwardson 《Neuroscience letters》1982,33(3):317-322
Synaptosomes have been prepared from human brain obtained at autopsies carried out up to 24 h postmortem (p.m.). They showed generally good retention of morphology, as well as accumulation of tissue potassium and linear rates of oxygen uptake. In response to veratrine depolarization they showed increased respiration rate, decreased tissue potassium content and the specific release of transmitter amino acids. Regression analysis indicated that metabolically and functionally active preparations may be obtained up to ca. 25 h p.m. Preparations obtained from patients dying with brain injury were inactive. 相似文献
7.
The pro-inflammatory cytokine interleukin-1β (IL-1β) is released by cells during injury and stress, and increased neuronal expression of IL-1β is a feature of age-related neurodegeneration. We have recently reported that IL-1β has a biphasic effect on the K+-induced rise in intracellular Ca2+ concentration ([Ca2+]i) in cortical synaptosomes, exerting an inhibitory effect on the K+-induced rise in [Ca2+]i at lower (3.5 ng/mL) concentrations and a stimulatory effect on the K+-induced rise in [Ca2+]i at higher (100 ng/mL) concentrations. In the present study, we observed that the K+-induced rise in [Ca2+]i was inhibited to a similar extent by the lower concentration of IL-1β in cortical synaptosomes prepared from young (3-month-old), middle-aged (12-month-old) and aged (24-month-old) rats. In contrast, cortical synaptosomes prepared from the aged rats exhibited an increased susceptibility to the higher concentration of IL-1β, resulting in a marked elevation in [Ca2+]i. We propose that the age-related increase in neuronal concentration of IL-1β promotes a dramatic elevation in [Ca2+]i following membrane depolarization, thereby altering Ca2+ homeostasis and exacerbating neuronal vulnerability to excitotoxicity. 相似文献
8.
G. N. Kryzhanovskii V. I. Fedorova R. N. Glebov R. M. Kulygina O. P. Sakharova 《Bulletin of experimental biology and medicine》1975,79(4):367-370
It was shown by electrophoresis on polyacrylamide gel that the content of proteins with low electrophoretic mobility rises in a Triton extract of the fractions of synaptic structures from the spinal cord tissue of rats with local tetanus, whereas no change was found in the protein spectrum in the dodecyl sulfate extract. In experiments in vitro tetanus toxin stimulated the incorporation of lysine-H3 into total proteins of cortical synaptosomes.Laboratory of General Pathology of the Nervous System, Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 79, No. 4, pp. 19–22, April, 1975. 相似文献
9.
E. V. Semenov 《Bulletin of experimental biology and medicine》1978,86(3):1168-1170
The effect of the central cholinolytic benactyzine and the cholinomimetic arecoline on the uptake of45Ca by rat brain synaptosomes was studied in vitro. Benactyzine was shown to cause biphasic changes (a decrease followed by an increase) in the intensity of uptake of the isotope, whereas arecoline led to a rapid initial increase in45Ca uptake. Benactyzine was shown to depress the effect of arecoline and depolarization on uptake of the isotope. It is concluded that the increase in45Ca uptake through the action of arecoline is connected with activation of Nachannels. Benactyzine, on the other hand, reduces the permeability of the these channels for45Ca and activates the Ca-channels proper.(Presented by Academician of the Academy of Medical Sciences of the USSR S. S. Golikov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 9, pp. 301–304, September, 1978. 相似文献
10.
K. Fink E. Schlicker A. Neise M. Göthert 《Naunyn-Schmiedeberg's archives of pharmacology》1990,342(5):513-519
Summary Rat brain cortex slices or synaptosomes preincubated with 3H-serotonin were superfused with physiological salt solution (which, in the case of slices, contained citalopram, an inhibitor of serotonin uptake), and the effects of histamine and related drugs on the evoked tritium overflow were studied.The electrically (3 Hz) evoked tritium overflow from slices was inhibited by histamine and the H3 receptor agonists R-(–)--methylhistamine and N-methylhistamine (pIC12.5 values: 6.41, 7.28 and 6.12, respectively), but not affected by the H1 receptor agonist 2-(2-thiazolyl)ethylamine and the H2 receptor agonist dimaprit (each at 10 mol/l). The concentration-response curve for histamine was shifted to the right by the H3 receptor antagonists impromidine, burimamide and thioperamide (apparent pA2 values: 7.45, 5.97 and 7.88, respectively); the concentration-response curve of serotonin for its inhibitory effect on the electrically evoked overflow was not affected by the three drugs (apparent pA2 values: < 5.5, < 5.5 and < 6.5). Given alone, impromidine, thioperamide and a low concentration of burimamide facilitated the electrically evoked overflow. In slices superfused with K+-rich, Ca2+-free solution containing tetrodotoxin throughout and in synaptosomes superfused with Ca2+-free solution, histamine inhibited the overflow evoked by introduction of Ca2+ (in synaptosomes, simultaneously with an increased amount of K+). In either tissue, the effect of histamine was counteracted by thioperamide.The results provide evidence that exogenous and probably also endogenous histamine inhibits serotonin release in the rat brain cortex via presynaptic histamine H3 receptors.Send offprint requests to E. Schlicker at the above address 相似文献