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Showing 2 results for Yavari
The Prevalence and Antibiotic Susceptibility of Shigella in Patients Referred to Health Center Iaboratory of Isfahan Medical University, 2006
R Nosoohian, M Yavari, A Ajami, M Sadegh,
Volume 1, Issue 1 (Spring - Summer 2007 [PERSIAN] 2007)
Abstract

Abstract Background and objectives :Epidemic dysentery, which can be caused by different organisms, is a major problem in developing countries. The cause variability and drug resistance make the treatment difficult. This study was carried out to determine the prevalence and antimicrobial susceptibility patterns of Shigella in Isfahan reference laboratory. Materials and Methods: In this descriptive study,200 stool samples referred to Isfahan Reference Laboratory were examined to detect possible microorganisms and their antibiotic sensitivity. Results:The Shigella and Salmonella infections rates were 17% and 0.5%. Shigella which is the most frequent cultured organism(97% of bacterial samples) includes: 79% Sd1, 15% Shigella Flexneri and 5% Shigella Sunnei. None of the samples was infected by Ecoli O157H7 or Entamoeba histolitica. The most effective ntibioticwas Ciprofloxacin (no resistance was seen to this antibiotic). Conclusion: The most important cause of bacterial dysentery in this study was shigellosis (sd1). Antibiotic resistance to ampicillin, Amoxiclav and Cotrimoxasole was quite high. This necessitates avoiding to empirical treatment of dysentery. Keywords: Dysentery, Antibiotic resistance, Salmonella, Shigella, Ecoli


Upregulated A20 (TNFAIP3) expression during respiratory syncytial virus infection in mice
Bahman Aghcheli , Romina Yavarinamini , Alireza Tahamtan ,
Volume 20, Issue 1 (Jan-Feb 2026)
Abstract
Background: Severe lower respiratory tract infections in infants and young children are frequently caused by respiratory syncytial virus (RSV), with the degree of illness strongly associated with disproportionate inflammatory activity. The signaling protein A20 (TNFAIP3) functions to inhibit NF-κB pathway activation, suggesting a possible role in tempering RSV-triggered lung inflammation. In this study, we assessed how RSV infection alters A20 gene expression in the lungs using a mouse model system.
Methods: Of the twelve female BALB/c mice allocated for the study, half were administered RSV intranasally at a concentration of 3 × 106 plaque-forming units (PFU), while the remaining six served as uninfected controls. All animals were humanely euthanized five days post-infection. Upon collection, lung tissue samples were immediately processed. The relative expression levels of messenger RNA (mRNA) for the TNFAIP3 gene, which encodes the A20 protein, were subsequently quantified using real-time reverse transcription polymerase chain reaction (RT-PCR).
Results: Analysis by quantitative PCR revealed that A20 expression was significantly higher in the lungs of RSV-infected mice compared with uninfected controls at day 5 post-infection (P = 0.0048).
Conclusion: The upregulation of A20 in RSV-infected mice suggests its potential role in modulating post-viral pulmonary inflammation.
 

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