ABSTRACT
Background: Alcohol and tobacco are known teratogens. Historically, more severe prenatal alcohol exposure (PAE) and prenatal tobacco exposure (PTE) have been examined as the principal predictor of neurodevelopmental alterations, with little incorporation of lower doses or ecological contextual factors that can also impact neurodevelopment, such as socioeconomic resources (SER) or adverse childhood experiences (ACEs). Here, a novel analytical approach informed by a socio-ecological perspective was used to examine the associations between SER, PAE and/or PTE, and ACEs, and their effects on neurodevelopment. Methods: N = 313 mother-child dyads were recruited from a prospective birth cohort with maternal report of PAE and PTE, and cross-sectional structural brain neuroimaging of child acquired via 3T scanner at ages 8-11 years. In utero SER was measured by maternal education, household income, and home utility availability. The child's ACEs were measured by self-report assisted by the researcher. PAE was grouped into early exposure (<12 weeks), continued exposure (>=12 weeks), and no exposure controls. PTE was grouped into exposed and non-exposed controls. Results: Greater access to SER during pregnancy was associated with fewer ACEs (maternal education: ß = -0.293,p = 0.01; phone access: ß = -0.968,p = 0.05). PTE partially mediated the association between SER and ACEs, where greater SER reduced the likelihood of PTE, which was positively associated with ACEs (ß = 1.110,p = 0.01). SER was associated with alterations in superior frontal (ß = -1336.036, q = 0.046), lateral orbitofrontal (ß = -513.865, q = 0.046), caudal anterior cingulate volumes (ß = -222.982, q = 0.046), with access to phone negatively associated with all three brain volumes. Access to water was positively associated with superior frontal volume (ß=1569.527, q = 0.013). PTE was associated with smaller volumes of lateral orbitofrontal (ß = -331.000, q = 0.033) and nucleus accumbens regions (ß = -34.800, q = 0.033). Conclusion: Research on neurodevelopment following community-levels of PAE and PTE should more regularly consider the ecological context to accelerate understanding of teratogenic outcomes. Further research is needed to replicate this novel conceptual approach with varying PAE and PTE patterns, to disentangle the interplay between dose, community-level and individual-level risk factors on neurodevelopment.
ABSTRACT
OBJECTIVE: To investigate the effects of dezocine on pediatric anesthesia emergence delirium (PAED) and Ramsay sedation scores in patients undergoing Nuss procedures (minimally invasive surgery for repairing pectus excavatum). METHODS: Altogether, 100 patients with pectus excavatum who underwent Nuss procedures in our hospital were selected and randomly divided into group A (n=50) and group B (n=50). General anesthesia was carried out for each patient, with an anaesthetic of sufentanil for group A, and dezocine plus sufentanil for group B. The visual analogue scale (VAS) score and Ramsay sedation score were recorded at extubation (T0), 10 min after extubation (T1), 20 min after extubation (T2), 30 min after extubation (T3) and 60 min after extubation (T4) for assessment of pain intensity and sedative effect; PAED scale score was applied to observe the emergence delirium at awakening, 15 min after awakening and 30 min after awakening. Quality of recovery-15 (QoR-15) scale score was used to evaluate the quality of early rehabilitation 1 d after operation and 2 d after operation. The occurrence of adverse reactions was recorded. RESULTS: The VAS scores at T0, T1, T2, T3 and T4 in group B were lower than those in group A, and there was statistical significance between group A and group B (P<0.001). VAS scores at T1, T2 and T3 were lower than those recorded at T0 in both groups (P<0.01), while no significant difference was noted at other time points (P>0.05). Ramsay sedation scores were increased at T0, T1, T2, T3 and T4 in group B in comparison to that in group A (all P<0.001), while the scores recorded at T4 in group A and T3 and T4 in group B were increased compared with those recorded at T0 (all P<0.01), and there was no significant difference at other time points (all P>0.05). Compared with group A, PAED scores in group B were downregulated at each time point after wakening up (all P<0.01), while QoR-15 scores in group B were increased at 1 d and 2 d after surgery (all P<0.05); there was no significant difference in adverse reactions between the two groups (all P>0.05). CONCLUSION: Sufentanil combined with dezocine is efficacious in general analgesia and sedation, which can reduce emergence agitation, improves the quality of rehabilitation and is relatively safe for patients undergoing minimally invasive repairing of pectus excavatum.
ABSTRACT
Prenatal alcohol exposure (PAE) interferes with neurodevelopment. The brain is particularly susceptible to the adverse consequences of prenatal alcohol exposure, and numerous studies have documented changes to brain anatomy and function, as well as consequences for cognition, behavior, and mental health. Studies in typically developing individuals have shown that the brain undergoes dynamic developmental processes over an individual's lifespan. Furthermore, magnetic resonance imaging (MRI) studies in other neurodevelopmental and psychiatric disorders have shown that their developmental trajectories differ from the typical pattern. Therefore, to understand long-term clinical outcomes of fetal alcohol spectrum disorders (FASD), it is necessary to investigate changes in neurodevelopmental trajectories in this population. Here we review studies that have used MRI to evaluate changes in brain structure and function over time via cross-sectional or longitudinal methods in individuals with PAE. Research demonstrates that individuals with PAE have atypical cortical and white matter microstructural developmental trajectories through childhood and adolescence. More research is needed to understand how factors such as sex and postnatal experiences may further mediate these trajectories. Furthermore, nothing is known about the trajectories beyond young adulthood.
ABSTRACT
The mechanism of sevoflurane preconditioning-induced neuroprotection is poorly understood. This study was aimed at identifying microRNAs (miRNAs) involved in the protective effect of sevoflurane preconditioning against hypoxic injury using the miRCURYTM LNA Array. The screened differentially expressed miRNAs were further validated using qRT-PCR. Finally, after transfection of miRNA (miR-101a or miR-34b) mimics or inhibitor, MTT and flow cytometry assays were used to evaluate cell survival and apoptosis in sevoflurane preconditioning. qRT-PCR confirmed the changes in expression of differentially expressed miRNAs that were screened by the microarray: down-regulation of rno-miR-101a, rno-miR-106b, and rno-miR-294 and up-regulation of rno-miR-883, rno-miR-16, and rno-miR-34b. MiR-101a and miR-34b were the most differentially expressed miRNAs. Sevoflurane preconditioning-inhibited apoptosis and preconditioning-enhanced cell viability of PC12 cells were significantly attenuated by transfection of miR-101a mimetic or miR-34b inhibitors, but were significantly enhanced by transfection of miR-34b mimetic. Therefore, a number of miRNAs, including miR-101a and miR-34b, might play important roles in the neuroprotection induced by sevoflurane preconditioning. Such miRNAs might provide novel targets for preventive and therapeutic strategies against cerebral ischemia-reperfusion injury.