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Full‐thickness cutaneous trauma, due to the lack of dermis, leads to difficulty in epithelialization by keratinocytes, developing a fibrotic scar, with less elasticity than the original skin, which may have disorders in predisposed individuals, resulting in hypertrophic scar and keloids. Biomedical materials have excellent characteristics, such as good biocompatibility and low immunogenicity, which can temporarily replace traditional materials used as primary dressings. In this work, we developed two dermal matrices based on Nile tilapia collagen, with (M_GAG) and without (M) glycosaminoglycans, using a sugarcane polymer membrane as a matrix support. To assess the molecular mechanisms driving wound healing, we performed qualitative proteomic analysis on the wound bed in an in vivo study involving immunocompetent murine models at 14 and 21 days post‐full‐thickness skin injury. Gene Ontology and Pathway analysis revealed that both skins were markedly represented by modulation of the immune system, emphasizing controlling the acute inflammation response at 14 and 21 days post‐injury. Furthermore, both groups showed significant enrichment of pathways related to RNA and protein metabolism, suggesting an increase in protein synthesis required for tissue repair and proper wound closure. Other pathways, such as keratinization and vitamin D3 metabolism, were also enriched in the groups treated with M matrix. Finally, both matrices improved wound healing in a full post‐thick skin lesion. However, our preliminary molecular data reveals that the collagen‐mediated healing matrix lacking glycosaminoglycan (M) exhibited a phenotype more favorable to tissue repair, making it more suitable for use before skin grafts. [ABSTRACT FROM AUTHOR]

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COVID-19 is an infectious disease caused by the SARS-CoV-2 virus, which induces a high release of pro-inflammatory chemokines and cytokines, leading to severe systemic disorders. Further, evidence has shown that recovered COVID-19 patients still have some symptoms and disorders from COVID-19. Physical exercise can have many health benefits. It is known to be a potent regulator of the immune system, which includes frequency, intensity, duration, and supervised by a professional. Given the confinement and social isolation or hospitalization of COVID-19 patients, the population became sedentary or opted for physical exercise at home, assuming the guarantee of the beneficial effects of physical exercise and reducing exposure to SARS-CoV-2. This study aimed to investigate the effects of a supervised exercise protocol and a homebased unsupervised exercise protocol on chemokine and cytokine serum levels in recovered COVID-19 patients. This study was a prospective, parallel, twoarm clinical trial. Twenty-four patients who had moderate to severe COVID-19 concluded the intervention protocols of this study. Participants were submitted to either supervised exercise protocol at the Clinical Hospital of the Federal University of Pernambuco or home-based unsupervised exercise for 12 weeks. We analyzed serum levels of chemokines (CXCL8/IL-8, CCL5/RANTES, CXCL9/ MIG, CCL2/MCP-1, and CXCL10/IP-10) and cytokines (IL-2, IL-4, IL-6, IL-10, IL-17A, TNF-α, and IFN-γ). Before the interventions, no significant differences were observed in the serum levels of chemokines and cytokines between the supervised and home-based unsupervised exercise groups. The CXCL8/IL-8 (p = 0.04), CCL2/MCP-1 (p = 0.03), and IFN-γ (p = 0.004) levels decreased after 12 weeks of supervised exercise. In parallel, an increase in IL-2 (p = 0.02), IL-6 (p = 0.03), IL-4 (p = 0.006), and IL-10 (p = 0.04) was observed after the supervised protocol compared to pre-intervention levels. No significant differences in all the chemokines and cytokines were found after 12 weeks of the home-based unsupervised exercise protocol. Given the results, the present study observed that supervised exercise was able to modulate the immune response in individuals with post-COVID-19, suggesting that supervised exercise can mitigate the inflammatory process associated with COVID-19 and its disorders. Clinical trial registration: https://ensaiosclinicos.gov.br/rg/RBR-7z3kxjk, identifier U1111-1272-4730. [ABSTRACT FROM AUTHOR]

Objectives: This study investigated the relationship between single-nucleotide polymorphisms (SNPs) in cytokine genes and the susceptibility to Squamous Intraepithelial Lesions (SIL), cervical cancer and HPV infection through a systematic review with meta-analysis. To verify the effect of SNPs, we also analyzed the transcription factor binding affinity using bioinformatics tools. Methods: Seven electronic databases (MEDLINE, Scielo, BIREME, PubMed, Scopus, Web of Science and Science Direct) were searched for case–control studies. Results: A total of 35 relevant case–control studies were meta-analyzed, including 7 cytokine genes and 15 SNPs. SNPs in IL-17A (rs2275913, rs3748067); IL-17 F (rs763780); IL-12A (rs568408); IL-12B (rs3212227); TNFA (rs1800629, rs361525); IL-1B (rs16944); IL-6 (rs1800795); IL-10 (rs1800896) genes were associated with increased risk for cervical cancer. No association was observed between meta-analyzed polymorphisms and SIL. Additional bioinformatics analysis suggested a possible transcriptional regulation pathway of the TNFA and IL-10 genes through the MZF1 (TNFA −308 G > A and IL-10 − 1082A>G) and ZNF263 (TNFA −238 G > A) transcription factors binding. Conclusion: Overall, 10 SNPs in cytokine genes were associated with increased risk for cervical cancer. Therefore, in our meta-analysis, these SNPs demonstrated to be potential biomarkers for predicting or identifying cases of high risk for SIL and cervical cancer. [ABSTRACT FROM AUTHOR]

Background: Chikungunya virus (CHIKV) is a global concern, inducing chikungunya fever and trigging an arthritogenic chronic phase beyond some severe forms. Outcomes of CHIKV infections in humans are dependent on genetic variations. Here, a systematic review was performed to show evidence of genetic variations on infection outcomes of patients. Methods: Searches were performed in Scopus, SciELO, MEDLINE/PubMed, Web of Science, OneFile (GALE), Periódicos CAPES and ScienceDirect Journals databases. The PICOS approach was used to assess the eligibility of records. A meta-analysis was also conducted to show an association between described alleles/genes and CHIKV infection outcome. Results: Reviews of genetic variants were conducted on genes: CD 209, OAS1, OAS2, OAS3, MIF, TLR-3, TLR-7, TLR-8, MYD-88, KIR, HLA-B; HLA-C; DRB1 and DQB1. Studies were performed on Gabon, Singapore, and India, including Indians, Malay, Gabonese and Chinese ethnicities and published between 2009–2017. The meta-analysis was performed with DRB1 *01; *03; *04; *07; *10; *11; *13; *14 and *15 and DQB1 *02; *03; *05 and *06 alleles with Indian population sample. Sampling power was >80% and a significant positive association between DRB1*14 and CHIKV infection was found (OR = 1.67, 95% CI = 1.04–2.67; p =.03). Conclusion: Majority of the studies were conducted in India. Meta-analysis suggests that DRB1*14 is related to the susceptibility of symptomatic CHIKV infection in Indian population. The literature about CHIKV infection and genetic variations is scarce. The precise role of genetic variation in CHIKV is not clear yet. Further studies are necessary to provide more concrete evidences. [ABSTRACT FROM AUTHOR]

Lovastatin is a drug in the statin class which acts as a natural inhibitor of 3-hydroxy-3-methylglutaryl, a coenzyme reductase reported as being a potential therapeutic agent for several diseases: Alzheimer's, multiple sclerosis, osteoporosis and due to its anti-cancer properties. Aspergillus terreus is known for producing a cholesterol reducing drug. This study sets out to evaluate the production of lovastatin by Brazilian wild strains of A. terreus isolated from a biological sample and natural sources. Carbon and nitrogen sources and the best physicochemical conditions using factorial design were also evaluated. The 37 fungal were grown to produce lovastatin by submerged fermentation. A. terreus URM5579 strain was the best lovastatin producer with a level of 13.96 mg/L. Soluble starch and soybean flour were found to be the most suitable substrates for producing lovastatin (41.23 mg/L) and biomass (6.1 mg/mL). The most favorable production conditions were found in run 16 with 60 g/L soluble starch, 15 g/L soybean flour, pH 7.5, 200 rpm and maintaining the solution at 32 °C for 7 days, which led to producing 100.86 mg/L of lovastatin and 17.68 mg/mL of biomass. Using natural strains and economically viable substrates helps to optimize the production of lovastatin and promote its use. [ABSTRACT FROM AUTHOR]