BackgroundPenile carcinoma (PC) is a rare, highly mutilating disease, common in developing countries. The evolution of penile cancer includes at least two independent carcinogenic pathways, related or unrelated to HPV infection.ObjectivesTo estimate the prevalence, identify HPV genotypes, and correlate with clinicopathological data on penile cancer.MethodsA retrospective cohort study involving 183 patients with PC undergoing treatment in a referral hospital in Goiânia, Goiás, in Midwestern Brazil, from 2003 to 2015. Samples containing paraffin embedded tumor fragments were subjected to detection and genotyping by INNO-LiPA HPV. The clinicopathological variables were subjected to analysis with respect to HPV positivity and used prevalence ratio (PR), adjusted prevalence ratio (PRa) and 95% confidence interval (CI) as statistical measures.ResultsThe prevalence of HPV DNA in PC was 30.6% (95% CI: 24.4 to 37.6), high-risk HPV 24.9% (95% CI: 18.9 to 31.3), and 62.5% were HPV 16. There was a statistical association between the endpoints HPV infection and HPV high risk, and the variable tumor grade II-III (p = 0.025) (p = 0.040), respectively. There was no statistical difference in disease specific survival at 10 years between the HPV positive and negative patients (p = 0.143), and high and low risk HPV (p = 0.325).ConclusionsThe prevalence of HPV infection was 30.6%, and 80.3% of the genotypes were identified as preventable by anti-HPV quadrivalent or nonavalent vaccine. HPV infections and high-risk HPV were not associated with penile carcinoma prognosis in this study.

Background The coronavirus disease (COVID-19) pandemic has impacted health services and healthcare systems worldwide. Studies have shown that hospital admissions for causes related to chronic non-communicable diseases (NCDs) have decreased significantly during peak pandemic periods. An analysis of the impact of the COVID-19 pandemic on hospital admissions for NCDs is essential to implement disability and mortality mitigation strategies for these groups. Therefore, this study aimed to analyze the impact of the COVID-19 pandemic on hospital admissions for NCDs in Brazil according to the type of NCD, sex, age group, and region of Brazil. Methods This is an ecological study conducted in Brazil. Data on hospital admissions from January 1, 2017 to May 31, 2021 were extracted from the Unified Health System’s Hospital Admissions Information System. The hospital admission rates per 100,000 thousand inhabitants were calculated monthly according to the type of NCD, sex, age group, and region of Brazil. Poisson regression models were used to analyze the impact of the COVID-19 pandemic on the number of hospital admissions. In this study, the pre-pandemic period was set from January 1, 2017 to February 29, 2020 and the during-pandemic from March 1, 2020 to May 31, 2021. Results There was a 27.0% (95.0%CI: -29.0; -25.0%) decrease in hospital admissions for NCDs after the onset of the pandemic compared to that during the pre-pandemic period. Decreases were found for all types of NCDs—cancer (-23.0%; 95.0%CI: -26.0; -21.0%), diabetes mellitus (-24.0%; 95.0%CI: -25.0%; -22.0%), cardiovascular diseases (-30.0%; 95.0%CI: -31.0%; -28.0%), and chronic respiratory diseases (-29.0%; 95.0%CI: -30.0%; -27.0%). In addition, there was a decrease in the number of admissions, regardless of the age group, sex, and region of Brazil. The Northern and Southern regions demonstrated the largest decrease in the percentage of hospital admissions during the pandemic period. Conclusions There was a decrease in the hospitalization rate for NCDs in Brazil during the COVID-19 pandemic in a scenario of social distancing measures and overload of health services.

Invasive aspergillosis is a common fungal infection in immunocompromised individuals. Some studies have shown that tolllike receptor and dectin-1 genetic polymorphisms may alter signaling pathways, thus increasing an individual's susceptibility to invasive aspergillosis. We investigated the pertinent literature to determine whether polymorphisms in the genes encoding tolllike receptors and dectin-1 increase the susceptibility to invasive aspergillosis. This study systematically reviewed the literature using the databases PubMed/PMC, Scopus, and Web of Science using the keywords invasive aspergillosis, polymorphism, Toll-like, and Dectin-1. From the initial search, 415 studies were found and according to our inclusion and exclusion criteria, eight studies were selected. Several studies described single-nucleotide polymorphisms (SNPs) that are associated with a greater susceptibility to invasive aspergillosis. These SNPs were found in the genes that encode toll-like receptors 1, 3, 4, and 5 and the gene that encodes dectin-1; upon activation, both cellular receptors initiate a signaling cascade that can result in the production of cytokines and chemokines. Thus, our literature review uncovered a significant association between polymorphisms in the genes that encode toll-like receptors and dectin-1 and invasive aspergillosis. More studies should be performed to better understand the relationship between toll-like receptor and dectin-1 genetic polymorphisms and invasive aspergillosis susceptibility.

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Resumo: A fibromialgia é uma disfunção neuroendócrina e reumática subsequente ou associada a dores difusas, insônia, fadiga e dores musculares generalizadas. Apesar de inúmeros estudos, métodos diagnósticos e tratamentos eficazes não são relatados para a fibromialgia. A diminuição dos níveis de serotonina (5-HT, 5-hidroxitriptamina) pode ocasionar maior sensibilidade aos estímulos da dor e acredita-se que a fibromialgia seja o resultado de mudanças anormais no processamento sensorial da dor. Este estudo teve como objetivo avaliar a frequência alélica e genotípica de um polimorfismo na região promotora do gene que codifica o transportador de serotonina (5-HTT) em um grupo de 24 mulheres diagnosticadas com fibromialgia e 20 controles saudáveis. Amostras de sangue periférico das pacientes e controles foram submetidas à extração de DNA e o polimorfismo genético foi avaliado por meio da reação em cadeia da polimerase. Os resultados foram comparados usando o teste exato de Fisher. As frequências alélicas obtidas para as pacientes com fibromialgia e controles foram respectivamente: alelo longo (L) 40,0% e 29,1%; alelo curto (S) 60% e 70,8% (p=0,4105). As frequências genotípicas obtidas para as pacientes com fibromialgia e controles foram respectivamente: L/L 12,5% e 15,0%; L/S 45,8% e 20,0%; S/S 41,6% e 65,0% (p=0,1900). As frequências alélicas e genotípicas obtidas para pacientes com fibromialgia e controles não diferiram significativamente neste estudo. Uma vez que a FM é uma patologia complexa e multifatorial, a análise de uma única variável genética parece ser insuficiente para explicar a etiologia da doença. Palavras-chave: Fibromialgia. Serotonina. Polimorfismo. Região promotora. Proteína transportadora membranar plasmática de serotonina.