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91.
小鼠持续性脑缺血后NMDA受体亚单位表达的变化 总被引:7,自引:1,他引:6
目的:研究小鼠持续性脑缺血后不同脑区NMDA受体亚单位表达的变化及其与病理损伤之间的联系。方法:采用大脑中动脉阻断法制作小鼠持续性脑缺血模型,取缺血后不同时间的皮层、海马、皮层下脑组织,用免疫印迹技术测定NMDA受体亚单位ζ1和ε1及ε2蛋白的含量。同时作冰冻切片和苏木素伊红染色,计算相应脑区神经元密度。结果:NMDA受体ζ1和ε1及ε2亚单位表达的改变发生于缺血后5h内,皮层下3个亚单位表达均明显增加,海马则各亚单位表达变化不一。脑梗塞灶和相关脑区神经元密度显著减小均出现于缺血后5h,相关脑区神经元死亡严重程度依次为皮层下组织和海马CA1区及大脑颞叶皮层Ⅲ-Ⅳ层。结论:小鼠持续性脑缺血,缺血侧脑组织NMDA受体亚单位ζ1和ε1及ε2表达的变化发生在明显的病理损害之前,表达变化程度因脑区不同,与相关脑区神经元损害的程度相应。 相似文献
92.
Simona Cabib Claudio Castellano Vincenzo Cestari Umberto Filibeck Stefano Puglisi-Allegra 《Psychopharmacology》1991,105(3):335-339
Pretreament with small, per se ineffective doses of the selective D1 antagonist SCH 23390 inhibited hyperactivity induced by cocaine. On the other hand, the classic neuroleptic haloperidol and the selective D2 antagonist metoclopramide prevented the stimulatory effects of cocaine on locomotion only at hypokinetic doses, while the atypical neuroleptic (–)-sulpiride, a selective D2 antagonist, did not produce significant effects when administered at the hypokinetic dose of 12 mg/kg. Finally, at low doses (–)-sulpiride dose-dependently potentiated the locomotor-stimulating effects of cocaine, an effect that is not shared either with haloperidol or with metoclopramide. These results are discussed in terms of different roles of DA receptor subtypes in the modulation of the stimulant effects of cocaine on locomotion. 相似文献
93.
用放免法检测乙型慢性活动性肝炎病人的红细胞c3b受体(KBCCR1).结果:病人RBCCR1明显低于献血员(P<0.05);抗-HBs特异性免疫复合物阳性病人RBCCR1明显低于阴性病人(P<0.01),与红细胞C3b受体花环试验检测结果一致。表明乙型慢性活动性肝炎病人RBCCR1数量减少,活性下降。其原因可能是特异性循环免疫复合物占据了RBCCR1空位,使CR1活性下降。 相似文献
94.
Central activation of excitatory amino acid receptors has been implicated in neuropathic pain following nerve injury. In a rat model of painful peripheral mononeuropathy, we compared the effects of non-competitive NMDA receptor antagonists (MK 801 and HA966) and a non-NMDA receptor antagonist (CNQX) on induction and maintenance of thermal hyperalgesia induced by chronic constrictive injury (CCI) of the rat common sciatic nerve. Thermal hyperalgesia to radiant heat was assessed by using a foot-withdrawal test and NMDA/non-NMDA receptor antagonists were administered intrathecally onto the lumbar spinal cord before and after nerve injury. Four daily single treatments with 20 nmol HA966 or CNQX beginning 15 min prior to nerve ligation (pre-injury treatment), reliably reduced thermal hyperalgesia in CCI rats on days 3, 5, 7 and 10 after nerve ligation. Thermal hyperalgesia was also reduced in CCI rats receiving a single post-injury treatment with HA966 (20 or 80 nmol) or MK 801 (5 or 20 nmol) on day 3 after nerve ligation when thermal hyperalgesia was well developed. In contrast, a single post-injury CNQX (20 or 80 nmol) treatment failed to reduce thermal hyperalgesia or to potentiate effects of HA966 or MK 801 (5 or 20 nmol) on thermal hyperalgesia in CCI rats. Moreover, multiple post-injury CNQX treatments utilizing the same dose regime as employed for the pre-injury treatment attenuated thermal hyperalgesia but only when the treatment began 1 or 24 h (but not 72 h) after nerve ligation.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
95.
Véronique Strijckmans Michel Bottlaender Humin Luo Michèle Ottavianil Daniel W. McPherson Christian Loc'h Chantal Fuseau Furn F. Knapp Bernard Mazière 《European journal of nuclear medicine and molecular imaging》1997,24(5):475-482
We studied the potential of three radiobrominated isomers of BrQNP, (Z(-,-)-[76Br]BrQNP,E(-,-)-[76Br]BrQNP andE(-,+)-[76Br]BrQNP), as suitable radioligands for imaging of central muscarinic cholinergic receptors in the human brain. These radioligands were stereospecifically prepared by electrophilic radiobromodestannylation of the respective tributylstannyl precursors using no-carrier-added [76Br]BrNH4 and peracetic acid. Preliminary pharmacological characterizations were determined by biodistribution, autoradiography, competition, displacement and metabolite studies in rats. The (-,-)-configuration presented important specific uptakes in brain muscarinic cholinergic receptor (mAChR)-rich structures and in heart, low metabolization rates and an apparent M2 selectivity. The (-,+)-configuration revealed more rapid clearance, lower uptake, a higher metabolization rate and an apparent M1 selectivity. Reversibility of the binding was confirmed for the three radiotracers. Positron emission tomography in the living baboon brain revealed high and rapid uptake in the brain and accumulation in the mAChR-rich structures studied. At 30 min p.i., theE(-,-)-radiotracer reached a plateau in cortex, pons and thalamus with concentrations of 29%, 24% and 19% ID/l, respectively.Z(-,-)-[76Br]BrQNP also accumulated in these structures, reaching a maximal uptake (27% ID/l) in the cortex 2 h p.i. At 5 min p.i. a plateau (17% ID/l) was only observed in the cortex for theE(-,+)-[76Br]BrQNP; by contrast, the other structures showed slow washout. After 3 weeks, the (-,-)-radiotracers were studied in the same baboon pretreated with dexetimide (1 mg/kg), a well-known muscarinic antagonist. In all the mAChR structures, the highly reduced uptake observed after this preloading step indicates that these radiotracers specifically bind to muscarinic receptors.Z(-,-)-[76Br]BrQNP, which is displaced in higher amounts from M2 mAChR-enriched structures, reveals an M2 affinity. The two isomers having the (-,-)-configuration are potential probes for investigating central muscarinic receptors. The absolute configuration on the acetate chiral centre influences their muscarinic subtype selectivity and thecis-trans isomerism of the vinyl moiety affects their specific fixation. 相似文献
96.
Marina Quartu Maria Pina Serra Annalisa Manca Paolo Follesa Rossano Ambu Marina Del Fiacco 《International journal of developmental neuroscience》2003,21(6):309-320
The immunohistochemical occurrence of the high affinity neurotrophin (NT) receptors trkA, trkB, and trkC is shown in the pre-term newborn, infant, and adult human post-mortem cerebellum. Immunoreactive neuronal perikarya and processes were observed in all specimens examined, where they appeared unevenly distributed in the cerebellar cortical layers and deep nuclei, and showed regional differences among cerebellar lobules and folia. The trk receptor-antibodies, tested by Western blot on human cerebellum homogenates, revealed multiple immunoreactive bands for trkA and single bands for trkB and trkC. The results obtained show the tissue localization of the trk receptor-like immunoreactivity in the human cerebellum from prenatal to adult age. The analysis for codistribution of the receptors with the relevant ligand and among the receptors in discrete cortical and deep nuclei tissue fields shows a wide variety of conditions, from a good similarity in terms of type and density of labeled structures, to a lack of correspondence, and suggests the possibility of colocalization of trk receptors with the relevant neurotrophin and among them in the cerebellar cortex. These results sustain the concept that the neurotrophin trophic system participates in the development, differentiation, and maintenance of the human cerebellar connectivity and support the possibility of a multifactorial trophic support for the neurotrophins through target-derived and local mechanisms. 相似文献
97.
E. V. Borisova D. Yu. Rusakov S. K. Sudakov 《Bulletin of experimental biology and medicine》1992,114(3):1328-1332
98.
Summary Insulin binding to trophoblast plasma membranes and the placental glycogen content were measured in twelve healthy women, in eleven well-controlled gestational diabetic women who were treated either with diet alone (n=4) or with insulin (n=7) and in 18 women with well-controlled overt diabetes mellitus (six White B; four White C; eight White D). The competitive binding assay was carried out with 22 concentrations of unlabelled insulin. Binding data were analysed by a non-linear direct model fitting procedure assuming one non-cooperative binding site. Maximum specific binding was unchanged in the total collective of gestational diabetic women, but was decreased by 30% in those treated with diet (6.2±2.2%) and increased by 90% in insulin-treated women (16.4±10.2%) as compared to the control subjects (8.7±2.5%). The diet-treated women had only 40% as many and those treated with insulin had more than twice as many receptors compared to control subjects on a per mg protein basis and if expressed per total placenta. In patients with overt diabetes mellitus maximum specific binding (18.5±10.6 %) was higher (p<0.05) due to more receptors compared to control subjects but was similar to the insulin-treated gestational diabetic patients. Maximum specific binding and receptor concentrations did not correlate linearly with maternal plasma insulin levels. Receptor affinities were virtually similar in all groups (1.8·109 l/mol). The placental glycogen content was reduced (p<0.05) to about 80% of that of control subjects in the diet-treated collective, whereas it was unchanged compared to control subjects in the insulin-treated gestational diabetic women despite a 40% increase (p<0.001) of the maternal-to-cord serum glucose ratio. In overt diabetic patients the maternal-to-cord serum glucose ratio and the placental glycogen content were higher (p<0.05) than in the control subjects. We conclude that trophoblast plasma membranes from gestational diabetic women treated with diet alone express less and those from women treated with insulin express more insulin receptors than those from a healthy control group in vitro. These differences could not have been disclosed without consideration of the mode of treatment. Trophoblast plasma membranes from overt diabetic women have more insulin receptors than those from healthy control subjects. 相似文献
99.
Prenatal Stress Increases the Hypothalamo-Pituitary-Adrenal Axis Response in Young and Adult Rats 总被引:11,自引:0,他引:11
Chantal Henry Mohamed Kabbaj Hervé Simon Michel Le Moal Stefania Maccari 《Journal of neuroendocrinology》1994,6(3):341-345
Prenatal stress is considered as an early epigenetic factor able to induce long-lasting alterations in brain structures and functions. It is still unclear whether prenatal stress can induce long-lasting modifications in the hypothalamo-pituitary-adrenal axis. To test this possibility the effects of restraint stress in pregnant rats during the third week of gestation were investigated in the functional properties of the hypothalamo-pituitary-adrenal axis and hippocampal type I and type II corticosteroid receptors in the male offspring at 3, 21 and 90 days of age. Plasma corticosterone was significantly elevated in prenatally-stressed rats at 3 and 21 days after exposure to novelty. At 90 days of age, prenatally-stressed rats showed a longer duration of corticosterone secretion after exposure to novelty. No change was observed for type I and type II receptor densities 3 days after birth, but both receptor subtypes were decreased in the hippocampus of prenatally-stressed offspring at 21 and 90 days of life. These findings suggest that prenatal stress produces long term changes in the hypothalamo-pituitary-adrenal axis in the offspring. 相似文献
100.
F. W. BACH 《Acta anaesthesiologica Scandinavica》1997,41(1):133-140
We have known the endogenous opioid peptide β-endorphin for 20 years. Surprisingly, our knowledge of the physiological role of this peptide and its receptors in modulation of pain perception is still fragmentary. Whereas most studies have tried to elucidate the physiological role of β-endorphin by reversing evoked responses by the opioid antagonist naloxone, this review focuses on quantification of release of β-endorphin in the brain as the approach to define physiological and pathophysiological roles of β-endorphin in relation to nociception. Using a lateral ventricle-cisterna magna perfusion model in the anesthetized rat, it was shown that depolarization of neurons in the arcuate nucleus of the hypothalamus, where β-endorphin is produced, was followed by release of β-endorphin to the cerebrospinal fluid compartment. Intense activation of spinal nociceptive pathways by intrathecal capsaicin injections also led to β-endorphin release. It is concluded that there may still be good reason to quantify β-endorphin in human cerebrospinal fluid to elucidate the role of β-endorphin in pain perception. 相似文献