BACKGROUND:Fibromyalgia syndrome,as a common rheumatic disease,is related to central sensitization and immune abnormalities.However,the specific mechanism has not been elucidated,and there is a lack of specific diagnostic markers.Exploring the possible pathogenesis of this disease has important clinical significance. OBJECTIVE:To screen the potential diagnostic marker genes of fibromyalgia syndrome and analyze the possible immune infiltration characteristics based on bioinformatics methods,such as weighted gene co-expression network analysis(WGCNA),and machine learning. METHODS:Gene expression profiles in peripheral serum of fibromyalgia syndrome patients and healthy controls were obtained from the gene expression omnibus(GEO)database.The differentially co-expressed genes were screened in the expression profile by differential analysis and WGCNA analysis.Least absolute shrinkage and selection operator(LASSO)and support vector machine-recursive feature elimination(SVM-RFE)machine learning algorithm were further used to identify hub biomarkers,and draw receiver operating characteristic curve(ROC)to evaluate the accuracy of diagnosing fibromyalgia syndrome.Finally,single sample gene set enrichment analysis(ssGSEA)and gene set enrichment analysis(GSEA)were used to evaluate the immune cell infiltration and pathway enrichment in patients with fibromyalgia syndrome. RESULTS AND CONCLUSION:Eight down-regulated differentially expressed genes(DEGs)were obtained after differential analysis of the GSE67311 dataset according to the conditions of log2|(FC)|>0 and P<0.05.After WGCNA analysis,497 genes were included in the module(MEdarkviolet)with the highest positive correlation(r=0.22,P=0.04),and 19 genes were included in the module(MEsalmon2)with the highest negative correlation(r=-0.41,P=6×10-5).After intersecting DEGs and the module genes of WGCNA,seven genes were obtained.Four genes were screened out by LASSO regression algorithm and five genes were screened out by SVM-RFE machine learning algorithm.After the intersection of the two,three core genes were identified,which were germinal center associated signaling and motility like,integrin beta-8,and carboxypeptidase A3.The areas under the ROC curve of the three core genes were 0.744,0.739,and 0.734,respectively,indicating that they have good diagnostic value and can be used as biomarkers for fibromyalgia syndrome.The results of immune infiltration analysis showed that memory B cells,CD56 bright NK cells,and mast cells were significantly down-regulated in patients with fibromyalgia syndrome compared with the control group(P<0.05),and were significantly positively correlated with the above three biomarkers(P<0.05).The enrichment analysis suggested that there were nine fibromyalgia syndrome enrichment pathways,mainly related to olfactory transduction pathway,neuroactive ligand-receptor interaction,and infection pathway.The above results showed that the occurrence and development of fibromyalgia syndrome are related to the involvement of multiple genes,abnormal immune regulation,and multiple pathways imbalance.However,the interactions between these genes and immune cells,as well as their relationships with various pathways need to be further investigated.

AIM:This study aims to investigate the regulatory effects of caffeic acid phenethyl ester(CAPE)on metabotropic glutamate receptor 5(mGluR5)and tyrosine kinase Fyn,and to explore its role in alleviating neuroinflam-mation and pathological features of Alzheimer disease(AD).METHODS:In vitro,the murine neuroblastoma N2a cell line was treated with amyloid β-protein 42 oligomers(Aβ42Os;10 nmol/L to 10 μmol/L)for 24 h.Cell viability was as-sessed by MTT assay.Western blot analyzed mGluR5 expression and Fyn phosphorylation(Tyr416).Pharmacological modulators(CHPG/MPEP)were used to evaluate mGluR5-mediated inflammatory cytokine regulation(qPCR)and Fyn ac-tivation.In vivo,wild-type(WT)and 5×FAD mice(WT,WT+CAPE,5×FAD and 5×FAD+CAPE)were analyzed for AD-related proteins,neuroinflammation(ELISA),glial activation(GFAP/Iba-1 immunofluorescence),and β-amyloid deposi-tion(thioflavin S).RESULTS:(1)Treatment with 1 μmol/L Aβ42Os increased mGluR5 expression(P<0.01)and Fyn phosphorylation(P<0.01)without affecting N2a cell viability.Intracerebral Aβ42Os injection similarly up-regulated hip-pocampal mGluR5 and Fyn(P<0.01).(2)MPEP reduced mGluR5 expression(P<0.01)and Fyn phosphorylation(P<0.01),while suppressing tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)mRNA levels(P<0.01).(3)CAPE decreased mGluR5-Fyn activation in N2a cells,neurons,and 5×FAD mice(P<0.01).(4)CAPE-treated 5×FAD mice exhibited reduced neuroinflammation markers(GFAP,Iba-1,TNF-α,IL-1β,and IL-6),Aβ plaques,and p-APP levels(P<0.01).CONCLUSION:Treatment with CAPE inhibits Aβ42Os-induced mGluR5-Fyn signaling activation,thereby attenuating neuroinflammation and the pathology associated with AD.

The symptom science model identifies complex symptoms and measures their phenotypic characteristics.It provides an in-depth analysis of symptom behaviors and biological mechanisms,aiding healthcare professionals in early symptom detection and initiating appropriate diagnostic and treatment measures.The model supports personalized interventions,aiming to achieve precision care and ultimately improve patient health.This study reviews the development and scope of the symptom science model,analyzes its current applications in chronic kidney disease,and explores its implications for symptom management in this condition.The aim is to offer insights and references for the scientific management of chronic kidney disease symptoms.

Objective:To analyze the characteristics of patients with pneumoconiosis complicated with chronic obstructive pulmonary disease (COPD), and to explore the comorbidity of pneumoconiosis and COPD and its influencing factors.Methods:From October to December 2022, 255 pneumoconiosis patients admitted to an occupational disease prevention and control hospital from January 2018 to December 2021 were selected as the study subjects. According to whether the pneumoconiosis patients were complicated with COPD or not, they were divided into pneumoconiosis and COPD comorbidity group and pneumoconiosis group. The general condition and dust exposure of the two groups of patients were analyzed, and the relationship between different types and different periods of pneumoconiosis and COPD comorbidity was analyzed by multivariate logistic regression.Results:A total of 255 subjects were collected, including 64 patients with comorbidity of pneumoconiosis and COPD, and the comorbidity rate was 25.1%. There were 186 males (72.9%) and 69 females (27.1%), ranging in age from 35 to 90 (63.79±11.79) years, and working age from 1 to 45 (20.31±10.57) years. The comorbidity of pneumoconiosis and COPD increased with the increase of working age (χ 2trend=8.19, P=0.004), and the comorbidity rate for COPD with working age of more than 30 years was 37.7% (23/61). The comorbidity rate of pneumoconiosis and COPD also increased with the increase of the stage of pneumoconiosis (χ 2trend=13.14, P<0.001), and the comorbidity rate of pneumoconiosis and COPD in the stage Ⅲ was as high as 44.0% (11/25). The cumulative dust exposure was negatively correlated with forced expiratory volume in one second/forced vital capacity (FEV 1/FVC), and the linear regression equation y=-0.04 x+78.4. Multivariate logistic regression analysis showed that the length of services ≥30 years ( OR=3.30, 95% CI: 1.15-9.52) and stageⅡ ( OR=3.05, 95% CI: 1.03-9.04) were the risk factors for comorbidity between pneumoconiosis and COPD ( P<0.05) . Conclusion:The comorbidity rate of pneumoconiosis and COPD is high. Working age, pneumoconiosis stage and cumulative dust exposure are the main influencing factors of pneumoconiosis and COPD comorbidity, so more attention should be paid to the comorbidity of pneumoconiosis and COPD.

AIM:This study aims to investigate the regulatory effects of caffeic acid phenethyl ester(CAPE)on metabotropic glutamate receptor 5(mGluR5)and tyrosine kinase Fyn,and to explore its role in alleviating neuroinflam-mation and pathological features of Alzheimer disease(AD).METHODS:In vitro,the murine neuroblastoma N2a cell line was treated with amyloid β-protein 42 oligomers(Aβ42Os;10 nmol/L to 10 μmol/L)for 24 h.Cell viability was as-sessed by MTT assay.Western blot analyzed mGluR5 expression and Fyn phosphorylation(Tyr416).Pharmacological modulators(CHPG/MPEP)were used to evaluate mGluR5-mediated inflammatory cytokine regulation(qPCR)and Fyn ac-tivation.In vivo,wild-type(WT)and 5×FAD mice(WT,WT+CAPE,5×FAD and 5×FAD+CAPE)were analyzed for AD-related proteins,neuroinflammation(ELISA),glial activation(GFAP/Iba-1 immunofluorescence),and β-amyloid deposi-tion(thioflavin S).RESULTS:(1)Treatment with 1 μmol/L Aβ42Os increased mGluR5 expression(P<0.01)and Fyn phosphorylation(P<0.01)without affecting N2a cell viability.Intracerebral Aβ42Os injection similarly up-regulated hip-pocampal mGluR5 and Fyn(P<0.01).(2)MPEP reduced mGluR5 expression(P<0.01)and Fyn phosphorylation(P<0.01),while suppressing tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)mRNA levels(P<0.01).(3)CAPE decreased mGluR5-Fyn activation in N2a cells,neurons,and 5×FAD mice(P<0.01).(4)CAPE-treated 5×FAD mice exhibited reduced neuroinflammation markers(GFAP,Iba-1,TNF-α,IL-1β,and IL-6),Aβ plaques,and p-APP levels(P<0.01).CONCLUSION:Treatment with CAPE inhibits Aβ42Os-induced mGluR5-Fyn signaling activation,thereby attenuating neuroinflammation and the pathology associated with AD.

The symptom science model identifies complex symptoms and measures their phenotypic characteristics.It provides an in-depth analysis of symptom behaviors and biological mechanisms,aiding healthcare professionals in early symptom detection and initiating appropriate diagnostic and treatment measures.The model supports personalized interventions,aiming to achieve precision care and ultimately improve patient health.This study reviews the development and scope of the symptom science model,analyzes its current applications in chronic kidney disease,and explores its implications for symptom management in this condition.The aim is to offer insights and references for the scientific management of chronic kidney disease symptoms.

Objective:To analyze the characteristics of patients with pneumoconiosis complicated with chronic obstructive pulmonary disease (COPD), and to explore the comorbidity of pneumoconiosis and COPD and its influencing factors.Methods:From October to December 2022, 255 pneumoconiosis patients admitted to an occupational disease prevention and control hospital from January 2018 to December 2021 were selected as the study subjects. According to whether the pneumoconiosis patients were complicated with COPD or not, they were divided into pneumoconiosis and COPD comorbidity group and pneumoconiosis group. The general condition and dust exposure of the two groups of patients were analyzed, and the relationship between different types and different periods of pneumoconiosis and COPD comorbidity was analyzed by multivariate logistic regression.Results:A total of 255 subjects were collected, including 64 patients with comorbidity of pneumoconiosis and COPD, and the comorbidity rate was 25.1%. There were 186 males (72.9%) and 69 females (27.1%), ranging in age from 35 to 90 (63.79±11.79) years, and working age from 1 to 45 (20.31±10.57) years. The comorbidity of pneumoconiosis and COPD increased with the increase of working age (χ 2trend=8.19, P=0.004), and the comorbidity rate for COPD with working age of more than 30 years was 37.7% (23/61). The comorbidity rate of pneumoconiosis and COPD also increased with the increase of the stage of pneumoconiosis (χ 2trend=13.14, P<0.001), and the comorbidity rate of pneumoconiosis and COPD in the stage Ⅲ was as high as 44.0% (11/25). The cumulative dust exposure was negatively correlated with forced expiratory volume in one second/forced vital capacity (FEV 1/FVC), and the linear regression equation y=-0.04 x+78.4. Multivariate logistic regression analysis showed that the length of services ≥30 years ( OR=3.30, 95% CI: 1.15-9.52) and stageⅡ ( OR=3.05, 95% CI: 1.03-9.04) were the risk factors for comorbidity between pneumoconiosis and COPD ( P<0.05) . Conclusion:The comorbidity rate of pneumoconiosis and COPD is high. Working age, pneumoconiosis stage and cumulative dust exposure are the main influencing factors of pneumoconiosis and COPD comorbidity, so more attention should be paid to the comorbidity of pneumoconiosis and COPD.

Beta-thalassemia major(β-TM)is an inherited disease caused by a defect in the synthesis of globin. The disease requires long-term blood transfusion and iron chelator treatment, which can cause various secondary changes in the body and eye tissues. Compared with normal peers, β-TM patients will show changes in the eye such as steeper corneal curvature, shallower anterior chamber, increased lens thickness, shorter axial length, and reduced tear secretion. At the same time, nutritional deficiencies and the use of iron chelator drugs will increase the risk of complicated cataract and retinal degeneration, thus affecting the quality of life of β-TM patients.This article combines relevant domestic and foreign literatures to explore and review the changes in the eye of β-TM patients, with a view to providing valuable insights for clinical practice.

AIM:To evaluate corrective effect and stability of corneal morphology in patients with moderate to high myopia after 2a treatment of femtosecond laser assisted laser in situ keratomileusis(FS-LASIK)Xtra.METHODS:Retrospective case-control study. A total of 30 cases(58 eyes)Patients with moderate to high myopia combined with astigmatism who planned to undergo refractive surgery in our hospital from August 2019 to August 2020 were included, and different types of surgery were performed respectively based on the relevant index of keratoconus screening in the preoperative corneal topography. They were divided into FS-LASIK group and Xtra group, with 15 cases(29 eyes)in each group. Uncorrected visual acuity(UCVA), best corrected visual acuity(BCVA), spherical equivalent(SE)and the corneal curvature of the anterior and posterior surfaces of different diameters(3, 5 and 7 mm)measured by Sirius three-dimensional corneal topography were observed preoperatively and 3 mo, 1 and 2 a postoperatively.RESULTS: The UCVA of the two groups of patients at different time points after surgery was significantly increased compared with preoperatively(both P<0.01), and there was no difference in UCVA and SE between the two groups(P>0.05). After 2 a postoperatively, residual astigmatism was -0.25-0 D in 25 eyes(86%)of the FS-LASIK Xtra group and 24 eyes(83%)of the FS-LASIK group. The actual corrected SE and expected corrected SE of both groups were positively correlated(both P<0.05). There were differences in corneal curvature on the surface of different diameter areas(3, 5, and 7 mm)between the two groups at 3 mo, 1, and 2 a postoperatively compared with preoperatively. After 1 and 2 a postoperatively, the corneal posterior surface curvature of the FS-LASIK Xtra group with corneal diameter of 3 and 5 mm was higher than that of the FS-LASIK group(P<0.05).CONCLUSIONS:FS-LASIK Xtra has good safety, efficacy and predictability in correcting patients with moderate to high myopia.

Objective:To investigate the impact of pumpkin polysaccharide(PP)on hypoxia/reoxygenation(H/R)-induced myocardial cell(H9C2)injury by regulating Nrf2/γ-GCS pathway.Methods:HR cell models were established,and the concentration of pumpkin polysaccharide(PP)was determined.H9C2 cells were grouped into Control group,H/R group,pumpkin polysaccharide group(PP group,2 mg/L PP),Nrf2 inhibitor group(ML385 group,2.0 μmol/L ML385),and PP+ML385 group(2.0 mg/L PP+2.0 μmol/L ML385),the apoptosis,mitochondrial membrane potential changes,oxidative stress(LDH,MDA,SOD,ROS),the lev-els of inflammatory factors(TNF-α,IL-6,IL-1β)and the protein expressions of Nrf2 and γ-GCS in H9C2 cells were detected,respec-tively.Results:Compared with Control group,H/R group had changes in cell morphology,the cell injury and mitochondrial membrane potential decreased,the H9C2 cell viability,SOD and protein expression levels of Nrf2 and γ-GCS were significantly decreased,while the apoptosis rate,LDH,MDA,ROS,and levels of TNF-α,IL-6 and IL-1β were significantly increased(P<0.05);compared with H/R group,the cell injury in PP group was reduced,the mitochondrial membrane potential was restored,the H9C2 cell viability,SOD and protein expression levels of Nrf2 and γ-GCS were significantly increased,and the apoptosis rate,LDH,MDA,ROS,and levels of TNF-α,IL-6 and IL-1β were significantly decreased(P<0.05),the effect of ML385 was opposite to that of PP,and ML385 could reverse the antioxidant and anti-inflammatory effects of PP.Conclusion:PP up-regulates the Nrf2/γ-GCS pathway to exert antiox-idant and anti-inflammatory effects,and reduces H/R-induced H9C2 cell injury.