miR-205-5p plays a vital role in the inflammation of allergic rhinitis (AR). The study is designed to investigate the effects and mechanism of miR-205-5p in AR in vivo and in vitro. An OVA-induced mice model and anti-DNP IgE-induced RBL-2H3 cell model were established. The pathological alterations in the nasal mucosa were evaluated by hematoxylin-eosin (HE) staining. IgE and histamine levels were detected by corresponding kits and the expressions of PEBP1, High mobility group box-1 (HMGB1) and Toll-like receptor 4 (TLR4) were detected by western blot. The association of miR-205-5p and PEBP1 was determined by dual-luciferase reported assay. β-hexosaminidase activity was to evaluate the degranulation of RBL-2H3 cell. The pathological injury of nasal mucosa was significantly improved by miR-205-5p inhibition compared to AR mice. Following the treatment of miR-205-5p inhibitor, the levels of helper T cell (Th1) cytokines, interleukin (IL)-2 and interferon-γ (IFN-γ) were increased, while the levels of Th2 cytokines, IL-4 and IL-13, as well as the levels of IgE and histamine were markedly decreased in AR mice. We further found that miR-205-5P inhibition induced increased expression of PEBP1 and decreased expressions of HMGB1and TLR4. In vitro, miR-205-5P was verified to bind to PEBP1. PEBP1 silencing led to the reverse of miR-205-5p effects on decreasing the levels of β-hexosaminidase activity and histamine, as well as the expressions of HMGB1 and TLR4 on anti-DNP IgE-induced RBL-2H3 cells. Our results indicate that miR-205-5P inhibition may ameliorate pathological injury via PEBP1. MiR-205-5P/ PEBP1 could be potential drug targets in AR

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 OVAinduced 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.

Syndromic deafness caused by PTPN11 gene mutation has gradually come into the public’s view. In the past, many people did not understand its application mechanism and role and only focused on non-syndromic deafness, so the research on syndromic deafness is not in-depth and there is a large degree of lack of research in this area. In order to let the public know more about the diagnosis and gene function of deafness caused by PTPN11 gene mutation syndrome, this paper used deep learning technology to study the diagnosis and gene function of deafness caused by syndrome with the concept of intelligent medical treatment, and finally drew a feasible conclusion. This paper provided a theoretical and practical basis for the diagnosis of deafness caused by PTPN11 gene mutation syndrome and the study of gene function. This paper made a retrospective analysis of the clinical data of 85 deaf children who visited Hunan Children’s Hospital,P.R. China from January 2020 to December 2021. The conclusion were as follows: Children aged 1–6 years old had multiple syndrome deafness, while children under 1 year old and children aged 6–12 years old had relatively low probability of complex deafness; girls were not easy to have comprehensive deafness, but there was no specific basis to prove that the occurrence of comprehensive deafness was necessarily related to gender; the hearing loss of patients with Noonan Syndrome was mainly characterized by moderate and severe damage and abnormal inner ear and auditory nerve; most of the mutation genes in children were located in Exon1 and Exon3, with a total probability of 57.65%. In the course of the experiment, it was found that deep learning was effective in the diagnosis of deafness with PTPN11 gene mutation syndrome. This technology could be applied to medical diagnosis to facilitate the diagnosis and treatment of more patients with deafness with syndrome. Intelligent medical treatment was also becoming a hot topic nowadays. By using this concept to analyze and study the pathological characteristics of deafness caused by PTPN11 gene mutation syndrome, it not only promoted patients to find diseases in time, but also helped doctors to diagnose and treat such diseases, which was of great significance to patients and doctors. The study of PTPN11 gene mutation syndrome deafness was also of great significance in genetics. The analysis of its genes not only enriched the gene pool, but also provided reference for future research.

Allergic rhinitis is a common chronic disease, and its high incidence has a great negative impact on the quality of life of many people, especially children. In this paper, through in-depth analysis of NOS2 gene polymorphism, the protective mechanism of NOS2 gene against AR was studied to provide theoretical and scientific basis for the diagnosis of children with AR. It was concluded that the concentration of Immunoglobulin E (IgE) in rs2297516 was 0.24 IU/mL compared with that in normal children. rs3794766 specific IgE concentration in the children group was increased by 0.36 IU/mL, which was higher than that in the healthy children group; the difference of rs7406657 specific IgE concentration between the children group and the healthy group was 0.03 IU/mL. The total serum IgE concentration in the healthy children group was lower than that in the infant group, and the change of Rs3794766 was the least, followed by rs2297516 and rs7406657. This means that rs7406657 is the highest, rs2297516 had general genetic correlation with AR patients, and rs3794766 had the least genetic correlation with AR patients. Among the three groups of SNP loci, the healthy children group was higher than the patient children group, indicating that AR reduces the gene frequency of the three loci, and the reduction of gene frequency will also increase the susceptibility of children to AR, because the frequency of gene occurrence will affect the gene sequence. In conclusion, smart medicine and gene SNPS can promote the detection and treatment of AR.