Body weight abnormalities, including overweight, obesity, and underweight, have become a dual public health challenge in Chinese adults: overweight and obesity lead to a variety of chronic complications, while underweight increases the risks of malnutrition, sarcopenia, and organ dysfunction. To systematically address these issues, multidisciplinary experts in endocrinology, sports science, nutrition, and psychiatry from various regions have held multiple weight management seminars. Based on the latest epidemiological data and clinical evidence, they expanded the guideline to include assessment and intervention strategies for underweight, in addition to the core content of obesity management. This guideline outlines the etiological mechanisms, evaluation methods, and multidimensional management strategies for overweight and obesity, covering key areas such as diagnosis and assessment, medical nutrition therapy, exercise prescription, pharmacological intervention, and psychological support. It is intended to provide a scientific and standardized approach to weight management across the adult population, aiming to curb the rising prevalence of obesity, mitigate complications associated with abnormal body weight, and improve nutritional status and overall quality of life.

Background::Intrauterine growth restriction (IUGR) is associated with adverse metabolic outcomes during adulthood. Histone modifications and changes in DNA methylation-affected genes are important for fetal development. This study aimed to investigate the epigenetic mechanisms in IUGR.Methods::IUGR models were established in Sprague–Dawley rats using a maternal nutritional restriction approach during pregnancy. The abundance of insulin-like growth factor 2 (IGF2), phosphoinositide 3-kinase (PI3K), AKT serine/threonine kinase 2 (AKT2), and peroxisome proliferators-activated receptor gamma coactivator 1 alpha (PGC-1α) was examined by real-time polymerase chain reaction (RT-PCR) and Western blotting analysis. Chromatin immunoprecipitation RT-PCR was employed to analyze histone modification in CCCTC-binding factor (CTCF) 1–4 binding sites of the Igf2/H19 imprinting control region (ICR). The methylation states of CTCF1–4 binding sites were studied by pyrosequencing. Results::The IUGR models were constructed successfully. Igf2 mRNA abundance in the placenta, fetal liver, and newborn liver was decreased in the IUGR group ( P <0.01). Meanwhile, as compared with the control group, the expression levels of AKT2, PI3K, and PGC-1α were lower in newborn and 8-week-old livers in the IUGR group ( P <0.05). In addition, knocking down Igf2 reduced the protein expression levels of AKT2-phosphorylation and PGC-1α ( P <0.05). In CTCF binding sites 1-4 of the Igf2/ H19 ICR, acetylated histones H3 (AcH3) enrichment was significantly lower in CTCF1-3 in newborn and 8-week-old IUGR rats. Histone H3 tri-methylated lysine 4 (H3K4me3) enrichment was significantly lower in the CTCF1–4 of newborn and 8-week-old IUGR groups ( P <0.01). H3K9me2 enrichment was significantly higher in the IUGR group ( P <0.01). The CpG dinucleotide methylation levels of CTCF1 and CTCF3, but not those of CTCF2 and CTCF4 binding sites in IUGR rat fetal, 4-week old, and 8-week-old livers decreased significantly ( P <0.05). Conclusion::The methylation status and histone modification in the Igf2/H19 ICR are related to growth and lipid metabolism via the PGC-1α/PI3K/AKT2 pathway in IUGR rats.

Objective To explore the T/NK cell-related differentially expressed genes(T/NK-DEGs)related to the prognosis of liver cancer based on the single-cell RNA-seq data,gene expression data and clinical information in the GEO and TCGA databases,and construct the prognostic model of liver cancer.Methods The single-cell RNA-seq data and gene expression matrices of liver cancer were obtained from the GEO database.The TCGA-LIHC cohorts,including mRNA expression data,clinical information,survival infor-mation,and somatic mutation data,were obtained from the TCGA database.Based on the two databases,the prognostic model of liver cancer patients was constructed by the bioinformatics method,and the performance of the model was predicted.Results Two T/NK-DEGs,PTTG1 and UBE2C,were identified to be associated with the prognosis of liver cancer and a prognostic model of liver cancer was constructed based on them.According to the risk score,the patients were divided into the high-risk score group and low-risk score group,in which the patients with high-risk score had a worse prognosis than those with low-risk score.The areas under the receiv-er operating characteristics(ROC)curve(AUCROC)of the prognostic model at 1-year,3-year and 5-year time points were 0.685,0.647 and 0.594,respectively.The higher risk score was correlated with the advanced pathological stage(Ⅰstage,Ⅱstage,andⅢstage)and T-stage(T1,T2,and T3)(P＜0.05).The prognostic model was able to predict the proportion of tumor infiltrating immune cells,and the sensitivity of immunotherapy and chemotherapy drugs in patients with liver cancer.Conclusion The constructed prog-nostic model in this study has an important role in the prediction of individualized survival and clinical treatment response of patients with liver cancer.

Objective To explore the T/NK cell-related differentially expressed genes(T/NK-DEGs)related to the prognosis of liver cancer based on the single-cell RNA-seq data,gene expression data and clinical information in the GEO and TCGA databases,and construct the prognostic model of liver cancer.Methods The single-cell RNA-seq data and gene expression matrices of liver cancer were obtained from the GEO database.The TCGA-LIHC cohorts,including mRNA expression data,clinical information,survival infor-mation,and somatic mutation data,were obtained from the TCGA database.Based on the two databases,the prognostic model of liver cancer patients was constructed by the bioinformatics method,and the performance of the model was predicted.Results Two T/NK-DEGs,PTTG1 and UBE2C,were identified to be associated with the prognosis of liver cancer and a prognostic model of liver cancer was constructed based on them.According to the risk score,the patients were divided into the high-risk score group and low-risk score group,in which the patients with high-risk score had a worse prognosis than those with low-risk score.The areas under the receiv-er operating characteristics(ROC)curve(AUCROC)of the prognostic model at 1-year,3-year and 5-year time points were 0.685,0.647 and 0.594,respectively.The higher risk score was correlated with the advanced pathological stage(Ⅰstage,Ⅱstage,andⅢstage)and T-stage(T1,T2,and T3)(P＜0.05).The prognostic model was able to predict the proportion of tumor infiltrating immune cells,and the sensitivity of immunotherapy and chemotherapy drugs in patients with liver cancer.Conclusion The constructed prog-nostic model in this study has an important role in the prediction of individualized survival and clinical treatment response of patients with liver cancer.

Body weight abnormalities, including overweight, obesity, and underweight, have become a dual public health challenge in Chinese adults: overweight and obesity lead to a variety of chronic complications, while underweight increases the risks of malnutrition, sarcopenia, and organ dysfunction. To systematically address these issues, multidisciplinary experts in endocrinology, sports science, nutrition, and psychiatry from various regions have held multiple weight management seminars. Based on the latest epidemiological data and clinical evidence, they expanded the guideline to include assessment and intervention strategies for underweight, in addition to the core content of obesity management. This guideline outlines the etiological mechanisms, evaluation methods, and multidimensional management strategies for overweight and obesity, covering key areas such as diagnosis and assessment, medical nutrition therapy, exercise prescription, pharmacological intervention, and psychological support. It is intended to provide a scientific and standardized approach to weight management across the adult population, aiming to curb the rising prevalence of obesity, mitigate complications associated with abnormal body weight, and improve nutritional status and overall quality of life.

BACKGROUND: Intrauterine growth restriction (IUGR) is associated with adverse metabolic outcomes during adulthood. Histone modifications and changes in DNA methylation-affected genes are important for fetal development. This study aimed to confirm the epigenetic mechanisms in IUGR. METHODS: IUGR models were established in Sprague-Dawley rats using a maternal nutritional restriction approach during pregnancy. The abundance of insulin-like growth factor 2 (IGF2), phosphoinositide 3-kinase (PI3K), AKT serine/threonine kinase 2 (AKT2), and PPAR gamma coactivator 1 alpha (PGC-1α) was examined by real-time polymerase chain reaction (RT-PCR) and Western blotting analysis. Chromatin immunoprecipitation RT-PCR was employed to analyze histone modification in CCCTC-binding factor (CTCF)1-4 binding sites of the IGF2/H19 imprinting control region (ICR). The methylation states of CTCF1-4 binding sites were studied by pyrosequencing. RESULTS: The IUGR models were constructed successfully. IGF2 mRNA abundance in the placenta, fetal liver, and newborn liver was decreased in the IUGR group (P <0.01). Meanwhile, as compared with the control group, the expression levels of AKT2, PI3K, and PGC-1α were lower in newborn and 8-week-old livers in the IUGR group (P <0.05). In addition, knocking down IGF2 reduced the protein expression levels of AKT2-P and PGC-1α (P <0.05). In CTCF binding sites 1-4 of the IGF2/H19 ICR, AcH3 enrichment was significantly lower in CTCF1-3 in newborn and 8-week-old IUGR rats. H3K4me3 enrichment was significantly lower in the CTCF1-4 of newborn and 8-week-old IUGR groups (P <0.01). H3K9me2 enrichment was significantly higher in the IUGR group (P <0.01). The CpG dinucleotide methylation levels of CTCF1 and CTCF3, but not those of CTCF2 and CTCF4 binding sites in IUGR rat fetal, 4-week old, and 8-week-old livers decreased significantly (P <0.05). CONCLUSION The methylation status and histone modification in the IGF2/H19 ICR are related to growth and lipid metabolism via the PGC-1α/PI3K/AKT2 pathway in IUGR rats.

Objective To study the anticancer effects of Qilou Pill-containing serum on human hepatocellular carcinoma HepG2 cells in vitro and its mechanism.Methods Human hepatoma HepG2 cells were cultured in vitro and divided into the control group and the low,medium and high dose groups of Qilou Pills,and each group was treated with corresponding serum containing drugs.The proliferation and apoptosis of HepG2 cells were detected by CCK-8 method and Annexin V-FITC/PI double staining.The mRNA and protein expression levels of P53,P21,Caspase-3,Bax and Bcl-2 were detected by real-time fluorescence quantitative PCR and Western blot,respectively.Results ① Qilou Pill-containing serum inhibited the proliferation of human hepatoma HepG2 cells in a concentration and time dependent manner,with statistical significance compared with the control group(P<0.01).②Qilou Pill drug-containing serum could promote the apoptosis of human hepatoma HepG2 cells,and the promoting effect was more significant with the increase of drug concentration.The difference between medium and high dose groups and control group was statistically significant(P<0.01),while the difference between low dose group was not significant(P>0.05).③Compared to the control group,the mRNA expressions of P53,P21,Caspase-3 and Bax in Qilou Pill serum increased with the increase of drug dose,while the Bcl-2 mRNA showed the opposite trend,with statistical significance(P<0.05 or P<0.01).④Compared with the control group,the protein expression levels of P53,P21,Caspase-3 and Bax in Qilou Pill-containing serum dose groups were increased,and showed an increasing trend with the increase of drug dose(P<0.05 or P<0.01).On the contrary,the expression level of Bcl-2 protein decreased gradually with the increase of drug dose,and the difference was statistically significant(P<0.01).Conclusion Qilou Pills can inhibit the proliferation of human hepatoma HepG2 cells and promote their apoptosis by participating in the transmission of P53 signalling pathway,so as to play a role in the treatment of hepatoma.

Objective To study the anticancer effects of Qilou Pill-containing serum on human hepatocellular carcinoma HepG2 cells in vitro and its mechanism.Methods Human hepatoma HepG2 cells were cultured in vitro and divided into the control group and the low,medium and high dose groups of Qilou Pills,and each group was treated with corresponding serum containing drugs.The proliferation and apoptosis of HepG2 cells were detected by CCK-8 method and Annexin V-FITC/PI double staining.The mRNA and protein expression levels of P53,P21,Caspase-3,Bax and Bcl-2 were detected by real-time fluorescence quantitative PCR and Western blot,respectively.Results ① Qilou Pill-containing serum inhibited the proliferation of human hepatoma HepG2 cells in a concentration and time dependent manner,with statistical significance compared with the control group(P<0.01).②Qilou Pill drug-containing serum could promote the apoptosis of human hepatoma HepG2 cells,and the promoting effect was more significant with the increase of drug concentration.The difference between medium and high dose groups and control group was statistically significant(P<0.01),while the difference between low dose group was not significant(P>0.05).③Compared to the control group,the mRNA expressions of P53,P21,Caspase-3 and Bax in Qilou Pill serum increased with the increase of drug dose,while the Bcl-2 mRNA showed the opposite trend,with statistical significance(P<0.05 or P<0.01).④Compared with the control group,the protein expression levels of P53,P21,Caspase-3 and Bax in Qilou Pill-containing serum dose groups were increased,and showed an increasing trend with the increase of drug dose(P<0.05 or P<0.01).On the contrary,the expression level of Bcl-2 protein decreased gradually with the increase of drug dose,and the difference was statistically significant(P<0.01).Conclusion Qilou Pills can inhibit the proliferation of human hepatoma HepG2 cells and promote their apoptosis by participating in the transmission of P53 signalling pathway,so as to play a role in the treatment of hepatoma.

Objective : To explore the protective effect and mechanism of salvianolic acid salt on acute lung injury induced by one lung ventilation(OLV) in rabbits. Methods : 24 rabbits were randomly divided into three groups : control group , model group and treatment group , with 8 rabbits in each group. The W/D value of lung was measured , and the morphological changes of lung tissue were observed by HE staining and electron microscopy; The contents of arachidonic acid(AA) , leukotriene B4( LTB4) , thromboxaneA2( TXA2) and prostacyclin 2( PGI2) in rabbit lung tissue were detected by ELISA ; The expressions of cyclooxygenase⁃2(COX⁃2) ,5 ⁃lipoxygenase(5 ⁃LOX) in lung tissue were detected by RT⁃qPCR; The expressions of COX⁃2 , 5 ⁃LOX , clara cell secretory protein(CCSP) and cytoplasmic phospholipase A2(C⁃PLA2) in lung tissue were detected by Western blot. Results : The W/D ratio of model group was higher than that of control group , but decreased after treatment ( P < 0. 05) ; HE staining showed that in the model group , the capillaries were dilated and congested , there were red exudates in the alveoli , the walls of alveoli were thickened , and inflammatory cells were infiltrated , but the treatment of salvianolic acid salt was relieved ; The mitochondria swelling , crista breaking and even disappearing were observed by transmission electron microscope in the model group , and alveolar epithelial cell Ⅰ (AT⁃ Ⅰ ) ultrastructural damage in the treatment group significantly improved compared with that in the model group ; The AA , LTB4 , TXA2 and PGI2 contents in the treatment group were lower than those in the model group (P < 0. 05) . RT⁃qPCR showed that the expression of 2 and 5 ⁃LOX decreased after Salvianolic acid salt treatment (P < 0. 05) ; Western blot showed that the expression of COX⁃2 , 5 ⁃LOX and C ⁃PLA2 in treatment group was lower than that in model group , while the expression of CCSP increased (P < 0. 05 ) . Conclusion Salvianolic acid salt has protective effect on lung injury induced by one⁃lung ventilation. Its mechanism may be related to down⁃regulation of COX⁃2 , 5 ⁃LOX and C ⁃PLA2 expression , up⁃regulation of CCSP expression.

OBJECTIVE: To explore the correlation between the genotypes and metabolic markers and microstructure of bones in children with Gitelman syndrome (GS). METHODS: For 15 children with GS and 10 healthy individuals, baseline data and bone metabolic markers including parathyroid hormone, alkaline phosphatase, osteocalcin, N-terminal propeptide of type I procollagen, beta isomer of the C-terminal telopeptide of type I collagen and 25-hydroxyvitamin D, high-resolution peripheral quantitative computed tomography indicators (volumetric bone mineral density, bone microstructure indicators) were collected. Genetic testing was carried out to determine their genotypes. RESULTS: The volumetric bone mineral density, bone geometry and bone microstructure parameters of the GS group were better than those of the healthy controls (P<0.05). Variants of the SLC12A3 gene were identified in 9 of the 15 patients but none of the 10 healthy controls. CONCLUSION The phenotype of GS children is influenced by the interaction of genetic variants, though the phenotype associated with high frequency mutations showed no specificity. There is also a correlation between their genotype and the bone microstructure.
Biomarkers ; Bone and Bones ; Child ; Collagen Type I/genetics* ; Genotype ; Gitelman Syndrome ; Humans ; Osteocalcin/genetics* ; Peptide Fragments ; Solute Carrier Family 12, Member 3