Traditional treatment for type 1 diabetes mellitus （T1DM） primarily involves insulin replacement， yet some patients encounter issues such as significant blood glucose fluctuations， high risk of hypoglycemia， and weight gain. In recent years， the adjuvant therapeutic role of non-insulin hypoglycemic drugs in T1DM has gradually gained attention. This article reviews the mechanisms of action and clinical research progress of five types of non-insulin hypoglycemic drugs in the treatment of T1DM： amylin analogues （pramlintide）， biguanides （metformin）， sodium-glucose co-transporter 2 inhibitor， dipeptidyl peptidase-4 inhibitor， and glucagon-like peptide-1 receptor agonist. It is found that these drugs can enhance clinical benefits for T1DM patients by improving insulin sensitivity， delaying gastric emptying， promoting urinary glucose excretion， and regulating incretin levels， thereby reducing glycated hemoglobin levels， decreasing insulin dosage， and managing body weight. Simultaneously， these drugs also present limitations such as low patient compliance due to complex dosing regimens， increased risk of diabetic ketoacidosis， and heterogeneity in glycemic control. Future research could focus on developing individualized treatment strategies， combining pharmacogenomics with novel biomarkers to precisely identify subpopulations of patients who may benefit， and delving into the potential value of these drugs in delaying diabetic vascular complications and improving patients’ quality of life.

Childhood simple obesity has become a significant public health issue in China. Modern medicine primarily relies on lifestyle interventions and often suffers from poor long-term compliance， while pharmacological options are limited and associated with potential adverse effects. Traditional Chinese Medicine （TCM） has a long history in the prevention and management of this condition， demonstrating eight distinct advantages， including systematic theoretical foundation， diversified therapeutic approaches， definite therapeutic efficacy， high safety profile， good patient compliance， comprehensive intervention strategies， emphasis on prevention， and stepwise treatment protocols. Additionally， TCM is characterized by six distinctive features： the use of natural medicinal substances， non-invasive external therapies， integration of medicinal dietetics， simple exercise regimens， precise syndrome differentiation， and diverse dosage forms. By combining internal and external treatments， TCM facilitates individualized regimen adjustment and holistic regulation， demonstrating remarkable effects in improving obesity-related metabolic indicators， regulating constitutional imbalance， and promoting healthy behaviors. However， challenges remain， such as inconsistent operational standards， insufficient high-quality clinical evidence， and a gap between basic research and clinical application. Future efforts should focus on accelerating the standardization of TCM diagnosis and treatment， conducting multicenter randomized controlled trials， and fostering interdisciplinary integration， so as to enhance the scientific validity and international recognition of TCM in the prevention and treatment of childhood obesity.

Objective: To explore the therapeutic effects of different surgical methods for temporomandibular joint disc reduction and anchoring surgery, providing reference for optimizing this surgical procedure. Method: The study was approved by the hospital ethics committee. 173 patients (195 joints) who underwent temporomandibular joint disc repositioning and anchoring surgery were selected for retrospective analysis. Patients were categorized into groups A (traditional preauricular incision-scalpel/tissue scissors anterior attachment release), 35 patients (40 joints), B (traditional preauricular incision-plasma bipolar radiofrequency electrode anterior attachment release), 42 patients (46 joints), C (revised tragus incision - scalpel/tissue scissors anterior attachment release), 50 patients (58 joints), and D (revised tragus incision-plasma bipolar radiofrequency electrode anterior attachment release), 46 patients (51 joints). After a 6-month postoperative follow-up, the differences in maximum mouth opening (MMO), visual analogue scale (VAS), effective rate of joint disc reduction, incidence of preauricular numbness, obvious scars among patients in each group at 1, 3, and 6 months were compared postoperatively. Results: After surgery, the MMO of all four groups of patients initially shrunk and then gradually increased compared to before surgery. At the 1-month follow-up after surgery, the plasma bipolar radiofrequency release (B+D) group had a smaller impact on the patient’s MMO compared to the surgical knife/tissue scissors release (A+C) group (P < 0.05). Postoperative VAS scores for all four groups showed a gradual decrease from pre-operative levels, with the (B+D) group scoring significantly lower in the first month post-surgery compared to the (A+C) group (P < 0.05). Six months post-surgery, the rate of joint disc reduction of the four groups were higher than 95%, with no significant differences observed between the groups (P > 0.05). Patients in the revised tragus incision (C+D) group experienced a lower rate of preauricular numbness compared to those in the traditional preauricular incision (A+B) group (4.59% vs. 12.79%, P < 0.05), The incidence of obvious scars in the (C+D) group was significantly lower than that in the (A+B) group (3.67% vs. 23.26%, P < 0.05). Conclusion The revised tragus incision is superior to traditional preauricular incision in terms of protecting the auriculotemporal nerve and the scars were more inconspicuous. Further, the plasma bipolar radiofrequency electrode is superior to the scalpel/tissue scissors in terms of mouth opening recovery and pain control. For temporomandibular joint disc reduction and anchoring surgery, a modified tragus incision combined with plasma bipolar radiofrequency electrode to release the anterior attachment of the joint disc can be recommended as a surgical option.

Taxifolin (TAX) is a natural compound known for its liver protection effect, but the mechanism remains unknown. Phosphorylated proteomics analyses discovered that the phosphorylation level of NDRG1 at T328 was a key event of TAX-improved liver fibrosis. We established models with NDRG1 knockout (KO) in vivo and in vitro, demonstrating that NDRG1 KO attenuated the development of hepatocyte injury, and combining NDRG1 KO and TAX administration did not result in a reduction in protection against liver injury. Cellular thermal shift assay and surface plasma resonance analysis showed that TAX directly binds to NDRG1 rather than its upstream kinase, subsequently demonstrating that TAX regulated phosphorylation of NDRG1 at T328 through binding to its C289 site. NDRG1 T328A (phosphorylated mutation) and T328E (mimic phosphorylation) in vivo and in vitro confirmed that pNDRG1_T328 exacerbates hepatocyte injury along with DNA damage, inflammatory response, and apoptosis, thereby contributing to hepatic stellate cells (HSCs) activation. In contrast, TAX can inhibit the above pathological abnormalities and block hepatocyte injury-triggered HSCs activation and fibrosis. Overall, TAX is a potent liver protection drug primarily targeting NDRG1 and inhibiting pNDRG1_T328 in hepatocytes.

Objective: To investigate the clinical symptoms, laboratory tests, and treatment strategies of a case of fetal/neonatal alloimmune thrombocytopenia (FNAIT) complicated with piperacillin drug antibody. Methods: The platelet antibodies in the mother were screened and identified by ELISA. The HLA antigens of the newborn were genotyped through PCR-SSO, while the specificity of HLA antibodies in the mother was determined using a Single Antigen kit. The drug antibody was detected by a piperacillin kit. Results: Maternal antibodies against paternally-derived platelet antigens were detected. The HLA genotypes of the newborn were identified as HLA A 33∶03 and HLA B 58∶01. The mother exhibited strong positive antibodies against the specific platelet antigens of the newborn, namely anti-HLA-A33 and anti-HLA-B58 antibodies. The piperacillin antibody was detected in the newborn. Following treatment of continuous intravenous immunoglobulin (IVIG), platelet transfusions, red blood cell transfusions and discontinuation of piperacillin treatment, the platelet count and hemoglobin levels increased in the newborn. Conclusion: The newborn in this case was diagnosed with FNAIT complicated by the presence of anti-HLA-A33 and anti-HLA-B58 antibodies, as well as drug-induced hemolytic anemia caused by piperacillin drug antibody. The condition is more complicated under the influence of dual immune antibodies. Laboratory detection techniques such as platelet antibody and drug antibody tests can assist in early clinical diagnosis. At the same time, more active drug and blood transfusion treatments should be given in clinical practice to improve the prognosis.

Objective: To investigate the clinical symptoms, laboratory tests, and treatment strategies of a case of fetal/neonatal alloimmune thrombocytopenia (FNAIT) complicated with piperacillin drug antibody. Methods: The platelet antibodies in the mother were screened and identified by ELISA. The HLA antigens of the newborn were genotyped through PCR-SSO, while the specificity of HLA antibodies in the mother was determined using a Single Antigen kit. The drug antibody was detected by a piperacillin kit. Results: Maternal antibodies against paternally-derived platelet antigens were detected. The HLA genotypes of the newborn were identified as HLA A 33∶03 and HLA B 58∶01. The mother exhibited strong positive antibodies against the specific platelet antigens of the newborn, namely anti-HLA-A33 and anti-HLA-B58 antibodies. The piperacillin antibody was detected in the newborn. Following treatment of continuous intravenous immunoglobulin (IVIG), platelet transfusions, red blood cell transfusions and discontinuation of piperacillin treatment, the platelet count and hemoglobin levels increased in the newborn. Conclusion: The newborn in this case was diagnosed with FNAIT complicated by the presence of anti-HLA-A33 and anti-HLA-B58 antibodies, as well as drug-induced hemolytic anemia caused by piperacillin drug antibody. The condition is more complicated under the influence of dual immune antibodies. Laboratory detection techniques such as platelet antibody and drug antibody tests can assist in early clinical diagnosis. At the same time, more active drug and blood transfusion treatments should be given in clinical practice to improve the prognosis.

Objective To establish radioresistant human non-small cell lung cancer NCI-H460R model cells and evaluate the sensitivity of these radioresistant cells to a ferroptosis inducer. Methods Radioresistant cell lines, designated as NCI-H460 R20Gy and NCI-H460 R116Gy, were generated by subjecting parental NCI-H460 cells to fractionated irradiation with varying cumulative doses. Both parental cells and the established radioresistant cell lines were each randomly divided into four groups and exposed to irradiation at 0, 2, 4, and 6 Gy, respectively. Successful establishment of the radioresistant cell lines was confirmed by colony formation assay. Subsequently, cells were treated with increasing concentrations of the ferroptosis inducer RSL-3 to assess differential sensitivity between parental and radioresistant cells to ferroptosis. Results In comparison to the parental NCI-H460 cells (D_0WT=1.2), both NCI-H460 R116Gy and NCI-H460 R20Gy cells exhibited radioresistance, with NCI-H460 R116Gy demonstrating a stronger radioresistance (D_0R116Gy=1.5) than NCI-H460 R20Gy (D_0R20Gy=1.4). Furthermore, NCI-H460 R116Gy cells exhibited increased sensitivity to RSL-3 relative to the parental cells (P < 0.001), while NCI-H460 R20Gy cells did not display a significant difference in sensitivity to RSL-3. Conclusion Human non-small cell lung cancer cells with radioresistance induced by a high cumulative irradiation dose exhibit increased sensitivity to the glutathione peroxidase 4-specific ferroptosis inducer RSL-3. This finding provides an experimental basis for optimizing combined treatment regimens involving radiotherapy and RSL-3 for non-small cell lung cancer patients with radiotherapy resistance.

Guided by Academician Zhang Boli's theory of "dampness， turbidity， phlegm， and fluid-related diseases"，this paper elaborated on the pathogenesis and syndrome differentiation treatment of heart failure from the perspective of the "spleen-mitochondria". It analyzed the essential similarities between "spleen-mitochondria" and "dampness， turbidity， phlegm， and fluid-related diseases"， as well as their close association with the onset of heart failure. Furthermore，it explored the connection between spleen function and mitochondrial function in traditional Chinese medicine （TCM），positing that the spleen's role in transportation and transformation is analogous to mitochondrial material metabolism and energy conversion，with spleen deficiency closely related to mitochondrial dysfunction. It thus concluded that mitochondrial material metabolism and energy conversion represent the microscopic essence of the spleen's role in transportation and transformation，and mitochondrial dysfunction is a contributing factor to pathological products like dampness and turbid phlegm，which are closely associated with the occurrence of heart failure. The four elements of dampness，turbidity，phlegm，and fluid are a series of related symptoms resulting from abnormal fluid transportation and transformation，serving as both factors in the onset of heart failure and the core pathological basis for its deterioration. Therefore，during the treatment of heart failure，it is essential to regulate mitochondrial function. Early intervention should focus on eliminating dampness and turbidity to improve mitochondrial function and restore normal energy metabolism. In the middle and late stages，emphasis should be placed on resolving phlegm，promoting blood circulation，warming Yang，and reducing water retention to alleviate mitochondrial damage and improve cardiac function. Supporting Qi and strengthening the spleen should be a continuous approach，and treatment should be adjusted to enhance mitochondrial function and stabilize the condition，thereby improving prognosis. This paper discussed the role of the spleen and mitochondria in the pathogenesis of heart failure，examined the evolution of heart failure mechanisms from the perspective of dampness， turbidity， phlegm， and fluid-related diseases，and proposed a phased treatment strategy. It enriched the theory of dampness， turbidity， phlegm， and fluid-related diseases and offered new strategies for heart failure treatment. However，in practical application，TCM strategies for treating heart failure need to be integrated with modern medical approaches to provide a more solid scientific foundation for treatment.

Objective:It is of great significance to analyze the expression characteristics of immune-related genes in pancreatic cancer and their relationship with prognosis,construct and verify a reliable prognostic model,and explore prognostic methods of pancreatic cancer from the perspective of immune microenvironment.Methods:GSEA enrich-ment analysis of differentially expressed genes in pancreatic cancer was performed to identify key immune-related pathways and genes.The genes involved in the immune pathway were screened through the STRING database and combined with univariate Cox regression and LASSO regression analysis.Three key genes,RIPK2,IRAK2 and CXCL11,were finally identified to construct the prognostic model.The accuracy of the model was evaluated using ROC curves and calibration curves,and verified in an independent verification set(GSE57495).At the same time,the expression pat-terns of key genes in the immune microenvironment were analyzed by single-cell RNA sequencing,and the expression levels of these genes were verified in pancreatic cancer cell lines by RT-qPCR.Results:The expressions of RIPK2,IRAK2 and CXCL11 in pancreatic cancer cell lines were higher than those in normal pancreatic cancer cells(P<0.05).The model based on these three genes divided the patients into a high-risk group(n=87)and a low-risk group(n=89),and the difference in survival time between the high-risk group and the low-risk group was statistically significant(P<0.001).Risk score was correlated with G stage,N stage and tumor residue(P<0.01).Single-cell analysis showed that the ex-pression of these genes was highest in tumor-associated macrophages(mean>0.5)and correlated with regulatory T cells and macrophage infiltration(P<0.05).Multivariate analysis showed that risk score was correlated with overall sur-vival after adjusting for clinical factors(P=0.0014).Conclusion:Based on three key immune-related genes(RIPK2,IRAK2 and CXCL11),we successfully constructed a model to accurately predict the prognosis of pancreatic cancer pa-tients,revealing the important role of these genes in the tumor immune microenvironment,and providing new insights and theoretical basis for pancreatic cancer prognosis assessment and immunotherapy research.