Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
 
Articles by Amany H. Mansour
Total Records ( 2 ) for Amany H. Mansour
  Amany H. Mansour , Tawfik R. Elkhodary , Rokia Anwar , Maha Ragab Habeeb and Mohammed Amin Mohammed
  Hepatocellular Carcinoma (HCC) is the major form of primary liver cancer and the third leading cause of cancer mortality worldwide. HCC is frequently diagnosed at an advanced stage, resulting in rather poor survival rates. CD133, a trans-membrane glycoprotein, is an important cell surface marker for both stem cells and Cancer Stem Cells (CSCs) in various tissues including the liver. CD133 has been used as the Tumor Initiating Cells (TICs) marker in HCC. Further identification and characterization of CSCs or TICs in HCC are necessary to better understand hepatic carcinogenesis. So, the objective of this study was to estimate the level of the specific markers as CD133 and transforming growth factor β (TGF-β) in HCC. Fifty peripheral blood samples were collected from HCC patients. The CD133 protein expression was analyzed by flow cytometry and TGF-β levels were assayed by ELISA. This study revealed a higher expression of CD133+cells in all HCC patients. The expression of CD133+cells was positively correlated with clinical, pathological and laboratory parameters. A mild to moderate positive correlation was found with tumor size, male gender, pathological grade, Hepatitis C virus and Alpha-fetoprotein and showed a strong positive correlation between age, TGF-β, Lymph node metastasis, portal vein tumor thrombosis and CD133+cells in peripheral blood. CD133+cells might represent true CSCs in HCC which could allow a better understanding of HCC initiation and progression, as well as possibly bear great therapeutic implications. Moreover, the multifunctional cytokine TGF-β plays a crucial role in the regulation of CD133 expression in HCC.
  Mohammed Amin Mohammed , Alaa Mahamad A. Hakeem El-Gamal , Nesreen Moustafa Omar , Abdelhadi M. Shebl , Amany H. Mansour , Sherin Mohamed Abd El-Aziz , Gamal Othman and Soad Amin Mohammed
  The major challenge in inflammatory bowel disease is to achieve a sensitive and specific non invasive diagnostic marker. Recently, S100A12 (Calgranulin C) have been established to be elevated in the feces of patients with IBD. The objective was to investigate the utility of fecal S100A12, in comparison to fecal Calprotectin and standard inflammatory markers, as a screening and distinguishing marker for IBD and Irritable Bowel Syndrome (IBS) in patients with chronic diarrhea. Stool samples were obtained from 173 individuals presenting with gastrointestinal symptoms requiring endoscopy. Fecal S100A12, fecal Calprotectin and serum S100A12 levels were measured and correlated to final diagnosis and standard tests (ESR, CRP, platelet count, albumin, perinuclear anti-neutrophil and antineutrophil cytoplasmic antibodies. Full colonoscopy with histopathological examination was performed. Patients diagnosed with IBD had elevated fecal S100A12 (median 49.7 mg kg-1) and Calprotectin (median 385 mg kg-1) levels compared with the patients without IBD (n = 35, S100A12: Median 4.6 mg kg-1, p<0.0001, Calprotectin: Median 30.5 mg kg-1; p<0.0001). Both the sensitivity and specificity of fecal S100A12 (cutoff 8 mg kg-1) for the detection of IBD were 93.91 and 97%, respectively whereas fecal Calprotectin (cutoff 35 mg kg-1) gave a sensitivity of 93.96% and a specificity of 84.2%. Both fecal markers were superior to the sensitivities and specificities of any standard inflammatory test. Both fecal S100A12 and Calprotectin are sensitive markers of gastrointestinal inflammation but fecal S100A12 provided exceptional specificity in distinguishing patients with IBD from patients without IBD.
 
 
 
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility