Prepubertal oral exposure to relevant doses of acrylamide impairs the testicular antioxidant system in adulthood, increasing protein carbonylation and lipid peroxidation.

The increased prevalence of human infertility due to male reproductive disorders has been linked to extensive exposure to chemical endocrine disruptors. Acrylamide (AA) is a compound formed spontaneously during the thermal processing of some foods that are mainly consumed by children and adolescents. We previously found that prepubertal exposure to AA causes reduced sperm production and functionality. Oxidative stress is recognized as the main cause of reduced sperm quality and quantity. In this sense, our objective was to evaluate the expression and activity of genes related to enzymatic antioxidant defense, nonprotein thiols, lipid peroxidation (LPO), protein carbonylation (PC) and DNA damage in the testes of rats exposed to acrylamide (2.5 or 5 mg/kg) from weaning to adult life by gavage. For the AA2.5 and AA5 groups, there were no alterations in the transcript expression of genes related to enzymatic antioxidant defense. The enzymatic activities and metabolic parameters were also not affected in the AA2.5 group. For the AA5 group, the enzymatic activities of G6PDH and GPX were reduced, SOD was increased, and protein carbonylation (PC) was increased. Data were also evaluated by Integrate Biomarker Response (IBRv2), a method to analyze and summarize the effects on biomarkers between doses. The IBRv2 index was calculated as 8.9 and 18.71 for AA2.5 and AA5, respectively. The following biomarkers were affected by AA2.5: decreased enzymatic activities of G6PDH, SOD, and GPX, increased GST and GSH, increased LPO and PC, and decreased DNA damage. For AA5, decreased enzymatic activities of G6PDH, GST, CAT and GPX, increased SOD and GSH, increased PC, and decreased LPO and DNA damage were observed. In conclusion, AA exposure during the prepubertal period causes imbalances in the testicular enzymatic antioxidant defense, contributing to the altered spermatic scenario in the testes of these rats.

Norovirus Epidemiology and Genotype Circulation during the COVID-19 Pandemic in Brazil, 2019-2022.

Norovirus stands out as a leading cause of acute gastroenteritis (AGE) worldwide, affecting all age groups. In the present study, we investigated fecal samples from medically attended AGE patients received from nine Brazilian states, from 2019 to 2022, including the COVID-19 pandemic period. Norovirus GI and GII were detected and quantified using RT-qPCR, and norovirus-positive samples underwent genotyping through sequencing the ORF1/2 junction region. During the four-year period, norovirus prevalence was 37.2%, varying from 20.1% in 2020 to 55.4% in 2021. GII genotypes dominated, being detected in 92.9% of samples. GII-infected patients had significantly higher viral concentrations compared to GI-infected patients (median of 3.8 × 107 GC/g and 6.7 × 105 GC/g, respectively); and patients aged >12-24 months showed a higher median viral load (8 × 107 GC/g) compared to other age groups. Norovirus sequencing revealed 20 genotypes by phylogenetic analysis of RdRp and VP1 partial regions. GII.4 Sydney[P16] was the dominant genotype (57.3%), especially in 2019 and 2021, followed by GII.2[P16] (14.8%) and GII.6[P7] (6.3%). The intergenogroup recombinant genotype, GIX.1[GII.P15], was detected in five samples. Our study is the first to explore norovirus epidemiology and genotype distribution in Brazil during COVID-19, and contributes to understanding the epidemiological dynamics of norovirus and highlighting the importance of continuing to follow norovirus surveillance programs in Brazil.

Diagnostic Accuracy of the Short Physical Performance Battery for Detecting Frailty in Older People.

BACKGROUND: The Short Physical Performance Battery (SPPB) is widely used to predict negative health-related outcomes in older adults. However, the cutoff point for the detection of the frailty syndrome is not yet conclusive. OBJECTIVE: The aim of this study was to determine the diagnostic value of the SPPB for detecting frailty in community-dwelling older adults. DESIGN: This was a population-based cross-sectional study focusing on households in urban areas. A total of 744 people who were 65 years old or older participated in this study. METHODS: Frailty was determined by the presence of 3 or more of the following components: unintentional weight loss, self-reported fatigue, weakness, low level of physical activity, and slowness. Diagnostic accuracy measures of the SPPB cutoff points were calculated for the identification of frailty (individuals who were frail) and the frailty process (individuals who were considered to be prefrail and frail). Receiver operating characteristic curves were constructed. Odds ratios for frailty and the frailty process and respective CIs were calculated on the basis of the best cutoff points. A bootstrap analysis was conducted to confirm the internal validity of the findings. RESULTS: The best cutoff point for the determination of frailty was ≤ 8 points (sensitivity = 79.7%; specificity = 73.8%; Youden J statistic = 0.53; positive likelihood ratio = 3.05; area under the curve = 0.85). The best cutoff point for the determination of the frailty process was ≤ 10 points (sensitivity = 75.5%; specificity = 52.8%; Youden J statistic = 0.28; positive likelihood ratio = 1.59; area under the curve = 0.76). The adjusted odds of being frail and being in the frailty process were 7.44 (95% CI = 3.90-14.19) and 2.33 (95% CI = 1.65-3.30), respectively. LIMITATIONS: External validation using separate data was not performed, and the cross-sectional design does not allow SPPB predictive capacity to be established. CONCLUSIONS: The SPPB might be used as a screening tool to detect frailty syndrome in community-dwelling older adults, but the cutoff points should be tested in another sample as a further validation step.