Non-genetic forms of antimicrobial (drug) resistance can result from cell-to-cell variability that is not encoded in the genetic material. Data from recent studies also suggest that non-genetic mechanisms can facilitate the development of genetic drug resistance. We speculate on how the interplay between non-genetic and genetic mechanisms may affect microbial adaptation and evolution during drug treatment. We argue that cellular heterogeneity arising from fluctuations in gene expression, epigenetic modifications, as well as genetic changes contribute to drug resistance at different timescales, and that the interplay between these mechanisms enhance pathogen resistance. Accordingly, developing a better understanding of the role of non-genetic mechanisms in drug resistance and how they interact with genetic mechanisms will enhance our ability to combat antimicrobial resistance.

Background: Enterococcus spp. are part of the normal flora of humans and animals. The nosocomial pathogenicity of Enterococcus spp. has emerged in recent years and has caused great concern due to developing of resistance to many antimicrobial agents. Objectives: The current study aimed to determine the resistance pattern and the type of virulence genes in Enterococcus spp. isolated from Milad hospital of Tehran, Iran. Materials and Methods: The current observational study was conducted from Apr 2014 to Feb 2015 on a total of 149 Enterococcus species isolated from Milad hospital in Tehran, Iran. The antibiotic susceptibility pattern of the bacteria was determined by the disc diffusion method for eight antibiotics. Minimum inhibitory concentration (MIC) of vancomycin was also done using agar-dilution assay by clinical and laboratory standards institute (CLSI) recommendations. The sodA, esp, cyl, ace and gelE genes were detected by polymerase chain reaction (PCR) assay. Results: About 37.5%, 73%, 86.6%, 35.8%, 69%, 60.8%, 45% and 79% of the isolates were resistant to vancomycin, tetracycline, gentam-

The World Health Organization acknowledges tuberculosis as a global threat.Tuberculosis infection is one of the top 10 causes of death worldwide. Nanotechnology and microbiology researchers are looking for new and safe nano drugs for eliminating Mycobacterium tuberculosis, the causative agent of tuberculosis. In this study, AgZnO nano-crystals (AgZnONCs) is synthesized via the decomposition of the precursor of oxalate method. Characterization of AgZnONCs were evaluated. Next, various concentrations of AgZnONCs, as well AgZnONCs+Rifampicin, were prepared. The MTT assay was employed to study the viability of human macrophage cell lines (THP-1) exposed to AgZnONCs. The bactericidal effects of AgZnONCs and AgZnONCs+Rifampicin were studied by Minimum Bactericidal Concentration (MBC) test. Subsequently, THP-1 were infected by H 37 Rv strain of M. tuberculosis (H 37 RvMtb). Also, bactericidal effects of AgZnONCs and AgZnONCs+Rifampicin were compared with ex-vivo conditions. The MBC of AgZnONCs and AgZnONCs+Rifampicin were ratios of 1:4 and 1:32 respectively (p-value <0.05). Also, more than 50% and 80% of THP-1 were alive in ratios of 1:4 and 1:32 in the presence of AgZnONCs, respectively. All phagocytic H 37 RvMtb were killed in the presence of AgZnONCs+Rifampicin (p-value <0.05),

In this study, gold nanoshell (GNS) were synthesised utilising the Halas method. The obtained nanoparticles (NPs) were characterised by Fourier-transform infrared (FTIR) spectroscopy, scanning electron microscopy (SEM), transmission electron microscopy (TEM), UV-Vis spectroscopy and dynamic light scattering. FTIR spectra demonstrated the successful functionalisation of silica NP with 3-aminopropyl trimethoxysilane. SEM and TEM images showed the morphology and diameter of the synthesised silica NPs (137 ± 26 nm) and GNS. UV-Vis spectrum illustrated the maximum absorbance of the resultant GNS and their average hydrodynamic diameter was 159 nm. For in vitro study, HCT-116 cells were exposed to gold nanoshells and intense pulsed light in different experiment groups. The results showed that exposing the cells to nanoshells and 30 s irradiation would efficiently decrease the viability percentage of the cells to about 30% compared with the control. A continued exposure of 4 min decreased the viability of the cancer cells to 20%. The results demonstrated that photothermal therapy would be promising in treatment of colon cancer cells utilising gold nanoshells.