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| 1 | Ultrastructure and histochemistry of rat myocardial capillary endothelial cells in response to diabetes and hypertension显示文摘Insufficient growth and rarefaction of capillaries, followed by endothelial dysfunction may represent one of the mostcritical mechanisms involved in heart damage. In this study we examined histochemical and ultrastructural changes inmyocardial capillary endothelium in two models of heart failure streptozotocin-induced diabetes mellitus (STZ) and NO-deficient hypertension in male Wistar rats. Diabetes was induced by a single i.v. dose of STZ (45 mg/kg) and chronic 9-week stage was analysed. To induce NO-deficient hypertension, animals were treated with inhibitor of NO synthase L-nitroarginine methylester (L-NAME) (40 mg/kg) for 4 weeks. Left ventricular tissue was processed for enzyme cata-lytic histochemistry of capillary alkaline phosphatase (AlPh), dipeptidyl peptidase IV (DPP IV), and endothelial NOsynthase/NADPH-diaphorase (NOS) and for ultrastructural analysis. In diabetic and hypertensive rats, lower/absentAlPh and DPP IV activities were found in focal micro-areas. NOS activity was significantly reduced and persisted onlylocally. Quantitative evaluation demonstrated reduction of reaction product intensity of AlPh, DPP and NOS by 49.50%,74.36%, 20.05% in diabetic and 62.93%, 82.71%, 37.65% in hypertensive rats. Subcellular alterations of endothelialcells were found in heart of both groups suggesting injury of capillary function as well as compensatory processes.Endothelial injury was more significant in diabetic animals, in contrast the adaptation was more evident in hypertensiveones. Concluding: both STZ-induced diabetes- and NO-deficient hypertension-related cardiomyopathy were accompa-nied by similar features of structural remodelling of cardiac capillary network manifested as angiogenesis and angiopathy.The latter was however, predominant and may accelerate disappearance of capillary endothelium contributing to myo-cardial dysfunction. | Ludmila OKRUHLICOVA Narcis TRIBULOVA1 Peter WEISMANN Ruzena SOTNIKOVA | 2005 | Cell Research2005，15，7： | 4 |
| 2 | Intestinal schistosomiasis in Uganda at high altitude(>1400 m):malacological and epidemiological surveys on Mount Elgon and in Fort Portal crater lakes reveal extra preventive chemotherapy needs显示文摘Background:Intestinal schistosomiasis is of public health importance in Uganda but communities living above 1400 m are not targeted for control as natural transmission is thought unlikely.To assess altitudinal boundaries and at-risk populations,conjoint malacological and epidemiological surveys were undertaken on Mount Elgon(1139 m-3937 m),in Fort Portal crater lakes and in the Rwenzori Mountains(1123 m-4050 m).Methods:Seventy freshwater habitats[Mount Elgon(37),Fort Portal crater lakes(23),Rwenzori Mountains(8)and Lake Albert(2)]were inspected for Biomphalaria species.Water temperature,pH and conductivity were recorded.A parasitological examination of 756 schoolchildren[Mount Elgon(300),Fort Portal crater lakes(456)]by faecal microscopy of duplicate Kato-Katz smears from two consecutive stool samples was bolstered by antigen(urine-CCA dipstick)and antibody(SEA-ELISA)diagnostic assays.Results:Biomphalaria spp.was found up to 1951 m on Mount Elgon and 1567 m in the Fort Portal crater lakes.Although no snail from Mount Elgon shed cercariae,molecular analysis judged 7.1%of snails sampled at altitudes above 1400 m as having DNA of Schistosoma mansoni;in Fort Portal crater lakes three snails shed schistosome cercariae.Prevalence of intestinal schistosomiasis as measured in schoolchildren by Kato-Katz(Mount Elgon=5.3%v.Fort Portal crater lakes=10.7%),CCA urine-dipsticks(18.3%v.34.4%)and SEA-ELISA(42.3%v.63.7%)showed negative associations with increasing altitude with some evidence of infection up to 2000 m.Conclusions:Contrary to expectations,these surveys clearly show that natural transmission of intestinal schistosomiasis occurs above 1400 m,possibly extending up to 2000 m.Using spatial epidemiological predictions,this now places some extra six million people at-risk,denoting an expansion of preventive chemotherapy needs in Uganda. | Michelle CStanton Moses Adriko Moses Arinaitwe Alison Howell Juliet Davies Gillian Allison EJames LaCourse Edridah Muheki Narcis BKabatereine J.Russell Stothard | 2017 | Infectious Diseases of Poverty2017，6，1： | 3 |
| 3 | Coffee and non‐alcoholic fatty liver disease: Brewing evidence for hepatoprotection?显示文摘 | Shaohua Chen Narci C Teoh Shiv Chitturi Geoffrey C Farrell | 2014 | J Gastroenterol Hepatol2014，，3： | 2 |
| 4 | Post-hepatectomy liver regeneration in the context of bile acid homeostasis and the gut-liver signaling axis显示文摘Background:Liver regeneration following partial hepatectomy(PHx)is a complicated process involving multiple organs and several types of signaling networks.The bile acid-activated metabolic pathways occupy an auxiliary yet important chapter in the entire biochemical story.PHx is characterized by rapid but transient bile acid overload in the liver,which constitutes the first wave of proliferative signaling in the remnant hepatocytes.Bile acids trigger hepatocyte proliferation through activation of several nuclear receptors.Following biliary passage into the intestines,enterocytes reabsorb the bile acids,which results in the activation of farnesoid X receptor(FXR),the consequent excretion of fibroblast growth factor(FGF)19/FGF15,and its release into the enterohepatic circulation.FGF19/FGF15 subsequently binds to its cognate receptor,fibroblast growth factor receptor 4(FGFR4)complexed withβ-klotho,on the hepatocyte membrane,which initiates the second wave of proliferative signaling.Because some bile acids are toxic,the remnant hepatocytes must resolve the potentially detrimental state of bile acid excess.Therefore,the hepatocytes orchestrate a bile acid detoxification and elimination response as a protective mechanism in concurrence with the proliferative signaling.The response in part results in the excretion of(biotransformed)bile acids into the canalicular system,causing the bile acids to end up in the intestines.Relevance for patients:Recently,FXR agonists have been shown to promote regeneration via the gut-liver axis.This type of pharmacological intervention may prove beneficial for patients with hepatobiliary tumors undergoing PHx.In light of these developments,the review provides an in-depth account of the pathways that underlie post-PHx liver regeneration in the context of bile acid homeostasis in the liver and the gut-liver signaling axis. | Lianne de Haan Sarah Jvan der Lely Anne-Loes K.Warps Quincy Hofsink Pim B.Olthof Mark J.de Keijzer Daniel A.Lionarons Lionel Mendes-Dias Bote G.Bruinsma Korkut Uygun Hartmut Jaeschke Geoffrey C.Farrell Narci Teoh Rowan Fvan Golen Tiangang Li Michal Heger | 2018 | Journal of Clinical & Translational Research2018，4，1： | 2 |
| 5 | Inflammation and oxidative stress caused might lead to left ventricular diastolic and hypertension by nitric oxide synthase uncoupling systolic dysfunction in patients with显示文摘 | Zsuzsanna Szelenyi Adam Fazakas Gabor Szenasi Melinda KiSS Narcis Tegze Bertalan CsabaFekete Eszter Nagy Imre Bodo Balint Nagy Attila Molvarec Attila Patocs Lilla Pepo Zoltan Prohatszka Andras Vereckei | 2015 | Journal of Geriatric Cardiology2015，12，1： | 2 |
| 6 | Is peritoneal drainage neces- sary in childhood perforated appendicitis A comparative study显示文摘 | Narci A Karaman I Karaman A | 2007 | J Pediatr Snrg2007，6，42： | 1 |
| 7 | Surgical treatment for laryngotracheal stenosis in the pediatric patient显示文摘 | Contencin P Fligny I | 1990 | Arch Otolaryngol Head Neck Surg1990，116，： | 1 |
| 8 | Efficient Production of Hydrogen over Supported Cobalt Catalysts from Ethanol Steam Reforming 显示文摘 | Jordi Llorca Narcis Homs Joaquim Sales Pilar Ramtrez de la Piscina | 2002 | Catalysis2002，209，2： | 1 |
| 9 | CO 2 hydrogenation to methanol over CuZnGa catalysts prepared using microwave-assisted methods显示文摘 | Weijie Cai Pilar Ramirez de la Piscina Jamil Toyir Narcis Homs | 2014 | Catalysis Today2014，，： | 1 |
| 10 | Obesity and diabetes accelerate hepatocarcinogenesis via hepatocyte proliferation independent of NF-κB or Akt/mTORC1显示文摘Background:There are strong links between obesity,diabetes and hepatocellular carcinoma(HCC),but molecular mechanisms remain unclear.Aim:We tested the proposed involvement of NF-κB,IL-6/STAT3 and Akt/mTORC1 before onset(at 3 months)and at onset(6 months)of accelerated hepatocarcinogenesis in DEN-injected obese and diabetic foz/foz compared to lean wildtype(Wt)mice,and also studied the hepatocyte proliferative response to DNA damage between the obese and lean lines.Methods:Male foz/foz and Wt littermates fed normal chow were DEN-injected(10mg/kg i.p.)at age 12-15 days.To test the effect of mTOR inhibitor on growth of dysplastic hepatocytes,a separate cohort of DEN-injected foz/foz mice was administered rapamycin(4 mg/kg body weight/day).Results:foz/foz mice developed obesity,hyperinsulinemia,diabetes,adipokine dysregulation and fatty liver,without increased serum or liver TNF-αor serum IL-6.All DEN-injected foz/foz mice developed HCC by 6 mths vs.0/10 lean Wt.At 3 mths,there were more dysplastic hepatocytes in DEN-injected foz/foz than Wt,with increased liver injury(serum ALT),hepatocyte apoptosis(M30-positive cells)and proliferation(cyclin D1,cyclin E,PCNA),but neither NF-κB nor STAT3 activation.foz/foz livers exhibited upregulation of DNA damage sensors ATM and ATR,with inadequate cell cycle checkpoint controls(CHK1,CHK2,p53,p21).Akt and mTORC1 were highly activated in livers from foz/foz vs.Wt mice.Despite such activation,rapamycin failed to reduce growth of dysplastic hepatocytes.Conclusions:Accelerated DEN-induced HCC in obese/diabetic mice is linked to enhanced growth of dysplastic hepatocytes that cannot be attributed to NF-κB or IL-6/STAT3 activation,nor to sustained mTORC1 activation.The critical mechanism for obesity-enhanced hepatocarcinogenesis lies in the disconnection between hepatocellular injury with DNA damage,and an unrestrained proliferative response.Relevance for patients:This study supports the epidemiological data linking obesity,diabetes and fatty liver disease with increased risk for developing HCC.The findings also suggest that mTORC1 inhibition may not be beneficial in the prevention of obesity-related hepatocarcinogenesis. | Evi Arfianti Claire Z Larter Seungsoo Lee Vanessa Barn Geoffrey Haigh Matthew M.Yeh George NIoannou Narci C.Teoh Geoffrey C.Farrell | 2016 | Journal of Clinical & Translational Research2016，2，1： | 1 |
| 11 | ArchDB:automated protein loop classification as a tool for structural genomics 显示文摘 | JORDI ESPADALER NARCIS FERNANDEZ-FUNENTES ANTONIO HERMOSO | 2004 | Nucleic Acids Research2004，32，： | 1 |
| 12 | Transnasal endoscopic treatment of choanal atresia without prolonged stenting显示文摘 | Van Den AbT Francois M Narcy P | 2002 | Arch Otolaryngol Head Neck Surg2002，128，8： | 1 |
| 13 | New ee显示文摘 | Diana Ciolacu Ana Maria Oprea Narcis Anghel | 2012 | Mater Sci Eng C2012，32，3： | 1 |
| 14 | Effects of Mediterranean climate annual varia- bility on stream biological quality assessment using macroinverte- brate communities 显示文摘 | Munn A Narcis P | 2011 | Ecological Indicators2011，11，： | 1 |
| 15 | The role of mean platelet volume in the diagnosis of acute appendicitis: a retrospective case-controlled study 显示文摘 | Narci H Turk E Karagulle E | 2013 | Iran Red Crescent Med J2013，15，11： | 1 |
| 16 | Carbon- carbon composites prepared by a rapid densification process I: Synthesis and physico-chemical data 显示文摘 | BRUNETON E NARCY B OBERLIN A | 1997 | Carbon1997，35，1011： | 1 |
| 17 | Brief, intermediate and prolonged ischemia in the isolated crystalloid perfused rat heart: relation between susceptibility to arrhythmias and degree of ultrastructural injury显示文摘 | Ravingerova T Narcis T Slezak J | 1995 | J Mol Cell Cardiol1995，27，9： | 1 |
| 18 | Is peritoneal drainagenecessary in childhood perforated appendicitis- -a comparativestudy显示文摘 | Narci A Karaman I Karaman A | 2007 | J Pediatr Surg2007，42，11： | 1 |
| 19 | New ee显示文摘 | Diana Ciolacu Ana Maria Oprea Narcis Anghel | 2012 | Mater Sci Eng C2012，32，3： | 1 |
| 20 | The role of mean platelet volume in the diagnosis of acute appendicitis:a retrospectivecase-controlled study显示文摘 | Narci H Turk E Karagulle E | 2013 | Iran Red Crescent Med J2013，15，11： | 1 |
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