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71.
目的 评价一种新型寰枢椎内固定系统的生物力学性能.方法 选取12头猪颈椎标本制作寰枢椎不稳模型,采用该新型内固定系统进行固定,测量三维运动范围,并与寰枢椎椎弓根钉棒系统进行比较.结果 新型寰枢椎内固定系统的特点是设计新颖、操作简单、使用安全;生物力学实验结果表明其在旋转、屈伸及侧弯状态的活动度与寰枢椎椎弓根钉棒差异无统...  相似文献   
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BACKGROUND: This study was designed to confirm our previous findings that nonalcoholic offspring from families with alcohol-dependent individuals have greater hypothalamic-pituitary-adrenal axis activation induced by opioid blockade compared with nonalcoholic subjects without a family history of alcohol dependence. METHODS: Sixty-four nonalcoholic subjects aged 18 to 25 years were enrolled in the protocol. Twenty-seven subjects were offspring from families with alcohol dependence and were designated as family history-positive subjects (FHP). Thirty-seven subjects were biological offspring of non-alcohol-dependent parents and were designated as family history-negative subjects (FHN). Subjects received naloxone hydrochloride (0, 50, 125, 375, and 500 microg/kg) in double-blind, randomized order; adrenocorticotropin (ACTH) and cortisol were monitored over 120 min. RESULTS: No hormone differences at baseline or during placebo administration were identified between FHP and FHN subjects. FHP subjects had greater ACTH and cortisol response to opioid receptor blockade induced by naloxone hydrochloride compared with FHN subjects. CONCLUSIONS: These observations confirm previous findings that differences in ACTH and cortisol dynamics between FHP and FHN subjects can be unmasked by opioid receptor blockade.  相似文献   
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BACKGROUND: Prenatal ethanol exposure alters the development of the hypothalamic-pituitary-adrenal (HPA) axis, resulting in HPA hyper-responsiveness to stressors in adulthood. Prenatal ethanol exposure also alters the development and activity of the serotoninergic (5-HT) system. We have previously shown that 5-HT(1A) and 5-HT(2A/C) receptor-mediated behavioral and physiological function are altered in fetal ethanol-exposed offspring. As there are extensive interactions between the HPA axis and the 5-HT system, the present study tested the hypothesis that prenatal ethanol exposure would alter 5-HT(1A) and 5-HT(2A/C) receptor-mediated HPA function. METHODS: The 5-HT(1A) agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.2 mg/kg), and the 5-HT(2A/C) agonist, (+)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI; 0.3 mg/kg), or vehicle (1 mL/kg) were administered to adult female and male offspring from prenatal ethanol-exposed (E), pair-fed control (PF), and ad libitum-fed control (C) dams. The plasma concentration of adrenocorticotropin (ACTH) and corticosterone (CORT) were determined at 0, 15, 30, 60, and 120 minutes postinjection. In addition, corticotropin releasing hormone (CRH) mRNA expression in the paraventricular nucleus of the hypothalamus, and 5-HT(1A) and 5-HT(2A/C) receptor mRNA expression in the hippocampus and prefrontal cortex, respectively, were determined by in situ hybridization. RESULTS: Ethanol-exposed females showed a blunted ACTH response to 8-OH-DPAT at 15 and 30 minutes, and conversely, an increased ACTH response to DOI at all time points postinjection, compared with PF and C females. Differences among E, PF, and C males failed to reach significance. Centrally, however, DOI resulted in a trend toward lower CRH mRNA levels in E and PF compared with C females, but higher CRH mRNA levels in E compared with control males. There were no differences among prenatal groups in 5-HT(2A) receptor expression in the prefrontal cortex following either 8-OH-DPAT or DOI treatment. However, following 8-OH-DPAT, hippocampal 5-HT(1A) receptor expression was higher in E than in PF females in CA1, with a trend toward higher expression in E than in C females in CA2, whereas following DOI, a prenatal group by subfield interaction suggests lower 5-HT(1A) mRNA levels in E and PF compared with C females in CA1 and the dentate gyrus. CONCLUSIONS: These data are the first to demonstrate that prenatal ethanol exposure has differential long-term effects on 5-HT(1A)-mediated and 5-HT(2A)-mediated neuroendocrine function in females and males, and suggest a sex-specific ethanol-induced alteration in the interaction between the HPA axis and the serotonin system.  相似文献   
77.
目的探讨寰枢椎(C1、C2)不稳或脱位对椎动脉血流动力学的影响。方法对37例经手术证实为寰枢椎不稳或脱位患者(病例组)及30例正常人(对照组),应用彩色多普勒超声观察椎动脉的管腔、结构走行及血流动力学情况,分别测量C1、C2间和C5、C6间椎动脉血流速度、阻力指数(RI),并对同侧椎动脉两处的检查结果进行对比分析。结果病例组中30例患者C1、C2间椎动脉血流速度、RI较C5、C6增加[分别为(67.3±22.8)cm/s对(47.4±20.5)cm/s,P<0.01;0.76±0.08对0.62±0.11,P<0.05],5例患者减低,2例患者无变化。椎动脉血流变化者中25例表现为一侧椎动脉,10例表现为双侧椎动脉。对照组双侧椎动脉C1、C2间血流速度、RI与C5、C6间差异无统计学意义。结论寰枢椎不稳或脱位导致椎基底动脉供血不足,表现为单侧椎动脉。病变处血流速度和RI增高是该类患者椎动脉彩色多普勒超声特征性改变,对诊断具有重要价值。  相似文献   
78.
Objective: As the initiation and acceleration of alcohol use commonly occurs during adolescence, the etiological basis for this phenomenon is of critical importance. Using the diathesis‐stress model as a framework, this review will evaluate the emerging evidence implicating the limbic–hypothalamic–pituitary–adrenal (LHPA) axis in the development of alcohol use disorder (AUD). Method: Searches were conducted of the PubMed/Medline, PsycInfo, PsycBooks, Cochrane and ISI Web of Science databases, using a specified set of search terms. Results: Genetic liabilities, antenatal stress/anxiety or exposure to addictive substances, exposure to maltreatment or other traumatic events in childhood and psychiatric illness in childhood/adolescence can all increase the risk, or diathesis, for AUD. Greater LHPA dysfunction may serve as a marker for higher diathesis levels in youth. When exposed to stressors in adolescence, high‐risk youth (or those with greater LHPA dysfunction) may use alcohol and/or other substances to cope with stressors and, in turn, become more vulnerable to AUD. Conclusion: Evidence suggests that LHPA dysfunction and stress play an important role in the development of AUD. Genetic liabilities, antenatal insults, maltreatment, and psychiatric illness appear to increase LHPA dysfunction, raising risk for AUD. Further research is needed to clarify the complex interplay among adverse developmental experiences, LHPA dysfunction, and the development of AUD in adolescents.  相似文献   
79.
Background: Fetal Alcohol Spectrum Disorder (FASD) is associated with numerous neurobehavioral alterations, as well as disabilities in a number of domains, including a high incidence of depression and anxiety disorders. Prenatal alcohol exposure (PAE) also alters hypothalamic‐pituitary‐adrenal (HPA) function, resulting in increased responsiveness to stressors and HPA dysregulation in adulthood. Interestingly, data suggest that pre‐existing HPA abnormalities may be a major contributory factor to some forms of depression, particularly when an individual is exposed to stressors later in life. We tested the hypothesis that exposure to stressors in adulthood may unmask an increased vulnerability to depressive‐ and anxiety‐like behaviors in PAE animals. Methods: Male and female offspring from prenatal alcohol (PAE), pair‐fed (PF), and ad libitum‐fed control (C) treatment groups were tested in adulthood. Animals were exposed to 10 consecutive days of chronic mild stress (CMS), and assessed in a battery of well‐validated tasks sensitive to differences in depressive‐ and/or anxiety‐like behaviors. Results: We report here that the combination of PAE and CMS in adulthood increases depressive‐ and anxiety‐like behaviors in a sexually dimorphic manner. PAE males showed impaired hedonic responsivity (sucrose contrast test), locomotor hyperactivity (open field), and alterations in affiliative and nonaffiliative social behaviors (social interaction test) compared to control males. By contrast, PAE and, to a lesser extent, PF, females showed greater levels of “behavioral despair” in the forced swim test, and PAE females showed altered behavior in the final 5 minutes of the social interaction test compared to control females. Conclusions: These data support the possibility that stress may be a mediating or contributing factor in the psychopathologies reported in FASD populations.  相似文献   
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