简介:摘要目的分析儿童急性偏瘫患者与正常对照之间血清成纤维细胞生长因子水平的差异。方法应用酶联免疫吸附双抗体夹心法(ELISA)检测52例儿童急性偏瘫患者(感染23例,颅脑损伤18例,脑血管11例)及50例健康对照者的血清b-FGF水平。结果疾病组和对照组血清b-FGF水平差异有统计学意义(P<0.05)。不同病因的急性偏瘫患者组间血清b-FGF水平差异无统计学意义(P>0.05)。结论儿童急性偏瘫患者血清b-FGF明显升高,恢复期更为显著,提示b-FGF等细胞因子可能在血管炎症反应/局部脑血管闭塞及血管闭塞后新生血管形成等儿童急性偏瘫的病理机制中具有重要作用。
简介:AbstractFibroblast growth factor 21 (FGF21) is a fasting or stress inducible metabolic hormone produced mainly in the liver. It plays important roles in regulating both glucose and lipid homeostasis via interacting with a heterodimeric receptor complex comprising FGF receptor 1 (FGFR1) and β-klotho (KLB). For the past decade, great effort has been made on developing FGF21 derivatives or specific FGF21 receptor agonists into therapeutic agents for various metabolic disorders including type 2 diabetes (T2D), obesity, and more importantly, nonalcoholic fatty liver disease (NAFLD). Here we have reviewed FGF21 gene and protein structures, its expression pattern, cellular signaling cascades that mediate FGF21 production and function. We have then summarized the six clinical trials utilizing four FGF21 analogues. Finally, two recent literatures on the development of GLP-1 and FGF21 dual agonists were presented briefly.
简介:AbstractObjective:To explore the levels of fibroblast growth factor 23 (FGF23) during pregnancy and its relationship with intrauterine growth restriction (IUGR).Methods:Pregnant rats were classified into an ad libitum rat chow group (ad libitum rat chow, AD group, n = 25) and an undernutrition group (50% of their daily food requirement, UN group, n= 25). The levels of maternal serum FGF23, tissue homogenate FGF23, and bone gla protein in fetal rats, and placental FGF23 mRNA and protein expression were examined by enzyme-linked immunosorbent assay, real-time qPCR analysis respectively. Finally, the effect of recombinant FGF23 on the viability of MG-63 cells was determined by cell proliferation assay. Data were analyzed with independent two-tailed t test and one-way analysis of variance. Spearman rank-order correlation coefficients (continuous variables) was performed to determine the relationship of results.Results:The diet restriction induced IUGR in rat offsprings, and the UN group exhibited a significantly lower FGF23 level (P < 0.05, n= 5). The FGF23 level was increased and peaked in maternal serum on gestation day (GD) 15, but peaked in fetal and placenta on GD20. Moreover, the tissue homogenate levels of FGF23 and bone gla protein in fetal rats in both groups were positively correlated (r= 0.923, P < 0.05; r= 0.925, P < 0.05, respectively, n = 15), FGF23 was localized to both decidual and labyrinth zones, with remarkably higher expression on GD20, P < 0.05, n= 5. In vitro, recombinant human FGF23 enhanced MG-63 cell viability, P < 0.05, n= 5.Conclusion:Prenatal undernutrition could decrease the FGF23 expression in fetal rats caused by the mother through the placenta, and induced the IUGR and hindered the ossification. And the FGF23 levels are peaked on GD15 mother but peaked on GD20 placenta and fetuses, these might be associated with the over compensation of maternal placenta on GD20.
简介:AbstractIn the past decades, skeletal muscle has become the focus of numerous studies due to its potential physiological role as an endocrine organ secreting hundreds of myokines. Among these myokines, fibroblast growth factor 21 (FGF21) and irisin are novel hormone polypeptides sending signals to regulate the function of specific organs, like skeletal muscle, liver, pancreas, and adipose tissue. Both hormones have been reported to normalize glucose, improve insulin resistance, and promote lipid homeostasis, thereby preventing the development of metabolic disorders, such as obesity and diabetes. Besides preserving pancreatic β-cell functions, FGF21 also protects pancreatic acini from inflammation and reduces proteotoxic stress via facilitating digestive enzyme secretion. Meanwhile, irisin is found to inhibit the pancreatic cancer cell growth as well. This review attempts to focus on the current knowledge of FGF21 and irisin and their effective roles in pancreas including pancreatic β- and acinar cells under various physiological conditions, its anti-diabetic actions, and the clinical implications.
简介:摘要2例FGF12基因变异所致早发型婴儿癫痫性脑病患儿就诊年龄分别为4月龄(男)和2月龄(女),分别于2018年9月和2019年4月收入广州市妇女儿童医疗中心,均为新生儿期出现反复抽搐,主要表现为癫痫发作形式多样,恶化期为痉挛后强直,伴或不伴痉挛发作,另伴有喂养困难和运动发育迟缓以及难治性肺炎。2例患儿均有FGF12基因杂合变异,变异位点分别为p.R52H和p.R114H。1例患儿因重症肺炎死亡,1例患儿加用钠离子通道阻滞剂后癫痫控制,运动发育进步,脑电图好转。
简介:摘要对2020年2月在山东大学齐鲁儿童医院住院治疗的1例早发性癫痫性脑病患儿进行回顾性分析。患儿,女,4月龄时因"反复抽搐发作4个月、喂养困难1个月"入院。患儿出生1 d起病,发作类型为强直发作,发育严重落后,脑电图示多灶放电,后转为高度失律,头颅影像学阴性,3月龄时出现喂养困难。基因检测结果示FGF12基因新发杂合错义突变(Arg114His)。多种抗癫痫药物、生酮饮食治疗均无效,加用苯妥英钠后2个月未发作。患儿发作控制后可自行进食,但智力运动发育无进步。FGF12基因突变致早发性癫痫性脑病预后不佳,发作较难控制,应尽早应用苯妥英钠等钠离子通道阻滞剂。
简介:摘要目的分析微小RNA-203(microRNA-203,miR-203)和成纤维细胞生长因子-2(fibroblast growth factors-2,FGF-2)在儿童血管瘤(hemangioma of infancy,HOI)中的表达水平并探讨其临床意义。方法选取2016年3月至2017年8月收治的55例HOI患者为HOI组,并将其分为增殖期(31例)与消退期(24例),另以术后正常组织标本为对照组(34例)。采用实时荧光定量PCR(qRT-PCR)检测各组miR-203与FGF-2 mRNA表达水平,免疫组织化学法检测FGF-2蛋白表达情况。观察的临床指标包括血管生长素(angiogenin,ANG)、血管内皮生长因子(vascular endothelial growth factor,VEGF)、碱性成纤维细胞生长因子(basic fibroblast growth factor,bFGF)、糖皮质激素受体α(glucocorticoid receptor α,GRα)、糖皮质激素受体β(glucocorticoid receptor β,GRβ)。Pearson法比较分析HOI组患儿各指标间的相关性;Logistic多因素回归法分析HOI发生的相关影响因素。结果与对照组(1.01±0.15)相比,HOI组miR-203(0.73±0.24)表达水平显著降低(P<0.05),且增殖期(0.72±0.21)显著高于消退期(0.59±0.19)(P<0.05);HOI组FGF-2 mRNA(2.38±0.74)表达水平显著高于对照组(1.02±0.14)(P<0.05),且消退期(2.37±0.79)显著高于增殖期(2.03±0.68)(P<0.05);Pearson分析显示miR-203与FGF-2、ANG、VEGF、bFGF呈显著负相关(P<0.05),而FGF-2与之呈显著正相关(P<0.05);Logistic分析显示miR-203与FGF-2表达水平是HOI发生的影响因素。结论miR-203在HOI中低表达,而FGF-2呈高表达,两者在HOI分期中表达变化比较差异显著,对临床诊断HOI及治疗具有重要意义。
简介:目的探讨成纤维细胞生长因子-2(FGF-2)和拓扑异构酶Ⅱ(ToPoⅡ)在小细胞肺癌(SCLC)中的表达情况及二者的相关性。方法采用EnVision两步法检测64例SCLC组织、20例癌旁组织中FGF-2和ToPoⅡ蛋白的表达水平。采用Westernblotting、RT-PCR法检测外源性FGF-2对人SCLC细胞株NCL-H446中ToPoⅡ蛋白及mRNA表达水平的影响。结果SCLC组织中FGF-2和ToPoⅡ阳性表达率分别为68.75%(44/64)和79.69%(51/64),显著高于癌旁组织的15.0%和10.0%(P〈0.01);FGF-2和ToPoⅡ表达与淋巴结转移和临床分期密切相关(P〈0.05),与性别、年龄和吸烟情况无关(P〉0.05);两者表达在SCLC中呈正相关(r=0.497,P〈0.01)。FGF-2可以上调NCL-H446细胞中ToPoⅡ蛋白和mRNA的表达。结论FGF-2和ToPoⅡ之间可能存在共同作用通路,FGF-2可能通过ToPoⅡ促进SCLC的发生、发展。
简介:无
简介:摘要目的研究成纤维细胞生长因子4(FGF4)下调对人肺癌A549细胞增殖与凋亡的影响及其机制。方法采用免疫荧光技术检测A549细胞中FGF4蛋白的表达,设计并合成干扰FGF4表达的小干扰RNA(siFGF4),转染人肺癌A549细胞,将细胞分为3组:空白对照组、阴性对照组和siFGF4组,收集各组转染48 h细胞,CCK-8法检测细胞的增殖能力,流式细胞术检测细胞凋亡率,Hoechst 33258染色观查细胞凋亡,蛋白质印迹法检测Bcl-2和Bax的表达。结果CCK-8结果显示,siFGF4组细胞增殖能力明显受到抑制(51.10%±3.51%),与空白对照组(99.05%±3.11%)和siNC组(99.00%±3.59%)比较,差异有统计学意义(F=46.73,P<0.05)。流式细胞仪检测结果显示,siFGF4组细胞凋亡率为59.99%±5.52%,高于空白对照组(2.98%±2.24%)及siNC组(4.76%±2.05%),差异有统计学意义(F=67.54,P<0.01)。蛋白质印迹法结果显示,与空白对照组及siNC组相比,siFGF4组Bcl-2的蛋白表达水平明显降低(F=51.53,P<0.01),Bax的蛋白表达水平明显升高(F=41.33,P<0.05)。结论下调人肺癌A549细胞FGF4基因表达有望为肺癌基因靶向治疗提供新的靶位。
简介:摘要目的探讨代谢综合征(MS)患者血清成纤维细胞生长因子19(FGF19)水平的变化及其在诊断MS中的意义。方法将175例门诊及住院MS患者按代谢指标异常个数分为3个代谢指标异常组(Ⅲ组)、4个代谢指标异常组(Ⅳ组)、5个代谢指标异常组(Ⅴ组),分别为68、57、50例。40例体检正常人群作为正常对照组(NC组)。采用酶联免疫法测定各组血清FGF19浓度,同时测量身高、体重、腰围、血压,测定血脂、空腹及餐后2 h血糖、空腹胰岛素、血清C反应蛋白含量。采用多元逐步回归法分析FGF19相关影响因素,通过绘制ROC曲线确定FGF19在诊断MS中的阈值。结果NC、Ⅲ、Ⅳ、Ⅴ组受试者血清FGF19水平逐渐降低,差异均有统计学意义(P<0.05)。多元逐步回归分析显示,体重指数、血清总胆固醇、糖化血红蛋白、腰围是MS患者FGF19水平变化的独立影响因素(P<0.05)。ROC曲线分析显示,FGF19诊断代谢综合征的曲线面积为0.849(P<0.01),阈值为115.4 pg/ml,灵敏度为0.875,特异度为0.667。结论随着MS代谢异常指标个数的增多,FGF19水平降低,且与肥胖、糖脂代谢紊乱相关,可能是预测及诊断MS发病的指标。
简介:摘要成纤维细胞生长因子23(FGF23)是一种新型内分泌因子,主要在成骨细胞及骨细胞中表达,许多研究发现其与辅因子Klotho蛋白结合后可作用于肾脏、甲状旁腺等组织,参与骨矿物质代谢。不仅如此,近年来FGF23在骨骼外的作用也逐渐被发现,如FGF23与甲状腺疾病、糖尿病等。因此了解FGF23的生物学特征、调节机制以及其与相关疾病的关系,对疾病的诊断、治疗具有重要的临床意义。本文就FGF23与磷代谢性疾病、甲状旁腺功能亢进症、Groves病、骨质疏松症、糖尿病、铁代谢等代谢疾病的关系进行综述。
简介:目的:探讨结直肠癌组织中FGF20的表达及其与微血管密度之间的相关性。方法:免疫组织化学染色和WesternBlot方法检测结直肠癌组织及正常肠黏膜组织中FGF20的表达或CD34的表达,分析FGF20在癌组织及正常肠黏膜组织中的表达差异以及与临床病理之间的相关性,探讨FGF20的表达与结直肠癌组织中微血管密度的相关性。结果:免疫组织化学和WesternBlot结果均提示结直肠癌组织中FGF20表达显著高于正常肠黏膜组织(P〈0.01);癌组织中FGF20的表达与肿瘤浸润(P〈0.05)及淋巴结转移(P〈0.05)密切相关,与分化程度及肝转移无明显相关(P〉0.05);癌组织中FGF20的表达与癌组织中微血管密度呈显著正相关(P〈0.05)。结论:FGF20在结直肠癌微血管形成中发挥重要作用,进而促进结直肠癌的发生、发展及远处转移,为明确FGF20在结直肠癌微血管形成中的作用以及深入探讨FGF20促进微血管形成的分子机制提供实验依据。