Objectives: Pseudomonas aeruginosa is known as a leading cause of nosocomial infections worldwide. Antimicrobial resistance and biofilm production, as two main virulence factors of P. aeruginosa, are responsible for the persistence of prolonged infections. In this study, antimicrobial susceptibility pattern and phenotypic and genotypic characteristics of biofilm of P. aeruginosa were investigated. Results: A total of 80 clinical P. aeruginosa isolates were obtained. Isolates showed resistance to all antibiotics with a rate from 12.5% (n = 10) against amikacin and piperacillin/tazobactam to 23.75% (n = 19) to levofloxacin. Multidrugresistant P. aeruginosa accounted for 20% (n = 16). 83.75% (n = 67) of isolates showed biofilm phenotype. All three biofilm-related genes were found simultaneously in 87.5% (n = 70) of P. aeruginosa and 13.5% (n = 10) of the isolates had none of the genes tested. From the results of the present study, combination therapy including an anti-pseudomonal beta-lactam (piperacillin/tazobactam or ceftazidime) and an aminoglycoside or carbapenems (imipenem, meropenem) with fluoroquinolones in conjunction with an aminoglycoside can be used against Pseudomonas infections. However, reasonable antimicrobial use and high standards of infection prevention and control are essential to prevent further development of antimicrobial resistance. Combination strategies based on the proper anti-pseudomonal antibiotics along with anti-biofilm agents can also be selected to eradicate biofilm-associated infections.

Current anti-hepatitis B virus (HBV) regimen do not meet ideal result due to emerging resistance strains, cytotoxicity, and unfavorable adverse effects. In chronic HBV infection, high rates of sub-viral particles (SVPs) bearing HBV surface antigen (HBsAg) is a major obstacle regarding to raise effective immune responses and subsequently virus clearance. Development of potent HBsAg secretion inhibitors would provide a better insight into HBV immunopathogenesis and therapy. Investigating new non-toxic HBsAg secretion inhibitors targeting either viral or cellular factors could restore the immune response to remove virally infected hepatocytes after inhibiting SVPs. In this study, we overview several classes of HBV inhibitors with focus on their limitations and advantages over anti-HBsAg secretion potential.

To be effective, therapeutic cancer vaccines should stimulate both an effective cell-mediated and a robust cytotoxic CD8+ T-cell response against human papillomavirus (HPV)-infected cells to treat the pre-existing tumors and prevent potential future tumors. In this study, the therapeutic experiments were designed in order to evaluate antitumor effect against the syngeneic TC-1 tumor model. The anti-tumor efficacy of a HPV-16 E7 DNA vaccine adjuvanted with melatonin (MLT) was evaluated in a C57BL/6 mouse tumor model by measuring tumor growth post vaccination and the survival rate of tumor-bearing mice, analyzing the specific lymphocyte proliferation responses in control and vaccinated mice by MTT assay. The E7-specific cytotoxic T cells (CTL) were analyzed by lymphocyte proliferation and lactate dehydrogenates (LDH) release assays. IFN-γ, IL-4 and TNF-α secretion in splenocyte cultures as well as vascular endothelial growth factor (VEGF) and IL-10 in the tumor microenvironment were assayed by ELISA. Our results demonstrated that subcutaneous administration of C57BL/6 mice with a DNA vaccine adjuvanted with MLT dose-dependently and significantly induced strong HPV16 E7-specific CD8+ cytotoxicity and IFN-γ and TNF-α responses capable of reducing HPV-16 E7-expressing tumor volume. A significantly higher level of E7-specific T-cell proliferation was also found in the adjuvanted vaccine group. Furthermore, tumor growth was significantly inhibited when the DNA vaccine was combined with MLT and the survival time of TC-1 tumor bearing mice was also significantly prolonged. In vivo studies further demonstrated that MLT decreased the accumulation of IL-10 and VEGF in the tumor microenvironment of vaccinated mice. These data indicate that melatonin as an adjuvant augmented the cancer vaccine efficiency against HPV-associated tumors in a dose dependent manner.