BACKGROUND:Growth hormone (GH) reduces visceral adiposity, increases lean body mass, and improves the lipid profile in obese adults. However, high-dose GH regimens have been associated with frequent adverse effects. The efficacy and safety of low-dose GH treatment in obese individuals without GH deficiency remain unclear. This study aims to evaluate the effects of recombinant human growth hormone (rhGH) on body composition, lipid profile, glucose metabolism, and adverse events in this population. METHODS:A systematic review and meta-analysis were conducted in accordance with the PRISMA statement. PubMed, Cochrane Library, and EMBASE databases were systematically searched up to December 2024. Eligible studies included randomized controlled trials (RCTs) involving obese individuals without GH deficiency, with at least one endpoint related to body composition, lipid profile, or glucose metabolism. The study protocol was registered in the International Prospective Register of Systematic Reviews (PROSPERO, #CRD42023464234). RESULTS:A total of 10 RCTs involving 420 participants were included. The mean age of participants ranged from 18 to 65 years, and treatment durations varied from 4 to 72 weeks. Low-dose rhGH therapy resulted in a significant reduction in visceral adipose tissue (SMD: -0.34, 95%CI: -0.57 to -0.12, p = 0.003) and a significant increase in thigh muscle area (MD: 6.33 cm2, 95%CI: 1.72 to 10.95, p = 0.007) compared to placebo. Additionally, fasting glucose levels were modestly elevated (MD: 4.18 mg/dL, 95%CI: 0.68 to 7.67, p = 0.02). No serious adverse events were reported in association with low-dose rhGH treatment across the included studies. CONCLUSIONS:Low-dose rhGH therapy significantly reduces visceral fat and enhances thigh muscle mass in obese individuals without GH deficiency. These findings suggest that low-dose rhGH may offer therapeutic potential for sarcopenic obesity, warranting further investigation in larger, longer-term studies.

Background Type 2 diabetes (T2D) and chronic gastritis/duodenitis (CGD) are both strongly associated with the onset of depression. However, the impact of T2D-CGD comorbidity on incident depression and all-cause mortality remains unclear. Method This retrospective cohort study utilized data from 387,149 participants in the UK Biobank to examine the relationship between T2D-CGD comorbidity, incident depression, and all-cause mortality. Outcome Patients with T2D are more likely to develop CGD compared to those without T2D (OR = 2.10, 95% CI = [1.97, 2.24]). T2D-CGD comorbidity was identified as a significant risk factor for both incident depression (adjusted HR = 2.29, 95% CI = [1.84, 2.85]) and all-cause mortality (adjusted HR = 2.57, 95% CI = [2.28, 2.88]). The synergistic effect of T2D and CGD on all-cause mortality was 1.92 times that of their individual effects combined (synergy index = 1.92, 95% CI = [1.56, 2.31]). The comorbidity was associated with a higher risk of depression and all-cause mortality within 15 years of disease onset. White matter hyperintensity, particularly near the cerebral ventricles, partially mediated the relationship between T2D-CGD comorbidity and incident depression. Interpretation Integrated screening and long-term monitoring strategies should be prioritized for population with the comorbidity of T2D and CGD, as it significantly elevates the risk of both incident depression and all-cause mortality. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement BH has received funding from the National Natural Science Foundation of China [grant number 82302148]. YY has received funding from the Key Science and Technology Program of Shaanxi Province [grant number 2023-YBSF-331] and Fourth Military Medical University [grant number 2023XC045]. GBC has received funding from the National Natural Science Foundation of China [grant number 82471936]. ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: The study used ONLY openly available human data that were originally located at UK Biobank. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes All data produced are available online at UK Biobank.

Aims:Sex differences in the incidence of thyroid nodules (TNs) are broadly recognized, but further analysis is lacking. Thus, the aim of this study was to evaluate the association between TNs and anthropometric parameters in type 2 diabetic males and females. Materials and Methods:This cross-sectional study included 747 patients with type 2 diabetes mellitus (T2DM). All patients underwent clinical examination, thyroid ultrasound, laboratory tests, anthropometrics and body composition. Multivariable logistic regression assessed factors associated with TNs, and a simple nomogram was finally developed. Results:In total, the incidence of TNs was 36.95% (276/747) and was significantly higher in females (52.75%) than in males (27.85%). Age was positively correlated with TNs risk in patients with T2DM (males: OR = 4.141, 95% CI [1.999-8.577], females: OR = 4.630, 95% CI [1.845-11.618]). Obesity (OR = 2.655, 95% CI [1.257-5.607]) and hyperuricemia (OR = 1.997, 95% CI [1.030-3.873]) were only associated with the risk of TNs independent of other risk factors in type 2 diabetic females, as well as other obesity factors such as weight, BMI, waist-hip ratio, percent body fat, visceral curve area, and upper arm circumference, but not in type 2 diabetic males. However, the diameter of the largest thyroid nodule was only related to age (R = 0.226, p < 0.01). Finally, the nomogram for evaluating TNs in female T2DM patients was established, and the C-index of the nomogram was 0.704 (95% CI [0.89-0.94]). Conclusion:TNs occur with a significantly higher frequency in type 2 diabetic females than in males, especially those with hyperuricemia and obesity. Modifiable metabolic factors, such as obesity and hyperuricemia, are a major focus for improving TNs risk in women.

OBJECTIVE:Type 2 diabetes mellitus (T2DM) is a significant risk factor for mild cognitive impairment (MCI). Here, we identified a T2DM-specific effective connectivity (EC) network, the dynamic features of which could be used to distinguish T2DM patients with MCI from healthy controls (HC) and correlation with cognitive performance. METHODS:Local and multicentered T2DM patients and matched HC who underwent functional magnetic resonance imaging were recruited. Their static and dynamic effective connectivity were compared. The relationships between connectome characteristics and cognitive performance were also evaluated. RESULTS:The nodes of the T2DM-related static causality network included the anterior central gyrus, tail of the parahippocampal gyrus, posterior superior temporal sulcus, posterior central parietal lobe, posterior central gyrus and V5 region of the occipital lobe. The V5 region of the visual cortex was the core node. In the multicentered dataset, compared with the HC group, the T2DM with MCI group had significantly greater fractional window and mean dwell time. Fractional windows of the state, which was dominated by the interaction of the nodes from SomMot_Network, Limbic_Network, Default_Network, in the T2DM-specific network increased with poorer cognitive performance in T2DM with MCI patients. CONCLUSION:Our findings provide insights into the neurobiological mechanisms of the cognitive impairment of T2DM patients from a dynamic network perspective, which may ultimately inform more targeted and effective strategies to prevent MCI.

Episodic memory decline is a common complication of type 2 diabetes (T2D). To comprehensively explore the neural mechanisms underlying it, we aimed to explore the sequence that episodic memory-related behavioral and brain-imaging biomarkers appear abnormal in the progression of T2D. We enrolled 62 healthy controls and 110 patients with T2D. The California Verbal Learning Test, Montreal cognitive assessment, and Stroop color word test was used to assess the episodic memory, general cognitive function, and executive function. Principal component analysis was applied to extract behavioral biomarkers. Imaging biomarkers included structural and functional MRI features of the entorhinal cortex-hippocampus and hippocampus-anterior cingulate cortex pathways. We used a novel discriminative event-based model to determine the sequence that memory-related biomarkers appear abnormal and estimate the stage of memory decline. T2D patients exhibited poorer memory, general cognitive function, and executive function compared to healthy controls after controlling age, sex, and education level. In the progression of T2D, functional interaction between brain regions showed abnormalities first, followed by memory tests, the cerebral spontaneous neural activity, and finally the gray matter volume. Besides, abnormalities appeared earlier in the entorhinal cortex than in the anterior cingulate cortex. Later stage of memory decline was distributed in older patients with T2D and was associated with higher systolic blood pressure, postprandial blood glucose, and low-density lipoprotein. In T2D, behavioral and brain imaging biomarkers of episodic memory appear abnormal in a specific sequence, and the stage of memory decline was closely associated with old age and vascular risk factors. NCT02420470, ClinicalTrials.gov ( https://www.clinicaltrials.gov/ ).

Objectives Type 2 diabetes (T2D) and chronic gastritis/duodenitis (CGD) are both strongly associated with the onset of depression. However, the impact of T2D-CGD comorbidity on incident depression remains unclear. Methods This prospective cohort study utilized data from 387 149 participants in the UK Biobank to examine the relationship between T2D-CGD comorbidity and incident depression. Results Patients with T2D exhibited a significantly higher likelihood of developing CGD than those without T2D (odds ratio = 2.10, 95% CI = [1.97, 2.24]). Both T2D and CGD were independently associated with an increased risk of incident depression, with their comorbidity demonstrating the strongest associations (adjusted hazard ratio = 2.29, 95% CI = [1.84, 2.85]). Notably, the comorbidity was linked to an elevated risk of depression within 15 years of disease onset. White matter hyperintensity, particularly near the cerebral ventricles, partially mediated the relationship between T2D-CGD comorbidity and incident depression. Conclusions Integrated screening and long-term monitoring strategies should be prioritized for population with the comorbidity of T2D and CGD, as it significantly elevates the risk of incident depression. White matter hyperintensity can serve as an imaging biomarker for detecting the risk of depression in patients with T2D-CGD comorbidity.

AIM:High rates of dropout and binge eating triggered by restrictive diet limit the effectiveness of dietary interventions in type 2 diabetes mellitus (T2DM). However, it remains unclear what the potential central underpinnings of T2DM-specific dietary behavior characteristics are. METHODS:41 T2DM patients and 43 matched healthy controls (HC) who underwent resting state functional MRI were enrolled to screen for the suspicious network by effective connectivity (EC) analysis and to explore its dynamic temporal and neurovascular coupling properties. Additionally, the timeline of neuropathological changes during T2DM progression was evaluated. RESULTS:Increased uncontrolled eating, internal and external loci of hunger were found in T2DM. EC of the frontoparietal cortex-putamen-cerebellum network was significantly higher in T2DM patients (P = 0.023). The fractional windows (P = 0.009) and mean dwell time (P = 0.009) of the densest state were significantly higher in T2DM patients. Neurovascular decoupling of the frontoparietal cortex-putamen-cerebellum network was correlated with these T2DM-specific eating behavior characteristics. Neurovascular decoupling coefficient of right putamen (Putamen_R) changed at the very beginning of T2DM. CONCLUSION:The frontoparietal cortex-putamen-cerebellum network was the suspicious T2DM-related abnormal eating pattern network. Neurovascular decoupling of the network, especially that of Putamen_R, occurred early and might serve as a biomarker for abnormal eating patterns in T2DM patients.

Type 2 diabetes (T2D) and chronic gastritis/duodenitis (CGD) are both associated with the onset of depression and mortality. However, the impact of T2D-CGD comorbidity on incident depression and mortality remains unclear. This retrospective cohort study utilized data from 387,149 participants in the UK Biobank to examine the relationship between T2D-CGD comorbidity, incident depression, and all-cause mortality. Patients with T2D are more likely to develop CGD compared to those without T2D (odds ratio = 2·10, 95% CI = [1·97, 2·24]). T2D, CGD, and their comorbidity each independently increased risks of depression incidence and all-cause mortality, with T2D-CGD showing the strongest associations for both (depression incidence: adjusted hazard ratio [aHR] = 2·29, 95% CI = [1·84, 2·85]; all-cause mortality: aHR = 2·57, 95% CI = [2·28, 2·88]). The synergistic effect of T2D and CGD on all-cause mortality was 1·92 times that of their individual effects combined (synergy index = 1·92, 95% CI = [1·56, 2·31]). The comorbidity was associated with a higher risk of depression and all-cause mortality within 15 years of disease onset. White matter hyperintensity, particularly near the cerebral ventricles, partially mediated the relationship between T2D-CGD comorbidity and incident depression. Integrated screening and long-term monitoring strategies should be prioritized for population with the comorbidity of T2D and CGD, as it significantly elevates the risk of both incident depression and all-cause mortality.

Background The role of stress hyperglycemia ratio (SHR) on the prognosis of spontaneous intracerebral hemorrhage (ICH) in patients with different diabetic status has not been elucidated. This study aimed to evaluate the prognostic value of SHR and admission blood glucose (ABG) for the short- and long-term mortality in diabetic and nondiabetic populations with ICH. Method Participants with ICH were retrospectively retrieved from the Medical Information Mart for Intensive Care (MIMIC-IV). The primary outcome was all-cause 30-day and 1-year mortality. The association of SHR and ABG with the primary outcomes in diabetic and nondiabetic cohorts were assessed by Cox proportional hazard regression. Results Overall, 1029 patients with a median age of 71.09 (IQR: 60.05–81.97) were included. Among them, 548 (53%) individuals were male, and 95 (19%) as well as 323 (31%) ones experienced the 30-day and 1-year mortality, respectively. After adjusting for confounding variables, individuals in quintile 5 of SHR had significantly higher risk of the 30-day and 1-year mortality than those in quintile 1 in the whole cohort (30-day mortality: HR 3.33, 95%CI 2.01–5.51; 1-year mortality: HR 2.09, 95% CI 1.46-3.00) and in nondiabetic patients (30-day mortality: HR 4.55, 95%CI 2.33–8.88; 1-year mortality: HR 3.06, 95%CI 1.93–4.86), but no significant difference was observed in diabetic patients. Similar results were observed for ABG as a categorical variable. As continuous variable, SHR was independently correlated with the 30-day and 1-year mortality in both of the diabetic and nondiabetic cohorts (30-day mortality: HR 2.63, 95%CI 1.50–4.60. 1-year mortality: HR 2.12, 95%CI 1.33–3.39), but this correlation was only observed in nondiabetic cohort for ABG (HR 1.00, 95%CI 0.99–1.01 for both of the 30-day and 1-year mortality). Moreover, compared with ABG, SHR can better improve the C-statistics of the original models regarding the 30-day and 1-year outcomes, especially in patients with diabetes ( p < 0.001 in all models). Conclusion SHR might be a more useful and reliable marker than ABG for prognostic prediction and risk stratification in critically ill patients with ICH, especially in those with diabetes.

This research aimed to investigate the association between various anthropometric indexes and metabolic syndrome (MetS) and evaluate their predictive effectiveness for MetS. Data from the China National Diabetes and Metabolic Disorders Survey (CNDMDS) were analyzed, including 44,557 adults aged 20 years and above. Eleven anthropometric indexes were assessed for their association with the prevalence of MetS. MetS diagnosis was based on the Joint Interim Statement (JIS) criteria, and the discriminatory ability of each index was evaluated using receiver operating characteristic (ROC) curve analysis. Among Chinese adults, the crude prevalence of MetS was 29.92%. All anthropometric indexes included in the analysis were significantly and positively associated with the prevalence of MetS (all p-trend < 0.0001). ROC curve analysis indicated that, among males, WC and AVI were the most effective indexes for discriminating MetS, while in females, WC and AVI also demonstrated the highest discriminative power. In the entire population, WHtR and BRI showed higher maximal Youden index values, with AUC values both at 0.83. WHtR and BRI exhibit comparable diagnostic value in predicting MetS in the general population. Considering the simplicity of calculation and measurement, WHtR is recommended as the primary screening index for MetS.

Background/Objectives: This study aims to investigate the effects of 4-methylumbelliferone (4-MU) on islet morphology, cell phenotype and function, and to explore possible mechanisms of β cell regeneration. Methods: The Type 1 diabetes (T1D) model was induced by continuous dose injection of streptozotocin (STZ), and mice were treated with 4-MU for 3 weeks. Plasma insulin level, islet cell phenotype and immune infiltration were determined by IPGTT, ELISA, HE and immunofluorescence. The Ins2Cre/+/Rosa26-eGFP transgenic mice model was used to detect β identity change. Primary rodent islets were incubated with 4-MU or vehicle in the presence or absence of STZ, AO/PI staining, and a scanning electron microscope (SEM), PCR and ELISA were used to evaluated islet viability, islet morphology, the specific markers of islet β cells and insulin secretion. Results: Treatment with 4-MU significantly decreased blood glucose and increased plasma insulin levels in STZ-induced diabetes. The plasma insulin level in the STZ group was 7.211 ± 2.602 ng/mL, which was significantly lower than the control group level (26.94 ± 4.300 ng/mL, p < 0.001). In contrast, the plasma insulin level in the STZ + 4-MU group was 22.29 ± 7.791 ng/mL, which was significantly higher than the STZ group (p < 0.05). The 4-MU treatment increased islet and β cells numbers and decreased α cell numbers in STZ-induced diabetes. Conclusions: Islet inflammation as indicated by insulin and CD3 was caused by infiltrates, and the β cell proliferation as indicated by insulin and Ki67 was boosted by 4-MU. β cell dedifferentiation was inhibited by 4-MU as assessed by insulin and glucagon double-positive cells and confirmed by Ins2Cre/+/Rosa26-eGFP mice. In cultured primary rodent islets, 4-MU restored islet viability, protected islet morphology, inhibited β-cell dedifferentiation, and promoted insulin secretion. The benefits of 4-MU in T1D have been proved to be associated with β cells self-replication, dedifferentiation inhibition and immune progression suppression, which help to maintain β cell mass.

Background The correlation between the triglyceride-glucose index (TyG) and the prognosis of ischemic stroke has been well established. This study aims to assess the influence of the TyG index on the clinical outcomes of critically ill individuals suffering from intracerebral hemorrhage (ICH).Methods Patients diagnosed with ICH were retrospectively retrieved from the Medical Information Mart for Intensive Care (MIMIC-IV) and the eICU Collaborative Research Database (eICU-CRD). Various statistical methods, including restricted cubic spline (RCS) regression, multivariable logistic regression, subgroup analysis, and sensitivity analysis, were employed to examine the relationship between the TyG index and the primary outcomes of ICH.Results A total of 791 patients from MIMIC-IV and 1,113 ones from eICU-CRD were analyzed. In MIMIC-IV, the in-hospital and ICU mortality rates were 14% and 10%, respectively, while in eICU-CRD, they were 16% and 8%. Results of the RCS regression revealed a consistent linear relationship between the TyG index and the risk of in-hospital and ICU mortality across the entire study population of both databases. Logistic regression analysis revealed a significant positive association between the TyG index and the likelihood of in-hospital and ICU death among ICH patients in both databases. Subgroup and sensitivity analysis further revealed an interaction between patients' age and the TyG index in relation to in-hospital and ICU mortality among ICH patients. Notably, for patients over 60 years old, the association between the TyG index and the risk of in-hospital and ICU mortality was more pronounced compared to the overall study population in both MIMIC-IV and eICU-CRD databases, suggesting a synergistic effect between old age (over 60 years) and the TyG index on the in-hospital and ICU mortality of patients with ICH.Conclusions This study established a positive correlation between the TyG index and the risk of in-hospital and ICU mortality in patients over 60 years who diagnosed with ICH, suggesting that the TyG index holds promise as an indicator for risk stratification in this patient population.

Download This Paper Open PDF in Browser Add Paper to My Library Share: Permalink Using these links will ensure access to this page indefinitely Copy URL Copy DOI

DACH1 is an important component of the retinal determinate gene network (RDGN), which regulates the expression of target genes by directly binding or interacting with other factors. DACH1 shows inhibitory effects in most tumors, but its role in papillary thyroid carcinoma is unclear and warrants further investigation. We assessed the expression of DACH1 in different tissues and correlation with immune infiltration by The Cancer Genome Atlas (TCGA) and Tumor Immune Estimation Resource (TIMMER2.0 databases). The effects of DACH1 on the proliferation and migration of TPC-1 and Bcpap cells were assessed by cell viability assay, colony formation assay, wound healing assay, transwell migration assay, and flow cytometry. Finally, the effects of DACH1 on CXCL8, CXCL10, and CXCL12 expression in Nthy-ori-3-1, TPC-1 and Bcpap cells were assessed by enzyme-linked immunosorbent assay kit and real-time polymerase chain reaction, respectively. The results showed that DACH1 was differentially expressed in different tumors and tissues. Basal expression of DACH1 was lower in thyroid and papillary thyroid carcinoma than in other normal tissues and corresponding tumors, and positively correlated with CD8 + T cell infiltration. In Nthy-ori-3-1, TPC-1 and Bcpap cells, overexpression of DACH1 inhibited cell migration and proliferation, and the opposite results was obtained by knocking down DACH1 using small interfering RNA. We also demonstrated that DACH1 regulated chemokines CXCL8, CXCL10, and CXCL12, thereby modulating tumor immunity.

Objectives: To explore the relationship between serum uric acid (UA) and high-density lipoprotein cholesterol (HDL-C) ratio (UHR) and metabolic syndrome (MetS) in nondiabetic individuals.Methods: A total of 15,760 nondiabetic participants were screened from the China National Diabetes and Metabolic Disorders Study. Pearson correlation was used to determine the correlation between the components of MetS and UHR, HDL-C, and UA. Receiver operating characteristic curves were used to evaluate the ability of UHR, HDL-C, and UA to identify MetS in the nondiabetic population.Results: A total of 6,386 men and 9,374 women were enrolled in this study. There were 1,480 (23.2%) men and 1,828 (19.5%) women with MetS. UHR significantly correlated with the components of MetS in men and women, especially with waist circumference and triglyceride. In men, although HDL-C showed a higher specificity index, UHR presented higher sensitivity index and area under the curve (AUC) than HDL-C (P = 0.0001) and UA (P < 0.0001), with AUC (95% CI) of 0.762 (0.752-0.773). Higher AUCs of UHR relative to HDL-C and UA were also observed in the age groups <40 and 40-59 years. There was no significant difference in AUC between UHR and HDL-C in the age group >= 60 years (P = 0.370). However, similar results were not observed in women.Conclusion: UHR significantly correlated with the components of MetS and could serve as a novel and reliable marker for identifying the population at a high risk of MetS in nondiabetic men, especially in younger adults.

BackgroundInsulin-like growth factor binding protein-1 (IGFBP-1) is considered a decline in polycystic ovary syndrome (PCOS), but it remains controversial that whether such reduction is attributed to obesity.AimsThis systematic review aims to explore whether IGFBP-1 is reduced in PCOS, and whether such reduction is associated with obesity.ResultsOur pooled study included 12 studies with a total of 450 participants. IGFBP-1 levels in PCOS were significantly lower than that in non-PCOS (SMD (95%CI)=-0.49(-0.89, -0.09), P=0.02). No significant difference in IGFBP-1 levels between patients with or without PCOS classified by BMI. Whilst, stratification by PCOS status revealed a significant decrease in IGFBP-1 in overweight (SMD (95%CI)=-0.92(-1.46, -0.37), P=0.001). When comparing fasting insulin in the same way, PCOS patients had significantly elevated fasting insulin level but not statistically declined IGFBP-1 after classified by BMI.ConclusionThis meta-analysis provides evidence that the decrease of IGFBP-1 in PCOS was more strongly influenced by comorbid obesity than by PCOS itself. Additionally, contrast to previous findings that insulin significantly suppresses IGFBP-1, our results suggested that the suppression of PCOS-related hyperinsulinemia on IGFBP-1 seemed diminished. Overall, our work may provide a novel perspective on the mechanism between insulin and IGFBP-1 underlying PCOS development.

As adolescents spend increasing amounts of time away from home, parental trust should become important. Little is known about how trust develops, however. We propose that parental trust is primarily based on knowledge. In this study, we pitted three types of knowledge of the child against each other in the prediction of parental trust: knowledge of feelings and concerns; of past delinquency; and of daily activities. Results showed that knowledge of daily activities was more important than knowledge of past delinquency. In further analyses, knowledge of daily activities that came from the child's spontaneous disclosure was most closely linked to parental trust. These findings add support to a recent re-interpretation of parental “monitoring” as parental knowledge that mainly comes from spontaneous child disclosure. Additionally, the role of parental trust for dysfunctional family relations was examined and it was found that the relations between the child's delinquency and family dysfunction were mediated by parental trust. Finally, even though there was substantial agreement between parents and children about parental trust in the child, the individual's unique perspectives were important. Family dysfunction from the child's perspective was based on whether they believed that their parents trusted them, and parental perceptions of family dysfunction were based on their own trust in the child.

目的:血清促甲状腺激素(TSH)在甲状腺乳头状癌(PTC)中的作用及机制尚不明确,本研究主要探讨TSH对甲状腺细胞系及乳头状癌细胞系的作用.方法:体外培养人甲状腺细胞系和乳头状癌细胞系,分别给予不同剂量(0 mU/L、5 mU/L及20 mU/L)的TSH干预.通过MTS及流式细胞术,观察TSH对甲状腺及乳头状癌细胞系增殖和细胞周期的作用;通过RNA-seq、ELISA检测TSH对细胞因子的影响;通过实时荧光定量PCR及Western blot寻找潜在的作用靶点.结果:MTS及流式细胞术结果显示,TPC-1和Nthy-ori-3-1细胞经TSH干预后增殖指数下降,20 mU/L浓度的TSH干预组细胞周期缩短.ELISA结果显示TPC-1中TSH下调CXCL8,上调CXCL10,而CXCL12的表达无明显变化.在Nthy-ori-3-1细胞中CXCL8和CXCL10的表达也观察到类似的结果,但CXCL12表达受到TSH的抑制.TSH可使Nthy-ori-3-1和Bcpap细胞中细胞命运决定因子(DACHl)的表达呈剂量依赖性上调,且TSH可抑制Bcpap中BRAF(V600E)以及Nthy-ori-3-1和TPC-1中BRAF的表达.结论:综上所述,我们并未发现TSH对甲状腺癌细胞有明显的促肿瘤作用.相反,本研究提示TSH可能呈部分抗癌作用.因此,TSH对甲状腺的致癌作用仍有待进一步研究.

Purpose Metabolic syndrome (Mets) is a pathological condition that includes many abnormal metabolic components and requires a simple detection method for rapid use in a large population. The aim of the study was to develop a diagnostic model for Mets in a Chinese population with noninvasive anthropometric and demographic predictors. Patients and methods Least absolute shrinkage and selection operator (LASSO) regression was used to screen predictors. A large sample from the China National Diabetes and Metabolic Disorders Survey (CNDMDS) was used to develop the model with logistic regression, and internal, internal-external and external validation were conducted to evaluate the model performance. A score calculator was developed to display the final model. Results We evaluated the discrimination and calibration of the model by receiver operator characteristic (ROC) curves and calibration curve analysis. The area under the ROC curves (AUCs) and the Brier score of the original model were 0.88 and 0.122, respectively. The mean AUCs and the mean Brier score of 10-fold cross validation were 0.879 and 0.122, respectively. The mean AUCs and the mean Brier score of internal-external validation were 0.878 and 0.121, respectively. The AUCs and Brier score of external validation were 0.862 and 0.133, respectively. Conclusions The model developed in this study has good discrimination and calibration performance. Its stability was proved by internal validation, external validation and internal-external validation. Then, this model has been displayed by a calculator which can exhibit the specific predictive probability for easy use in Chinese population.

Objective:To investigate the relationship between changes of weight status after becoming overweight in young adults and middle-aged and weight loss ratio and the risk of hypertension in middle-aged and elderly population.Methods:Participants aged 40-79 years old were selected from China National Diabetes and Metabolic Disorders Survey. Weight loss ratio was defined as (maximum weight-current weight)/maximum weight. The association between changes of weight status after becoming overweight in young adults and middle-aged and weight loss ratio and the risk of hypertension was examined by using multivariate logistic regression.Results:A total of 7 623 cases of hypertension were diagnosed among 19 823 study participants. (1) Compared with normal weight group(18.5 kg/m 2≤both MAXBMI and BMI<24.0 kg/m 2), the OR(95% CI) of hypertension for continuous overweight group from young adults(both MAXBMI and BMI≥24.0 kg/m 2, 18 years≤age of maximum weight<40 years), continuous overweight group from middle-aged(both MAXBMI and BMI≥24.0 kg/m 2, 40 years≤age of maximum weight<60 years) were 2.66(2.38-2.96) and 2.79(2.56-3.03), and the OR(95% CI) for past overweight from young adults(MAXBMI ≥24.0 kg/m 2, 18.5 kg/m 2≤BMI<24.0 kg/m 2, 18 years ≤ age of maximum weight<40 years), past overweight from middle-aged (MAXBMI≥24.0 kg/m 2, 18.5 kg/m 2≤BMI<24.0 kg/m 2, 40 years≤age of maximum weight<60 years) were 1.20(1.04-1.37) and 1.58(1.40-1.78). (2)Compared with weight loss ratio<5%, weight loss ratio ≥5% was associated with decreased risk of hypertension in normal weight (18.5 kg/m 2≤MAXBMI<24.0 kg/m 2) and overweight(MAXBMI≥24.0 kg/m 2) population. Conclusion:Overweight in young adults and middle-aged is associated with increased risk of hypertension in middle-aged and aged population regardless of current BMI. Weight loss of 5% or more from maximum body weight may be a protective factor against hypertension regardless of MAXBMI.