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1.
丁酸对人结肠癌细胞株SW1116增殖及分化状态的影响 总被引:9,自引:0,他引:9
目的:探讨结肠中膳食纤维的酵解产物丁酸对人结肠癌细胞株生长、增殖及分化状态的影响。方法:将传代人结肠癌SW1116细胞株接种于不含及合不同浓度(2、3、4、7、10 mmol/L)丁酸的培养基中。经6、24、48和72h后,用四唑蓝(MTT)法测定细胞增殖率、细胞匀浆中癌胚抗原(CEA)及和碱性磷酸酶(ALP)的表达;同时用电镜观察细胞形态的改变。结果:丁酸对SW1116细胞株的生长抑制作用呈浓度依赖性,在所观察的丁酸浓度及时限内,最高抑制率达53.9%。同时丁酸能大大增加SW1116细胞CEA和ALP的表达;当丁酸浓度≥7mmol/L和培养时间≥48h时,二者增加最为显著(P<0.001)。电镜显示丁酸能使细胞表面微绒毛明显增多。结论:丁酸能抑制SW1116细胞株的生长并诱导其分化。 相似文献
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Węglarz L. Dzierżewicz Z. Orchel A. Szczerba J. Jaworska-Kik M. Wilczok T. 《Scandinavian journal of gastroenterology》2013,48(1):73-79
Background: Although Desulfovibrio desulfuricans species, besides existing in the natural environment, is also found in the human digestive tract, no information is currently available on its role in the intestinal ecosystem and its activity in regard to the intestinal mucosa. Bacterial products (lipopolysaccharides, LPSs) are generally known for their ability to trigger inflammatory response by stimulating cytokine expression, such as interleukin-8 (IL-8). Methods: Colonic Caco-2 cells were exposed to LPSs isolated from the soil type and intestinal wild strains of D. desulfuricans bacteria. The amount of IL-8 secreted was measured by ELISA. The effects of sodium butyrate and cell preincubation with sodium butyrate on the IL-8 secretion in response to LPSs were also analysed. Results: LPSs from D. desulfuricans down-regulated IL-8 secretion by the cells. Incubation of these cells with butyrate alone resulted in a dose-dependent stimulation of IL-8 release. Butyrate also modulated IL-8 secretion by cells stimulated with LPSs. Conclusions: Our findings suggest the lack of inflammatory response of intestinal mucosa in the presence of LPSs of D. desulfuricans. This response can be conditioned by the natural bacterial product, butyrate, which exerts a stimulatory effect on the IL-8 secretion and modulates its release in response to LPSs. 相似文献
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长久以来,膳食纤维被认为可以降低结直肠肿瘤发生风险.膳食纤维做为益生元,被肠内益生菌酵解,可产生多种短链脂肪酸,降低肠内致癌物浓度,加速致癌物的排出,影响胆汁酸代谢.但有少数前瞻性研究结果并不支持该假说,其抗结直肠肿瘤作用的机制尚需要进一步研究. 相似文献
6.
Dietary resistant starch and chronic inflammatory bowel diseases 总被引:5,自引:0,他引:5
Jacobasch G Schmiedl D Kruschewski M Schmehl K 《International journal of colorectal disease》1999,14(4-5):201-211
These studies were performed to test the benefit of resistant starch on ulcerative colitis via prebiotic and butyrate effects.
Butyrate, propionate, and acetate are produced in the colon of mammals as a result of microbial fermentation of resistant
starch and other dietary fibers. Butyrate plays an important role in the colonic mucosal growth and epithelial proliferation.
A reduction in the colonic butyrate level induces chronic mucosal atrophy. Short-chain fatty acid enemas increase mucosal
generation, crypt length, and DNA content of the colonocytes. They also ameliorate symptoms of ulcerative colitis in human
patients and rats injected with trinitrobenzene sulfonic acid (TNBS). Butyrate, and also to a lesser degree propionate, are
substrates for the aerobic energy metabolism, and trophic factors of the colonocytes. Adverse butyrate effects occur in normal
and neoplastic colonic cells. In normal cells, butyrate induces proliferation at the crypt base, while inhibiting proliferation
at the crypt surface. In neoplastic cells, butyrate inhibits DNA synthesis and arrests cell growth in the G1 phase of the
cell cycle. The improvement of the TNBS-induced colonic inflammation occurred earlier in the resistant starch (RS)-fed rats
than in the RS-free group. This benefit coincided with activation of colonic epithelial cell proliferation and the subsequent
restoration of apoptosis. The noncollagenous basement membrane protein laminin was regenerated initially in the RS-fed group,
demonstrating what could be a considered lower damage to the intestinal barrier function. The calculation of intestinal short-chain
fatty acid absorption confirmed this conclusion. The uptake of short-chain fatty acids in the colon is strongly inhibited
in the RS-free group, but only slightly reduced in the animals fed with RS. Additionally, RS enhanced the growth of intestinal
bacteria assumed to promote health. Further studies involving patients suffering from ulcerative colitis are necessary to
determine the importance of RS in the therapy of a number of intestinal diseases and the maintenance of health.
Accepted: 11 August 1999 相似文献
7.
目的:观察0.05%丙酸氟替卡松乳膏治疗湿疹的临床疗效。方法:将我院收治的55例湿疹患者随机分为两组,观察组28例患者采用0.05%丙酸氟替卡松乳膏治疗,对照组27例患者采用0.1%丁酸氢化可的松软膏治疗,比较分析两组的疗效。结果:观察组总有效率为92.9%,对照组为66.7%,两组问有显著性差异(χ2=5.8928,P〈0.05),两组均无明显不良反应发生。结论:0.05%丙酸氟替卡松乳膏治疗湿疹疗效满意,且不良反应少,值得临床关注。 相似文献
8.
Fangyan Wang Zengyou Jin Kaiyi Shen Tingting Weng Zhisong Chen Jiahui Feng Zhengzheng Zhang Jiaming Liu Xiaolong Zhang Maoping Chu 《The American journal of emergency medicine》2017,35(3):402-409
Objectives
The depressed heart function is the main complication to cause death of septic patients in clinic. It is urgent to find effective interventions for this intractable disease. In this study, we investigated whether butyrate could be protective for heart against sepsis and the underlying mechanism.Methods
Mice were randomly divided into three groups. Model group challenged with LPS (30 mg/kg, i.p.) only. Butyrate group received butyrate (200 mg/kg·d) for 3 days prior to LPS administration (30 mg/kg). Normal group received saline only. 6 h and 12 h after LPS administration were chosen for detection the parameters to estimate the effects or mechanism of butyrate pretreatment on heart of sepsis.Results
The data showed that septic heart depression was attenuated by butyrate pretreatment through improvement of heart function depression (P < 0.01) and reduction of morphological changes of myocardium. The overexpression of proinflammatory factors, TNF-α, IL-6 and LTB4, in heart tissues induced by sepsis was significantly alleviated by butyrate pretreatment (P < 0.01). As oxidative stress indicators, SOD and CAT activity, and MDA content in heart were deteriorated by LPS challenge, which was noticeably ameliorated by butyrate pretreatment (P < 0.01 or P < 0.05).Conclusions
In conclusion, pretreatment with butyrate attenuated septic heart depression via anti-inflammation and anti-oxidation. 相似文献9.