Objective To explore the effects of S100 calcium-binding protein A9 (S100A9) gene knockout on the phenotype of systemic lupus erythematosus (SLE) in mice and to clarify the role of S100A9 in the pathogenesis of SLE. Methods Ten female C57BL/6 wild-type and S100A9 knockout (S100A9-KO ) mice were selected, with five wild-type and five S100A9-KO B6 mice receiving imiquimod (IMQ) cream to establish SLE mouse model. The other five wild-type and five S100A9-KO B6 mice were treated as control groups by wiping the skin of the right ear with a cotton swab. After 8 weeks, the mice were sacrificed. The serum was collected from each mouse to detect the levels of anti-double-stranded DNA (dsDNA) antibodies, immunoglobulin G (IgG), B cell activating factor (BAFF), and interleukin 6 (IL-6) using ELISA. The levels of serum creatinine were determined using a sarcosine oxidase method. Urine was collected to measure urinary protein concentration. Kidneys were collected and stained with hematoxylin and eosin (H&E) for evaluating histological changes. Results After IMQ treatment, the length and weight of spleen, levels of serum creatinine, anti-dsDNA antibodies, IgG, BAFF, IL-6, and urinary protein in the IMQ B6 group and IMQ S100A9-KO B6 group were significantly higher than those of the control groups. Lupus-like changes including increased glomerular volume and tubular epithelial swelling were observed in kidneys from the IMQ and IMQ S100A9-KO groups. However, compared with the IMQ B6 group, the IMQ S100A9-KO B6 group exhibited milder levels of serum and urine indicators as well as the lupus-like symptoms. Conclusion IMQ could induce lupus-like symptoms in both wild-type B6 mice and S100A9-KO B6 mice, but the lesions in S100A9 knockout mice are milder. Theses results suggested that S100A9 is involved in and promotes the pathogenesis of SLE.
Animals ; Lupus Erythematosus, Systemic/chemically induced* ; Female ; Calgranulin B/genetics* ; Mice, Knockout ; Mice, Inbred C57BL ; Phenotype ; Mice ; Interleukin-6/blood* ; Disease Models, Animal ; Antibodies, Antinuclear/blood* ; B-Cell Activating Factor/blood* ; Immunoglobulin G/blood* ; Kidney/pathology*

Objective To evaluate the impact of the growth speed of cerebral infarction on the occurrence of symptomatic intracranial hemorrhage(sICH)in patients with acute anterior circulation ischemic stroke after mechanical thrombectomy.Methods The clinical data of patients with acute ischemic stroke(AIS),who received mechanical thrombectomy at the First Affiliated Hospital of Soochow University of China from June 2016 to December 2022,were retrospectively analyzed.After thrombectomy,the patients were divided into sICH group and non-sICH group according to Heidelberg criteria.The clinical data and imaging findings were compared between the two groups.Multivariate logistic regression analysis was used to identify the independent risk factors for sICH after thrombectomy,and the area under the receiver operating characteristic curve(AUC)was used to evaluate the efficacy of the growth speed of cerebral infarction in predicting sICH.Results A total of 218 patients were enrolled in this study,sICH group had 23 patients and non-sICH group had 195 patients.The differences in NIHSS score,collateral circulation status,core infarction volume,and growth speed of cerebral infarction between the two groups were statistically significant(all P＜0.05).Multivariate logistic regression analysis showed that rapid growth speed of cerebral infarction was an independent risk factor for sICH occurring after mechanical thrombectomy.For predicting sICH,the sensitivity and specificity of the growth speed of cerebral infarction were 78.3％and 69.7％respectively,with an AUC of 0.751 and a predicted value of 7.6 mL/h.Conclusion The rapid growth speed of cerebral infarction is a predictive factor for sICH occurring after mechanical thrombectomy in patients with acute anterior circulation ischemic stroke.The risk of sICH becomes higher after mechanical thrombectomy when the growth speed of cerebral infarction is faster than 7.6 mL/h.

Objective:To investigate the effect of 5F on proliferation and apoptosis of human pancreatic cancer.Methods:The pcDNA3.1-PUMAAS and pcDNA3.1 were transfected into AsPC-1 cells by Lipofectamine 2000 methods,stable transfected clony was chosen through G418.AsPC-1 cells were divided into three groups:transfected pcDNA3.1-PUMAAS,transfected pcDNA3.1 and control group without transfection AsPC-1 cells.Three groups was treated with serial concentrations(8.875,37.5,142?mol/L,respectively)of 5F 10?L.MTT assay was used to observe the inhibitory actions of 5F on AsPC-1 cells.The apoptotic rate of the cells was detected by flow cytometry.And the apoptosis was assessed by Hoechst 33258 dye staining and TUNEL staining.The expression of PUMA protein was detected by Western blotting and RT-PCR.Results:The inhibitory action on cell growth was seen in AsPC-1 control cells and pcDNA3.1-cells dealing with 5F.It could also promote the occurrence of apoptosis.5F inhibited the proliferation of AsPC-1 cells in a concentration-dependent manner.The apoptosis induced by 5F was accompanied with the up-regulation of PUMA.In cells treated with 5F,the apoptosis rate decreased greatly and proliferation rate increased compared with the AsPC-1 control cells and pcDNA3.1-cells dealing with 5F.The expression of PUMA was decreased greatly comparing with pcDNA3.1-cells treated with 5F,Conclusion:5F can depress the proliferation of AsPC-1 cell in vitro,mainly through the induction of apoptosis,and it was a potential agent for pancreatic cancer chemotherapy,the mechanism was probably related to its effect on the regulation of PUMA expression.