Possible associations between Zika virus infection and hearing loss were observed during the epidemic in the Americas. To describe the auditory alterations, pathogenesis and recommendations for follow-up in individuals with prenatal or acquired Zika virus infection. Bibliographic research conducted in March/2018-April/2019 at the main available databases. Article selection, data extraction and quality evaluation were carried out by two independent reviewers. Studies containing auditory evaluation of patients with congenital or acquired Zika virus infection; and/or hypotheses or evidences on the pathophysiology of auditory impairment associated with Zika virus; and/or recommendations on screening and follow-up of patients with auditory impairment by Zika virus were included. A total of 27 articles were selected. Sensorineural and transient hearing loss were reported in six adults with acquired Zika virus infection. Of the 962 studied children, 482 had microcephaly and 145 had diagnostic confirmation of Zika virus; 515 of the 624 children with auditory evaluation performed only screening tests with otoacoustic emissions testing and/or automated click-stimuli auditory brainstem response testing. Studies in prenatally exposed children were very heterogeneous and great variations in the frequency of altered otoacoustic emissions and automated click-stimuli auditory brainstem response occurred across the studies. Altered otoacoustic emissions varied from 0% to 75%, while altered automated click-stimuli auditory brainstem response varied from 0% to 29.2%. Sensorineural, retrocochlear or central origin impairment could not be ruled out. One study with infected mice found no microscopic damage to cochlear hair cells. Studies on the pathogenesis of auditory changes in humans are limited to hypotheses and recommendations still include points of controversy. The available data are still insufficient to understand the full spectrum of the involvement of the auditory organs by Zika virus, the pathogenesis of this involvement or even to confirm the causal association between auditory involvement and virus infection. The screening and follow-up recommendations still present points of controversy.
To evaluate the effect of high-fidelity simulation of pediatric emergencies compared to case-based discussion on the development of self-confidence, theoretical knowledge, clinical reasoning, communication, attitude, and leadership in undergraduate medical students. 33 medical students were allocated to two teaching methods: high-fidelity simulation (HFS, n = 18) or case-based discussion (CBD, n = 15). Self-confidence and knowledge tests were applied before and after the interventions and the effect of HFS on both outcomes was estimated with mixed-effect models. An Objective Structured Clinical Examination activity was conducted after the interventions, while two independent raters used specific simulation checklists to assess clinical reasoning, communication, attitude, and leadership. The effect of HFS on these outcomes was estimated with linear and logistic regressions. The effect size was estimated with the Hedge's g. Both groups had an increase in self-confidence (HFS 59.1 × 93.6, p < 0.001; CDB 50.5 × 88.2, p < 0.001) and knowledge scores over time (HFS 45.1 × 63.2, p = 0.001; CDB 43.5 × 56.7, p-value < 0.01), but no difference was observed between groups (group*time effect in the mixed effect models adjusted for the student ranking) for both tests (p = 0.6565 and p = 0.3331, respectively). The simulation checklist scores of the HFS group were higher than those of the CBD group, with large effect sizes in all domains (Hedges g 1.15 to 2.20). HFS performed better than CBD in developing clinical reasoning, communication, attitude, and leadership in undergraduate medical students in pediatric emergency care, but no significant difference was observed in self-confidence and theoretical knowledge.
Aim: To describe NR3C1 exon-1F methylation and cortisol levels in newborns. Materials & methods: Preterm ≤1500 g and full-term infants were included. Samples were collected at birth and at days 5, ... Plain language summary We investigated the methylation of a gene, NR3C1 exon-1F, and cortisol levels in newborns. DNA methylation is a biochemical process that can modify gene activity. In the case... Tweetable abstract Preterm infants have higher rates of NR3C1 gene methylation and cortisol levels at birth than term infants, but this difference reverses over time in the first 3 months of life. ...
Background/Objectives: Prematurity is a significant global health concern, often associated with neurodevelopmental challenges. Solute Carrier Family 6 Member 4 (SLC6A4), the gene encoding the serotonin transporter, a key component in serotonin reuptake in the synaptic cleft, plays a key role in stress response and neurodevelopment. Epigenetic regulation of stress-related genes, such as SLC6A4, influences neonatal stress adaptation and developmental outcomes. This study aimed to quantify and compare DNA methylation levels at 13 CpG sites in the promoter region of the SLC6A4 gene between preterm and term neonates at three time points. Methods: A cohort of 46 preterm infants and a cohort of 49 full-term infants were analyzed. Blood samples collected at birth (D0), the fifth day (D5), and the thirtieth day (D30) were used to analyze DNA methylation, using bisulfite conversion and pyrosequencing. Results: Significant differences in SLC6A4 methylation were observed. At D0, CpGs 12 and 13 showed higher methylation in preterm infants. CpG 9 showed lower methylation in preterm infants at D5. Extremely preterm infants had the highest values of methylation at the three time points. Longitudinal mixed-effects analysis revealed distinct temporal patterns between groups. Total and site-specific methylation at CpGs 2, 8, and 9 increased over time in full-term infants, while methylation remained stable over time in very preterm and extremely preterm infants. Conclusions: This study reveals significant differences in SLC6A4 methylation between very preterm, extremely preterm, and full-term infants, highlighting the impact of prematurity and early-life stress on the epigenome. These findings contribute to improving our understanding of the epigenetic mechanisms shaping neurodevelopment and stress adaptation in neonates.
This study aims to describe neurological, visual, and auditory findings in children whose mothers had confirmed Zika virus (ZIKV) infection during pregnancy, with most of these children not presenting congenital microcephaly; Methods: an observational, longitudinal, and prospective study was conducted in Rio de Janeiro, Brazil, from March 2015 to January 2017, involving children with in utero exposure to Zika virus, following from birth up to 30 months of age. Results: Of the 2882 pregnant women admitted, 116 had a suspected ZIKV infection, of whom 33 had laboratory confirmation. Only one child presented with congenital microcephaly. Despite this, neurodevelopment delay was observed in 36.4% of children evaluated, radiological abnormalities in 29.1%, auditory abnormalities in 8.3%, and ophthalmological abnormalities in 10%. Conclusions: Newborns of mothers with confirmed ZIKV infection during pregnancy may present with varying degrees of visual, auditory, and neurological impairment, despite the presence of congenital microcephaly.
Aim: Promoter methylation of LINE-1 may be affected by prematurity, but there is little evidence in the literature.Materials & methods: Blood from premature and full-term neonates on days 0, 5, 30 and 90 was analyzed for DNA methylation percentage in a promoter region of the LINE-1, after bisulfite conversion and pyrosequencing.Results: Premature infants, as a whole, showed significantly lower methylation percentage at birth, but this difference diminished over time. However, the subgroup of extremely premature (<28 weeks gestational age) had higher methylation percentages, similar to full-term newborns.Conclusion: This research underscores the critical role of prematurity on the methylation pattern of LINE-1. These findings underline the complexity of epigenetic regulation in prematurity and emphasize the need for further studies.