Objective To identify meaningful objective examination methods by analyzing the results of vari-ous objective examinations of children with recurrent vertigo(RVC).Methods Fifty children with RVC(29 in ver-tigo attacking group,21 in vertigo non-attacking group)and 20 children without RVC were selected.All partici-pants underwent a series of relevant objective examinations,the results of each examination were statistically ana-lyzed and the characteristic differences of each examination between the RVC group and the control group were ob-tained.Results ① The abnormal rate of sleep SpO2,high stimulation rate ABR and AHI in the RVC group were significantly higher than those in the control group(P＜0.05).② The abnormal rate of sleep SpO2 and high stimu-lation rate ABR in the vertigo attacking group were higher than those in the vertigo non-attacking group.There was a statistical difference between the two groups(P＜0.05).③ Pure tone audiometry(or conditioned play audiome-try),acoustic immittance,cranial MRI,positional test and vHIT were normal in both RVC group and normal con-trol group.Conclusion Continuous sleep SpO2 and high stimulation rate ABR are correlated with RVC,especially RVC during vertigo attacking.AHI is correlated with RVC,but not with the onset of vertigo.Clinically,continu-ous sleep SpO2 monitoring,PSG and high stimulation rate ABR can be used as auxiliary examinations for the diagno-sis of RVC.

Objective:To explore the relationship between sleep status and the disease in children with recurrent vertigo（RVC） by analyzing the objective sleep condition of children with recurrent vertigo. Methods:According to the diagnostic criteria of RVC, 50 children with RVC and 20 normal controls without RVC were selected. According to the vertigo questionnaire score, the RVC group was divided into mild, moderate and severe groups according to severity. Continuous polysomnography（PSG） was performed for all participants, and SPSS 25.0 statistical software was used to analyze the monitoring results. Results:①There were significant differences in sleep time of each period, total sleep time and sleep efficiency between RVC group and control group（P<0.05）, but there was no significant difference in sleep latency（P>0.05）. The specific manifestations were that the proportion of sleep time in N1 and N2 phases increased, the proportion of sleep time in N3 and REM phases decreased, the total sleep time and sleep efficiency decreased in RVC group. ②The abnormal rate of sleep apnea hypopnea index, that is, the proportion of AHI≥5 times/h and the abnormal rate of lowest blood oxygen saturation in RVC group were higher than those in normal control group. There was significant difference between the two groups（P<0.05）. ③There were significant differences in the proportion of AHI≥5 times/h and lowest SpO2 among mild group, moderate group and severe group（P<0.05）. ④There was no significant correlation between the degree of vertigo and the abnormal rate of AHI in children with RVC, but there was a negative correlation between the degree of vertigo and the abnormal rate of lowest SpO2 in children with RVC. Conclusion:Children with RVC are often accompanied by sleep disorders, clinicians should pay attention to both the symptoms of vertigo and sleep condition in children. Polysomnography is non-invasive and operable, providing a new idea to the auxiliary examination of RVC in children. It is of certain clinical significance for the comprehensive treatment of children with RVC to actively improve vertigo symptoms and pay attention to improving sleep quality.
Humans ; Child ; Polysomnography ; Sleep Apnea, Obstructive/diagnosis* ; Sleep ; Dizziness ; Vertigo/diagnosis*

Objective:To investigate the efficacy of recombinant human interferon α2b in the adjuvant treatment of neonatal pneumonia.Methods:A total of 60 children with neonatal pneumonia who received treatment in Lingbi County People's Hospital from January 2020 to January 2022 were included in this study. They were randomly divided into study and control groups ( n = 30/group). The control group was treated with conventional therapy and the study group was treated with recombinant human interferon α2b and conventional therapy. All children were treated for 7 days. The time to clinical symptom remission, total response rate, and inflammatory factor levels were compared between the two groups. Results:Before treatment, there were no significant differences in general data between the study and control groups (all P > 0.05). After treatment, the time to body temperature recovery, rale disappearance, cough disappearance, and shortness of breath disappearance in the study group were (4.03 ± 1.27) days, (5.13 ± 1.72) days, (4.96 ± 1.64) days, and (5.45 ± 1.52) days, respectively, which were significantly shorter than (5.13 ± 1.52) days, (6.73 ± 1.85) days, (6.73 ± 1.82) days, and (6.82 ± 1.74) days, respectively in the control group ( t = 3.04, 3.46, 3.95, 3.24, all P < 0.05). The total response rate in the study group was 93.3% (28/30), which was significantly higher than 80.0% (24/30) in the control group, and clinical efficacy was better in the study group than that in the control group ( Z = 2.40, P = 0.016). High-sensitivity C-reactive protein, procalcitonin, interleukin-6, and serum amyloid A in the study group were (2.96 ± 0.84) mg/L, (0.72 ± 0.33) μg/L, (6.25 ± 2.18) mg/L, and (3.48 ± 1.13) mg/L, respectively, which were significantly lower than (4.02 ± 1.53) mg/L, (1.16 ± 0.47) μg/L, (8.04 ± 2.06) ng/L, and (6.42 ± 2.03) mg/L, respectively in the control group ( t = 3.32, 4.19, 3.26, 6.93, all P < 0.05). Conclusion:Recombinant human interferon α2b for the adjuvant treatment of neonatal pneumonia can shorten the time to clinical symptom remission, decrease inflammatory factor levels, and improve clinical efficacy.

Objective:To explore the method of establishing a modified demyelination and myelination regeneration model induced by dicyclohexanone oxalyl dihydrazone (CPZ) in mice with multiple sclerosis (MS), and to analyze the image markers of demyelination and myelination regeneration in mouse MS model.Methods:After the intragastrically administered with sodium carboxymethyl cellulose (CMCNa) for one week, a total of 30 C57BL/6 male mice were randomly divided into the control group ( n=10), the demyelination group ( n=10), and the remyelination group ( n=10). The mice of the control group were immediately performed MR scanning and pathological specimen obtaining; the mice in the demyelination group were administered with intragastrical CPZ-CMCNa once a day for 6 weeks for inducing demyelination, then received MR scanning and specimen obtaining with the same protocols used in control group; the mice in the remyelination group were administered with intragastrical CPZ-CMCNa once a day for six weeks for demyelination, then CPZ was withdrawn and normal diet was given for another four weeks. Then MR scanning and specimen obtaining were performed with the same protocols used in the other two groups. Regions of interest (ROIs) were set at the rostrum of corpus callosum (rCC), the bilateral normal appearing white matters (NAWM) of the rostrum of corpus callosum, and the bilateral cerebral cortex (Cx). The normalized T 2WI (T 2-normalized), fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD) values were compared among the three groups by one-way ANOVA. Results:The demyelination and remyelination mice model of MS were successfully established. The T 2-normalized values of rCC in control group, demyelination group and remyelination group were 0.47±0.03, 0.72±0.04, 0.54±0.04, respectively, with statistically significant difference found ( F=90.511, P<0.05). Post-hoc multiple comparisons showed significant differences among those groups ( P<0.05). There was no significant difference of T 2-normalized value in NAWM and Cx among the three groups ( P>0.05). Moreover, there were significant differences in the FA values (0.36±0.04, 0.29±0.03, and 0.32±0.05), the MD values [(0.572±0.015), (0.598±0.034), and (0.626±0.043)×10 -3 mm 2/s], the AD values [(0.79±0.04), (0.77±0.06), and (0.83±0.04)×10 -3 mm 2/s], and the RD values [(0.46±0.02), (0.51±0.03), and (0.53±0.05)×10 -3 mm 2/s] of rCC of the control group, the demyelination group, and the remyelination group (all P<0.05). Significant difference was found in FA values between the demyelination group and the control group ( P<0.05), and in MD values between the remyelination group and the control group ( P<0.05), as well as in AD values between the remyelination group and the demyelination group ( P<0.05). There were also significant differences in RD values between the remyelination group and the control group, and the demyelination group and the control group (all P<0.05). However, no significant difference was found in all diffusion tensor imaging (DTI) metrics of NAWM and Cx among the three groups (all P>0.05). The LFB-eosin staining showed that the myelin sheath of rCC was lost in the demyelination group, and the rCC was partially regenerated and repaired in the remyelination group. Conclusion:The modified CPZ-CMCNa model can selectively induce demyelination and remyelination of rCC, and the changes of demyelination and remyelination of rCC in the modified CPZ-CMCNa model can be quantitatively detected by T 2WI combined with DTI, which might provide related theoretical basis for the study on dynamic changes of MS lesions.

Objective:To investigate the role of NOD-like receptor protein 3 (NLRP3) in the regulation of phagocytosis in Vibrio vulnificus ( V. vulnificus)-infected macrophages. Methods:Expression profiles of phagocytosis-related genes in PBS- and V. vulnificus-infected J774A.1 cells were analyzed by RNA-Seq. NLRP3-knockout (NLRP3 KO) J774A.1 cells were constructed using CRISPR-Cas9 gene-editing system. The phagocytosis of V. vulnificus and pHrodo RED-labelled Escherichia coli ( E. coli) bioparticles in parental and NLRP3 KO J774A.1 cells was detected by flow cytometry. Real-time PCR was performed to measure the expression of Fgr2 b gene at mRNA level in PBS- and V. vulnificus-treated parental and NLRP3 KO J774A.1 cells. Results:The expression of 18 phagocytosis-related genes was upregulated in V. vulnificus-infected J774A.1 cells than in PBS-treated J774A.1 cells ( P<0.05). There was a 5 bp deletion in the exon 2 of NLRP3 gene in NLRP3 KO J774A.1 cells, resulting in frameshift mutation and complete loss of NLRP3 expression. NLRP3 KO J774A.1 cells exhibited enhanced phagocytosis of V. vulnificus and pHrodo RED-labelled E. coli bioparticles than parental J774A.1 cells ( P<0.05). Besides, the expression of Fgr2 b gene at mRNA level was significantly increased in V. vulnificus-infected NLRP3 KO J774A.1 cells than in parental J774A.1 cells ( P<0.05). Conclusions:The phagocytosis of V. vulnificus in macrophages could be negatively regulated by NLRP3, which was possibly mediated through the regulation of Fgr2 b gene expression.

Objective:To explore the effects of maternal pre-pregnancy body mass index (BMI) and gestational weight gain and its subtypes on the risk of preeclampsia.Methods:Pregnant women delivered in the Department of Obstetrics and Gynecology of the First Affiliated Hospital of Shanxi Medical University from March 2012 to September 2016 were selected as the research subjects. According to the inclusion and exclusion criteria, 9 274 pregnant women were included. 901 preeclampsia pregnant women were selected as the case group, and 8 373 non-preeclampsia pregnant women were selected as the control group. General demographic characteristics, pre-pregnancy weight, height, lifestyle during pregnancy, reproductive history, and disease history of pregnant women were collected, and pre-pregnancy BMI and gestational weight gain were calculated. Unconditional logistic regression was used to analyze the relationship between pre-pregnancy BMI and weight gain during pregnancy and PE and its clinical subtypes.Results:Among the 901 preeclampsia after inclusion and exclusion, 401 cases were diagnosed as early-onset PE (EOPE), 500 cases were late-onset PE (LOPE), 178 cases were Mild PE (MPE), and 723 cases were severe PE (SPE). There were statistically significant differences between PE and non-PE pregnant women in terms of maternal age, residence, parity, family history of gestational diabetes and hypertension ( P<0.05). After adjusting for the above factors, the logistic regression analysis results showed that pre-pregnancy BMI<18.5 kg/m 2 and inadequate gestational weight gain were protective factors for PE ( OR=0.74, 95% CI: 0.56-0.98; OR=0.78, 95% CI: 0.62-0.99), while pre-pregnancy BMI≥24.0 kg/m 2 and excessive gestational weight gain were risk factors for PE ( OR=1.82, 95% CI: 1.54-2.14; OR=1.82, 95% CI: 1.54-2.15). After subtype analysis on PE, the results showed that pre-pregnancy BMI<18.5 kg/m 2 was a protective factor for EOPE and MPE ( OR=0.52, 95% CI: 0.32-0.83; OR=0.47, 95% CI: 0.23-0.97), while pre-pregnancy BMI≥24.0 kg/m 2 and excessive gestational weight gain were risk factors for clinical subtypes of PE. After stratification according to pre-pregnancy BMI, excessive gestational weight gain was the risk factor for PE ( OR=1.86, 95% CI: 1.51-2.30; OR=1.90, 95% CI: 1.39-2.60) in pregnant women 18.5 kg/m 2≤BMI<24.0 kg/m 2 and ≥24.0 kg/m 2. Inadequate gestational weight gain ( OR=0.55, 95% CI: 0.34-0.89) was a protective factor for PE in pregnant women with pre-pregnancy BMI≥24.0 kg/m 2. Excessive gestational weight gain ( OR=4.05, 95% CI: 1.20-13.69) was a risk factor for EOPE in pregnant women with pre-pregnancy BMI<18.5 kg/m 2. Excessive gestational weight gain was a risk factor for the clinical subtype of PE in pregnant women 18.5 kg/m 2≤BMI<24.0 kg/m 2 before pregnancy. Inadequate gestational weight gain was a protective factor for EOPE and MPE ( OR=0.39, 95% CI: 0.19-0.80; OR=0.29, 95% CI: 0.11-0.77) in pregnant women with pre-pregnancy BMI≥24.0 kg/m 2. Excessive weight gain was a risk factor for EOPE, LOPE and SPE ( OR=1.60, 95% CI: 1.06-2.42; OR=2.20, 95% CI: 1.44-3.37; OR=2.28, 95% CI: 1.58-3.29). Conclusions:Pre-pregnancy BMI and gestational weight gain affect the risk of preeclampsia and its clinical subtypes. In contrast, the influence of gestational weight gain on preeclampsia varies among different pre-pregnancy BMI groups. Therefore, it is recommended to pay attention to the changes in pre-pregnancy BMI and gestational weight gain simultaneously to reduce preeclampsia.

Objective:The aim of this study is to investigate the relationship between fat mass and obesity associated ( FTO) gene polymorphism and the risk of gestational diabetes mellitus (GDM), and provide clues and basis for the study of GDM mechanism. Methods:The case group of GDM pregnant women who delivered at the First Affiliated Hospital of Shanxi Medical University from March 1, 2012 to July 30, 2014 were selected, and matched the control group among non-GDM pregnant women by age, gestational age and residential address, and 324 cases and 318 controls were finally included. DNA was extracted and genotyped, and min P test and unconditional logistic regression model were used to estimate the relationship between FTO gene polymorphism and GDM. Results:At gene level, we did not find the association between FTO and the risk of GDM ( P>0.05). After adjusted for family history of diabetes, pre-pregnancy body mass index and multiple comparisons using false discovery rate method, unconditional logistic regression analysis showed that pregnant women who carried the rs11075995 TT genotype ( OR=0.59, 95 %CI: 0.35-0.89), rs3826169 GG genotype ( OR=0.59, 95 %CI: 0.35-0.88), and rs74245270 GA genotype ( OR=0.69, 95 %CI: 0.49-0.98), GA or AA genotype( OR=0.70, 95 %CI: 0.50-0.97) had reduced risk of GDM. However, pregnant women who carried the rs74018601 GA genotype ( OR=1.51, 95 %CI: 1.07-2.12), GA or AA genotype ( OR=1.46, 95 %CI: 1.06-2.02), rs7205009 AA genotype ( OR=1.83, 95 %CI: 1.18-2.86), GA or AA genotype ( OR=1.53, 95 %CI: 1.08-2.19), and rs9888758 AG genotype ( OR=1.43, 95 %CI: 1.02-2.00) had elevated risk of GDM. Conclusion:The polymorphisms of FTO gene rs11075995,rs3826169, rs74245270, rs74018601, rs7205009 and rs9888758 were associated with the risk of GDM.

Objective:To investigate the relationship between folic acid supplementation and the risk of preeclampsia (PE).Methods:A total of 9 048 pregnant women were selected from the First Hospital of Shanxi Medical University in Taiyuan from March 2012 to September 2016. Among them, 882 pregnant women with PE were divided into case group, and 8 166 pregnant women without PE were divided into control group. Information on demographic characteristics, folic acid supplementation, maternal complications, and other factors were collected by face-to-face interviews after child birth in the hospital. Unconditional logistic regression analyses were used to investigate the relationship between folic acid supplementation and the risk of PE and the effects of pre-pregnancy BMI on the relationship of folic acid supplementation with the risk of PE.Results:Compared with nonusers, folic acid supplement users had reduced risk of PE ( OR=0.79, 95 %CI: 0.64-0.96). Folic acid supplementation before and during pregnancy were negatively related with the risk of PE ( OR=0.63, 95 %CI: 0.49-0.81). Pregnant women who used folic acid tablets only or used both folic acid tablets and multivitamin containing folic acid had reduced risk of PE ( OR=0.81, 95 %CI: 0.66-0.99; OR=0.64, 95 %CI: 0.49-0.85). No significant relationship was observed in the multivitamin group. Supplemental folic acid doses of <400, 400, and >400 μg/d were related with reduced risk of PE ( OR=0.62, 95 %CI: 0.42-0.91; OR=0.81, 95 %CI: 0.66-0.99; OR=0.68, 95 %CI: 0.49-0.94). After stratified by pre-pregnancy BMI, pregnant women who used folic acid supplementation, those with pre-pregnancy BMI<24.0 kg/m 2 had reduced risk of PE ( OR=0.75, 95 %CI: 0.59-0.96). However, no significant relationship was observed in women with pre-pregnancy BMI≥24.0 kg/m 2. Conclusions:Folic acid supplementation before and during pregnancy were related with reduced risk of PE. Pre-pregnancy BMI might affect the relationship between folic acid supplementation and the risk of PE. Appropriate folic acid supplementation should be recommend for women with different pre-pregnancy BMI.

Exposure of airborne particulate matter (PM) with an aerodynamic diameter less than 2.5 lm (PM2.5) is epidemiologically associated with lung dysfunction and respiratory symptoms, including pulmonary fibrosis. However, whether epigenetic mechanisms are involved in PM2.5-induced pulmonary fibrosis is currently poorly understood. Herein, using a PM2.5-induced pulmonary fibrosis mouse model, we found that PM2.5 exposure leads to aberrant mRNA 5-methylcytosine (m5C) gain and loss in fibrotic lung tissues. Moreover, we showed the m5C-mediated regulatory map of gene functions in pulmonary fibrosis after PM2.5 exposure. Several genes act as m5C gain-upregulated factors, probably critical for the development of PM2.5-induced fibrosis in mouse lungs. These genes, including Lcn2, Mmp9, Chi3l1, Adipoq, Atp5j2, Atp5l, Atpif1, Ndufb6, Fgr, Slc11a1, and Tyrobp, are highly related to oxidative stress response, inflammatory responses, and immune system processes. Our study illustrates the first epitranscrip-tomic RNA m5C profile in PM2.5-induced pulmonary fibrosis and will be valuable in identifying biomarkers for PM2.5 exposure-related lung pathogenesis with translational potential.

Objective: To explore the effect of lipopolysaccharide intervention program on Legionella pneumonia. Methods: C3H/HeN mice (6-8 weeks old) were used as experimental animals. The mice were randomly divided into lipopolysaccharide intervention, non-lipopolysaccharide intervention and control groups. Each group was again divided into three time points: 12 h, 24 h and 48 h. Mice in the lipopolysaccharide intervention group were intraperitoneally injected with E. coli lipopolysaccharide (100 ng per mice), and the rest groups were intraperitoneally injected with normal saline. After 24 hours, mice in the lipopolysaccharide intervention and the non-intervention groups mice were infected with Legionella by tracheal injection and the control group was given the same amount of saline. All the mice were killed at 12, 24 and 48 hours respectively. The mice were anatomized, lungs of the mice were separated and weighed. Organ coefficients (lung weight/body weight of mice) were calculated. 1 ml Orbital blood was collected. Toll-like receptor 4 (TLR4) levels of peripheral blood mononuclear cells were measured by flow cytometry. The contents of TNF-α and IL-1β in the upper left lung lobe were measured by ELISA. Results: In the lung organs, the coefficients of lipopolysaccharide non-intervention group were higher than the other groups and there was no significant difference seen between the lipopolysaccharide intervention group and the controls. TLR4 peaked at 12 hours in both the lipopolysaccharide intervention and the non-intervention groups while the TLR4 level in the intervention group was higher than that in the non-intervention group. There were no significant differences appeared on the TLR4 expression levels between the two Legionella pneumonia modelled groups at 24 or 48 hours. There was no significant difference seen regarding the concentration of TNF-α and IL-1β between the intervention and the control groups. The secretion levels of TNF-α and IL-1β in the non-intervention group were higher than those in the intervention group at each time point. Conclusion The lipopolysaccharide intervention program may alleviate the inflammatory symptoms of Legionella infection.