Diabetic kidney disease （DKD） is one of the more common chronic kidney diseases，and its causes are complex. DKD is very easy to progress to end-stage renal disease，and the current therapeutic effect still needs to be improved. As an important excretive organ of the human body， the kidney has physiological functions such as discharging metabolic waste， regulating fluid balance， and maintaining the stability of the body's internal environment. These highly complex biochemical processes all depend on the energy support provided by mitochondria. Mitochondrial dysfunction is a key factor causing kidney injury， and the imbalance of mitochondrial homeostasis is an important link leading to mitochondrial dysfunction. The occurrence and development of DKD are often accompanied by the imbalance of mitochondrial homeostasis in renal cells. Mitochondrial autophagy， as a means of regulating mitochondrial homeostasis， is very important for the prevention and treatment of DKD. The PTEN-induced putative kinase 1 （PINK1）/Parkin pathway is one of the most classical pathways to regulate mitochondrial autophagy. Recent studies have found that some drugs can regulate the PINK1/Parkin signaling pathway to target mitochondrial homeostasis and exert renoprotective effects. In particular， traditional Chinese medicine has a significant effect on early and middle stage DKD by regulating PINK1/Parkin pathway-mediated mitochondrial autophagy. This article discussed the mechanism of PINK1/Parkin pathway in mitochondrial autophagy and DKD and reviewed the effect of PINK1/Parkin pathway-mediated mitochondrial autophagy on DKD. At the same time， it explored the therapeutic effect of traditional Chinese and western medicine on DKD mediated by PINK1/Parkin-mediated mitochondrial autophagy， aiming to broaden the ideas of traditional Chinese and western medicine for the prevention and treatment of DKD from the perspective of PINK1/Parkin regulating mitochondrial autophagy.

Diabetic kidney disease （DKD） is one of the more common chronic kidney diseases，and its causes are complex. DKD is very easy to progress to end-stage renal disease，and the current therapeutic effect still needs to be improved. As an important excretive organ of the human body， the kidney has physiological functions such as discharging metabolic waste， regulating fluid balance， and maintaining the stability of the body's internal environment. These highly complex biochemical processes all depend on the energy support provided by mitochondria. Mitochondrial dysfunction is a key factor causing kidney injury， and the imbalance of mitochondrial homeostasis is an important link leading to mitochondrial dysfunction. The occurrence and development of DKD are often accompanied by the imbalance of mitochondrial homeostasis in renal cells. Mitochondrial autophagy， as a means of regulating mitochondrial homeostasis， is very important for the prevention and treatment of DKD. The PTEN-induced putative kinase 1 （PINK1）/Parkin pathway is one of the most classical pathways to regulate mitochondrial autophagy. Recent studies have found that some drugs can regulate the PINK1/Parkin signaling pathway to target mitochondrial homeostasis and exert renoprotective effects. In particular， traditional Chinese medicine has a significant effect on early and middle stage DKD by regulating PINK1/Parkin pathway-mediated mitochondrial autophagy. This article discussed the mechanism of PINK1/Parkin pathway in mitochondrial autophagy and DKD and reviewed the effect of PINK1/Parkin pathway-mediated mitochondrial autophagy on DKD. At the same time， it explored the therapeutic effect of traditional Chinese and western medicine on DKD mediated by PINK1/Parkin-mediated mitochondrial autophagy， aiming to broaden the ideas of traditional Chinese and western medicine for the prevention and treatment of DKD from the perspective of PINK1/Parkin regulating mitochondrial autophagy.

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.

Objective: To investigate the expressions of GPR15 and FOXP3 in colorectal carcinoma(CRC) tissues and their clinical prognostic values. Methods : A total of 132 patients with CRC underwent radical surgery were collected. The control group selected the normal mucosal tissues more than 5 cm away from the edge of the cancer focus. Immunohistochemistry(Envision two-step method) was used to detect the expression levels of GPR15 and FOXP3 in CRC and adjacent tissues, and analyze their relationships with clinicopathological factors of colorectal cancer. Kaplan-Meier method was used to draw the survival curve to analyze the correlation between the expressions of GPR15 and FOXP3 and the survival prognosis of patients with CRC. The factors influencing prognosis of patients with colorectal cancer were analyzed by Cox regression. Results : The immunohistochemistry showed that the expression levels of GPR15 and FOXP3 in CRC were significantly higher than those in normal colorectal mucosal tissues(P<0.05). The expression of GPR15 in CRC tissues was correlated with location, nerve invasion and TNM stage; FOXP3 expression was correlated with sex(P<0.05).Both expressions were not significantly correlated with the clinicopathologic features of age, tumor size, differentiation degree, tissue type, depth of invasion, tumor budding, vascular invasion and lymph node metastasis. Correlation analysis showed that there was no significant correlation between GPR15 and FOXP3 expression(Kappa=-0.019,P>0.05). The survival prognosis of GPR15 positive group was significantly worse than that of negative group(log-rank: χ2=4.3,P=0.039);while the survival prognosis of FOXP3 positive group was significantly better than that of negative group(log-rank: χ2=7.3,P=0.007).Age ≤55 years, positive GPR15 and negative FOXP3 were independent risk factors for poor prognosis in patients with CRC(P<0.05). Conclusion The expression levels of GPR15 and FOXP3 in CRC are significantly higher than those in paracancer tissues, GPR15 and FOXP3 are expected to become new tumor markers for early screening, accurate treatment and prognosis assessment of CRC.

Cancer is one of the major diseases of high morbidity and mortality worldwide,and its therapeutic approaches are facing great challenges.Immunotherapy,especially the activation of innate immunity represented by the cGAS-STING signaling pathway,is the current research hotspot in tumor immunotherapy.Activation of innate immune response by gas therapy is the latest development in tumor therapeutic approaches,especially the use of gas signaling molecules(NOx CO,H2S and SO2)to activate the cGAS-STING signaling pathway to induce intrinsic immunity of the organism,which leads to anti-tumor immunotherapy.Although intrinsic immunity activated by gas signaling molecules plays an important role in tumor immunotherapy,few reviews have been reported on its association with the cGAS-STING signaling mechanism.In this paper,we will comprehensively describe how gas signaling molecules damage the mitochondrial matrix and DNA damage through oxidative/nitrosative stress,thereby activating the cGAS-STING signaling pathway and triggering the innate immune cascade,aiming to summarize the process of activation of anti-tumor immune effects by gas signaling molecules,and to provide more references for the gas therapies in the future anti-tumor immunity research.

Breast cancer is the leading cause of cancer-related mortality among women worldwide and has drawn extensive research attention.Owing to its molecular heterogeneity,drug resistance,and low therapeutic response,single-modality treatments often fail to achieve satisfactory efficacy or broad applicability.Combination therapy,designed based on the pathophysiological characteristics,related signaling pathways,and biomarkers of breast cancer,has emerged as a promising approach for improving therapeutic outcomes.With the advancement of research on combination strategies,the understanding of their molecular mechanisms—particularly key signaling pathways and biomarkers—has become increasingly important.However,comprehensive reviews addressing these molecular mechanisms and synergistic strategies remain scarce.This article summarizes recent advances in combination therapy for breast cancer,providing a comprehensive review of recent combination therapies for breast cancer and their underlying molecular mechanisms,and focusing on key signaling pathways involved in combination therapy and synergistic strategies,thereby providing theoretical insights and reference for researchers,graduate students,and clinicians engaged in the development of novel combination therapeutic strategies for breast cancer and related malignancies.

Objective To investigate a rapid detection method for compressed Nitrous oxide(N2O).Methods The GC-MS system was employed under conventional chromatographic conditions(without replacing standard columns or utilizing headspace sampling)by directly injecting a small gas sample for analysis.N2O identification was performed via NIST spectral library matching,while qualitative and quantitative purity assessments were achieved by monitoring the relative abundance variation of the characteristic fragment ion m/z 30 to eliminate CO2 interference.Results The fragment ion m/z 30 demonstrated specificity for N2O identification.A linear correlation was observed between the peak area of m/z 30 and N2O purity(y=22.741x-1.4565,R2=0.912 6),enabling quantitative purity determination.Additionally,the abundance of m/z30 exhibited a correlation with N2O in CO2 mixtures(y=0.7787x-0.0387,R2=0.722 2).Conclusion Conventional N2O identification typically requires dedicated GC-MS systems,gas-specific chromatographic columns,and headspace sampling.This study successfully utilized routine chromatographic conditions for organic toxicant screening to achieve rapid N2O analysis.The proposed method holds practical significance for compressed N2O identification in forensic and analytical applications.

Cancer is one of the major diseases of high morbidity and mortality worldwide,and its therapeutic approaches are facing great challenges.Immunotherapy,especially the activation of innate immunity represented by the cGAS-STING signaling pathway,is the current research hotspot in tumor immunotherapy.Activation of innate immune response by gas therapy is the latest development in tumor therapeutic approaches,especially the use of gas signaling molecules(NOx CO,H2S and SO2)to activate the cGAS-STING signaling pathway to induce intrinsic immunity of the organism,which leads to anti-tumor immunotherapy.Although intrinsic immunity activated by gas signaling molecules plays an important role in tumor immunotherapy,few reviews have been reported on its association with the cGAS-STING signaling mechanism.In this paper,we will comprehensively describe how gas signaling molecules damage the mitochondrial matrix and DNA damage through oxidative/nitrosative stress,thereby activating the cGAS-STING signaling pathway and triggering the innate immune cascade,aiming to summarize the process of activation of anti-tumor immune effects by gas signaling molecules,and to provide more references for the gas therapies in the future anti-tumor immunity research.

Breast cancer is the leading cause of cancer-related mortality among women worldwide and has drawn extensive research attention.Owing to its molecular heterogeneity,drug resistance,and low therapeutic response,single-modality treatments often fail to achieve satisfactory efficacy or broad applicability.Combination therapy,designed based on the pathophysiological characteristics,related signaling pathways,and biomarkers of breast cancer,has emerged as a promising approach for improving therapeutic outcomes.With the advancement of research on combination strategies,the understanding of their molecular mechanisms—particularly key signaling pathways and biomarkers—has become increasingly important.However,comprehensive reviews addressing these molecular mechanisms and synergistic strategies remain scarce.This article summarizes recent advances in combination therapy for breast cancer,providing a comprehensive review of recent combination therapies for breast cancer and their underlying molecular mechanisms,and focusing on key signaling pathways involved in combination therapy and synergistic strategies,thereby providing theoretical insights and reference for researchers,graduate students,and clinicians engaged in the development of novel combination therapeutic strategies for breast cancer and related malignancies.

Objective To investigate a rapid detection method for compressed Nitrous oxide(N2O).Methods The GC-MS system was employed under conventional chromatographic conditions(without replacing standard columns or utilizing headspace sampling)by directly injecting a small gas sample for analysis.N2O identification was performed via NIST spectral library matching,while qualitative and quantitative purity assessments were achieved by monitoring the relative abundance variation of the characteristic fragment ion m/z 30 to eliminate CO2 interference.Results The fragment ion m/z 30 demonstrated specificity for N2O identification.A linear correlation was observed between the peak area of m/z 30 and N2O purity(y=22.741x-1.4565,R2=0.912 6),enabling quantitative purity determination.Additionally,the abundance of m/z30 exhibited a correlation with N2O in CO2 mixtures(y=0.7787x-0.0387,R2=0.722 2).Conclusion Conventional N2O identification typically requires dedicated GC-MS systems,gas-specific chromatographic columns,and headspace sampling.This study successfully utilized routine chromatographic conditions for organic toxicant screening to achieve rapid N2O analysis.The proposed method holds practical significance for compressed N2O identification in forensic and analytical applications.