Objective To understand the application effect of early screening scale and behavioral intervention effect in children with autism spectrum disorder (ASD). Methods A total of 348 children with suspected ASD were selected and evaluated using the Modified Checklist for Autism in Toddlers (M-CHAT) and Autism Behavior Checklist (ABC). The evaluation results were compared with those from the Diagnostic and Statistical Manual of Mental Disorders (DSM-V). Children enrolled were given Early start Denver model (ESDM) intervention. The evaluation results of Gesell Developmental Scale and Autism Treatment Evaluation Checklist (ATEC) scores were compared before and after intervention. Results The sensitivity, specificity, accuracy and Kappa value of M-CHAT for evaluating ASD in children aged 1-3 years were 89.53%, 90.70%, 89.92% and 0.78. The corresponding values of ABC were 78.49%, 81.40%, 79.46% and 0.56. The sensitivity, specificity, accuracy and Kappa value of M-CHAT for evaluating children aged >3-6 years were 87.30%, 77.78%, 84.44% and 0.64. The corresponding values of ABC were 85.71%, 77.78%, 83.33% and 0.62. The sensitivity and accuracy of M-CHAT were higher than ABC for evaluating ASD in children aged 1-3 years (P<0.05). There were no significant differences in sensitivity, specificity and accuracy between M-CHAT and ABC for evaluating ASD in children aged 3-6 years (P>0.05). After intervention, development quotients (DQ) of personal-social aspects, adaptability, language, gross motor, and fine motor of children with ASD were higher than those before intervention (P<0.05). ATEC scores for language, behavior, sensation, and social contact of children with ASD were lower than those before intervention (P<0.05). Conclusion M-CHAT and ABC both can be used for early screening of ASD in children, especially M-CHAT. Early behavioral intervention can effectively improve the condition and developmental level of children with ASD.

ObjectiveTo explore the impacts of material type and loading volume of rigid containers on the hydrogen peroxide low temperature plasma sterilization of thoracoscopic instruments, to identify the best rigid containers and loading volume of thoracoscopic instruments. MethodsThoracoscopic instruments sterilized by STERRAD^® 100NX hydrogen peroxide low temperature plasma in Shanghai Pulmonary Hospital affiliated to Tongji University from August to September 2024 were selected as the research items. According to the material of rigid containers, the instruments were divided into polyethylene case group (A), stainless steel case group (B) and silicone resin case group (C). In terms of the loading volume, the rigid containers were divided into (loading capacity <80%) groups of 8, 10 and 12 instruments. The results of physical monitoring, the first type of chemical indicator card monitoring, and the five types of card luminal chemical process challenge device (PCD) monitoring of the 9 groups of A8, A10, A12, B8, B10, B12, C8, C10 and C12 were compared and evaluated. ResultsCompared to A8, A10 A12, C8, C10 or C12 groups, the thoracoscope instruments in the stainless steel containers in B8, B10 or B12 group had higher hydrogen peroxide concentrations and shorter elapsed time in the pressure check phases 1 and phases 2, with the differences statistically significant (P<0.05), followed by the silicone resin case group and the polyethylene case group. The nine groups of physical parameter monitoring, the first type of chemical indicator monitoring, and the five types of chemical PCD monitoring for lumen sterilization achieved 100% qualification rates, and there were no significant differences in the qualified rates of sterilization among the 9 groups (P>0.05). ConclusionWhen using hydrogen peroxide low temperature plasma to sterilize thoracoscopic instruments, it is recommended to use stainless steel or silicone resin rigid containers with a controlled loading capacity (≤12) to ensure optimal sterilization quality.

BACKGROUND:The imbalance between proliferation and apoptosis of chondrocytes plays an important role in the occurrence and development of osteoarthritis. Previous studies have found that hsa-miR-3202 is involved in regulating the proliferation and apoptosis of various cells. However,no studies have explored the correlation between hsa-miR-3202 and osteoarthritis.OBJECTIVE:To investigate the expression of hsa-miR-3202 in osteoarthritic chondrocytes and its effect on the proliferation and apoptosis of chondrocytes. METHODS:(1) MicroRNAs differentially expressed in osteoarthritic chondrocytes were screened by biogenic analysis. Based on the current research situation at home and abroad,hsa-miR-3202 was selected for follow-up studies,and its target genes were predicted by gene ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment. (2) Human normal chondrocyte cell lines C28/I2 in logarithmic growth phase were selected and randomly divided into four groups for culture:in normal group,cells were cultured in normal medium for 24 hours,the medium was then changed to normal medium for another 6 hours of culture,and changed to normal medium for subsequent culture;in lipopolysaccharide group,cells were cultured in lipopolysaccharide-containing medium for 24 hours,the medium was then changed to normal medium for another 6 hours,and changed to normal medium for subsequent culture;in lipopolysaccharide+NC group,cells were cultured in lipopolysaccharide-containing medium for 24 hours,and then transfected with has-miR-3202 mimics control for 6 hours,and the medium was change to normal medium for subsequent culture;in lipopolysaccharide+hsa-miR-3202 mimics group,cells were cultured in lipopolysaccharide-containing medium for 24 hours and then transfected with has-miR-3202 mimics for 6 hours,and the medium was changed to normal medium for subsequent culture. After further 48 hours of culture,the expression level of hsa-miR-3202 was detected by fluorescence quantitative PCR and cell apoptosis was detected by flow cytometry. After further culture of 0-72 hours,cell proliferation activity was detected by cell counting kit-8. RESULTS AND CONCLUSION:Bioinformatics analysis results indicated that hsa-miR-3202 was significantly down-regulated in osteoarthritic chondrocytes. GO functional enrichment and KEGG pathway enrichment showed that the function of hsa-miR-3202 target gene was closely related to cell growth and apoptosis. The results of in vitro cell experiments showed that compared with the normal group,the expression level of hsa-miR-3202 and proliferation ability of chondrocytes were significantly decreased in the lipopolysaccharide group (P<0.05),while the apoptotic rate was significantly increased (P<0.05). Compared with the lipopolysaccharide group,the expression level of hsa-miR-3202 and proliferation ability of chondrocytes were significantly increased in the lipopolysaccharide+hsa-miR-3202 mimics group (P<0.05),while the apoptotic rate was significantly decreased (P<0.05). To conclude,the expression of hsa-miR-3202 is down-regulated in osteoarthritic chondrocytes to inhibit cell proliferation and promote cell apoptosis,thus affecting the occurrence and development of osteoarthritis.

Objective:This study aims to conduct a systematic review and network meta-analysis comparing the safety and efficacy of endoscopic versus surgical treatments for gastroesophageal reflux disease (GERD).Methods:Randomized controlled trials were identified through systematic searches of MEDLINE, Embase, Web of Science, and CNKI. Both direct effect models and Bayesian random-effects network meta-analysis were used to compare treatments directly and indirectly. The following types of studies were included : (1) RCTs involving endoscopic or surgical treatment for adult GERD patients aged ≥18 years with no previous history of gastroesophageal surgery; (2) studies comparing two or more treatment methods, including different endoscopic or surgical procedures, proton pump inhibitor (PPI) therapy, and/or sham surgery; and (3) articles published in Chinese or English. Review articles and conference abstracts were excluded.Results:A total of 47 randomized controlled trials were enrolled, and 43 studies were network meta-analyzed. Both endoscopic and surgical treatments significantly reduced postoperative PPI use compared to PPI therapy ( P <0.05). Among all treatment modalities, laparoscopic Nissen fundoplication (LNF, SUCRA=0.84) demonstrated the highest efficacy, followed by laparoscopic Toupet fundoplication (LTF, SUCRA=0.71) and anterior partial fundoplication (APF, SUCRA=0.70). Transoral incisionless fundoplication (TIF) demonstrated the best outcomes in relieving heartburn (SUCRA=0.87) and bloating (SUCRA=0.86) symptoms. The overall safety of surgical treatment was comparable to that of PPI therapy. However, LNF was associated with a higher incidence of postoperative dysphagia and gas-related symptoms, whereas TIF had a lower risk of postoperative complications. Conclusions:Both endoscopic and surgical treatments are effective for GERD. LNF provides the highest rate of medication discontinuation but carries a higher risk of postoperative complications. TIF offers better relief of heartburn and bloating with fewer complications.

Oral and maxillofacial tumors significantly impact human health,with oral squamous cell carcinoma(OSCC)being par-ticularly prevalent among head and neck tumors.At present,traditional research in this area has largely relied on genomics,pro-teomics,and transcriptomics,which involve the homogenization of tissue specimens and result in the loss of critical temporal and spatial tissue information.In contrast,spatial metabolomics,an emerging field,allows for the in-situ analysis of fresh tissue sam-ples,preserving this essential information.This article reviews the application of spatial metabolomics in OSCC research,highlight-ing its potential to enhance understanding of cancer pathogenesis directly within the tissue context.

Objective:This study aims to conduct a systematic review and network meta-analysis comparing the safety and efficacy of endoscopic versus surgical treatments for gastroesophageal reflux disease (GERD).Methods:Randomized controlled trials were identified through systematic searches of MEDLINE, Embase, Web of Science, and CNKI. Both direct effect models and Bayesian random-effects network meta-analysis were used to compare treatments directly and indirectly. The following types of studies were included : (1) RCTs involving endoscopic or surgical treatment for adult GERD patients aged ≥18 years with no previous history of gastroesophageal surgery; (2) studies comparing two or more treatment methods, including different endoscopic or surgical procedures, proton pump inhibitor (PPI) therapy, and/or sham surgery; and (3) articles published in Chinese or English. Review articles and conference abstracts were excluded.Results:A total of 47 randomized controlled trials were enrolled, and 43 studies were network meta-analyzed. Both endoscopic and surgical treatments significantly reduced postoperative PPI use compared to PPI therapy ( P <0.05). Among all treatment modalities, laparoscopic Nissen fundoplication (LNF, SUCRA=0.84) demonstrated the highest efficacy, followed by laparoscopic Toupet fundoplication (LTF, SUCRA=0.71) and anterior partial fundoplication (APF, SUCRA=0.70). Transoral incisionless fundoplication (TIF) demonstrated the best outcomes in relieving heartburn (SUCRA=0.87) and bloating (SUCRA=0.86) symptoms. The overall safety of surgical treatment was comparable to that of PPI therapy. However, LNF was associated with a higher incidence of postoperative dysphagia and gas-related symptoms, whereas TIF had a lower risk of postoperative complications. Conclusions:Both endoscopic and surgical treatments are effective for GERD. LNF provides the highest rate of medication discontinuation but carries a higher risk of postoperative complications. TIF offers better relief of heartburn and bloating with fewer complications.

Oral and maxillofacial tumors significantly impact human health,with oral squamous cell carcinoma(OSCC)being par-ticularly prevalent among head and neck tumors.At present,traditional research in this area has largely relied on genomics,pro-teomics,and transcriptomics,which involve the homogenization of tissue specimens and result in the loss of critical temporal and spatial tissue information.In contrast,spatial metabolomics,an emerging field,allows for the in-situ analysis of fresh tissue sam-ples,preserving this essential information.This article reviews the application of spatial metabolomics in OSCC research,highlight-ing its potential to enhance understanding of cancer pathogenesis directly within the tissue context.

BACKGROUND:The imbalance between proliferation and apoptosis of chondrocytes plays an important role in the occurrence and development of osteoarthritis. Previous studies have found that hsa-miR-3202 is involved in regulating the proliferation and apoptosis of various cells. However,no studies have explored the correlation between hsa-miR-3202 and osteoarthritis.OBJECTIVE:To investigate the expression of hsa-miR-3202 in osteoarthritic chondrocytes and its effect on the proliferation and apoptosis of chondrocytes. METHODS:(1) MicroRNAs differentially expressed in osteoarthritic chondrocytes were screened by biogenic analysis. Based on the current research situation at home and abroad,hsa-miR-3202 was selected for follow-up studies,and its target genes were predicted by gene ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment. (2) Human normal chondrocyte cell lines C28/I2 in logarithmic growth phase were selected and randomly divided into four groups for culture:in normal group,cells were cultured in normal medium for 24 hours,the medium was then changed to normal medium for another 6 hours of culture,and changed to normal medium for subsequent culture;in lipopolysaccharide group,cells were cultured in lipopolysaccharide-containing medium for 24 hours,the medium was then changed to normal medium for another 6 hours,and changed to normal medium for subsequent culture;in lipopolysaccharide+NC group,cells were cultured in lipopolysaccharide-containing medium for 24 hours,and then transfected with has-miR-3202 mimics control for 6 hours,and the medium was change to normal medium for subsequent culture;in lipopolysaccharide+hsa-miR-3202 mimics group,cells were cultured in lipopolysaccharide-containing medium for 24 hours and then transfected with has-miR-3202 mimics for 6 hours,and the medium was changed to normal medium for subsequent culture. After further 48 hours of culture,the expression level of hsa-miR-3202 was detected by fluorescence quantitative PCR and cell apoptosis was detected by flow cytometry. After further culture of 0-72 hours,cell proliferation activity was detected by cell counting kit-8. RESULTS AND CONCLUSION:Bioinformatics analysis results indicated that hsa-miR-3202 was significantly down-regulated in osteoarthritic chondrocytes. GO functional enrichment and KEGG pathway enrichment showed that the function of hsa-miR-3202 target gene was closely related to cell growth and apoptosis. The results of in vitro cell experiments showed that compared with the normal group,the expression level of hsa-miR-3202 and proliferation ability of chondrocytes were significantly decreased in the lipopolysaccharide group (P<0.05),while the apoptotic rate was significantly increased (P<0.05). Compared with the lipopolysaccharide group,the expression level of hsa-miR-3202 and proliferation ability of chondrocytes were significantly increased in the lipopolysaccharide+hsa-miR-3202 mimics group (P<0.05),while the apoptotic rate was significantly decreased (P<0.05). To conclude,the expression of hsa-miR-3202 is down-regulated in osteoarthritic chondrocytes to inhibit cell proliferation and promote cell apoptosis,thus affecting the occurrence and development of osteoarthritis.

Multiple sclerosis (MS) is a neuroinflammatory demyelinating disease, mediated by pathogenic T helper 17 (Th17) cells. However, the therapeutic effect is accompanied by the fluctuation of the proportion and function of Th17 cells, which prompted us to find the key regulator of Th17 differentiation in MS. Here, we demonstrated that the triggering receptor expressed on myeloid cells 2 (TREM-2), a modulator of pattern recognition receptors on innate immune cells, was highly expressed on pathogenic CD4-positive T lymphocyte (CD4⁺ T) cells in both patients with MS and experimental autoimmune encephalomyelitis (EAE) mouse models. Conditional knockout of Trem-2 in CD4⁺ T cells significantly alleviated the disease activity and reduced Th17 cell infiltration, activation, differentiation, and inflammatory cytokine production and secretion in EAE mice. Furthermore, with Trem-2 knockout in vivo experiments and in vitro inhibitor assays, the TREM-2/zeta-chain associated protein kinase 70 (ZAP70)/signal transducer and activator of transcription 3 (STAT3) signal axis was essential for Th17 activation and differentiation in EAE progression. In conclusion, TREM-2 is a key regulator of pathogenic Th17 in EAE mice, and this sheds new light on the potential of this therapeutic target for MS.
Animals ; Humans ; Mice ; CD4-Positive T-Lymphocytes/pathology* ; Cell Differentiation ; Encephalomyelitis, Autoimmune, Experimental/metabolism* ; Mice, Inbred C57BL ; Multiple Sclerosis ; Th1 Cells/pathology*

Objective:To study the role and specific mechanisms of glucose-6-phosphate dehydrogenase (G6PD), a key enzyme for glycometabolism, mediated reduction stress in arsenic-induced malignant transformation of cells.Methods:Immortalized human skin keratinocyte-forming cells (HaCaT cells) were treated with sodium arsenite (NaAsO 2) at a concentration of 0.0 (control group) and 1.0 μmol/L (arsenic group), and malignant transformation indicators were tested using cell growth kinetics assay, cell scratch assay, and soft agar colony formation assay. At different stages of arsenic treatment (0, 1, 7, 14, 21, 28, 35 passages of cells), the effects of NaAsO 2 on glycometabolism in HaCaT cells were determined using corresponding reagent kits and Western blot, including glucose-6-phosphate (G6P), lactate, acetyl CoA, G6PD levels, as well as protein expression levels of hexokinase 2 (HK-2), 6-phosphofructose-2-kinase/fructose-2, 6-diphosphatase 3 (PFKFB3), pyruvate dehydrogenase kinase 1 (PDK1), 6-phosphoglucose dehydrogenase (PGD), and G6PD. Mitochondria were extracted, and the effects of NaAsO 2 on HaCaT cells and mitochondrial redox [reduced nicotinamide adenine dinucleotide phosphate (NADPH)/nicotinamide adenine dinucleotide phosphate (NADP +) ratio, reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio] were determined using corresponding reagent kits. The effect of G6PD on reduction stress and NaAsO 2-induced malignant transformation of HaCaT cells was determined using small interfering RNA (siRNA) intervention method. Results:Compared 1.0 μmol/L NaAsO 2-cultured HaCaT cells up to 35 generations (T-HaCaT cells) with matching passage 0.0 μmol/L NaAsO 2-cultured HaCaT cells [(33.797 ± 0.280) h, 0.177 ± 0.015, 13.667 ± 2.625], the multiplication time [(24.042 ± 0.479) h] was shorter ( t = 30.45, P < 0.001), the cell migration rate (0.396 ± 0.039) was higher ( t = 9.08, P < 0.001), and the number of colonies formed in soft agar (73.667 ± 4.450) was higher ( t = 20.11, P < 0.001). Compared with matching passage control group cells and 0 generation of the same group, G6P level in the arsenic group was higher at passages 1, 7, 14, 21, 28 and 35 ( P < 0.05), lactate and G6PD levels were higher at passages 14, 21, 28 and 35 ( P < 0.05), acetyl CoA level was lower at passages 21, 28 and 35 ( P < 0.05), and protein expression levels of HK-2, PFKFB3, PDK1, PGD, and G6PD were higher at passages 7, 14, 21, 28 and 35 ( P < 0.05). The NADPH/NADP + ratio of cells was higher at passages 1, 14, 21, 28 and 35 ( P < 0.05), GSH/GSSG ratio was higher at passages 21, 28 and 35 ( P < 0.05). The ratio of mitochondrial NADPH/NADP + was higher at passages 1, 7, 21, 28 and 35 ( P < 0.05), the GSH/GSSG ratio was higher at passages 1, 7, 14, 21, 28 and 35 ( P < 0.05). G6PD expression was silenced by siRNA in T-HaCaT cells, compared with the T-HaCaT con siRNA-treated group, the T-HaCaT G6PD siRNA-treated group had lower NADPH/NADP + and GSH/GSSG ratios in both cells and mitochondria ( P < 0.05), longer cell multiplication time, lower cell migration rate, and fewer soft agar colonies ( P < 0.05). Conclusion:During the malignant transformation of HaCaT cells induced by NaAsO 2, G6PD and other enzymes related to glycometabolism are activated, leading to reprogramming of glycometabolism, resulting in an imbalance of cell redox homeostasis and enhanced reduction stress in cells and mitochondria, thereby promoting NaAsO 2 induced malignant transformation of HaCaT cells.