Graves病患者^131I治疗前后血清IL-8水平的变化及相关研究

通过测定G raves病（GD）患者^131I治疗前后血清IL-8水平及FT3/IL-8和FT4/IL-8比值的变化,并分析比较治疗前后血清IL-8与TRAb及甲状腺功能变化,探求IL-8与GD发生、发展机制的关系及可否将其作为判断GD治疗疗效及预后的指标。共检测138份血样,其中,40名为正常对照,98例为GD患者。采用放射免疫法（R IA）检测血清TT3、TT4、FT3、FT4、TRAb及IL-8含量,采用免疫放射定量分析法（IRMA）对hTSH进行检测。结果显示：①GD初发组治疗前,血清IL-8水平明显高于对照组（P〈0.01）;治疗后3个月、6个月血清IL-8检测值明显降低（P〈0.01）,治疗后18个月,血清IL-8接近正常水平;②GD复发组血清IL-8水平明显高于对照组和缓解组（P〈0.01）;③GD患者血清FT3/IL-8和FT4/IL-8比值较对照组明显增高,治疗后3个月下降至对照组水平;④GD患者血清IL-8水平与TRAb呈正相关。结论：①GD患者的免疫功能恢复滞后于其本身的甲状腺功能;②FT3/IL-8和FT4/IL-8比值较IL-8单一指标更符合甲状腺的功能状况;③IL-8可能在GD的发病中起重要作用,可作为GD患者^131I治疗后观察疗效、判断预后及了解免疫功能恢复状况的有效指标。     

Graves病131I治疗后一年内缓解和早发甲减患者血清IL-18和TRAb的变化分析

探讨131I治疗后一年内GD患者甲减的免疫功能状态的改变.采用CLIA、IRMA和EIA方法,监测41例GD患者131I治疗前后血清白细胞介素-18(IL-18)、促甲状腺素受体抗体(TRAb)、TPOAb的含量和甲状腺重量(TDW)变化.41例GD患者分为甲减组13例和缓解组28例.结果表明治疗前两组GD患者血清IL-18和TRAb水平明显升高,与对照组比较均有显著性差异(P＜0.01,P(0.05),两组间比较,血清FT3、FT4、sTSH、TDW和131I剂量均无显著性差异(P＞0.05).治疗后两组血清IL-18明显下降,甲减组血清sTSH升高明显(P＜0.01),而缓解组TDW明显减少(P＜0.05).两组患者治疗后的TRAb水平仍然较高(P＜0.05).IL-18与FT3、FT4和TDW呈正相关(r=0.372,P＜0.01;r=0.312,P(0.01;r=0.371,P＜0.01),与sTSH呈负相关(r=-0.224,P＜0.01).甲减组TPOAb升高的病例治疗前为4/13,治疗后为6/13;缓解组治疗前为10/28,治疗后为12/28.131I治疗后6～12个月内辐射对患者免疫系统的调控产生的直接影响较小,血IL-18含量变化如结合TRAb、TPOAb指标了解甲状腺Th1/Th2型免疫应答状态,对疗效观察和预后判断有阶段性指导作用.     

131I治疗对Graves''''病患者近期红细胞免疫功能的影响

目的观察131I治疗对Graves'病(GD)患者红细胞免疫功能(EIF)的影响.方法检测并比较56例GD患者经131I治疗前及治疗后1周、1月、3月、6月和12个月时血清TT3、TT4、TSH、FT3、FT4、TSH以及红细胞C3b受体花环率(RBC-C3bRR)、红细胞免疫复合物花环率(RBC-ICR),45例健康成人作为对照组.结果 131I治疗后3月、6月和12月,GD患者TT3、TT4、FT3、FT4、RBC-C3bRR较治疗前明显下降,TSH和RBC-ICR较治疗前明显升高;RBC-C3bRR与TT3、TT4、FT3、FT4水平呈负相关,RBC-ICR与TT3、TT4、FT3、FT4水平呈正相关.结论131I治疗能增强机体红细胞免疫功能;EIF与甲状腺激素水平之间存在显著相关性,其检测可作为GD病人免疫状态、疗效评价指标.     

中药协同131I治疗Graves病的临床研究

探讨中药石麦清液协同131I治疗Graves病(GD)的疗效及给药方法.GD患者100例随机分为A组:131I治疗,B组:131I 石麦清液治疗,服131I后7d服石麦清液20mL每天3次共40d.以治疗前和治疗后30d、90d测定血清FT3、FT4和TSH并选择8种症状,采用Kupperman四级评分评估.结果表明B组临床症状提前改善,安全渡过131I治疗一月后出现的FT3、FT4反跳性升高,A组30d后临床症状重于治疗前,FT3、FT4高于治疗前.B组90d临床症状显著改善,FT3、FT4和TSH测值正常,A组临床症状改善,但FT3、FT4低于正常,TSH高于正常.30d后B组安全渡过高危期,90d治疗后,减轻甲状腺功能减退症发病率疗效优于A组.石麦清液无毒性、安全和可在临床推广应用.     

^131I治疗36例Graves病伴白细胞减少患者的临床疗效观察

为探讨^131I治疗对Graves病（GD）伴白细胞（WBC）减少患者或服用ATD后出现白细胞减少的GD患者的疗效,给予36例GD伴白细胞减少的患者^131I治疗,并分别测定患者治疗前和治疗后1个月、3个月、6个月的血常规、甲状腺激素水平等相关指标。结果显示^131I治疗3个月后,FT3、FT4水平明显降低,TSH升高,与治疗前比较有显著性差异（P〈0.05）;^131I治疗后3个月,外周血白细胞水平逐渐恢复,与治疗前比较有显著性差异（P〈0.05）。^131I治疗GD伴白细胞减少是一种安全可靠、疗效肯定的治疗方法,应尽早选用。     

Graves病131I治疗前后甲状腺自身抗体的变化及其临床意义

测定放射性131I治疗前后Graves病患者血清甲状腺球蛋白抗体(TGAb)和甲状腺过氧化物酶抗体(TPOAb)的变化,探讨131I治疗Graves病的疗效及影响早发甲低的因素.将334例Graves病患者按131I治疗前TGAb、TPOAb水平分为阳性组202例(TGAb＞115IU/mL,TPOAb＞34IU/mL)和阴性组132例(TGAb＜115IU/mL,TPOAb＜34IUmL),并对其治疗前及治疗后3、6、9及12个月的血清FT3、FT4、TSH及TGAb、TGAb水平进行动态观察.治疗后1年, 甲低发生率分别为阳性组23.8%,阴性组11.4%, 两组间甲低发生率有显著差异(P＜0.01).并且随着131I治疗后时间的推移, TPOAb、TGAb的阳性率逐渐降低.早发甲低与治疗前TGAb、TPOAb水平有关, 测定血清中TGAb、TPOAb浓度对Graves病患者131I治疗前调整给药剂量可提供参考, 并且131I治疗Graves病可以降低患者甲状腺激素自身抗体水平, 促进其自身免疫状态的改善和恢复.     

碳酸锂联合131I治疗甲亢性心脏病的研究

观察碳酸锂对甲亢性心脏病患者131I治疗后血清甲状腺激素水平的影响及对甲亢性心脏病的治疗效果。将138例拟行131I治疗的甲亢性心脏病患者随机分为单独使用131I治疗组（对照组）和131I＋碳酸锂组（试验组）。试验组服131I的同时开始服用碳酸锂0.25g,3次/日,共十天。均于131I治疗前和治疗后15d、30d、90d分别检查血清FT3、FT4,观察90天的甲亢性心脏病治疗效果。使用单因素方差分析各组组内和组间差别。结果发现,对照组治疗后15d,血清FT4水平高于治疗前,以后逐渐下降;试验组131I治疗后血清FT3和FT4水平均低于治疗前并逐渐下降,甲亢性心脏病症状加重病例较对照组明显少。碳酸锂可降低甲亢性心脏病患者131I治疗后血清甲状腺激素水平,131I联合碳酸锂治疗甲亢性心脏病疗效好,是治疗甲亢心的理想方法。     

不同甲状腺功能状态下甲状腺CT值及甲状腺摄131I率变化规律

目的 通过观察不同甲状腺功能状态下甲状腺CT值和甲状腺摄131I率间变化规律,为进一步探讨Graves病(GD)患者甲状腺CT值与甲状腺摄131I率间关系奠定基础.方法 受检者选自廊坊市人民医院核医学科2007年3月至2009年12月门诊首诊患者及我院正常体检人群,按甲状腺功能不同分为甲亢组、甲减组和正常组,分别测定甲状腺激素水平、甲状腺CT值和摄131I率,其结果分别与甲状腺功能正常组做对照,各组数据以均数±标准差((x)±s)表示,行方差分析.结果 与正常组比较:①甲亢组,甲状腺激素TT36.38±2.34nmol/L、TT4 195±37.25nmol/L、FT3 10.17±2.76pmoL/L、FT438.94±11.23 pmol/L均明显升高,TSH0.11±0.88 μU/mL降低,P均＜0.01;甲状腺摄131I率2h 44±9％、4h 58±16％、24h 76±15％,各时间点均明显增高,P均＜0.01;甲状腺CT值78±13HU降低,P＜0.01.②甲减组,甲状腺激素水平TT30.57±0.14nmol/L、TT426.03±8.55nmol/L、FT3 1.37±0.84pmol/L、FT44.72±1.39pmol/L均明显降低,TSH 15.67±8.95μU/mL增高,P均＜0.01;甲状腺摄131Ⅰ率2h5.7±2.3％、4h3.8±1.3％、24h 2.6±1.1％,各时间点均明显降低,P均＜0.01;甲状腺CT值53±16HU降低,P＜0.01.结论 不同甲状腺功能状态下甲状腺CT值和甲状腺摄131I率间存在一定变化规律,该规律与甲状腺病理改变和甲状腺滤泡内I-含量变化密切相关.     

131I治疗甲亢合并周期性麻痹疗效初步分析

评价131I治疗甲亢合并周期性麻痹(TPP)的疗效,对8例TPP患者用131I治疗,测定治疗前后血清指标.结果表明:血清钾降低,TT3、TT4、FT3、FT4均升高,131I治疗见效快,疗程短,治愈率高,治疗后6个月治愈率75%(6/8),12个月后治愈率100%(8/8),是TPP治疗的首选.     

血清CXCL10在131I治疗Graves病中的测定意义

目的:旨在探讨CXCL10的检测在放射性碘治疗Graves病中的临床应用价值.方法:ELISA分别测定初诊的甲亢患者以及甲亢患者131I治愈后的血清CXCL10的水平,并与正常对照组比较,随后作统计分析CXCL10水平与FT3、FT4是否存在一定的相关性.结果:甲亢患者的CXCL10水平显著高于正常对照组,在131I治愈后的血清水平显著下降,降至正常水平;CXCL10水平与FT3、FT4浓度呈正相关.结论:CXCL10水平与甲状腺的功能密切相关,可作为评判甲亢患者131I治疗效果的有价值的指标.     

CaO-MgO-P_2O_5-SiO_2-CaF_2系统自硬性玻璃的研究

为研究钙离子、镁离子在体内环境中对自硬性玻璃结晶行为的影响,为自硬性生物活性玻璃的临床应用提供依据,本文设计了CaO-P2O5-SiO2-CaF2(Ca-glass)和CaO-MgO-P2O5-SiO2-CaF2(CaMg-glass)系统玻璃并使用模拟体液(simulated body flu id,SBF)进行了研究。首先采用磷酸氢二氨[(NH4)2HPO4]/[NH4H2PO4]硬化液与Ca-glass、CaMg-glass制成硬化体,然后使用X射线衍射(XRD)、扫描电镜(SEM)、失重、力学分析等方法,研究硬化体在SBF中的结晶性、降解性和力学性能。实验结果表明,玻璃粉末与磷酸铵缓冲溶液反应形成了磷酸铵钙[(NH4)2.Ca(HPO4)2.H2O]硬化体。硬化体经过SBF浸泡,Ca-glass系统硬化体中部分磷酸铵钙转化成羟基磷灰石,而CaMg-glass系统硬化体仍然为磷酸铵钙。Ca-glass与CaMg-glass硬化体在SBF中浸泡28天分别降解19.4%和31.3%,抗压强度分别为93.14MPa和64.52MPa。镁离子的歧化作用是导致Ca-glass、CaMg-glass硬化体结晶性能、降解性能以及力学性能差别的主要原因。     

2-Perbromomethyl-2-oxazoline: a novel trifunctional initiator for the ring-opening polymerization of 2-methyl-2-oxazoline

Polymerization of 2-methyl-2-oxazoline was carried out using a trifunctional initiator, 2-perbromomethyl-2-oxazoline. The degree of polymerization (DP) of the resulting polymer was very close to the feed mole ratio of the monomer to initiator. The number-average molecular weight M?_n increased linearly with conversion, indicating the living nature of the propagating chain end. ¹H NMR and end-group analyses results are consistent with the proposal that the polymer possesses a star-shaped structure.     

Corticosteroid-interleukin 2 interactions: inhibition of binding of interleukin 2 to interleukin 2 receptors.

PHA activated human peripheral blood mononuclear cells (MNC) were incubated with human interleukin 2 (IL-2) in the absence or in the presence of 10(-6)-10(-9) M hydrocortisone (HC). HC suppressed the proliferative response of the activated MNC to highly purified human leucocyte IL-2 in a dose dependent manner. This suppression was in full accordance with an inhibition of the IL-2 binding capacity, whereby the high affinity binding sites were reduced by 85%, while the low affinity sites were less affected. The mechanism by which HC inhibits the binding of IL-2 is still unknown. Evidence is presented that HC binds only weakly to IL-2. We conclude that HC interferes with the IL-2 binding by modulating the binding and/or signal processing function of the IL-2 receptor.     

13C NMR spectroscopy of 2-formamido-2-methylpropyl acrylate and poly(2-formamido-2-methylpropyl acrylate)

The synthesis and characterization of 2-formamido-2-methylpropyl acrylate (FMPA) is reported. ¹³C NMR spectra of FMPA in CDCl₃, CD₃OD, DMSO-d₆, DMF-d₇, and D₂O exhibit two pairs of lines for all seven carbon atoms at room temperature; the ratio of the two conformers varies moderately with solvent (21 : 79 to 41 : 59). The conformers are believed to involve strong internal hydrogen bonding which is not completely broken even by the addition of trifluoroacetic acid to CDCl₃ (1/1, v/v). However, the pairs of lines coalesce in turn as the temperature is raised to 120°C in DMSO-d₆. FMPA was polymerized at 35°C in DMF and CHCl₃, using a free radical initiator and the polymer was characterized by ¹³C NMR spectroscopy.     

Isolation of a novel KIR2DL3-specific mAb: comparative analysis of the surface distribution and function of KIR2DL2, KIR2DL3 and KIR2DS2

In recent years an increasing number of sequences coding for new KIRs have been described. However, the limited availability of mAbs with unique KIR specificities has hindered an exhaustive assessment of their actual function, HLA-specificity, expression at the cell surface and distribution in different cell populations. In this study we report the generation of a novel mAb (ECM41) specific for KIR2DL3 molecules. By the use of cell transfectants expressing one or other KIR we show that this reagent allows discrimination of KIR2DL3 from other GL183 mAb-reactive molecules such as KIR2DL2 and KIR2DS2. Moreover we show that this novel mAb can be used to assess the surface expression and distribution of KIR2DL3 in different polyclonal NK populations and in NK cell clones. Along this line, we were able to analyze the HLA class I specificity of NK clones expressing either KIR2DL3 or KIR2DL2, two inhibitory receptors that were so far serologically undistinguishable. Finally, the combined use of GL183 and ECM41 mAbs in redirected killing assays allowed us to investigate the functional outcome of the simultaneous engagement of KIR2DL3 and KIR2DS2 in NK cell clones co-expressing KIRs that display opposite (inhibitory vs activating) function.     

肌肽减轻H_2O_2诱导的N2a细胞损伤

目的探究肌肽对H2O2诱导的N2a细胞损伤的保护作用及其机制。方法将N2a细胞分为对照组、损伤组(给予H2O2)和肌肽保护组(预先加入肌肽)。用相差显微镜观察了细胞形态,用免疫荧光染色和免疫印迹实验检测细胞AKT1和FAS-L的蛋白表达。结果肌肽显著增加了N2a细胞增殖能力(P0.05);与对照组比较,H2O2损伤组细胞形态发生明显改变,细胞皱缩,胞膜变厚并出现发泡现象;而肌肽保护组细胞形态较损伤组明显改善;免疫荧光染色和免疫印迹实验显示,损伤组AKT1的表达显著低于对照组,FAS-L的表达显著高于对照组。而肌肽保护组AKT1的表达显著高于对照组,FAS-L的表达显著低于对照组(P0.05)。结论肌肽能够减轻N2a细胞对H2O2诱导的细胞损伤。     

An apparent KIR2DS2-negative KIR2DL2-positive genotype discloses the novel allele KIR2DS2*00104

KIR2DS2*00104 lacks a distinctive synonymous substitution of KIR2DS2 in nucleotide 418 that affects KIR genotyping.     

Synthesis and copolymerization of macromonomers based on 2-nonyl- and 2-phenyl-2-oxazoline

Several macromonomers were prepared by cationic ring-opening polymerization of 2-nonyl- and 2-phenyl-2-oxazoline using different techniques of functionalization. Introduction of the unsaturated functional group directly via a suitable termination agent proved to be superior to the use of a phenol-functionalized initiator and to the introduction of hydroxyl end groups via hydrolysis of the reactive cationic chain end and subsequent esterification with methacryloyl chloride. The macromonomers were characterized by spectroscopic techniques as well as GPC. One of the 4-vinylbenzyl-terminated macromonomers was copolymerized with MMA in different ratios. The copolymerization parameter r₁ was determined to be 0.75. The resulting graft copolymers were characterized regarding number of grafts per chain, molar mass, and glass transition temperature.     

NDRG2对肝癌细胞HepG2凋亡的诱导作用

目的：探讨NDRG2对肝癌细胞HepG2凋亡的诱导作用。方法：用RT-PCR获取NDRG2基因。测序判断正确后，将其克隆入含绿色荧光蛋白(GFP)基因的真核表达载体pIRES2-EGFP中，并转染NDRG2表达阴性的HepG2细胞。用光镜观察转染细胞的形态变化；荧光显微镜观察NDRG2蛋白的定位；流式细胞仪分析细胞周期的改变；透射电镜进一步观察细胞超微结构的改变。结果：获得了NDRG2基因，成功地构建了pIRES2-EGFP-NDRG2真核表达载体。转染HepG2细胞后，细胞生长受抑，结构破坏并死亡。荧光显微镜观察到NDRG2在胞质中表达，流式细胞仪检测出现G1期阻滞和凋亡峰，透射电镜观察到典型的细胞凋亡特征。结论：NDRG2基因具有诱导HepG2细胞凋亡的作用，其机制有待进一步研究。     

Synthesis and polymerization of 2-cyano-2-methyltrimethylene carbonate

2-Cyano -methyltrimethylene carbonate (CMTC, 2 ) was synthesized starting from 2-methylacrolein (6), propionaldehyde (8) or 2-hydroxymethyl-2-methyl-1,3-propanediol (9). A key position in this synthesis is held by 2,2-bis(hydroxymethyl)propionitrile ( 3 ), which in a first step, is reacted — in conjunction with 2,2-dimethyl-1,3-propanediol ( 20 0) — with diphenyl carbonate ( 17 ) to result in a statistical copolycarbonate. Ring-closing depolymerization of this polymer, with a catalyst based on tin, yields in a second step the title monomer, CMTC (2), along with 2,2-dimethyltrimethylene carbonate (DTC, 1b ). Separation of the two monomers can be achieved by selective solubilization of the latter in toluene. Polymerization of CMTC is performed preferentially by using weak nucleophiles as initiators, such as Et₂AlOEt, Al(O-secBu)₃ or MgBu₂, since strong nucleophiles such as BuLi or ZnEt₂ tend to give side reactions with the cyano group. Copolymerization of CMTC with DTC results in statistical copolymers. With Et₂AlOEt as initiator copolymers with Bernoulli statistics are obtained, with a ratio of diads DTC/DTC : (DTC/CMTC + CMTC/DTC) : CMTC/CMTC equal to 1:2:1 for equimolar feed composition. With MgBu₂ as initiator and the same feed composition, a copolymer with the diad ratio 1:5:1 is obtained. Poly(CMTC) is a crystalline polymer with a melting point of 132.9°C and a glass transition temperature of 68.8 °C.