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61.
产后抑郁症与孤啡肽及单胺类递质的相关性研究   总被引:21,自引:1,他引:20  
目的 探讨孤啡肽 (OFQ)及单胺类递质与产后抑郁症的关系。方法 采用放射免疫法测定 2 5名健康产妇 (对照组 )及 17例产后抑郁症妇女 (抑郁组 )静脉血中孤啡肽及单胺类递质含量。结果 ①抑郁组及对照组血孤啡肽含量分别为 (2 7 39± 6 0 4 )ng/L及 (10 37± 3 6 5 )ng/L ,与对照组相比 ,抑郁组孤啡肽含量显著升高 (P <0 0 1) ;抑郁组及对照组血 5 羟色胺 (5 HT)含量分别为 (0 93± 0 2 1) μmol/L及 (1 4 3± 0 36 ) μmol/L ,二者间有显著差异 (P <0 0 5 ) ;抑郁组血多巴胺 (DA)含量为 (2 15± 0 4 1) μmol/L ,显著低于对照组 (P <0 0 5 )。②抑郁组孤啡肽与5 HT及DA含量呈显著负相关 (r为 0 6 0 1及 0 5 93,P <0 0 5 )。③抑郁组爱丁保产后抑郁量表总分 (EPDS)与OFQ含量呈显著正相关 (r为 0 5 12 ,P <0 0 5 ) ,与 5 HT、DA含量呈显著负相关 (r分别为 - 0 5 71及 - 0 5 2 6 ,P <0 0 5 )。结论 孤啡肽与产后抑郁症的发生发展密切相关。  相似文献   
62.
孤啡肽对内吗啡肽-1抗伤害感受作用的影响   总被引:1,自引:0,他引:1  
目的:观察孤啡肽对内吗啡肽-1在痛觉控制方面的影响。方法:采用侧脑室、鞘内同时注射孤啡肽和内吗啡肽-1,运用热辐射甩尾和醋酸扭体测痛,观察孤啡肽对内吗啡肽-1抗伤害感受效应的影响。结果:侧脑室注射孤啡肽可拮抗内吗啡肽-1的抗伤害感受效应,而鞘内注射孤啡肽可增强内吗啡肽-1的抗伤害感受效应。结论:孤啡肽在脊髓上和脊髓水平均可影响内阿片肽的抗伤害感受效应,但作用机制可能不同。  相似文献   
63.
子宫内膜异位不孕患者血孤啡肽及泌乳素水平的相关研究   总被引:3,自引:1,他引:2  
目的探讨子宫内膜异位症(内异症)不孕患者血孤啡肽及泌乳素水平的变化及意义。方法采用放射免疫法测定29例内异症不孕妇女(不孕组)、32例内异症妊娠妇女(妊娠组),23例单纯输卵管阻塞不孕妇女(对照组)及30例健康妇女(正常组)血孤啡肽及泌乳素的含量。结果(1)不孕组妇女血孤啡肽及泌乳素的含量分别为(28.44±6.55)ng.L-1和(42.33±9.92)μg.L-1,妊娠组妇女血孤啡肽及泌乳素的含量分别为(18.26±5.13)ng.L-1和(29.32±8.51)μg.L-1,对照组分别为(10.18±3.64)ng.L-1和(18.05±4.77)μg.L-1,正常组分别为(11.35±3.71)ng.L-1和(16.14±4.46)μg.L-1。(2)内异症不孕组及妊娠组妇女血孤啡肽水平显著高于对照组及正常组(P<0.01及P<0.05),且不孕组与妊娠组间差异也有显著性(P<0.05)。(3)不孕组及妊娠组妇女血泌乳素含量高于对照组及正常组(P<0.01及P<0.05),且不孕组水平显著也高于妊娠组(P<0.05)。(4)内异症不孕组血孤啡肽及泌乳素水平显著正相关(P<0.01)。结论孤啡肽及泌乳素与子宫内膜异位不孕的发生、发展密切相关。  相似文献   
64.
目的进一步阐明孤啡吠在痛觉调制中的作用。方法;本实验在大鼠电刺激甩尾测痛模型上.观察了侧脑室(icu)及路内(it)注射孤啡肽对芬太尼镇痛效应的影响。结果:icu及it注射孤啡吠后可减弱芬太尼镇痛效应。结论:孤啡肽的致痛敏作用可能与其对抗由μ受体介导的痛抑制效应有关。  相似文献   
65.
Effects of orphanin FQ on endomorphin-1 induced analgesia   总被引:4,自引:0,他引:4  
Orphanin FQ (also known as nociceptin) is a 17-amino-acid peptide which acts as a potent endogenous agonist of the orphan opioid receptor-like (ORL1) receptor. Endomorphin-1, a 4-amino-acid peptide discovered recently, is a potent and selective endogenous agonist for the mu-opiate receptor. In the present study, the effect of OFQ or/and endomorphin-1 on the response to noxious thermal stimuli was observed using the tail-flick test in rats. Intracerebroventricular (i.c.v.) administration of OFQ (1, 5 microg) could shorten tail-flick latency; In contrast, intrathecal (i.t.) administration of OFQ (1, 2 or 10 microg) could increase the latency; i.c.v. (1, 2, 5 microg) or i.t. (0.2, 2, 5 microg) administration of endomorphin-1 dose-dependently increased the latency, indicating an analgesic effect. Furthermore, OFQ (0.1-5 microg) when intraventricularly injected together with endomorphin-1 (5 microg), could dose-dependently reverse the analgesia induced by the latter. On the contrary, OFQ (1 microg) intrathecally injected together with endomorphin-1 (0.2 microg) could further increase the tail-flick latency. The results showed that OFQ at the supraspinal level produces hyperalgesia and is antagonistic to endomorphin-1, while at the spinal level it produces analgesia and is synergic with endomorphin-1. Different interaction mechanism between OFQ and endomorphin-1 in the brain and the spinal cord is thus suggested.  相似文献   
66.
67.
Nociceptin/orphanin FQ (N/OFQ), the endogenous ligand of the NOP opioid receptor (previously referred to as ORL1 or OP4 receptor), exerts a variety of behavioral effects. N/OFQ as well as the synthetic NOP receptor agonist Ro 64-6198 have been reported to possess antistress properties and to elicit a pronounced hyperphagic effect in freely feeding rats. These findings have raised our interest to investigate possible interactions in the control of ingestive behavior between N/OFQ and corticotropin-releasing factor (CRF), which is well known to be a major mediator of stress and to possess anorectic properties. These studies have shown that intracerebroventricular injections of N/OFQ or of Ro 64-6198 reverse the anorectic action evoked by intracerebroventricular administration of CRF. The anti-anorectic effect of N/OFQ or Ro 64-6198 is antagonized by the selective NOP receptor antagonist [Nphe1]N/OFQ1-13NH2, providing evidence that it is mediated by this receptor. The effect occurs at doses that are not hyperphagic per se and is clearly selective versus the anorectic action of CRF since N/OFQ or Ro 64-6198 do not influence the anorectic effect of Escherichia coli lipopolysaccharide (LPS). Neither N/OFQ nor Ro 64-6198 shows affinity for CRF receptors, suggesting that NOP receptor agonists might act as functional antagonists of CRF with regard to its anorectic action. Microinjection studies have revealed that the bed nucleus of the stria terminalis (BNST) is highly sensitive to the anorectic action of CRF, as well as to the anti-anorectic action of N/OFQ; pretreatment with 0.025-0.25 microg/site of N/OFQ into the BNST blocked the anorectic action of 0.1 microg/site of CRF given in the same area. On the other hand, intra-BNST microinjection of 0.025-0.25 microg/site of N/OFQ did not modify basal food intake. Thus, the BNST may be the site where the functional antagonism between N/OFQ and CRF takes place. These findings raise interest for the N/OFQ-NOP receptor system as a pharmacological target to block the anorectic effect of CRF. In comparison to CRF receptor antagonists, NOP receptor agonists may have the advantage of not inhibiting the hypothalamic-pituitary-adrenal (HPA) axis.  相似文献   
68.
Rationale: Central injections of nociceptin (NC) stimulate feeding in rats. Objective: The present study evaluated the effect of N-terminal partial sequences or analogues of NC on food intake in male Wistar rats, to characterize pharmacologically the NC receptor mediating the hyperphagic effect. Methods: NC and related peptides were injected into the lateral (LV) or third (3V) cerebroventricle in freely feeding rats. Results: In the LV, NC stimulated feeding. The N-terminal fragment NC(1–13)NH2 proved to be the least active sequence with hyperphagic activity; NC(1–12)NH2 and NC(1–9)NH2 were inactive. [Phe1ψ(CH2-NH)Gly2]NC(1–13)NH2 ([F/G)]NC(1–13)NH2), an analogue of NC(1–13)NH2, markedly stimulated feeding and, coadministered in the LV with NC, never reduced the hyperphagic effect of the natural sequence. These findings suggest that [F/G)]NC(1–13)NH2, which has been reported to act as a NC receptor antagonist in peripheral tissues, be- haves as a full agonist at the central NC receptors controlling feeding. The hyperphagic potencies of NC and [F/G)]NC(1–13)NH2 were much higher following injection into the 3V than in the LV. Another analogue of NC(1–13)NH2, namely [Nphe1]NC(1–13)NH2, injected into the 3V did not stimulate feeding, but reduced the effect of NC. [Nphe1]NC(1–13)NH2 at a dose of 16.8 nmol/rat significantly reduced, and at 168 nmol/rat almost completely abolished the effect of NC (1.68 nmol/rat). The latter dose of [Nphe1]NC(1–13)NH2 significantly reduced also feeding induced by food deprivation, but did not modify the hyperphagic effect of neuropeptide Y (0.3 nmol/rat). Conclusions: The present results confirm the orexigenic effect of NC in freely feeding rats and indicate that [Nphe1]NC(1–13)NH2 may represent a selective NC receptor antagonist to study the physiological and pathophysiological role of NC in feeding behaviour. Received: 18 July 1999 / Final version: 30 September 1999  相似文献   
69.
We characterized nociceptive discharges induced by mechanical stimulation and the modulating effects of orphanin FQ on noxious responses in the rat brain stem gigantocellular reticular nucleus (Gi). A pressure pulse of constant force and rising rate was delivered by a mechanical stimulator with feedback control, allowing responses to be analyzed statistically. A pressure pulse of 300 g, which evoked C-fiber mediated nerve responses, was delivered to the tail. Two excitatory (45/58) and one inhibitory (13/58) types of extracellular unit discharges were recorded in Gi. One of the excitatory types was a phasic discharge (13/45) elicited at the onset and/or the end of stimulation. Latencies of the phasic discharges (0.104±0.1 s) were shorter than those of other type (tonic) discharges (0.43±0.2 s). The tonic discharges (32/45), which frequently persisted past the end of stimulation without adaptation, were classified into two groups. The first group of tonic type units (23/45) was high threshold, like nociceptive specific neurons in the primary sensory cortex, while the second group of neurons (9/45) responded to a wide range of stimulus intensities. The mean frequency, response duration and spike numbers gradually increased with stimulus intensity change in all nine neurons. The neurons encode mechanical stimulus intensity with discharge frequency, response duration and evoked spike numbers. Local injection of orphanin FQ (200 ng/2 μl) changed high threshold tonic type spike numbers in a biphasic manner, i.e., there was an early phase suppression (5–30 min, p=0.016) and a late phase enhancement (30–60 min, p=0.027). In contrast, phasic type discharges did not show an altered discharge pattern in response to orphanin FQ. Thus, orphanin FQ affects small fiber-mediated nociceptive responses and may behave as a complex modulator of pain systems in the brain stem. Electronic Publication  相似文献   
70.
Spontaneous transient outward currents have been found in peripheral neurons and smooth muscle cells, but rarely in central neurons. Using a nystatin-perforated patch clamp technique, we succeeded in recording spontaneous transient outward currents in mouse dentate gyrus granule cells. Nociceptin/orphanin FQ increased the amplitude and frequency of transient outward currents. We consider modulation of spontaneous transient outward currents to be a new means to regulate cell activity in central neurons, and studied their characteristics and mechanism of augmentation. The whole-cell current-voltage relationship showed outward rectification and the reversal potential was close to the equilibrium potential for K+. The frequency of spontaneous transient outward currents increased at depolarized potentials. Tetraethylammonium, iberiotoxin and a Ca2+ chelator BAPTA-AM inhibited spontaneous transient outward currents. These results suggest the involvement of large-conductance Ca2+-activated K+ channels. Single-channel recordings in the inside-out configuration revealed Ca2+-activated K+ channels with a conductance ranging from 82 to 352 pS. The augmenting effect of nociceptin/orphanin FQ was cancelled by [Phe1psi(CH2-NH)Gly2]Nociceptin(1-13)NH2. Cd2+ did not affect the transient outward currents or augmentation by nociceptin/orphanin FQ. Whereas nociceptin/orphanin FQ, theophylline and cyclic ADP ribose induced transient outward currents with short duration observed under control conditions, inositol 1,4,5-trisphosphate induced transient outward currents with long duration, in addition to those with short duration. Ryanodine inhibited nociceptin/orphanin FQ from augmenting spontaneous transient outward currents. Our data suggest that Ca2+ sparks transiently activate large-conductance Ca2+-activated K+ channels to induce transient outward currents. Nociceptin/orphanin FQ probably sensitizes ryanodine receptors and increases transient outward currents to reduce cell excitability.  相似文献   
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