ObjectiveTo explore the clinical efficacy and mechanism of Bupi Qingfei prescription （BPQF） in treating stable bronchiectasis in the patients with syndromes of lung-spleen Qi deficiency and phlegm-heat accumulation in the lungs. MethodsA randomized， double-blind， placebo-controlled trial was conducted. Patients were randomized into BPQF and placebo control （PC） groups. On the basis of conventional Western medicine treatment， the BPQF granules and placebo were respectively administered at 10 g each time， twice a day， for a course of 24 weeks. The TCM symptom scores， Quality of Life Questionnaire for Bronchiectasis （QOL-B） scores， lung function indicators， T lymphocyte subsets， level of inflammatory factors in the sputum， level of neutrophil elastase （NE） in the sputum， and occurrence of adverse reactions were observed before and after treatment in the two groups. ResultsA total of 64 patients completed the study， encompassing 32 in the BPQF group and 32 in the PC group. After treatment， the BPQF group showed decreased TCM symptom scores （P<0.01）， increased QOL-B scores （P<0.01）， and declined levels of tumor necrosis factor （TNF）-α and NE （P<0.05， P<0.01）. The PC group showed decreased TCM symptom （except spleen deficiency） scores （P<0.01）， increased the QOL-B health cognition and respiratory symptom domain scores （P<0.05， P<0.01）， and a declined TNF-α level （P<0.01）. Moreover， the BPQF group had lower TCM symptom （except chest tightness） scores （P<0.05， P<0.01）， higher QOL-B （except treatment burden） scores （P<0.05， P<0.01）， and lower levels of interleukin-6 and TNF-α （P<0.05） than the PC group. Neither group showed serious adverse reactions during the treatment process. ConclusionBPQF can ameliorate the clinical symptoms of stable bronchiectasis patients who have lung-spleen Qi deficiency or phlegm-heat accumulation in the lungs by regulating the immune balance and inhibiting airway inflammatory responses.

To investigate the clinical features and peripheral blood immune cell subsets ofelderly (≥60 years old) onset rheumatoid arthritis (EORA) patients.

The incidence of cutaneous squamous cell carcinoma (CSCC) is increasing rapidly. This study discussed the effects of artesunate (ART) on CSCC cell proliferation and migration via the solute carrier family 7 member 11 (SLC7A11)-glutathione peroxidase 4 (GPX4) pathway. MTT assessed cell viability and analyzed the IC50 value (69.26 μM). Accordingly, human CSCC cells (A431) were cultured in vitro, and treated with 70 μM ART, Ferrostatin-1, oe-SLC7A11, and C646, with cell biological behavior assessed.The potential targets of ART were predicted. p53 acetylation and protein stability and ART-p300 binding were examined. Thymusless nude mice were subcutaneously inoculated with A431 cells, and treated with ART and C646. ART-treated A431 cells showed weakened proliferation, migration, lactate dehydrogenase levels, oxidized glutathione/glutathione ratio, reactive oxygen species, malondialdehyde, and active Fe2+ levels, which could be reversed by suppressing ferroptosis. ART promoted p53 acetylation and protein stability and curbed the SLC7A11-GPX4 pathway by targeting p300. ART stimulated ferroptosis via the SLC7A11-GPX4 pathway, thereby repressing CSCC cell proliferation and migration, which were counteracted by p300 inhibition. ART regulated the SLC7A11-GPX4 pathway by up-regulating the p300-p53 axis, thereby hindering tumor growth in vivo. Collectively, ART inhibits CSCC proliferation and migration by modulating the SLC7A11-GPX4 pathway through the p300-p53 axis.

The incidence of cutaneous squamous cell carcinoma (CSCC) is increasing rapidly. This study discussed the effects of artesunate (ART) on CSCC cell proliferation and migration via the solute carrier family 7 member 11 (SLC7A11)-glutathione peroxidase 4 (GPX4) pathway. MTT assessed cell viability and analyzed the IC50 value (69.26 μM). Accordingly, human CSCC cells (A431) were cultured in vitro, and treated with 70 μM ART, Ferrostatin-1, oe-SLC7A11, and C646, with cell biological behavior assessed.The potential targets of ART were predicted. p53 acetylation and protein stability and ART-p300 binding were examined. Thymusless nude mice were subcutaneously inoculated with A431 cells, and treated with ART and C646. ART-treated A431 cells showed weakened proliferation, migration, lactate dehydrogenase levels, oxidized glutathione/glutathione ratio, reactive oxygen species, malondialdehyde, and active Fe2+ levels, which could be reversed by suppressing ferroptosis. ART promoted p53 acetylation and protein stability and curbed the SLC7A11-GPX4 pathway by targeting p300. ART stimulated ferroptosis via the SLC7A11-GPX4 pathway, thereby repressing CSCC cell proliferation and migration, which were counteracted by p300 inhibition. ART regulated the SLC7A11-GPX4 pathway by up-regulating the p300-p53 axis, thereby hindering tumor growth in vivo. Collectively, ART inhibits CSCC proliferation and migration by modulating the SLC7A11-GPX4 pathway through the p300-p53 axis.

The incidence of cutaneous squamous cell carcinoma (CSCC) is increasing rapidly. This study discussed the effects of artesunate (ART) on CSCC cell proliferation and migration via the solute carrier family 7 member 11 (SLC7A11)-glutathione peroxidase 4 (GPX4) pathway. MTT assessed cell viability and analyzed the IC50 value (69.26 μM). Accordingly, human CSCC cells (A431) were cultured in vitro, and treated with 70 μM ART, Ferrostatin-1, oe-SLC7A11, and C646, with cell biological behavior assessed.The potential targets of ART were predicted. p53 acetylation and protein stability and ART-p300 binding were examined. Thymusless nude mice were subcutaneously inoculated with A431 cells, and treated with ART and C646. ART-treated A431 cells showed weakened proliferation, migration, lactate dehydrogenase levels, oxidized glutathione/glutathione ratio, reactive oxygen species, malondialdehyde, and active Fe2+ levels, which could be reversed by suppressing ferroptosis. ART promoted p53 acetylation and protein stability and curbed the SLC7A11-GPX4 pathway by targeting p300. ART stimulated ferroptosis via the SLC7A11-GPX4 pathway, thereby repressing CSCC cell proliferation and migration, which were counteracted by p300 inhibition. ART regulated the SLC7A11-GPX4 pathway by up-regulating the p300-p53 axis, thereby hindering tumor growth in vivo. Collectively, ART inhibits CSCC proliferation and migration by modulating the SLC7A11-GPX4 pathway through the p300-p53 axis.

Objective To explore the mediating role of occupational well-being in the relationship between professional identity and safety behavior among nurses. Methods A total of 1 006 nurses from ten tertiary general hospitals in eight provincial administrative regions were selected as the research subjects using convenient sampling method. Their safety behavior, professional identity and occupational well-being were investigated using Nurse Safety Behavior Scale, Nurse Professional Identity Scale and Occupational Well-being Scale. Structural equation modeling was performed using AMOS 26.0 to examine the mediating effect of occupational well-being in the relationship between professional identity and safety behavior among nurses. Results The scores for safety behavior, professional identity, and occupational well-being were (53.0±6.1), (123.7±21.2) and (90.8±13.1), respectively. Safety behavior was positively correlated with both professional identity and occupational well-being (correlation coefficients were 0.50 and 0.50, respectively, both P<0.01). Professional identity was positively correlated with occupational well-being (correlation coefficient was 0.51, P<0.01). The multiple linear regression analysis results showed that the higher the professional identity and occupational well-being of nurses, the higher the level of safety behavior (both P<0.05). The result of mediating effect shows that the total effect of occupational identity on safety behavior was 0.498 [95% confidence interval (CI) was 0.405-0.576], and occupational well-being played a mediating role between professional identity and safety behavior among nurses with the mediation effect of 0.156 (95%CI was 0.112-0.205), accounting for 31.33% of the total effect. Conclusion The safety behavior of nurses is at a moderate level. Both professional identity and occupational well-being can affect the safety behavior of nurses. Professional identity can increase the safety behavior of nurses by affecting occupational well-being.

OBJECTIVE: To investigate the predictive value of early lactate/albumin ratio (LAR) combined with quick sequential organ failure assessment (qSOFA) for the 28-day prognosis of patients with sepsis caused by emergency community-acquired pneumonia (CAP). METHODS: The clinical data of patients with sepsis caused by CAP admitted to the department of emergency of Beijing Haidian Hospital from June 2021 to August 2022 were retrospectively analyzed, including gender, age, comorbidities, lactic acid (Lac), serum albumin (Alb), LAR, procalcitonin (PCT) within 1 hour, and 28-day prognosis. Patients were divided into two groups based on 28-day prognosis, and risk factors affecting patients' prognosis were analyzed using univariate and multivariate Cox regression methods. Patients were divided into two groups according to the best cut-off value of LAR, and Kaplan-Meier survival curves were used to analyze the 28-day cumulative survival of patients in each group. Time-dependent receiver operator characteristic curve (ROC curve) were plotted to analyze the predictive value of sequential organ failure assessment (SOFA), acute physiology and chronic health evaluation II (APACHE II), and qSOFA+LAR score on the prognosis of patients with sepsis caused by CAP at 28 days. The area under the curve (AUC) was calculated and compared. RESULTS: A total of 116 patients with sepsis caused by CAP were included, of whom 80 survived at 28 days and 36 died, 28-day mortality of 31.0%. There were no statistically significant differences in age, gender, comorbidities, pH, platelet count, and fibrinogen between the survival and death groups, and there were significantly differences in blood urea nitrogen (BUN), white blood cell count (WBC), hemoglobin, Lac, Alb, PCT, D-dimer, LAR, as well as qSOFA score, SOFA score, and APACHE II score. Univariate Cox regression analyses showed that BUN, WBC, pH, Lac, Alb, PCT, LAR, qSOFA score, SOFA score, and APACHE II score were associated with mortality outcome. Multifactorial Cox regression analysis of the above variables showed that BUN, WBC, PCT, and APACHE II score were independent risk factors for 28-day death in the emergency department in patients with sepsis caused by CAP [hazard ratio (HR) were 1.081, 0.892, 1.034, and 1.135, respectively, all P < 0.05]. The best cut-off value of early LAR for predicting the 28-day prognosis of sepsis patients was 0.088, the Kaplan-Meier survival curve showed that the 28-day cumulative survival rate of sepsis patients in the LAR ≤ 0.088 group was significantly higher than that in the LAR > 0.088 group [82.9% (63/76) vs. 42.5% (17/40), Log-Rank test: χ² = 22.51, P < 0.001]. The qSOFA+LAR score was calculated based on the LAR cut-off value and qSOFA score, and ROC curve analysis showed that the AUCs of SOFA score, APACHE II score, and qSOFA+LAR score for predicting 28-day death of patients with sepsis caued by CAP were 0.741, 0.774, and 0.709, respectively, with the AUC of qSOFA+LAR score slightly lower than those of SOFA score and APACHE II score, but there were no significantly differences. When the best cut-off value of qSOFA+LAR score was 1, the sensitivity was 63.9% and the specificity was 80.0%. CONCLUSION The qSOFA+LAR score has predictive value for the 28-day prognosis of patients with sepsis caused by CAP in the emergency department, its predictive value is comparable to the SOFA score and the APACHE II score, and it is more convenient for early use in the emergency department.
Emergency Service, Hospital/statistics & numerical data* ; Sepsis/etiology* ; Prognosis ; Community-Acquired Pneumonia/mortality* ; Organ Dysfunction Scores ; Predictive Value of Tests ; Lactic Acid/blood* ; Serum Albumin, Human/analysis* ; Biomarkers/blood* ; Retrospective Studies ; Hospital Mortality ; Kaplan-Meier Estimate ; APACHE ; Procalcitonin/blood* ; ROC Curve ; Area Under Curve ; Humans

Objective To investigate the role of lncSIL in transforming growth factor-β1(TGF-β1)-induced alveo-lar epithelial interstitial transformation(EMT)and its related signaling pathways.Methods Western blot was used to detect the effect of lncSIL silencing on the expression of E-cadherin(E-cad),alpha-smooth muscle actin(α-SMA)and Collagen I(Col I)in the process of EMT induced by TGF-β1.LncSIL interacting proteins were ana-lyzed by RNA pulldown.Western blot was used to detect the effect of overexpression or silencing of lncSIL on the expression of its target gene enhancer of zeste homolog 2(EZH2)and its downstream factors P21 and cyclin-de-pendent kinase 6(CDK6).Flow cytometry was used to analyze the effect of lncSIL on cell cycle progression.Re-sults After lncSIL silencing,the expression of α-SMA and Col I increased,the expression of E-cad decreased.RNA pulldown assay showed that EZH2 was the target protein that interacted with lncSIL,and the expression of EZH2 increased after silencing lncSIL,the expression of EZH2 downstream gene P21 decreased,CDK6 increased.Flow cytometry showed that the number of cells in S phase significantly increased.When lncSIL was overexpressed,the expression of EZH2 and CDK6 was down-regulated,the expression of P21 was up-regulated,and the number of S phase cells significantly decreased.Conclusion LncSIL inhibits TGF-β1-induced alveolar epithelial cell mesen-chymal transition by negatively regulating EZH2/P21/CDK6 signaling pathway to inhibit cell cycle progression.

Objective To investigate the protective effect of the compound drug Weng-Li-Tong(WLT)against cisplatin(CDDP)-induced hepatocyte injury.Methods A cellular injury model was established by treating murine hepatocyte line BNL CL.2 with CDDP(80 μmol/L).Experimental groups were divided as follows:CDDP group(modeling only),WLT group(intervention with 1 g/L WLT),WLT+CDDP group(co-administration of CDDP and 1 g/L WLT),and a control group(normal culture).The protective effect of the compound drug WLT on CDDP-mediated hepatocyte injury was evaluated using CCK-8 assay,PI staining,crystal violet staining,Western blotting,reactive oxygen species(ROS)detection,and apoptosis analysis.Results Compared with the control group,the number of dead cells increased significantly(P＜0.001)in the CDDP group,but no cytotoxicity was observed in the WLT group.The hepatocyte morphology in the WLT+CDDP group showed improvement with no obvious shrinkage compared to the CDDP group,as evidenced by the reduced proportion of PI-positive cells.Crystal violet staining results also indicated a higher cell count in the WLT+CDDP group than in the CDDP group,suggesting the protective effect of WLT against CDDP-mediated liver injury.Under CDDP intervention,the expression of the apoptosis-related protein Cleaved Caspase-3 increased.However,in the WLT+CDDP group,the expression of Cleaved Caspase-3 decreased,while the expression of the anti-apoptotic protein Bcl-2 increased.Additionally,compared to the CDDP group,the WLT+CDDP group showed a reduction in ROS production[DCFH-DA staining positive rate(％):56.20±1.65 vs.44.57±0.31]and a decrease in the proportion of apoptotic cells[proportion of early and late apoptotic cells(％):43.60±0.44 vs.19.57±0.78;33.30±1.02 vs.14.83±0.57].Conclusion The compound drug WLT exhibits a protective effect against CDDP-mediated hepatocyte injury,suggesting potential therapeutic value in acute liver injury models.

Methylation modification is one of the most common epigenetic modification regulation in eukaryotes, including histone methylation, DNA methylation, RNA methylation, etc., which plays an important regulatory role in physiological processes and pathologic occurrence and development. Tooth root development is carried out by both epithelial and mesenchymal cells and involves a variety of cell-molecular interactions. In recent years, a large number of studies have found that methylation plays a key role in the regulation of tooth root development and expands the mechanism network of tooth root development. In this paper, we review the role and mechanism of methylation modification during root development.