Periodontitis and rheumatoid arthritis (RA) are chronic inflammatory diseases that share similar inflammatory mechanisms and characteristics. Programmed cell death (PCD) has recently garnered attention for its crucial role in regulating inflammation and maintaining tissue homeostasis, as well as for its potential to link these two diseases. The various forms of PCD--including apoptosis, pyroptosis, and necroptosis--are closely controlled by signaling pathways such as Toll-like receptor 4 (TLR4) /NF-κB and MAPK. These pathways determine cell fate and influence inflammatory responses, tissue destruction, and repair, and they both play important roles in the pathogenesis of RA and periodontitis. In periodontitis, periodontal pathogens such as Porphyromonas gingivalis (P. gingivalis) and its virulence factors, including lipopolysaccharide (LPS), induce pyroptosis and necroptosis in immune cells such as macrophages via the TLR4/NF-κB pathway, which leads to an excessive release of pro-inflammatory cytokines such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α. Concurrently, these pathogens inhibit the normal apoptotic process of immune cells, such as neutrophils, prolonging their survival, exacerbating immune imbalance, and aggravating periodontal tissue destruction. Similarly, in RA synovial tissue, fibroblast-like synoviocytes (FLS) acquire apoptosis resistance through signaling pathways such as the Bcl-2 family, JAK/STAT, and NF-κB, allowing for the consistent proliferation and secretion of matrix metalloproteinases and pro-inflammatory cytokines. Meanwhile, the continuous activation of pyroptotic pathways in neutrophils and macrophages results in the sustained release of IL-1β, further exacerbating synovial inflammation and bone destruction. Notably, dysregulated PCD fosters inter-organ crosstalk through shared inflammatory mediators and metabolic networks. Damage-associated molecular patterns (DAMPs) and cytokines that originate from periodontal lesions can spread systemically, influencing cell death processes in synovial and immune cells, thereby aggravating joint inflammation and bone erosion. By contrast, systemic inflammation in RA can upregulate osteoclastic activity or interfere with the normal apoptosis of periodontal cells via TNF-α and IL-6, ultimately intensifying periodontal immune imbalance. This review highlights the pivotal bridging role of PCD in the pathogenesis of both periodontitis and RA, providing a reference for therapeutic strategies that target cell death pathways to manage and potentially mitigate these diseases.

Objective To explore the effect of fine particulate matter (PM_2.5) in Taiyuan City on short-term pulmonary function in elderly patients with chronic obstructive pulmonary disease (COPD). Methods Among the 1 015 elderly COPD patients admitted to the respiratory departments of five general hospitals in Taiyuan City from December 2021 to December 2023 were retrospectively selected for research; medical records, air pollutant data and meteorological data were analyzed; the relationship between PM_2.5 and lung function indicators and air pollutants was analyzed; the impact of PM_2.5 on lung function and its lag effect were analyzed; the cumulative effect of PM_2.5 concentration on the risk of pulmonary ventilation dysfunction was analyzed; The influence of gender and age on the relationship between PM_2.5 and patients ' short-term pulmonary function was analyzed. Results PM_2.5, respirable particulate matter (PM₁₀), sulfur dioxide (SO₂), carbon monoxide (CO) were negatively correlated with average temperature and average humidity (P<0.05) ; Nitrogen dioxide (NO₂), ozone (O₃) were negatively correlated with average temperature (P<0.05) ; There was a positive correlation among PM_2.5, PM₁₀, SO₂, CO, NO₂, and O₃ (P<0.05) ; Elevated PM_2.5 is an independent risk factor for decreased lung function and increased air pollutants (P<0.05) ; At lag0 and lag1, PM_2.5 concentration was negatively correlated with lung function in a dose-response manner (P<0.05); daily average PM_2.5 concentration at lag0 was a dangerous effect (P<0.05). Conclusion The impact of PM_2.5 concentration on lung function has a certain time lag. An increase in PM_2.5 concentrations can lead to a decline in lung function.

OBJECTIVE To explore the effects of leonurine on growth arrest-specific protein-6 （GAS6）/Axl signaling pathway， and clarify its mechanism of alleviating myocardial injury in rats with coronary heart disease. METHODS The rat model of coronary heart disease was constructed； successfully modeled rats were randomly separated into model group， leonurine low- dose and high-dose groups （intragastric administration of leonurine 25， 100 mg/kg+intraperitoneal injection of normal saline 75 mg/kg）， and leonurine high-dose+GAS6/Axl signaling pathway inhibitor group （intragastric administration of leonurine 100 mg/kg+ intraperitoneal injection of R428 75 mg/kg）， with 12 rats in each group. Additional 12 normal rats were selected as control group. Each administration group was given relevant medicine； control group and model group were given a constant volume of normal saline intragastrically and intraperitoneally， once a day， for 48 consecutive days. After administration， the heart function of rats， and serum levels of inflammatory factors and myocardial injury markers were detected； the pathological morphology of myocardial tissue was observed； the myocardial cell apoptosis rate， the expressions of apoptosis and GAS6/Axl signaling pathway-related proteins were determined. RESULTS Compared with control group， model group showed disorders in the arrangement of myocardial cells and myocardial fibers， hypertrophy of myocardial cells， and nuclear condensation； left ventricular ejection fraction， left ventricular fractional shortening， ratio of early-diastolic and late-diastolic motion velocity of the mitral ring， the protein expression of GAS6， B-cell lymphoma 2/B-cell lymphoma 2 associated X protein and phosphorylated Axl/Axl ratios were decreased significantly （P＜0.05）. The levels of tumor necrosis factor-α， interleukin-1β， interleukin-6， creatine kinase isoenzyme， troponin Ⅰ and myoglobin， the cell apoptosis rate， and cleaved caspase-3/caspase-3 ratio were increased significantly （P＜0.05）. Leonurine could obviously improve the above pathological conditions and detection indicators （P＜0.05）， and the effect of leonurine high-dose group was more significant than that of leonurine low-dose group （P＜0.05）； R428 treatment could reverse the ameliorating effect of high-dose of leonurine on myocardial injury in rats with coronary heart disease （P＜0.05）. CONCLUSIONS Leonurine can alleviate myocardial injury in rats with coronary heart disease， and its mechanism of action is related to the activation of the GAS6/Axl signaling pathway.

This paper summarizes Professor SHI Zaixiang's clinical experience in treating high fever caused by sepsis using Chaihu Guizhi Ganjiang Decoction （柴胡桂枝干姜汤）. He holds that the key pathogenesis of sepsis involves constrained heat in the shaoyang and internal accumulation of water and fluids. The clinical manifestations such as high fever， chills， and alternating sensations of cold and heat are attributed to pathogenic heat constrained in the shaoyang. Meanwhile， soft tissue edema and serous cavity effusions are due to shaoyang dysfunction and internal water retention. In clinical practice， treating sepsis-related high fever requires addressing both the shaoyang-constrained heat and the associated edema and effusions. The therapeutic approach focuses on harmonizing the shaoyang and resolving internal fluids， using Chaihu Guizhi Ganjiang Decoction as the base formula with flexible modifications. Professor SHI emphasizes that this formula shows a rapid antipyretic effect， particularly in cases where multiple anti-infective treatments have failed.

Objective To retrieve and integrate relevant evidence on the prevention and nursing of neonatal intraoperative acquired pressure and provide a reference basis for nursing practice.Methods According to the"6S"model retrieval strategy,we searched for published articles including the following topic words,such as prevention,assessment,management,and nursing care of neonatal intra-operative pressure injury from establishment of databases until August 2,2023.We got the related references from clinical decision-making websites,guidelines network,professional association websites,domestic and foreign databases.Results Totally 14 articles were included,including 1 clinical decision support,4 clinical guidelines,3 evidence summaries,2 systematic reviews and 4 expert consensuses.Finally,31 pieces of best evidence were summarized from 5 aspects of risk factors,risk assessment,observation and preventive measures,nursing measures after the occurrence of pressure injury,education and training.Conclusion Multidisciplinary collaborative participation based on the obtained evidence is an effective strategy,which can be applied to the prevention and nursing care of neonatal intraoperative acquired pressure injury.Appropriate preventive and nursing programs should be made according to the actual situation and clinical environment,so as to reduce the incidence of neonatal intraoperative acquired pressure injury and to ensure the safety of neonatal perioperative nursing care.

Objective To construct a theoretical model of venous thromboembolism(VTE)risk perception in pregnant women,so as to provide a scientific basis for promoting pregnant women to form a correct risk perception of VTE and actively take preventive behaviors.Methods A qualitative research approach guided by the procedural grounded theoiy was adopted.Data were collected by a semi-structured deep interview on 18 pregnant women who received prenatal examination in the outpatient department of a tertiary A obstetrics and gynecology hospital in Nanjing from June to July 2023,and the data were analyzed by three-level coding and continuous comparison method.Results The VTE risk perception of pregnant women was affected by 6 factors including social coupling system,self health status,life behavior habits,knowledge on disease,compliance behavior and emotional stimulation.Pregnant women perceived VTE risk from 3 aspects:threats to maternal and child safety,increased family economic burden and increased time cost,impact on social roles.Thus,3 health behavior decisions were formed,including taking preventive behaviors,overcoming implementation barriers,and seeking knowledge behaviors,in order to reduce their own risk of VTE,and prevent the occurrence of VTE.Conclusion The theoretical model of VTE risk perception of pregnant women can guide medical staff to comprehensively consider the influencing factors of VTE risk perception of pregnant women,optimize the form and content of VTE health education,give pregnant women individualized and sustainable VTE prevention guidance,and strengthen pregnant women's perception of VTE risk and the benefits of preventive behavior,so as to actively take the correct health behavior decisions.

Objective:To assess the prognostic impact of frailty on elderly inpatients with heart failure.Methods:This prospective cohort study enrolled 121 in elderly patients with heart failure from Beijing Hospital, the General Hospital of the People's Liberation Army, and Beijing Tsinghua Changgung Hospital between September 2018 and April 2019.Patients were assessed for frailty using the Fried frailty phenotype and categorized into frail and non-frail groups.Follow-ups were conducted at 3-, 6-, and 12-months post-enrollment through clinic visits or phone calls to record adverse events.Composite endpoints include all-cause mortality and rehospitalization duo to deterioration of heart failure.Results:The study included 121 patients with an average age of 78.0±7.4 years, of whom 71(58.7%)were male and 57(47.1%)were classified as frail.Compared to the non-frail group, the frail group had lower estimated glomerular filtration rates[49.5±20.7 ml/(min·1.73m 2) vs.(64.0±27.1)ml/(min·1.73m 2)], lower scores in Basic Activities of Daily Living[5.0(4.0, 6.0) vs.6.0(5.0, 6.0)], Instrumental Activities of Daily Living[2.0(1.3, 7.8) vs.7.0(5.0, 8.0)], and Mini-Mental State Examination[26.0(16.0, 28.0) vs.27.0(22.3, 29.0)], all P<0.05.They also experienced longer hospital stays[10.5(6.0, 18.8)days vs.8.0(6.0, 11.8)days, P=0.008].During the follow-up period, the incidence of composite endpoint events was significantly higher in the frail group(43.9% vs.25.0%, P=0.029).Kaplan-Meier survival analysis demonstrated that the one-year incidence of composite endpoint events was significantly higher in the frail group( P=0.013).Multivariable Cox regression analysisindicated that frailty was an independent risk factor for composite endpoint events( HR=2.201, 95% CI: 1.089-4.447, P=0.028). Conclusions:Frailty is an independent risk factor for poor outcomes in elderly hospitalized patients with heart failure and should be considered a crucial factor in clinical assessment and treatment strategies.

ObjectiveTo investigate the potential effect of ursodeoxycholic acid （UDCA） in the prevention and treatment of COVID-19 in patients with chronic hepatitis B. MethodsClinical data were collected from 324 patients with chronic hepatitis B who were treated in Beijing Ditan Hospital， Capital Medical University， from January to December 2022， and according to whether UDCA was administered， they were divided into UDCA group and control group. The propensity score matching （PSM） method was used to balance the confounding factors such as age， sex， and chronic complications， and the two groups were compared in terms of SARS-CoV-2 infection rate， symptoms， and recovery time after COVID-19. The two groups were also compared in terms of related laboratory markers （white blood cell count ［WBC］， hemoglobin ［Hb］， platelet count ［PLT］， alanine aminotransferase ［ALT］， aspartate aminotransferase ［AST］， albumin ［Alb］， alkaline phosphatase ［ALP］， total bilirubin ［TBil］， triglyceride ［TG］， and total cholesterol ［TC］）， vaccination， and the incidence rate of liver disease symptoms after COVID-19. The independent-samples t test was used for comparison of normally distributed continuous data between two groups， and the Mann-Whitney U test was used for comparison of data with skewed distribution between the two groups； the chi-square test and the continuously corrected chi-square test were used for comparison of categorical data between two groups. The binary Logistic regression model was used for univariate and multivariate analyses to investigate the influencing factors for COVID-19 after matching. ResultsThere were 87 patients in the UDCA group and 237 patients in the control group， and after PSM， there were 78 patients in the UDCA group and 137 patients in the control group， with good balance between the two groups. There was a significant difference in SARS-CoV-2 infection rate between the UDCA group and the control group ［82.1% （64/78） vs 95.6% （131/137）， χ²=10.847， P=0.001］. After COVID-19， compared with the control group， the UDCA group had a significantly lower proportion of the patients with chill （10.9% vs 38.9%， χ²=16.124， P<0.001） and cough （56.3% vs 74.8%， χ²=6.889， P=0.009）. There was a significant difference between the UDCA group and the control group in the proportion of the patients with a recovery time of ≤7 days after COVID-19 （79.7% vs 61.1%， χ²=6.760， P=0.009）. Both univariate and multivariate logistic regression analyses showed that UDCA was an independent influencing factor for COVID-19 （odds ratio=0.21 and 0.17， both P<0.05）. ConclusionUDCA is an protective factor against COVID-19 in patients with chronic hepatitis B and can alleviate related symptoms to some extent and shorten the recovery time， and therefore， it has an important value in the prevention and treatment of COVID-19.

OBJECTIVE: To explore the regulatory mechanism of human hepatocyte apoptosis induced by lysosomal membrane protein Sidt2 knockout. METHODS: The Sidt2 knockout (Sidt2^-/-) cell model was constructed in human hepatocyte HL7702 cells using Crispr-Cas9 technology.The protein levels of Sidt2 and key autophagy proteins LC3-II/I and P62 in the cell model were detected using Western blotting, and the formation of autophagosomes was observed with MDC staining.EdU incorporation assay and flow cytometry were performed to observe the effect of Sidt2 knockout on cell proliferation and apoptosis.The effect of chloroquine at the saturating concentration on autophagic flux, proliferation and apoptosis of Sidt2 knockout cells were observed. RESULTS: Sidt2^-/- HL7702 cells were successfully constructed.Sidt2 knockout significantly inhibited the proliferation and increased apoptosis of the cells, causing also increased protein expressions of LC3-II/I and P62(P < 0.05) and increased number of autophagosomes.Autophagy of the cells reached a saturated state following treatment with 50 μmol/L chloroquine, and at this concentration, chloroquine significantly increased the expressions of LC3B and P62 in Sidt2^-/- HL7702 cells. CONCLUSION Sidt2 gene knockout causes dysregulation of the autophagy pathway and induces apoptosis of HL7702 cells, and the latter effect is not mediated by inhibiting the autophagy-lysosomal pathway.
Humans ; Lysosome-Associated Membrane Glycoproteins/metabolism* ; Autophagy ; Apoptosis ; Hepatocytes ; Lysosomes/metabolism* ; Chloroquine/pharmacology* ; Nucleotide Transport Proteins/metabolism*

Objective:To evaluate the association of different biomarkers with frailty in elderly hospitalized patients.Methods:In this cross-sectional study, a total of 319 elderly patients aged 65 years or older hospitalized in Beijing Hospital between September 2018 and February 2019 were enrolled.Patients had a mean age of(75.0±6.6)years and 151(47.3%)were women.Based on the Fried phenotype, patients were divided into a non-frail group(244 cases, 76.5%)and a frail group(75 cases, 23.5%). The clinical characteristics and biomarker levels of the two groups were compared.The association of different biomarkers with frailty was evaluated by using the receiver operating characteristic(ROC)curve.The Youden index was used for the optimal cutoff values and the area under the curve(AUC)were calculated.AUCs of different biomarkers were compared to assess their correlations with frailty.Results:Hemoglobin, lipid levels(triglycerides, total cholesterol and low-density lipoprotein cholesterol), and prealbumin were significantly lower in the frail group than in the non-frail group( P<0.05), while N-terminal pro-B type natriuretic peptide(NT-proBNP)and high-sensitivity C reactive protein(hsCRP)levels were significantly higher than in the non-frail group( P<0.05). Thyrotropin(TSH)and free triiodothyronine(FT3)levels were significantly lower( P<0.05)and trans-triiodothyronine(rT3)was significantly higher( P<0.05)in the frail group.The combination of six biomarkers[hemoglobin, prealbumin, hsCRP, 25-dihydroxy vitamin D3[25(OH)D3], rT3 and NT-pro BNP]had the most powerful correlation with frailty(AUC=0.705, 95% CI: 0.652-0.755), but the correlation was not significantly different from that of the combination of 3 markers(hemoglobin, rT3 and hsCRP)(ROC=0.010, 95% CI: -0.0106-0.0306, P>0.05). Either of the two combinations was significantly better than the combination of 2 markers(hemoglobin and rT3)(ROC=0.143, 95% CI: 0.0406-0.245; ROC=0.153, 95% CI: 0.0498-0.256; all P<0.01). Conclusions:Hemoglobin, lipids, prealbumin, TSH and FT3 levels decrease while NT-proBNP and hsCRP levels increase in elderly hospitalized frail patients.The 6-biomarker combination[hemoglobin, prealbumin, hsCRP, 25(OH)D3, rT3 and NT-pro BNP]and 3-biomarker combination(hemoglobin, rT3 and hsCRP)have better correlation with frailty than the 2-biomarker combination(hemoglobin and rT3).