首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   551篇
  免费   54篇
  国内免费   42篇
  2024年   3篇
  2023年   30篇
  2022年   27篇
  2021年   47篇
  2020年   30篇
  2019年   28篇
  2018年   30篇
  2017年   26篇
  2016年   17篇
  2015年   19篇
  2014年   24篇
  2013年   36篇
  2012年   14篇
  2011年   23篇
  2010年   21篇
  2009年   14篇
  2008年   18篇
  2007年   17篇
  2006年   14篇
  2005年   16篇
  2004年   12篇
  2003年   14篇
  2002年   9篇
  2001年   10篇
  2000年   10篇
  1999年   7篇
  1998年   3篇
  1997年   7篇
  1996年   15篇
  1995年   6篇
  1994年   7篇
  1993年   4篇
  1992年   8篇
  1991年   7篇
  1990年   12篇
  1989年   8篇
  1988年   5篇
  1987年   4篇
  1986年   6篇
  1985年   6篇
  1984年   11篇
  1983年   3篇
  1982年   4篇
  1980年   3篇
  1979年   3篇
  1977年   2篇
  1976年   2篇
  1974年   1篇
  1973年   2篇
  1972年   1篇
排序方式: 共有647条查询结果,搜索用时 62 毫秒
11.
12.
电刺激乌拉坦麻醉的大鼠下丘脑外侧区(LH)可使缰核(Hb)内51.0%的单位兴奋,15.7%的单位抑制,其中发生兴奋反应的单位有15.4%可被逆行激活。双侧Hb内微量注射利多卡因,电刺激LH引起的升压反应可被阻断42.0±28.0%;反之,双侧LH内微量注射利多卡固,电刺激Hb引起的升压反应可被阻断62.0±26.4%。结果表明,LH与Hb在血压调节中相互依赖,具有协同作用。  相似文献   
13.
躯体传入冲动抑制中枢性心肌缺血的脊髓机制   总被引:1,自引:1,他引:0  
朱伟建  张荣宝 《生理学报》1991,43(2):141-148
本工作在58只尿酯-氯醛糖麻醉,三碘季铵酚制动,人工呼吸,切断迷走神经的兔上进行。结果显示:电刺激正中神经(MN)和腓深神经(DPN)均能抑制或部分抑制下丘脑背内侧核(DMH)诱发的缺血性心电 ST 段偏移,以刺激 MN 的抑制作用更为明显。蛛网膜下腔注射(ith)吗啡(40μg)也能抑制这种缺血性心电变化。ith 纳洛酮(20μg)则可阻断刺激 MN 对中枢性心肌缺血的抑制作用。完整兔在刺激左侧 MN 或 DPN 后,用放射免疫技术测得胸 2—5(T_2-5)节段两侧中间外侧柱(IML)中亮氨酸脑啡肽(LENK)含量明显增加。在颈1(C_1)水平横断脊髓,以同样参数刺激左侧 MN,同侧胸髓 IML 中 LENK 含量明显增加,而对侧胸髓 IML 中 LENK 含量无明显改变;刺激一侧 DPN,T_(2-5)的两侧 IML 中 LENK 含量均无明显变化。上述结果表明,刺激 MN 与 DPN 均能抑制 DMH 诱发的中枢性心肌缺血,但以MN 作用较明显。我们推测这种抑制作用可能与通过脊上机制双侧性增加 IML 中 LENK 含量有关,MN 的抑制作用可能尚包括直接激活胸髓内的脑啡肽系统,增加同侧 IML 中 LENK含量,加强了对交感输出活动的抑制作用。  相似文献   
14.
刺激蓝斑对下丘脑弓状核单位放电的影响   总被引:2,自引:0,他引:2  
本研究室以往工作表明,下丘脑弓状核(ARC)和蓝斑(LC)在痛觉调制和针刺镇痛中具有重要作用。本实验观察刺激 LC 对清醒制动大鼠 ARC 单位放电的影响。ARC 单位对刺激LC 的反应以抑制为主,在38个单位中有23个单位呈现抑制反应。ARC 单位对外周伤害性刺激的反应以兴奋为主,在27个单位中有20个单位呈现兴奋反应。刺激 LC 可以使 ARC 单位的伤害性反应的持续时间明显缩短。α_2受体激动剂(氯压啶)和α_1受体阻断剂(酚苄明)能加快ARC 单位的平均放电频率,而β-受体激动剂(异丙基肾上腺素)和β受体阻断剂(心得安)则无明显影响。这些结果提示 LC 的去甲肾上腺素能神经元对 ARC 神经元的作用是通过α受体实现的。  相似文献   
15.
Summary The afferent pathways to the nucleus basalis prosencephali of the pigeon were studied by use of the horseradish peroxidase (HRP) technique. It was confirmed that this nucleus receives a direct pathway from the nucleus sensorius principalis nervi trigemini and that, as in the starling, it receives a direct input from the nucleus lemnisci lateralis, pars ventralis, an auditory relay. Totally novel is the finding that the nucleus basalis prosencephali is the target of a direct pathway originating in the medullary nucleus vestibularis superior. All three pathways bypass the thalamus. From within the telencephalon the nucleus basalis prosencephali also receives fibres from the tuberculum olfactorium and the peri-ectostriatal belt, suggestive of olfactory and visual input. Marked cell bodies were also found in the neostriatum frontolaterale. It is assumed that these arose from HRP uptake by axons of the tractus fronto-archistriatalis that course through the nucleus basalis prosencephali to the anterodorsal archistriatum. Marked fibres and bouton-like formations were observed in the latter structure. The afferents to the nucleus basalis prosencephali are discussed in conjunction with the probable role of the nucleus as a sensorimotor coordinator of the pecking/feeding behaviour of the pigeon.  相似文献   
16.
17.
As an alternative to dichotomous keys, tabular keys are used for taxonomic identification. With the use of computers, keys based on the Bayes formula can also be made available more widely. For the development of a key, the maximum a posterior probability (MAP) for a taxon is important because it allows to evaluate the quality of a key. If it is low, the taxon is hard to distinguish from other taxa. In this paper, we show that finding MAP in a Bayesian key is NP-hard. Estimates for MAP or other measures have to be used for the estimation of the quality of a Bayesian key.  相似文献   
18.
本工作采用离体孵育技术,观察大鼠下丘脑薄片(含有室旁核和视上核)释放精氨酸加压素(AVP)和糖皮质激素(GC)及其他甾体激素对AVP释放的快速影响。结果如下:(1)大鼠下丘脑薄片经过90min的恢复之后,在长达6h的孵育过程中能够相当稳定地释放AVP,释放量为9.06±1.23pg/min;(2)皮质酮(B)在20min内可明显地抑制AVP的释放,在10-7—10-4mol/L范围内呈剂量-效应关系;(3)在同一剂量(10-6mol/L),皮质醇、17β-雌二醇和睾丸酮也可快速地抑制AVP的释放,而相同剂量的地塞米松、醛固酮、孕酮、RU486和胆固醇却无此效应;(4)RU486(10-7—10-3mol/L)对AVP的释放没有影响,但却能(10-5—10-3mol/L)部分地阻断B的快速抑制效应。这些结果表明,GC对大鼠下丘脑AVP的释放具有不通过传统的基因组机制的快速抑制效应,此种抑制效应可能与GC的负反馈调节作用有关。  相似文献   
19.
Ouabain-blocked toad urinary bladders were maintained in Na+-free mucosal solutions, and a depolarizing solution of high K+ activity containing only 5 mM Na+ on the serosal side. Exposure to mucosal sodium (20 mM activity) evoked a transient amiloride-blockable inward current, which decayed to near zero within one hour. The apical sodium conductance increased in the initial phase of the current decay and decreased in the second phase. The conductance decrease required Ca2+ to be present on the serosal side and was more rapid when the mucosal Na+ activity was higher. At 20 mM mucosal Na+ and 3 mM serosal Ca2+ the initial (maximal) rate of inhibition amounted to 20% in 10 min. The conductance decrease could be accelerated by raising the serosal Ca2+ activity to 10 mM. The inhibition reversed on lowering the serosal Ca2+ to 3 μM and, in addition, the mucosal Na+ to zero. Exposure of the mucosal surface to the ionophore nystatin abolished the Ca2+ sensitivity of the transcellular conductance, showing that the Ca2+-sensitive conductance resides in the apical membrane. The data imply that in the K+-depolarized epithelia, cellular Ca2+, taken up from the serosal medium by means of a Na+-Ca2+ antiport, cause feedback inhibition by blockage of apical Na+ channels. However, the rate of inhibition is small, such that this regulatory mechanism will have little effect at 1 mM serosal Ca2+ and less than 20 mM cellular Na+.  相似文献   
20.
Summary Antisera raised against ACTH (1–39), -endorphin and the 16K proopiocortin were used, in association with the immunoperoxidase reaction, to localize positively-staining cell bodies and nerve fibres in the hypothalamus of the rat. Antigens, cross-reactive against anti-ACTH (1–39) serum were detected in a fibre system in the rostro-dorsal hypothalamus situated between the optic chiasm and the third ventricle while immunoreactive 16K-like material was present in fibres localized in the caudal hypothalamus, dorso-lateral to the arcuate nucleus. This latter system was also associated with the appearance of ACTH (1–39) and ACTH (17–39) immunoreactivity.Cells of the arcuate nucleus stained positively for ACTH (1–39), 16K antigen and -endorphin, and on examining adjacent thin sections it was observed that cells that contained 16K antigen-like material, also gave a positive immunoreaction with ACTH (1–39) and -endorphin antisera. In the magnocellular system, cells of the supraoptic (SON) and paraventricular (PVN) nuclei also gave a positive immunoreaction with anti-ACTH (1–39), 16K antigen and -endorphin serum. As in the case of the arcuate nucleus, common cells stained for these three antigens.On the basis of the precursor theory for the synthesis of ACTH, 16K antigen and -endorphin, it was not unexpected to find these three fragments of pro-opiocortin localized together in cells of the arcuate nucleus. That ACTH (1–39), 16K antigen and -endorphin-like materials are present in the magnocellular neurosecretory system would suggest that cells of the SON and PVN are not only involved in the synthesis of neurophysin and the neurohypophysial hormones, but also of some products of the pro-opiocortin molecule. Whether the biochemical nature of the ACTH and -endorphin in cells of the SON and PVN is identical to that of anterior pituitary origin remains to be established, as does the biosynthetic relationship between neurophysin and oxytocin/ vasopressin and these fragments of pro-opiocortin.Drs. M.M. Wilkes, S.S.C. Yen, G. Pelletier, B.A. Eipper and R. Walter are thanked for supplying some of the antisera and antigens used in this study. Thanks also go to Ciba-Geigy Ltd. and Organon Inc. for supplies of ACTH (17–39) and ACTH (1–24) respectively. This work was financed by The Medical Research Council of New Zealand  相似文献   
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号