Meta-Analysis of Biofilm Formation, Antibiotic Resistance Pattern, and Biofilm-Related Genes in Pseudomonas aeruginosa Isolated from Clinical Samples

Resistant microorganisms such as Pseudomonas aeruginosa grow by developing biofilms in hospitals. We aimed to investigate the biofilm formation and the frequencies of biofilm-related genes and their associations with antibiotic resistance pattern in P. aeruginosa isolated from Iranians' clinical samples. This review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We conducted a systematic literature search in scientific databases using medical subject heading terms, including "Pseudomonas aeruginosa,""biofilm formation,""biofilm-related genes,""antibiotic resistance,"and "prevalence,"to obtain related articles published from 1st January, 2000, to 30th March, 2019. The studies reporting the prevalence of biofilm formation, the frequencies of biofilm-related genes, and the antibiotic resistance pattern in P. aeruginosa retrieved from Iranian patients were included. Meta-analysis was performed using the Comprehensive Meta-Analysis software. The pooled rate of biofilm formation was calculated as 86.5 (95 confidence interval CI: 79-91.6). The combined frequencies of strong, moderate, and weak biofilms were 51% (95% CI: 37.4-64.4), 29.2% (95% CI: 20.9-39.1), and 25.4% (95% CI: 11.5-47.2), respectively. The pooled prevalence of laslR, algD, algU, ppyR, and pelF genes were 93.6% (95% CI: 88.1-96.6), 91.4% (95% CI: 80.8-96.4), 89.3% (95% CI: 85.2-92.3), 98.7% (95% CI: 96.5-99.6), and 93% (95% CI: 82.7-97.3), respectively. The highest combined antibiotic resistance rates of P. aeruginosa isolates were against piperacillin/tazobactam (90%). This study showed that biofilm formation was higher in multidrug-resistant (MDR) P. aeruginosa than non-MDRs. A significant correlation was observed between biofilm formation and antibiotic resistance in 50% of studies included in this review. © Copyright 2020, Mary Ann Liebert, Inc., publishers 2020

The biological basis and clinical significance of hormonal imprinting, an epigenetic process

The biological phenomenon, hormonal imprinting, was named and defined by us (Biol Rev, 1980, 55, 47-63) 30 years ago, after many experimental works and observations. Later, similar phenomena were also named to epigenetic imprinting or metabolic imprinting. In the case of hormonal imprinting, the first encounter between a hormone and its developing target cell receptor—usually at the perinatal period—determines the normal receptor-hormone connection for life. However, in this period, molecules similar to the target hormone (members of the same hormone family, synthetic drugs, environmental pollutants, etc), which are also able to bind to the receptor, provoke faulty imprinting also with lifelong—receptorial, behavioral, etc.,—consequences. Faulty hormonal imprinting could also be provoked later in life in continuously dividing cells and in the brain. Faulty hormonal imprinting is a disturbance of gene methylation pattern, which is epigenenetically inherited to the further generations (transgenerational imprinting). The absence of the normal or the presence of false hormonal imprinting predispose to or manifested in different diseases (e.g., malignant tumors, metabolic syndrome) long after the time of imprinting or in the progenies