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51.
温热与顺铂以不同的时序性联合对人肺巨细胞癌细胞抑制作用的实验研究 总被引:1,自引:0,他引:1
目的探讨42℃热疗与化疗药物顺铂联合作用于肺癌细胞时,在进行化疗的同时何时进行热疗疗效最好,从而为临床治疗提供实验依据。方法利用MTT法测定单纯42℃热疗组、单纯化疗组以及不同时间结合点的热化疗组对人肺巨细胞癌细胞(PLA801D)的抑制率。结果42℃热疗与化疗药物顺铂(DDP)同时作用时,对肺癌细胞的抑制率最强(55.73%),不仅优于单纯热疗组(3.13%)、单纯化疗组,也优于先化疗后热疗组和先热疗后化疗组(P均<0.000)。结论顺铂与42℃热疗同时作用较其他结合方式对肺癌细胞的毒性作用更强。 相似文献
52.
Changes in tissue-plasminogen activator mRNA expression following cortical ablation in the rat brain 总被引:2,自引:0,他引:2
Kohmura E Yuguchi T Sakaki T Nonaka M Fujinaka T Hayakawa T Yoshimine T 《Journal of molecular neuroscience : MN》2000,14(1-2):53-59
Tissue plasminogen activator (tPA) has been used to treat acute thrombotic lesions. Roles other than the activation of fibrinolytic
pathways have been suggested for tPA in the mature brain. We used the in situ hybridization technique to investigate the changes in tPA mRNA expression within the brain after cortical ablation. We found
that expression of tPA mRNA started to increase diffusely in the cortex ipsilateral to the injury 6 h after ablation. This
increase had become prominent 24 h after ablation. On d 5, the expression of tPA mRNA had returned to that of the control
animals except for the area near the injury. We also found that administration of MK-801 before injury suppressed the increase
of tPA mRNA in the ipsilateral cortex. These results suggest that the increase in tPA mRNA is likely to be mediated via activation
of NMDA receptors. 相似文献
53.
Olfactory bulbectomy (OBX) transects the glutamatergic efferents from the olfactory bulbs, and the changes of glutamatergic N-methyl-D-aspartate (NMDA) receptor-mediated function are though to be involved in the behavioral deficits seen in OBX rats. In the present study, irritability scores in OBX male Wistar rats were correlated with discrete regional effects on NMDA receptor function measured using a [3H] MK-801 binding assay. Irritability scores, measured before and for 2 weeks after OBX, showed a gradual increase in irritability after OBX. A reduction of the NMDA receptor density was observed in the cerebral cortex and amygdala 16 days after OBX, but not in the striatum, olfactory tubercle, entorhinal cortex, and hippocampus. These results demonstrate that OBX causes changes in the NMDA receptor system in certain brain regions and suggest that these changes may be responsible for the behavioral deficits of OBX rats. 相似文献
54.
Nagatomo I Hashiguchi W Tominaga M Akasaki Y Uchida M Takigawa M 《Brain research》2001,888(2):306-310
To clarify the role of nitric oxide (NO) in the pathogenesis of seizures in susceptible EL mice, we investigated effects of three drugs potentially related to NO production, MK-801, dantrolene, and FK506, on convulsive seizures and brain NO metabolites (NOx). MK-801 or dantrolene, but not FK506, suppressed convulsive seizures in EL mice; only MK-801 reduced NOx in the brain. Our results suggested involvement of the N-methyl-D-aspartate receptor-channel complex and intracellular calcium mobilization, but not calcineurin, in the convulsions of EL mice. 相似文献
55.
A Model of Status Epilepticus Induced by Intermittent Electrical Stimulation of the Deep Prepyriform Cortex in Rats 总被引:1,自引:0,他引:1
56.
The effect of different ligands for the GABA-BZD receptor and the NMDA receptor were studied in rats trained to discriminate (?)-nicotine (1.9 μmol/kg) from saline in a standard two-bar operant conditioning paradigm with food reinforcement. MK-801 (0.03–0.3 μmol/kg), flumazenil (10–30 μmol/kg), and Ro 15–4513 (3–10 μmol/kg) did not generalize to (?)-nicotine on nicotine-trained rats, and when tested as antagonists they did not block the nicotine cue. Diazepam (3–10 μmol/kg) and ethanol (11–22 mmol/kg) did not have any effect by themselves, but they significantly attenuated the nicotine cue by 53 and 65%, respectively, without affecting the response rates of the animals. Pre-treatment with flumazenil (30 μmol/kg) reversed the effect of diazepam but it did not reverse the effect of ethanol on the discriminative stimulus properties of (?)-nicotine. The effect of ethanol was not blocked by Ro 15–4513 (10 μmol/kg). These data indicate that diazepam and ethanol modulate the expression of the nicotine cue and that the effect of diazepam is mediated via a benzodiazepine receptor mechanism. © Wiley-Liss, Inc. 相似文献
57.
Takeshi Yanase Shuichi Hara Toshiji Mukai Fumi Kuriiwa Nobuhisa Iwata Sadao Kano Takahiko Endo 《Brain research》1998,798(1-2)
Intracerebroventricular administration of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) or kainate caused a rise of the temperature of the brain and the rectum in urethane-anesthetized rats. An AMPA–kainate receptor antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX), significantly suppressed the AMPA- and kainate-induced rises of brain and rectal temperatures. An N-methyl-
-aspartate receptor antagonist, MK-801, also suppressed the rises of the brain and rectal temperatures induced by AMPA or kainate, but the profiles of the suppressive effects of MK-801 were different between rats treated with AMPA and kainate. An antipyretic agent, indomethacin, completely suppressed the AMPA-induced rises of brain and rectal temperatures. Although indomethacin completely suppressed the kainate-induced rise of the rectal temperature as well, the brain temperature was still raised. These findings suggest that distinct mechanisms may be involved in the temperature rise of the brain and the rectum mediated through AMPA and kainate receptor stimulation. 相似文献
58.
Repeated administration of methamphetamine (METH) results in damage to nigrostriatal dopaminergic neurons. Both competitiveN-methyl-d-aspartate (NMDA) receptor antagonists and use-dependent cation channel blockers attenuate METH-induced damage. The objectives of the present study were to examine whether comparable reductions in METH-induced damage could be obtained by compounds acting at strychnine-insensitive glycine receptors on the NMDA receptor complex. Four injections of METH (5 mg/kg i.p.) resulted in a 70.9% depletion of striatal dopamine (DA) and 62.7% depletion of dihydroxyphenylacetic acid (DOPAC) content, respectively. A significant protection against METH-induced DA and DOPAC depletion was afforded by the use-dependent channel blocker, MK-801. The competitive glycine antagonist 7-chlorokynurenic acid (7-Cl-KA), the low efficacy glycine partial agonist (+)-3-amino-1-hydroxy-2-pyrrolidone ((+)-HA-966), and the high efficacy partial glycine agonist 1-aminocyclopropane-car☐ylic acid (ACPC) were ineffective against METH-induced toxicity despite their abilities to attenuate glutamate-induced neurotoxicity under both in vivo and in vitro conditions. These results indicate that glycinergic ligands do not possess the same broad neuroprotective spectrum as other classes of NMDA antagonists. 相似文献
59.
Potent Analgesia Induced in Rats by Combined Action at PCP and Polyamine Recognition Sites of the NMDA Receptor Complex 总被引:4,自引:0,他引:4
Terence J. Coderre 《The European journal of neuroscience》1993,5(4):390-393
The present study was performed to examine the analgesic effects of the intrathecal administration of agents acting at various sites in the N -methyl- d -aspartic acid (NMDA) receptor complex on the nociceptive responses to s.c. formalin injection in rats. Both the competitive NMDA receptor antagonist 2-amino-5-phosphonovaleric acid (APV) and the non-competitive NMDA antagonist dizocilpine maleate (MK-801) produced dose-dependent analgesic effects in the late, but not the early, phase of the formalin test. The polyamine antagonist ifenprodil, and the strychnine-insensitive glycine antagonists DCQX and 7-chlorokynurenic acid, failed to produce any analgesic effects in either the early or the late phase of the formalin test. The analgesic effects of APV were enhanced slightly by combined administration with a non-analgesic dose of glycine, and the analgesic effects of MK-801 were dramatically potentiated by combined adminstration of a non-analgesic dose of the polyamine spermine. The results indicate that much more potent analgesia can be produced in the formalin test by a combination of open channel blockers (such as MK-801) with agonists acting at the polyamine site, than by a single treatment with antagonists to either glycine allosteric or polyamine sites within the NMDA receptor complex. 相似文献
60.
Wilhelmus J.H.J. Meijerink Patricia E. Molina Charles H. Lang Naji N. Abumrad 《Brain research》1996,706(1):123
Previous studies have indicated that excitatory amino acids are involved in the analgesic and addictive properties of morphine. However, their role in the morphine-induced alterations in glucose metabolism is not known. This study assessed the contribution of NMDA receptor activation to the morphine-induced hormonal and metabolic alterations in conscious unrestrained chronically catheterized rats. Whole body glucose flux was assessed with a primed constant intravenous infusion of [3-3H]glucose in rats pretreated with the NMDA-receptor antagonist MK-801 (0.25 mg/kg, intraarterial) or an equal volume (1.5 ml) of sterile saline (0.9% ) administered 15 min prior to i.c.v. injection of H2O (Con; 5 μl) or morphine sulfate (80 μg). No significant alterations were noted in metabolic and hormonal parameters of H2O injected rats. i.c.v. morphine increased the plasma glucose concentration (60%), hepatic glucose production (Ra; 60%) and whole body glucose utilization (Rd; 53%), but did not alter the glucose metabolic clearance rate (MCR). MK-801 alone resulted in transient hyperglycemia (25%), stimulation of glucose Ra (60%) and glucose Rd (53%), and a significant (30%) increase in MCR. MK-801 pretreatment blunted the morphine-induced hyperglycemia and the increased glucose Ra and Rd. Morphine increased the plasma concentration of epinephrine (4-fold), norepinephrine (2-fold) and corticosterone (67%); however, no alterations in plasma insulin and glucagon were detected. MK-801 pretreatment, blunted the morphine-induced increase in corticosterone and norepinephrine, and elicited a significant rise in insulin concentrations. These results indicate that activation of the NMDA receptors contributes to the morphine-induced hyperglycemia and hormonal alterations. Furthermore, this response appears partially mediated by activation of sympathetic outflow and suppression of insulin release, which is blunted by inhibition of NMDA receptors. 相似文献