SUMMARYThis study tests the hypothesis that peroxisome proliferator activated receptor-γ coactivator 1α (PGC-1α) and the integrity of gap junctions (GJs) were suppressed and the number of apoptotic bodies was increased in remote viable areas of left ventricle following acute myocardial infarction (AMI), which can be reversed by losartan therapy. Open chest surgery was consecutively performed on 32 adult male Sprague-Dawley rats. These rats were classified into 4 groups (n = 8/each group): group I, AMI (by ligation of left coronary artery (LCA) without treatment); group II, AMI with losartan 20 mg/kg/day; group III, sham control (without LAD ligation); and group IV, sham control with losartan 20 mg/kg/day. Echocardiography was performed on day 1 prior to AMI and on day 14 just before the rats were to be sacrificed for cellular and molecular studies. The results showed that mRNA expression of PGC-1α, integrated area (µm 2 ) of clustered connexin43 (Cx43) spots, and Cx43 GJs were substantially down-regulated and the number of apoptotic bodies was markedly increased in nontreated AMI rats compared with healthy control and losartan-treated AMI rats on day 14 following AMI (all values of P < 0.001). Additionally, day14 left ventricular (LV) ejection fraction was significantly lower in nontreated AMI rats than in healthy control and losartan-treated AMI rats (all values of P < 0.0001).Down-regulation of GJs and PGC-1α gene expression and cellular death were frequently observed in remote viable areas of LV following AMI. Losartan therapy reversed the adverse effects of AMI and preserved LV function. (Int Heart J 2007; 48: 533-546)
BackgroundCanine distemper virus (CDV) is present worldwide and produces a lethal systemic infection of wild and domestic Canidae. Pre-existing antibodies acquired from vaccination or previous CDV infection might interfere the interpretation of a serologic diagnosis method. In addition, due to the high similarity of nucleic acid sequences between wild-type CDV and the new vaccine strain, current PCR derived methods cannot be applied for the definite confirmation of CD infection. Hence, it is worthy of developing a simple and rapid nucleotide-based assay for differentiation of wild-type CDV which is a cause of disease from attenuated CDVs after vaccination. High frequency variations have been found in the region spanning from the 3'-untranslated region (UTR) of the matrix (M) gene to the fusion (F) gene (designated M-F UTR) in a few CDV strains. To establish a differential diagnosis assay, an amplification refractory mutation analysis was established based on the highly variable region on M-F UTR and F regions.ResultsSequences of frequent polymorphisms were found scattered throughout the M-F UTR region; the identity of nucleic acid between local strains and vaccine strains ranged from 82.5% to 93.8%. A track of AAA residue located 35 nucleotides downstream from F gene start codon highly conserved in three vaccine strains were replaced with TGC in the local strains; that severed as target sequences for deign of discrimination primers. The method established in the present study successfully differentiated seven Taiwanese CDV field isolates, all belonging to the Asia-1 lineage, from vaccine strains.ConclusionsThe method described herein would be useful for several clinical applications, such as confirmation of nature CDV infection, evaluation of vaccination status and verification of the circulating viral genotypes.
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