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Golden Retriever muscular dystrophy (GRMD) is the most representative model for studying Duchenne muscular dystrophy (DMD) in humans, owing its phenotypic expression. DMD is a recessive disorder linked to the X chromosome in which the loss of dystrophin induces progressive weakness and degeneration of the skeletal and cardiac muscles, which lead to replacement by connective and adipose tissues. Onset of clinical signs occurs between 2 and 5 years of age, and many patients die from heart or respiratory failure. The main studies concerning dystrophic Golden Retrievers (DGR) sought to elucidate the pathophysiology of the disease and its clinical implications to develop therapies and alternative treatments to improve the quality of life and increase longevity of DMD patients. This review presents an overview of relevant contributions of the DGR model for elucidating DMD in humans.

The Golden Retriever muscular dystrophy (GRMD) is one of the best models of Duchenne muscular dystrophy (DMD), with similar genotypic and phenotypic manifestations. Progressive proliferation of connective tissue in the endomysium of the muscle fibers occurs in parallel with the clinical course of the disease in GRMD animals. Previous studies suggest a relationship between mast cells and the deposition of fibrous tissue due to the release of mediators that recruit fibroblasts. The aim of this study was to evaluate the presence of mast cells and their relationship with muscle injury and fibrosis in GRMD dogs of different ages. Samples of muscle groups from six GRMD and four control dogs, aged 2 to 8 months, were collected and analyzed. The samples were processed and stained with HE, toluidine blue, and Azan trichrome. Our results showed that there was a significant increase in infiltration of mast cells in all muscle groups of GRMD dogs compared to the control group. The average number of mast cells, as well as the deposition of fibrous tissue, decreased with age in GRMD dogs. In the control group, all muscle types showed a significant increase in the amount of collagenous tissue. This suggests increased mast cell degranulation occurred in younger GRMD dogs, resulting in increased interstitial space and fibrous tissue in muscle, which then gradually decreased over time as the dogs aged. However, further studies are needed to clarify the role of mast cells in the pathogenesis of fibrosis.

Invasive non-typhoidal Salmonella (iNTS) from the clonal type ST313 (S. Typhimurium ST313) is the major cause of invasive salmonellosis disease in Africa. Recently in Brazil, iNTS ST313 strains have been isolated from different sources, but there is a lack of understanding the mechanisms behind how these gut bacteria are able to break the gut barrier and reach the patient’s bloodstream. Herein, we compared 13 S. Typhimurium ST313 strains genomes isolated from human-blood cultures investigating aspects of virulence and resistance mechanisms. RNAseq analyses were also performed between the clinical blood isolate and SL1344 prototype, which belongs to ST19 and it was originally isolated from human feces. That analysis reveals here 15-upregulated genes related to pathogenesis in S. Typhimurium ST313 compared to SL1344 (ST19) such as sopD2, sifB, pipB, amongst others. We have also compared these clinical with non-clinical isolates from Brazil, a total of 22 genomes were studied by single nucleotide polymorphism (SNPs). The epidemiological analysis of 22 genomes of S. Typhimurium ST313 strains grouped them into three distinct clusters (A, B and C) by SNP analysis, where cluster A comprised five, the group B six, and the group C 11. The 13 clinical blood isolates were all resistant to streptomycin, 92. 3% strains were resistant to ampicillin and 15.39% strains were resistant to kanamycin. The resistance genes acrA, acrB, mdtK, emrB, emrR, mdsA and mdsB related to the production of efflux pumps were detected in all (100%) strains studied, similar to pathogenic traits investigated. In conclusion, we evidenced the S. Typhimurium ST313 strains isolated in Brazil are different of the African strains ST313. The elevated frequencies of virulence genes such as sseJ, sopD2 and pipB are a major concern in these Brazilian isolates, showing a higher pathogenic potential.

Introduction: Water treatment deficit and poor health, hygiene and sanitation infrastructure can contribute to disease transmission by dissemination of contaminants and microorganisms. As an alternative, carbon-based materials coated with antimicrobial molecules have been proposed for water treatment, but few supporting data are available so far. Hence, this study investigates the potential use of PAN-based activated carbon fibers (ACF) decorated with silver nanoparticles in water treatment.Methods: Silver nanoparticles were incorporated into the material using a cheap and electroless method. Field emission scanning electron microscopy (FEGSEM), Raman spectroscopy and X-ray photoelectron spectroscopy (XPS) characterized the whole material. The textile was mounted on a water filter prototype and had its capacity to remove bacterial (Escherichia coli) and fungal (Candida albicans, Aspergillus niger and Penicillium funiculosum) cells evaluated. Composition and toxicity of the filtered water were determined.Results: Water filtered by Ag@ACF for 2 and 24 h contained 0.254 mg/L and 0.964 mg/L Ag, respectively. Ag@ACF filtering successfully removed E. coli, C. albicans, and A. niger from the suspensions, but not P. funiculosum. Treated water was non-toxic for Vero cells and Drosophila melanogaster, but toxic for Raphidocelis subcapitata. Ag@ACF showed efficient microbial elimination when applied in water treatment. Silver nanoparticles released in aqueous medium may be responsible for R. subcapitata toxicity. Future studies should be conducted to reduce silver nanoparticles release from the carbon fiber.