Objective: To explore the effect of different obesity indicators in predicting cardiovascular and cerebrovascular diseases (CVD) risk among patients with type 2 diabetes mellitus (T2DM), so as to provide the evidence for the early identification of CVD risk among T2DM patients. Methods: The patients with T2DM under community management in Qingpu District, Shanghai Municipality were selected as the study subjects in January 2025. Basic information such as gender, age, and blood glucose control status were collected through the Shanghai Chronic Disease Information Management System, while history of CVD were obtained from residents' electronic health records and the Shanghai Disease Control Information Platform. Obesity was assessed using body mass index (BMI), waist circumference (WC), BMI combined with WC, waist-to-height ratio (WHtR), and triglyceride (TG) combined with WC indicators. The association between obesity and CVD was analyzed using multivariable logistic regression models. The predictive effect of each obesity indicators for CVD was evaluated using the area under the receiver operating characteristic curve (AUC). Results: A total of 4 367 patients with T2DM were included, including 2 121 males (48.57%) and 2 246 females (51.43%). The average age was (68.71±8.05) years. The prevalence of CVD was 44.49%. Multivariable logistic regression analysis showed that after adjusting for age, education level, history of hypertension, duration of T2DM, use of glucose-lowering medications, renal function, and blood glucose control status, obese T2DM patients had a 389.4% increased risk of CVD compared to those with normal BMI; centrally obese T2DM patients had a 100.4% increased risk compared to those with normal WC; T2DM patients with isolated general obesity and compound obesity had 161.0% and 241.1% increased risks of CVD, respectively, compared to those with normal BMI and WC; centrally obese T2DM patients had a 100.4% increased risk compared to those with normal WHtR; T2DM patients with normal TG-high WC and high TG-high WC phenotypes had 83.1% and 68.8% increased risks of CVD, respectively, compared to those with normal TG and normal WC (all P<0.05). BMI had the highest AUC, at 0.714, with sensitivity and specificity of 0.675 and 0.642, respectively. This was followed by BMI combined with WC, which had an AUC of 0.707, with sensitivity and specificity of 0.635 and 0.679, respectively. Conclusions Obesity defined by BMI, WC, BMI combined with WC, WHtR, and TG combined with WC increases the risk of CVD among patients with T2DM. BMI and BMI combined with WC have better predictive effect in predicting CVD risk among patients with T2DM, and can be used as the primary obesity indicators for CVD risk screening.

Abdominal aortic aneurysm (AAA) is a deadly condition of the aorta, carrying a significant risk of death upon rupture. Currently, there is a dearth of efficacious pharmaceutical interventions to impede the advancement of AAA and avert it from rupturing. Here, we investigated dihydromyricetin (DHM), one of the predominant bioactive flavonoids in Ampelopsis grossedentata (A. grossedentata), as a potential agent for inhibiting AAA. DHM effectively blocked the formation of AAA in angiotensin II-infused apolipoprotein E-deficient (ApoE^-/-) mice. A combination of network pharmacology and whole transcriptome sequencing analysis revealed that DHM's anti-AAA action is linked to heme oxygenase (HO)-1 (Hmox-1 for the rodent gene) and hypoxia-inducible factor (HIF)-1α in vascular smooth muscle cells (VSMCs). Remarkably, DHM caused a robust rise (∼10-fold) of HO-1 protein expression in VSMCs, thereby suppressing VSMC inflammation and oxidative stress and preserving the VSMC contractile phenotype. Intriguingly, the therapeutic effect of DHM on AAA was largely abrogated by VSMC-specific Hmox1 knockdown in mice. Mechanistically, on one hand, DHM increased the transcription of Hmox-1 by triggering the nuclear translocation and activation of HIF-1α, but not nuclear factor erythroid 2-related factor 2 (NRF2). On the other hand, molecular docking, combined with cellular thermal shift assay (CETSA), isothermal titration calorimetry (ITC), drug affinity responsive target stability (DARTS), co-immunoprecipitation (Co-IP), and site mutant experiments revealed that DHM bonded to HO-1 at Lys243 and prevented its degradation, thereby resulting in considerable HO-1 buildup. In summary, our findings suggest that naturally derived DHM has the capacity to markedly enhance HO-1 expression in VSMCs, which may hold promise as a therapeutic strategy for AAA.

The prevalence of Class III malocclusion varies among different countries and regions. The populations from Southeast Asian countries (Chinese and Malaysian) showed the highest prevalence rate of 15.8%, which can seriously affect oral function, facial appearance, and mental health. As anterior crossbite tends to worsen with growth, early orthodontic treatment can harness growth potential to normalize maxillofacial development or reduce skeletal malformation severity, thereby reducing the difficulty and shortening the treatment cycle of later-stage treatment. This is beneficial for the physical and mental growth of children. Therefore, early orthodontic treatment for Class III malocclusion is particularly important. Determining the optimal timing for early orthodontic treatment requires a comprehensive assessment of clinical manifestations, dental age, and skeletal age, and can lead to better results with less effort. Currently, standardized treatment guidelines for early orthodontic treatment of Class III malocclusion are lacking. This review provides a comprehensive summary of the etiology, clinical manifestations, classification, and early orthodontic techniques for Class III malocclusion, along with systematic discussions on selecting early treatment plans. The purpose of this expert consensus is to standardize clinical practices and improve the treatment outcomes of Class III malocclusion through early orthodontic treatment.
Humans ; Malocclusion, Angle Class III/classification* ; Orthodontics, Corrective/methods* ; Consensus ; Child

Objective:To analyze the influencing factors of thyroid volume in children aged 8 - 10 in Yunnan Province, and provide scientific basis for improving iodine deficiency disorders monitoring.Methods:From March to July 2020, in 129 counties (cities, districts) under the jurisdiction of Yunnan Province, each county (city, district) was divided into 5 sampling areas based on east, west, south, north, and middle. One township was selected from each area, and 40 non-boarding children aged 8 - 10 from one primary school were selected from each township (age balanced, half male and half female) as survey subjects. One random urine sample and household edible salt samples were collected for urine iodine and salt iodine testing, and physical examination and thyroid volume measurement were conducted for children. The influencing factors of thyroid volume were analyzed using Pearson correlation.Results:A total of 24 934 urine samples were collected from children, with a median urine iodine of 233.2 μg/L. A total of 24 933 household edible salt samples were collected from children, the median salt iodine was 24.17 mg/kg, and the qualified rate of iodized salt was 96.63% (24 003/24 839); A total of 24 937 children were examined of their thyroid gland, with a median thyroid volume of 2.62 ml and a goiter rate of 1.12% (280/24 937). Among them, there were 12 410 boys and 12 527 girls, with thyroid volumes of 2.61 and 2.64 ml, respectively. The thyroid volume of boys was positively correlated with age, height, weight, body mass index, body surface area, and salt iodine ( r = 0.15, 0.21, 0.26, 0.18, 0.25, 0.03, P < 0.001). The thyroid volume of girls was positively correlated with age, height, weight, body mass index, and body surface area ( r = 0.17, 0.26, 0.28, 0.17, 0.27, P < 0.001). Conclusion:Children aged 8 - 10 in Yunnan Province are at an iodine excess level; the age, weight, height, body mass index, and body surface area are influencing factors of thyroid volume.

Objective To explore the clinical significance of long non-coding RNA(lncRNA)VIM-AS5 expres-sion in human breast cancer tissues and its regulatory mechanism involved in cancer cell proliferation and mi-gration.Methods The Lnc2Cancer 3.0 database was used to analyze the expression of VIM-AS5 in breast cancer tissues and its correlation with the clinical stage and survival time of breast cancer patients.RT-qPCR was used to detect the expression of VIM-AS5 in breast cancer cell lines BT-549,MDA-MB-435,MDA-MB-231 and CAL-51.Plasmid with VIM-AS5 overexpression and negative control were all transfected into CAL-51 cells through liposome recorded as VIM-AS5 group and NC group,respectively.The proliferation and migration of CAL-51 cells were detected by colony formation assay and scratch healing method,respectively.Dual-lucif-erase reporter gene experiment verified the targeting relationship between VIM-AS5 and miR-500a.RT-qPCR was used to detect the expression of miR-500a in CAL-51 cells.Western blot was used to detect the expression of JAK/STAT3 pathway in CAL-51 cells.Results The expression of VIM-AS5 in breast cancer tissues was significantly lower than that in adjacent tissues(P＜0.01).VIM-AS5 expression was negatively correlated with the clinical stage of breast cancer patients(P＜0.01).The survival time of breast cancer patients with low VIM-AS5 expression was significantly shorter than that of breast cancer patients with high VIM-AS5 ex-pression(P＜0.01).Compared with mammary epithelial cell line MCF-10 A cells,VIM-AS5 expression was significantly reduced in breast cancer cells(P＜0.01).The counting number of colony formed in the VIM-AS5 group was significantly lower than that in the NC group(P＜0.01).The cell migration rate in the VIM-AS5 group was significantly lower than that in the NC group(P＜0.01).Dual-luciferase reporter gene experiment confirmed that miR-500a was the target gene of VIM-AS5(P＜0.01).VIM-AS5 can negatively regulate the expression of miR-500a(P＜0.01).Compared with the NC group,the expression of JAK/STAT3 pathway proteins JAK,p-STAT3,c-Myc,Bcl-2,and CDK3 in CAL-51 cells of the VIM-AS5 group were significantly decreased.Conclusions VIM-AS5 is low-expressed in breast cancer cells,and up-regulation of VIM-AS5 may inhibit the proliferation and migration of breast cancer cells CAL-51 by targeting at miR-500a/JAK/STAT3 pathway.

Objective To understand the characteristics and temporal trends of stroke incidence in the household population of Shanghai's Qingpu District and to provide a basis for the development of comprehensive prevention and control strategies. Methods The stroke case database for Qingpu District from 2017-2022 was obtained from the Shanghai Stroke and Acute Myocardial Infarction Registry and Reporting Information System. The average age of onset, incidence rate, standardised incidence rate, and constitutive ratio were calculated. Independent samples t-tests were used for comparisons between groups, 2-tests and 2-trend tests for comparisons of rates, and the Joinpoint regression model for calculating the annual percentage change (APC) to analyse the temporal trend of rates. Results Between 2017 and 2022, the average age of stroke onset in the household population of Shanghai's Qingpu District was 73.69±11.60 years. The average annual incidence rate was 556.62/100 000, with an average annual standardised incidence rate of 333.76/100000. There was an increasing trend in the incidence and standardised incidence of stroke in males (APC=7.06%, t=3.44, P=0.03, APC=5.32%, t=3.04, P=0.04). The incidence of stroke increases with age, with cases mainly concentrated in those aged 65 years and above, accounting for 79.47%. Ischemic stroke dominates the stroke typology, accounting for 91.08% of cases, while the incidence of hemorrhagic stroke shows an increasing trend (APC=4.64%, t=4.59, P=0.01). Conclusion The occurrence of stroke in the general population of Shanghai’s Qingpu District is concerning. The study indicates that males, individuals aged 65 years and above, and ischaemic stroke are significant factors that require attention for stroke prevention and control.

Objective:To explore the effects of genistein-3'-sodium sulfonate (GSS) on on motor function and brain autophagy levels in Parkinson disease (PD) model mice.Methods:Forty C57BL/6J mice were randomly divided into control group, model group, low-dose GSS group (0.15 mg/kg), medium-dose GSS group (0.50 mg/kg) and high-dose GSS group (1.50 mg/kg), with 8 mice in each group.Mice in the model group and the high, medium, and low-dose GSS groups were injected intraperitoneally with 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine to establish the PD mouse model, then mice in high, medium and low-close GSS group were intraperitoneally injected with corresponding doses of GSS (once a day for 21 days). The mice in model group were injected with equal volume 0.9% sodium chloride solution(once a day for 21 days), while the control group mice were fed normally.After 21 days, the motor and cognitive abilities of mice were evaluated by gait analysis, open field test, rotarod test, and modified Y maze test.Western blot was used to detect the expression levels of LC3-Ⅱ and Beclin-1 proteins in the cerebral cortex and striatum tissues of mice.SPSS 26.0 software was used for data analysis.One-way ANOVA was used for normal distribution data comparison among multiple groups, and LSD test was used for further pairwise comparisons, while Kruskal-Wails H test was used for non normal distribution data comparison. Results:(1) Gait analysis showed that there were statistically significant differences in the stride length of left forelimb, left hindlimb, right hindlimb( F=5.93, 6.21, 3.78, all P<0.01) and regularity index( H=14.409, P<0.01). The regularity index of the model group mice was lower than that of the control group ( P<0.05), and the regularity indexes of the low, medium, and high-dose GSS groups were all higher than that of the model group (all P<0.05). (2)In the open field test, there were statistically significant differences in the total distance and speed of movement among the 5 groups ( F=5.49, 5.49, both P<0.01). The total distance and speed of movement in the model group were both lower than those in the control group (both P<0.05). The total distance and speed of movement in the medium-dose GSS group( (2 395.57±319.35) cm, (7.98±1.06) cm/s) and high-dose GSS group ((2 386.51±396.00) cm, (7.95±1.32) cm/s) were higher than those of the model group ((1 863.31±278.96) cm, (6.21±0.93) cm/s) and the low-dose GSS group ((1 956.90±297.15) cm, (6.52±0.99) cm/s) (all P<0.05). (3) In the rotarod test and modified Y maze test, there were significant differences in latency to fall and residence time among the 5 groups ( F=58.41, 9.90, both P<0.01). The latency to fall and residence time of model group were lower than those of control group (both P<0.05), while those in the medium-dose and high-dose GSS groups were higher than those in the model group and low-dose GSS group (all P<0.05). (4) Western blot results showed that there were significant differences in the expression levels of LC3-Ⅱ/LC3-Ⅰ ratio ( F=8.17, 15.47, both P<0.01)and Beclin-1 protein( F=29.07, 20.54, both P<0.01) in cerebral cortex and striatum among the five groups.The LC3-Ⅱ/LC3-Ⅰ ratio and Beclin-1 protein levels in the cerebral cortex ((0.51±0.14), (0.46±0.06)) and striatum ((0.58±0.09), (0.55±0.10)) of the model group were lower than those in the control group (cerebral cortex: (1.00±0.10), (1.00±0.05), striatumm: (1.00±0.06), (1.00±0.25), all P<0.01). The LC3-Ⅱ/LC3-Ⅰratio and Beclin-1 protein in the medium-dose GSS group were higher than those in the model group, low-dose and high-dose GSS groups in both cerebral cortex and striatum (all P<0.05). The level of Beclin-1 of cerebral cortex in model group was lower than those in various doses of GSS group(all P<0.05). There were no statistically significant differences of Beclin-1 protein levels between the model group mice and various doses of GSS groups in striatum (all P>0.05). Conclusion:GSS can improve the motor and cognitive functions of PD model mice, and the mechanism may be related to the upregulation of autophagic activity in the cerebral cortex and striatum of mice.

Chronic heart failure(CHF)is a common and frequent clinical condition with complex pathogenesis.The micro-inflammatory state exists in the development of CHF and is manifested by a continuous increase in inflammatory proteins and inflammatory cytokines in the circulation,affecting the body's metabolism and immune function.Micro-inflammatory state of CHF belongs to the syndrome of deficiency in nature and excess in superficiality in the TCM field.The basic pathogenesis of CHF is"deficiency qi retention";the nature is the deficiency of heart energy and the superficiality is retention of qi,blood stagnation,phlegm,water and dampness,with"deficiency,stagnation and water"running throughout the disease.Therefore,based on the theory of"deficiency qi retention",this article took"reinforcing deficiency and removing stagnation"as its basic treatment method,regulated the body's immunity and inflammatory indicators such as serum high-sensitivity C-reactive protein,tumor necrosis factor-α,in order to alleviate the micro-inflammatory state,which is of great significance for the prevention and treatment of CHF.