Abstract In recent years, the prevalence of overweight and obesity among children and adolescents has risen rapidly, posing a serious threat to their physical and mental health. To provide scientific, systematic, and standardized weight management guidance for overweight and obese children and adolescents, the study focuses on the core concept of healthy lifestyle intervention, integrates multidisciplinary expert opinions and research findings,and proposes a comprehensive multidisciplinary intervention framework covering scientific exercise intervention, precise nutrition and diet, optimized sleep management, and standardized psychological support. It calls for the establishment of a multi agent collaborative management mechanism led by the government, implemented by families, fostered by schools, initiated by individuals, optimized by communities, reinforced by healthcare, and coordinated by multiple stakeholders. Emphasizing a child and adolescent centered approach, the consensus advocates for comprehensive, multi level, and personalized guidance strategies to promote the internalization and maintenance of a healthy lifestyle. It serves as a reference and provides recommendations for the effective prevention and control of overweight and obesity, and enhancing the health level of children and adolescents.

Abstract Asthma is a well-characterized heterogeneous disease marked by airway remodeling and chronic airway inflammation. Clinically, the treatment of asthma primarily relies on hormonal drugs. However, the long-term use of these medications can lead to significant side effects. Mitophagy is a biological process that selectively transports damaged mitochondria to lysosomes for degradation. Recent research has revealed the crosstalk between mitophagy and asthma. Accordingly, taking mitophagy as an entry point, summarizing the key molecular mechanisms and regulators of mitophagy in asthma will facilitate the development of novel intervention targets and strategies for asthmatic treatment.

Objective:To observe the effect of Liuzijue on post-stroke fatigue patients with the type of Qi deficiency and blood stasis and the effect of pulmonary function.Method:From March 2022 to March 2023,a total of 68 post-stroke fatigue patients with Qi deficiency and blood stasis who were hospitalized in the Affiliated Rehabilitation Hospital of Fujian University of Traditional Chinese Medicine and met the criteria were selected,the patients were divided into therapy group(n=34)and control group(n=34)according to random number table.The control group was treated with conventional reha-bilitation combined with conventional respiratory therapy,the therapy group was treated with conventional reha-bilitation combined with Liuzijue,30 minutes/time,5 times/week,a total of 12 weeks.The fatigue severity scale score(FSS),Qi Deficiency Syndrome and Blood Stasis factor diagnostic scale score,vital capacity(VC),forced vital capacity(FVC),peak expiratory flow(PEF),and maximal voluntary ventilation(MVV)were assessed in both groups before and after treatment.Result:After 12 weeks of treatment,the FSS scores and the Qi deficiency syndrome and blood stasis factor di-agnostic scale score exhibited significant differences in the therapy group compared with those before treatment(P＜0.05),and significant improvement compared with those in the control group(P＜0.05).The significant differ-ences were found in the VC、FVC、PEF and MVV of both two groups between before and after treatment(P＜0.05),and the degree of improvement was more pronounced in the therapy group.Conclusion:The Liuzijue applied to post-stroke fatigue patients with Qi deficiency and blood stasis can better improve the fatigue score and Qi deficiency syndrome and blood stasis score,as well as improve the level of pulmonary function of patients,which is worthy of clinical application.

Objective:To investigate the inpact of thyroid cancer-derived cancer-associated fibroblasts(CAF) autophagy on papillary thyroid cancer(PTC).Methods:CAF and normal fibroblasts were isolated from cancerous and adjacent normal thyroid tissues from four PTC patients. Expressions of fibroblast activation protein(FAP) and α-smooth muscle actin in cells were assessed. Conditioned medium of CAF and normal fibroblasts were prepared and used to culture PTC cells. The effects of CAF and normal fibroblasts on survival, proliferation, migration, invasion and iodine uptake of PTC cells were evaluated through cell proliferation assay, cell scratch assay, cell invasion assay, and cell iodine uptake assay. The autophagy level of CAF was also evaluated. Autophagy inhibition and activation were used to regulate the autophagy of CAF, and then their effects on PTC cell proliferation, migration and invasion were further evaluated. The in vivo effect of CAF autophagy on PTC xenograft tumor growth was evaluated.Results:CAF exhibited higher FAP expression and basal autophagy levels. PTC cells co-cultured with CAF-conditioned media showed enhanced proliferation, migration, invasion, and reduced iodine uptake. Autophagy inhibition reduced these effects, while autophagy activation further promoted them. In vivo, inhibiting CAF autophagy suppressed tumor growth.Conclusions:CAF promotes PTC cell malignancy through autophagy activation, enhancing proliferation, migration, and invasion while reducing iodine uptake.

A 15-year-old boy developed abdominal pain and melena two weeks after COVID-19 infection, which was followed by gross hematuria and proteinuria. Laboratory studies revealed significantly elevated inflammatory markers. Endoscopic examinations showed multiple jejunal and ileal ulcers. Renal biopsy suggested mesangial proliferative glomerulonephritis with crescent formation, necrosis of capillary loops, and mesangial IgA deposits. IgA vasculitis without purpura was considered as a possible diagnosis, and the treatment with prednisone led to remission of both gastrointestinal and renal diseases.

Objective To establish a homozygous zebrafish map3k15 knockout line using CRISPR/Cas9 gene editing technology so to provide an animal model for investigation of potential role of map3k15 in renal diseases.Methods 1)Analyzing the expression pattern of map3k15 in zebrafish;2)Establishing a homozygous map3k15 knockout zebrafish line using CRISPR/Cas9;3)Observing the phenotypic effects of map3k15 deficiency in ze-brafish.Results 1)map3k15 was expressed in the zebrafish pronephros,and map3k15/map3k15 protein was found highly conserved across species;2)map3k15-/-mutant zebrafish model was constructed with+2 bp mutation and+1 bp mutation;3)map3k15 mutant zebrafish exhibited edema in yolk sac,pericardium and head during embryonic development.Conclusions A homozygous zebrafish map3k15 knockout line is successfully developed which may provide an important model for future research on the role of map3k15 in renal development and disease.

To investigate the association between neutrophil to lymphocyte ratio (NLR) andestimated glomerular filtration rate (eGFR) in patients with diabetes using large-scale data.

Kidney disease constitutes a significant global public health issue,with its associated healthcare burden escalating annually.Lipid metabolism disorders play a crucial role in the onset and progression of various kidney diseases.Given the diversity of lipid species and the complexity of metabolic pathways,traditional research methods often fall short in fully elucidating the intricate roles of lipids in kidney diseases.In this context,lipido-mics,the systematic analysis of lipid molecules and their metabolic alterations in biological samples,emerges as a powerful tool with unique research value and clinical potential.This review summarizes the latest findings in lipido-mics across various kidney diseases and discusses the challenges encountered in clinical application and future research directions.

Kidney disease constitutes a significant global public health issue,with its associated healthcare burden escalating annually.Lipid metabolism disorders play a crucial role in the onset and progression of various kidney diseases.Given the diversity of lipid species and the complexity of metabolic pathways,traditional research methods often fall short in fully elucidating the intricate roles of lipids in kidney diseases.In this context,lipido-mics,the systematic analysis of lipid molecules and their metabolic alterations in biological samples,emerges as a powerful tool with unique research value and clinical potential.This review summarizes the latest findings in lipido-mics across various kidney diseases and discusses the challenges encountered in clinical application and future research directions.

A 66-year-old female patient with lung adenocarcinoma was treated with crizotinib [the first-generation anaplastic lymphoma kinase (ALK) inhibitors] 250 mg twice daily. Prior to treatment, the patient's liver and kidney functions were normal. One month after treatment, her serum creatinine (Scr) was 85 μmol/L, and alanine aminotransferase (ALT) was 115 U/L. After discontinuing crizotinib for 10 days, both Scr and ALT returned to normal. One month later, the patient underwent a right lower lobectomy. Crizotinib was restarted postoperatively, and she developed symptoms of lower limb edema and poor appetite. After more than 3 months of treatment, her Scr increased to 129 μmol/L, ALT was 96 U/L, and aspartate aminotransferase (AST) was 83 U/L. Crizotinib was then switched to alectinib (the second-generation ALK inhibitors) 600 mg orally twice daily, and the patient's gastrointestinal symptoms and liver function were rapidly improved. However, her Scr continued to increase gradually (140-150 μmol/L). Renal biopsy pathology indicated IgA nephropathy and acute tubular injury. After 4 months of alectinib treatment, Scr was 174 μmol/L, and the drug was promptly discontinued. One month after discontinuation, Scr decreased to 125 μmol/L. Due to tumor progression, the patient restarted alectinib at a reduced dose (300 mg twice daily). Three months later, Scr increased to 177 μmol/L. Subsequently, alectinib was replaced with lorlatinib (the third-generation ALK inhibitors) 100 mg once daily due to tumor progression. After 6 months of treatment, the tumor condition was controlled, and Scr decreased to 124 μmol/L.