RESUMO
Objective:To investigate the effect of botulinum toxin type A on children with odorihidrosis.Methods:From March 2017 to February 2021, 121 children with odorihidrosis, including 48 males and 73 females, aged 13 to 17 (15.9±1.2) years, were admitted to the Burn and Plastic Surgery Department of the 980 Hospital of PLA. There were 24 cases in mild group, 50 cases in moderate group and 47 cases in severe group. Botulinum toxin A was injected into 20-50 points on each side, and 1 U was injected into each point. The total amount of botulinum toxin A was 50-100 U on both sides.Results:Three groups of children were evaluated for efficacy, 24 cases of mild group was significantly effective in 23 cases, accounting for 95.8%. In the moderate group, 46 (92.0%) of 50 cases showed obvious effect. 49 cases (98.0%) were effective; In the severe group, 40 cases (85.1%) showed obvious effect and 45 cases (95.7%) were effective. Three groups of children with different efficacy had no statistical significance ( P>0.05). The significant efficiency in mild and moderate groups was higher than that in severe group, and the difference was statistically significant ( P<0.05). Conclusions:Botulinum toxin type A is effective in the treatment of children with mild and moderate bromhidrosis, and is worthy of clinical application.
RESUMO
BackgroundUnderstanding the host genetic architecture and viral immunity contributes to the development of effective vaccines and therapeutics for controlling the COVID-19 pandemic. Alterations of immune responses in peripheral blood mononuclear cells play a crucial role in the detrimental progression of COVID-19. However, the effects of host genetic factors on immune responses for severe COVID-19 remain largely unknown. MethodsWe constructed a powerful computational framework to characterize the host genetics-influenced immune cell subpopulations for severe COVID-19 by integrating GWAS summary statistics (N = 969,689 samples) with four independent scRNA-seq datasets (N = 606,534 cells). ResultsWe found that 34 risk genes were significantly associated with severe COVID-19, and the number of highly-expressed genetics-risk genes increased with the severity of COVID-19. Three cell-subtypes that are CD16+monocytes, megakaryocytes, and memory CD8+T cells were significantly enriched by COVID-19-related genetic association signals. Notably, three causal risk genes of CCR1, CXCR6, and ABO were specifically expressed in these three cell types, respectively. CCR1+CD16+monocytes and ABO+ megakaryocytes with significant up-regulated genes including S100A12, S100A8, S100A9, and IFITM1 confer higher risk to the cytokine storms among severe patients. CXCR6+ memory CD8+ T cells exhibit a notable polyfunctionality of multiple immunologic features, including elevation of proliferation, migration, and chemotaxis. Moreover, we observed a prominent increase in cell-cell interactions of both CCR1+ CD16+monocytes and CXCR6+ memory CD8+T cells in severe patients compared to normal controls among both PBMCs and lung tissues, and elevated interactions with epithelial cells could contribute to enhance the resident to lung airway for against COVID-19 infection. ConclusionsWe uncover a major genetics-modulated immunological shift between mild and severe infection, including an increase in up-regulated genetic-risk genes, excessive secreted inflammatory cytokines, and functional immune cell subsets contributing high risk to severity, which provides novel insights in parsing the host genetics-influenced immune cells for severe COVID-19.
