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.

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.

Diamond-Blackfan anemia(DBA),also known as congenital pure red cell aplasia,is a rare genetic disorder characterized by bone marrow failure,congenital anomalies,and severe red blood cell abnormalities.The rarity of the condition,and consequently limited patient pool and scarcity of research models,means that the pathogenic mechanisms associated with genetic mutations in DBA remain uncertain,and the clinical treatment options are limited.This review synthesizes the findings from zebrafish,mouse,and human cellular models of DBA mutations.We clarify the pathogenic mechanisms and monitor the progression of drugs into clinical trials,thereby aiding further in-depth explorations into the etiology and therapeutic advancements for DBA.

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.

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 identify long non-coding RNA (lncRNA) associated with rheumatoid arthritis-associated interstitial lung disease (RA-ILD) and investigate their mechanisms. Methods Peripheral blood samples were collected from RA-ILD patients (n＝3), RA patients without lung involvement (n＝3), and healthy controls (n＝3). Next-generation sequencing was performed to screen differentially expressed lncRNA. A human fibrotic lung cell model was established by inducing the MRC-5 cell line with transforming growth factor-β (TGF-β). Following siRNA-mediated knockdown of target genes, changes in inflammatory and oxidative stress-related genes were analyzed via real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). Western blotting and dual-luciferase reporter (DLR) assays were used to validate protein expression, ubiquitination levels, and nuclear translocation of oxidative stress regulators, and antioxidant response element (ARE) transcriptional activity. Rescue experiments were conducted to confirm the role of target lncRNA in oxidative stress and inflammation in fibrotic lung cells. Results High-throughput sequencing revealed significant downregulation of LINC00638 in RA-ILD patients. Knockdown of LINC00638 markedly reduced transcriptional levels of interleukin (IL)-4, nuclear factor erythroid-2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and superoxide dismutase 2 (SOD2), while increasing IL-6, IL-1β, interferon-γ (IFN-γ), and reactive oxygen species (ROS) levels. Furthermore, LINC00638 knockdown decreased Nrf2 protein expression, increased its ubiquitination, reduced nuclear translocation, and suppressed ARE transcriptional activity. In MRC-5 cells, LINC00638 knockdown combined with N-acetylcysteine treatment restored Nrf2 and HO-1 levels while reducing IL-6 expression. Conclusions LINC00638 suppresses inflammatory responses in RA-ILD by activating the Nrf2/ARE antioxidant signaling pathway, suggesting its potential as a therapeutic target for diagnosis and treatment.

BACKGROUND:It has been confirmed that the mixing of decellularized matrix and polymer electrospinning can not only improve the structural properties of fibers,but also preserve the biological decellularized of decellularized matrix.However,there is no relevant report on the preparation of skin tissue engineering scaffolds by electrospinning polyurethane and decellularized skin matrix. OBJECTIVE:To investigate the reparative effect of a decellularized skin matrix/polyurethane blended fibrous scaffold on rat skin defects. METHODS:Polyurethane electrospun fibrous scaffold and decellularized skin matrix/polyurethane blended fibrous scaffold were fabricated using the electrospinning technique.The fiber structure was observed under scanning electron microscope.Rat adipose mesenchymal stem cells were inoculated on two kinds of scaffolds respectively.The morphology of the scaffolds was observed under scanning electron microscope.Three full-thickness skin defects of 1 cm×1 cm were fabricated on the back of 10 SD rats.Polyurethane electrospun fibrous scaffolds(control group)and decellularized skin matrix/polyurethane blended fibrous scaffolds(experimental group)were implanted in two of the defects,and no material was implanted in the remaining defects(blank control group).The skin wound healing was observed at 1,2,and 3 weeks after operation.At 3 weeks after implantation,the wound was stained with hematoxylin and eosin and the scar area was calculated. RESULTS AND CONCLUSION:(1)Under scanning electron microscope,the two kinds of electrospun fibers were reticulated,and the rat adipose mesenchymal stem cells attached to the fibers on the two kinds of scaffolds,and the adhesion was good.(2)With the extension of the postoperative time,the skin wounds of each group gradually healed.By week 3 after the operation,the skin wounds of the experimental group and the control group were basically healed,and small ulcers could be seen on the wounds of the blank control group.Hematoxylin-eosin staining of skin wounds showed that the epidermal coverage of the wound was basically complete in the control group and the experimental group,and fibroblast growth and inflammatory cell infiltration could be seen in the dermis.In addition,the collagen fibers of the wound in the experimental group were abundant and arranged in a regular order,basically parallel to the epidermal surface.The wound epidermis of blank control group was still defective.The scar area of the experimental group was smaller than that of the other two groups(P<0.05,P<0.01).(3)These results indicate that the decellularized skin matrix/polyurethane blended fibrous scaffold can effectively repair full-thickness skin defects and improve scar formation in rats.

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 investigate LI Dongyuan's theory of"any deficiency of spleen and stomach is a disease of the blood"and provide reference for modern clinical practice.[Methods]Taking Discussion on Internal and External Injuries,Treatise on Spleen and Stomach,Orchid Chamber of Secrets and Invention of Medicine as references,it starts from the connotation of"any deficiency of spleen and stomach is a disease of the blood",and explores the etiology and pathogenesis of the diseases,the theoretical construction and the clinical application respectively.[Results]Taking Inner Canon of Yellow Emperor and Zhongjing's academic thought as the source,absorbing CHENGs' and ZHU Xi's ideas of science.Being inspired by his teacher ZHANG Yuansu,and driven by his own clinical practice,LI Dongyuan put forward the academic thought of"any deficiency of spleen and stomach is a disease of the blood".From the Treatise on Spleen and Stomach-Treatise on the Prosperity and Decline of Spleen and Stomach,"any deficiency of spleen and stomach is a disease of the blood",which is a pathological state caused by the deficiency of spleen and stomach Qi and the weakness of elevation due to the disorders of emotions and moods,overwork and overdose,and uncontrolled diets,there fore causes insufficient blood production and too much blood consumption,and then leads to the deficiency of blood and Yin,and the essence of which is the disordered ascending,descending,floating and sinking of the human body's Qi.In treatment,LI Dongyuan always based on regulating blood,to restore the body's Qi,and harmonize Qi and blood as the goal,with"blood replenishment must have Yang Qi,Qi and blood double tonic""rising Yang must be in response to the time of the day,and make good use of the wind herbs""relieving heat must protect the Yin and blood,moderation in attacking and destroying".[Conclusion]Exploring this theory can help to view the relationship between Qi and blood from a new perspective,better grasp LI Dongyuan's academic thinking,and provide reference for the treatment of spleen and stomach diseases and blood diseases.