longitudinal-evaluation-auditory-speech-performance-pediatric

Longitudinal Evaluation of Auditory and Speech Performance in Pediatric Cochlear Implant Recipients Using IT-MAIS, MESP, CAP, and SIR Scales

Considerable variability in auditory and speech outcomes among pediatric cochlear implant (CI) recipients has raised ongoing debate regarding whether ...

Central South University (Hunan Children's Hospital)

Long noncoding RNA nuclear enriched abundant transcript 1 (lnc-NEAT1) and its target microRNA-125a (miR-125a) are reported to regulate immune and inflammation process in allergic rhinitis (AR). Hence, this study intended to investigate the correlation between lnc-NEAT1 and miR-125a expressions, as well as their clinical values in pediatric AR patients.

Aberrant expressions of circulating lncRNA NEAT1 and microRNA-125a are linked with Th2 cells and symptom severity in pediatric allergic rhinitis.

Allergic rhinitis (AR) threatens patient survival. CD4 T cells play key roles in AR progression. Long non-coding RNAs (lncRNAs) are key regulators of cell differentiation. Therefore, we investigated the molecular mechanism of the lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in AR. Expression levels of MALAT1, microRNA (miR)-135b-5p, interleukin-4 (IL-4), and GATA-binding protein 3 (GATA-3) in the nasal mucosa of AR patients were quantified. CD4 T cells were isolated from the peripheral blood of healthy volunteers and treated with ovalbumin (OVA) and Th2 inducers. After MALAT1 and miR-135b-5p levels changed in CD4 T cells, the proportion of IL-4-expressing cells and the levels of IL-4 and GATA-3 in OVA-induced CD4 T cells were determined. Binding relationships among MALAT1, miR-135b-5p, and GATA-3 were predicted and verified. Rescue experiments were performed to confirm the role of the MALAT1/miR-135b-5p/GATA-3 axis in Th2 differentiation of CD4 T cells. MALAT1, IL-4, and GATA-3 expression was upregulated, whereas miR-135b-5p expression was downregulated, in patients with AR. MALAT1 knockdown or miR-135b-5p overexpression in CD4 T cells notably decreased the proportion of IL-4-expressing cells and downregulated GATA-3 and IL-4 expression in OVA-induced CD4 T cells. MALAT1 and GATA-3 exhibited competitive binding toward miR-135b-5p. MALAT1 facilitated CD4 T cell Th2 differentiation via the miR-135b-5p/GATA-3 axis. MALAT1 facilitated AR development by facilitating CD4 T cell Th2 differentiation via the miR-135b-5p/GATA-3 axis. This study may provide guidance for clinical treatment of AR.

Long non-coding RNA MALAT1 promotes Th2 differentiation by regulating microRNA-135b-5p/GATA-3 axis in children with allergic rhinitis.

Hypoxic-ischemic encephalopathy (HIE) represents a leading cause of morbidity and mortality among neonates. However, the underlying molecular mechanisms of HIE remain largely elusive. A HIE animal model was established, and neural stem cells (NSCs) underwent oxygen-glucose deprivation/reoxygenation (OGD/R) to mimic HIE in vitro. The HIE-induced brain injury was evaluated using a battery of assessments, including the Morris water maze test, wire hanging test, cylinder test, TTC, TUNEL, IHC, and IF staining. Subsequently, the expressions of budding uninhibited by benzimidazoles related 1 (BUBR1) and signal transducer and activator of transcription 3 (STAT3) were examined using immunoblotting and qRT-PCR. Furthermore, the interaction between BUBR1 and STAT3 was confirmed through co-immunoprecipitation assays. BUBR1 was observed to be downregulated in both the HIE model and in NSCs subjected to OGD/R. Notably, the restoration of BUBR1 expression was found to alleviate the detrimental effects of HIE, primarily by facilitating nerve regeneration. Further investigation revealed that BUBR1 also mitigated OGD/R-induced apoptosis in NSCs. Mechanistically, BUBR1 was shown to regulate the phosphorylation of STAT3, a crucial transcription factor involved in cell survival and regeneration. Moreover, BUBR1 alleviated OGD/R-induced apoptosis of NSCs and promoted nerve regeneration to protect HIE by regulating STAT3 phosphorylation. BUBR1 facilitated nerve regeneration by modulating STAT3 phosphorylation, thereby alleviating HIE.

BUBR1 Facilitated Nerve Regeneration by Modulating STAT3 Phosphorylation, Thereby Alleviating HIE in Neonatal Mice.

Hypoxic-ischemic encephalopathy (HIE) is an irreversible brain injury attributable to impaired blood oxygen delivery in the brain after perinatal asphyxia. The pathogeny of HIE is very complex, and there is still shortage of effective treatment. DA5-CH is a novel dual receptor agonist of glucose dependent insulin stimulating polypeptide (GIP) and glucagon like peptide-1 (GLP-1). However, the function and mechanism of DA5-CH in HIE remain unclear. In this paper, cultured cortical neurons were exposed to oxygen-glucose deprivation (OGD) and neonatal rats were subjected to hypoxic-ischemic damage to explore the protective effects of DA5-CH. Our work revealed that DA5-CH markedly increased cell viability, reduced intracellular ROS levels and DNA damage, and decreased cell apoptosis in OGD-treated cultured cortical neurons. In vivo, DA5-CH treatment significantly improved cognitive dysfunction and neuronal damage, decreased the infarct volume and neuronal death of hypoxic-ischemic (HI) neonatal rats. In addition, DA5-CH decreased TNFα, IL-1β and IL-6 levels in cortical tissue of HI neonatal rats and in microglia cells subjected to OGD. Moreover, DA5-CH treated microglia medium increased the cell viability, but decreased apoptosis of cortical neurons. DA5-CH suppressed NLRP3 inflammasome activation through inactivation of the TLR2/NF-κB signalling pathway. Furthermore, the protective effects of DA5-CH on the hypoxic-ischemic brain injury were antagonized by nigericin (an NLRP3 agonist). Taken together, our findings revealed that DA5-CH alleviates neonatal hypoxic-ischemic encephalopathy by inhibiting TLR2/NF-κB/NLRP3 mediated-neuroinflammation.

Novel GLP-1/GIP Dual Receptor Agonist Alleviates Neonatal Hypoxic-Ischemic Encephalopathy by Inhibiting TLR2/NF-κB/NLRP3 Mediated-Neuroinflammation : The role of DA5-CH in neonatal hypoxic-ischemic encephalopathy.

Article	Year
Aberrant expressions of circulating lncRNA NEAT1 and microRNA-125a are linked with Th2 cells and symptom severity in pediatric allergic rhinitis. Journal of clinical laboratory analysis\| PubMed ID: 35064698	2022
Long non-coding RNA MALAT1 promotes Th2 differentiation by regulating microRNA-135b-5p/GATA-3 axis in children with allergic rhinitis. The Kaohsiung journal of medical sciences\| PubMed ID: 36149748	2022
BUBR1 Facilitated Nerve Regeneration by Modulating STAT3 Phosphorylation, Thereby Alleviating HIE in Neonatal Mice. Cell biology international\| PubMed ID: 40470792	2025
Novel GLP-1/GIP Dual Receptor Agonist Alleviates Neonatal Hypoxic-Ischemic Encephalopathy by Inhibiting TLR2/NF-κB/NLRP3 Mediated-Neuroinflammation : The role of DA5-CH in neonatal hypoxic-i... Neurochemical research\| PubMed ID: 40673927	2025

Xionghui Wu

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