Objective:To investigate the potential of praeruptorin A (PA) in alleviating inflammatory damage in sepsis through the inhibition of ferritin expression.Methods:C57BL/6 mice were intraperitoneally injected with lipopolysaccharide (LPS) to establish the model of sepsis. After 6 and 12 h of PA intervention, serum levels of inflammatory cytokines IL-6 and TNF-α were measured by ELISA. Kidney tissues were collected at 72 h for HE staining to assess inflammatory cell infiltration and tissue damage. Human neutrophils were divided into four groups: control, LPS, ferritin, and LPS+ ferritin groups. After 12 h of intervention, qRT-PCR was used to detect the expression of IL-6 and TNF-α mRNA. In order to observe the effect of PA on the expression of inflammatory cytokines and ferritin, human neutrophils were grouped into control, LPS, and LPS+ PA (2/3/4 μmol/L) groups. After 12 h of intervention, qRT-PCR was performed to measure the expression of IL-1β, IL-6, TNF-α, and ferritin mRNA; ELISA was used to quantify the levels of IL-1β, IL-6, and TNF-α in culture supernatants; Western blot was used to analyze the expression of ferritin. Molecular docking was conducted to verify interactions between PA and ferritin.Results:Significant inflammatory cell recruitment, tissue damage, and elevated serum levels of IL-6 and TNF-α ( P<0.01) were observed in mice with LPS-induced sepsis. PA significantly inhibited cytokine secretion ( P<0.01) and alleviated tissue injury in sepsis mice. In human neutrophil models, ferritin upregulated the expression of IL-6 and TNF-α mRNA ( P<0.01); LPS stimulation alone increased the expression of IL-1β, IL-6, TNF-α, and ferritin at both mRNA and protein levels ( P<0.01), while co-stimulation with PA (3/4 μmol/L) significantly reversed the aforementioned results ( P<0.01). Molecular docking confirmed there were interaction sites between PA and ferritin. Conclusion:PA inhibits the release of inflammatory cytokines and alleviates tissue damage in sepsis, and the potential mechanism may involve modulating ferritin expression to suppress inflammatory responses.

Objective:To investigate the potential of praeruptorin A (PA) in alleviating inflammatory damage in sepsis through the inhibition of ferritin expression.Methods:C57BL/6 mice were intraperitoneally injected with lipopolysaccharide (LPS) to establish the model of sepsis. After 6 and 12 h of PA intervention, serum levels of inflammatory cytokines IL-6 and TNF-α were measured by ELISA. Kidney tissues were collected at 72 h for HE staining to assess inflammatory cell infiltration and tissue damage. Human neutrophils were divided into four groups: control, LPS, ferritin, and LPS+ ferritin groups. After 12 h of intervention, qRT-PCR was used to detect the expression of IL-6 and TNF-α mRNA. In order to observe the effect of PA on the expression of inflammatory cytokines and ferritin, human neutrophils were grouped into control, LPS, and LPS+ PA (2/3/4 μmol/L) groups. After 12 h of intervention, qRT-PCR was performed to measure the expression of IL-1β, IL-6, TNF-α, and ferritin mRNA; ELISA was used to quantify the levels of IL-1β, IL-6, and TNF-α in culture supernatants; Western blot was used to analyze the expression of ferritin. Molecular docking was conducted to verify interactions between PA and ferritin.Results:Significant inflammatory cell recruitment, tissue damage, and elevated serum levels of IL-6 and TNF-α ( P<0.01) were observed in mice with LPS-induced sepsis. PA significantly inhibited cytokine secretion ( P<0.01) and alleviated tissue injury in sepsis mice. In human neutrophil models, ferritin upregulated the expression of IL-6 and TNF-α mRNA ( P<0.01); LPS stimulation alone increased the expression of IL-1β, IL-6, TNF-α, and ferritin at both mRNA and protein levels ( P<0.01), while co-stimulation with PA (3/4 μmol/L) significantly reversed the aforementioned results ( P<0.01). Molecular docking confirmed there were interaction sites between PA and ferritin. Conclusion:PA inhibits the release of inflammatory cytokines and alleviates tissue damage in sepsis, and the potential mechanism may involve modulating ferritin expression to suppress inflammatory responses.

Objective:To examine the factors that contribute to memory impairment in elderly stroke patients and develop a predictive model.Methods:One hundred stroke patients from the First People's Hospital of Changzhou were selected to assess the incidence of memory impairment using the Montreal cognitive assessment memory index score(MoCA-MIS).Univariate analysis and multivariate Logistic regression were performed to determine the factors influencing memory impairment in these patients.Additionally, the correlation among relevant scale scores was examined, and a prediction model was developed.Results:In the study, 49 patients(49.0%)did not exhibit memory impairment.Patients with memory impairment were found to have higher proportions of individuals over 75 years old, elevated levels of triglyceride(TG), total cholesterol(TC), low-density lipoproteins cholesterol(LDL-C), and National Institute of Health Stroke Scale(NIHSS)scores compared to those without memory impairment.Conversely, patients without memory impairment had higher proportions of individuals with more than 9 years of education, higher levels of high-density lipoprotein cholesterol(HDL-C), mini-mental state examination(MMSE)scores, Rivermead behavioural memory test-Ⅱ(RBMT-Ⅱ)scores, and picture-based memory impairment screen(PMIS)scores(all P<0.05).Furthermore, Montreal cognitive assessment-memory index(MoCA-MIS)scores in stroke patients with memory impairment showed negative correlations with NIHSS scores, TG, and LDL-C, while showing positive correlations with HDL-C, MMSE scores, RBMT-Ⅱ scores, and PMIS scores(all P<0.05).Multifactorial Logistic regression analysis indicated that years of education, TG, HDL-C, NIHSS score, MMSE score, RBMT-Ⅱ score, PMIS score, and the location of the lesion in the cortex or temporal lobe were significant factors influencing memory impairment in stroke patients(all P<0.05).The receiver operating characteristic curve(ROC)analysis revealed an area under curve(AUC)of 0.955(95% CI: 0.921-0.977)for the prediction model of memory impairment in stroke patients, with a Yoden index of 0.841. Conclusions:The risk of memory impairment in stroke patients is associated with education years and blood lipid levels.Factors such as high education level, active cognitive function, and memory training serve as protective factors against memory impairment.The prediction model developed using these influencing factors demonstrates high predictive accuracy for post-stroke memory impairment.

ObjectiveTo explore the features and assessment for far space neglect in left spatial neglect patients after right brain stroke. MethodsFrom January to October, 2021, 30 left unilateral spatial neglect (USN) patients after right stroke (patients, n = 30) from Beijing Bo'ai Hospital and healthy volunteers matching with gender, age and level of education (controls, n = 30) were evaluated with line cancelation (LC), star cancelation (SC) and line bisection (LB) tests, nearly and far away. The 25 controls were evaluated with LB on the second day. ResultsNo line or star was omissed in the controls. Both the deviation and percentage were more in the patients than in the controls (|t| > 4.319, P < 0.001). Both the deviation and percentage were less different for all the test (|Z| < 1.638, t = -1.282, P > 0.05) between nearly and far away, except the deviation of LB (t = -4.994, P < 0.001). The ICC of test-retest was above 0.462 (P < 0.01). ConclusionRight brain stroke patients with USN may present far spatial neglect, which can be assessed with LB.

Objective:To test the utility of monofilament cutaneous threshold testing among patients with impaired touch sensation caused by central nervous system injury.Methods:Thirty stroke survivors and 30 patients with spinal cord injury were recruited. Monofilament threshold testing and cotton wool tests were performed on the bilateral forehead, face, palms and dorsum of feet among the stroke survivors. Among those with a spinal cord injury both tests were performed on each side of the L 4, L 5 and S 1 vertebrae. One week later, all were retested. Intra-class correlation coefficients (ICCs) were used to quantify the test-retest reliability of the tests. Kappa values were calculated to determine the degree of agreement between them. Stepwise multiple linear regressions were evaluated to examine the relationship between touch perception thresholds and age, height, gender, type of injury and injured site. Results:①The ICC for the monofilament test was between 0.74 and 0.95, higher than that of the cotton wool test (ICC: 0.60 to 0.83). ②The kappa value between the monofilament and cotton wool tests was 0.550, indicating good agreement. ③The types of injury and injured sites were independent correlates of the touch perception thresholds, but there was no significant correlation between the touch perception thresholds and age, height, gender or group.Conclusions:The monofilament cutaneous threshold test has good test-retest reliability, better than the cotton wool test. Therefore, it may be useful as a tool for assessing impaired touch sensation caused by central nervous system injury.

Objective To explore the relationship between positive rate of de novo donor specific antibody (dnDSA ) and human leukocyte antigen (HLA ) mismatch after kidney transplantation and explore the impact of dnDSA upon long-term graft survival and rejection .Methods Retrospective analysis was conducted for clinical data of 101 kidney transplant recipients .Based upon HLA antibody and dnDSA ,they were divided into three groups of HLA-(n=70) ,dnDSA- (n=23) and dnDSA+(n=8) .Rejection and graft survival were recorded for evaluating the impact of dnDSA on rejection and graft survival and observing the differences among all groups .Results The mismatchs of HLA-A/B and HLA-DR were more frequent than HLA-and dnDSA-groups(P=0 .047 , P=0 .010)and graft survival was lower in dnDSA+ group than HLA-and dnDSA-groups (P=0 .001) .The rejection rate was higher in dnDSA+ group (62 .5％ ) than HLA- group (8 .57％ ) and dnDSA-group (8 .69％ ) . The difference was statistically significant (P=0 .013) . Pathological examination indicated microcirculatory inflammation (glomerulonephritis & trichodangiitis ) and damage (multilayer change of capillary basement membrane) occurred frequently in dnDSA + group and C4d remained positive . However ,scar ,arterial fibrosis or tubulointerstitial inflammation was not correlated with dnDSA . Conclusions HLA mismatch is correlated with dnDSA positivity . And dnDSA may reduce graft survival and enhance rejection rate . Rejection mediated by dnDSA is often accompanied by microcirculatory inflammation and C4d positivity .