ObjectiveThis study aimed to investigate the action mechanism by which Banxia Xiexintang （BXT） inhibits epithelial-mesenchymal transition （EMT） in chronic atrophic gastritis （CAG） rats by regulating the interleukin-17（IL-17）/extracellular regulated protein kinases（ERK）/CCAAT enhancer binding protein β（C/EBPβ）signaling pathway， thereby providing new theoretical evidence for the treatment of CAG with classic traditional Chinese medicine formulas. MethodsA CAG rat model was established by using the combined factor method. After successful modeling， the rats were randomly divided into the model group， low-， medium-， and high-dose groups （0.549， 1.098， 2.196 g·kg^-1， respectively） of BXT， and the positive drug group （vitacoenzyme， 0.3 g·kg^-1）. A normal control group was also set up. After 8 weeks of intervention， the pathological changes of gastric tissue were evaluated. The enzyme-linked immunosorbent assay （ELISA） was used to detect the contents of IL-17， tumor necrosis factor-α （TNF-α）， cyclooxygenase-2 （COX-2）， and C/EBPβ in serum， as well as the contents of EMT markers in gastric mucosal tissue including E-cadherin， N-cadherin， and vimentin. The immunohistochemistry method was employed to determine the localization and protein expression levels of IL-17， p-ERK， and C/EBPβ in gastric mucosal tissue. Western blot was used to detect the protein expressions of C/EBPβ， ERK， and its phosphorylated form （p）-ERK in gastric mucosa. Real-time polymerase chain reaction （Real-time PCR） was applied to measure the mRNA expression levels of ERK， COX-2， and C/EBPβ in gastric mucosa. ResultsCompared with those in the normal control group， the rats in the model group showed gastric mucosal glandular atrophy and inflammatory cell infiltration. The protein and their related mRNA expressions of C/EBPβ， ERK， and p-ERK in gastric mucosa were significantly increased （P<0.05，P<0.01）. The levels of IL-17， TNF-α， COX-2， and C/EBPβ in serum were significantly increased （P<0.01）. The contents of N-cadherin and vimentin in gastric mucosal tissue were significantly increased， while the content of E-cadherin was significantly decreased （P<0.01）. Compared with the model group， after intervention with different doses of BXT， the pathological damage of the gastric mucosa was improved to varying degrees. The protein and mRNA expressions of C/EBPβ， ERK， and p-ERK in gastric mucosa were significantly reduced （P<0.05，P<0.01）. The levels of IL-17， TNF-α， COX-2， and C/EBP β in serum were significantly decreased （P<0.01）. The contents of N-cadherin and vimentin in gastric mucosa tissue were decreased， while the content of E-cadherin was increased （P<0.05，P<0.01）. ConclusionBXT can effectively improve the pathological damage of gastric mucosal tissue in CAG rats. Its action mechanism may be related to reducing the levels of IL-17 and TNF-α in serum， regulating the IL-17/ERK/C/EBPβ signaling pathway and inhibiting the EMT process.

AIM:To evaluate the accuracy of a portable non-contact tonometer(PNCT)compared with a traditional non-contact tonometer(NCT)in measuring intraocular pressure(IOP)at different levels.METHODS:Patients who presented to Ningbo Eye Hospital between January 2025 and January 2026 were retrospectively included. All patients underwent measurements using PNCT, NCT, and Goldmann applanation tonometry(GAT). Based on the GAT measurements, the patients were categorized into a low IOP group(IOP≤16 mmHg), a moderate IOP group(16 mmHg0.05). Spearman correlation analysis revealed that the IOP values measured by both PNCT and NCT were positively correlated with those measured by GAT(rs=0.86 and 0.84, respectively, P<0.05). Intraclass correlation coefficient(ICC)analysis demonstrated an ICC of 0.89 between PNCT and GAT(P<0.05), and 0.88 between NCT and GAT(P<0.05), with an overall ICC of 0.88 among the three instruments(P<0.05). Bland-Altman analysis indicated a mean bias of 0.1 mmHg [95% limits of agreement(LoA): -7.3 to 7.6 mmHg] between PNCT and GAT, and a mean bias of 0.1 mmHg(95%LoA: -8.4 to 8.6 mmHg)between NCT and GAT. Based on the GAT measurements, the eyes were categorized into a low IOP group(60 eyes, 32.6%, IOP≤16 mmHg), a moderate IOP group(63 eyes, 34.2%, 16 mmHg0.05), whereas the difference between NCT and GAT showed a positive correlation with CCT(rs=0.23, P<0.05).CONCLUSION:The IOP measurements obtained by PNCT, NCT, and GAT demonstrated strong correlation and good agreement, with PNCT being less influenced by CCT. However, as IOP levels increased, the measurement errors of both PNCT and NCT also increased. Therefore, PNCT and NCT readings should only serve as references and cannot replace GAT.

Objective To explore the effect of competitive respiratory training in patients undergoing abdominal contrast-enhanced magnetic resonance imaging(MRI).Methods A total of 115 patients who un-derwent abdominal contrast-enhanced MRI in the hospital from October 2021 to April 2022 were randomly as-signed to the control group(n=64)and the experimental group(n=51).The control group received routine one-on-one respiratory training,while the experimental group received a competitive respiratory training,wherein the first of the two individuals to achieve qualified breath-holding would undergo scanning first.The duration of respiratory training and scanning,as well as abdominal MRI image quality,were compared between the two groups.Image quality was assessed based on respiratory motion artifact scores,anatomical detail scores,and the percentage of sequences affected by respiratory motion artifacts.Results The average duration of respiratory training in the experimental group was significantly shorter than that in the control group[(39.90±14.26)s vs.(71.31±20.96)s,P=0.001].The difference in total scan time of the abdomen and up-per abdomen was not statistically significant(P＞0.05).The respiratory motion artifact score was higher in the experimental group compared to the control group(P＜0.05).The anatomical detail scores for both the FIESTA and LAVA sequences were higher in the experimental group than in the control group(P＜0.05),while no significant difference was found for the T1 sequence score(P＜0.05).The percentage of sequences affected by respiratory motion artifacts was significantly lower in the experimental group than in the control group(P=0.006).Conclusion Competitive respiratory training can shorten the duration of respiratory train-ing,improve breath-hold quality and persistence,reduce respiratory motion artifacts,and consequently enhance image quality in abdominal contrast-enhanced MRI.

In order to explore the effect of PGD2/DP1 receptor pathway on the expression of cyto-kines and injury-related factors in Escherichia coli(E.coli)induced bovine bone marrow derived macrophages,an in vitro model of E.coli induced bovine bone marrow derived macrophages was established.The effects of DP1 receptor agonist on phagocytosis and killing ability,mRNA expres-sion,secretion of pro-inflammatory cytokines(TNF-α,IL-1β)and activation of signaling pathway(MAPK,NF-κB)in cow bone marrow derived macrophages induced by E.coli were examined.The results showed that compared with the E.coli infection group,the phagocytosis and killing ability of BW-245C+E.coli group and 15 d-PGJ2+E.coli group were enhanced(P＜0.01).Compared with the blank control group,mRNA expression was at a higher level(P＜0.001),and the secre-tion of pro-inflammatory cytokines(TNF-α,IL-1β)was significantly increased after adding E.coli solution.The mRNA expression of BW-245C+E.coli group and 15 d-PGJ2+E.coli group were significantly decreased(P＜0.001),and the secretion of pro-inflammatory cytokines(TNF-α,IL-1β)was significantly decreased(P＜0.001).and signaling pathway(MAPK,NF-κB)were sig-nificantly down-regulated(P＜0.001).This study showed that DP1receptor agonist plays an inhib-itory role in the inflammatory response of cow bone marrow-derived macrophages induced by E.coli.This finding provides a potential target for future treatment of cow endometritis,laying the foundation for the development of novel anti-inflammatory treatment strategies.

OBJECTIVE To evaluate the efficacy and mechanism of Kai-Xin-San in improving intestinal function damage in-duced by intragastric administration of fluoxetine in chronic unpredictable mild stress(CUMS)depression model mice.METHODS A CUMS depression mouse model was established and treated with fluoxetine(9 mg·kg-1·d-1),low-dose(1.5 g·kg-1·d-1)and high-dose(4.5 g·kg-1·d-1)Kai-Xin-San,fluoxetine combined with low-dose(9 mg·kg-1·d-1+1.5 g·kg-1·d-1)and high-dose(9 mg·kg-1·d-1+4.5 g·kg-1·d-1)Kai-Xin-San,and mosapride combined with fluoxetine(2 mg·kg-1·d-1+9 mg·kg-1·d-1)for 28 consecutive days.The body weight of mice was measured;the food utilization was calculated and the serum D-xylose content was measured to evaluate the intestinal mucosal absorption capacity of mice;HE staining was used to evaluate the intestinal structural dam-age of mice;TUNEL staining was used to evaluate the intestinal tissue apoptosis of mice;ELISA was used to detect the expression lev-els of brain gut peptides such as vasoactive intestinal peptide(VIP),gastrin(MTL),substance P(SP)and Ghrelin in the intestine of mice;Western blot was used to detect the expression of apoptosis signaling pathway proteins.RESULTS Compared with the model group,fluoxetine significantly reduced the body weight of mice after 2 weeks of administration(P<0.05);the food utilization and ser-um D-xylose content of mice were significantly reduced after 4 weeks of administration(P<0.05),and the intestinal villi of depressed mice were damaged(P<0.05)and intestinal epithelial apoptosis of mice was enhanced(P<0.01);the expression of VIP in the small intestine of mice was upregulated(P<0.05),and the expression of MTL,SP and Ghrelin was downregulated(P<0.05,P<0.01);cleaved Caspase-3/Caspase-3 and cleaved Caspase-9/Caspase-9 in the intestinal apoptosis signaling pathway of mice were upregulat-ed(P<0.05,P<0.01).Compared with the fluoxetine group,the body weight of mice was significantly increased after 2 weeks of com-bined use of Kai-Xin-San and fluoxetine(P<0.05,P<0.01).After 4 weeks of combined use of high-dose Kai-Xin-San and fluoxe-tine,the food utilization and serum D-xylose expression of mice were significantly increased(P<0.05);intestinal villus damage was improved(P<0.05);intestinal epithelial tissue apoptosis was significantly reduced(P<0.01);small intestinal VIP expression was significantly downregulated(P<0.01),and the expression of MTL,SP and Ghrelin was significantly upregulated(P<0.05);cleaved Caspase-3/Caspase-3 and cleaved Caspase-9/Caspase-9 in the apoptosis signaling pathway were significantly reduced(P<0.05,P<0.01).CONCLUSION Kai-Xin-San has the effect of improving the gastrointestinal motility and intestinal absorption function dam-age caused by fluoxetine in depressed mice.Its mechanism may be related to improving the expression of brain gut peptide in the small intestine and inhibiting intestinal villi damage and intestinal tissue apoptosis.

Objective:To evaluate the role of uncoupling protein 2 in dexmedetomidine-induced alleviation of myocardial ischemia-reperfusion (I/R) injury in diabetic mice.Methods:SPF C57BL/6 male mice, aged 6-8 weeks, weighing 20-25 g, in which the model of type 2 diabetes mellitus was established by high-fat feeding combined with intraperitoneal injection of streptozotocin, were used in this study. Ninety diabetic mice were divided into 5 groups ( n=18 each) by a random number table method: sham operation group (S group), myocardial I/R group, myocardial I/R+ UCP2 inhibitor genipin group (I/R+ G group), myocardial I/R+ dexmedetomidine group (I/R+ D group) and myocardial I/R+ dexmedetomidine+ UCP2 inhibitor genipin group (I/R+ DG group). Myocardial I/R injury model was established by ligating the left anterior descending coronary artery of diabetic mice for 60 min followed by 120 min of reperfusion. Dexmedetomidine 20 μg/kg was intraperitoneally injected at 5 min prior to reperfusion in I/R+ D group. Genipin 100 mg/kg was intraperitoneally injected at 14 h prior to ischemia, and dexmedetomidine 20 μg/kg was intraperitoneally injected at 5 min prior to reperfusion in I/R+ D+ G group. The concentrations of cardiac troponin I (cTnI), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-10 in serum were detected by enzyme-linked immunosorbent assay at 120 min of reperfusion. The myocardial tissue was obtained for determination of the myocardial infarct size, the level of reactive oxygen species (ROS) (by flow cytometry), and the expression of UCP2, nuclear factor kappa B (NF-κB) inhibitory protein α (IκBα), phosphorylated IκBα (p-IκBα), NF-κB p65 and phosphorylated NF-κB p65 (p-NF-κB p65) (by Western blot) and for observation of the morphological structure of the myocardial tissue. The cardiac function was evaluated by echocardiography at 24 h of reperfusion. Results:Compared with group S, the percentage of myocardial infarct size and level of ROS were significantly increased, the concentrations of cTnI, TNF-α, IL-6 and IL-10 were increased, the expression of UCP2 was up-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were increased, the stroke volume (SV), ejection fraction (EF), and left ventricular fractional shortening (FS) were decreased ( P<0.05), and the myocardial structure was severely damaged in group I/R. Compared with group I/R, the percentage of myocardial infarct size and level of ROS were significantly decreased, the concentrations of cTnI, TNF-α and IL-6 were decreased, the concentration of IL-10 was increased, the expression of UCP2 was up-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were decreased, the SV, EF and FS were increased ( P<0.05), and the pathological damage was significantly attenuated in group I/R+ D. Compared with group I/R+ D, the percentage of myocardial infarct size and level of ROS were significantly increased, the concentrations of cTnI, TNF-α and IL-6 were increased, the concentration of IL-10 was decreased, the expression of UCP2 was down-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were increased, the SV, EF and FS were decreased ( P<0.05), and the pathological damage was aggravated in group I/R+ D+ G. Conclusions:Dexmedetomidine may ameliorate myocardial I/R injury by up-regulating UCP2 expression in the myocardium and inhibiting mitochondrial ROS-mediated inflammatory responses in diabetic mice.

Objective:To evaluate the role of uncoupling protein 2 in dexmedetomidine-induced alleviation of myocardial ischemia-reperfusion (I/R) injury in diabetic mice.Methods:SPF C57BL/6 male mice, aged 6-8 weeks, weighing 20-25 g, in which the model of type 2 diabetes mellitus was established by high-fat feeding combined with intraperitoneal injection of streptozotocin, were used in this study. Ninety diabetic mice were divided into 5 groups ( n=18 each) by a random number table method: sham operation group (S group), myocardial I/R group, myocardial I/R+ UCP2 inhibitor genipin group (I/R+ G group), myocardial I/R+ dexmedetomidine group (I/R+ D group) and myocardial I/R+ dexmedetomidine+ UCP2 inhibitor genipin group (I/R+ DG group). Myocardial I/R injury model was established by ligating the left anterior descending coronary artery of diabetic mice for 60 min followed by 120 min of reperfusion. Dexmedetomidine 20 μg/kg was intraperitoneally injected at 5 min prior to reperfusion in I/R+ D group. Genipin 100 mg/kg was intraperitoneally injected at 14 h prior to ischemia, and dexmedetomidine 20 μg/kg was intraperitoneally injected at 5 min prior to reperfusion in I/R+ D+ G group. The concentrations of cardiac troponin I (cTnI), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-10 in serum were detected by enzyme-linked immunosorbent assay at 120 min of reperfusion. The myocardial tissue was obtained for determination of the myocardial infarct size, the level of reactive oxygen species (ROS) (by flow cytometry), and the expression of UCP2, nuclear factor kappa B (NF-κB) inhibitory protein α (IκBα), phosphorylated IκBα (p-IκBα), NF-κB p65 and phosphorylated NF-κB p65 (p-NF-κB p65) (by Western blot) and for observation of the morphological structure of the myocardial tissue. The cardiac function was evaluated by echocardiography at 24 h of reperfusion. Results:Compared with group S, the percentage of myocardial infarct size and level of ROS were significantly increased, the concentrations of cTnI, TNF-α, IL-6 and IL-10 were increased, the expression of UCP2 was up-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were increased, the stroke volume (SV), ejection fraction (EF), and left ventricular fractional shortening (FS) were decreased ( P<0.05), and the myocardial structure was severely damaged in group I/R. Compared with group I/R, the percentage of myocardial infarct size and level of ROS were significantly decreased, the concentrations of cTnI, TNF-α and IL-6 were decreased, the concentration of IL-10 was increased, the expression of UCP2 was up-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were decreased, the SV, EF and FS were increased ( P<0.05), and the pathological damage was significantly attenuated in group I/R+ D. Compared with group I/R+ D, the percentage of myocardial infarct size and level of ROS were significantly increased, the concentrations of cTnI, TNF-α and IL-6 were increased, the concentration of IL-10 was decreased, the expression of UCP2 was down-regulated, the p-IκBα/IκBα ratio and p-NF-κB p65/NF-κB p65 ratio were increased, the SV, EF and FS were decreased ( P<0.05), and the pathological damage was aggravated in group I/R+ D+ G. Conclusions:Dexmedetomidine may ameliorate myocardial I/R injury by up-regulating UCP2 expression in the myocardium and inhibiting mitochondrial ROS-mediated inflammatory responses in diabetic mice.

BACKGROUND:Some studies have shown a potential relationship between dietary intake and osteoarthritis,but whether there is a causal relationship between food preferences and osteoarthritis is still unknown.There is currently no large-scale genome-wide association study on dietary preferences and osteoarthritis in China.OBJECTIVE:To explore the causal association between dietary preferences and osteoarthritis in European populations,in order to provide a theoretical basis for the prevention of osteoarthritis and to provide reference data for the identification of high-risk groups for hip and knee osteoarthritis in China.METHODS:A total of 20 dietary preference genetic statistics datasets were selected to screen for exposure factor-related instrumental variables.The dataset for osteoarthritis was selected for the ending.After exclusion of the instrumental variables related to confounders,the two-sample Mendelian randomized causal association analysis was conducted mainly by inverse variance weighted analysis,and other four statistical methods were used as supplements.Sensitivity test was performed for the results.RESULTS AND CONCLUSION:(1)The results of the inverse variance weighted analysis showed that preference for barbecue(OR=1.204,95％CI:1.058-1.370,P=0.005),beef(OR=1.167,95％CI:1.034-1.317,P=0.012),chicken(OR=1.399,95％CI:1.119-1.749,P=0.003),pork chops(OR=1.218,95％CI:1.039-1.427,P=0.015)and coffee(OR=1.133,95％CI:1.037-1.238,P=0.006)were risk factors for osteoarthritis of the knee and hip joints,vegetables(OR=0.893,95％CI:0.827-0.964,P=0.004),and vinegar(OR=0.897,95％CI:0.812-0.991,P=0.032)were protective factors for knee-hip osteoarthritis.(2)The results of the sensitivity analysis showed that the instrumental variables included in the analysis without horizontal pleiotropy and bias,and the corresponding inverse variance weighted analysis of effects model was used according to the results of the heterogeneity analysis.(3)The results of this study provide certain reference value in the research on the relationship between dietary preferences and hip and knee osteoarthritis,but only included human whole genome association study data from European populations,and the validity of the research results in other races remains to be tested.Moreover,no stratification was performed on gender,age and other health status.It is difficult to completely rule out the bias from population stratification in the research results.In the future,larger-scale and more finely classified sample data are still needed to carry out relevant causal relationship research.

BACKGROUND:Some studies have shown a potential relationship between dietary intake and osteoarthritis,but whether there is a causal relationship between food preferences and osteoarthritis is still unknown.There is currently no large-scale genome-wide association study on dietary preferences and osteoarthritis in China.OBJECTIVE:To explore the causal association between dietary preferences and osteoarthritis in European populations,in order to provide a theoretical basis for the prevention of osteoarthritis and to provide reference data for the identification of high-risk groups for hip and knee osteoarthritis in China.METHODS:A total of 20 dietary preference genetic statistics datasets were selected to screen for exposure factor-related instrumental variables.The dataset for osteoarthritis was selected for the ending.After exclusion of the instrumental variables related to confounders,the two-sample Mendelian randomized causal association analysis was conducted mainly by inverse variance weighted analysis,and other four statistical methods were used as supplements.Sensitivity test was performed for the results.RESULTS AND CONCLUSION:(1)The results of the inverse variance weighted analysis showed that preference for barbecue(OR=1.204,95％CI:1.058-1.370,P=0.005),beef(OR=1.167,95％CI:1.034-1.317,P=0.012),chicken(OR=1.399,95％CI:1.119-1.749,P=0.003),pork chops(OR=1.218,95％CI:1.039-1.427,P=0.015)and coffee(OR=1.133,95％CI:1.037-1.238,P=0.006)were risk factors for osteoarthritis of the knee and hip joints,vegetables(OR=0.893,95％CI:0.827-0.964,P=0.004),and vinegar(OR=0.897,95％CI:0.812-0.991,P=0.032)were protective factors for knee-hip osteoarthritis.(2)The results of the sensitivity analysis showed that the instrumental variables included in the analysis without horizontal pleiotropy and bias,and the corresponding inverse variance weighted analysis of effects model was used according to the results of the heterogeneity analysis.(3)The results of this study provide certain reference value in the research on the relationship between dietary preferences and hip and knee osteoarthritis,but only included human whole genome association study data from European populations,and the validity of the research results in other races remains to be tested.Moreover,no stratification was performed on gender,age and other health status.It is difficult to completely rule out the bias from population stratification in the research results.In the future,larger-scale and more finely classified sample data are still needed to carry out relevant causal relationship research.

Escherichia coli(E.coli)is a key pathogenic bacterium responsible for postpartum endo-metritis,with its colonization in the reproductive tract closely associated with endometrial damage and disruption of the ovarian cycle.This ultimately leads to infertility,causing significant economic losses to the dairy industry.Macrophages play a pivotal role in the inflammatory response.This study aims to investigate the mRNA expression profile of bovine bone marrow-derived macropha-ges following E.coli infection using RNA sequencing(RNA-seq)technology.Additionally,it seeks to identify the biological functions and signaling pathways of differentially expressed genes(DEGs)through Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analyses.The results demonstrated that E.coli infection induced differential expression of 4 522 genes,with 2 141 upregulated and 2 381 downregulated.These genes were primarily asso-ciated with inflammatory responses,where TLR2,TLR4,NLRP3,and PTGS2 played pivotal roles.PGD2 synthesis was mediated by TLR2,TLR4,and NLRP3.Transcriptome sequencing of bovine bone marrow-derived macrophages infected with E.coli and treated with a PGD2 inhibitor revealed a marked downregulation of TLR2 and TLR4 gene expression.qPCR validation results were highly consistent with the RNA-seq findings.This study elucidates the interactive regulatory roles of TLR2,TLR4,and NLRP3 in conjunction with PGD2,which collectively modulate bovine endome-tritis.These findings offer significant molecular insights that enhance our understanding of the pathological mechanisms underlying bovine endometritis,thereby informing its prevention and treatment strategies.