母体缺氧诱导因子-1α水平及胎盘血流变化与胎儿生长受限的相关性

目的研究母体缺氧诱导因子-1α(HIF-1α)水平和胎盘血流量与胎儿生长受限(FGR)发生和发展的相关性。方法以2014年10月至2017年10月于该院就诊的60例FGR患者作为研究组,另取同期就诊的60例健康孕妇作为对照组,检测两组研究对象孕20、24、28、32、36周和分娩前母体静脉血及分娩时胎儿脐静脉血中HIF-1α水平,监测各时间节点胎盘血流搏动指数(PI)、血流阻力指数(RI)和脐动脉收缩期峰值与舒张末期流速比值(S/D)的动态变化,分析胎儿分娩后母体胎盘组织HIF-1α表达水平,统计孕妇妊娠不良事件发生情况。结果研究组孕妇孕20、24、28、32、36周和分娩前血清HIF-1α水平均明显高于对照组,差异均有统计学意义(P0.05);且研究组孕妇分娩后胎盘组织切片染色HIF-1α表达水平光密度值明显高于对照组,胎儿脐静脉血HIF-1α水平明显高于对照组,差异均有统计学意义(P0.05);两组孕妇胎盘动脉血流PI、RI和S/D均随孕周增加而呈逐渐减小趋势,且研究组孕妇孕20、24、28、32、36周和分娩前母体胎盘动脉血流PI、RI和S/D均明显高于对照组,差异均有统计学意义(P0.05);孕妇静脉血HIF-1α水平、胎儿脐静脉血HIF-1α水平、分娩后母体胎盘组织HIF-1α水平,胎盘血流PI、RI和S/D均与FGR呈正相关(P0.05);研究组孕妇妊娠不良反应事件总体发生率明显高于对照组,差异有统计学意义(P0.05)。结论孕妇HIF-1α水平升高及胎盘血流PI、RI和S/D升高会增加孕妇妊娠并发症和妊娠不良事件发生率。     

血管内皮生长因子、基质细胞衍生因子-1在胎儿生长受限体内的表达

目的:探讨血管内皮生长因子(VEGF)、基质细胞衍生因子-1(SDF-1)在胎儿生长受限(FGR)机制中的作用.方法:对正常足月妊娠孕妇(正常足月妊娠组)及FGR患者(FGR组)的胎盘行免疫组织化学检测VEGF、SDF-1表达水平.并同时检测相应孕妇体内血清VEGF、SDF-1浓度.结果:免疫组织化学结果显示正常足月妊娠组和FGR组胎盘组织滋养细胞中均有VEGF和SDF-1表达,VEGF、SDF-1的表达强度依次为0.25±0.00、0.20 ±0.00及0.21 ±0.00、0.13 ±0.00.正常足月妊娠组和FGR组孕妇血清中SDF-1、VEGF浓度水平依次为(289.12±30.41)、(120.53 ±32.58)和(524.07 ±43.51)、(257.46 ±40.51)pg/mL,显示正常足月妊娠组孕妇胎盘组织VEGF、SDF-1表达强度和体内VEGF、SDF-1表达水平均显著高于FGR组.结论:SDF-1及VEGF在维持正常妊娠方面发挥重要的作用,当 SDF-1及VEGF表达水平异常,可能出现FGR等病理妊娠情况.     

乙型肝炎相关肝细胞癌患者血清AFP、VEGF、AFU水平与微血管侵犯的相关性分析

目的 分析乙型肝炎相关肝细胞癌患者血清甲胎蛋白(AFP)、血管内皮生长因子(VEGF)、岩藻糖苷酶(AFU)水平及与微血管侵犯(MVI)的相关性.方法 选择2017年11月至2019年11月该院收治的乙型肝炎相关肝细胞癌患者235例,根据是否发生MVI分为MVI组(108例)和无MVI组(127例),同时根据MVI病理特征将MVI组患者分为低危组(M1期,20例)、中危组(M2期,31例)和高危组(M3期,57例),检测血清AFP、VEGF、AFU水平,采用Spearman相关分析乙型肝炎相关肝细胞癌患者血清AFP、VEGF、AFU水平与MVI的相关性,绘制受试者工作特征(ROC)曲线,分析血清AFP、VEGF、AFU诊断乙型肝炎相关肝细胞癌MVI的效能.结果 MVI组患者血清AFP、VEGF、AFU水平明显高于无MVI组患者(P<0.05);高危组患者血清AFP、VEGF、AFU水平明显高于低危组、中危组患者,中危组患者明显高于低危组患者(P<0.05);相关性分析显示,乙型肝炎相关肝细胞癌患者血清AFP、VEGF、AFU水平与MVI均呈正相关(P<0.05);ROC曲线分析显示,AFP、VEGF、AFU诊断乙型肝炎相关肝细胞癌患者发生MVI的曲线下面积(AUC)分别为0.867、0.924和0.904,3项指标联合检测的AUC为0.958,均高于单项指标检测.结论 乙型肝炎相关肝细胞癌患者血清AFP、VEGF、AFU水平明显上升,其水平与MVI呈正相关,联合检测血清AFP、VEGF、AFU对于诊断乙型肝炎相关肝细胞癌MVI具有较高的效能.     

肝细胞生长因子在胎儿生长受限孕妇胎盘组织的表达及其意义

目的：探讨肝细胞生长因子（HGF）在胎儿生长受限孕妇胎盘组织中的表达及其对胎盘滋养细胞凋亡的影响。方法：选取胎儿生长受限（FGR）孕妇42例及正常晚孕孕妇（对照组）38例,采用逆转录聚合酶联反应、免疫印迹的方法,检测胎盘组织中HGF和Fas基因mRNA及蛋白表达水平。结果：胎盘组织HGFmRNA和蛋白的表达水平,FGR组明显低于对照组（P〈0.05）;FasmRNA和蛋白在胎盘组织中的表达水平,FGR组明显高于对照组（P〈0.05）。胎盘HGF的表达与Fas的表达呈负相关。结论：胎盘组织HGF低表达和F as高表达可能是FGR胎盘滋养细胞凋亡的一个重要影响因素。     

孕妇血清IL-6、sVEGFR-1预测早发型胎儿生长受限最佳分娩时机的临床价值

目的筛查孕妇血清中与早发型胎儿生长受限(FGR)有关的细胞因子谱,并探讨血清白细胞介素-6(IL-6)、可溶性血管内皮生长因子受体-1(sVEGFR-1)与FGR胎儿最佳分娩时机的关系。方法选取2020年4-12月该院早发型FGR的单胎妊娠孕妇162例作为FGR组,另选取同期20例胎儿发育正常妊娠26~32周的孕妇作为对照组。方案1:随机选择FGR组与对照组各20份血清标本,采用Bio-Plex Pro悬液芯片技术检测血清细胞因子谱。方案2:将FGR组其余142例孕妇根据分娩时间分为诊断FGR 2周内分娩组(102例)和诊断FGR 2周后分娩组(40例),采用酶联免疫吸附试验检测血清细胞因子水平。采用Logistic回归模型分析血清细胞因子对FGR分娩时间的影响,采用受试者工作特征(ROC)曲线评估血清细胞因子谱预测FGR孕妇2周内分娩的价值。结果与FGR孕妇分娩时间相关的因素包括羊水过少、子痫前期、胎心监护异常、脐动脉或导管静脉舒张末期血流缺失/逆流;血清IL-6、sVEGFR-1、胎盘生长因子(PLGF)、可溶性CD40配体(sCD40L)、瘦素水平与早发型FGR孕妇分娩时机有关(P<0.05)。与诊断FGR 2周后分娩组相比,诊断FGR 2周内分娩组孕妇血清IL-6、sVEGFR-1、sCD40L、瘦素水平均升高,而血清PLGF水平降低(P<0.05);Logistic回归模型分析显示,血清IL-6、sVEGFR-1水平升高是早发型FGR 2周内分娩的独立影响因素(P<0.05)。ROC曲线分析结果显示,血清IL-6、sVEGFR-1单独和联合检测预测FGR 2周内分娩的曲线下面积分别为0.778(95%CI:0.693~0.864)、0.844(95%CI:0.780~0.908)、0.875(95%CI:0.815~0.936)。结论孕妇血清IL-6、sVEGFR-1水平升高分别与羊水过少及子痫前期相关,检测血清IL-6、sVEGFR-1水平可以预测早发型FGR最佳分娩时机。     

血管内皮生长因子与妊娠期糖尿病围产儿结局关系的研究

目的探讨妊娠期糖尿病孕妇(GDM)血清血管内皮生长因子(VEGF)水平与围产儿结局间的关系,并观察VEGF受体(VEGFR)在胎盘组织中的蛋白表达。方法招募在孕龄24～28周被诊断患有GDM的孕妇,总数为100例,另招募50例相应年龄的正常孕妇作为研究对照。抽取孕妇的血样,测量糖化指标:血糖、糖化血红蛋白(HbA1c)、VEGF。分娩后立即收集胎盘低温保存,用于分析组织中VEGFR蛋白的表达。并收集母婴临床信息,根据围产儿结局异常与否分为围产儿正常组和围产儿异常组。结果 (1)GDM组孕妇血清VEGF水平、HbA1c、空腹血糖值均明显高于正常孕妇组(P<0.05)。(2)同一GDM经干预治疗后妊娠晚期时血糖明显降低,HbA1c与对照组比较差异无统计学意义(P>0.05),但血清VEGF水平仍保持较高水平。(3)与围产儿正常的母亲相比,对于发生围产儿异常的GDM组母亲,二者血清当中的VEGF水平有显著性的差异(P<0.05)。(4)采用Logistic回归法对两组的VEGF表达水平进行分析,所得结果说明VEGF是GDM围产儿结局异常的危险因子(OR=5.196,P<0.001,95%CI:1.845～14.610)。(5)用Western印迹法测定胎盘组织中VEGFR蛋白表达量在GDM围产儿结局异常组亦较高。结论孕妇高VEGF血症是GDM围产儿结局的一个不利因素,高VEGF水平可作为GDM不良围产儿结局的预测指标。     

促血管生成素-2与胎儿生长受限发病的关系

目的:探讨促血管生成素-2(Ang-2)在母血、脐血血清中的水平和在胎盘组织上的表达与胎儿生长受限(FGR)发病的关系。方法:选取剖宫产分娩足月FGR患儿的孕妇30例作为实验组,同期剖宫产分娩正常足月婴儿的孕妇30例作为对照组。采用酶联免疫法(ELISA)测定母血和脐血血清中Ang-2的水平;采用免疫组织化学方法(SP法)检测孕妇胎盘组织中Ang-2的表达。结果:(1)实验组和对照组母血血清中Ang-2的水平分别为(8.86±0.43)ng/mL、(19.31±0.25)ng/mL。实验组和对照组脐血血清中Ang-2的水平分别为(10.92±0.41)ng/mL、(22.28±0.23)ng/mL;实验组和对照组胎盘组织中Ang-2的表达分别为118.17±1.59、151.64±1.64。实验组母血和脐血血清中Ang-2的水平和胎盘组织中Ang-2的表达均显著低于对照组(P<0.01)。(2)实验组胎盘组织中Ang-2的表达与母血血清Ang-2水平呈正相关(r=0.93,P<0.01);实验组胎盘组织中Ang-2的表达与脐血血清Ang-2水平呈正相关(r=0.93,P<0.01);母血血清中Ang-2水平与脐血血清中Ang-2水平呈正相关(r=0.99,P<0.01)。结论:母血和脐血血清中Ang-2水平均降低和胎盘组织中Ang-2表达降低可能参与了FGR的发病过程。     

PAPP-A、PLGF、sFlt-1预测妊娠期高血压疾病发病风险价值的研究

目的探讨妊娠相关蛋白A(PAPP-A)、胎盘生长因子(PLGF)、可溶性血管内皮生长因子(sFlt-1)在预测妊娠期高血压疾病发病风险中的价值。方法采用酶联免疫法(ELISA)检测66例孕妇不同孕周的血清PAPP-A、PLGF和sFlt-1水平。其妊娠期高血压组33例(观察组),正常妊娠组33例。采用荧光定量PCR及Western blot方法分别检测胎盘组织中PLGF、sFlt-1 mRNA及蛋白表达。结果在孕程的全部采血孕周,观察组孕妇血清sFlt-1水平均明显高于对照组,而PLGF均低于对照组。观察组各孕周内sFlt-1/PLGF均显著高于对照组。观察组胎盘组织sFlt-1 mRNA及蛋白表达水平明显高于对照组;PLGF mRNA及蛋白表达水平明显低于对照组。结论孕妇血清中PAPP-A、PLGF、sFlt-1水平变化能够作为诊断和预测妊娠期高血压疾病的临床客观指标。     

妊娠高血压综合征血管内皮生长因子表达与围产儿结局的关系

目的　探讨在妊娠高血压综合征 (简称妊高征 )发病中血管内皮生长因子 (VEGF)对围产儿结局的影响。方法　分别采用酶联免疫吸附试验检测 4 0例妊高征孕妇的静脉血VEGF水平 ,免疫组化检测胎盘及蜕膜组织VEGF及CD34表达情况 ,详细记录围产儿的情况。并以 35例正常孕妇作对照。结果　①妊高征组孕妇的外周血VEGF水平及胎盘组织微血管密度 (MVD)明显低于正常妊娠组 (P <0 . 0 5 ) ;②两组胎盘绒毛滋养叶细胞和蜕膜组织中均有VEGF阳性表达 ,胎盘组织强阳性表达高于蜕膜。轻度妊高征与对照组比较 ,其胎盘组织VEGF强阳性表达的差异无显著性意义 ;而中度和重度妊高征与对照组相比 ,VEGF强阳性表达明显降低 ,其差异有显著性意义 (P <0 .0 5 )。各组孕妇蜕膜组织中的VEGF的表达强度的差异无显著性意义 ;③孕妇外周血VEGF水平与新生儿评分有关 ,与新生儿出生体重 (r =0 . 2 9;P <0 . 0 5 )和胎盘重量 (r =0 34;P <0 . 0 1)均存在直线正相关关系 ;与胎儿胎龄无明显关系。结论　妊高征孕妇血清VEGF水平和胎盘组织MVD降低 ,胎盘组织VEGF表达明显下降 ,VEGF可能对围产儿的结局有一定影响。     

重度子痫前期孕妇血清Endocan 表达水平及其对胎儿生长受限的预测价值

目的 探讨重度子痫前期患者血清内皮细胞特异性分子(Endocan)表达水平对胎儿生长受限(fetal growthrestriction, FGR)的预测价值。方法 选取2020 年6 月~2021 年12 月于陕西省人民医院分娩的90 例重度子痫前期并发胎儿生长受限(FGR)孕妇为实验组,160 例重度子痫前期未并发FGR 孕妇为对照组。收集两组患者的临床资料,采用酶联免疫吸附法测定血清Endocan 的表达。采用Logistic 回归分析重度子痫前期FGR 发病的独立危险因素;采用ROC曲线分析Endocan 对重度子痫前期FGR 的预测价值。结果 实验组血清Endocan 表达(449.18±166.68pg/ml)显著高于对照组(331.44±63.07pg/ml),差异有统计学意义(t=7.99,P ＜ 0.05);Logistic 多因素回归分析,血清Endocan、舒张压及24h 尿蛋白是子痫前期FGR 发病的独立危险因素,这3 个危险因素联合检测对预测重度子痫前期孕妇FGR 发病的价值最高,ROC 曲线下面积为0.828(95%CI: 0.773~0.884)。结论 血清Endocan 是重度子痫前期FGR 发病的独立危险因素,其联合舒张压及尿蛋白检测对预测重度子痫孕妇FGR 的发病有一定价值。     

转化生长因子-β、碱性成纤维生长因子和血小板衍生生长因子在骨折愈合中的表达

目的:观察转化生长因子-β(TGF-β)、碱性成纤维细胞生长因子(bFGF)和血小板衍生生长因子(PDGF)在骨折愈合中的表达和分布情况,进而探讨其作用机制。方法:选用SD大鼠制作胫骨骨折愈合模型,伤后不同时期处死取材,分别进行组织学和TGF-β、bFGF和PDGF免疫组化染色观察。结果:(1)伤后3d开始形成原始骨痂。1周时肉芽组织中的间质细胞开始分化为软骨细胞,软骨形成后再进行软骨内化骨。4周时形成连接骨折端的桥接骨痂。(2)伤后早期血肿中炎性细胞表达bFGF、PDGF。伤后1周骨膜增殖细胞、肉芽组织中的成纤维细胞、内皮细胞、骨端骨细胞以及原始骨痂成骨细胞表达TGF-β、bFGF和PDGF。伤后2周软骨细胞表达TGF-β、bFGF和PDGF。结论:TGF-β、bFGF和PDGF有着各自的表达和分布特点,并共同调解骨原细胞的增殖和成骨细胞、软骨细胞的分化,最终完成骨折愈合。     

Detection of intrauterine growth retardation in twins using individualized growth assessment: I. Evaluation of growth outcome at birth.

The growth of 17 sets of twins was evaluated at 2 to 3 week intervals from 15 weeks to delivery by measurement of the head circumference, abdominal circumference, and thigh circumference, and estimation of weight. The birth characteristics of these twins were compared to those predicted by Rossavik growth models, derived from second-trimester ultrasound measurements, using the Growth Potential Realization Index (GPRI) and by comparison to population standards. Newborns were classified as normal or intrauterine growth retarded (IUGR) based on their Neonatal Growth Assessment Score, determined from GPRI values. All normal twins had birth weights that were appropriate-for-gestational-age and had few abnormal birth measurements. The birth weight differences between normal twin fetuses were all < 20%. IUGR twins were both small for gestational age (78%) and appropriate-for-gestational-age (22%), and all had 3 or 4 abnormal GPRI values. In only 40% of the cases was the birth-weight difference between a normal and an IUGR twin > 20%. No single anatomic parameter evaluated at birth adequately separated the normal twins from those with IUGR. These results indicate the need for multiple parameter Individualized Growth Assessment in the detection of IUGR in twins.     

抚触对早产儿体格发育及血生长激素、胰岛素样生长因子-1水平的影响

目的:观察抚触对早产儿体格发育及血生长激素、胰岛素样生长因子-1水平的影响。方法:收集病情平稳的住院早产儿58例,随机分为抚触组(28例)及对照组(30例),观察两组早产儿体重、身长、头围发育情况,测定两组生后第2 d及第30 d空腹血中生长激素、胰岛素样生长因子-1水平。结果:生后30 d抚触组体重及胰岛素样生长因子-1水平较对照组明显升高;而头围、身长及生长激素水平差异无统计学意义。结论:新生儿抚触有助于早产儿体重增长及胰岛素样生长因子的分泌。     

肥厚腰椎黄韧带中成纤维细胞生长因子、转化生长因子及结缔组织生长因子的表达

背景：腰椎黄韧带肥厚是临床上引起腰椎管狭窄的主要因素之一,但其分子机制仍不是非常清楚。目的：分析纤维化相关细胞因子碱性成纤维细胞生长因子、转化生长因子β1和结缔组织生长因子在腰椎黄韧带肥厚过程中的作用。方法：取临床手术所取黄韧带,对照组6例（椎管内占位且无腰椎不稳患者黄韧带）、突出组（单纯腰椎间盘突出症患者黄韧带）6例、腰椎管狭窄症组6例。采用实时定量RT-PCR的方法检测各组黄韧带中碱性成纤维细胞生长因子、转化生长因子β1、结缔组织生长因子及Ⅰ、Ⅲ、Ⅴ型胶原蛋白的mRNA含量,分析3个细胞因子在黄韧带肥厚过程中的作用。结果与结论：腰椎管狭窄症组碱性成纤维细胞生长因子mRNA表达均明显高于突出组和对照组（均P 〈0.05）;腰椎管狭窄症组转化生长因子β1mRNA在3组中的表达明显高于对照组和突出组（均P 〈0.01）;结缔组织生长因子 mRNA 3组间差异无显著性意义（P 〉0.05）。腰椎管狭窄症组Ⅰ型胶原蛋白mRNA表达明显高于突出组和对照组（均P 〈0.05）;Ⅲ型胶原蛋白、Ⅴ型胶原蛋白mRNA表达3组之间差异无显著性意义（P 〉0.05）。结果说明碱性成纤维细胞生长因子、转化生长因子β1在腰椎黄韧带肥厚形成过程中有重要作用,引起黄韧带肥厚的主要胶原产物为Ⅰ型胶原蛋白。     

Prediction of normal fetal growth by the Rossavik growth model using two scans before 27 weeks, menstrual age

Individual growth curve standards for five fetal anatomic parameters (head and abdominal circumferences, head and abdominal cubes, and femur diaphysis length) and estimated fetal weight were prospectively developed in 70 pregnant women who delivered infants with growth considered appropriate-for-menstrual age. For this purpose, we used the Rossavik growth model (P = c(t) kappa + s(t], model specification functions previously reported, and the data of two scans before 27.0 weeks of menstrual age, separated by an interval of at least 5 weeks. The anatomic parameters and estimated weights of these fetuses in the last 14 weeks of gestation were found to have values close to their projected standards. Whereas there was a significant, although small, systematic error of overprediction for most of the parameters and estimated fetal weight, deviations between observed and expected values were, with few exceptions, within the ranges established by Deter for normal growth. This study demonstrates that the Rossavik growth model could be used to predict normal fetal growth in a sample of patients different from those from which the model was developed.     

Individual growth curve standards in twins: growth in the second trimester

To provide a more detailed assessment of the growth of twins, the individual second trimester growth patterns of six fetal parameters [HC, AC, FDL, ThC, head cube (A) and abdominal cube (B)] were studied in fourteen sets of normal twins (six monozygotic and eight dizygotic) and sixteen normal singletons using the Rossavik growth model [P = c(t)(k + s(t)]. Comparisons of start points and coefficient c values indicated no statistically significant differences in the growth processes of twins and singletons in early pregnancy and no detectable effect of zygocity. Comparisons of second trimester growth within sets of twins and randomly paired singletons revealed the presence of differences in feto-placental support. A significant effect of differences in genetic growth potential or maternal support could not be demonstrated, however. These results suggest that with respect to growth, normal twins in the second trimester can be treated as two singletons in the same mother.     

A simple, rapid immunometric assay for determination of functional and growth hormone-occupied growth hormone-binding protein in human serum

We present a sensitive time-resolved fluorometric immunofunctional assay (TR-FIA) for direct quantitation of functional growth hormone-binding protein (GHBP), using an immunoassay kit for growth hormone (GH-DELFIA). In addition to the immobilized GH antibody, one monoclonal antibody against GHBP was used. This anti-GHBP was labelled with the chelate of europium. The assay was performed in one step. The detection limit for GHBP was 0.044 nmol L^–1 (NBS + 3 SD). The calibration curve was linear in the interval 0.11–8.03 nmol L^?1. Average intra-assay coefficient of variation (CV) was 3.44%. Average interassay CV at GHBP concentrations 0.563 nmol L^?1 and 1.40 nmol L^?1 were 12% and 6.3% respectively. Analytical recovery in serum ranged from 76% to 127% with a mean of 101 ± 3.6%. Serum GHBP in 102 normal subjects ranged from 0.513 to 3.772 nmol L ¹ and was positively related to body mass index (P < 0.001). In growth hormone-deficient sera GHBP was higher than in control subjects (1.751 ± 0.179 nmol L^?1 and 1.257 ± 0.140 nmol L^?1 respectively, P < 0.001). Acromegalic patients had lower levels of GHBP than controls (0.946 ± 0.251 and 1.234 ± 0.144 nmol L^?1 respectively, P = 0.005). This assay also allowed detection of GH-complexed GHBP in serum. These results were in agreement with theoretical values calculated from the measured GH and the functional GHBP concentrations. Results were compared with data obtained by a recently reported, validated ligand immunofunctional assay (LIFA), which is fundamentally different. There was a significant linear relationship between the results from the two assays (r = 0.89, P = 0.001). The slope of the regression line was 0.65. In conclusion, this new convenient GHBP TR-FIA provides a sensitive and precise method for detecting total GHBP as well as complexed GHBP in human serum, and allows easy processing of large numbers of samples.     

Expression of hepatocyte growth factor, keratinocyte growth factor and their receptors in experimental chronic pancreatitis

BACKGROUND: Hepatocyte (HGF) and Keratinocyte growth factors (KGF) are key factors of tissue organization and regeneration. These peptide growth factors and their receptors c-met and keratinocyte growth factor receptor (KGFR) are overexpressed in pancreatic cancer. AIM: Expression and localization of ligands and receptors were investigated during the development of experimental chronic pancreatitis. METHODS: Chronic pancreatitis was induced in rats by intravenous injection of dibutyltin dichloride. One to 60 days after treatment, the expression of growth factors and receptors was analysed by competitive polymerase chain reaction, Western blot analysis and immunohistochemistry. RESULTS: HGF mRNA expression increased (10-fold) until days 7-14 followed by a decrease to control level. Expression of c-met mRNA constantly increased (15-fold). KGF and KGFR mRNA expression were increased after 14-28 days (5-fold) and then returned to control levels. mRNA expression patterns correlated with changes in the protein expression, whereas protein levels of KGF remained unchanged. Ligands were localized in mesenchymal cells and their receptors on epithelial cells. CONCLUSIONS: The significant increase of HGF and c-met expression suggests an essential role of this growth factor in the morphological changes during the development of chronic pancreatitis. Changes in the expression of KGF and KGFR are less pronounced.     

Effect of measurement variability on Rossavik growth model specification and prediction of growth outcome at birth.

We have studied how variability in second-trimester ultrasound measurements affects the process of fetal growth evaluation based on individual fetal growth curve standards specified by Rossavik growth models. The head and abdominal short axes of two second-trimester scans of a patient with normal fetal growth were increased or decreased by increments ranging from 0.1 cm to values equal to the two standard deviations of the interobserver variability for these measurements--i.e., 0.3 cm for head short axis and 0.4 cm for abdominal short axis. The largest increments affected the Growth Potential Realization Index for weight at birth by 1% to 13% when applied to head short axis, and by 2% when applied to abdominal short axis. In contrast, the same increments had little effect (1%) on the Growth Potential Realization Indices for head and abdominal circumferences. Whereas 0.1-cm increments had no effect on any of the individual growth models or predicted birth characteristics, some combinations of these small errors involving both head and abdominal short axes changed the Growth Potential Realization Index for weight by as much as 15%, and those for head and abdominal circumferences by 3% and 8%, respectively. Under some scenarios, fetal growth status could be falsely classified as normal or abnormal. These results show that the reliability of individualized growth assessment depends to a great extent on excellent ultrasound technique, at least for certain parameters.