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| 1 | Intestinal alkaline phosphatase in the colonic mucosa of children with inflammatory bowel disease显示文摘AIM:To investigate intestinal alkaline phosphatase(iAP) in the intestinal mucosa of children with inflammatory bowel disease(IBD).METHODS:Colonic biopsy samples were taken from 15 newly diagnosed IBD patients and from 10 healthy controls.In IBD patients,specimens were obtainedboth from inflamed and non-inflamed areas.The iAP mRNA and protein expression was determined by reverse transcription-polymerase chain reaction and Western blotting analysis,respectively.Tissue localization of iAP and Toll-like receptor(TLR) 4 was investigated by immunofluorescent staining.RESULTS:The iAP protein level in the inflamed mucosa of children with Crohn's disease(CD) and ulcerative colitis(UC) was significantly decreased when compared with controls(both P < 0.05).Similarly,we found a significantly decreased level of iAP protein in the inflamed mucosa in CD compared with non-inflamed mucosa in CD(P < 0.05).In addition,the iAP protein level in inflamed colonic mucosa in patients with UC was decreased compared with non-inflamed mucosa in patients with CD(P < 0.05).iAP protein levels in the non-inflamed mucosa of patients with CD were similar to controls.iAP mRNA expression in inflamed colonic mucosa of children with CD and UC was not significantly different from that in non-inflamed colonic mucosa with CD.Expression of iAP mRNA in patients with noninflamed mucosa and in controls were similar.Co-localization of iAP with TLR4 showed intense staining with a dotted-like pattern.iAP was present in the inflamed and non-inflamed mucosa of patients with CD,UC,and in control biopsy specimens,irrespective of whether it was present in the terminal ileum or in the colon.However,the fluorescent signal of TLR4 was more pronounced in the colon compared with the terminal ileum in all groups studied.CONCLUSION:Lower than normal iAP protein levels in inflamed mucosa of IBD patients may indicate a role for iAP in inflammatory lesions in IBD.Based on our results,administration of exogenous iAP enzyme to patients with the active form of IBD may be a therapeutic option. | Kriszta Molnár dám Vannay Beáta Szebeni Nóra Fanni Bánki Erna Sziksz ron Cseh Hajnalka Gyrffy Péter László Lakatos Mária Papp András Arató Gábor Veres | 2012 | World Journal of Gastroenterology2012，18，25： | 5 |
| 2 | CYP24A1 inhibition facilitates the anti-tumor effect of vitamin D3 on colorectal cancer cells显示文摘AIM:The effects of vitamin D3 have been investigated on various tumors, including colorectal cancer (CRC). 25-hydroxyvitamin-D3-24-hydroxylase (CYP24A1), the enzyme that inactivates the active vitamin D3 metabolite 1,25-dihydroxyvitamin D3 (1,25-D3), is considered to be the main enzyme determining the biological halflife of 1,25-D3. During colorectal carcinogenesis, the expression and concentration of CYP24A1 increases significantly, suggesting that this phenomenon could be responsible for the proposed efficacy of 1,25-D3 in the treatment of CRC. The aim of this study was to investigate the anti-tumor effects of vitamin D3 on the human CRC cell line Caco-2 after inhibition of the cytochrome P450 component of CYP24A1 activity. METHODS:We examined the expression of CYP24A1 mRNA and the effects of 1,25-D3 on the cell line Caco-2 after inhibition of CYP24A1. Cell viability and proliferation were determined by means of sulforhodamine-B staining and bromodeoxyuridine incorporation, respectively, while cytotoxicity was estimated via the lactate dehydrogenase content of the cell culture supernatant. CYP24A1 expression was measured by realtime reverse transcription polymerase chain reaction. A number of tetralone compounds were synthesized to investigate their CP24A1 inhibitory activity. RESULTS:In response to 1,25-D3, CYP24A1 mRNA expression was enhanced significantly, in a time- and dose-dependent manner. Caco-2 cell viability and proliferation were not influenced by the administration of 1,25-D3 alone, but were markedly reduced by coadministration of 1,25-D3 and KD-35, a CYP24A1-inhibiting tetralone. Our data suggest that the mechanism of action of co-administered KD-35 and 1,25-D3 does not involve a direct cytotoxic effect, but rather the inhibition of cell proliferation. CONCLUSION:These findings demonstrate that the selective inhibition of CYP24A1 by compounds such as KD-35 may be a new approach for enhancement of the anti-tumor effect of 1,25-D3 on CRC. | János P Kósa Péter Horváth János Wlfling Dóra Kovács Bernadett Balla Péter Mátyus Evelin Horváth Gábor Speer István Takács Zsolt Nagy Henrik Horváth Péter Lakatos | 2013 | World Journal of Gastroenterology2013，19，17： | 5 |
| 3 | Increased duodenal expression of mi R-146a and-155 in pediatric Crohn's disease显示文摘AIM: To evaluate the role of micro RNA(mi R)-146 a,-155 and-122 in the duodenal mucosa of pediatric patients with Crohn's disease(CD) and the effect of transforming growth factor-β(TGF-β) on these mi Rs in duodenal epithelial and fibroblast cells.METHODS: Formalin-fixed, paraffin-embedded biopsies derived from the macroscopically inflamed(CD inflamed: n = 10) and intact(CD intact: n = 10) duodenal mucosa of pediatric CD patients and control children(C: n = 10) were examined. Expression of mi R-146 a,-155 and-122 was determined by realtime polymerase-chain reaction(PCR). The expression of the above mi Rs was investigated in recombinant human TGF-β(1 nmol/L, 24 h) or vehicle treated small intestinal epithelial cells(CCL-241) and primary duodenal fibroblast cells derived from healthy children as well.RESULTS: Expression of mi R-146 a was significantly higher in the inflamed duodenal mucosa compared to the intact duodenal mucosa of children with CD(CD inflamed: 3.21 ± 0.50 vs CD intact: 0.62 ± 0.26, p ≤ 0.01) and to the control group(CD inflamed: 3.21 ± 0.50 vs C: 1.00 ± 0.33, p ≤ 0.05). The expression of mi R-155 was significantly increased in the inflamed region of the duodenum compared to the control group(CD inflamed: 4.87 ± 1.02 vs Control: 1.00 ± 0.40, p ≤ 0.001). The expression of mi R-122 was unchanged in the inflamed or intact mucosa of CD patients compared to controls. TGF-β treatment significantly decreased the expression of mi R-155 in small intestinal epithelial cells(TGF-β: 0.7 ± 0.083 vs Control: 1 ± 0.09, p ≤ 0.05) and also the expression of mi R-146a(TGF-β: 0.67 ± 0.04 vs Control: 1 ± 0.15, p ≤ 0.01) and mi R-155(TGF-β: 0.72 ± 0.09 vs Control: 1 ± 0.06, p ≤ 0.05) in primary duodenal fibroblasts compared to corresponding vehicle treated controls. TGF-β treatment did not influence the expression of mi R-122.CONCLUSION: The elevated expression of mi R-146 a and-155 in the inflamed duodenal mucosa of CD patients suggests the role of these mi Rs in the pathomechanism of inflammatory bowel disease. Antiinflammatory TGF-β plays an important role in the regulation of the expression of these mi Rs. | Dániel Szucs Nóra Judit Béres Réka Rokonay Kriszta Boros Katalin Borka Zoltán Kiss András Arató Attila J Szabó ádám Vannay Erna Sziksz Csaba Bereczki Gábor Veres | 2016 | World Journal of Gastroenterology2016，22，26： | 2 |
| 4 | 卒中介入治疗培训指南:国际多学会共识文件显示文摘1背景
缺血性卒中是全球人口死亡和残疾的首要原因。很多急性大血管闭塞(emergent large vesselocclusion,ELVO)患者都会遗留长期残疾。事实上,这些颅内大动脉闭塞经常会导致大面积脑损伤,进而造成患者死亡或严重致残。 | Lavine SD Cockroft K Hoh B Bambakidis N Khalessi AA Woo H Riina H Siddiqui A Hirsch JA Chong W Rice H Wenderoth J Mitchell P Coulthard A Signh TJ Phatorous C Khangure M Klurfan P ter Brugge K Iancu D Gunnarsson T Pongpech S Rodesch G Soderman M Taylor A Krings T Orbach D Picard L Suh DC Zheng HQ Jansen O Muto M Szikora I Pierot L Brouwer P Gralla J Renowden S Andersson T Fiehler J Turjman F White P Januel AC Spelle L Kulcsar Z Chapot R Biondi A Dima S Taschner C Szajner M Krajina A Sakai N Matsumaru Y Yoshknura S Ezura M Fujinaka T Iihara K Ishii A Higashi T Hirohata M Hyodo A Ito Y Kawanishi M Kiyosue H Kobayashi E Kobayashi S Kuwayama N Matsumoto Y Miyachi S Murayama Y Nagata I Nakahara I Nemoto S Niimi Y Oishi H Satomi J Satow T Sugiu K Tanaka M Terada T Yamagami H Diaz O Lylyk P Jayaraman MV Patsalides A Gandhi CD Lee SK Abruzzo T Albani B Ansari SA Arthur AS Baxter BW Bulsara KR Chen M Almandoz JE Fraser JF Heck DV Hetts SW Hussain MS Klucznik RP Leslie-Mawzi TM Mack WJ McTaggart RA Meyers PM Mocco J Prestigiacomo CA Pride GL Rasmussen PA Starke RM Sunenshine PJ Tarr RW Frei DF Pabo M Nogueira RG Zaidat OO Jovin T Linfante I Yavagal D Liebeskind D Novakovic R Pongpech S 许岩 孙瑞 郭芮兵 | 2017 | 国际脑血管病杂志2017，25，5： | 2 |
| 5 | 生理性线粒体破碎是心脏适应能量需求增加的正常现象显示文摘线粒体在心脏中起着双重作用:负责满足能量需求和调节细胞凋亡。通常认为,线粒体的分裂和碎裂是病理性应激(如缺血)的结果,是线粒体质量差的指标,并导致线粒体自噬和细胞死亡。然而,最近的研究表明,抑制裂变也导致线粒体功能减弱和心脏损害,说明裂变对维持心脏和线粒体生物能量平衡十分重要。 | 刘莉 叶鹏 Coronado M Fajardo G Nguyen K Zhao M Kooiker KB Jung G Hu DQ Reddy S Sandoval E Stotland A Gottlieb RA Bernstein D | 2018 | 中华高血压杂志2018，26，1： | 2 |
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