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1.
Int J Cardiol Heart Vasc ; 31: 100648, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-33088900

RESUMO

AIMS: The aim of this study was to examine the association of influenza infection and vaccination with extent of cardiac damage during acute myocardial infarctions (AMIs) as measured by serum biomarkers and left ventricular ejection function (LVEF) in patients. METHODS: Post-hoc analysis was performed on data from a prospective case-control study of influenza and AMI, conducted in a tertiary care hospital in Sydney, Australia. We included 275 cases of AMI, aged ≥ 40 years admitted to the cardiology during the study period. RESULTS: Mean and median CK-MB levels were significantly higher among unvaccinated group compared to vaccinated group (p value < 0.05). Troponin levels were also higher among unvaccinated group compared to vaccinated group; although not statistically significant. Troponin and CKMB values were not statistically different among influenza positive cases and influenza negative cases. Large size infarcts were less frequent among vaccinated cases compared to unvaccinated cases (25% vs 35.5%) and were more frequent among influenza positive cases compared to influenza negative cases (35.3% vs 31.5%), however differences were not statistically significant. LVEF was lower among vaccinated cases compared to unvaccinated cases (62.5% vs. 52.8%) and influenza positive cases compared to influenza negative cases (58.8% vs 55.4), however differences were not significant. CONCLUSION: Lower CKMB levels among vaccinated groups showed that influenza vaccine may have a protective effect against large infarcts, therefore influenza vaccination should be recommended for high risk groups. The study suggests an association of larger infarcts with influenza infection, but larger studies are required to confirm this.

2.
Retrovirology ; 3: 92, 2006 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-17169163

RESUMO

BACKGROUND: Protein methylation is recognized as a major protein modification pathway regulating diverse cellular events such as protein trafficking, transcription, and signal transduction. More recently, protein arginine methyltransferase activity has been shown to regulate HIV-1 transcription via Tat. In this study, adenosine periodate (AdOx) was used to globally inhibit protein methyltransferase activity so that the effect of protein methylation on HIV-1 infectivity could be assessed. RESULTS: Two cell culture models were used: HIV-1-infected CEM T-cells and HEK293T cells transfected with a proviral DNA plasmid. In both models, AdOx treatment of cells increased the levels of virion in culture supernatant. However, these viruses had increased levels of unprocessed or partially processed Gag-Pol, significantly increased diameter, and displayed reduced infectivity in a MAGI X4 assay. AdOx reduced infectivity equally in both dividing and non-dividing cells. However, infectivity was further reduced if Vpr was deleted suggesting virion proteins, other than Vpr, were affected by protein methylation. Endogenous reverse transcription was not inhibited in AdOx-treated HIV-1, and infectivity could be restored by pseudotyping HIV with VSV-G envelope protein. These experiments suggest that AdOx affects an early event between receptor binding and uncoating, but not reverse transcription. CONCLUSION: Overall, we have shown for the first time that protein methylation contributes towards maximal virus infectivity. Furthermore, our results also indicate that protein methylation regulates HIV-1 infectivity in a complex manner most likely involving the methylation of multiple viral or cellular proteins and/or multiple steps of replication.


Assuntos
Adenosina/análogos & derivados , Adenosina/farmacologia , HIV-1/patogenicidade , Metiltransferases/antagonistas & inibidores , Ácido Periódico/farmacologia , Proteínas/metabolismo , Adenosina/química , Linhagem Celular , Proteínas de Fusão gag-pol/metabolismo , Produtos do Gene vpr/metabolismo , HIV-1/efeitos dos fármacos , HIV-1/ultraestrutura , Células HeLa , Humanos , Metilação , Linfócitos T/virologia , Vírion/efeitos dos fármacos , Vírion/metabolismo , Produtos do Gene vpr do Vírus da Imunodeficiência Humana
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