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 investigate the therapeutic mechanism of Dingkun Dan(DKD)in polycystic ovary syndrome(PCOS)by examining the effects of microRNA-30d-5p on ovarian granulosa cells(GCs).Methods A PCOS rat model was established using dehydroepiandrosterone(DHEA).Normal rat GCs and PCOS rat GCs were cultured in vitro and divided into four groups:blank control group,model group,low-dose DKD group,and high-dose DKD group.After grouping,GCs viability was assessed using the methyl thiazolyl tetrazolium(MTT)assay,GCs apoptosis was analyzed by flow cytometry,and the gene expression of transforming growth factor β1(TGF-β1),Smad2,Smad3,and microRNA-30d-5p in GCs was measured by real-time polymerase chain reaction(RT-PCR),protein expression of TGF-β1,Smad2,and Smad3 in GCs was detected by Western Blot.Results Compared with the blank control group,the model group exhibited significantly decreased GCs viability,increased GCs apoptosis,upregulated mRNA and protein expression of TGF-β1,Smad2,and Smad3,and downregulated microRNA-30d-5p expression,the differences were statistically significant(P＜0.01).Compared with the model group,both low-and high-dose DKD groups showed increased GCs viability,reduced GCs apoptosis,downregulated mRNA and protein levels of TGF-β1 Smad2 and Smad3,elevated microRNA-30d-5p expression,and the differences were statistically significant(P＜0.05 or P＜0.01).Conclusion DKD promotes GCs proliferation by targeting Smad2 via microRNA-30d-5p,suggesting a potential therapeutic role in PCOS-related ovulatory dysfunction.

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 evaluate the role of spinal serum and glucocorticoid-inducible kinase 1(SGK-1)/Kalirin-7/N-methyl-D-aspartate receptor 2B(NR2B) signaling pathway in the type 2 diabetic neuropathic pain(DNP) in rats.Methods:Clean-grade male Sprague-Dawley rats, aged 6 weeks, weighing 120-160 g, were randomized to receive a normal diet(normal control group [group C, n=12]) or a high-fat and high-glucose diet( n=60). Diabetes mellitus was induced by single intraperitoneal injection of streptozotocin 35 mg/kg after 8 weeks of a high-fat and high-glucose diet. The successful DNP model was defined as a decrease in the pain threshold(mechanical paw withdrawal threshold [MWT] and thermal paw withdrawal latency [TWL]) to less than 85% of the baseline value in type 2 diabetic rats. Twelve non-DNP(pain threshold above 85% of the baseline value) rats with type 2 diabetes mellitus were randomly selected and included in non-DNP group(NDNP group). Thirty-six rats with DNP were divided into 3 groups( n=12 each) using a random number table method: DNP group, DNP plus SGK1 inhibitor GSK-650394 group(DNP+ G group), and DNP plus solvent control group(DNP+ SC group). At day 14 after STZ injection, GSK-650394(10 μl) 300 nmol/L was intrathecally injected once a day for 14 consecutive days in DNP+ G group. DNP group did not receive any treatment, and the rats in DNP+ SC group received intrathecal injection of the equal volume of dimethyl sulfoxide. The MWT and TWL were measured after 8 weeks of feeding, at 14 days after STZ injection, and at 3, 7 and 14 days after intrathecal injection(at 17, 21 and 28 days after STZ injection). After 7 days of intrathecal injection, the lumbar enlargement tissues of the spinal cord were collected for determination of the expression of SGK-1, phosphorylated SGK-1(Ser422-SGK1), Kalirin-7, phosphorylated NR2B(Tyr1472-NR2B), and NR2B by Western blot. The ratios of Ser422-SGK1 to SGK1 and Tyr1472-NR2B to NR2B were calculated. Results:Compared with C group, the MWT was significantly decreased and TWL was shortened at 14 days after STZ injection and at the corresponding time points of intrathecal injection, and the ratios of spinal Ser422-SGK1 to SGK1 and Tyr1472-NR2B to NR2B were increased, and the expression of Kalirin-7 was up-regulated in DNP group( P<0.05), and no statistically significant change was found in the aforementioned parameters in NDNP group( P>0.05). Compared with DNP group, the MWT was significantly increased and TWL was prolonged at 3, 7 and 14 days of intrathecal injection, the ratios of Ser422-SGK1 to SGK1 and Tyr1472-NR2B to NR2B in the spinal cord tissue were decreased, Kalirin-7 expression was down-regulated( P<0.05), and no statistically significant differences were found in the aforementioned parameters in DNP+ SC group( P>0.05). Conclusions:The enhanced phosphorylation of SGK-1 in the spinal cord of DNP rats may play an important role in the occurrence and maintenance of DNP probably by activating the Kalirin-7/NR2B signaling pathway.

Objective To observe changes in voltage-dependent anion channel 3(VDAC3)in a mouse model of sepsis-induced myocardial injury and to explore its potential mechanism.Methods Twenty male C57BL/6J mice were divided randomly into a Sham group and Sepsis group,respectively(n=10 mice per group).Sepsis was induced by the cecal ligation and puncture(CLP).Serum levels of interleukin(IL)-6,tumor necrosis factor(TNF)-α,creatine kinase MB(CK-MB),and cardiac troponin T(cTnT)were detected by enzyme-linked immunosorbent assay.Pathological changes in heart tissue were observed by hematoxylin and eosin staining.Structural and functional changes in the heart were evaluated by echocardiography.Changes in total glutathione,reduced glutathione(GSH),oxidized glutathione,and malondialdehyde(MDA)in heart tissue were detected by spectrophotometry.The morphological structure of mitochondria in mouse cardiomyocytes was observed by transmission electron microscopy.Expression levels of IL-6,IL-1β,VDAC3,glutathione peroxidase 4(GPX4),solute carrier family 7 member 11(SLC7A11),lipocalin-2(LCN2),and prostaglandin-endoperoxide synthase 2(PTGS2)mRNA were detected by real-time quantitative polymerase chain reaction and the localization and expression of VDAC3 and GPX4 proteins in mouse heart tissue were detected by immunofluorescence staining.The correlations between VDAC3 mRNA and GPX4,SLC7A11,PTGS2,LCN2,IL-6,and IL-1β mRNA were analyzed.Expression levels of VDAC3,GPX4,and SLC7A11 proteins were detected by Western blot.Results IL-6,TNF-α,CK-MB,and cTnT levels were significantly higher in the Sepsis group compared with the Sham group(P＜0.05).In the Sepsis group,myocardial fibers were torn,the ventricular wall was thickened and edematous,the mitochondrial membrane was ruptured,and mitochondrial cristae were broken or absent.GSH levels were significantly reduced in the Sepsis group(P＜0.05)and the lipid peroxide MDA was increased in the Sepsis group(P＜0.05)compared with the Sham group.VDAC3,GPX4 and SLC7A11 mRNA and protein levels were all lower in the Sepsis group compared with the Sham group(P＜0.05),while expression levels of IL-6,IL-1β,LCN2,and PTGS2 mRNA were increased(P＜0.05).VDAC3 mRNA was positively correlated with GPX4 and SLC7A11 mRNA levels,and negatively correlated with LCN2,PTGS2,IL-6,and IL-1β.Conclusions VDAC3 expression decreases in myocardial injury,and it may participate in the occurrence of sepsis-induced myocardial injury by regulating ferroptosis.

Objective:To evaluate the role of spinal serum and glucocorticoid-inducible kinase 1(SGK-1)/Kalirin-7/N-methyl-D-aspartate receptor 2B(NR2B) signaling pathway in the type 2 diabetic neuropathic pain(DNP) in rats.Methods:Clean-grade male Sprague-Dawley rats, aged 6 weeks, weighing 120-160 g, were randomized to receive a normal diet(normal control group [group C, n=12]) or a high-fat and high-glucose diet( n=60). Diabetes mellitus was induced by single intraperitoneal injection of streptozotocin 35 mg/kg after 8 weeks of a high-fat and high-glucose diet. The successful DNP model was defined as a decrease in the pain threshold(mechanical paw withdrawal threshold [MWT] and thermal paw withdrawal latency [TWL]) to less than 85% of the baseline value in type 2 diabetic rats. Twelve non-DNP(pain threshold above 85% of the baseline value) rats with type 2 diabetes mellitus were randomly selected and included in non-DNP group(NDNP group). Thirty-six rats with DNP were divided into 3 groups( n=12 each) using a random number table method: DNP group, DNP plus SGK1 inhibitor GSK-650394 group(DNP+ G group), and DNP plus solvent control group(DNP+ SC group). At day 14 after STZ injection, GSK-650394(10 μl) 300 nmol/L was intrathecally injected once a day for 14 consecutive days in DNP+ G group. DNP group did not receive any treatment, and the rats in DNP+ SC group received intrathecal injection of the equal volume of dimethyl sulfoxide. The MWT and TWL were measured after 8 weeks of feeding, at 14 days after STZ injection, and at 3, 7 and 14 days after intrathecal injection(at 17, 21 and 28 days after STZ injection). After 7 days of intrathecal injection, the lumbar enlargement tissues of the spinal cord were collected for determination of the expression of SGK-1, phosphorylated SGK-1(Ser422-SGK1), Kalirin-7, phosphorylated NR2B(Tyr1472-NR2B), and NR2B by Western blot. The ratios of Ser422-SGK1 to SGK1 and Tyr1472-NR2B to NR2B were calculated. Results:Compared with C group, the MWT was significantly decreased and TWL was shortened at 14 days after STZ injection and at the corresponding time points of intrathecal injection, and the ratios of spinal Ser422-SGK1 to SGK1 and Tyr1472-NR2B to NR2B were increased, and the expression of Kalirin-7 was up-regulated in DNP group( P<0.05), and no statistically significant change was found in the aforementioned parameters in NDNP group( P>0.05). Compared with DNP group, the MWT was significantly increased and TWL was prolonged at 3, 7 and 14 days of intrathecal injection, the ratios of Ser422-SGK1 to SGK1 and Tyr1472-NR2B to NR2B in the spinal cord tissue were decreased, Kalirin-7 expression was down-regulated( P<0.05), and no statistically significant differences were found in the aforementioned parameters in DNP+ SC group( P>0.05). Conclusions:The enhanced phosphorylation of SGK-1 in the spinal cord of DNP rats may play an important role in the occurrence and maintenance of DNP probably by activating the Kalirin-7/NR2B signaling pathway.

Objective To observe changes in voltage-dependent anion channel 3(VDAC3)in a mouse model of sepsis-induced myocardial injury and to explore its potential mechanism.Methods Twenty male C57BL/6J mice were divided randomly into a Sham group and Sepsis group,respectively(n=10 mice per group).Sepsis was induced by the cecal ligation and puncture(CLP).Serum levels of interleukin(IL)-6,tumor necrosis factor(TNF)-α,creatine kinase MB(CK-MB),and cardiac troponin T(cTnT)were detected by enzyme-linked immunosorbent assay.Pathological changes in heart tissue were observed by hematoxylin and eosin staining.Structural and functional changes in the heart were evaluated by echocardiography.Changes in total glutathione,reduced glutathione(GSH),oxidized glutathione,and malondialdehyde(MDA)in heart tissue were detected by spectrophotometry.The morphological structure of mitochondria in mouse cardiomyocytes was observed by transmission electron microscopy.Expression levels of IL-6,IL-1β,VDAC3,glutathione peroxidase 4(GPX4),solute carrier family 7 member 11(SLC7A11),lipocalin-2(LCN2),and prostaglandin-endoperoxide synthase 2(PTGS2)mRNA were detected by real-time quantitative polymerase chain reaction and the localization and expression of VDAC3 and GPX4 proteins in mouse heart tissue were detected by immunofluorescence staining.The correlations between VDAC3 mRNA and GPX4,SLC7A11,PTGS2,LCN2,IL-6,and IL-1β mRNA were analyzed.Expression levels of VDAC3,GPX4,and SLC7A11 proteins were detected by Western blot.Results IL-6,TNF-α,CK-MB,and cTnT levels were significantly higher in the Sepsis group compared with the Sham group(P＜0.05).In the Sepsis group,myocardial fibers were torn,the ventricular wall was thickened and edematous,the mitochondrial membrane was ruptured,and mitochondrial cristae were broken or absent.GSH levels were significantly reduced in the Sepsis group(P＜0.05)and the lipid peroxide MDA was increased in the Sepsis group(P＜0.05)compared with the Sham group.VDAC3,GPX4 and SLC7A11 mRNA and protein levels were all lower in the Sepsis group compared with the Sham group(P＜0.05),while expression levels of IL-6,IL-1β,LCN2,and PTGS2 mRNA were increased(P＜0.05).VDAC3 mRNA was positively correlated with GPX4 and SLC7A11 mRNA levels,and negatively correlated with LCN2,PTGS2,IL-6,and IL-1β.Conclusions VDAC3 expression decreases in myocardial injury,and it may participate in the occurrence of sepsis-induced myocardial injury by regulating ferroptosis.

Objective: To provide high-quality clinical evidence of the efficacy of Tibetan medicine Honghua Ruyi (HHRY) pills for endometriosis-associated dysmenorrhea. Methods: This study constitutes a multicenter, randomized, double-blind, placebo-controlled trial encompassing a three-menstrual cycle intervention followed by a three-menstrual cycle follow-up period. A total of 164 eligible females with endometriosis-associated dysmenorrhea were randomly divided into HHRY pills and placebo groups in a 1:1 ratio. The primary outcome included dysmenorrhea symptoms assessed using Visual Analog Scale (VAS) scores and quality of life, whereas the secondary outcome measures included the maximum VAS for non-menstrual pelvic pain, duration of pain episodes (in days), frequency and quantity of the consumption of ibuprofen sustained-release capsules (or other non-steroidal anti-inflammatory drugs), and days off work/study for staff/student due to dysmenorrhea, ovarian cyst, and/or pelvic nodule size. The safety was monitored throughout the treatment period. All the analyses were based on the intention-to-treat principle. For continuous outcomes, simple or multiple linear regressions were used to estimate the differences between the HHRY pills and placebo groups, with categorical data expressed as the number and percentage of occurrences. Differences were compared using the chi-square test or Fisher's exact test. The predefined analysis was adjusted for concomitant treatment, a variable considered to be associated with outcomes but unaffected by treatment allocation. Estimates of treatment effects were reported with 95% confidence intervals. Two-tailed P values ≤ .05 were considered statistically significant. Conclusion Positive results from this trial, upon completion would provide robust evidence for the efficacy and safety of HHRY pills in treating dysmenorrhea in patients with endometriosis.

[摘 要] 目的：探讨程序性死亡受体-1（PD-1）单抗联合顺铂或吉西他滨在KRAS基因突变非小细胞肺癌（NSCLC）A549细胞移植瘤小鼠模型治疗中的作用。方法：构建免疫系统-肿瘤双人源化A549细胞小鼠移植瘤模型，将60只小鼠按随机数字表法分成6组（10只/组），分别为对照组（200 μL/kg PBS）、PD-1单抗组（20 mg/kg PD-1单抗）、顺铂组（3 mg/kg顺铂）、PD-1单抗+顺铂组（20 mg/kg PD-1单抗+3 mg/kg顺铂）、吉西他滨组（30 mg/kg吉西他滨）和PD-1单抗+吉西他滨组（20 mg/kg PD-1单抗+30 mg/kg吉西他滨）。TUNEL和DAPI双染色法检测移植瘤组织中细胞凋亡水平，测量移植瘤体积和质量并计算肿瘤生长抑制率，免疫组化法检测移植瘤微血管密度（MVD）。结果：成功构建免疫系统-肿瘤双人源化NSCLC A549细胞小鼠移植瘤模型，PD-1单抗+顺铂组移植瘤的细胞凋亡率、肿瘤生长抑制率均最高，移植瘤体积、质量和MVD均最小，与其他5组小鼠比较差异均有统计学意义（均P<0.05）。结论：顺铂与PD-1单抗具有协同活性，而吉西他滨拮抗PD-1单抗的治疗作用。提示PD-1单抗联合顺铂对KRAS突变NSCLC A549细胞移植瘤小鼠的疗效更好。

Objective To explore the risk factors of apathy and correlations with cognitive function in patients with hypertension combined with cerebral small vessel disease(CSVD).Methods Totally 141 patients with hypertension combined with CSVD were prospectively enrolled and were divided into apathy group(n=43)and non-apathy group(n= 98)according to neuropsychiatric inventory-apathy scale(NPI-Apathy)scores.The general data,imaging marker scores and total imaging burden scores were compared between groups.In hypertension combined with CSVD patients,multivariate logistic regression analysis was performed to screen the independent risk factors of apathy,and Spearman correlation analysis was also performed to observe the correlation of apathy and cognitive function.Results The patients'age,high density lipoprotein cholesterol(HDL-C),Fazekas scores of lateral periventricular white matter hyper-intensity(WMH),cerebral microbleed of depth/infratentorial and total imaging burden scores of apathy group were all higher,while mini-mental state examination(MMSE)and Montreal cognitive assessment(MoCA)scores were both lower than those of non-apathy group(all P＜0.05).HDL-C and Fazekas scores of lateral periventricular WMH were both independent risk factors for apathy(both P＜0.05),while NPI-Apathy scores were moderately negatively correlated with cognitive function in patients with hypertension combined with CSVD(r=-0.543,-0.484,both P＜0.001).Conclusion HDL-C and Fazekas scores of lateral periventricular WMH were both independent risk factors for apathy in patients with hypertension combined with CSVD.The more severe the apathy,the lower the cognitive function.