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Although the spread of plasmid-mediated antibiotic-resistant bacteria is a public health concern, food contamination with plasmid-mediated antibiotic-resistant Escherichia coli has not been well investigated in Vietnam. The aim of this study was to describe the prevalence of colistin-resistant, carbapenem-resistant and endemic blaCTX−M in extended-spectrum β-lactamase (ESBL)-producing E. coli isolates. Colistin- and carbapenem-resistant ESBL-producing E. coli were isolated from chickens in Vietnam and Japan. The results showed that 52% and 93% of Vietnamese chicken was isolated with colistin-resistant and AmpC/ESBL-producing E. coli, respectively, while 52.7% of Japanese chickens were isolated with AmpC/ESBL-producing E. coli. Carbapenem-resistant E. coli has not been isolated in Vietnam or Japan. Genotyping revealed that colistin-resistant E. coli harboured mcr-1, and most of the AmpC/ESBL-related genes were blaCTX−M−55 and blaCTX−M−65 together with blaTEM in Vietnamese chickens, and blaCMY−2 in Japanese chickens. Multidrug resistance analysis showed that ESBL-producing E. coli isolates were more resistant to quinolones, streptomycin, and chloramphenicol compared with colistin-resistant E. coli isolates from Vietnam, suggesting selection in ESBL-producing E. coli for multiple antibiotic resistance genes. In conclusion, colistin-resistant E. coli was detected in about half of the chicken meat samples, the majority of which were found to harbour mcr-1. The high prevalence of ESBL-producing E. coli has remained constant across the last five years, and the predominant blaCTX−M for ESBL-producing E. coli was found to be blaCTX−M−55 or blaCTX−M−65, with the coexistence of blaTEM in Vietnam. Our results can be implemented in monitoring systems to combat the development of antimicrobial resistance.

Bacterial blight is one of the most devastating rice diseases that cause huge economic loss worldwide. The cause of rice blight is Gram negative bacteria Xanthomonas oryzae pv. oryzae (X. oryzae pv. Oryzae). Since both silver nanoparticles and chitosan have antibacterial, antifungal and growth-stimulating effect, this work has focused on synthesizing chitosan stabilized silver nanoparticles (AgCSs) with small sizes and in vitro evaluating antibacterial activity against X. oryzae pv. oryzae bacteria. AgCSs were chemically synthesized by reducing silver nitrate by borohydride sodium in the presence of chitosan with optimization of the concentration of the reactants. AgCSs were characterized by UV/vis absorption spectra, field emission scanning electronic microscopy (FESEM), ImageJ software, zeta potential measurement, Fourier-transform infrared spectroscopy (FTIR) and X-ray diffraction. AgCSs have spherical configuration and narrow size distributions with different average sizes from 15 nm to 25 nm depending on the initial concentration of silver nitrate. All AgCSs colloidal systems were stable and exhibited no tendency for coagulation more than 5 months. It was the first time that chitosan-stabilized silver nanoparticles were assessed the in vitro antibacterial activity against bacterial blight VXO_281 strain. The disc diffusion method demonstrated that the smallest size silver nanoparticles (AgCS1) showed high antibacterial effect against the X. oryzae pv. oryzae VXO_281 strain with a concentration of more than 5 µg/mL and the inhibition zone was dose-dependent. The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of AgCS1 against X. oryzae pv. oryzae VXO_281 were 2.5 µg/mL and 20 µg/mL, respectively.

Aim Early life stress can induce epigenetic changes through genetic and environmental interactions and is a risk factor for depression. Brain-derived neurotrophic factor (BDNF) has been implicated in the pathophysiology of depression and antidepressant drug action. We investigated epigenetic changes at the BDNF exon I promoter in the hippocampus of adult rats subjected to maternal separation (MS) during early life and treated with an antidepressant drug as adults. Methods Rat pups were subjected to MS from postnatal day 1 to 21 and received chronic escitalopram (ESC) as adults. We assessed the effects of MS and ESC on BDNF exon I and DNA methyltransferases (DNMTs) mRNA levels (quantitative reverse-transcription polymerase chain reaction [qRT-PCR]), acetylated histone H3 and MeCP2 binding to the BDNF promoter I (chromatin immunoprecipitation followed by real-time PCR), and BDNF protein levels (enzyme-linked immunosorbent assay). Results The levels of BDNF protein, exon I mRNA, histone H3 acetylation, and DNMT1 and DNMT3a mRNA were altered in the MS group compared with the control group. Significant decreases were observed in the BDNF protein, exon I mRNA, and histone H3 acetylation levels and significant increases in DNMT1 and DNMT3a mRNA levels. The comparison between the MS + ESC and MS groups revealed significant increases in BDNF protein, exon I mRNA, and histone H3 acetylation levels and significant decreases in MeCP2 and DNMT1 and DNMT3a mRNA levels. Conclusion These findings indicate that MS induced epigenetic changes at the BDNF exon I promoter and these changes were prevented by antidepressant drug treatment during adulthood.

The group II metabotropic glutamate 2/3 (mGlu2/3) receptor antagonist LY341495 produces antidepressant-like effects by acting on mammalian target of rapamycin complex 1 (mTORC1) signaling and α-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors in rodent. We investigated whether LY341495 affects neuroplasticity via these mechanisms in rat primary hippocampal cultures under conditions of dexamethasone (DEX)-induced neurotoxicity. Ketamine was used for comparison. Hippocampal cultures were treated with LY341495 under conditions of DEX-induced toxicity. Changes in mTORC1-mediated proteins were determined by Western blotting analyses. Changes in dendritic outgrowth and spine density were evaluated via immunostaining. LY341495 significantly prevented DEX-induced decreases in the levels of mTORC1, 4E-BP1, and p70S6K phosphorylation as well as the levels of the synaptic proteins. These effects were blocked by pretreatment with the AMPA receptor inhibitor 2,3-dihydroxy-6-nitro-7sulfamoyl-benzo(f)quinoxaline (NBQX) and the mTORC1 inhibitor rapamycin. LY341495 significantly attenuated DEX-induced decreases in dendritic outgrowth and spine density. Pretreatment with rapamycin and NBQX blocked these effects of LY341495. Further analyses indicted that induction of BDNF expression produced by LY341495 was blocked by pretreatment with NBQX and rapamycin. LY341495 has neuroplastic effects by acting on AMPA receptor-mTORC1 signaling under neurotoxic conditions. Therefore, activation of AMPA receptor and mTORC1 signaling, which enhance neuroplasticity, may be novel targets for new antidepressants.

Early life stress can induce epigenetic changes through genetic and environmental interactions and is a risk factor for depression. Brain-derived neurotrophic factor (BDNF) has been implicated in the pathophysiology of depression and antidepressant drug action. We investigated epigenetic changes at the BDNF exon I promoter in the hippocampus of adult rats subjected to maternal separation (MS) during early life and treated with an antidepressant drug as adults.Rat pups were subjected to MS from postnatal day 1 to 21 and received chronic escitalopram (ESC) as adults. We assessed the effects of MS and ESC on BDNF exon I and DNA methyltransferases (DNMT) mRNA levels (quantitative reverse-transcription polymerase chain reaction), acetylated histone H3, and MeCP2 binding to the BDNF promoter I (chromatin immunoprecipitation followed by real-time polymerase chain reaction), and BDNF protein levels (enzyme-linked immunosorbent assay).The levels of BDNF protein, exon I mRNA, histone H3 acetylation, and DNMT1 and DNMT3a mRNA were altered in the MS group compared with the control group. Significant decreases were observed in the BDNF protein, exon I mRNA, and histone H3 acetylation levels and there were significant increases in DNMT1 and DNMT3a mRNA levels. The comparison between the MS + ESC and MS groups revealed significant increases in BDNF protein, exon I mRNA, and histone H3 acetylation levels and significant decreases in MeCP2 and DNMT1 and DNMT3a mRNA levels.These findings indicate that MS induced epigenetic changes at the BDNF exon I promoter and these changes were prevented by antidepressant drug treatment during adulthood.

Acute encephalitis syndrome (AES) is associated with high morbidity and mortality, and affects both children and adults. The main etiologic agent is Japanese encephalitis virus (JEV); however, there are also reports of Dengue virus (DENV) encephalitis. The objectives of this study were to determine the proportion of patients with encephalitis due to JEV during the 2014 outbreak in Son La Province in Vietnam and to explore the association of DENV in non-JEV viral encephalitis cases. Of 90 patients, 6 (6.7%) were positive for anti-JEV immunoglobulin M (IgM), 5 (5.6%) were positive for anti-DENV IgM, 30 (33.3%) were positive for both anti-JEV and anti-DENV IgM, and 56 (62.2%) were positive for flavivirus immunoglobulin G (IgG). In 5 patients with AES, who had positive anti-DENV IgM results in at least one of the paired serum samples, DENV was confirmed by neutralization testing. The incidence of JEV infection was high. There is still a need to maintain and strengthen the national JEV immunization program. This noticeable occurrence of DENV infection was not reported in Son La Province in 2013?2014. Our data suggested that in addition to JEV, DENV was also a causative agent of AES in 2014 in Son La Province, and this finding also confirmed the local occurrence of DENV infection., Japanese Journal of Infectious Diseases, 70(4), pp.357-361; 2017