Objective To screen and analyze biomarkers of comorbidity in nonalcoholic fatty liver disease(NAFLD)and colorectal cancer(CRC)based on bioinformatics so as to explore the mechanism of comorbidity.Methods After data related to NAFLD and CRC were downloaded from the public database(GEO),gene set enrichment analysis(GSEA)was performed for all genes to screen the expression pathways,and the common differentially expressed genes of both genes were annotated by GO and KEGG functions.Subsequently,PPI protein interaction network was constructed using STRING online database to screen key genes,and transcription factor-gene regulatory network was constructed based on key genes,and biomarker genes were identified using LASSO regression.Finally,the transcription factor prediction analysis of key genes and SCD was conducted through Network Analyst database,and the transcription factor network was constructed.Results GSEA analysis revealed that signaling pathways such as TNF-α and IL-6-JAK-STAT3 were activated in NAFLD patients.The 17 common differentially expressed genes were mainly enriched in biological processes such as bivalent inorganic cation homeostasis and neutrophil chemotaxis in GO analysis.KEGG pathway analysis showed that common differentially expressed genes were mainly concentrated in IL-17 signaling pathway.The protein interaction network screened out five key genes:TREM1,FPR1,IL1RN,S100A9,and S100A8.IL1RN and SCD,identified by LASSO regression,were validated as biomarker genes using external datasets and immunohistochemistry data from the human protein atlas(HPA)database,showing high expression in CRC tissues.A transcription factor-key comorbidity gene regulatory network was constructed using Network Analyst.Conclusion The genes for comorbidities between NAFLD and colorectal cancer discovered by bioinformatics reveal the potential pathogenesis of comorbidities,and provide ideas for cancer screening and early diagnosis of colorectal cancer in NAFLD patients.

This consensus was developed by the Orthodontic Society of the Chinese Stomatological Association to provide a systematic, scientific, and practical guideline for informed consent in orthodontic care. Orthodontic treatment is typically lengthy, highly individualized, and involves multiple factors such as growth and development, occlusal function, and facial esthetics. Rapid technological advances and diverse risk profiles make the traditional reliance on orthodontist experience or institutional templates insufficient to ensure patients′ full understanding and autonomous decision-making. To address this, the expert panel conducted extensive reviews of domestic and international guidelines, analyzed representative dispute cases, and performed multicenter patient-clinician surveys. Using a multi-round Delphi method, the group established a standardized informed consent framework covering the initial consultation, treatment, and retention phases. The consensus emphasizes that informed consent is not only a fundamental legal and ethical requirement but also a key step in building trust, improving patient compliance, and enhancing treatment satisfaction. Orthodontists should clearly and comprehensively explain treatment plans, potential risks, uncertainties, and associated costs, while respecting the autonomy of patients or guardians, and maintain continuous communication and dynamic evaluation throughout the treatment process. The release of this consensus provides unified and authoritative guidance for clinical orthodontics, helping to standardize informed consent, enhance its transparency, safeguard patient rights, reduce medical risks, and promote high-quality, sustainable development of orthodontic practice.

This consensus was developed by the Orthodontic Society of the Chinese Stomatological Association to provide a systematic, scientific, and practical guideline for informed consent in orthodontic care. Orthodontic treatment is typically lengthy, highly individualized, and involves multiple factors such as growth and development, occlusal function, and facial esthetics. Rapid technological advances and diverse risk profiles make the traditional reliance on orthodontist experience or institutional templates insufficient to ensure patients′ full understanding and autonomous decision-making. To address this, the expert panel conducted extensive reviews of domestic and international guidelines, analyzed representative dispute cases, and performed multicenter patient-clinician surveys. Using a multi-round Delphi method, the group established a standardized informed consent framework covering the initial consultation, treatment, and retention phases. The consensus emphasizes that informed consent is not only a fundamental legal and ethical requirement but also a key step in building trust, improving patient compliance, and enhancing treatment satisfaction. Orthodontists should clearly and comprehensively explain treatment plans, potential risks, uncertainties, and associated costs, while respecting the autonomy of patients or guardians, and maintain continuous communication and dynamic evaluation throughout the treatment process. The release of this consensus provides unified and authoritative guidance for clinical orthodontics, helping to standardize informed consent, enhance its transparency, safeguard patient rights, reduce medical risks, and promote high-quality, sustainable development of orthodontic practice.

Objective To screen and analyze biomarkers of comorbidity in nonalcoholic fatty liver disease(NAFLD)and colorectal cancer(CRC)based on bioinformatics so as to explore the mechanism of comorbidity.Methods After data related to NAFLD and CRC were downloaded from the public database(GEO),gene set enrichment analysis(GSEA)was performed for all genes to screen the expression pathways,and the common differentially expressed genes of both genes were annotated by GO and KEGG functions.Subsequently,PPI protein interaction network was constructed using STRING online database to screen key genes,and transcription factor-gene regulatory network was constructed based on key genes,and biomarker genes were identified using LASSO regression.Finally,the transcription factor prediction analysis of key genes and SCD was conducted through Network Analyst database,and the transcription factor network was constructed.Results GSEA analysis revealed that signaling pathways such as TNF-α and IL-6-JAK-STAT3 were activated in NAFLD patients.The 17 common differentially expressed genes were mainly enriched in biological processes such as bivalent inorganic cation homeostasis and neutrophil chemotaxis in GO analysis.KEGG pathway analysis showed that common differentially expressed genes were mainly concentrated in IL-17 signaling pathway.The protein interaction network screened out five key genes:TREM1,FPR1,IL1RN,S100A9,and S100A8.IL1RN and SCD,identified by LASSO regression,were validated as biomarker genes using external datasets and immunohistochemistry data from the human protein atlas(HPA)database,showing high expression in CRC tissues.A transcription factor-key comorbidity gene regulatory network was constructed using Network Analyst.Conclusion The genes for comorbidities between NAFLD and colorectal cancer discovered by bioinformatics reveal the potential pathogenesis of comorbidities,and provide ideas for cancer screening and early diagnosis of colorectal cancer in NAFLD patients.

To summarize the progress in BNCT dose verification method in the world and discusses their development prospects. Boron neutron capture therapy (BNCT) utilizes the specific capture reaction between the neutrons and boron drugs enriched in tumor cells to selectively kill tumor cells. In order to verify the accuracy of the radiotherapy plan and ensure the therapeutic effect on patients, it is necessary to measure the dose before treatment and compare the experimental radiation dose with the planned dose. The current BNCT dose measurement method mainly include point dose measurement method based on ionization chambers, thermoluminescence dosimeters and activation foils, two-dimensional dose measurement method based on films, and three-dimensional dose measurement method based on gel dosimeters.

Purpose: Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) play a key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanism of SLC26A2 in the proliferation and inflammatory factor production of HASMCs. Materials and Methods: We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhood acute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with plateletderived growth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferation was detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migration and production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses. Results: SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs. Conclusion These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma and airway inflammation.

Purpose: Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) play a key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanism of SLC26A2 in the proliferation and inflammatory factor production of HASMCs. Materials and Methods: We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhood acute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with plateletderived growth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferation was detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migration and production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses. Results: SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs. Conclusion These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma and airway inflammation.

KylinRay-IMRT is the advanced radiotherapy treatment planning module of accurate radiotherapy system (KylinRay) aiming to provide accurate and efficient plan design platform. In this paper the system design, main functions and key technologies of KylinRay-IMRT were introduced. KylinRay-IMRT supports three dimensional conformal radiotherapy (3D-CRT), intensity modulated radiotherapy (IMRT) and many other types of treatment plan design with function modules including patient data management, image registration and fusion, image contouring, image three dimensional reconstruction and visualization, three dimensional conformal radiotherapy planning, intensity modulated radiotherapy planning, plan evaluation and comparison, and report print. KylinRay-IMRT has been tested by the national standard YY/T 0889-2013, the results showed that the performance of KylinRay-IMRT can fully meet the standard requirements.
Humans ; Radiotherapy Dosage ; Radiotherapy Planning, Computer-Assisted ; Radiotherapy, Conformal ; Radiotherapy, Intensity-Modulated ; Tomography, X-Ray Computed

Objective: To study the change of STAT1 expression in the anterior cingulate cortex on rats under orthodontic force, and to further explore the roles of STAT1 and related JAK-STAT1 signaling pathway in the mediation and regulation of pain during tooth movement. Methods: 112 male Sprague-Dawley (SD) rats (225±25 g) were used in this study. They were randomly divided into experimental groups (96 rats) and control groups (16 rats). All rats were installed bilateral maxillary device for tooth movement models. Rats in the experimental groups were applied 80g orthodontic force on both sides and were divided into six subgroup 4 h, 12 h, 24 h, 2 d, 3 d, 7 d, with 16 rabbits in each subgroup. The control groups were only installed the same orthodontic devices, without the application of orthodontic force. Brain tissue of the anterior cingulate cortex was isolated after 4 h, 12 h, 24 h, 2 d, 3 d, 7 d since experiment, and the expression level of STAT1 and p-STAT1 was analyzed with the method of immunofluorescence and PCR. Results : For the immunofluorescence result, there was significant difference in STAT1 expression between control groups and different experimental groups at different time points in total (P < 0.05). The STAT1 expression amount in the 4 h group decreased significantly when compared with the control group (P < 0.05); to the 2 d group, the difference is still statistically significant (P < 0.01). 3 d group, 7 d group and control group had no statistically significant difference. The STAT1 expression amount in 4 h group, 12 h group, 24 h group was significantly lower than that in 3 d and 7 d groups, differences were statistically significant (P < 0.05). The STAT1 expression in the 2 d group was significantly lower than that of 7 d (42.35 ± 5.77) group, the difference was statistically significant (P < 0.05). There was significant difference in p-STAT1 expression between control groups and different experimental groups at different time points in total (F = 623.518, P < 0.05). The p-STAT1 expression amount in experimental groups were higher than that in the control group (P < 0.05). The p-STAT1 expression in 4 h group was lower than that in 12 h and 24 h group and higher than that in 2 d, 3 d and 7 d groups, of which the differences were statistically significant (P < 0.05). The p-STAT1 expression in 12 h group was lower than that in 24 h group and higher than that in 2 d, 3 d and 7 d groups, of which the differences were statistically significant (P < 0.05). For the PCR result, the expression of mRNA in STAT1 of experimental groups of 4 h, 12 h, 24 h, 2 d, 3 d, 7 d and the control groups were not statistically significant (P > 0.05). Conclusions After applying orthodontic force, the expression of STAT1 decreased transiently and the expression of p-STAT1 increased transiently. The reduction of STAT1 was probably caused by the phosphorylation of STAT1 and decrease in the translation level of STAT1, rather than changes in the transcriptional levels. The orthodontic pain might be related with the activation of STAT1 into phosphorylated STAT1.

Objective To investigate the effects of Wuling Powder on insulin resistance of C57BL/6J mice induced by high lipid diet, and discuss the mechanism. Methods C57BL/6J mice were randomly divided into six groups:normal group, model group, rosiglitazone group, Wuling Powder in low, middle, and high dose groups, 10 mice per group. Besides the normal group, other five groups were fed with high fat and sugar diet, with a purpose to establish insulin resistance model. Normal group and model group were given pure water. Rosiglitazone group received a gavage with rosiglitazone of 0.75 mg/kg. Wuling Power low, middle, and high groups received gavage with Wuling Power of 1.23, 3.69, 11.07 g/kg, respectively, the does volume was 0.2 mL/10 g, once a day. The weight and abdominal girth were detected every week. At the end of the sixth week, mice were given 12-hour fasting, and their eyeball were taken for blood. The body weight, length, and fat in abdomen and both kidneys were detected. Paraffin section was made with HE staining. FPG and FINS of each group were detected. ISI and IRI were calculated, and TC and TG were detected. Results Compared with the model group, Wuling Powder can significantly reduce the body weight and abdominal girth of mice (P<0.01, P<0.001), improve liver fatty degeneration, lower the FPG, FINS, TCH, TG, IRI, and increase the ISI in mice (P<0.05, P<0.01). Conclusions Wuling Powder has the effect of preventing insulin resistance of C57BL/6J mice induced by high lipid diet.