Slater, J. G., D. E. Protsenko, N. Carbone, J. P. Jones, and B. J. F. Wong,
"Acoustic response of cartilage during laser-mediated stress relaxation",
IEEE Journal of selected topics in quantum electronics, vol. 11, issue 4: IEEE, pp. 846-853, 2005.
Abstractn/a
Ayad, A.E., Hamed, and E. S. Hamdy,
"Adenosine preconditioning for myocardial preservation in off-pump coronary artery bypass surgery",
Egyptian Journal of Anaesthesia,, vol. 2005,21, issue 1, pp. 21-25, 2005.
Kapiel, T., B. Rhodes, F. Dane, and X. Zhang,
"Advances in watermelon breeding",
Journal of New Seeds, vol. 6, no. 4: Taylor & Francis, pp. 289–319, 2005.
Abstractn/a
Deogun, J. S., S. Das, H. S. Hamza, and S. Goddard,
"An algorithm for boundary discovery in wireless sensor networks",
International Conference on High-Performance Computing: Springer, Berlin, Heidelberg, pp. 343-352, 2005.
Abstractn/a
g Zekri, A. - R. N. a, A. A. c Bahnassy, M. A. Hafez, A. M. R. f El-Shehaby, G. M. d Sherif, H. M. e Khaled, and N. b Zakhary,
"Alterations of the fragile histidine triad gene in hepatitis C virus-associated hepatocellular carcinoma",
Journal of Gastroenterology and Hepatology (Australia), vol. 20, no. 1, pp. 87-94, 2005.
AbstractBackground and Aim: The present study was conducted to address whether homozygous deletion (HZD) or transcriptional alterations of the fragile histidine triad (FHIT) gene play a role in the development and progression of hepatitis C virus-associated hepatocellular carcinoma (HCC). Methods: Homozygous deletion of the FHIT gene at exons 3-9 was assessed as well as mRNA FHIT expression using reverse transcription polymerase chain reaction. The study included 23 samples of HCC, 11 on top of cirrhosis and 12 non-cirrhotic, in addition to five cases with chronic active hepatitis (CAH), as well as seven morphologically normal tissues distant to the tumor (NDT) and 10 normal liver samples from liver transplantation donors. Results: Homozygous deletion was found in 18 of 23 HCC cases. The highest incidence of deletion was detected in exon 9 (52.0%) and the lowest in exon 7 (4.3%). Ten of the 18 cases (55.5%) showed deletion in more than one exon, eight in two exons, one in three exons and one in five exons. There was a significant association between HZD of exons 5 and 9 and HCC arising on top of cirrhosis (P = 0.041 and 0.006, respectively) as well as between exons 8 and 9 and the presence of CAH (P = 0.029 and 0.034, respectively). Aberrant FHIT transcripts were detected in 15 HCC cases (65.2%), 13 of them showed complete reduction of the mRNA transcripts and two showed abnormal bands. Sequence analysis of abnormal-sized transcripts revealed that they were generated by the fusion of exons 5 and 7 as well as exons 7 and 9. In contrast, six of the seven NDT samples tested (85.6%) showed HZD in one or more exons. None of the normal liver samples from liver transplantation donors showed any changes. The highest incidence of HZD was detected in exon 9 (five of six cases representing 83.3%) and the lowest was in exon 4 (one of six cases representing 16.7%). Four cases showed the same aberrant FHIT HZD in both NDT and matched HCC. Conclusions: The results of the present study indicate that the FHIT gene is a frequent target in hepatitis C virus-associated HCC and that alterations affecting this gene could be an early event in this type of neoplasm as they were detected in cirrhotic and CAH patients. However, this should be confirmed by a larger, extended study including more cases of cirrhotic and CAH patients as well as matched tumor and normal samples. © 2005 Blackwell Publishing Asia Pty Ltd.
g Zekri, A. - R. N. a, A. A. c Bahnassy, M. A. Hafez, A. M. R. f El-Shehaby, G. M. d Sherif, H. M. e Khaled, and N. b Zakhary,
"Alterations of the fragile histidine triad gene in hepatitis C virus-associated hepatocellular carcinoma",
Journal of Gastroenterology and Hepatology (Australia), vol. 20, no. 1, pp. 87-94, 2005.
AbstractBackground and Aim: The present study was conducted to address whether homozygous deletion (HZD) or transcriptional alterations of the fragile histidine triad (FHIT) gene play a role in the development and progression of hepatitis C virus-associated hepatocellular carcinoma (HCC). Methods: Homozygous deletion of the FHIT gene at exons 3-9 was assessed as well as mRNA FHIT expression using reverse transcription polymerase chain reaction. The study included 23 samples of HCC, 11 on top of cirrhosis and 12 non-cirrhotic, in addition to five cases with chronic active hepatitis (CAH), as well as seven morphologically normal tissues distant to the tumor (NDT) and 10 normal liver samples from liver transplantation donors. Results: Homozygous deletion was found in 18 of 23 HCC cases. The highest incidence of deletion was detected in exon 9 (52.0%) and the lowest in exon 7 (4.3%). Ten of the 18 cases (55.5%) showed deletion in more than one exon, eight in two exons, one in three exons and one in five exons. There was a significant association between HZD of exons 5 and 9 and HCC arising on top of cirrhosis (P = 0.041 and 0.006, respectively) as well as between exons 8 and 9 and the presence of CAH (P = 0.029 and 0.034, respectively). Aberrant FHIT transcripts were detected in 15 HCC cases (65.2%), 13 of them showed complete reduction of the mRNA transcripts and two showed abnormal bands. Sequence analysis of abnormal-sized transcripts revealed that they were generated by the fusion of exons 5 and 7 as well as exons 7 and 9. In contrast, six of the seven NDT samples tested (85.6%) showed HZD in one or more exons. None of the normal liver samples from liver transplantation donors showed any changes. The highest incidence of HZD was detected in exon 9 (five of six cases representing 83.3%) and the lowest was in exon 4 (one of six cases representing 16.7%). Four cases showed the same aberrant FHIT HZD in both NDT and matched HCC. Conclusions: The results of the present study indicate that the FHIT gene is a frequent target in hepatitis C virus-associated HCC and that alterations affecting this gene could be an early event in this type of neoplasm as they were detected in cirrhotic and CAH patients. However, this should be confirmed by a larger, extended study including more cases of cirrhotic and CAH patients as well as matched tumor and normal samples. © 2005 Blackwell Publishing Asia Pty Ltd.
Khayyal, M. T., M. A. El-Ghazaly, D. M. Abdallah, S. N. Okpanyi, and O. Kelber,
"Analgesics. Anti-inflammatories. Antiphlogistics. Antirheumatic Drugs-Mechanisms Involved in the Anti-inflammatory Effect of a Standardized Willow Bark Extract",
Arzneimittelforschung, vol. 55, no. 11: Aulendorf [Germany]: Editio Cantor, pp. 677–687, 2005.
Abstractn/a
Khayyal, M. T., M. A. El-Ghazaly, D. M. Abdallah, S. N. Okpanyi, and O. Kelber,
"Analgesics. Anti-inflammatories. Antiphlogistics. Antirheumatic Drugs-Mechanisms Involved in the Anti-inflammatory Effect of a Standardized Willow Bark Extract",
Arzneimittelforschung, vol. 55, issue 11: Aulendorf [Germany]: Editio Cantor, pp. 677-687, 2005.
Abstractn/a