sTfR对慢性炎症患者并发缺铁性贫血的诊断价值

目的:探讨血清可溶性转铁蛋白受体(sTfR)水平对慢性炎症患者并发缺铁性贫血与慢性炎症患者并发非缺铁性贫血的鉴别诊断价值.方法:采用散射免疫比浊法定量测定非贫血对照组,单一原因造成的缺铁性贫血(IDA)、慢性炎症并发缺铁性贫血患者、慢性炎症并发非缺铁性贫血患者sTfR浓度.采用t检验和ROC曲线评价sTfR的诊断价值.结果:非贫血对照组与单一原因造成的IDA sTfR浓度有显著性差异(P＜0.05),AUC=0.965,有较高的诊断准确度.慢性炎症并发缺铁性贫血患者与慢性炎症并发非缺铁性贫血患者sTfR浓度有显著性差异(P＜0.05);AUC=0.834,有一定的准确度.结论:sTfR浓度对单一原因造成的IDA和慢性炎症并发缺铁性贫血患者有较高的诊断准确性;并且根据不同的临床资料选用不同的阈值用于诊断.     

LDH及sTfR在成人急性溶血性贫血中的意义

目的 探讨血清乳酸脱氢酶(lactic dehydrogenase,LDH)及可溶性血清转铁蛋白受体(soluable transferritin receptor,sTfR)在无慢性贫血史成人急性溶血性贫血(acute hemolutic anemia,AHA)诊断中的意义.方法 无慢性溶血性疾病史的32例成人急性溶贫患者采用酶标比色法测定血清LDH水平,ELISA方法检测血清sTfR水平并与正常体检者进行比较分析.结果 急性溶贫患者血清sTfR水平为49.3±13.1 nmol/L,对照组为15.5 ±2.1 nmol/L,两组比较有统计学差异(P＜0.05);急性溶贫患者血清LDH水平为531.1 ±111.2 IU/L,对照组为105.5 ±42.1 IU/L,两组比较有统计学差异(P＜0.05);不同程度AHA患者血清LDH及sTfR不同.结论 血清LDH、sTfR活性可作为无慢性溶血性疾病成人AHA诊断筛选.     

可溶性血清转铁蛋白受体和血清铁在诊断妊娠妇女缺铁性贫血中的比较

目的比较可溶性血清转铁蛋白受体(soluble transferrin receptor,sTfR)和血清铁(serum iron,SI)两种检测指标,在诊断妊娠妇女缺铁性贫血中的灵敏度和特异性.方法采用免疫分析法和比色法测定30例贫血妊娠妇女和30例贫血妊娠妇女和30例健康妊娠妇女的sTfR水平的SI水平,并对实验数据进行分析和比较.结果30例贫血妊娠妇女的sTfR平均值是31.3860±6.7990nmol/L,高于临界值28.1mmol/L(P＜0.05),属于贫血范围;SI的平均值是9.53±4.2622nmol/L,与临界值9nmol/L没有差异,属于正常范围.30例正常妊娠妇女的sTfR平均值是25.2080±6.9032nmol/L,小于临界值28.1nmol/L(P＜0.05),属于正常范围;SI的平均值是13.3733±4.8359nmol/L,高于临界值属于正常范围(P＜0.01).贫血妊娠妇女的sTfR水平明显高于正常妊娠妇女的sTfR水平(P＜0.01)、SI水平明显低于正常妊娠妇女(P＜0.01).sTfR、SI测定妊娠妇女缺铁性贫血的灵敏度分别是70%和53.3%、特异性分别是83.3%和80.0%.结论在诊断妊娠妇女缺铁性贫血,两种指标的特异性都比较高,但sTfR测定比SI测定灵敏性高、能更正确地对妊娠妇女是否缺铁做出正确判断.     

MCV、MCH、RDW及SF在地中海贫血及与缺铁性贫血鉴别中的应用价值

目的探讨平均红细胞体积(Mean corpuscular volume,MCV)、平均红细胞血红蛋白量(Mean corpuscular hemoglobin,MCH)、红细胞分布宽度(RDW)及血清铁蛋白(Serum ferritin,SF)在鉴别缺铁性贫血和地中海贫血中的价值。方法收集广东省妇幼保健院2013年1月~2015年12月确诊为地中海贫血的患者120例(地贫组),缺铁性贫血的患者100例(IDA组),另收集60例健康志愿者(对照组),检测所有患者的血常规五分类和血清铁蛋白。结果地贫组和IDA组患者MCV和MCH均低于对照组,差异有统计学意义(P0.05);地贫组MCV低于IDA组,差异有统计学意义(P0.05);IDA组SF低于地贫组和对照组,差异有统计学意义(P0.05),地贫组SF值高于对照组(P0.05);地贫组和IDA组患者MCH值都低于对照组,差异有统计学意义(P0.05);IDA组患者RDW值高于地贫组和对照组,差异有统计学意义(P0.05)。同时多个项目联合检测更能提高鉴别诊断的效率,跟基因诊断金标准相比MCV、MCH、RDW及SF联合检测筛查地中海贫血的灵敏度为90.8%,特异度为90.0%。结论 MCV、MCH、RDW及SF在鉴别缺铁性贫血和地中海贫血中有重要的参考价值,对预防和降低重型地贫患儿的出生有着重要的意义。     

孕妇MCV、RDW、SF检测的临床应用价值

目的了解和探讨孕妇缺铁性贫血与红细胞平均体积（MCV）、红细胞分布宽度（RDW）、血清铁蛋白（SF）检测对妊娠合并缺铁性贫血的相关性及诊断价值。方法采用血细胞分析仪测定MCV和RDW,采用电化学发光仪测定血清铁蛋白,并对结果进行相关统计学分析。结果RDW、SF中度贫血组与正常对照组比较有显著性差异（P（0.05）,两贫血组与正常对照组比较有显著性差异（P（0.05）。SF测定缺铁性贫血的敏感性达88.4%,3项联合检测的敏感性高达96.6%。结论孕妇在妊娠中期检测SF是铁营养状态监测的一个敏感指标,而MCV、RDW、SF三项联合检测能显著提高缺铁性贫血的诊断率。     

可溶性转铁蛋白受体与血清铁蛋白在慢性炎症性疾病合并缺铁性贫血诊断中的价值比较

目的：探讨可溶性转铁蛋白受体（Soluble tranferrin receptor,sTfR）与血清铁蛋白（Serum ferritin,SFer）在慢性炎症性疾病合并缺铁性贫血（Iron deficiency anemia,IDA）诊断中的价值。方法：随机选取我院2009年8月至2011年6月收治的29例患有慢性炎症性疾病伴IDA患者,31例慢性炎症性疾病无贫血患者,以及28例健康人,进行SFer,sTfR检测。结果：sTfR在慢性炎症性疾病合并IDA组明显升高,与慢性炎症性疾病无贫血组比较有显著性差异（P〈0.01）;SFer在慢性炎症性疾病合并IDA组有降低,与慢性炎症性疾病无贫血组比较无显著性差异（P〉0.05）。结论：血清sTfR的测定较SFer更能准确反映体内铁贮存情况,对慢性炎症性疾病合并IDA的诊断具有指导意义。     

缺铁性贫血患者输注PRC前后血清EPO和SF水平的观察

目的：探讨缺铁性贫血患者输注悬浮红细胞（PRC）前后血清红细胞生成素（EPO）和铁蛋白（SF）水平的变化。方法：应用放射免疫分析对35例缺铁性贫血患者进行了输注PRC前后血清EPO和SF水平的检测,并以30名正常健康人作比较。结果：缺铁性贫血患者在输注PRC前血清EPO水平显著高于正常人组（P〈0.01）,而血清SF则显著低于正常人组（P〈0.01）;经治疗2周后血清EPO水平与正常人比较无显著性差异（P〉0.05）,血清SF与正常人比较仍有显著性差异（P〈0.05）。结论：输注PRC对缺铁性贫血的疗效具有重要的临床价值。     

再生障碍性贫血患者治疗前后血清TNF-α、VEGF和TSGF检测的临床意义

目的：探讨了再生障碍性贫血患者治疗前后血清TNF-α、VEGF和TSGF水平的变化及意义。方法：应用放射免疫分析、酶免法和化学法对33例再生障碍性贫血患者进行了血清TNF-α、VEGF和TSGF检测,并与35例正常健康人作比较。结果：再生障碍性贫血患者在治疗前血清TNF-α、TSGF水平非常显著地高于正常人组（P〈0.01）,而血清VEGF水平则非常显著地低于正常人组（P〈0.01）,血清TNF-α和TSGF水平与VEGF水平呈明显负相关（r=-0.5192、-0.6018,P〈0.01）,经治疗3个月后与正常人组比较仍有差异（P〈0.05）。结论：检测再生障碍性贫血患者血清TNF-α、VEGF和TSGF水平的变化对了解病情、指导治疗具有重要的临床价值。     

慢性再生障碍性贫血患者CD28共刺激分子及Fas的表达

再生障碍性贫(ap]astic anemia,AA)简称再障,是免疫介导的造血抑制的综合病症,其中又以慢性再生障碍性贫血(chronic aplastic anend8,CAA)患者多见.本文旨在观测CAA患者外周血共刺激分子CD28及Fas(CD95)的表达水平.     

缺铁性贫血患者输注PRC前后血清SF、FA和VitB12水平的临床意义

目的：探讨了缺铁性贫血（IDA）患者输注悬浮红细胞（PRC）前后血清铁蛋白（SF）、叶酸（FA）和维生素B12（VitB12）水平的变化。方法：应用放射免疫分析对32例缺铁性贫血患者进行了输注PRC前后血清SF、FA和VitB12水平测定,并以35名正常健康人作比较。结果：缺铁性贫血患者在输注PRC前血清SF水平非常显著地低于正常人组（P〈0.01）,而血清FA、VitB12水平显著高于正常人组（P〈0.01）,经治疗2周后除SF水平与正常人比较仍有差异外（P〈0.05）,而FA和VitB12水平则与正常人比较无显著性差异（P〉0.05）。结论：输注PRC对缺铁性贫血患者具有一定的治疗作用,有重要的临床价值。     

PCR诱导猴免疫缺陷病毒SF2、SF3位点突变和转染研究

目的研究猴免疫缺陷病毒（ｓｉｍｉａｎｉｍｍｕｎｏｄｅｆｉｃｉｅｎｃｙｖｉｒｕｓ,ＳＩＶ）ＬＴＲ区ＳＦ２或ＳＦ３位点结构与病毒转录活性的关系。方法利用ＬＴＲ５端引物和含ＳＦ２或ＳＦ３部位双点突变的中间引物,首次用ＰＣＲ扩增长度约０．６ｋｂ的ＳＩＶｍａｃ２３９ＬＴＲ５端ＤＮＡ片段,经纯化后,作为正向引物,再次用ＰＣＲ扩增长度约１．１ｋｂ的ＬＴＲ全段（９２０９～１０２７９）并将其连接到ＰＢＳ－ＳＩＶｍａｃ２３９３端病毒的重组质粒上,后者再经ＳｐｈⅠ切点与ＳＩＶｍａｃ２３９５端病毒连接。用突变的病毒转染外周血淋巴细胞（ＰＢＬ）,用ＥＬＩＳＡ法动态测定培养液中ＳＩＶ核心蛋白Ｐ２７浓度。结果与ＳＩＶｍａｃ２３９株相比,ＳＦ２或ＳＦ３突变株在转染后,其核心蛋白Ｐ２７水平无明显降低。结论两步ＰＣＲ诱导突变是一种简单有效的方法;ＳＦ２或ＳＦ３位点结构对于ＳＩＶｍａｃ２３９在外周血淋巴细胞中的转录活性可能不具重要的影响     

缺铁合并感染儿童铁剂治疗前后血清可溶性转铁蛋白受体及转铁蛋白的变化

目的探讨血清可溶性转铁蛋白受体(sTfR)、转铁蛋白(Tf)在缺铁合并急性感染儿童(IDAI)口服铁剂治疗前后的变化规律.方法将病例分成IDAI组、单纯缺铁性贫血(IDA)组及IDAI治疗组.IDAI组给口服铁剂3w.采用速率散射免疫比浊法,测定初诊时及治疗3w后患儿血清sTfR、Tf、铁蛋白(SF)水平.部分病例采用常规铁染色观察骨髓储存铁.结果 IDAI组和IDA组患儿sTfR、Tf均显著高于对照组(P<0.01),这两组间无显著差异(P>0.05),IDAI患儿经治疗后血色素(Hb)升高但尚未正常时,sTfR、Tf已降至对照组水平,治疗前后差异显著(P<0.01).结论 sTfR、TF对诊断早期铁缺乏特异,敏感,测定结果不受感染因素干扰,是临床诊断早期缺铁合并感染儿童,指导铁剂治疗及疗效监测的可靠指标.     

肝细胞生长因子研究进展

查阅近二十年国外有关HGF/SF文献,基本弄清了HGF/SF的分子结构及组织分布,说明了HGF/SF的调节和cmet受体及两者的关系,揭示了HGF/SF的生物活性、HGF/SF和肿瘤扩散以及与肝再生的关系.因此,HGF/SF在肝再生中起主要作用;是肾再生的关键因子;可促进伤口愈合;通过增加恶性细胞的侵袭性,HGF/SF可能作为肿瘤转移的重要因素之一.     

Diverse and potent activities of HGF/SF in skin wound repair

Genetic studies in the mouse have highlighted essential roles for several growth factors in skin repair and have offered a rationale for their use in therapy. The present study shows that the plasminogen-related growth factor HGF/SF (hepatocyte growth factor/scatter factor) promotes wound repair in homozygous diabetic db/db mice by recruiting neutrophils, monocytes, and mast cells to the wound; by promoting the migration of endothelial cells to the injured area; and by enhancing keratinocyte migration and proliferation. As a result, granulation tissue formation, wound angiogenesis, and re-epithelialization are all increased. The results demonstrate that HGF/SF affects and sustains all key cellular processes responsible for wound repair and point to a unique potential of this molecule for the therapy of chronic skin wounds.     

Purification and characterization of pre-mRNA splicing factor SF2 from HeLa cells

SF2, an activity necessary for 5' splice site cleavage and lariat formation during pre-mRNA splicing in vitro, has been purified to near homogeneity from HeLa cells. The purest fraction contains only two related polypeptides of 33 kD. This fraction is sufficient to complement an S100 fraction, which contains the remaining splicing factors, to splice several pre-mRNAs. The optimal amount of SF2 required for efficient splicing depends on the pre-mRNA substrate. SF2 is distinct from the hnRNP A1 and U1 snRNP a polypeptides, which are similar in size. Endogenous hnRNA copurifies with SF2, but this activity does not appear to have an essential RNA component. SF2 appear to be necessary for the assembly or stabilization of the earliest specific prespliceosome complex, although in the absence of other components, it can bind RNA in a nonspecific manner. SF2 copurifies with an activity that promotes the annealing of complementary RNAs. Thus, SF2 may promote specific RNA-RNA interactions between snRNAs and pre-mRNA, between complementary snRNA regions, and/or involving intramolecular pre-mRNA helices. Other purified proteins with RNA annealing activity cannot substitute for SF2 in the splicing reaction.     

Novel association to the proprotein convertase PCSK7 gene locus revealed by analysing soluble transferrin receptor (sTfR) levels

The level of body iron storage and the erythropoietic need for iron are indicated by the serum levels of ferritin and soluble transferrin receptor (sTfR), respectively. A meta-analysis of five genome-wide association studies on sTfR and ferritin revealed novel association to the PCSK7 and TMPRSS6 loci for sTfR and the HFE locus for both parameters. The PCSK7 association was the most significant (rs236918, P = 1.1 × 10E-27) suggesting that proprotein convertase 7, the gene product of PCSK7, may be involved in sTfR generation and/or iron homeostasis. Conditioning the sTfR analyses on transferrin saturation abolished the HFE signal and substantially diminished the TMPRSS6 signal while the PCSK7 association was unaffected, suggesting that the former may be mediated by transferrin saturation whereas the PCSK7-associated effect on sTfR generation appears to be more direct.     

缺血性脑卒中患者血清hsCRP和SF水平

目的：研究血清超敏C反应蛋白（highsensitivity C reactive protein,hsCRP）和血清铁蛋白（SF）在缺血性脑卒中患者中的变化及意义。方法：对120例缺血性脑卒中患者和100例健康人应用散射比浊法测定血清hsCRP和SF浓度。结果：缺血性脑卒中患者血清中hsCRP和SF浓度与正常对照组相比明显增高,差异具有显著统计学意义（P〈0．01）。结论：血清hsCRP和SF在缺血性脑卒中发生时增高,两者可作为缺血性脑卒中独立的危险因素和预示因子。     

Co-expression of VEGF, c-Met and HGF/SF in secondary pleural tumors

Tumor angiogenesis is influenced by a large number of angiogenic factors among which vascular endothelial growth factor (VEGF) is one of the most important cytokines. Together with hepatocyte growth factor/scatter factor (HGF/SF), c-Met receptor forms a paracrine signaling system. The aim was to study the characterization of the proteins, VEGF, c-Met and HGF/SF with expression pattern and possible co-expression in secondary pleural tumors. Biopsy specimens of the pleural region from 70 patients were chosen and analyzed using immunohistochemistry and in situ hybridization. In the investigated tumors, a marked intracytoplasmic expression, sometimes over-expression of VEGF, c-Met and HGF/SF was detected. This expression was not connected to certain tumor types or a certain histogenetic origin of the tumor. These results indicate a role of these factors in angiogenesis. The synthesis of VEGF and c-Met within the tumor cells was established by in situ hybridization. There was a significant co-expression of VEGF and c-Met/HGF. Thus, autocrine stimulation of these angio-genetically effective systems may be present here. Importantly, the autocrine mechanism between over-expressed c-Met and HGF/SF in malignant tumors, already preferred by other authors, with demonstration of the proteins in the same tumor cells, has to be assumed in the process of pleural metastatic spread. Simultaneous synthesis of these three different proteins is also possible via the plasminogen-urokinase system. VEGF is reported to increase vascular permeability, which in turn causes pleural effusions. The results presented here may be the basis for possible future palliative therapeutical strategies in malignant pleural effusions.