Background:Infections caused by strains with multi-drug resistance are difficult to treat with standard antibiotics. Garlic is a powerful remedy to protect against infections of many bacteria, fungi and viruses. However, little is known about the potentials of fresh garlic extract (FGE) to improve the sensitivity of multi-drug resistant strains to antibiotics.Objectives:In this study, we used the disk diffusion method to investigate the antimicrobial activities of FGE and the combination of antibiotics with FGE, on methicillin-resistant Staphylococcus aureus (MRSA), Pseudomonas aeruginosa and Candida albicans, to evaluate the interactions between antibiotics and FGE.Materials and Methods:Clinical isolates were isolated from clinical specimens obtained from the inpatients at the First Affiliated Hospital of Xi’an Jiaotong University Health Science Center. The isolates consisted of MRSA, (n = 30), C. albicans (n = 30) and P. aeruginosa (n = 30). Quality control for CLSI (Clinical and Laboratory Standards Institute) disk diffusion was performed using S. aureus ATCC®25923, C. albicans ATCC®90028 and P. aeruginosa ATCC®27853. The 93 microorganisms were divided into four groups in a factorial design: control (deionized water), FGE, antibiotics without FGE, and antibiotics with FGE. Next, antibacterial activity was evaluated by measuring the diameter of inhibition zones according to performance standards for antimicrobial susceptibility testing of the Clinical and Laboratory Standards Institute (CLSI, formerly NCCLS).Results:Fresh garlic extract displayed evident inhibition properties against C. albicans and MRSA, yet weak inhibition properties against P. aeruginosa. Additionally, FGE showed the potential to improve the effect of antibiotics on antibiotic resistant pathogens. The synergism of fluconazole and itraconazole with FGE on C. albicans yielded larger sized inhibition zones compared with fluconazole and itraconazole without FGE (P < 0.01). The factorial analysis represents intense positive interaction effects (P < 0.01). The synergism of cefotaxime and ceftriaxone with FGE on P. aeruginosa yielded larger sized inhibition zones than cefotaxime and ceftriaxone without FGE (P < 0.01). The factorial analysis represents intense positive interaction effects (P < 0.01).Conclusions:The results suggest that FGE can improve the antibiotic sensitivity of these pathogens to some antibiotics.

Hereditary hearing impairment is a clinically and genetically heterogeneous disease. Whole‐exome sequencing was performed on seven affected and six unaffected members in a large Chinese family with autosomal‐dominant nonsyndromic hearing loss. The pathogenic variant of the gene encoding human topoisomerase IIβ TOP2B (c.G4837C:p.D1613H) was cosegregated with hearing loss in this pedigree and another two variants of TOP2B were detected in 66 sporadic patients with hearing loss. top2b knockdown led to significant defects in zebrafish inner ears and caused downregulation of akt which resulted in inactivation of PI3K‐Akt signalling. As a result, supporting cell and hair cell numbers were reduced through inhibition of the PI3K‐Akt pathway. Therefore, we hypothesized that mutations in TOP2B can cause autosomal‐dominant nonsyndromic hearing impairment through inhibition of the PI3K‐Akt signalling pathway. Database The whole‐exome sequence data in the study are available at the Sequence Read Archive database (NCBI) under the accession numbers , , , , , , , , , , . and , respectively.

Drug addiction is a recurrent, chronic brain disease. The existing treatment methods have limitations, such as poor adherence and inability to completely avoid relapse. Histidine triad nucleotide‐binding protein 1 (HINT1) is involved in many neuropsychiatric diseases, such as schizophrenia, pain, and drug dependence. Studies have confirmed that there is a genetic link between HINT1 and addictions such as nicotine and cocaine. However, there is no research on the role of HINT1 protein in morphine addiction at home and abroad. Thus, we designed this project by constructing different types of morphine addiction animal models, including conditioned place preference and behavioral sensitization. We comprehensively examined the participation of HINT1 protein in key brain regions associated with addiction, including prefrontal cortex, nucleus accumbens, corpus striatum, and hippocampus, in different stages of different models. In addition, we used HINT1 knockout mice to establish the above models and physical dependence model to investigate the effect of HINT1 protein deletion on morphine addiction‐related behaviors. We found that HINT1 has varying degrees of involvement in different stages of multiple addictive animal models. The absence of HINT1 can attenuate morphine‐mediated addictive behavior to a certain extent and can alleviate the withdrawal symptoms of morphine.

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