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121.
采用放射免疫分析技术测定了强啡肽A(DynA)对烫伤大鼠淋巴细胞内cAMP和cGMP含量的影响,并观察了其与免疫功能的关系,旨在探讨DynA调节烫伤大鼠免疫功能的机制。结果表明,烫伤大鼠脾淋巴细胞转化与白细胞介素2(IL-2)的生成明显降低,脾淋巴细胞内cAMP的含量明显升高,而cGMP的含量无明显变化。烫伤大鼠血清可抑制正常大鼠淋巴细胞转化功能和IL-2的生成,并使淋巴细胞内cAMP含量升高。DynA可增强烫伤大鼠淋巴细胞转化和IL-2的生成,降低细胞内cAMP含量,钠洛酮可翻转DynA的这种作用。DynA还可改善烫伤大鼠血清对淋巴细胞转化功能的抑制作用,降低烫伤大鼠血清引起的淋巴细胞内cAMP含量升高。提示DynA可增强烫伤大鼠的免疫功能,且这种作用与淋巴细胞内第二信使cAMP改变有关。 相似文献
122.
123.
Effects of melanocortin receptor ligands on ethanol intake and opioid peptide levels in alcohol-preferring AA rats 总被引:1,自引:0,他引:1
Ploj K Roman E Kask A Hyytiä P Schiöth HB Wikberg JE Nylander I 《Brain research bulletin》2002,59(2):97-104
Melanocortin (MC) peptides are suggested to play a role in opiate dependence, where they antagonise the addictive properties of opiates. To further study the involvement of the MCs in drug dependence, we analysed the effects of the MC(4)-receptor antagonist HS014 (1 nmol/rat), and the non-selective MC-receptor agonist MTII (1 nmol/rat), using i.c.v. administration, on ethanol intake in alcohol-preferring AA rats. The rats had access to ethanol during 40 days, resulting in a mean ethanol intake of 6.6 g/kg/day, before treatment. One group received only artificial cerebrospinal fluid solution. MTII caused a reduction in ethanol intake and ethanol preference, whereas HS014 was without effect. No effect on water intake was observed. A decrease in food intake was detected after MTII, whereas HS014 induced an increase in food intake. Analysis of dynorphin B and Met-enkephalin-Arg(6)Phe(7) immunoreactive levels revealed that MTII and HS014 altered opioid peptide levels in several brain areas and the pituitary gland of the rats with an established ethanol intake. This is the first report showing that manipulation of the MC-receptor system changes ethanol intake in chronically ethanol-drinking AA rats. In addition, manipulation of the MC system modulates ethanol-induced changes in opioid peptide levels. 相似文献
124.
Non-selective opioid receptor antagonists are increasingly used in the treatment of alcohol dependence. The clinical effects are significant but the effect size is rather small and unpleasant side effects may limit the benefits of the compounds. Ligands acting at μ- and/or δ- receptors can alter the voluntary intake of ethanol in various animal models. Therefore, the attenuating effects of selective opioid receptor ligands on ethanol intake may be of clinical interest in the treatment of alcoholism. The objective of this study was to examine the effects of a selective κ-receptor agonist, U50,488H on voluntary ethanol intake in the rat. We used a restricted access model with a free choice between an ethanol solution (10% v/v) and water. During the 3-days baseline period, the rats received a daily saline injection (1 ml/kg, i.p.) 15 min before the 2 h access to ethanol. The animals had free access to water at all times. The control group received a daily saline injection during the 4-days treatment-period, whereas the treatment groups received a daily dose of U50,488H (2.5, 5.0 or 10 mg/kg per day). Animals treated with U50,488H dose-dependently decreased their ethanol intake. The effect of the highest dose of U50,488H was reduced by pre-treatment with the selective κ-antagonist nor-binaltorphimine (nor-BNI). These results demonstrate that activation of κ-opioid receptors can attenuate voluntary ethanol intake in the rat, and the data suggest that the brain dynorphin/κ-receptor systems may represent a novel target for pharmacotherapy in the treatment of alcohol dependence. 相似文献
125.
Dynorphin-(1-17) (dynorphin A) significantly reduced the linear locomotion, rearing and grooming behaviors in mice using a newly devised multi-dimensional behavioral analyser. The behaviors inhibited by dynorphin A were dose-dependently antagonized by prior treatment with naloxone. The results suggest that dynorphin A-induced behavioral depression is mediated via opioid receptors in the mouse brain. 相似文献
126.
用放射免疫分析检测胃角部癌组织阿片肽含量,结果表明亮—脑啡肽含量在癌中心和边缘处明显升高,以前者为甚,癌周3cm处则与对照相近;强啡肽A_(1—13)和β—内啡肽含量以癌中心处降低最为显著,边缘处次之,癌周3cm处接近正常;但是胃癌组血浆阿片肽含量与对照组无显著差异.揭示胃癌发生发展可能与阿片肽含量变化有关. 相似文献
127.
Dynorphin is a potent opioid peptide. Using a highly sensitive radioimmunoassay we have measured the levels of immunoreactive (ir) dynorphin in the cortex, hypothalamus, anterior and posterior pituitary in hyperthyroid and hypothyroid rats. Ir dynorphin levels were increased in the cortex of hypothyroid animals and decreased in the hypothalamus of hyperthyroid rats. 相似文献
128.
We have performed a longitudinal study of the content of the putative neurotransmitter substances, enkephalin, dynorphin, and acetylcholine (ACh), in the cochlea of the Fischer 344 rat. It is the first study of transmitters in the rat cochlea over an extended time span. This study also provides biochemical verification of the presence of ACh in cochlear tissues. No change was seen in the cochlear content of these transmitter candidates up to 24 months of age. 相似文献
129.
Neurotransmitter receptors that control the release of opioid peptides in the spinal cord may play an important role in pain modulation. Norepinephrine, released by a descending pathway originating in the brainstem, is a powerful inducer of analgesia in the spinal cord. Adrenergic α2C receptors are present in opioid-containing terminals in the dorsal horn, where they could modulate opioid release. The goal of this study was to investigate this possibility. Opioid release was evoked from rat spinal cord slices by incubating them with the sodium channel opener veratridine in the presence of peptidase inhibitors (actinonin, captopril and thiorphan), and was measured in situ through the internalization of μ-opioid receptors in dorsal horn neurons. Veratridine produced internalization in 70% of these neurons. The α2 receptor agonists clonidine, guanfacine, medetomidine and UK-14304 inhibited the evoked μ-opioid receptor internalization with IC50s of 1.7 μM, 248 nM, 0.3 nM and 22 nM, respectively. However, inhibition by medetomidine was only partial, and inhibition by UK-14304 reversed itself at concentrations higher than 50 nM. None of these agonists inhibited μ-opioid receptor internalization produced by endomorphin-2, showing that they inhibited opioid release and not the internalization itself. The inhibitions produced by clonidine, guanfacine or UK-14304 were completely reversed by the selective α2C antagonist JP-1203. In contrast, inhibition by guanfacine was not prevented by the α2A antagonist BRL-44408. These results show that α2C receptors inhibit the release of opioids in the dorsal horn. This action may serve to shut down the opioid system when the adrenergic system is active. 相似文献
130.
RATIONALE: Endocannabinoid, opioid, and dopamine systems interact to exhibit cannabinoid receptor neuromodulation of opioid peptides and D(4) dopamine receptor gene expression in CB(1)-cannabinoid-deficient mouse striatum. OBJECTIVE: Using CB(1)-transgenic mice, we examine primary age-sex influences and interactions on opioid and dopamine system members' gene expression in striatum. MATERIALS AND METHODS: Real-time quantitative polymerase chain reaction was used to analyze gene expression of opioid peptides [preproenkephalin (PPENK); preprodynorphin (PPDYN)], opioid receptors [delta-opioid receptor (delta-OR); mu-opioid receptor (micro-OR)] and dopamine receptor subtypes (D(1) through D(5)) in male/female CB(1)(+/+)/CB(1)(-/-) mice striata at two adult ages [young (60-90 days); old (140-300 days)]. RESULTS: (1) Increased PPENK and PPDYN, owing to genotype [CB(1)(+/+) vs. CB(1)(-/-)], depended on sex. When genotype-independent, they depended on sex (PPENK) or age (PPDYN). (2) delta-OR was age-dependent (higher in old). (3) micro-OR, owing to genotype, was age-dependent [higher in old CB(1)(-/-) males]. When genotype-independent, it depended on sex (higher in females). (4) Female D(1) was genotype-independent and age-dependent, while male D(1) was higher in old over young CB(1)(+/+) mice. (5) D(5), owing to genotype, was sex-dependent [higher in young female CB(1)(-/-) mice]. (6) D(2), genotype-independent, was higher in old over young male mice. (7) Young female D(3) was higher in CB(1)(-/-) over CB(1)(+/+) mice. Male D(3) was age-dependent (higher in old mice). (8) D(4), owing to genotype, was sex-dependent [higher in CB(1)(-/-) over CB(1)(+/+) females]. Genotype-independent D(4) was sex-dependent in young mice (higher in females) and age-dependent in males (higher in old). CONCLUSIONS: Greater striatal expression is genotype-dependent in females (opioid-peptides, D(3), D(4), D(5)) and genotype-independent in both females (PPENK, mu-OR, D(4)) and old males (PPDYN, delta-OR, D(2), D(3), D(4)). 相似文献