ABSTRACT
The transcription factor nuclear factor of kappa-light-chain-enhancer of activated B cells (NF-κB) is expressed in brown adipocytes, but its role remains largely unknown in the cells. This issue was addressed in current study by examining NF-κB in brown adipocytes in vitro and in vivo. NF-κB activity was increased by differentiation of brown adipocytes through elevation of p65 (RelA) expression. The transcriptional activity of NF-κB was induced by the cold stimulation with an elevation in S276 phosphorylation of p65 protein. Inactivation of NF-κB in brown adipocytes made the knockout mice [uncoupling protein 1 (Ucp1)-CreER-p65f/f, U-p65-KO] intolerant to the cold environment. The brown adipocytes exhibited an increase in apoptosis, a decrease in cristae density and uncoupling activity in the interscapular brown adipose tissue (iBAT) of p65-KO mice. The alterations became severer after cold exposure of the KO mice. The brown adipocytes of mice with NF-κB activation (p65 overexpression, p65-OE) exhibited a set of opposite alterations with a reduction in apoptosis, an increase in cristae density and uncoupling activity. In mechanism, NF-κB inhibited expression of the adenine nucleotide translocase 2 (ANT2) in the control of apoptosis. Data suggest that NF-κB activity is increased in brown adipocytes by differentiation and cold stimulation to protect the cells from apoptosis through down-regulation of ANT2 expression.
ABSTRACT
IF1 (ATPIF1) is a nuclear DNA-encoded mitochondrial protein whose activity is inhibition of the F
ABSTRACT
Aims: To determine resistance rates and patterns of certain uropathogens, including E. coli, Klebsiella spp. and Pseudomonas spp., isolated from hospitalized urinary tract infections patients, to aminoglycoside antibiotics and to detect the most prevalent plasmidmediated aminoglycoside modifying enzymes (AMEs). Methods: Uropathogenic isolates (150) were recovered from urine specimens of hospitalized UTI patients in Cairo, Egypt and identified by conventional methods. The recovered uropathogens (E. coli, Klebsiella spp. and Pseudomonas spp.) were tested for their susceptibility to gentamicin, tobramycin, amikacin, neomycin, netilmicin, and kanamycin by disc diffusion method. Plasmid-mediated aminoglycoside resistance was determined by transformation experiments as well as by using plasmids as templates for PCR screening of the AMEs-coding genes aph(3')-I, aac(6')-I, aac(3)-I, aac(3)-II and ant(2'')-I in all resistant isolates. Results: Of a total of 150 uropathogenic clinical isolates, 110 isolates were of the above mentioned genera and were selected for the current study. Sixty three isolates (57.2%) were resistant to at least one aminoglycoside antibiotic. Highest and lowest resistance rates were observed to kanamycin (53.6%) and amikacin (7.2%), respectively. The resistance rates to gentamicin, neomycin, tobramycin and netilmicin were 33.6%, 24.5%, 23.6% and 14.5%, respectively. AMEs-coding genes were detected on the plasmids of 93.6% of resistant isolates with prevalence rates of 53.9% for ant(2'')-I, 38% for both aac(6')-I and aac(3)-II and 33.3% for aph(3')-I, while aac(3)-I gene was not detected in any of the tested resistant isolates. Double and triple combinations of AMEs-coding genes were detected in ich49.2% of resistant isolates. Conclusion: A high prevalence of plasmid-mediated resistance to aminoglycoside antibiotics in Gram negative uropathogens from hospitalized patients was observed. Uropathogens may represent potential reservoirs of panaminoglycoside resistance in hospitals, having on their plasmids combinations of AMEs-coding genes. Good infection control measures in Egyptian hospitals together with periodic screening of prevalence rates of different resistance genes are required.
ABSTRACT
OBJECTIVE To study 6 kinds of aminoglycoside-modifying enzymes (AMEs) genes in Chryseobacterium spp isolates. METHODS The isolates were identified by API20NE Gram-negative identification cards,and the susceptibility of antimicrobial agents was detected by MIC kits ( bioM?rieux ) 6 AMEs genes of 2 strains of Chryseobacterium spp were measured by PCR,and verified by DNA sequencing and sequence analysis. RESULTS In the 2 strains,2 kinds of resistant genes [aac(6′)-Ⅱ and ant(2″)-Ⅰ] were positive,and 4 kinds genes of AMEs [aac (6′)-Ⅰb,aac(3)-Ⅱ,ant(3″)-Ⅰ and aac(3)-Ⅰ] were negative.The amplicons were purified,sequenced and analyzed with BLAST 2.0 and found to be identical to aac(6′)-Ⅱ and ant(2″)-Ⅰ. CONCLUSIONS There are AMEs in Chryseobacterium spp isolates. This is the first report on AMEs genes [coexistance of aac(6′)-Ⅱ and ant(2″)-Ⅰ] in Chryseobacterium spp.