Project description:Members of the genus Acinetobacter drag attention due to their importance in microbial pathology and biotechnology. OmpA is a porin with multifaceted functions in different species of Acinetobacter. In this study we identified this protein in Acinetobacter sp. SA01, an efficient phenol degrader strain, in different cellular and sub-cellular compartments (such as OM, OMV, biofilm and extracellular environment). Differential expression of proteins, including OmpA, under two conditions of phenol and ethanol supplementation was assessed using shotgun proteomics.
Project description:Studies of expression of mechanims of defense of the Acinetobacter sp.5-2Ac.02 from airborne hospital environment under stress conditions, such as SOS response (ROS response, heavy metals resistant mechanisms, peptides), as well as Quorum network (acetoin cluster and aromatics biodegradation cluster). Characterization functional of AcoN-like as negative regulator protein from acetoin cluster in Acinetobacter spp. Strains
Project description:Transcriptome analysis of RNA samples from whole heart Transverse aortic constriction (TAC) is a well-established method for studying the pathomechanisms of heart failure in animal models of cardiac hypertrophy. A number of studies have shown that the treatment of heart failure in this animal model of cardiac hypertrophy suggests that hypertrophy and fibrosis may be reversible. However, since TAC-release protocols that improve hemodynamics by releasing physical stenosis remain undefined, the histological characteristics and molecular biological regulatory mechanisms of the reversibility of cardiac hypertrophy and fibrosis are unknown. Therefore, this study aimed to establish a TAC release model and investigate the reversibility and plasticity mechanisms of myocardial hypertrophy, fibrosis, and angiogenesis. Four weeks post-TAC surgery, TAC release was conducted by cutting the aortic stenosis sutures. The TAC group exhibited severe myocardial hypertrophy, fibrosis, and increased angiogenesis, along with diastolic dysfunction. Conversely, the TAC-release group showed reduced hypertrophy and fibrosis, and improved diastolic function. Gene expression analysis highlighted Regulator of Calcineurin 1 as a key player in cardiac function and histological changes post-TAC release. Rcan1 knockdown exacerbated myocardial hypertrophy and fibrosis in the TAC-release group. This study sheds light on the functional, structural, and histological changes in the heart induced by TAC release and elucidates some of its regulatory mechanisms.
