ObjectiveTo investigate the effect and predictive value of systemic inflammatory markers on pathological complete response (pCR) after neoadjuvant chemotherapy (NACT) for locally advanced breast cancer (LABC). MethodsThe clinicopathologic data of female patients with LABC who received NACT and radical surgical resection in the Department of Breast Surgery, Affiliated Hospital of Southwest Medical University from February 2019 to February 2022 were retrospectively analyzed. The factors affecting pCR after NACT were analyzed by the multivariate logistic regression and the prediction model was established. The efficiency of the prediction model was evaluated by receiver operating characteristic (ROC) curve and area under the ROC curve (AUC). ResultsA total of 98 patients were gathered, of which 29 obtained pCR, with a pCR rate of 29.6%. The multivariate analysis of binary logistic regression showed that the patients with non-menopausal status, negative estrogen receptor (ER), chemotherapy+targeted therapy, and systemic immune-inflammation index (SII) <532.70 (optimal critical value) were more likely to obtain pCR after NACT (P<0.05). The prediction model was established according to logistic regression analysis: Logit (P)=0.697–2.974×(menopausal status)–1.932×(ER status)+3.277×(chemotherapy regimen)–2.652×(SII). The AUC (95%CI) of the prediction model was 0.914 (0.840, 0.961), P<0.001. ConclusionsIt is not found that other inflammatory indicators such as neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and lymphocyte-to-monocyte ratio are associated with pCR after NACT. But SII is an important predictor of pCR after NACT for LABC and has a good predictive efficiency.
Objective To explore the therapeutic effect of rehabilitation therapy combined with computer-aided design and computer-aided manufacture (CAD/CAM) of orthopedic insoles on deputy scaphoid inflammation. Methods We selected the patients with deputy scaphoid inflammation who had treated in Sichuan Province Orthopedic Hospital between July 2018 and February 2020. The patients were randomly divided into control group and experimental group by drawing lots. The control group received rehabilitation therapy, while the experimental group received rehabilitation therapy combined with CAD/CAM orthopedic insoles. The clinical efficacy was tested at the 5th and 12th weeks after treatment, and the foot pain was assessed by Visual Analogue Scoring (VAS), and the foot function was assessed by the American Orthopaedic Foot and Ankle Association (AOFAS) scale. Results A total of 78 patients were included, and 3 patients dropped out. There was no significant difference in sex, age, weight or course of disease between the two groups (P>0.05). Before treatment, there was no statistically significant difference in VAS score (t=0.329, P=0.743) or AOFAS score (t=0.431, P=0.668) between the two groups. At the 5th and 12th weeks after treatment, the VAS score of the experimental group was lower than that of the control group (t=4.517, 5.299; P<0.001), and the AOFAS score was higher than that of the control group (t=6.239, 5.779; P<0.001). Over time, the VAS score of the two groups decreased (P<0.05), while the AOFAS score increased (P<0.05). Conclusion Rehabilitation therapy combined with CAD/CAM of orthopedic insoles have better curative effect than traditional rehabilitation therapy for deputy scaphoid inflammation.
Currently, approximately one-third of epilepsy patients exhibit resistance to anti-seizure medications (Anti-seizure medications, ASMs), which can only alleviate symptoms, but cannot completely cure the condition. Consequently, the development of new ASMs from an understanding of epilepsy pathogenesis has emerged as an urgent social issue. The role of neuroinflammation in various neurological diseases has garnered significant attention as a popular research topic both domestically and internationally. Numerous studies have corroborated the involvement of neuroinflammation in the onset and progression of epilepsy. The biological target, Translocator protein 18 kDa (TSPO), is considered as a marker of neuroinflammation and is intricately involved in the entire neuroinflammatory response. Investigating the function of TSPO in epilepsy neuroinflammation can potentially uncover new treatment targets. At present, the exact mechanism of TSPO in epilepsy neuroinflammation remains unclear, thus necessitating a comprehensive summary and overview. This article reviewed the advancements made in TSPO research within the realm of neuroinflammation and its role in epileptic neuroinflammation, aiming to contribute novel insights for the identification of related targets and pathways for epilepsy treatment.
Objective To investigate and analyze the relationships among glucagon-like peptide-1 (GLP-1) level, chronic inflammation, and atherosclerosis in patients with non-alcoholic fatty liver disease (NAFLD). Methods From October 2016 to February 2017, using cross-sectional investigation, the GLP-1 level, chronic inflammation, and atherosclerosis were investigated in 80 subjects (40 NAFLD patients in NAFLD group, and 40 non-fatty liver disease participants in control group) who underwent physical examination at Xi’an Road Community Hospital. Results Compared with those in the control group, GLP-1 fasting level in patients with NAFLD [(9.09±1.03) vs. (9.15±1.06) pmol/L, P=0.807] and postprandial plasma GLP-1 [(15.96±3.37) vs. (17.46±4.76) pmol/L, P=0.108] had no changes. The correlations of GLP-1 level with chronic inflammation and insulin resistance (IR) were not significant either. The increased risk of carotid intima-media thickness related cardiovascular disease (CVD) in the NAFLD group was greater than that in the control group, and the difference was statistically significant [22 (55.0%)vs.13 (32.5%), P=0.043]. When the plasma lipoprotein-associated phospholipase A2 level increased, the risk of NAFLD increased [odd ratio (OR)=1.16, 95% confidence interval (CI) (1.02, 1.32), P=0.023]. Plasma ceramide kinase (CERK) in the NAFLD group was lower than that in the control group, and the difference was statistically significant [(12.36±2.45) vs. (18.33±3.71) ng/mL, P<0.001]. When the plasma CERK level of the fasting plasma was elevated, the risk of NAFLD decreased [OR=0.30, 95%CI (0.12, 0.78), P=0.014]. The homeostasis model assessment of insulin resistance (HOMA-IR) in the NAFLD group was higher than that in the control group, and the difference was statistically significant (2.46±2.53 vs. 1.11±0.66, P=0.002). The Matsuda index in the NAFLD group was less than that in the control group, and the difference was statistically significant (5.88±4.09 vs. 10.46±7.90, P=0.002). When HOMA-IR increased, the risk of NAFLD increased [OR=2.75, 95%CI (2.49, 3.12), P=0.036]. Conclusions Plasma GLP-1 level is not a sensitive indicator of chronic inflammation and IR in patients with NAFLD. Patients with NAFLD are in an increased risk of atherosclerosis and CVD. It suggests that NAFLD might be involved in chronic inflammation and IR. Chronic inflammation can cause IR, and then chronic inflammation and IR can cause NAFLD and subclinical atherosclerosis. In return for this, NAFLD increases chronic inflammation and IR.
Objective To investigate the relationship between delayed diagnosis time (time from symptom onset to diagnosis) in patients with chronic obstructive pulmonary disease (COPD) and the burden of type 2 inflammation (defined as the persistent inflammatory status assessed by blood EOS counts, EOS%, and Fractional exhaled nitric oxide(FeNO) among other biomarkers).MethodsThis study was a single-center, observational study that included patients with COPD first diagnosis at the respiratory outpatient department of our hospital from June 2023 to December 2024. Asthma-COPD overlap (ACO) were identified according to the 2017 Spanish COPD guidelines. Clinical data were collected, including gender, age, delayed diagnosis time, acute exacerbations in the past year, pulmonary function tests, exhaled nitric oxide (FeNO), and type 2 inflammatory markers such as blood eosinophil counts (EOS). The correlation between the delayed diagnosis time and type 2 inflammation burden, as well as its influencing factors, were analyzed. Results A total of 195 patients were included, with 98 cases of COPD and 97 cases of ACO. The mean delayed diagnosis time was 18.0 (2.8, 37.5) months for the overall patients, 24.0 (1.0, 60.0) months for COPD, and 16.5 (3.0, 36.0) months for ACO, with no significant difference between the COPD and ACO groups (P>0.05). The median blood EOS counts, EOS%, andFeNO levels were 180 cells/μL, 1.9%, and 18 ppb in the COPD group, respectively, compared to 350 cells/μL, 4.7%, and 28 ppb in the ACO group, indicating higher type 2 inflammation levels in the ACO group (all P<0.001). A significant correlations were found between the disease course and the blood EOS counts and EOS% of the patients (respectively r=0.159, 0.152, all P<0.05).FeNO levels showed no significant correlation with delayed diagnosis time of COPD (P>0.05). Patients with a history of asthma and acute exacerbations in the past year had longer delayed diagnosis time and higher peripheral blood eosinophil counts (all P<0.05). Binary logistic regression analysis revealed that BMI and delayed diagnosis time were independent influencing factors for blood EOS counts (all P<0.05). ConclusionDelayed diagnosis of COPD was associated with aggravated type 2 inflammatory burden. Clinical practice should emphasize early recognition of COPD symptoms and implement prompt therapeutic interventions.
【Abstract】 Objective To investigate the effect of allogeneic bone marrow-derived mesenchymal stem cells ( BMSCs) transplantation on the airway inflammation and airway remodeling in chronic asthmatic mice. Methods Forty female BALB/c mice were equally randomized into four groups, ie. a normal control group, a BMSCs control group, an asthma model group, and a BMSCs transplantation group. BMSCs were generated from male donor mice, then the mice in the asthma model group and the BMSCs transplantation group were sensitized and challenged with OVA to establish chronic asthmatic mice model. Hematoxylin and eosin staining and Alcian blue-periodic acid-Schiff staining were used to analyze the effects on airway inflammation and airway remodeling after BMSC engraftment. The number of CD4 + CD25 + regulatory T cells in spleen was detected by flow cytometry. Results In lungs of the asthmamodel group, there were intensive inflammatory cells infiltration around airway and blood vessels, goblet cell proliferation, epithelial desquamation, patchy airway occlusion by hyperviscous mucus, and hypertrophy of airway smooth muscle.Airway inflammation and airway remodeling were significantly relieved in the BMSCs transplantation group.There was no obvious inflammatory cells infiltration in the airway and airway remodeling both in the normal control group and the BMSCs control group. The number of CD4 + CD25 + regulatory T cells in spleensignificantly decreased in the asthma model group compared with the two control groups ( P lt; 0. 05) , and significantly increased in the BMSCs transplantation group compared with the asthma model group ( P lt;0. 05) . There was no significant difference in the number of CD4 + CD25 + regulatory T cells in spleen betweenthe control groups and the BMSCs transplantation group. Conclusion BMSCs engraftment can up-regulate CD4 + CD25 + regulatory T cells and relieve airway inflammation and airway remodeling in asthmatic mice.
ObjectiveTo summarize the research progress of mesenchymal stem cells derived exosomes (MSCs-EXOs) in wound repair in recent years.MethodsThe literature about the role of MSCs-EXOs in wound repair at home and abroad was extensively consulted. The mechanism of MSCs-EXOs in wound repair and its clinical application prospects were summarized and analyzed.ResultsMSCs-EXOs can inhibit early inflammatory reaction, promote angiogenesis, proliferation, and migration of epithelial cells, regulate collagen synthesis, and inhibit scar proliferation in the later stage of wound healing. Compared with MSCs, MSCs-EXOs have many advantages, such as high stability, easy storage, non-tumorigenicity, no proliferation, easy quantitative use, and so on. It has broad clinical application prospects.ConclusionMSCs-EXOs can promote wound repair and hopefully develop into a clinical product to promote the repair of acute or chronic wounds.
Aortic dissection is one of the most devastating cardiovascular diseases. One of the most important pathological features of aortic dissection is local inflammatory response, including the infiltration of inflammatory cells, extracellular matrix degradation, and smooth muscle cell phenotype switch. Macrophages which are the core of the inflammatory response play an extremely pivotal role in the progression of inflammation and tissue remodeling. Macrophages can be artificially divided into M1 and M2 types, of which the M1-type promotes inflammation while the M2-type is associated with the regression of inflammation and tissue healing. Mastering the switch of phenotypic transformation of macrophages may be of great help in inhibiting the inflammation of aortic tissue and facilitating tissue healing, as well as the treatment of aortic dissection. In this paper, we focus on the polarization of macrophages and discuss the role of macrophages in aortic dissection, the polarization pathway and the effect of related polarizing agents on the treatment of aortic dissection.
The aim of the study is to identify the effects and underlying mechanisms of visfatin on inflammation and necroptosis in vascular endothelial cells. Human umbilical vein endothelial cells (HUVECs) were stimulated with visfatin or pretreated with Polyinosinic acid (LOX-1 inhibitor). By using the Western blot, RT-PCR, immunocytochemistry, enzyme-linked immunosorbent assay (ELISA), MTT and flow cytometry technique, the occurrence of inflammation and necroptosis in HUVECs were evaluated. Our results showed that 100 ng/mL visfatin significantly increased the mRNA and protein expression of monocyte chemotactic protein 1 (MCP-1) and LOX-1 after 24 hours’ treatment in HUVECs. However, pretreatment with Polyinosinic acid could significantly reduce the expression of MCP-1 compared with visfatin group. Additionally, 100 ng/mL visfatin could induce the production of necrotic features and increase the mRNA expression of BMF (one of the markers of necroptosis), while pretreating with Polyinosinic acid markedly downregulated the mRNA expression of BMF gene and promoted the cell proliferation. These results indicate that visfatin might induce inflammation and necroptosis via LOX-1 in HUVECs, suggesting that visfatin plays a central role in the development of atherosclerosis.
Objective To explore the association between the preoperative systemic immune-inflammation index (SII) and prognosis in non-small cell lung cancer (NSCLC) patients. Methods A comprehensive literature survey was performed on PubMed, Web of Science, EMbase, The Cochrane Library, Wanfang, and CNKI databases to search the related studies from inception to December 2021. The hazard ratio (HR) and 95% confidence interval (CI) were combined to evaluate the correlation of the preoperative SII with overall survival (OS), disease-free survival (DFS), and recurrence-free survival (RFS) in NSCLC patients. Results A total of 11 studies involving 9 180 patients were eventually included. The combined analysis showed that high SII levels were significantly associated with worse OS (HR=1.61, 95%CI 1.36-1.90, P<0.001), DFS (HR=1.50, 95%CI 1.34-1.68, P<0.001), and RFS (HR=1.17, 95%CI 1.04-1.33, P<0.001). Subgroup analyses also further verified the above results. Conclusion Preoperative SII is a powerful prognostic biomarker for predicting outcome in patients with operable NSCLC and contribute to prognosis evaluation and treatment strategy formulation. However, more well-designed and prospective studies are warranted to verify our findings.