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：摘要急性肾损伤（AKI）在世界范围内具有较高的发病率和病死率，且是慢性肾脏病（CKD）和进展为终末期肾脏病的危险因素，给患者带来日益沉重的健康负担。成纤维生长因子23（FGF23）和a-Klotho（以下称“Klotho”）通路是近年来的研究热点。AKI发生后，血清中FGF23水平迅速上升，Klotho表达下降。这两种指标的变化被认为是预测AKI发生及预后的新型生物预测标志。本文围绕FGF23和Klotho在AKI中的表达改变和相关机制进行综述。

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：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：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：摘要目的探讨原发性胆汁性肝硬化（PBC）患者血清成纤维细胞生长因子19（FGF19）、人Klotho蛋白（Klotho）及成纤维细胞肾脏因子受体蛋白4（FGFR4）表达的意义。方法选择中国科学院大学宁波华美医院2017年8月至2020年7月收治的PBC患者63例作为PBC组，另选择该院同期健康体检者51例作为对照组。采用酶联免疫吸附法测定血清FGF19、Klotho蛋白和FGFR4蛋白表达水平。结果PBC组血清FGF19［（178.86±21.28）ng/L］、FGFR4蛋白［（2.96±0.47）ng/L］均高于对照组的（69.93±12.12）ng/L和（1.21±0.35）ng/L，Klotho蛋白［（3.25±0.89）μg/L］低于对照组的（9.67±1.53）μg/L（t=32.51、27.98、22.08，均P < 0.05）。PBC组血清丙氨酸氨基转移酶（ALT）［（84.25±13.24）U/L］、天门冬氨酸氨基转移酶（AST）［（71.82±10.35）U/L］、碱性磷酸酶（ALP）［（278.93±32.45）U/L］均高于对照组的（23.76±3.42）U/L、（23.10±4.53）U/L和（76.81±16.36）U/L（t=31.75、31.26、40.48，均P < 0.05）。经受试者工作特征（ROC）曲线分析显示，FGF19诊断PBC灵敏度为76.67%，特异度为61.90%；Klotho蛋白诊断PBC灵敏度为58.82%，特异度为66.67%；FGFR4蛋白诊断PBC灵敏度为54.55%，特异度为76.67%。经Pearson分析，FGF19与FGFR4蛋白呈线性正相关（r=0.78，P < 0.05），而Klotho蛋白与FGFR4蛋白呈线性负相关（r=-0.72，P < 0.05）。结论PBC患者血清FGF19和FGFR4蛋白水平升高，而Klotho蛋白水平降低，且FGF19与FGFR4蛋白呈线性正相关，而Klotho蛋白与FGFR4蛋白呈线性负相关，该研究具备显著创新性和科学性。

简介：摘要目的探讨miR-125在鼻咽癌组织中的表达及其调控肿瘤细胞生物学特性的可能机制。方法收集2018年6月至2019年6月上海交通大学附属第六人民医院南院收治的鼻咽癌患者癌组织及癌旁组织各30例，通过荧光定量PCR法检测miR-125和成纤维细胞生长因子2(FGF-2)mRNA的表达。鼻咽癌细胞CNE-2转染miR-125 mimic(miR-125 mimic组)，并设阴性对照组(NC组)。Transwell小室实验检测细胞侵袭能力；划痕愈合实验检测细胞迁移能力；WST-1用于评估细胞的增殖活力；流式细胞术和电镜观察分别用于检测细胞的凋亡和自噬；双荧光素酶报告分析miR-125靶标；Western blotting检测相关蛋白的表达情况。结果鼻咽癌组织中miR-125 mRNA的相对表达量为0.692±0.316，明显低于癌旁组织的1.501±0.748(t＝5.242，P<0.001)；鼻咽癌组织中FGF-2 mRNA的相对表达量为1.317±0.552，明显高于癌旁组织的0.783±0.241(t＝7.360，P<0.001)。miR-125 mimic组CNE-2细胞中miR-125 mRNA的表达量为4.091±0.145，显著高于NC组的0.993±0.137(t＝85.062，P<0.001)。miR-125 mimic组完成转染48、96 h后，CNE-2细胞的增殖活性均显著低于NC组(0.891±0.214 vs. 1.295±0.245，t＝6.802，P<0.001；0.934±0.208 vs. 1.488±0.269，t＝8.924，P<0.001)。miR-125 mimic组的穿膜细胞数和细胞的迁移率分别为(36 000±3 820)个和(39.4±6.5)%，均显著低于NC组的(74 000±7 500)个和(102.7±10.6)%(t＝24.728，P<0.001；t＝27.883，P<0.001)。miR-125 mimic组CNE-2细胞凋亡率为(22.5±1.4)%，显著高于NC组的(1.4±0.5)%(t＝77.740，P<0.001)，且miR-125 mimic组细胞凋亡蛋白Bax的相对表达量为0.983±0.158，显著高于NC组的0.418±0.122(t＝15.503，P<0.001)，Bcl-2的相对表达量为0.688±0.174，显著低于NC组的1.013±0.109(t＝8.670，P<0.001)。电镜观察到miR-125过表达的CNE-2细胞出现自噬现象，miR-125 mimic组自噬蛋白LC3Ⅱ/LC3Ⅰ相对表达量比值为2.517±0.209，显著高于NC组的1.238±0.135(t＝28.156，P<0.001)。miR-125 mimic组FGF-2蛋白的表达量为0.504±0.118，显著低于NC组的1.228±0.134(t＝22.210，P<0.001)。双荧光素酶报告证实FGF-2是miR-125的靶基因。FGF-2基因质粒和miR-125 mimic共转染的CNE-2细胞完成转染12、24、48及96 h细胞增殖活性均显著高于miR-125 mimic转染细胞(均P<0.05)，细胞凋亡率显著低于miR-125 mimic转染细胞[(6.2±1.5)% vs. (17.6±2.4)%，t＝22.062，P<0.001]。结论miR-125在鼻咽癌组织中表达下降，过表达miR-125可能通过下调FGF-2抑制鼻咽癌细胞CNE-2的增殖、迁移和侵袭，促进CNE-2的凋亡与自噬。

简介：AbstractStroke is a devastating disease that occurs when a blood vessel in the brain is either blocked or ruptured, consequently leading to deficits in neurological function. Stroke consistently ranked as one of the top causes of mortality, and with the mean age of incidence decreasing, there is renewed interest to seek novel therapeutic treatments. The Scavenger Receptor Class B type 1 (SR-B1) is a multifunctional protein found on the surface of a variety of cells. Research has found that that SR-B1 primarily functions in an anti-inflammatory and antiatherosclerotic capacity. In this review, we discuss the characteristics of SR-B1 and focus on its potential correlation with the modifiable risk factors of stroke. SR-B1 likely has an impact on stroke through its interaction with smoking, diabetes mellitus, diet, physical inactivity, obesity, hypercholesterolemia, atherosclerosis, coronary heart disease, hypertension, and sickle cell disease, all of which are critical risk factors in the pathogenesis of stroke.

简介：AbstractBackground:Hepatitis B core-related antigen (HBcrAg) is a promising disease-monitoring marker for chronic hepatitis B (CHB). We investigated correlations between HBcrAg with antiviral efficacy and virological and histological variables.Methods:One hundred and forty-five CHB patients from the mainland of China between August 2013 and September 2016 who underwent liver biopsy received entecavir therapy and had paired liver biopsy at 78 weeks. We analyzed correlations between HBcrAg and virological and histological variables in hepatitis B e antigen (HBeAg)-positive and HBeAg-negative patients. We also explored the predictors of HBeAg loss after 78 weeks of antiviral therapy. Pearson correlation analysis and logistic forward stepwise regression were the main statistic methods.Results:HBeAg-positive patients (n = 93) had higher baseline HBcrAg (median 7.4 vs. 5.3 log10 U/mL P < 0.001) and greater HBcrAg declines (median 1.6 vs. 0.9 log10 U/mL P= 0.007) than HBeAg-negative patients after 78 weeks of therapy. At baseline, HBcrAg correlated with hepatitis B virus (HBV) DNA in both HBeAg-positive (r = 0.641, P < 0.001) and -negative patients (r = 0.616, P < 0.001), with hepatitis B surface antigen (HBsAg) in HBeAg-positive patients (r = 0.495, P < 0.001), but not with anti-hepatitis B virus core antibody (anti-HBc). Weak correlations existed between HBcrAg, histology activity index (HAI; r = 0.232, P= 0.025), and Ishak fibrosis score (r= -0.292, P= 0.005) in HBeAg-positive patients. At 78 weeks, significant correlations existed only between HBcrAg and anti-HBc in HBeAg-positive (r = -0.263, P = 0.014) and HBeAg-negative patients (r= -0.291, P= 0.045). Decreased HBcrAg significantly correlated with reduced HBV DNA (r= 0.366, P= 0.001; r= 0.626, P < 0.001) and HBsAg (r = 0.526, P = 0.001; r = 0.289, P = 0.044) in HBeAg-positive and -negative patients, respectively, and with reduced HAI in HBeAg-positive patients (r = 0.329, P = 0.001). Patients with HBeAg loss (n = 29) showed a larger reduction in HBcrAg than those without (median 2.3 vs. 1.3 log10 U/mL, P = 0.001). In multivariate analysis, decreased HBcrAg was an independent predictor of HBeAg loss (P = 0.005).Conclusions:HBcrAg reflects viral replication and protein production. Decreased HBcrAg could predict HBeAg loss after antiviral therapy.Trial registration:Clinical Trials.gov: NCT01962155; https://www.clinicaltrials.gov/ct2/show/NCT01962155?term=NCT01962155&draw=2&rank=1

简介：摘要目的探讨2型糖尿病(T2DM)合并下肢动脉疾病(LEAD)患者血清成纤维细胞生长因子-23(FGF-23)与骨钙素的关系。方法选择2017年11月到2018年5月在哈尔滨医科大学附属第一医院内分泌科住院的T2DM患者178例。通过彩色多普勒超声评估下肢动脉粥样硬化斑块程度。根据LEAD的发生情况，将患者分为单纯糖尿病组(98例)、糖尿病合并LEAD组(80例)，根据血管病变严重程度将糖尿病合并LEAD组再分为非闭塞组(55例)、闭塞组(25例)。对所有患者的一般资料进行收集整理；对患者的糖化血红蛋白、血脂、尿素氮、肌酐等生化指标以及空腹C肽进行测定。使用ELISA法检测血清FGF-23及血清骨钙素含量。应用logistic回归分析探讨LEAD的危险因素。结果与单纯糖尿病组相比，糖尿病合并LEAD组年龄、血尿素氮、肌酐、尿酸、胆固醇、甘油三酯、空腹C肽、FGF-23水平均升高(t＝2.036～6.249，P均<0.01)，且糖尿病合并LEAD组高血压病史(χ2＝11.193，P＝0.001)、神经病变史(χ2＝10.382，P＝0.001)、饮酒史(χ2＝4.589，P＝0.032)、颈动脉彩超阳性率(χ2＝33.386，P<0.001)也较高；但骨钙素水平降低(χ2＝4.189，P<0.001)。与非闭塞组相比，闭塞组骨钙素水平降低(t＝3.001，P<0.05)，FGF-23水平升高(t＝2.233，P<0.05)。Logistic回归分析发现，年龄(OR＝1.112，95% CI：1.041～1.188，P<0.05)、饮酒史(OR＝3.415，95% CI：1.116～10.452，P<0.05)、FGF-23(OR＝9.128，95% CI：3.610～23.080，P<0.05)、骨钙素(OR＝0.369，95% CI：0.223～0.612，P<0.05)和颈动脉粥样硬化(OR＝4.801，95% CI：1.552～14.855，P<0.05)是LEAD的独立影响因素。在整体和糖尿病合并LEAD组中，FGF-23水平与骨钙素水平均呈正相关(r＝0.327、0.585，P均<0.001)。结论T2DM合并LEAD患者血清骨钙素水平降低、血清FGF-23水平升高，且与LEAD的严重程度相关。T2DM合并LEAD患者血清FGF-23与血清骨钙素水平呈正相关。

简介：摘要目的探讨慢性肾脏病(CKD)患者成纤维细胞生长因子23(FGF23)基因多态性与肾功能损伤、血管钙化的相关性。方法选择2016年1月至2019年1月收治的270例CKD患者作为研究对象，依据肾小球滤过率变化情况分为稳定组和恶化组，依据血管钙化与否分为钙化组和非钙化组。选择同期来本院体检的健康人群50例作为对照组。以酶联免疫吸附法测定血清FGF23水平，以Sequenom Massarray系统测定基因位点rs7955866、rs13312756、rs3812822进行基因分型，分析各组基因型、等位基因分布，并采用Spearman相关性分析等位基因频率与血清FGF23水平、肾功能损伤程度和血管钙化的相关性。结果CKD患者血清FGF23水平[(434.8±68.9)pg/mL]显著高于对照组[(300.5±34.4)pg/mL，t＝20.911，P<0.001]，对照组、稳定组[(345.6±38.8)pg/mL]、恶化组[(552.3±85.4)pg/mL]、非钙化组[(336.4±34.3)pg/mL]和钙化组[(561.4±89.3)pg/mL]的血清FGF23水平比较，差异有统计学意义(P<0.05)。对照组、稳定组、恶化组、非钙化组和钙化组在基因位点rs7955866(AA、AG、GG)、rs3812822(CC、CT、TT)的基因型及等位基因频率比较，差异具有统计学意义(P<0.05)，而各组在基因位点rs13312756(CC、CG、GG)的基因型及等位基因频率比较，差异无统计学意义(P>0.05)。rs7955866位点基因A、rs3812822位点基因C的频率，与血清FGF23水平、肾功能损伤程度及血管钙化情况呈正相关(P<0.05)。结论血清FGF23水平与CKD患者肾功能损伤、血管钙化进展呈正相关。FGF23基因位点rs7955866、rs3812822、rs13312756存在遗传变异，其中rs7955866位点基因A、rs3812822位点基因C是肾功能损伤和血管钙化的危险因素。

简介：AbstractChronic hepatitis B virus (HBV) infection remains a global health burden. Timely and effective antiviral therapy is beneficial for patients with HBV infection. With existing antiviral drugs, including nucleos(t)ide analogs and interferon-alfa, patients can achieve viral suppression with improved prognosis. However, the rate of hepatitis B surface antigen loss is low. To achieve a functional cure and even complete cure in chronic hepatitis B patients, new antivirals need to be developed. In this review, we summarized the advantages and disadvantages of existing antiviral drugs and focused on new antivirals including direct-acting antiviral drugs and immunotherapeutic approaches.

简介：AbstractGroup B streptococcus (GBS) is a leading cause of neonatal infection. Maternal vaginal-rectal colonization with GBS during the intrapartum period is a prerequisite for GBS early-onset disease (EOD). The obstetric measures for effective prevention of GBS EOD include universal prenatal screening by vaginal-rectal culture, correct specimen collection and processing, appropriate implementation of intrapartum antibiotic prophylaxis, and coordination with pediatric care providers. It is now recommended to universal screen GBS between 360/7 and 376/7 weeks of gestation and to identify groups of women who are eligible for intravenous intrapartum antibiotic prophylaxis as a means of preventing GBS EOD.