Previous studies have shown that fibroblast growth factor 13 is downregulated in the brain of both Alzheimer’s disease mouse models and patients,and that it plays a vital role in the learning and memory.However,the u...Previous studies have shown that fibroblast growth factor 13 is downregulated in the brain of both Alzheimer’s disease mouse models and patients,and that it plays a vital role in the learning and memory.However,the underlying mechanisms of fibroblast growth factor 13 in Alzheimer’s disease remain unclear.In this study,we established rat models of Alzheimer’s disease by stereotaxic injection of amyloid-β(Aβ_(1-42))-induced into bilateral hippocampus.We also injected lentivirus containing fibroblast growth factor 13 into bilateral hippocampus to overexpress fibroblast growth factor 13.The expression of fibroblast growth factor 13 was downregulated in the brain of the Alzheimer’s disease model rats.After overexpression of fibroblast growth factor 13,learning and memory abilities of the Alzheimer’s disease model rats were remarkably improved.Fibroblast growth factor 13 overexpression increased brain expression levels of oxidative stress-related markers glutathione,superoxide dismutase,phosphatidylinositol-3-kinase,AKT and glycogen synthase kinase 3β,and anti-apoptotic factor BCL.Furthermore,fibroblast growth factor 13 overexpression decreased the number of apoptotic cells,expression of pro-apoptotic factor BAX,cleaved-caspase 3 and amyloid-βexpression,and levels of tau phosphorylation,malondialdehyde,reactive oxygen species and acetylcholinesterase in the brain of Alzheimer’s disease model rats.The changes were reversed by the phosphatidylinositol-3-kinase inhibitor LY294002.These findings suggest that overexpression of fibroblast growth factor 13 improved neuronal damage in a rat model of Alzheimer’s disease through activation of the phosphatidylinositol-3-kinase/AKT/glycogen synthase kinase 3βsignaling pathway.展开更多
The changes in the levels of serum interleukin-13 (IL-13) and nerve growth factor (NGF) in patients with systemic lupus erythematosus (SLE) and their clinical significance were investigated. Sandwich ELISA was used to...The changes in the levels of serum interleukin-13 (IL-13) and nerve growth factor (NGF) in patients with systemic lupus erythematosus (SLE) and their clinical significance were investigated. Sandwich ELISA was used to determine the levels of serum IL-13 and NGF in 35 SLE patients and 15 normal controls. The results showed that the levels of serum IL-13 (92.69±9.87 pg/ml) and NGF (339.69±25.60 pg/ml) in active SLE patients were significantly higher than those in inactive SLE patients (IL-13, 54.22±9.31 pg/ml; NGF, 300.89±33.51 pg/ml)(P<0.01). The inactive patients also had significantly increased serum levels of IL-13 and NGF as compared with normal controls (IL-13, 35.20±12.70 pg/ml; NGF, 111.40±32.54 pg/ml; P<0.05 and P<0.01, respectively). Spearman correlation analysis revealed that the serum IL-13 levels were correlated with disease activity index of SLE (SLEDAI), ESR and serum levels of C_3 (r= 0.813, 0.504, -0.605, respectively). The serum NGF levels were also correlated with above markers (r=0.442, 0.338, -0.463, respectively). The serum levels of IL-13 and NGF had a positive correlation (r=0.506, P<0.01). It was suggested that IL-13 and NGF might be involved in the pathogenesis of SLE and closely correlated with disease activity.展开更多
BACKGROUND： Inflammatory reaction correlates with sporadic intracranial aneurysm （IA）. Variation of tumor necrosis factor receptor superfamily 13B （TNFRSF13B）, an inflammatory mediator receptor, may associate wit...BACKGROUND： Inflammatory reaction correlates with sporadic intracranial aneurysm （IA）. Variation of tumor necrosis factor receptor superfamily 13B （TNFRSF13B）, an inflammatory mediator receptor, may associate with IA. OBJECTIVE： To explore the relationship between TNFRSF13B gene and sporadic IA, as well as the clinical characteristics of sporadic IA. DESIGN, TIME AND SETTING： Case-control study of genetic association was performed at the Experimental Technology Center of China Medical University from November 2006 to January 2008. PARTICIPANTS： A total of 367 patients with IA, confirmed by three-dimensional computed tomography angiography, magnetic resonance angiography, digital subtraction angiography, and neuro surgery, were admitted to the Department of Neurosurgery, First Affiliated Hospital of China Medical University from 2006 to 2007, and were selected as the case group. All patients were Han, with no family history of IA. In addition, a total of 396 non-lA patients were selected as control subjects. METHODS： Peripheral vein blood was harvested to extract whole blood genomic DNA. Genotyping and TNFRSF13B single nucleotide polymorphism （SNP） rs11078355 G〉A allele polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism. The relationship of TNFRSF13B SNP rs11078355 G〉A polymorphisms to IA and IA clinical characteristics were analyzed using the chi-square and two-sided test. MAIN OUTCOME MEASURES： TNFRSF13B SNP rs11078355 G〉A genotype distribution. RESULTS： In the IA patients, TNFRSF13B SNP rs11078355 G〉A genotype frequency was significantly increased （X2 = 16.306, odds ratio = 1.881,95% confidence interval = 1.382 2.560, P 〈 0.001）. In IA patients aged 〉 65 years, the frequency of TNFRSF13B SNP rs11078355 GA ＋ AA genotype was significantly greater than the GG genotype （X2 = 26.604, odds ratio = 5.248, 95% confidence interval = 2.662 10.345, P 〈 0.001）. CONCLUSION： The TNFRSF13B gene may associate with sporadic IA in Han Chinese populations In elderly patients, allele A may be an independent risk factor for IA, in addition to senile diseases, such as hypertension and diabetes mellitus.展开更多
目的:探究子痫前期患者血清胎盘蛋白-13(Placental protein 13,PP13)、基质金属蛋白酶抑制因子2(Tissue inhibitor of metalloproteinase,TIMP-2)、缺氧诱导因子-1α(Hypoxia inducible factor-1α,HIF-1α)水平与胎儿生长受限的相关性...目的:探究子痫前期患者血清胎盘蛋白-13(Placental protein 13,PP13)、基质金属蛋白酶抑制因子2(Tissue inhibitor of metalloproteinase,TIMP-2)、缺氧诱导因子-1α(Hypoxia inducible factor-1α,HIF-1α)水平与胎儿生长受限的相关性及临床意义。方法:选取2021年9月至2023年9月期间本院收治的94例子痫前期孕妇作为研究对象。根据孕妇分娩后胎儿的体重情况评估胎儿是否发生胎儿生长受限(Fetal growth restriction,FGR),将研究对象分为FGR组(n=31)和非FGR组(n=63)。另选取同期内的94例健康孕妇作为研究对象的对照组。对比三组血清PP13、TIMP-2、HIF-1α水平。分析血清PP13、TIMP-2、HIF-1α水平与FGR的相关性和独立影响因素。分析各指标对子痫前期患者FGR发生的预测价值。结果:FGR组的血清PP13水平明显低于非FGR组和对照组,非FGR组血清PP13水平低于明显对照组(P<0.05)。FGR组的血清TIMP-2和HIF-1α水平明显高于非FGR组和对照组,非FGR组的血清TIMP-2和HIF-1α水平明显高于对照组(P<0.05)。血清PP13水平与FGR发生呈负相关,血清TIMP-2、HIF-1α水平与FGR发生呈正相关(P<0.05)。血清PP13是FGR发生的独立保护因素,血清TIMP-2、HIF-1α是FGR发生的独立危险因素(P<0.05)。血清PP13、TIMP-2、HIF-1α水平联合预测FGR发生的曲线下面积(Area under the curve,AUC)明显大于各血清指标的单独预测(P<0.05)。结论:血清PP13、TIMP-2、HIF-1α水平与子痫前期患者FGR发生关系密切,各指标联合检测可为预测FGR发生提供有效参考。展开更多
目的 探讨血清孤独G蛋白偶联受体配体-13(solitary G protein-coupled receptor ligand-13,Apelin-13)、碱性成纤维细胞生长因子(fibroblast growth factor 2,FGF2)、中枢神经特异蛋白(central nervous system specific protein B,S100B...目的 探讨血清孤独G蛋白偶联受体配体-13(solitary G protein-coupled receptor ligand-13,Apelin-13)、碱性成纤维细胞生长因子(fibroblast growth factor 2,FGF2)、中枢神经特异蛋白(central nervous system specific protein B,S100B)水平与脑卒中后抑郁(post-stroke depression, PSD)的关系。方法 回顾性分析河南科技大学附属黄河医院/黄河三门峡医院2022年4月至2024年1月收治的260例脑卒中患者临床资料,随访1个月,参考17项汉密尔顿抑郁量表(Hamilton Depression Rating Scale, HAMD-17)评估结果统计PSD发生率,并将其分为发生组和未发生组,比较两组血清Apelin-13、FGF2、S100B水平及其他临床资料,采用Logistic回归模型分析PSD发生的影响因素;绘制受试者工作特征曲线(Receiver operating characteristic curve, ROC)评价血清Apelin-13、FGF2、S100B对PSD的预测价值。结果 PSD发生率为37.31%;与未发生组比较,发生组女性、糖尿病、左侧大脑半球病灶占比、美国国立卫生研究院卒中量表(national Institutes of health stroke scale, NIHSS)评分、同型半胱氨酸水平、系统性免疫炎症指数(systemic immune-inflammatory index, SII)、血清Apelin-13、S100B水平较高(P<0.05),月均可支配医疗费用、血清FGF2水平较低(P<0.05);月均可支配医疗费用(OR=0.732,95%CI:0.599~0.894)、左侧大脑半球病灶(OR=1.478,95%CI:1.159~1.885)、NIHSS评分(OR=1.293,95%CI:1.095~1.527)、同型半胱氨酸水平(OR=1.278,95%CI:1.058~1.542)、SII(OR=1.370,95%CI:1.133~1.657)、Apelin-13水平(OR=1.278,95%CI:1.086~1.503)、FGF2水平(OR=0.807,95%CI:0.689~0.946)、S100B水平(OR=1.357,95%CI:1.089~1.690)为PSD发生的影响因素(P<0.05);血清Apelin-13、FGF2、S100B联合预测PSD的灵敏度高于单独预测,曲线下面积(area under curve, AUC)高于单独预测方法(P<0.05),特异度与单独预测基本一致。结论 血清Apelin-13、FGF2、S100B水平与月均可支配医疗费用、左侧大脑半球病灶、NIHSS评分、同型半胱氨酸、SII可能是PSD发生的影响因素,且血清Apelin-13、FGF2、S100B可能对PSD有预测价值,其中联合预测价值更显著。展开更多
文摘Previous studies have shown that fibroblast growth factor 13 is downregulated in the brain of both Alzheimer’s disease mouse models and patients,and that it plays a vital role in the learning and memory.However,the underlying mechanisms of fibroblast growth factor 13 in Alzheimer’s disease remain unclear.In this study,we established rat models of Alzheimer’s disease by stereotaxic injection of amyloid-β(Aβ_(1-42))-induced into bilateral hippocampus.We also injected lentivirus containing fibroblast growth factor 13 into bilateral hippocampus to overexpress fibroblast growth factor 13.The expression of fibroblast growth factor 13 was downregulated in the brain of the Alzheimer’s disease model rats.After overexpression of fibroblast growth factor 13,learning and memory abilities of the Alzheimer’s disease model rats were remarkably improved.Fibroblast growth factor 13 overexpression increased brain expression levels of oxidative stress-related markers glutathione,superoxide dismutase,phosphatidylinositol-3-kinase,AKT and glycogen synthase kinase 3β,and anti-apoptotic factor BCL.Furthermore,fibroblast growth factor 13 overexpression decreased the number of apoptotic cells,expression of pro-apoptotic factor BAX,cleaved-caspase 3 and amyloid-βexpression,and levels of tau phosphorylation,malondialdehyde,reactive oxygen species and acetylcholinesterase in the brain of Alzheimer’s disease model rats.The changes were reversed by the phosphatidylinositol-3-kinase inhibitor LY294002.These findings suggest that overexpression of fibroblast growth factor 13 improved neuronal damage in a rat model of Alzheimer’s disease through activation of the phosphatidylinositol-3-kinase/AKT/glycogen synthase kinase 3βsignaling pathway.
文摘The changes in the levels of serum interleukin-13 (IL-13) and nerve growth factor (NGF) in patients with systemic lupus erythematosus (SLE) and their clinical significance were investigated. Sandwich ELISA was used to determine the levels of serum IL-13 and NGF in 35 SLE patients and 15 normal controls. The results showed that the levels of serum IL-13 (92.69±9.87 pg/ml) and NGF (339.69±25.60 pg/ml) in active SLE patients were significantly higher than those in inactive SLE patients (IL-13, 54.22±9.31 pg/ml; NGF, 300.89±33.51 pg/ml)(P<0.01). The inactive patients also had significantly increased serum levels of IL-13 and NGF as compared with normal controls (IL-13, 35.20±12.70 pg/ml; NGF, 111.40±32.54 pg/ml; P<0.05 and P<0.01, respectively). Spearman correlation analysis revealed that the serum IL-13 levels were correlated with disease activity index of SLE (SLEDAI), ESR and serum levels of C_3 (r= 0.813, 0.504, -0.605, respectively). The serum NGF levels were also correlated with above markers (r=0.442, 0.338, -0.463, respectively). The serum levels of IL-13 and NGF had a positive correlation (r=0.506, P<0.01). It was suggested that IL-13 and NGF might be involved in the pathogenesis of SLE and closely correlated with disease activity.
文摘BACKGROUND： Inflammatory reaction correlates with sporadic intracranial aneurysm （IA）. Variation of tumor necrosis factor receptor superfamily 13B （TNFRSF13B）, an inflammatory mediator receptor, may associate with IA. OBJECTIVE： To explore the relationship between TNFRSF13B gene and sporadic IA, as well as the clinical characteristics of sporadic IA. DESIGN, TIME AND SETTING： Case-control study of genetic association was performed at the Experimental Technology Center of China Medical University from November 2006 to January 2008. PARTICIPANTS： A total of 367 patients with IA, confirmed by three-dimensional computed tomography angiography, magnetic resonance angiography, digital subtraction angiography, and neuro surgery, were admitted to the Department of Neurosurgery, First Affiliated Hospital of China Medical University from 2006 to 2007, and were selected as the case group. All patients were Han, with no family history of IA. In addition, a total of 396 non-lA patients were selected as control subjects. METHODS： Peripheral vein blood was harvested to extract whole blood genomic DNA. Genotyping and TNFRSF13B single nucleotide polymorphism （SNP） rs11078355 G〉A allele polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism. The relationship of TNFRSF13B SNP rs11078355 G〉A polymorphisms to IA and IA clinical characteristics were analyzed using the chi-square and two-sided test. MAIN OUTCOME MEASURES： TNFRSF13B SNP rs11078355 G〉A genotype distribution. RESULTS： In the IA patients, TNFRSF13B SNP rs11078355 G〉A genotype frequency was significantly increased （X2 = 16.306, odds ratio = 1.881,95% confidence interval = 1.382 2.560, P 〈 0.001）. In IA patients aged 〉 65 years, the frequency of TNFRSF13B SNP rs11078355 GA ＋ AA genotype was significantly greater than the GG genotype （X2 = 26.604, odds ratio = 5.248, 95% confidence interval = 2.662 10.345, P 〈 0.001）. CONCLUSION： The TNFRSF13B gene may associate with sporadic IA in Han Chinese populations In elderly patients, allele A may be an independent risk factor for IA, in addition to senile diseases, such as hypertension and diabetes mellitus.
文摘目的:探究子痫前期患者血清胎盘蛋白-13(Placental protein 13,PP13)、基质金属蛋白酶抑制因子2(Tissue inhibitor of metalloproteinase,TIMP-2)、缺氧诱导因子-1α(Hypoxia inducible factor-1α,HIF-1α)水平与胎儿生长受限的相关性及临床意义。方法:选取2021年9月至2023年9月期间本院收治的94例子痫前期孕妇作为研究对象。根据孕妇分娩后胎儿的体重情况评估胎儿是否发生胎儿生长受限(Fetal growth restriction,FGR),将研究对象分为FGR组(n=31)和非FGR组(n=63)。另选取同期内的94例健康孕妇作为研究对象的对照组。对比三组血清PP13、TIMP-2、HIF-1α水平。分析血清PP13、TIMP-2、HIF-1α水平与FGR的相关性和独立影响因素。分析各指标对子痫前期患者FGR发生的预测价值。结果:FGR组的血清PP13水平明显低于非FGR组和对照组,非FGR组血清PP13水平低于明显对照组(P<0.05)。FGR组的血清TIMP-2和HIF-1α水平明显高于非FGR组和对照组,非FGR组的血清TIMP-2和HIF-1α水平明显高于对照组(P<0.05)。血清PP13水平与FGR发生呈负相关,血清TIMP-2、HIF-1α水平与FGR发生呈正相关(P<0.05)。血清PP13是FGR发生的独立保护因素,血清TIMP-2、HIF-1α是FGR发生的独立危险因素(P<0.05)。血清PP13、TIMP-2、HIF-1α水平联合预测FGR发生的曲线下面积(Area under the curve,AUC)明显大于各血清指标的单独预测(P<0.05)。结论:血清PP13、TIMP-2、HIF-1α水平与子痫前期患者FGR发生关系密切,各指标联合检测可为预测FGR发生提供有效参考。
