ObjectiveTo investigate somatization symptoms in adolescents during frequent earthquakes in Hefei， and to explore their correlation with earthquake experiences. MethodsA cross-sectional survey was used to select 324 adolescents in Hefei as the survey objects. The self-rating scale of somatization symptoms （SSS） and the fatigue intensity scale （FIS） were used to evaluate the somatization symptoms and fatigue degree of middle school students， and multivariate Logistic regression analysis was used to explore the related factors of somatization symptoms and fatigue among middle school students. ResultsA total of 324 adolescents were included， and the overall detection rate of somatization symptoms was 6.5%， and the detection rate of moderate or above fatigue was 20.1%. The results of regression analysis showed that adolescents who were concerned about the earthquake for a longer time （≥1 h） had a higher risk of somatization symptoms （OR=5.430， 95%CI： 1.547-19.058）， and adolescents who received pre-earthquake training had a lower degree of fatigue （OR=0.535， 95%CI： 0.292-0.981） （P<0.05）. ConclusionDuring the frequent earthquakes， adolescents have more somatization symptoms and fatigue. Therefore， it is crucial to enhance health education， reduce the emphasis on event-related reports， and implement earthquake prevention and disaster reduction training to improve the physical and mental health of adolescents.

ObjectiveTo investigate the mechanisms of Runmu Dihuang decoction （RMDHD） in treating perimenopausal dry eye with liver-kidney Yin deficiency syndrome based on the silent information regulator 3 （SIRT3）/hypoxia-inducible factor-1α （HIF-1α）/nuclear factor-κB （NF-κB） signaling pathway. MethodsSixty female Sprague-Dawley rats were randomly divided into six groups （n=10 per group）： Sham operation group， model group， sodium hyaluronate eye drop group， and low-， medium-， and high-dose RMDHD groups （5.625， 11.25， 22.50 g·kg^-1）. Except for the sham operation group， all rats underwent bilateral ovariectomy and were administered 0.1% benzalkonium chloride eye drops combined with long-term chronic irritation to establish a perimenopausal dry eye model with liver-kidney Yin deficiency syndrome. Drug administration began in the 11th week after modeling and continued for 21 days. General conditions， screen-grip test scores， tear secretion volume， tear film breakup time （TFBUT）， and corneal fluorescein staining were recorded. Serum levels of reactive oxygen species （ROS）， follicle-stimulating hormone （FSH）， estradiol （E₂）， and progesterone （PROG） were measured by enzyme-linked immunosorbent assay （ELISA）. Pathological changes in the lacrimal glands， corneas， and uteri were observed using hematoxylin-eosin （HE） staining. Protein expression levels of SIRT3， HIF-1α， phosphorylated NF-κB p65 （p-NF-κB p65）， and total NF-κB p65 in the lacrimal glands were detected by Western blot. The expression of inflammatory cytokines interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α） in the lacrimal glands was assessed by immunohistochemistry （IHC）. ResultsAfter model establishment， no significant differences were observed among the groups except the sham operation group. Compared with the sham operation group， the other groups exhibited slowed movement， dull responses， increased irritability， reduced body weight， elevated rectal temperature， decreased screen-grip test scores， reduced tear secretion， and significantly shortened TFBUT （P<0.05）. After treatment， compared with the model group， the sodium hyaluronate eye drop group and all RMDHD groups showed improved general conditions， significantly increased tear secretion （P<0.05）， prolonged TFBUT （P<0.05）， and elevated screen-grip test scores （P<0.05）. Serum ROS and FSH levels were significantly decreased， while E₂ and PROG levels were significantly increased （P<0.05）. Pathological damage to the cornea， lacrimal glands， and uterus was ameliorated. In addition， protein expression levels of SIRT3 and HIF-1α in the lacrimal glands were significantly upregulated （P<0.05）， whereas the expression of p-NF-κB p65， IL-1β， and TNF-α was significantly downregulated （P<0.05）. ConclusionRMDHD increases tear secretion and TFBUT， improves lacrimal gland and corneal injury， and alleviates dry eye symptoms in a perimenopausal dry eye rat model with liver-kidney Yin deficiency syndrome. The underlying mechanism may be related to regulation of the SIRT3/HIF-1α/NF-κB signaling pathway， inhibition of oxidative stress and inflammatory responses， and reduction of ocular surface tissue damage.

Objective:To investigate the hemodynamic characteristics of intracranial collateral circulation assessed non-invasively by TCD and their correlation with clinical prognosis in patients with severe carotid stenosis or occlusion.Methods:A retrospective cohort study design was used to include 96 patients with severe stenosis(≥70％)or occlusion of the unilateral internal carotid artery admitted from March 2021 to March 2024,who were divided into a well-compensated group(58 patients)versus a poorly-compensated group(38 patients)based on the ASITN/SIR collateral branch score.Hemodynamic parameters(PSV,EDV,MFV,PI,RI)were measured using TCD,and collateral circulation status was validated by digital subtraction angiography(DSA).Prognosis was evaluated over a 12-month follow-up.Logistic regression was used to analyze risk factors for poor prognosis.Results:The good collateral group exhibited significantly higher PSV(82.32±18.51 vs.56.45±15.32 cm/s)and MFV(56.93±12.33 vs.35.89±9.83 cm/s),and significantly lower PI(0.64±0.15 vs.0.82±0.21)and RI(0.43±0.08 vs.0.51±0.11)compared to the poor collateral group(all P＜0.001).TCD parameters showed strong correlations with ASITN/SIR grades(PSV:r=0.62;PI:r=-0.61,all P＜0.001).Multivariate analysis identified age ≥65 years(OR=1.06),hypertension(OR=3.07),PI ≥ 1.00(OR=17.25),and PSV ≤ 60 cm/s(OR=1.96)as independent risk factors for poor prognosis(all P＜0.05).Conclusion:The TCD multi-parameter model enables quantitative assessment of collateral circulation function,with PI ≥ 1.00 and PSV ≤ 60 cm/s serving as key predictors of adverse outcomes.The non-invasive and dynamic monitoring advantages of TCD provide critical insights for hemodynamic stratification and personalized intervention in patients with carotid stenosis or occlusion.

Aberrant expression of Colgalt1 is closely associated with tumorigenesis and tumor progres-sion;however,the mechanism by which it regulates macrophages to influence tumor development remains poorly understood.This study aimed to establish a macrophage-specific Colgalt1 gene knockout mouse model to delve into the mechanisms through which Colgalt1 modulates macrophage function and subse-quently affects the occurrence and progression of tumor-related diseases.Initially,Colgalt1flox+mice were generated using gene editing techniques,followed by crossing with Lyz2-Cre+mice,which exhibit tissue-specific expression in the myeloid lineage(including monocytes and mature macrophages).Through this strategy,mice with the genotype Colgalt1-/-Lyz2-Cre+were successfully obtained,achieving conditional knockout of the Colgalt1 gene in macrophages.Colgalt1flox/flox Lyz2-Cre-mice were used as control.PCR and agarose gel electrophoresis were employed to identify the Flox and Cre genotypes of the knockout mice.RT-qPCR and Western Blot techniques were utilized to detect the expression levels of Colgalt1 in BMDMs from knockout mice at both the mRNA and protein levels,respectively.Western Blot results re-vealed a significant downregulation of Colgaltl expression in BMDMs from knockout mice compared to controls(P＜0.01).RT-qPCR results demonstrated a significant reduction in Colgalt1 mRNA levels in BMDMs from knockout mice compared to contro1s(P＜0.001),while no significant differences in Col-galt1 mRNA expression were observed in liver,lung,or spleen tissues between the two groups.Addition-ally,immunohistochemistry was employed to detect Colgalt1 expression in liver-specific macrophages,re-vealing an absence of Colgalt l-positive staining in liver macrophages from knockout mice.HE staining was used to observe cellular morphology in liver tissues from both groups of mice,showing no significant differences in cellular morphology or obvious pathological changes in tissues and organs.Moreover,the o-verall survival of the mice was not affected.Finally,RT-qPCR was used to assess the expression of mac-rophage-related inflammatory factors in BMDMs from both groups of mice.The results indicated that com-pared to controls,knockout mice exhibited downregulated expression of TNF-α(P＜0.05)and signifi-cantly upregulated expression of IL-10(P＜0.01),Arginase1(P＜0.001),and CD206(P＜0.001)in BMDMs,suggesting an anti-inflammatory trend and M2 polarization of macrophages following Colgalt 1 knockout.In summary,this study successfully established a macrophage-specific Colgalt1 gene knockout mouse model,providing a more reliable experimental animal model for in-depth exploration of the specific roles of Colgalt1 in macrophage functional regulation and the pathogenesis of tumor-related diseases.This model holds promise for identifying novel therapeutic targets and strategies for tumors and other diseases.

Aim To establish the cells co-expressing 5-HT2C re-ceptor(5-HT2C R)and enhanced green fluorescent protein(EG-FP)-tagged nuclear factor of activated T cells 2(NFAT2)in U2OS cells.Methods The 5-HT2CR stably expressed U2OS-EGFP-NFAT2-5-HT2CR cells were screened by hygromycin B af-ter 5-HT2C plasmid was transfected into U2OS-EGFP-NFAT2 cells.The mRNA and protein expression of 5-HT2CR in the se-lected U2OS-EGFP-NFAT2-5-HT2CR cells were detected by RT-qPCR and Western blot.The activation of U2OS-EGFP-NFAT2-5-HT2CR cells was verified by nuclear translocation level assay.The effects of 5-HT,LSD,DOM,DOI,psilocybin(PSI),lisuride(LIS)on the U2OS-EGFP-NFAT2-5-HT2CR cells were detected by the high throughout screening assay.Results Among these cells,No 56 had the highest nuclear translocation function.5-HT2CR mRNA and protein were stably expressed in U2OS-EG-FP-NFAT2-5-HT2CR transfected cell line for 1-15 generations by RT-qPCR and Western blot.Vabicaserin increased the EGFP-NFAT2 nuclear translocation in U2OS-EGFP-NFAT2-5-HT2C R during 1-15 generations.The 5-HT2CR antagonist SB242084 significantly decreased EGFP-NFAT2 nuclear translocation in-duced by Vabicaserin in U2OS-EGFP-NFAT2-5-HT2CR cells.5-HT,LIS,PSI slightly increased the EGFP-NFAT2 nuclear trans-location in U2OS-EGFP-NFAT2-5-HT2C R cells,whereas LSD,DOI,DOM had no effect.Conclusions U2OS-EGFP-NFAT2-5-HT2CR cells co-expressing 5-HT2CR and EGFP-NFAT2 are es-tablished,which can be used for high throughout screening of chemicals and the study on the mechanism of the5-HT2CR.

Background:Duodenal papillary adenoma is a benign tumor with relatively low incidence but significant carcinogenesis potential.Despite the minimal invasiveness and low complication rate,endoscopic papillectomy is associated with a definite risk of recurrence for duodenal papillary adenoma.Investigating the driver genes of duodenal papillary adenoma and establishing predictive models for recurrence and malignant progression could facilitate the precision medicine.Aims:To identify the key driver genes for tumor occurrence,carcinogenesis and recurrence in duodenal papillary adenoma by integrating multi-dimensional bioinformatics approaches based on transcriptomics data,and validate clinically.Methods:Expression profiles of duodenal papillary adenoma and adenocarcinoma were obtained from the GEO database(including data sets GSE189035,GSE94919,GSE111156,and GSE102208).Differentially expressed genes(DEGs)between adenomatous and normal tissues were screened.Weighted gene co-expression network analysis(WGCNA)and pseudo-time analysis were combined to identify the core genes exhibiting an"initial rise followed by decline"expression pattern during the dynamic progression from normal tissue to adenoma and adenocarcinoma.Functional annotation,immune microenvironment profiling,and protein-protein interaction network analysis were performed to explore the tumor-promoting mechanisms of these core genes.Clinical validation was conducted using immunohistochemistry to estimate the gene expression level and its relationship with tumor recurrence.Results:A total of 469 common DEGs were identified.WGCNA revealed that the blue module(including 1 051 genes)was associated with adenoma development and progression(Cor=-0.29,0.15,and 0.11 for normal tissue,adenoma,and adenocarcinoma,respectively).Intersection with DEGs pinpointed four key genes:SLC12A2,BEST4,SLC37A2,and SOAT2.Pseudo-time analysis demonstrated that only SLC12A2 maintained sustained high expression in both adenoma and adenocarcinoma tissues.KEGG enrichment analysis indicated that SLC12A2 was linked to various malignant pathways(e.g.,PD-1/PD-L1 signaling pathway),and its high expression correlated with the reduced immune cell infiltration(e.g.,γδ T cells,CD8+T cells,etc.).Clinical validation by immunohistochemistry confirmed the trend of initial upregulation and subsequent downregulation of SLC12A2 expression in normal,adenoma,and adenocarcinoma tissues.Patients with tumor recurrence showed higher SLC12A2 expression level(P=0.004);likewise,SLC12A2 high expression was associated with an elevated recurrence risk(P=0.034).Conclusions:SLC12A2 serves as a critical driver of tumorigenesis and progression for duodenal papillary adenoma,and might be a promising biomarker for recurrence prediction.

Background:Duodenal papillary adenoma is a benign tumor with relatively low incidence but significant carcinogenesis potential.Despite the minimal invasiveness and low complication rate,endoscopic papillectomy is associated with a definite risk of recurrence for duodenal papillary adenoma.Investigating the driver genes of duodenal papillary adenoma and establishing predictive models for recurrence and malignant progression could facilitate the precision medicine.Aims:To identify the key driver genes for tumor occurrence,carcinogenesis and recurrence in duodenal papillary adenoma by integrating multi-dimensional bioinformatics approaches based on transcriptomics data,and validate clinically.Methods:Expression profiles of duodenal papillary adenoma and adenocarcinoma were obtained from the GEO database(including data sets GSE189035,GSE94919,GSE111156,and GSE102208).Differentially expressed genes(DEGs)between adenomatous and normal tissues were screened.Weighted gene co-expression network analysis(WGCNA)and pseudo-time analysis were combined to identify the core genes exhibiting an"initial rise followed by decline"expression pattern during the dynamic progression from normal tissue to adenoma and adenocarcinoma.Functional annotation,immune microenvironment profiling,and protein-protein interaction network analysis were performed to explore the tumor-promoting mechanisms of these core genes.Clinical validation was conducted using immunohistochemistry to estimate the gene expression level and its relationship with tumor recurrence.Results:A total of 469 common DEGs were identified.WGCNA revealed that the blue module(including 1 051 genes)was associated with adenoma development and progression(Cor=-0.29,0.15,and 0.11 for normal tissue,adenoma,and adenocarcinoma,respectively).Intersection with DEGs pinpointed four key genes:SLC12A2,BEST4,SLC37A2,and SOAT2.Pseudo-time analysis demonstrated that only SLC12A2 maintained sustained high expression in both adenoma and adenocarcinoma tissues.KEGG enrichment analysis indicated that SLC12A2 was linked to various malignant pathways(e.g.,PD-1/PD-L1 signaling pathway),and its high expression correlated with the reduced immune cell infiltration(e.g.,γδ T cells,CD8+T cells,etc.).Clinical validation by immunohistochemistry confirmed the trend of initial upregulation and subsequent downregulation of SLC12A2 expression in normal,adenoma,and adenocarcinoma tissues.Patients with tumor recurrence showed higher SLC12A2 expression level(P=0.004);likewise,SLC12A2 high expression was associated with an elevated recurrence risk(P=0.034).Conclusions:SLC12A2 serves as a critical driver of tumorigenesis and progression for duodenal papillary adenoma,and might be a promising biomarker for recurrence prediction.

OBJECTIVE: To investigate the management strategies of external fixation combined with microsurgical techniques for repairing complex foot and ankle wounds in children. METHODS: The clinical data of 9 children with complex foot and ankle wounds who met the selection criteria between June 2017 and December 2021 was retrospectively analyzed. There were 6 boys and 3 girls, aged 3-13 years, with an average of 7.4 years. The causes of injury included crush injury in 5 cases and traffic accident injury in 4 cases. The wound size ranged from 6 cm×5 cm to 25 cm×18 cm. The time from injury to surgery ranged from 3 to 8 hours, with an average of 5 hours. All cases underwent staged surgical treatment. Among the 3 cases requiring deformity correction, 2 cases initially underwent free anterolateral thigh flap transplantation for wound coverage and limb salvage, followed by circular external fixation combined with osteotomy to address postoperative limb deformity, while 1 case received osteotomy for tibial fracture realignment prior to local pedicled flap reconstruction. All the 6 cases with non-deformity correction underwent initial external fixation followed by secondary flap reconstruction for wound management. The American Orthopaedic Foot & Ankle Society (AOFAS) ankle-hindfoot score was used to evaluate the foot and ankle function of children. RESULTS: All children successfully achieved limb salvage postoperatively. Among the 6 non-deformity correction cases, all flaps survived with satisfactory wound healing and no infection was observed; fractures healed within 2.5-4.5 months, after which external fixators were removed for functional rehabilitation with favorable recovery. One case treated with circular external fixation combined with osteotomy achieved bone union at 4 months postoperatively, followed by fixator removal. One case undergoing osteotomy for tibial fracture realignment showed bone healing at 2.5 months post-correction, with subsequent fixator removal. One patient receiving bone lengthening developed infection at 1 week postoperatively, which was managed with multiple debridements, ultimately achieving bone union at 16 months postoperatively and followed by fixator removal. At last follow-up, all patients demonstrated satisfactory ankle-hindfoot functional recovery, with AOFAS ankle-hindfoot scores ranging from 80 to 90 (mean, 84.2). CONCLUSION The combination of external fixation and microsurgical techniques demonstrates significant advantages in reconstructing complex foot and ankle wounds in children. The synergistic interaction provides both mechanical stability and biological repair, enabling early functional rehabilitation while reducing infection risks.
Humans ; Child ; Male ; Female ; Adolescent ; Child, Preschool ; Foot Injuries/surgery* ; Ankle Injuries/surgery* ; Retrospective Studies ; External Fixators ; Microsurgery/methods* ; Plastic Surgery Procedures/methods* ; Surgical Flaps ; Fracture Fixation/methods* ; Osteotomy/methods* ; Treatment Outcome

OBJECTIVES: To investigate the molecular epidemiology of children with phenylketonuria (PKU) in Gansu, China, providing foundational data for intervention strategies. METHODS: A retrospective analysis was conducted on 1 159 PKU families who attended Gansu Provincial Maternity and Child Care Hospital from January 2012 to December 2024. Sanger sequencing, multiplex ligation-dependent probe amplification, whole exome sequencing, and deep intronic variant analysis were used to analyze the PAH gene. RESULTS: For the 1 159 children with PKU, 2 295 variants were identified in 2 318 alleles, resulting in a detection rate of 99.01%. The detection rates were 100% (914/914) in 457 classic PKU families, 99.45% (907/912) in 456 mild PKU families, and 96.34% (474/492) in 246 mild hyperphenylalaninemia families. The 2 295 variants detected comprised 208 distinct mutation types, among which c.728G>A (14.95%, 343/2 295) had the highest frequency, followed by c.611A>G (4.88%, 112/2 295) and c.721C>T (4.79%, 110/2 295). The cumulative frequency of the top 23 hotspot variants reached 70.28% (1 613/2 295), and most variant alleles were detected in exon 7 (29.19%, 670/2 295). CONCLUSIONS Deep intronic variant analysis of the PAH gene can improve the genetic diagnostic rate of PKU. The development of targeted detection kits for PAH hotspot variants may enable precision screening programs and enhance preventive strategies for PKU.
Humans ; Phenylketonurias/epidemiology* ; Female ; Male ; Retrospective Studies ; Phenylalanine Hydroxylase/genetics* ; Mutation ; Child, Preschool ; China/epidemiology* ; Child ; Infant

OBJECTIVES: To investigate the dynamic changes in serum microRNA-15b (miR-15b) and vascular endothelial growth factor (VEGF) in preterm infants with mild or moderate-to-severe bronchopulmonary dysplasia (BPD), as well as their value in assessing short-term neurodevelopment. METHODS: A retrospective analysis was conducted on the medical data of 156 preterm infants with BPD who were admitted to the neonatal intensive care unit from January 2020 to February 2023. According to the severity of BPD, they were divided into a mild group (n=88) and a moderate-to-severe group (n=68). Serum levels of miR-15b and VEGF were measured on postnatal days 1, 7, 14, and 28. Repeated measures analysis of variance was used to assess the dynamic changes in serum levels of miR-15b and VEGF. The mediating effect of VEGF between miR-15b and short-term neurological development was tested and analyzed using the stepwise regression method and the Bootstrap method. Logistic regression analysis was used to identify factors influencing adverse neurodevelopmental outcomes. RESULTS: In the mild group, there was a significant reduction in the serum level of miR-15b and a significant increase in VEGF over time (P<0.05), while in the moderate-to-severe group, there was a significant increase in miR-15b and a significant reduction in VEGF over time (P<0.05). Serum miR-15b and VEGF levels were important factors influencing neurodevelopmental outcomes, showing independent correlations (P<0.001). The mediating effect analysis indicated that miR-15b indirectly affected short-term neurodevelopment by inhibiting VEGF expression [indirect effect: -0.705 (95%CI: -1.178 to -0.372)], with the indirect effect accounting for 54.36% of the total effect. CONCLUSIONS There are different changing trends in serum levels of miR-15b and VEGF in preterm infants with mild and moderate-to-severe BPD. miR-15b primarily influences neurodevelopment through VEGF.
Humans ; Bronchopulmonary Dysplasia/physiopathology* ; MicroRNAs/blood* ; Vascular Endothelial Growth Factor A/blood* ; Infant, Newborn ; Infant, Premature/blood* ; Female ; Male ; Retrospective Studies ; Child Development ; Nervous System/growth & development*