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| 1 | Lipid-Lowering Agents in Nonalcoholic Fatty Liver Disease and Steatohepatitis: Human Studies显示文摘 | William Nseir Julnar Mograbi Murad Ghali | 2012 | Digestive Diseases and Sciences2012，，7： | 2 |
| 2 | Obesity as a risk factor for clostridium diffi- cile infection显示文摘 | Jihad B Raymond F Julnar M | 2013 | Clin Infect Dis2013，57，4： | 1 |
| 3 | Lipid-Lowering Agents in Nonalcoholic Fatty Liver Disease and Steatohepatitis: Human Studies显示文摘 | William Nseir Julnar Mograbi Murad Ghali | 2012 | Digestive Diseases and Sciences2012，，7： | 1 |
| 4 | Diuretic effect and mechanism of action of parsley显示文摘 | Sawsan Ibrahim Kreydiyyeh Julnar Usta | 2002 | Journal of Ethnopharmacology2002，，3： | 1 |
| 5 | Changes in sphingomyelinases, ceramide, Bax, Bcl 2 , and caspase-3 during and after experimental status epilepticus显示文摘 | Mohamad A. Mikati Michele Zeinieh Ralph Abi Habib Jimmy El Hokayem Amal Rahmeh Marwan El Sabban Julnar Usta Ghassan Dbaibo | 2008 | Epilepsy Research2008，，2： | 1 |
| 6 | Homozygous Mutations in the Conserved ATP Hinge Region of the Wilson Disease Gene: Association With Liver Disease显示文摘 | Kassem Barada Mazen El-Atrache Ihab I. El-Hajj Khaled Rida Jida El-Hajjar Ziyad Mahfoud Julnar Usta | 2010 | Journal of Clinical Gastroenterology2010，，6： | 1 |
| 7 | Wilson's disease in Lebanon and regional countries: Homozygosity and hepatic phenotype predominance显示文摘AIM To determine the phenotypes and predominant diseasecausing mutations in Lebanese patients with Wilson's disease,as compared to regional non-European data.METHODS The clinical profile of 36 patients diagnosed in Lebanon was studied and their mutations were determined by molecular testing.All patients underwent full physical exam,including ophthalmologic slit-lamp examination ultrasound imaging of the liver,as well as measurement of serum ceruloplasmin and 24-h urinaryCu levels.In addition,genetic screening using PCR followed by sequencing to determine disease-causing mutations and polymorphisms in the ATP7B gene was carried on extracted DNA from patients and immediate family members.Our phenotypic-genotypic findings were then compared to reported mutations in Wilson's disease patients from regional Arab and non-European countries. RESULTS Patients belonged to extended consanguineous families.The majority were homozygous for the disease-causing mutation,with no predominant mutation identified. The most common mutation,detected in 4 out of 13families,involved the ATP hinge region and was present in patients from Lebanon,Egypt,Iran and Turkey.Otherwise,mutations in Lebanese patients and those of the region were scattered over 17 exons of ATP7B.While the homozygous exon 12 mutation Trp939Cys was only detected in patients from Lebanon but none from the regional countries,the worldwide common mutation H1069Q was not present in the Lebanese and was rare in the region.Pure hepatic phenotype was predominant in patients from both Lebanon and the region(25%-65%).Furthermore,the majority of patients,including those who were asymptomatic,had evidence of some hepatic dysfunction.Pure neurologic phenotype was rare. CONCLUSION Findings do not support presence of a founder effect.Clinical and genetic screening is recommended for family members with index patients and unexplained hepatic dysfunction. | Kassem Barada Aline El Haddad Meghri Katerji Mustapha Jomaa Julnar Usta | 2017 | World Journal of Gastroenterology2017，23，36： | 0 |
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