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.

Objective To construct a differential diagnosis model for systemic lupus erythematosus(SLE)from other autoimmune diseases based on the conventional test indicators in clinical laboratory,so as to improve the diagnostic efficacy of the existing test indicators.Methods The data of 178 SLE patients(SLE group)and 196 patients with other autoimmune diseases(control group)diagnosed in Sichuan Provincial People's Hospital from Apr.2022 to Mar.2023 were retrospectively analyzed.The differences in the levels of 19 clinical routine indicators between the 2 groups were analyzed.The least absolute shrinkage and selection operator(LASSO)regression was used to screen for test indicators with non-zero coefficients.These indicators were then used in logistic regression to construct a Nomogram model for SLE differential diagnosis.Model performance was assessed using receiver operating characteristic(ROC)curves and decision curve analysis.Results The levels of anti-cardiolipin antibody immunoglobulin(Ig)G,anti-cardiolipin antibody IgA,high-sensitivity C reactive protein(hs-CRP),D-dimer,and thrombin time(TT)in the SLE group were significantly higher than those in the control group(all P＜0.05),while the levels of IgM,complement 3(C3),complement 4(C4),prothrombin time(PT),and activated partial thromboplastin time(APTT)in the SLE group were significantly lower than those in the control group(all P＜0.05).Through LASSO regression,IgM,C3 and C4 were selected as the most likely indicators with non-zero coefficients.Multivariate logistic regression analysis showed that the differential diagnosis model was Logit P=4.18-1.34 × IgM-1.70 × C3-6.61 × C4.The area under the curve of this model was 0.80(95％confidence interval 0.76-0.85),with a sensitivity of 0.77 and a specificity of 0.74.Decision curve analysis demonstrated favourable clinical utility within a threshold probability range of 0.2-0.9.Conclusion The present model,constructed using the clinical routine indicators,such as IgM,C3 and C4,is helpful for the differential diagnosis of SLE from other autoimmune diseases and has good clinical application value.

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.

Pancreatic cancer has a very poor prognosis.Early diagnosis and treatment are especially critical for improving its prognosis.Nanotechnology has been widely used in the diagnosis and treatment of pancreatic cancer.Relying on the unique physicochemical properties of nanoparticles and their rich surface modifications,effective enrichment of tumor sites can be achieved.Magnetic iron oxide nanoparticles(MIONPs)is one of the commonly used nanomaterials in the diagnosis and treatment of pancreatic cancer,and has good biocompatibility.Through special surface modification,it can be used in targeted diagnosis and treatment of pancreatic cancer.MIONPs can be used as a contrast agent for MRI,and by modifying the surface,they also can be used in targeted imaging of pancreatic cancer.And they can also be modified as a drug delivery system to achieve targeted delivery of drugs and improve therapeutic effects.However,the application of MIONPs in pancreatic cancer diagnosis and treatment still faces some challenges,such as nanotoxicity and cost issues.With the development of technology,MIONPs are expected to play an important role in the personalized diagnosis and treatment of pancreatic cancer.

Objective:To discuss the effect of exosome(Exo)microRNA-761(miR-761)on the epithelial-mesenchymal transition(EMT)process of the osteosarcoma(OS)cells by regulating tumor-associated macrophage(TAM)polarization,and to clarify its related mechanism.Methods:The miR-761 plasmid and negative control(miR-NC)plasmid were transfected into the HEK293 cells,and the non-transfected cells were regarded as control group.The transfection efficiency was detected using real-time fluorescence quantitative PCR(RT-qPCR)method.The Exo containing miR-761 was isolated,and the morphology of Exo was observed by transmission electron microscope.The concentration and size distribution of Exo samples were detected by nanoparticle analyzer,and the expression of Exo surface marker protein was detected by Western blotting method.The human monocyte leukemia THP-1 cells were stimulated with phorbol 12-myristate 13-acetate(PMA)to become the M0 macrophages,which were then treated with Exo containing miR-761 and co-cultured with the OS MG63 cells to establish the co-culture system.The experiment was divided into M0 group,TAM group,miR-761 NC group,and miR-761 Exo group.The M0 macrophages were collected from various groups,and the positive rates of M1 macrophage marker CD86 and M2 macrophage marker CD206 in various groups were detected by flow cytometry;the protein expression levels of M1 macrophage secreted factors interleukin-1β(IL-1β)and tumor necrosis factor-α(TNF-α)and M2 macrophage secreted factors interleukin-10(IL-10)and transforming growth factor-β1(TGF-β1)in various groups were detected by Western blotting method.The M0 macrophages were treated with Exo containing miR-761 and co-cultured with MG63 cells to establish the co-culture system.The experiment was divided into control group,TAM group,miR-NC Exo+TAM group,and miR-761 Exo+TAM group.The MG63 cells in various groups were collected,and the fluorescence intensities of E-cadherin and Vimentin in the MG63 cells in various groups were observed by immunofluorescence staining;the expression levels of E-cadherin,Vimentin,and EMT regulation-related transcription factors Twist1,Snail,and Slug proteins in the cells in various groups were detected by Western blotting method;the numbers of invasion and migration cells in various groups were detected by Transwell chamber assay.Results:The HEK293 cells containing miR-761 were successfully obtained by transfection experiments,and the Exo was isolated.Compared with M0 group,the positive rate of CD86 of the macrophages in TAM group was decreased(P＜0.05),while the positive rate of CD206 was increased(P＜0.05),the expression levels of IL-1β and TNF-α proteins were decreased(P＜0.05),while the expression levels of IL-10 and TGF-β1 proteins were increased(P＜0.05).Compared with TAM group,the positive rate of CD86 of the macrophages in miR-761 Exo group was increased(P＜0.05),while the positive rate of CD206 was decreased(P＜0.05),the expression levels of IL-1β and TNF-α proteins were increased(P＜0.05),while the expression levels of IL-10 and TGF-β1 proteins were decreased(P＜0.05).Compared with control group,the fluorescence intensity of E-cadherin in the MG63 cells in TAM group was decreased,while the fluorescence intensity of Vimentin was increased,the expression level of E-cadherin protein was decreased(P＜0.05),while the expression levels of Vimentin,Twist1,Snail,and Slug proteins were increased(P＜0.05),and the numbers of invasion and migration cells were increased(P＜0.05).Compared with TAM group,the fluorescence intensity of E-cadherin in the MG63 cells in miR-761 Exo+TAM group was increased,while the fluorescence intensity of Vimentin was decreased,the expression level of E-cadherin protein was increased(P＜0.05),while the expression levels of Vimentin,Twist1,Snail,and Slug proteins were decreased(P＜0.05),and the numbers of invasion and migration cells were decreased(P＜0.05).Conclusion:The exo-delivered miR-761 can inhibit the EMT process of the OS cells,thereby inhibiting the cell migration and cell invasion;its mechanism may be related to regulating TAM polarization.

Objective:To investigate the effect of copper chlorophyllin sodium salt(CHL)on the sensitivity of human pancreatic cancer cells in response to gemcitabine(GEM)therapy and on the therapeutic effect on pancreatic cancer cells that have developed GEM resistance.Methods:MIA GR(a pancreatic cancer cell line resistant to GEM)was induced by a low-dose continuous incremental method,and the half inhibitory concentration(IC50)of MIA WT and MIA GR to GEM treatment was detected by the CCK-8 method,and the resistance index was calculated;the difference in IC50 of CHL on the two types of cells was detected by the CCK-8 method after treating MIA WT and MIA GR cells with different concentrations of CHL,CCK-8 method was used to detect the difference in IC50 of CHL on the two types of cells;on the basis of IC50,MIA WT and MIA GR cells were intervened with CHL and(or)GEM with different multiplicity of IC50,respectively,and the growth inhibition curves of MIA WT and MIA GR cells were detected by the CCK-8 method under the intervention of CHL combined with GEM;After the intervention of MIA WT and MIA GR cells with CHL and(or)GEM at IC50,respectively,the effects on the proliferation of the two different cells were detected using the clone formation assay;the effects on cytotoxicity/activity were observed under fluorescence microscopy;and the effects on apoptosis were detected using flow cytometry.Finally,western blotting was used to detect the effects of CHL and(or)GEM interventions on the drug resistance-associated molecules P-glycoprotein(P-gp)and ribonucleotide reductase regulatory subunit M2(RRM2)in MIA GR cells,the and sensitivity-related molecule deoxycytidine kinase(DCK)on protein expression levels.Results:MIA GR cells were verified to be well drug resistant,with resistance indices of 549.1 and 667.9 after 48 h and 96 h after GEM intervention compared to homologous wild-type MIA WT cells,respectively;CHL intervention inhibited the proliferation of MIA GR cells more significantly compared to that of MIA WT cells;and CHL in combination with GEM exerted a more significant growth inhibitory effect compared to GEM alone in both MIA WT cells(P<0.001)and MIA GR cells(P<0.01).CHL significantly inhibited the tumor proliferation of MIA GR cells,and the inhibitory effect was more pronounced in both cells when combined with GEM(P<0.000 1);furthermore,compared to GEM alone,the intervention with CHL could cause more pronounced cytotoxicity(P<0.000 1)in both MIA WT and MIA GR cells.caused more pronounced cytotoxicity(P<0.000 1)and induced a higher percentage of apoptosis than GEM alone.The results of the western blotting assay showed that CHL intervention caused a decrease in the expression levels of P-gp and RRM2 proteins,as well as an increase in the protein expression level of DCK in MIA GR cells.Conclusion:CHL increases the sensitivity of pancreatic cancer cells to GEM and also induces a decrease in the resistance of drug-resistant pancreatic cancer cells to GEM.

Background and purpose:Pancreatic cancer is a highly aggressive solid tumor of the digestive system,with radical resection being unfeasible in approximately 80%of patients due to the absence of specific clinical manifestations in the early stages.The use of gemcitabine as a first-line chemotherapeutic agent has not significantly improved patient prognosis,primarily due to the development of chemoresistance.The precise mechanisms underlying gemcitabine resistance in pancreatic cancer remain unclear.This study aimed to explore potential biomarkers associated with gemcitabine chemoresistance in pancreatic cancer by utilizing gemcitabine-resistant cell lines and pathological pancreatic cancer tissues,in conjunction with data from online databases.Additionally,we analyzed follow-up data from pancreatic cancer patients to assess the impact of relevant targets on patient prognosis.Methods:In this study,gemcitabine-resistant cell lines were developed through stepwise induction using a gemcitabine concentration gradient.Second-generation high-throughput RNA-seq sequencing was conducted on these resistant cells,and bioinformatics analysis was employed to identify four pancreatic cancer genes from the Gene Expression Omnibus(GEO)datasets(GSE106336,GSE110580,GSE35141,and GSE140077).Co-expressed genes were screened using real-time fluorescence quantitative polymerase chain reaction(RTFQ-PCR),Western blot and immunohistochemistry to verify the expression levels of target molecules.Surgical specimens from 70 patients diagnosed with pancreatic adenocarcinoma at the First Affiliated Hospital of Xi'an Jiao Tong University between June 2018 and June 2021 were analyzed.These included 30 specimens resistant to gemcitabine,16 non-resistant specimens,and 24 normal pancreatic tissues as controls.Ethical approval was obtained(Ethical approval:2021 LunxuanKeZi No.457,No.XJTU1AF2021LSK-457).Clinical and prognostic information was collected,and the log-rank test was used to evaluate the relationship between target molecule expression and patient prognosis.Results:The half maximal inhibitory concentration(IC50)for gemcitabine was significantly higher in the gemcitabine-resistant cell strain(Mia GR)than in the wild-type cell line(Mia WT)(258.10 μmol/L vs 0.18 μmol/L),with a resistance index(RI)of 1 443.9.Transcriptome sequencing identified 3 985 differentially expressed genes,of which 25 were shared with the GEO datasets.Further analysis highlighted INPP4B as a key gene.RTFQ-PCR and Western blot confirmed that INPP4B mRNA and protein levels were significantly elevated in drug resistant cells compared to wild-type cells(P＜0.05).Immunohistochemical analysis revealed that INPP4B expression was significantly higher in drug resistant pancreatic cancer tissues compared to non-drug resistant tissues,and lower in normal tissues than in both cancerous tissue types.Kaplan-Meier curves demonstrated that patients with low INPP4B expression had significantly better progression-free survival(PFS)than those with high expression(HR=2.874,95%CI:1.262-6.544,P=0.013).Although patients with low INPP4B expression also showed better overall survival(OS),the difference was not statistically significant(HR=1.484,95%CI:0.518-4.250,P=0.465).Conclusion:INPP4B may serve as a potential biomarker for gemcitabine chemoresistance in pancreatic cancer and is associated with poor prognosis in drug resistant patients.Developing targeted assays and treatments for INPP4B could facilitate early identification of patients likely to exhibit resistance to gemcitabine therapy,thereby improving their prognosis.

Background and purpose:Pancreatic cancer is a highly aggressive solid tumor of the digestive system,with radical resection being unfeasible in approximately 80%of patients due to the absence of specific clinical manifestations in the early stages.The use of gemcitabine as a first-line chemotherapeutic agent has not significantly improved patient prognosis,primarily due to the development of chemoresistance.The precise mechanisms underlying gemcitabine resistance in pancreatic cancer remain unclear.This study aimed to explore potential biomarkers associated with gemcitabine chemoresistance in pancreatic cancer by utilizing gemcitabine-resistant cell lines and pathological pancreatic cancer tissues,in conjunction with data from online databases.Additionally,we analyzed follow-up data from pancreatic cancer patients to assess the impact of relevant targets on patient prognosis.Methods:In this study,gemcitabine-resistant cell lines were developed through stepwise induction using a gemcitabine concentration gradient.Second-generation high-throughput RNA-seq sequencing was conducted on these resistant cells,and bioinformatics analysis was employed to identify four pancreatic cancer genes from the Gene Expression Omnibus(GEO)datasets(GSE106336,GSE110580,GSE35141,and GSE140077).Co-expressed genes were screened using real-time fluorescence quantitative polymerase chain reaction(RTFQ-PCR),Western blot and immunohistochemistry to verify the expression levels of target molecules.Surgical specimens from 70 patients diagnosed with pancreatic adenocarcinoma at the First Affiliated Hospital of Xi'an Jiao Tong University between June 2018 and June 2021 were analyzed.These included 30 specimens resistant to gemcitabine,16 non-resistant specimens,and 24 normal pancreatic tissues as controls.Ethical approval was obtained(Ethical approval:2021 LunxuanKeZi No.457,No.XJTU1AF2021LSK-457).Clinical and prognostic information was collected,and the log-rank test was used to evaluate the relationship between target molecule expression and patient prognosis.Results:The half maximal inhibitory concentration(IC50)for gemcitabine was significantly higher in the gemcitabine-resistant cell strain(Mia GR)than in the wild-type cell line(Mia WT)(258.10 μmol/L vs 0.18 μmol/L),with a resistance index(RI)of 1 443.9.Transcriptome sequencing identified 3 985 differentially expressed genes,of which 25 were shared with the GEO datasets.Further analysis highlighted INPP4B as a key gene.RTFQ-PCR and Western blot confirmed that INPP4B mRNA and protein levels were significantly elevated in drug resistant cells compared to wild-type cells(P＜0.05).Immunohistochemical analysis revealed that INPP4B expression was significantly higher in drug resistant pancreatic cancer tissues compared to non-drug resistant tissues,and lower in normal tissues than in both cancerous tissue types.Kaplan-Meier curves demonstrated that patients with low INPP4B expression had significantly better progression-free survival(PFS)than those with high expression(HR=2.874,95%CI:1.262-6.544,P=0.013).Although patients with low INPP4B expression also showed better overall survival(OS),the difference was not statistically significant(HR=1.484,95%CI:0.518-4.250,P=0.465).Conclusion:INPP4B may serve as a potential biomarker for gemcitabine chemoresistance in pancreatic cancer and is associated with poor prognosis in drug resistant patients.Developing targeted assays and treatments for INPP4B could facilitate early identification of patients likely to exhibit resistance to gemcitabine therapy,thereby improving their prognosis.

Objective:To investigate the effect of copper chlorophyllin sodium salt(CHL)on the sensitivity of human pancreatic cancer cells in response to gemcitabine(GEM)therapy and on the therapeutic effect on pancreatic cancer cells that have developed GEM resistance.Methods:MIA GR(a pancreatic cancer cell line resistant to GEM)was induced by a low-dose continuous incremental method,and the half inhibitory concentration(IC50)of MIA WT and MIA GR to GEM treatment was detected by the CCK-8 method,and the resistance index was calculated;the difference in IC50 of CHL on the two types of cells was detected by the CCK-8 method after treating MIA WT and MIA GR cells with different concentrations of CHL,CCK-8 method was used to detect the difference in IC50 of CHL on the two types of cells;on the basis of IC50,MIA WT and MIA GR cells were intervened with CHL and(or)GEM with different multiplicity of IC50,respectively,and the growth inhibition curves of MIA WT and MIA GR cells were detected by the CCK-8 method under the intervention of CHL combined with GEM;After the intervention of MIA WT and MIA GR cells with CHL and(or)GEM at IC50,respectively,the effects on the proliferation of the two different cells were detected using the clone formation assay;the effects on cytotoxicity/activity were observed under fluorescence microscopy;and the effects on apoptosis were detected using flow cytometry.Finally,western blotting was used to detect the effects of CHL and(or)GEM interventions on the drug resistance-associated molecules P-glycoprotein(P-gp)and ribonucleotide reductase regulatory subunit M2(RRM2)in MIA GR cells,the and sensitivity-related molecule deoxycytidine kinase(DCK)on protein expression levels.Results:MIA GR cells were verified to be well drug resistant,with resistance indices of 549.1 and 667.9 after 48 h and 96 h after GEM intervention compared to homologous wild-type MIA WT cells,respectively;CHL intervention inhibited the proliferation of MIA GR cells more significantly compared to that of MIA WT cells;and CHL in combination with GEM exerted a more significant growth inhibitory effect compared to GEM alone in both MIA WT cells(P<0.001)and MIA GR cells(P<0.01).CHL significantly inhibited the tumor proliferation of MIA GR cells,and the inhibitory effect was more pronounced in both cells when combined with GEM(P<0.000 1);furthermore,compared to GEM alone,the intervention with CHL could cause more pronounced cytotoxicity(P<0.000 1)in both MIA WT and MIA GR cells.caused more pronounced cytotoxicity(P<0.000 1)and induced a higher percentage of apoptosis than GEM alone.The results of the western blotting assay showed that CHL intervention caused a decrease in the expression levels of P-gp and RRM2 proteins,as well as an increase in the protein expression level of DCK in MIA GR cells.Conclusion:CHL increases the sensitivity of pancreatic cancer cells to GEM and also induces a decrease in the resistance of drug-resistant pancreatic cancer cells to GEM.

Objective:To summarize the clinical experience of changing the membranous pulmonary system during extracorporeal membrane oxygenation(ECMO) in infants after congenital heart disease opration with cardiopulmonary bypass.Methods:From January to September in 2019, 6 cases of congenital heart disease with cardio-pulmonary bypass in our hospital were analyzed retrospectively, whose membrane obstruction occurred during ECMO treatment and replaced successfully.The hemodynamics and blood gas before and after replacement of ECMO system were observed, and the experience was summarized.Results:Six patients(3 males and 3 females), aging from 1 to 3 months and weighing from 3.0 to 4.9 kg, were received VA-ECMO adjuvant therapy.The ECMO system replacement process was smooth and took 175-209 s. The hemodynamic of the children was stable.The ECMO support time was 134-249 h. After the improvement of cardiac systolic function, all children were successfully withdrawn and survived.Conclusion:The improved method of liquid replacement in ECMO system can make full use of the blood components in the original system and avoid the loss of blood tangible components.According to the plan of rapid replacement, the risk of replacement will not be increased.