Systemic chronic inflammation associated with advancing age is closely linked to the onset and progression of multiple age-related diseases. This persistent inflammatory state, commonly termed inflammaging, reflects complex interactions between accumulated cellular damage and dysregulated immune responses. Inflammasomes are multiprotein complexes of the innate immune system that respond to cellular stress and damage and amplify inflammatory signaling. Their sustained or recurrent activation may contribute to the establishment and maintenance of inflammaging. This review focuses on the NLRP3 inflammasome and summarizes its activation mechanisms, regulatory pathways, and pathological significance within the aging microenvironment. Particular attention is given to neurodegenerative diseases, osteoarthritis, atherosclerosis, and type 2 diabetes, emphasizing shared activation mechanisms and tissue-specific effects. Although initiating stimuli differ among these conditions, several molecular events can contribute to NLRP3 inflammasome activation. Priming mediated by nuclear factor‑κB (NF‑κB) promotes the expression of NLRP3 and pro-interleukin-1β, whereas lysosomal damage, mitochondrial dysfunction, reactive oxygen species accumulation, mitochondrial DNA release, and potassium efflux can participate in activation pathways. These events are interconnected rather than obligatory sequential steps in every setting. Inflammasome assembly promotes caspase-1 activation, which facilitates interleukin-1β and interleukin-18 maturation and gasdermin D cleavage, potentially leading to pyroptosis. The relative contributions of these processes depend on cell type, tissue context, and disease stage. Within aging tissues, persistent damage signals and impaired cellular homeostasis may favor repeated inflammasome activation, establishing a cycle of inflammatory amplification and further tissue injury. However, the pathological consequences vary across organs. In neurodegenerative diseases, inflammasome signaling is associated with neuroinflammation and neuronal vulnerability; in osteoarthritis, it may contribute to joint inflammation and cartilage degeneration. In atherosclerosis, it is implicated in vascular inflammation and plaque progression, whereas in type 2 diabetes, it is linked to metabolic inflammation and impaired glucose homeostasis. These distinctions underscore the importance of interpreting shared molecular mechanisms within specific tissue environments. The review further discusses the therapeutic potential of targeting inflammasomes to mitigate inflammaging and associated disease processes. Strategies include inhibiting NLRP3 activation, modulating upstream stress and priming pathways, and limiting downstream inflammatory signaling or pyroptotic cell death. By interrupting shared mechanisms of inflammatory amplification, these approaches may offer opportunities for coordinated intervention across multiple age-related disorders. Nevertheless, mechanistic overlap does not imply uniform therapeutic responses, and benefits observed in experimental models should not be equated with established clinical efficacy or evidence of delayed human aging.Successful clinical translation will require careful consideration of disease stage, tissue specificity, treatment timing, and the consequences of prolonged interference with innate immune defenses. Long-term safety is particularly important for older populations and preventive applications. The limited availability of validated biomarkers of inflammasome activity also complicates patient stratification, assessment of target engagement, and monitoring of therapeutic responses. Future research should clarify causal relationships, identify contexts in which inflammasome inhibition is most beneficial, and establish reliable translational endpoints. Overall, inflammasomes represent an important link between aging-associated damage and chronic inflammatory amplification, supporting their investigation as shared targets for early intervention in multiple age-related diseases, while highlighting the need for disease-specific evaluation and rigorous assessment of benefits and risks.

Objective:To explore the application effect of a precision mode of reporting quantity under the background of procurement as quantity for medical materials on improving the management level for prediction of medical consumables.Methods:The fishbone diagram was applied to analyze the influence factors of reporting quantity in centralized procurement as quantity for medical materials.The work of reporting quantity were intervened according to predictive model for requirement,and management measures.The data of reporting quantity of centralized procurement of two kinds of medical materials(coronary artery stent and coronary artery dilation balloon)in clinical use at Peking Union Medical College Hospital between April 2021 and March 2024 were selected.According to different management modes for reporting quantity of consumables,the conventional mode was adopted to manage reporting quantity of consumables during April 2021 and March 2023,and precision mode was adopted to manage them during April 2023 and March 2024.Prediction deviation rate and execution deviation rate of the two kinds of modes of reporting quantity were compared.Results:The average prediction deviation rates for coronary artery stent and coronary artery dilation balloon of adopting precision mode for reporting quantity were respectively(12.19±2.64)%and(20.61±3.41)%,all of which were lower than those of conventional mode for reporting quantity,and the differences were significant(t=6.422,6.917,P<0.05).The average execution deviation rates were respectively(17.55±3.48)%and(25.85±2.56)%,all of which were lower than those of conventional mode for reporting quantity,and the differences were significant(t=7.148,7.436,P<0.05).Conclusion:Under the background of procurement as quantity for medical consumables,the precision mode for reporting quantity can enhance the precision for reporting quantity and the fine management level for the work of reporting quantity through establishes prediction model for quantity of procurement,and conducts effective management measures.

AIM To investigate the effects of Yunpi Tongchang Formula on intestinal mucosal barrier damage in rats with opioid-induced constipation(OIC)of Spleen-Kidney Yang Deficiency Syndrome.METHODS In contrast to the 10 rats of the blank group,the 50 rats of the modeling group were induced into models of OIC of Spleen-Kidney Yang Deficiency Pattern by 7 days consecutive administration of both subcutaneous loperamide injection and alternating gavage of activated carbon ice water and vinegar.Following successful modeling,rats were randomly allocated into the model group,the mosapride citrate tablet group(1.35 mg/kg),and the high-dose,medium-dose,and low-dose Yunpi Tongchang Formula groups(15.12,7.56,3.78 g/kg),with 8 mice in each group.Upon the completion of the 14 days treatment,the rats had their TCM Syndrome scores assessed;their fecal water content,initial black stool excretion time,and small intestine propulsion rate measured;their colon tissue morphology observed by HE staining;their serum levels of IL-6,TNF-α,and IL-1β detected by ELISA;their expressions of occludin and zonula occludens-1(ZO-1)in colon tissues detected by immunohistochemistry;their mRNA expressions of MyD88,TLR4 and NF-κB p65 in the colon tissues detected by RT-qPCR;and their protein expressions of MyD88,TLR4 and NF-κB p65 in the colon tissues detected by Western blot.RESULTS Compared to the blank group,the model group had higher TCM Syndrome scores(P＜0.01);lower fecal water content and small intestine propulsion rate(P＜0.05,P＜0.01);longer initial black stool excretion time(P＜0.01);more mucosal edema in colon tissue,obvious inflammatory infiltration,and glandular disorder;increased serum levels of IL-6,TNF-α and IL-1 β(P＜0.05);decreased colon expressions of ZO-1 and occludin(P＜0.01);and increased mRNA and protein expressions of TLR4,MyD88 and NF-κB p65(P＜0.01).Compared to the model group,both the medium-dose Yunpi Tongchang Formula group and the mosapride citrate tablet group demonstrated effectively reduced TCM syndrome scores(P＜0.01);increased fecal water content and small intestine propulsion rate(P＜0.05,P＜0.01);and shorter initial black stool excretion time(P＜0.01);improved colon mucosal edema and inflammatory infiltration;decreased serum levels of IL-6,TNF-α and IL-1β(P＜0.01);upregulated protein expressions of ZO-1 and occludin(P＜0.01);and downregulated mRNA and protein expressions of TLR4,MyD88 and NF-κB p65(P＜0.05,P＜0.01).CONCLUSION Yunpi Tongchang Formula significantly ameliorates constipation symptoms in OIC rat models of Spleen-Kidney Yang Deficiency Syndrome because of its efficacy in attenuating intestinal inflammation and preserving the integrity of intestinal epithelial barrier structure,with its mechanistic action in downregulating TLR4/MyD88/NF-κB signaling pathway activation.

Objective:To investigate the role of pyroptosis in T-2 toxin induced articular cartilage injury.Methods:A total of 145 SPF grade male Wistar rats were randomly divided into blank control group ( n = 45), solvent control group ( n = 45), and T-2 toxin group ( n = 55) based on body weight (50 - 70 g). The T-2 toxin group and the solvent control group were given 100 ng·g -1·d -1 T-2 toxin and an equal amount of anhydrous ethanol by gavage, respectively; the blank control group was fed routinely. Fifteen rats from each group were euthanized at 6, 12, and 24 weeks of intervention, and bilateral knee joints of the rats were collected. Pathological changes in rat knee articular cartilage were observed using hematoxylin and eosin staining. TdT-mediated dUTP nick-end labeling (TUNEL) staining was used to detect chondrocyte injury. Western blot was used to detect the protein expression of gasdermin D (GSDMD), cleaved N-terminal of gasdermin D (GSDMD-N), NOD like receptor thermal protein domain associated protein 3 (NLRP3), cysteinyl aspartate specific proteinase 1 (Caspase-1), interleukin 1β (IL-1β), interleukin 18 (IL-18), and apoptosis-associated spike-like protein containing CARD (ASC). Results:At 6, 12, and 24 weeks of intervention, the T-2 toxin group rats showed varying degrees of damage to the knee articular cartilage tissue, including a decrease in the number of chondrocytes and death. At 24 weeks of intervention, the TUNEL staining positivity rates of chondrocytes in the blank control group, solvent control group, and T-2 toxin group were (1.28 ± 0.45)%, (0.73 ± 0.27)%, and (4.01 ± 2.37)%, respectively, with statistically significant differences between the groups ( F = 6.11, P = 0.036); and the T-2 toxin group was higher than the blank control group ( P < 0.05). At 24 weeks of intervention, there were statistically significant differences in the expression levels of NLRP3, Caspase-1, GSDMD, GSDMD-N, and IL-1β proteins among the blank control group, solvent control group, and T-2 toxin group ( F = 3.81, 11.81, 6.74, 3.71, 155.49, P = 0.044, 0.003, 0.023, 0.036, 0.001); and the T-2 toxin group was higher than the blank control group ( P < 0.05). At different intervention cycles, there was no statistically significant difference in the expression levels of ASC and IL-18 proteins among the groups ( F = 0.78, 0.93, 3.73, 2.26, 0.88, 0.11, P > 0.05). Conclusion:The NLRP3/Caspase-1/GSDMD pathway mediated pyroptosis is involved in T-2 toxin induced articular cartilage injury in rats.

This study was a single-center cross-sectional investigation aimed at identifying risk factors for cognitive dysfunction in patients undergoing maintenance hemodialysis (MHD), with the goal of providing a basis for improving patient prognosis. Patients receiving MHD in the Blood Purification Center of Hainan Provincial People's Hospital from June 1 to June 30, 2023, were enrolled. Cognitive function was assessed using the Mini-Mental State Examination (MMSE), and potential risk factors for cognitive impairment were analyzed by using Logistic regression. A total of 278 patients were included, 69 patients (24.8%) of whom had cognitive impairment. Multivariate Logistic regression analysis indicated that the history of cerebrovascular disease ( OR=3.109, 95% CI 1.310-7.378, P=0.010), old age ( OR=1.077, 95% CI 1.040-1.115, P<0.001), low dialysis frequency ( OR=0.270, 95% CI 0.120-0.606, P=0.001), low academic qualification (using college/university as the control group: primary school group OR=26.960, 95% CI 7.519-96.673, P<0.001; Junior high school/technical secondary school group OR=4.264, 95% CI 1.330-13.650, P=0.015; High school group OR=9.554, 95% CI 2.861-31.904, P<0.001), high β2-microglobulin ( OR=1.609, 95% CI 1.044-2.480, P=0.031) and high C-reactive protein/albumin ( OR=2.672, 95% CI 1.226-5.826, P=0.013) were independent risk factors for cognitive impairment in MHD patients.

Objective To investigate the factors influencing global longitudinal strain(GLS)measured by cardiac magnetic resonance(CMR)in patients with acute ST-segment elevation myocardial infarction(STEMI).Methods Clinical data of 315 hospitalized patients diagnosed with acute STEMI who underwent percutaneous coronary intervention(PCI)at the First Medical Center of Chinese PLA General Hospital from June 2016 to September 2021 were retrospectively collected.After analyzing CMR images of all patients,GLS and other strain parameters were obtained,and then the patients were divided into two groups according to the median GLS.In order to balance gender and age differences,1:1 propensity score matching was performed,and 206 patients were eventually included:GLS>-11.3%group(indicating severe GLS impairment,n=103)and GLS≤-11.3%group(n=103).Baseline characteristics,laboratory indicators,coronary angiographic parameters,electrocardiogram(ECG)features,and CMR parameters were compared between the two groups.Variables showing significant differences were analyzed for their correlation with GLS.Multivariate logistic regression and multiple stepwise linear regression analyses were performed to identify factors associated with GLS impairment.Results Compared with GLS≤-11.3%group,GLS>-11.3%group had significantly higher peak levels of creatine kinase-MB(CK-MB)and troponin T(TnT)(P<0.001).A higher proportion of patients in GLS>-11.3%group had the left anterior descending artery(LAD)as the culprit vessel,while a lower proportion had the right coronary artery(RCA)as the culprit vessel(P<0.001).Additionally,GLS>-11.3%group had longer QRS duration(P<0.001)and a higher incidence of pathological Q waves(P=0.001).Regarding CMR parameters,GLS>-11.3%group exhibited larger global circumferential strain(GCS),infarct size(IS),and left ventricular end-systolic volume(LVESV),as well as lower global radial strain(GRS)and left ventricular ejection fraction(LVEF)(P<0.001).Multivariate logistic regression indicated that peak TnT(OR=1.092,P=0.001),LAD culprit vessel(OR=3.744,P<0.001),and QRS duration(OR=1.026,P<0.001)were significantly associated with severely impaired GLS.Multiple stepwise linear regression analysis showed that the logarithmic value of peak TnT,LAD as the culprit vessel,and the square root of QRS duration were linearly correlated with GLS values(adjusted R2=0.301,P<0.001),and these independent variables explained 30.1%of the variation in GLS.Conclusion Elevated peak TnT,prolonged QRS duration,and LAD as the culprit vessel are significantly associated with severe GLS impairment in STEMI patients,indicating more severe myocardial infarction and worse left ventricular function.

Objective To study the effects of Hedysarum polysaccharides polysaccharide(HPS)on the farnesoid X receptor(FXR)-fibroblast growth factor-19(FGF19)signaling pathway of diabetes rats.Methods Twelve Wistar male rats were randomly selected as the normal group,and the other rats were fed with a single intraperitoneal injection of streptozotocin(50 mg·kg-1 STZ)and a high sugar and high-fat diet to replicate the diabetes rat model.Model rats were randomly divided into model group,positive control group(given 400 mg·kg-1·d-1 suspension of Bifidobacterium quadruplex live bacterial tablets by gavage),experimental-H,-M,-L groups(given 200,100,and 50 mg·kg-1·d-1 doses of HPS suspension by gavage);normal group,and model group were given equal volume of purified water by gavage once a day for 8 consecutive weeks.Glucose(Glu)was detected by a blood glucose meter;and serum total glyceride(TG)and total cholesterol(TC)were detected by enzyme-linked immunosorbent assay reagent kit;the expressions of FXR、fibroblast growth factor receptors 4(FGFR4)relative mRNA expression level and protein were detected by real-time fluorescence quantitative polymerase chain reaction method and Western blot.Results The Glu concentrations in the normal group,model group,positive control group,and experimental-H groups were(7.66±0.61),(29.25±1.64),(23.31±3.02)and(19.31±5.13)mmol·L-1,respectively;the TG content were(957.00±113.73),(1 345.00±246.44),(958.00±96.53)and(964.00±130.22)μmol·L-1,respectively;the TC content were(161.65±4.53),(302.19±5.35),(236.09±5.14)and(165.58±2.58)μmol·L-1,respectively;the expression of FXR relative mRNA expression level were 1.00±0.06,0.48±0.02,0.67±0.04 and 0.92±0.04,respectively;the expression of FGFR4 relative mRNA expression level were 1.00±0.04,0.17±0.01,0.48±0.04 and 0.41±0.03;respectively.The above indexes of the model group were compared with the control group,and the above indexes of the control group and the experimental-H group were compared with the model group,and the differences were statistically significant(all P＜0.01).Conclusion HPS improves blood sugar,lowers blood lipids,and protects liver and intestinal tissues,possibly by regulating the FXR-FGF19 signaling pathway in intestinal tissue,and regulating bile acid synthesis.

Three evaluation methods were recommended for the key properties of the intravascular catheter lubricating coating such as stability,lubricity and integrity,including insoluble particle test method,friction test procedure and appearance detection method.Fifteen batches of microcatheters produced by different manufacturers were selected for testing to clarify the three methods in test principle,step,result,characteristic.References were provided for the design,production,evaluation and regulation of intravascular catheters with lubricant coatings.[Chinese Medical Equipment Journal,2025,46(1):66-72]

Objective:To evaluate the music perception ability and appraisal status of cochlear implant adult users, then to compare those with normal-hearing subjects.Methods:The Iowa Musical Background and Appreciation Questionnaire (IMBAQ) was conducted to evaluate 20 cases of post-lingual deafness cochlear implant recipients (9 males, 11 females) aged 12-61(mean=28.8 yrs). Those music perception abilities were tested via Music Perceptional Evaluation Platform. Two kinds of tone(C#3, C#5)were carried out in the music perception test, including the Just Noticeable Difference (JND) Test, the Pitch-Direction Discrimination (PDD) Test and the Melody Contour Identification (MCI) Test. Meanwhile, the timbre identification tests were received by both normal hearing and cochlear implant patients.Results:The total outcomes of cochlear implant recipients were inferior to the normal hearing subjects ( P<0.05). Both of the thresholds of JND ( P=0.001) and PDD ( P<0.001) had a significant difference, while comparing the two frequency values (C#3 and C#5) in cochlear implant adult users. IMBAQ results indicated the lower post-implantation music appreciation and engagement compared to pre-deafness levels. The longer duration of formal music training was positively correlated with better music perception performance in CI recipients. Conclusions:There still has a big gap between the cochlear implant group and normal hearing group in the music perception test. And different frequency value causes effect on the result of cochlear implant patient group.

Collagen is a major structural protein in the matrix of animal cells and the most widely distributed and abundant functional protein in mammals. Collagen’s good biocompatibility, biodegradability and biological activity make it a very valuable biomaterial. According to the source of collagen, it can be broadly categorized into two types: one is animal collagen; the other is recombinant collagen. Animal collagen is mainly extracted and purified from animal connective tissues by chemical methods, such as acid, alkali and enzyme methods, etc. Recombinant collagen refers to collagen produced by gene splicing technology, where the amino acid sequence is first designed and improved according to one’s own needs, and the gene sequence of improved recombinant collagen is highly consistent with that of human beings, and then the designed gene sequence is cloned into the appropriate vector, and then transferred to the appropriate expression vector. The designed gene sequence is cloned into a suitable vector, and then transferred to a suitable expression system for full expression, and finally the target protein is obtained by extraction and purification technology. Recombinant collagen has excellent histocompatibility and water solubility, can be directly absorbed by the human body and participate in the construction of collagen, remodeling of the extracellular matrix, cell growth, wound healing and site filling, etc., which has demonstrated significant effects, and has become the focus of the development of modern biomedical materials. This paper firstly elaborates the structure, type, and tissue distribution of human collagen, as well as the associated genetic diseases of different types of collagen, then introduces the specific process of producing animal source collagen and recombinant collagen, explains the advantages of recombinant collagen production method, and then introduces the various systems of expressing recombinant collagen, as well as their advantages and disadvantages, and finally briefly introduces the application of animal collagen, focusing on the use of animal collagen in the development of biopharmaceutical materials. In terms of application, it focuses on the use of animal disease models exploring the application effects of recombinant collagen in wound hemostasis, wound repair, corneal therapy, female pelvic floor dysfunction (FPFD), vaginal atrophy (VA) and vaginal dryness, thin endometritis (TE), chronic endometritis (CE), bone tissue regeneration in vivo, cardiovascular diseases, breast cancer (BC) and anti-aging. The mechanism of action of recombinant collagen in the treatment of FPFD and CE was introduced, and the clinical application and curative effect of recombinant collagen in skin burn, skin wound, dermatitis, acne and menopausal urogenital syndrome (GSM) were summarized. From the exploratory studies and clinical applications, it is evident that recombinant collagen has demonstrated surprising effects in the treatment of all types of diseases, such as reducing inflammation, promoting cell proliferation, migration and adhesion, increasing collagen deposition, and remodeling the extracellular matrix. At the end of the review, the challenges faced by recombinant collagen are summarized: to develop new recombinant collagen types and dosage forms, to explore the mechanism of action of recombinant collagen, and to provide an outlook for the future development and application of recombinant collagen.