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1.
Cebus monkeys of 3 different age groups were trained to perform an automated behavioral task (delayed response), intended to measure recent memory ability. In in initial study, the aged monkeys (18 years and older) exhibit prprogressively greater performance impairments (relative to young monkeys) as they were required to remember the location of a visual stimulus for increasingly longer durations (0 to 20 sec). This deficits replicated previously published results from aged Rhesus monkeys and appeared similar to the primary memory deficits reported in elderly humans and demented patients. In subsequent studies, the effects of three different cholinomimetics were evaluated for their ability to improve the aged monkey's performance on this task. Each monkey was tested under several acute doses of the cholinergic precursor, choline, the anticholinesterase, physostigmine, and the cholinergic muscarinic receptor agonist, arecoline. The results revealed clear differences in the ability of these drugs to improve performance on this task. Choline exerted no apparent effects in the aged monkeys at any dose tested. Physostigmine clearly enhanced performance in certain aged monkeys, but the optimal dose varied dramatically between subjects, replicating previously published results with aged Rhesus monkeys and humans. Arecoline produced clear improvement within a restricted dose range, with little variation in optimal dose between subjects. In addition to demonstrating differences in the effects of different cholinomimetics on memory performance in aged primates, these data also suggest a possible rationale for future investigations. Assuming that each of these drugs primarily affected cholinergic function in the manner conventionally attributed, these data suggest that, within the cholinergic system, the more directly one stimulates the receptor, the more one might expect robust and consistent effects on memory performance in aged subjects. 相似文献
2.
Widespread depletion of forebrain noradrenaline, produced by the intracerebral injection of 4 g of 6-hydroxydopamine into the fibres of the dorsal noradrenergic bundle, potentiated the catalepsy induced by 20 mg/kg of morphine and severely attenuated the catalepsy induced by two separate cholinergic agonists, arecoline and pilocarpine. It did not, however, affect haloperidol catalepsy at any of the four doses tested. These results suggest that cholinergic catalepsy may be critically dependent on an intact noradrenergic substrate, perhaps through cholinergic receptors located either presynaptically on noradrenergic terminals or on the cell bodies of origin in the locus coeruleus. Noradrenaline appears to play a modulatory role in morphine catalepsy, although other sites of action must also be involved. Ascending noradrenergic systems do not appear to influence haloperidol catalepsy. 相似文献
3.
槟榔碱抑制氧化型低密度脂蛋白诱导的小鼠巨噬细胞炎症因子表达及其机制 总被引:3,自引:0,他引:3
目的 观察槟榔碱对氧化型低密度脂蛋白诱导的小鼠巨噬细胞炎症因子表达的影响,并探讨其作用机制.方法不同浓度槟榔碱(10-6、10-5、10-4和10-3moL/L)处理细胞24 h,台盼兰拒染法观察细胞活力;氧化型低密度脂蛋白诱导小鼠巨噬细胞,同时给予槟榔碱处理,采用逆转录聚合酶链反应检测肿瘤坏死因子α、白细胞介素6和细胞间黏附分子1 mRNA的表达以及过氧化体增殖物激活型受体γ mRNA的表达.结果 槟榔碱处理细胞24h后,10-3 mol/L组细胞活力下降(P<0.01),而10-6、10-5和10-4 mol/L组对细胞活力无明显影响;10-6、10-5和10-4 mol/L槟榔碱分别处理细胞24 h后,对肿瘤坏死因子α、白细胞介素6和细胞间黏附分子1 mRNA的表达无明显影响;10-6mol/L槟榔碱与氧化型低密度脂蛋白共同处理细胞24 h后,细胞肿瘤坏死因子α、白细胞介素6和细胞间黏附分子1 mRNA的表达无显著改变,而10-5和10-4mol/L槟榔碱明显抑制氧化型低密度脂蛋白诱导的小鼠巨噬细胞肿瘤坏死因子α、白细胞介素6和细胞间黏附分子1 mRNA的表达,且10-5mol/L槟榔碱使氧化型低密度脂蛋白诱导的细胞内过氧化体增殖物激活型受体γ mRNA的表达增加(P<0.01).结论 槟榔碱抑制氧化型低密度脂蛋白诱导的巨噬细胞炎症因子表达,其作用机理可能是通过过氧化体增殖物激活型受体γ起作用. 相似文献
4.
Areca nut (Areca catechu) is chewed as a medical and psychoactive food by roughly 10% of the world population. Areca nut chewing may lead to low birth weight, premature delivery and impaired muscle development. Our previous study showed that arecoline, a major alkaloid in the areca nut, inhibited the myogenic differentiation of C2C12 myoblastic cells. The clustering of acetylcholine receptors (AChRs) in the postsynaptic membrane at the neuromuscular junction (NMJ) by agrin, a signaling protein released by motor neurons, is critical for the development of functional muscles. Here, we further investigate whether arecoline affects the AChR clustering using cultured C2C12 myotubes. Rhodamine-conjugated α-bungarotoxin was used to detect the presence of AChR clusters. Our results showed that arecoline inhibited the formation of agrin-induced AChR clusters and destabilized agrin-induced or spontaneous AChR cluster formation. In addition, arecoline inhibited the expression of myogenin in C2C12 myotubes. These results shed light on the important role of arecoline on the detrimental effect of areca nut to muscle development. 相似文献
5.
Central cholinergic systems have long been implicated in the modulation of learning and memory processes in animals and man. Drugs that affect the central cholinergic system have been found either to enhance or to hinder performance in tests of learning and memory. Few studies have evaluated the effects of different cholinergic drugs within a single experimental paradigm and with a relatively wide dose range. The studies reported here investigated the effects of cholinergic drugs with diverse modes of action on the retention of a passive avoidance response. Physostigmine, arecoline, oxotremorine, nicotine, and 4-aminopyridine were administered IP immediately following the acquisition of a one-trial passive avoidance task. All of the drugs were found to enhance 72-h retention of passive avoidance; however, the effective doses were different for each of the drugs studied. 相似文献
6.
槟榔灭钉螺增效成分的研究 总被引:2,自引:0,他引:2
对从槟榔(Areca catechu L.的干燥成熟种子)核中分离出的组分进行灭钉螺增效实验,研究表明,最有效成分为槟榔碱(Arecoline,Are.)。它与植物灭钉螺药商陆皂甙或化学灭钉螺药五氨酸钠等联合使用,可显著降低二者的投药量。 相似文献
7.
In two experiments tolerance development to the effects of arecoline on operant responding for a water reward was shown to be dose-dependent, complete tolerance developing to a daily dose of 4 mg/kg, but only partial tolerance developing to a daily dose of 8 mg/kg. However, rats chronically treated with the higher dose of arecoline were least affected by a challenge dose of oxotremorine (0.2 mg/kg); i.e. the high dose group exhibited the greatest cross-tolerance to oxotremorine. Moreover, atropine (4 mg/kg) pretreatment prior to arecoline (4 mg/kg) prevented cross-tolerance to oxotremorine, indicating that dispositional mechanisms are unlikely to be involved in tolerance to arecoline. 相似文献
8.
近年来,对槟榔的研究已不局限其对口腔的危害及对癌症的诱发,而逐渐扩展到其对人体其他主要器官及系统的影响。研究表明,槟榔果的主要成分槟榔碱可对男(雄)性的泌尿生殖系统以及女(雌)性泌尿生殖系统和妊娠造成损伤。对男(雄)性生殖系统,槟榔碱可导致活性氧簇增高并引起氧化应激反应。槟榔碱还可上调肿瘤坏死因子α水平及诱导环氧合酶2(COX-2)高表达,影响免疫系统进而对精子造成损伤。另外,槟榔碱通过多种途径刺激睾丸Leydig细胞分泌合成过量睾酮。对女(雌)性泌尿生殖系统及妊娠,槟榔碱可造成卵细胞损伤。孕妇长期咀嚼槟榔会影响新生儿出生结局,如低出生体质量和婴幼儿死亡。动物胚胎模型研究结果显示,槟榔碱可产生胚胎毒性,影响胚胎发育。对两性泌尿系统,槟榔碱诱导慢性肾病(CKD)的发生并致使膀胱癌进一步恶化。阐述槟榔碱对生殖和泌尿系统的损伤作用可进一步了解此类生物成分的危害,并能及时且有效地建立疾病的预防机制。 相似文献
9.
目的:合成含噻二唑噁二唑双杂环的槟榔碱衍生物,研究目标化合物体外舒张血管活性。方法:将化合物1a~e的吡啶环用碘甲烷季铵化得到相应的季铵盐,用NaBH4还原季铵盐得到目标物3a~e。采用离体血管条法研究目标化合物体外舒张血管活性。结果:合成了5个槟榔碱衍生物,目标化合物的结构经元素分析、IR、1HNMR、MS确证。在10μmol/L浓度下,化合物3a、3b、3c、3d、3e对离体血管舒张率分别为17.06%,27.35%,31.36%,27.32%和21.74%,在相同的条件下.槟榔碱的舒张率为21%。结论:噻二唑噁二唑双杂环可以作为槟榔碱酯基的生物电子等排体。 相似文献
10.
Cyr61 is associated with growth and progression of many types of tumors and is an independent poor prognostic indicator for oral cancer patients. Areca nut (AN) chewing is the most important etiological factor in the pathogenesis of oral cancer in India and many Southeast Asian countries. Yet, the molecular mechanisms involved in the AN-induced oral cancer remain largely unknown. In this study, we show that arecoline, a main alkaloid found in AN, stimulated Cyr61 synthesis in human gingival epithelial S-G cells. Constitutive overexpression of Cyr61 protein in oral epithelial cells during AN chewing may play a role in the pathogenesis of oral cancer. ERK inhibitor PD98059, N-acetyl-L-cysteine, Rho-associated protein kinase (ROCK) selective inhibitor Y-27632 and a geranylgeranyltransferase inhibitor reduced the arecoline-stimulated levels of Cyr61 protein by ~31%, 47%, 65% and 100%, respectively. Lovastatin also completely inhibited arecoline-induced Cyr61 synthesis and the inhibition is dose-dependent. Decreased of geranylgeranylated proteins could be the mechanism that lovastatin regulates Cyr61 synthesis and lovastatin could serve as a useful agent in controlling AN-induced oral cancer. 相似文献