Objective To construct a prediction model for the population with hypertension and diabetes to assess the risk of chronic kidney disease (CKD), and to provide a scientific basis for formulating targeted CKD prevention and control measures. Methods Based on physical examination data from community residents aged 60 years and above in Nanjing in 2022, 10 221 patients with hypertension and diabetes were selected as the study subjects. Variables associated with CKD prevalence were screened using univariate analysis, and further variable selection was performed using LASSO regression. Finally, a CKD risk prediction model was constructed based on logistic regression. The model's performance was evaluated using the ROC curve and calibration curve. Results The prevalence rate of CKD in the study population was 22.71%, with a mean age of 71.66 years. LASSO regression identified seven variables associated with CKD: age, blood urea nitrogen (BUN), hemoglobin, uric acid, triglyceride-glucose (TyG) index, urine protein-to-creatinine ratio (UPCR), and medical insurance type. The final logistic regression model incorporated six variables: age [OR=1.067 (95% CI: 1.058-1.076)], BUN [OR=1.377 (95% CI: 1.338-1.418)], hemoglobin [OR=0.992 (95% CI: 0.989-0.995)], uric acid [OR=1.004 (95% CI: 1.003-1.004)], TyG index [OR=1.445 (95% CI: 1.324-1.577)], and self-payment medical insurance [OR=1.732 (95% CI: 1.542-1.945)]. The model had an AUC of 0.759 (95% CI: 0.747-0.770) and a Brier score of 0.140 (95% CI: 0.136-0.145), indicating good predictive performance. The calibration curve showed good agreement between the predicted risk and the observed value. Conclusion The constructed LASSO-logistic regression risk prediction model in this study can effectively assess the risk of CKD in elderly individuals aged 60 years and above with hypertension and diabetes, providing a basis for early identification of high-risk individuals and the formulation of targeted CKD prevention and control measures.

OBJECTIVE: To standardize the operative procedure for tissue-engineered cartilage repair, by demonstrating surgical technique of arthroscopic implantation of decalcified cortex-cancellous bone scaffolds, and summarizing the surgical experience of the sports medicine department team at Peking University Third Hospital. METHODS: This article elaborates on surgical techniques and skills, focusing on the unabridged implantation technology and surgical procedure of decalcified cortex-cancellous bone scaffolds under arthroscopy: First, the patient was placed in the supine position. After anesthesia had been established, the surgeon established an arthroscope and explored the damaged area under the scope. After confirming the size and location of the injury site, the surgeon cleaned the damaged cartilage, and also trimmed the edges of the cartilage to ensure that the cut surface was smooth and stable. the surgeon performed the micro-fracture surgery in the area of cartilage injury, and then measured the size of the injured area under the scope. Next, the surgeon manually trimmed the tissue-engineered scaffold based on the measurements taken under the arthroscope, and then directly implanted the scaffold using a sleeve. A honeycomb-shaped fixator was used to implant absorbable nails to fix the scaffold. After the scaffold was installed, the knee was repeatedly flexed and extended for 10-20 times to ensure stability and range of motion. Finally, the arthroscope was withdrawn and the wound was closed. RESULTS: Decalcified cortex-cancellous bone scaffolds possessed unparalleled advantages over synthetic materials in terms of morphology and biomechanics. The cancellous bone part of the scaffold provided a three-dimensional, porous space for cell growth, while the cortical bone part offered the necessary mechanical strength. The surgery was performed entirely under arthroscopy to minimize invasiveness to the patient. Absorbable pins were used for fixation to ensure the stability of the scaffold. This technique could effectively improve the prognosis of the patients with cartilage injuries and standardized the surgical procedures for arthroscopic tissue-engineered scaffold operations in the patients with cartilage damage. CONCLUSION With the standard arthroscopic tissue-engineered scaffold repair technique, it is possible to successfully repair damaged cartilage, alleviate symptoms in the short term, and provide a more ideal long-term prognosis. The author and their team explain the surgical procedures for tissue-engineered scaffolds under arthroscopy, with the aim of guiding future clinical practice.
Tissue Engineering/methods* ; Humans ; Tissue Scaffolds ; Arthroscopy/methods* ; Cartilage, Articular/surgery*

Local anesthetics (LAs), such as articaine (AT), exhibit limited efficacy in inflammatory environments, which constitutes a significant limitation in their clinical application within oral medicine. In our prior research, we developed AT-17, which demonstrated effective properties in chronic inflammatory conditions and appears to function as a novel oral LA that could address this challenge. In the present study, we further elucidated the beneficial effects of AT-17 in acute inflammation, particularly in oral acute inflammation, where mitochondrial-related apoptosis played a crucial role. Our findings indicated that AT-17 effectively inhibited lipopolysaccharide (LPS)-induced nerve cell apoptosis by ameliorating mitochondrial dysfunction in vitro. This process involved the inhibition of mitochondrial reactive oxygen species (mtROS) production and the subsequent activation of the NRF2 pathway. Most notably, improvements in mitochondria-related apoptosis were key contributors to AT-17's inhibition of voltage-gated sodium channels. Additionally, AT-17 was shown to reduce mtROS production in nerve cells through the Na⁺/NCLX/ETC signaling axis. In conclusion, we have developed a novel local anesthetic that exhibits pronounced anesthetic functionality under inflammatory conditions by enhancing mitochondria-related apoptosis. This advancement holds considerable promise for future drug development and deepening our understanding of the underlying mechanisms of action.

OBJECTIVES: To explore the role of oxidative stress and immune infiltration in rheumatoid arthritis (RA). METHODS: RA datasets GSE55235 (10 RA vs 10 normal samples) and GSE55457 (13 RA vs 10 normal samples) from the GEO database were merged as the test set to identify the differentially expressed genes (DEGs) in RA using R. The DEGs were intersected with oxidative stress-related genes to obtain oxidative stress-associated DEGs. KEGG and GO enrichment analyses of the DEGs were performed, and the RA-related pathways and biological processes were analyzed using GSEA. A protein-protein interaction (PPI) network was constructed using STRING and Cytoscape, and the top 10 key genes were obtained using the Degree algorithm. The validation dataset GSE1919 from GEO database was used for ROC analysis of the key genes to obtain the core genes, and their correlations with infiltrating immune cells were analyzed using CIBERSORT. The results were verified by RT-qPCR for detecting expression levels of the core genes in RA and normal joint samples. RESULTS: We identified 89 oxidative stress-associated DEGs. Enrichment analysis suggested that these DEGs were involved in the biological processes including oxidative stress, chemical stress response, reactive oxygen species response, and lipopolysaccharide response. ROC analysis showed that the 5 core genes (STAT1, MMP9, MYC, CCL5, and JUN) all had AUC values >0.7, indicating their high diagnostic sensitivity and specificity for RA. These genes were closely correlated with immune cells, particularly T cells. RT-qPCR confirmed significant differential expressions of the core genes between RA and normal samples. CONCLUSIONS Oxidative stress and diverse immune responses are features of RA, and the immune responses contribute to activation of oxidative stress. The identified core genes can potential serve as new diagnostic markers for RA.
Arthritis, Rheumatoid/genetics* ; Oxidative Stress/genetics* ; Humans ; Computational Biology ; Protein Interaction Maps ; Gene Expression Profiling ; Gene Regulatory Networks

PURPOSE: To investigate the regulatory role of nerve injury-induced protein 1 (NINJ1) in the anti-inflammatory function of human umbilical cord mesenchymal stem cells (hUC-MSCs) co-stimulated by interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α). METHODS: hUC-MSCs were expanded in vitro using standard protocols, with stem cell characteristics confirmed by flow cytometry and multilineage differentiation assays. The immunomodulatory properties and cellular activity of cytokine-co-pretreated hUC-MSCs were systematically evaluated via quantitative reverse transcription RT-qPCR, lymphocyte proliferation suppression assays, and Cell Counting Kit-8 viability tests. Transcriptome sequencing, Western blotting and small interfering RNA interference were integrated to analyze the regulatory mechanisms of NINJ1 expression. Functional roles of NINJ1 in pretreated hUC-MSCs were elucidated through gene silencing combined with lactate dehydrogenase release assays, Annexin V/Propidium Iodide apoptosis analysis, macrophage co-culture models, and cytokine Enzyme-Linked Immunosorbent Assay. Therapeutic efficacy was validated in a cecal ligation and puncture-induced septic mouse model: 80 mice were randomly allocated into 4 experimental groups (n=20/group): sham group (laparotomy without cecal ligation); phosphate-buffered saline-treated group (cecal ligation and puncture (CLP) + 0.1 mL phosphate-buffered saline); hUC-MSCs (small interfering RNA (siRNA)-interferon-gamma and tumor necrosis factor-alpha co-stimulation (IT))-treated group (CLP + hUC-MSCs transfected with scrambled siRNA); and hUC-MSCs (siNINJ1-IT)-treated group (CLP + hUC-MSCs with NINJ1-targeting siRNA). RESULTS: hUC-MSCs demonstrated compliance with International Society for Cellular Therapy criteria, confirming their stem cell identity. IFN-γ/TNF-α co-pretreatment enhanced the immunosuppressive capacity of hUC-MSCs, accompanied by the reduction of cellular viability, while concurrently upregulating pro-inflammatory cytokines such as interleukin-6 and interleukin-1β. This co-stimulation significantly elevated NINJ1 expression in hUC-MSCs, whereas genetic silencing of NINJ1 effectively suppressed pro-inflammatory cytokine production and attenuated damage-associated molecular patterns release through inhibition of programmed plasma membrane rupture. Furthermore, the NINJ1 interference potentiated the ability of cytokine-pretreated hUC-MSCs to suppress LPS-induced pro-inflammatory responses in RAW264.7 macrophages. In cecal ligation and puncture-induced sepsis model, NINJ1-silenced hUC-MSCs exhibited enhanced therapeutic efficacy, manifested by reduced systemic inflammation and multi-organ damage. CONCLUSION Our findings shed new light on the immunomodulatory functions of cytokine-primed MSCs, offering groundbreaking insights for developing MSC-based therapies against inflammatory diseases via interfering the expression of NINJ1.
Mesenchymal Stem Cells/drug effects* ; Animals ; Interferon-gamma/pharmacology* ; Tumor Necrosis Factor-alpha/pharmacology* ; Humans ; Mice ; Umbilical Cord/cytology* ; Cells, Cultured ; Apoptosis ; Male

A variety of plants are used as Gymnadenia conopsea(L.)R.Br medicine in some areas.According to statistics,there are 7 genera and 16 species of Orchidaceae.There is confusion in medicinal varieties,which seriously affects drug safety and rational utilization of resources.Based on the national standards,this article conducted a textual research from the aspects of ancient herbs,modern monographs,the name of the reference,base,property and taste and efficacy and other aspects.The results showed that,the Gymnadenia conopsea(L.)R.Br medicine is named Erheten nai gar,and the Tibetan medicine is named Wangla,and most of the herbs take"Gymnadenia conopsea(L.)R.Br"as the name.The mainstream varieties of Gymnadenia conopsea(L.)R.Br,a plant of the genus Gymnadenia of Orchidaceae,were born in arid grassland or wetland and meadow,with palmlike roots,green stems and leaves and pink and white flowers.Gymnadenia conopsea(L.)R.Br is different in property and taste and efficacy when used as different ethnic medicines,but it has the commonness of tonifying kidney,producing sperm and strengthening yang and nourishing.The conclusion of textual research could provide references for the resource conservation,rational research and utilization,and artificial cultivation of Gymnadenia conopsea(L.)R.Br resources.

Chronic atrophic gastritis(CAG)is a chronic gastric disorder characterized by recurrent damage to the gastric mucosal epithelium,resulting in the reduction of intrinsic glands,with or without concurrent intestinal metaplasia.The"hyperactive stomach qi"theory,derived from Huang Di Nei Jing Su Wen Ji Zhu,proposes that the core pathogenesis of CAG lies in excessive stomach qi activity,grounded in the physiological principle of"strong yang qi in earth and weak yin qi in earth".This theory synthesizes the clinical manifestations and pathological progression of CAG,asserting that its development often involves intertwined pathological factors such as stagnation,dryness-heat,phlegm-dampness and stasis-toxicity.A triphasic therapeutic framework is proposed:the spleen qi deficiency phase,marked by impaired spleen transport function and dysregulated qi-fluid distribution,requiring spleen fortification and qi-fluid regulation;the hyperactive stomach qi phase,characterized by intensified stomach qi activity coupled with dryness-damp stagnation,necessitating stagnation resolution,dampness elimination and yin nourishment;the decline and disorder of middle qi phase,characterized by the deficiency of the middle qi,with phlegm,blood stasis and toxins forming the terminal stage.Treatment should focus on reinforcing the middle and restoring balance,detoxifying and dissipating accumulation.By exploring CAG pathogenesis and treatment through the lens of"hyperactive stomach qi",this study aimed to provide novel theoretical insights and therapeutic strategies for TCM in the prevention and treatment of CAG.

Objective To explore the application of DRG mortality risk stratification method in evaluating perioperative healthcare quality,analyzes the distribution characteristics and influencing factors of perioperative mortality patients,and provide decision-making support for reducing perioperative mortality.Methods Collect perioperative case data from a tertiary hospital in Jiangxi Province from 2021 to 2023,and classify the risk of death for different DRG group.A chi-square test was used for univariate analysis,and a logistic regression model was used to analyze the factors affecting perioperative patient mortality.Results Among the death cases,the medium-and high-risk groups accounted for the highest proportion(59.31%),and the ratio of male to female was 2.2∶1.0,the most cases were over 65 years old(57.60%),and the top five Core DRG disease groups are neurological disorders,circulatory disorders,early grouping disorders,digestive disorders,and hepatobiliary and pancreatic disorders.Critical condition,serious complications or comorbidities,operation grade,relative weight,age,gender,and hospital day were independent influencing factors of perioperative death.All differences were statistically significant(P＜0.05).Conclusion To reduce perioperative mortality risks,it is necessary to enhance the treatment capacity for critically ill patients,optimize the dynamic management mechanism for surgical grading,and strengthen the risk management of emergency surgical medical care.

Objective To explore the application of plasma 7 microRNA (miR7) testing in the differential diagnosis of very early-stage hepatocellular carcinoma (HCC). Methods This study is a multicenter real-world study. Patients with single hepatic lesion (maximum diameter≤2 cm) who underwent plasma miR7 testing at Zhongshan Hospital, Fudan University, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Anhui Provincial Hospital, and Peking University People’s Hospital between January 2019 and December 2024 were retrospectively enrolled. Patients were divided into very early-stage HCC group and non-HCC group, and the clinical pathological characteristics of the two groups were compared. The value of plasma miR7 levels, alpha-fetoprotein (AFP), and des-gamma-carboxy prothrombin (DCP) in the differential diagnosis of very early-stage HCC was evaluated using receiver operating characteristic (ROC) curves and area under the curve (AUC). In patients with both negative AFP and DCP (AFP＜20 ng/mL, DCP＜40 mAU/mL), the diagnostic value of plasma miR7 for very early-stage HCC was analyzed. Results A total of 64 528 patients from 4 hospitals underwent miR7 testing, and 1 682 were finally included, of which 1 073 were diagnosed with very early-stage HCC and 609 were diagnosed with non-HCC. The positive rate of miR7 in HCC patients was significantly higher than that in non-HCC patients (67.9% vs 24.3%, P＜0.001). ROC curves showed that the AUCs for miR7, AFP, and DCP in distinguishing HCC patients from the non-HCC individuals were 0.718, 0.682, and 0.642, respectively. The sensitivities were 67.85%, 43.71%, and 44.45%, and the specificities were 75.70%, 92.78%, and 83.91%, respectively. The pairwise comparison of AUCs showed that the diagnostic efficacy of plasma miR7 detection was significantly better than that of AFP or DCP (P＜0.05). Although its specificity was slightly lower than AFP and DCP, the sensitivity was significantly higher. Among patients negative for both AFP and DCP, miR7 maintained an AUC of 0.728 for diagnosing very early-stage HCC, with 67.82% sensitivity and 77.73% specificity. Conclusions Plasma miR7 testing is a potential molecular marker with high sensitivity and specificity for the differential diagnosis of small hepatic nodules. In patients with very early-stage HCC lacking effective molecular markers (negative for both AFP and DCP), miR7 can serve as a novel and effective molecular marker to assist diagnosis.

Objective To investigate the ameliorative effects and mechanisms of six types of tea(green tea,cyan tea,red tea,white tea,black tea and yellow tea)on metabolic disorders in obesity mice induced by high-fat diet(HFD).Methods Four-week-old male C57BL/6J mice were randomly divided into 8 groups with 7 mice per group.An HFD-induced obese mouse model was established,and the mice in control group maintained on standard diet followed by intragastric administration of different teas for 5 weeks.The body weight,liver weight ratio,fasting blood glucose,and lipid profile of the mice were measured to assess glucose and lipid metabolism.Serum inflammatory factors including IL-6,tumor necrosis factor-alpha(TNF-α)and oxidative stress markers[malondialdehyde(MDA)and superoxide dismutase(SOD)were measured.Additionally,liver histopathology and the expression of key glycolipid metabolism-related genes,adenosine monophosphate-activated protein kinase(AMPK)and carnitine palmitoyltransferase 1(CPT-1),were analyzed to explore underlying mechanisms.Results Cyan tea significantly suppressed weight gain,demonstrating superior weight control.White tea markedly reduced fasting blood glucose levels and decreased the area under the curve of oral glucose tolerance test(OGTT)and insulin tolerance test(ITT),indicating synergistic improvements in glucose metabolism and insulin sensitivity.Yellow tea exhibited exceptional anti-inflammatory and antioxidant effects,reducing hepatic IL-6 and MDA while enhancing SOD activity.Green tea activated the lipid oxidation pathway by upregulating AMPK/CPT-1 expression.All kinds of tea significantly attenuated hepatic lipid droplet accumulation.Conclusion All six types of tea alleviated metabolic disorders by reducing hepatic fat content in obesity mice.However,different types of tea exert their unique effects on improving metabolic disorders through differential mechanisms such as glucose metabolism regulation,lipid oxidation,and anti-inflammatory and antioxidant actions.