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Taha, A. A., I. M. Ibrahim, and M. L. Ibrahim, "Abdominal Vascular Injury during lumbar disc Surgery. ", The Egyptian Journal of Neurosurgery, , vol. 14, issue January 2004., pp. 16-22, 2004.
Mohammad, W. S., "Abdominal/adductor strength imbalance in soccer players with osteitis pubis", Journal of Men's Health, vol. 14, no. 3, pp. e33–e40, 2018. Abstract
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Mohammad, W. S., and W. M. Elsais, "ABDOMINAL/ADDUCTOR STRENGTH IMBALANCE IN SOCCER PLAYERS WITH OSTEITIS PUBIS", Journal of Men's Health, vol. 14, issue 3, pp. e33-e40, 2018. article.pdf
dalia mohamed kamel, abdominopelvic cavity concept in urinary incontinence rehabilitation, , germany, lap lambert academic publishing, 2016. scan_u1.jpgscan_u3.jpg
Abe, M., L. Abelmann, B. R. Acharya, S. Acharya, O. Acher, A. L. Adenot, S. Adenwalla, A. A. Adly, U. Adriano, M. Ahmadian, et al., Abe, M., AI Shames, N. Matsushita, and Y. Shimada. Ferromagnetic resonance study on magnetic homogeneity in spin-sprayed NiZn ferrite films highly permeable at gigahertz frequencies; T-MAG Sep 03 3142-3144, , Submitted. Abstract
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abeer ahmed abdelhady, abeer, , 2017. lglf-jnb.pdflglf_rb.pdf
Bahnassy, A. A., M. O. H. A. M. E. D. FAWZY, M. El-Wakil, A. - R. N. Zekri, A. Abdel-Sayed, and M. Sheta, "Aberrant expression of cancer stem cell markers (CD44, CD90, and CD133) contributes to disease progression and reduced survival in hepatoblastoma patients: 4-year survival data.", Translational research : the journal of laboratory and clinical medicine, vol. 165, issue 3, pp. 396-406, 2015 Mar. Abstract

Hepatoblastoma (HB) is an embryonal tumor of the liver in children. Prognosis and response to treatment in HB are highly variable. Cancer stem cells (CSCs) constitute a population of cells, which contribute to the development and progression of many tumors. However, their role in HB is not well defined yet. We assessed the prognostic and predictive values of some CSC markers in HB patients. Protein and messenger RNA expressions of the CSC markers CD133, CD90, and CD44 were assessed in 43 HB patients and 20 normal hepatic tissues using immunohistochemistry and quantitative real-time polymerase chain reaction. The expression levels of these markers were correlated to standard prognostic factors, patients' response to treatment, overall survival (OS), and disease-free survival (DFS). CD44, CD90, and CD133 proteins were detected in 48.8%, 32.6%, and 48.8% compared with 46.5%, 41.7%, and 58.1% RNA, respectively (concordance, 77.8%-96%). None of the normal tissue samples was positive for any of the markers. Significant correlations were reported between α-fetoprotein and both CD44 and CD133 (P = 0.02) as well as between tumor types CD90 and CD133 (P = 0.009). Reduced OS correlated with CD44, CD90, and CD133 expressions (P < 0.001), advanced stage (P < 0.001), response to treatment (P < 0.001), and total excision of the tumor. Reduced DFS correlated with CD44 and CD133 expressions (P < 0.001) only. In conclusion, CD133, CD44, and CD90 could be used as prognostic and predictive markers in HB. High expression of these markers is significantly associated with poor response to treatment and reduced survival. Moreover, complete surgical resection and systemic chemotherapy are essential to achieve good response and prolonged survival, especially in early stage patients.

Bahnassy, A. A., M. El-Sayed, N. M. Ali, O. Khorshid, M. M. Hussein, H. F. Yousef, M. A. Mohanad, A. - R. N. Zekri, and S. E. Salem, "Aberrant expression of miRNAs predicts recurrence and survival in stage-II colorectal cancer patients from Egypt", Applied Cancer Research, vol. 37, issue 39, pp. 1-13, 2017. bahnassy2017.pdf
Eissa, S., M. Swellam, I. M. El-Khouly, S. K. Kassim, H. Shehata, A. Mansour, M. Esmat, A. I. Nossier, M. A. Hamdy, N. M. Awad, et al., "Aberrant Methylation of RARb2 and APC Genes in Voided Urine as Molecular Markers for Early Detection of Bilharzial and Nonbilharzial Bladder Cancer", Cancer Epidemiol Biomarkers Prev; 20 (8): 1657, 2011. AbstractCU-PDF

Background: Bladder cancer cells illustrate major disruptions in their DNA methylation patterns as compared with normal ones. Authors aimed to identify epigenetic molecular markers in urine for early detection of bladder cancer. Materials and Methods: We retrospectively analyzed the methylation status

Mansour, W. Y., N. V. Bogdanova, U. Kasten-Pisula, T. Rieckmann, S. Kocher, K. Borgmann, M. Baumann, M. Krause, C. Petersen, H. Hu, et al., "Aberrant overexpression of miR-421 downregulates ATM and leads to a pronounced DSB repair defect and clinical hypersensitivity in SKX squamous cell carcinoma", Radiother Oncol, 2012/12/04, vol. 106, no. 1, pp. 147-54, Jan, 2013. Abstractmansour_2013.pdfWebsite

BACKGROUND: Cellular and clinical sensitivity to ionizing radiation (IR) is determined by DNA double-strand breaks (DSB) repair. Here, we investigate the molecular mechanism underlying the extreme response of a head and neck tumor case (SKX) to standard radiotherapy. METHODS: Immunofluorescence (IF) was used for the assessment of DSB repair, Western blot and real-time PCR for protein and mRNA expression, respectively. RESULTS: SKX cells exhibited a pronounced radiosensitivity associated with numerous residual gamma-H2AX foci after IR. This was not associated with lacking canonical repair proteins. SKX cells did not express any ATM protein. Accordingly, immunoblotting revealed no ATM kinase activity toward substrates such as p-SMC1, p-CHK2 and p-KAP1. Sequencing of all 66 exons of ATM showed no mutation. ATM mRNA level was moderately reduced, which could be reverted by 5'-Aza-C treatment but without restoring protein levels. Importantly, we demonstrated a post-transcriptional regulation in SKX cells via 6-fold enhanced levels of miR-421, which targets the 3'-UTR of ATM mRNA. Transfection of SKX cells with either anti-miR-421 inhibitor or a microRNA-insensitive ATM vector recovered ATM expression and abrogated the hyper-radiosensitivity. CONCLUSION: This is the first report describing microRNA-mediated down-regulation of ATM leading to clinically manifest tumor radiosensitivity.

Mansour, W. Y., N. V. Bogdanova, U. Kasten-Pisula, T. Rieckmann, S. Köcher, K. Borgmann, M. Baumann, M. Krause, C. Petersen, H. Hu, et al., "Aberrant overexpression of miR-421 downregulates ATM and leads to a pronounced DSB repair defect and clinical hypersensitivity in SKX squamous cell carcinoma", Radiotherapy and oncology, vol. 106, no. 1: Elsevier, pp. 147–154, 2013. Abstract
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Mansour, W. Y., N. V. Bogdanova, U. Kasten-Pisula, T. Rieckmann, S. Köcher, K. Borgmann, M. Baumann, M. Krause, C. Petersen, H. Hu, et al., "Aberrant overexpression of miR-421 downregulates ATM and leads to a pronounced DSB repair defect and clinical hypersensitivity in SKX squamous cell carcinoma.", Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, vol. 106, issue 1, pp. 147-54, 2013 Jan. Abstract

BACKGROUND: Cellular and clinical sensitivity to ionizing radiation (IR) is determined by DNA double-strand breaks (DSB) repair. Here, we investigate the molecular mechanism underlying the extreme response of a head and neck tumor case (SKX) to standard radiotherapy.

METHODS: Immunofluorescence (IF) was used for the assessment of DSB repair, Western blot and real-time PCR for protein and mRNA expression, respectively.

RESULTS: SKX cells exhibited a pronounced radiosensitivity associated with numerous residual γ-H2AX foci after IR. This was not associated with lacking canonical repair proteins. SKX cells did not express any ATM protein. Accordingly, immunoblotting revealed no ATM kinase activity toward substrates such as p-SMC1, p-CHK2 and p-KAP1. Sequencing of all 66 exons of ATM showed no mutation. ATM mRNA level was moderately reduced, which could be reverted by 5'-Aza-C treatment but without restoring protein levels. Importantly, we demonstrated a post-transcriptional regulation in SKX cells via 6-fold enhanced levels of miR-421, which targets the 3'-UTR of ATM mRNA. Transfection of SKX cells with either anti-miR-421 inhibitor or a microRNA-insensitive ATM vector recovered ATM expression and abrogated the hyper-radiosensitivity.

CONCLUSION: This is the first report describing microRNA-mediated down-regulation of ATM leading to clinically manifest tumor radiosensitivity.

El-Mougy, F. A., M. M. Yusuf, D. A. Omran, and S. A. Sharaf, "Aberrant p16INK4A methylation: Relation to viral related", South Asian journal of cancer, vol. 3, issue 1, pp. 1-4, 2014. southasianjcancer311-6131332_170153.pdf
El-Mougy, F. A., M. M. Youssef, D. A. Omran, S. A. Sharaf, H. H. El-Sayed, W. A. Rabie, and Elghobary A. Mohamed, "Aberrant p16INK4A methylation: Relation to viral related chronic liver disease and hepatocellular carcinoma", South Asian J Cancer. , vol. 3, issue 1, pp. 1-4, 2014.
El-Mougy, F. A., M. M. Youssef, D. A. Omran, S. A. Sharaf, H. H. El-Sayed, W. A. Rabie, and E. A. Mohame, Aberrant p16INK4A methylation: Relation to viral related chronic liver disease and hepatocellular carcinoma, , 2014.
El-Mougy, F. A., M. M. Youssef, D. A. Omran, S. A. Sharaf, H. H. El-Sayed, W. A. Rabie, E. A. Mohamed, and H. A. Elghobary, "Aberrant p16INK4A methylation: Relation to viral related chronic liver disease and hepatocellular carcinoma.", South Asian journal of cancer, vol. 3, issue 1, pp. 1-4, 2014 Jan. Abstract

BACKGROUND: Hepatocellular carcinoma (HCC) is currently the fifth most common solid tumor worldwide and the third leading cause of cancer related deaths. Several studies have shown that the tumor suppressor gene p16INK4A is frequently downregulated by aberrant methylation of the 5'-cytosine-phosphoguanine island within the promoter region.

AIM: To find out the frequency of methylated p16INK4A in the peripheral blood of HCC and cirrhotic patients and to evaluate its role in hepatocarcinogenesis.

PATIENTS AND METHODS: This study was performed on 58 subjects: 30 HCC patients, 20 cirrhotic patients, and eight healthy volunteers. Methylation of p16INK4A was examined using methylation specific polymerase chain reaction (PCR) (MSP). Comparison of quantitative variables between the study groups was done using Mann-Whitney U test for independent samples when not normally distributed. For comparing categorical data, Chi-square (χ(2)) test was performed. Exact test was used instead when the expected frequency was less than 5.

RESULTS: Methylation of p16INK4A was found in 6.7% of HCC patients, 5% of liver cirrhosis (LC) patients, and none of the healthy volunteers; 66.67% of the p16INK4A-methylated cases (2/3) were positive for anti-hepatitis C virus (HCV) antibodies (one of them had HCC). All HCC cases with aberrant p16INK4A methylation show very high serum alpha fetoprotein (AFP) level (9,080; 30,000 μg/mL). There were no significant associations between the status of p16INK4A methylation and tumor size.

CONCLUSION: Hypermethylation of p16INK4A was found to be infrequent among Egyptian patients with HCC.

El-Mougy, F. A., M. M. Youssef, D. A. Omran, S. A. Sharaf, H. H. El-Sayed, W. A. Rabie, E. A. Mohamed, and H. A. Elghobary, "Aberrant p16INK4A methylation: Relation to viral related chronic liver disease and hepatocellular carcinoma.", South Asian J Cancer, vol. 3, pp. 1-4, 2014.
Helmy, H. S., M. A. Senousy, A. El-Sahar, R. H. Sayed, M. A. Saad, and E. M. Elbaz, "Aberrations of miR-126-3p, miR-181a and sirtuin1 network mediate Di-(2- ethylhexyl) phthalate-induced testicular damage in rats: The protective role of hesperidin", Toxicology , vol. 433–434 , pp. 152406, 2020.
Helmy, H. T. S., M. A. Senousy, A. E. El-Sahar, R. H. Sayed, M. A. Saad, and E. M. Elbaz, "Aberrations of miR-126-3p, miR-181a and sirtuin1 network mediate Di-(2-ethylhexyl) phthalate-induced testicular damage in rats: The protective role of hesperidin.", Toxicology, vol. 433-434, pp. 152406, 2020. Abstract

Recently, oxidative stress was implicated in the environmental contaminant Di-(2-ethylhexyl) phthalate (DEHP)-induced testicular toxicity, however the mechanism is unclear. We investigated the role of oxidative stress-responsive microRNAs in DEHP-induced aberrations and the protective effect of the citrus flavonoid, hesperidin (HSP). Male Wistar rats were randomly allocated into four groups as vehicle-treated control, DEHP-alone group (500 mg/kg/day) for 30 days, and HSP (25 or 50 mg/kg) for 60 days; testicular damage was triggered by oral administration of DEHP (500 mg/kg/day) after thirty days of oral administration of HSP (25 or 50 mg/kg). DEHP administration reduced testis weight coefficient, serum testosterone, testicular 3β-hydroxysteroid dehydrogenase and antioxidant enzyme activities, and elevated serum fatty acid-binding protein-9, testicular malondialdehyde, and Bax/Bcl2 ratio. Aberrant testicular miR-126-3p and miR-181a expression was observed, along with decreased expression of sirtuin1 (SIRT1) and its targets; nuclear factor-erythroid 2-related factor2, haeme oxygenase-1, and superoxide dismutase2. HSP administration significantly ameliorated these changes and restored testicular function in a dose-dependent manner. We highlight a novel role of oxidative stress-miR-126/miR-181a-SIRT1 network in mediating DEHP-induced changes which were reversed by the antioxidant HSP.

Helmy, H. T. S., M. A. Senousy, A. E. El-Sahar, R. H. Sayed, M. A. Saad, and E. M. Elbaz, "Aberrations of miR-126-3p, miR-181a and sirtuin1 network mediate Di-(2-ethylhexyl) phthalate-induced testicular damage in rats: The protective role of hesperidin.", Toxicology, vol. 433-434, pp. 152406, 2020. Abstract

Recently, oxidative stress was implicated in the environmental contaminant Di-(2-ethylhexyl) phthalate (DEHP)-induced testicular toxicity, however the mechanism is unclear. We investigated the role of oxidative stress-responsive microRNAs in DEHP-induced aberrations and the protective effect of the citrus flavonoid, hesperidin (HSP). Male Wistar rats were randomly allocated into four groups as vehicle-treated control, DEHP-alone group (500 mg/kg/day) for 30 days, and HSP (25 or 50 mg/kg) for 60 days; testicular damage was triggered by oral administration of DEHP (500 mg/kg/day) after thirty days of oral administration of HSP (25 or 50 mg/kg). DEHP administration reduced testis weight coefficient, serum testosterone, testicular 3β-hydroxysteroid dehydrogenase and antioxidant enzyme activities, and elevated serum fatty acid-binding protein-9, testicular malondialdehyde, and Bax/Bcl2 ratio. Aberrant testicular miR-126-3p and miR-181a expression was observed, along with decreased expression of sirtuin1 (SIRT1) and its targets; nuclear factor-erythroid 2-related factor2, haeme oxygenase-1, and superoxide dismutase2. HSP administration significantly ameliorated these changes and restored testicular function in a dose-dependent manner. We highlight a novel role of oxidative stress-miR-126/miR-181a-SIRT1 network in mediating DEHP-induced changes which were reversed by the antioxidant HSP.

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