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| 1 | Dismicrobism in inflammatory bowel disease and colorectal cancer: Changes in response of colocytes显示文摘Patients with inflammatory bowel disease(IBD)have an increased risk of 10%-15%developing colorectal cancer(CRC)that is a common disease of high economic costs in developed countries.The CRC has been increasing in recent years and its mortality rates are very high.Multiple biological and biochemical factors are responsible for the onset and progression of this pathology.Moreover,it appears absolutely necessary to investigate the environmental factors favoring the onset of CRC and the promotion of colonic health.The gut microflora,or microbiota,has an extensive diversity both quantitatively and qualitatively.In utero,the intestine of the mammalian fetus is sterile.At birth,the intestinal microbiota is acquired by ingesting maternal anal or vaginal organisms,ultimately developing into a stable community,with marked variations in microbial composition between individuals.The development of IBD is often associated with qualitative and quantitative disorders of the intestinal microbial flora(dysbiosis).The healthy human gut harbours about10 different bacterial species distributed in colony forming units which colonize the gastrointestinal tract.The intestinal microbiota plays a fundamental role in health and in the progression of diseases such as IBD and CRC.In healthy subjects,the main control of intestinal bacterial colonization occurs through gastric acidity but other factors such as endoluminal temperature,competition between different bacterial strains,peristalsis and drugs can influence the intestinal microenvironment.The microbiota exerts diverse physiological functions to include:growth inhibition of pathogenic microorganisms,synthesis of compounds useful for the trophism of colonic mucosa,regulation of intestinal lymphoid tissue and synthesis of amino acids.Furthermore,mucus seems to play an important role in protecting the intestinal mucosa and maintaining its integrity.Changes in the microbiota composition are mainly influenced by diet and age,as well as genetic factors.Increasing evidence indicates that dysbiosis favors the production of genotoxins and metabolites associated with carcinogenesis and induces dysregulation of the immune response whichpromotes and sustains inflammation in IBD leading to carcinogenesis.A disequilibrium in gut microflora composition leads to the specific activation of gut associated lymphoid tissue.The associated chronic inflammatory process associated increases the risk of developing CRC.Ulcerative colitis and Crohn’s disease are the two major IBDs characterized by an early onset and extraintestinal manifestations,such as rheumatoid arthritis.The pathogenesis of both diseases is complex and not yet fully known.However,it is widely accepted that an inappropriate immune response to microbial flora can play a pivotal role in IBD pathogenesis. | Giovanni Tomasello Pietro Tralongo Provvidenza Damiani Emanuele Sinagra Benedetto Di Trapani Marie Noelle Zeenny Inaya Hajj Hussein Abdo Jurjus Angelo Leone | 2014 | World Journal of Gastroenterology2014，20，48： | 10 |
| 2 | Inflammatory bowel disease in rats:Bacterial and chemical interaction显示文摘AIM: To develop a novel model of colitis in rats, using a combination of iodoacetamide and enteropathogenic E. coli (EPEC), and to elucidate the pathophysiologic processes implicated in the development of ulcerative colitis (UC). METHODS: Male Sprague-Dawley rats (n = 158) were inoculated intrarectally on a weekly basis with 4 different combinations: (a) 1% methylcellulose (MC), (b) 100 μL of 6% iodoacetamide (IA) in 1% MC, (c) 200 μL containing 4 × 108 colony factor units (CFU) of EPEC, and (d) combined treatment of (IA) followed by bacteria (B) after 2 d. Thirty days post treatment, each of the four groups was divided into two subgroups; the inoculation was stopped for one subgroup and the other subgroup continued with biweekly inoculation until the end of the experiment. Colitis was evaluated by the clinical course of the disease, the macroscopic and microscopic alterations, activity of myeloperoxidase (MPO), and by TNF-α gene expression. RESULTS: Findings indicative of UC were seen in the combined treatment (IA + B) as well as the IA conti-nued treatment groups: the animals showed slow rate of increase in body weight, diarrhea, bloody stools, high colonic ulcer score, as well as histological altera- tions characteristic of UC, with an extensive inflamma- tory reaction. During the course of the experiment, the MPO activity was consistently elevated and the TNF-α gene expression was upregulated compared to the control animals. CONCLUSION: The experimental ulcerative colitis model used in the present study resembles, to a great extent, the human disease. It is reproducible with characteristics indicative of chronicity. | Inaya Abdallah Hajj Hussein Rania Tohme Kassem Barada Mostafa Hassan Mostafa Jean-Noel Freund Rosalyn A Jurjus Walid Karam Abdo Jurjus | 2008 | World Journal of Gastroenterology2008，14，25： | 2 |
| 3 | Fibmblasts in wound healing: transformation, integrin expression, motility and proliferation differences in syndecan - 1 deficient mice显示文摘 | Jurjus RA Liu YY Pal- Ghosh S | 2007 | Faseb Journal2007，5，21： | 1 |
| 4 | Clozapine and associated diabetes mellitus 显示文摘 | Popli AP Lonicki PE Jurjus GT | 1997 | J Clin Psychiatry1997，58，： | 1 |
| 5 | Animal models of inflammatory bowel disease显示文摘 | JURJUS A R KHOURY N N REIMUND J M | 2004 | Journal of Pharmacological and Toxicological Methods2004，50，2： | 1 |
| 6 | The prevalence of hypertension and its association with other cardiovascular disease risk factors in a representative sample of the Lebanese population 显示文摘 | Tohme RA Jurjus AR Estephan A | 2005 | Human Hypertension2005，19，： | 1 |
| 7 | Clozapine and associated diabetes mellitus显示文摘 | Popli AP Lonicki PE Jurjus GT | 1997 | J Clin Psychiatry1997，58，： | 1 |
| 8 | Animal models of inflammatory bowel disease 显示文摘 | Jurjus AR Khoury NN Reimund JM | 2004 | J Pharmacol Toxicol Methods2004，50，2： | 1 |
| 9 | Design for learning:adapting the microscopic anatomy laboratory to adult learners显示文摘 | Jurjus R A Krum J Goldman E F | 2013 | Anat Sci Educ2013，6，3： | 1 |
| 10 | Rat model of burn wound healing: Effect of botox显示文摘 | Abdallah Haji Hussein I Dali Balta N Jurjus RA | 2012 | J Biol Regul Homeost Agents2012，26，3： | 1 |
| 11 | Animal models of inflammatory bowel disease显示文摘 | Abdo R. Jurjus Naim N. Khoury Jean-Marie Reimund | 2004 | Journal of Pharmacological and Toxicological Methods2004，，2： | 1 |
| 12 | The prevalence of hypertension and its association with other cardiovascular disease risk factors in a representative sample of the Lebanese population 显示文摘 | Tohme RA Jurjus AR Estephan A | 2005 | J Hum Hypertens2005，19，11： | 1 |
| 13 | Endothelium and myocyte cellular insulin receptor alterations in a rat model of myocardial infarction显示文摘 | Jaroudi WA Jurjus AR El-Sabban ME | 2003 | Can J Physiol Pharmacol2003，81，3： | 1 |
| 14 | Animal models of inflarmmatorybowel disease显示文摘 | Khoury NN Reimund JM | 2004 | J Pharmacol Toxicol Methods2004，50，2： | 1 |
| 15 | Rat model of burn wound healing: effect of Botox显示文摘 | Abdallah Hajj Hussein l Dali Balta N Jurjus RA | 2012 | J Biological Regulat Homeostat Agents2012，26，3： | 1 |
| 16 | Animal models of inflam- matory bowel disease 显示文摘 | Jurjus AR Khoury NN Reimund JM | 2004 | Pharmacol Toxicol Meth2004，50，2： | 1 |
| 17 | Animal models of inflammatory bowel disease显示文摘 | Jurjus AR Khoury NN Reimund JM | 2004 | l Pharmacol Toxicol Mothods2004，50，： | 1 |
| 18 | Design for learning: Adapting the microscopic anatomy laboratory to adult learners显示文摘 | Jurjus RA Krum J Goldman EF | 2012 | Anat Sci Educ2012，，10： | 1 |
| 19 | Knowledge and practices regarding atherothrombosis in the Lebanese population显示文摘 | TOHME R JURJUS R ESTEPHAN A | 2006 | Prevention and Control2006，2，4： | 1 |
| 20 | Cellular changes in the postmortem hippocampus in major depression显示文摘 | Craig A. Stockmeier Gouri J. Mahajan Lisa C. Konick James C. Overholser George J. Jurjus Herbert Y. Meltzer Harry B.M. Uylings Lee Friedman Grazyna Rajkowska | 2004 | Biological Psychiatry2004，，9： | 1 |
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