molecular and antigenic tissue impact of viral infections on liver transplant patients with neonatal hepatitis

Pathogenesis of neonatal hepatitis relates to various underlying causes including viral infections. Both hepatotropic and non-hepatotropic viruses may induce liver failures in infants before birth, during delivery, or shortly after birth. The tissue impact of HCMV, HSV, HBV, HCV, and rotavirus and adenovirus infections was evaluated in studied infants with neonatal hepatitis. The history of viral infections was analyzed in paraffin-embedded biopsy and autopsy tissues of 22 infants with neonatal hepatitis between years 1996 and 2007, retrospectively. The tissue molecular presentation of HBV, HCV, HCMV, HSV, adenovirus, and rotavirus was evaluated by different qualitative simple and nested PCR and RT-PCR protocols. Immunohistochemistry [IHC] method was used for studying the antigenic prevalence of HSV-1, 2; HBV, HCMV and adenovirus infections. Also the laboratory liver indices of all patients with neonatal hepatitis were analyzed. The HBV and HSV genomes were detected in 3 [14%] of 22 infants. The rotavirus and HCV-RNA and also the HCMV-DNA were detected separately in 1 [4%] of 26 paraffin-embedded autopsy and biopsy tissues. The HBV and HSV-1 specific antigens were separately diagnosed in 1 [4%] of 26 neonatal samples by IHC protocols. Also the HSV-2 antigen was seen in 5 [23%] of 22 liver autopsy and biopsy specimens. Co-infections with HCMV, HSV, HBV, HCV, and rotavirus were detected in these infants with hepatitis. Diagnosis of single and mixed molecular and antigenic traces of HCMV, HSV, HBV, HCV and rotavirus underlines the etiologic role of these viruses in clinical pathogenesis of neonatal hepatitis

Endothelial nitric oxide synthase gene t-786c polymorphism in renal transplant recipients

Nitric oxide [NO] is a major mediator in vascular biology, regulating regional blood flow. NO and the enzymes required for its production contribute to ischemia-reperfusion injury. The T-786C functional polymorphism in the promoter region substantially reduces promoter activity of the endothelial nitric oxide synthase [eNOS] gene and compromises endothelial NO synthesis. To examine the association between T-786C [rs 2070744] single nucleotide polymorphism [SNP] in eNOS gene and the development of acute rejection in renal transplant patients. 60 renal transplant recipients [30 with episodes of acute rejection [ARs] and 30 without rejection [non-ARs]], between June 2008 and March 2010, were included in this study. The polymorphism was determined by PCR-restriction fragment-length polymorphism analysis. The distribution of the genotypes were TT/TC/CC 60%, 33.4%, 6.6%, and 43%, 46.7%, 13.3% in ARs and non-ARs, respectively [p=0.28]. The frequency of T-allele was 76.7% and 66.3%; and for C-allele was 66.6% and 33.3% in ARs and non-ARs, respectively [p=0.09]. There were no significant associations between these polymorphisms and acute and chronic kidney allograft rejection. We could not detect any significant association between polymorphism in T-786C of eNOS gene and the development of acute rejection