当归对高血压病患者血浆血栓素及前列环素水平的影响

目的 :探讨当归对高血压病 ( EH)患者血浆血栓素及前列环素的影响。方法 :将 60例 EH患者随机分为 A、B两组 ,各 30例 ,分别给予当归和安慰剂治疗 ,疗程均为 4周。另 60例正常健康人作为对照组。结果 :EH组的血浆血栓素 B2 ( Tx B2 )明显高于对照组 ,血浆 6-酮 -前列腺素 ( 6- keto-PGF1α)则显著降低。A组治疗后血浆 Tx B2 水平降低 ,6- keto- PGF1α升高 ( P<0 .0 1)。B组治疗前后无明显变化。结论 :当归能提高 EH患者血浆 6- keto- PGF1α,降低 Tx B2 。     

卡托普利对心力衰竭患者QT离散度及血浆AngⅡ,TXB2,6-keto-PGF1α影响

目的 :探讨卡托普利治疗慢性充血性心力衰竭 （CHF）对肾素 -血管紧张素系统和前列腺素系统及 QT离散度 （QTd）的影响。方法 :用放射免疫法测定 40例 CHF患者卡托普利治疗 2周前后血浆 Ang ,TXB2 ,6 - keto- PGF1α浓度 ;手工测量同步 12导联心电图 QTd。结果 :1卡托普利治疗 2周后 QTd无明显变化 ;2血浆 Ang ,TXB2 浓度和 TXB2 /6 - keto- PGF1α比值明显下降 ;6 - keto- PGF1α水平显著升高 ;3血浆 TXB2 的降低与 6 - keto- PGF1α的升高呈负相关 （r=- 0 .5 9,P<0 .0 1） ;平均动脉压的下降与 6 - keto- PGF1α的升高呈正相关 （r=0 .41,P<0 .0 5 ）。结论 :卡托普利 2周治疗有利于恢复心力衰竭患者体液内环境的稳定 ;但对 QTd无显著影响。     

法洛四联征患者血小板功能状态的研究

目的 :观察法洛四联征 ( TOF)患者血小板功能状态。方法 :采用放射免疫分析法测定 2 6例 TOF患者血浆及尿液中血栓素 A2 ( TXA2 )的代谢产物尿液中血栓素 B2 ( TXB2 )和前列环素( FGI2 )的代谢产物 6-酮 -前列腺素 1α( 6- keto- PGF1α)的含量 ,以及血浆α-颗粒膜蛋白 ( GMP- 14 0 )的含量 ,并与 14例年龄相匹配的正常健康者作对照。结果 :TOF组患者血浆及尿液中 TXB2 的水平显著高于对照组 ( P<0 .0 1) ;TXB2 与 6- keto- PGF1α的比值明显大于对照组 ( P<0 .0 1) ;TOF组血浆GMP- 14 0水平亦显著高于对照组 ( P <0 .0 1)。结论 :TOF患者体内 TXA2 与 PGI2 代谢失衡 ,GMP- 14 0释放增加 ,血小板呈激活状态 ,有利于血小板的粘附、聚集 ,参与血栓性疾病的发生。     

冠状动脉内直接注射硝基甘油抑制PTCA术后血小板的活化

目的 :研究冠状动脉内直接注射硝基甘油抑制 PTCA术后血小板的活化。方法 :应用放免法测定 38例稳定心绞痛患者 PTCA前后血小板膜表面 α-颗粒膜蛋白 （GMP- 140 ）分子数和血浆血栓素 B2 （Tx B2 ）、血浆 6 -酮 -前列腺素 F1α（6 - Keto- PGF1α）浓度 ,以及血小板衍化生长因子 （PDGF）和血小板聚集率。结果 :冠脉内直接注射硝基甘油的患者 PTCA前后上述指标无明显变化 ,而未用药的患者 PTCA术后 5 min血小板膜表面 GMP- 140及血浆 Tx B2 ,PDGF和血小板聚集率均明显增高 ,术后 10 m in达到高峰 ,30 m in降至正常。结论 :冠脉内直接注射硝基甘油可以抑制 PTCA术后血小板的活化     

苯那普利对心力衰竭者血浆血管紧张素Ⅱ血栓素B2和6酮—前列腺素浓度的影响

目的　探讨苯那普利治疗慢性充血性心力衰竭 (CHF)对肾素 -血管紧张素系统和前列腺素系统的影响。方法　用放射免疫法测定 40例 CHF患者苯那普利治疗 2周前后血浆血管紧张素 (Ang )、血栓素 B2 (TXB2 )、6酮 -前列腺素 (6- keto- PGF1 a)。结果　 CHF患者经苯那普利治疗 2周后血浆 Ang 、TXB2 浓度明显下降 ,6- keto-PGF1 a水平显著升高 ,TXB2 / 6- keto- PGF1 a比值明显下降 (P<0 .0 1) ;血浆 TXB2 的降低与 6- keto- PGF1 a升高呈负相关 (r=- 0 .5 9,P<0 .0 1) ;平均动脉压的下降与 6- keto- PGF1 a的升高呈负相关 (r=- 0 .41,P<0 .0 5 )。结论　苯那普利治疗 2周有利于恢复心力衰竭患者体内环境的稳定     

苯那普利对心力衰竭患者血浆血管紧张素Ⅱ、血栓素B_2和6酮-前列腺素浓度的影响

目的　探讨苯那普利治疗慢性充血性心力衰竭 (CHF)对肾素 -血管紧张素系统和前列腺素系统的影响。方法　用放射免疫法测定 40例 CHF患者苯那普利治疗 2周前后血浆血管紧张素 (Ang )、血栓素 B2 (TXB2 )、6酮 -前列腺素 (6- keto- PGF1 a)。结果　 CHF患者经苯那普利治疗 2周后血浆 Ang 、TXB2 浓度明显下降 ,6- keto-PGF1 a水平显著升高 ,TXB2 / 6- keto- PGF1 a比值明显下降 (P<0 .0 1) ;血浆 TXB2 的降低与 6- keto- PGF1 a升高呈负相关 (r=- 0 .5 9,P<0 .0 1) ;平均动脉压的下降与 6- keto- PGF1 a的升高呈负相关 (r=- 0 .41,P<0 .0 5 )。结论　苯那普利治疗 2周有利于恢复心力衰竭患者体内环境的稳定     

PTCA手术前后患者TNF,TGF和PGF水平分析

目的 :探讨 PTCA术前后血浆中肿瘤坏死因子 （TNF）、转化生长因子 （TGF-α） ,和 6 -酮 -前列腺素 F1α（6 - keto-PGF1α）的含量变化及临床意义。方法 :PTCA患者 38例 ,分别于术前、术后 4h,12 h,抽外周血测定 TNF,TGF-α和 6 - keto- PGF1α值 ,对照组选取 CAG正常者 2 2例。结果 :PTCA手术前后血浆中 TNF值均较 CAG正常组升高 ,TGF- α术前与 CAG正常组相同 ,术后升高。CAG正常组 6 - keto- PGF1α均高于 PTCA组 ,PTCA组术后只有轻度升高。放置支架越多 TNF,TGF- α值升高越明显 （P<0 .0 1）。结论 :PTCA术后的血管反应与免疫因素有关。     

肝硬化患者血浆血栓素B_2与6-酮-前列腺素F_1a测定的临床意义

报告80例肝硬化患者及30例对照组血浆血栓素 B(Tx B_2) 及6-酮-前列腺素 F_1α(6-酮-PGF_1α)测定结果,并分析两者比值与肝硬化的关系。结果提示肝硬化失代偿期患者血浆TxB_2浓度降低,6-酮-PGF_1α水平升高。     

原发性高血压患者血小板活化状态研究

目的 :探讨血小板活化与原发性高血压 (EH)的关系。方法 :观察 36例EH患者 (EH组 )和 2 5例正常人 (对照组 )的血小板α颗粒膜蛋白 14 0 (GMP 14 0 )在血小板膜表面的分子数和血浆中的含量 ,并同时测定了血浆血栓烷B2 (TxB2 )。结果 :EH组患者血小板膜表面GMP 14 0分子数和血浆中GMP 14 0浓度、血浆TxB2 浓度均显著高于对照组。未发现GMP 14 0与TxB2 在EH患者异常变化中的线性相关性。结论 :GMP 14 0与TxB2 反映了血小板活化在EH中的两种不同的重要作用     

慢性心力衰竭患者血清TXB2,6-k-PGF1α和前列腺素E2测定及其意义

目的 :探讨慢性心力衰竭 （CHF）患者血清血栓烷 B2 （TXB2 ）、6-酮 -前列腺素 F1α（6- k- PGF1α）和前列腺素E2 （PGE2 ）水平的变化及其临床意义。方法 :采用放射免疫法测定了 10 8例 CHF患者和 3 0例非慢性心力衰竭患者的血清 TXB2 、6- k- PGF1α和 PGE2 水平 ,进行对照分析。结果 :CHF组血清 TXB2 水平 （86± 8ng/L）显著高于对照组 （49± 6ng/L） （t=2 .3 68,P<0 .0 5 ） ,6- k- PGF1α水平 （49± 4ng/L）显著低于对照组 （80± 9ng/L） （t=3 .5 2 6,P<0 .0 1） ,PGE2 无显著差异 （P>0 .0 5 ）。 6- k- PGF1α与 PGE2 间呈显著正相关 （r=0 .3 16,P<0 .0 1）。 , , 度 CHF患者中 , 度组血清 TXB2 水平 （114± 18ng/L）显著高于 度组 （62± 8ng/L） （t=2 .3 68,P<0 .0 5 ） ,其他组间血清TXB2 ,6- k- PGF1α和 PGE2 水平无显著差异 （均 P>0 .0 5 ）。住院死亡组血清 TXB2 显著高于好转组 （t=2 .0 82 ,P<0 .0 5 ） ,6- k- PGF1α和 PGE2 水平无显著差异 （均 P>0 .0 5 ）。结论 :CHF组血清 TXB2 水平显著高于对照组 ,6- k-PGF1α水平显著低于对照组 ,6- k- PGF1α与 PGE2 间呈显著正相关 ,观察血清 TXB2 ,6- k- PGF1α和 PGE2 的变化 ,有助于 CHF患者的病理机制、病情进展和预后的研究     

Classification and characterization of hereditary types 2A, 2B, 2C, 2D, 2E, 2M, 2N, and 2U (unclassifiable) von Willebrand disease.

All variants of type 2 von Willebrand disease (VWD) patients, except 2N, show a defective von Willebrand factor (VWF) protein (on cross immunoelectrophoresis or multimeric analysis), decreased ratios for VWF:RCo/Ag and VWF:CB/Ag and prolonged bleeding time. The bleeding time is normal and FVIII:C levels are clearly lower than VWF:Ag in type 2N VWD. High resolution multimeric analysis of VWF in plasma demonstrates that proteolysis of VWF is increased in type 2A and 2B VWD with increased triplet structure of each visuable band (not present in types 2M and 2U), and that proteolysis of VWF is minimal in type 2C, 2D, and 2E variants that show aberrant multimeric structure of individual oligomers. VWD 2B differs from 2A by normal VWF in platelets, and increased ristocetine-induced platelet aggregation (RIPA). RIPA, which very likely reflects the VWF content of platelets, is normal in mild, decreased in moderate, and absent in severe type 2A VWD. RIPA is decreased or absent in 2M, 2U, 2C, and 2D, variable in 2E, and normal in 2N. VWD 2M is usually mild and characterized by decreased VWF:RCo and RIPA, a normal or near normal VWF multimeric pattern in a low resolution agarose gel. VWD 2A-like or unclassifiable (2U) is distinct from 2A and 2B and typically featured by low VWF:RCo and RIPA with the relative lack of high large VWF multimers. VWD type 2C is recessive and shows a characteristic multimeric pattern with a lack of high molecular weight multimers, the presence of one single-banded multimers instead of triplets caused by homozygosity or double hereozygosity for a mutation in the multimerization part of VWF gene. Autosomal dominant type 2D is rare and characterized by the lack of high molecular weight multimers and the presence of a characteristic intervening subband between individual oligimers due to mutation in the dimerization part of the VWF gene. In VWD type 2E, the large VWF multimers are missing and the pattern of the individual multimers shows only one clearly identifiable band, and there is no intervening band and no marked increase in the smallest oligomer. 2E appears to be less well defined, is usually autosomal dominant, and accounts for about one third of patients with 2A in a large cohort of VWD patients.     

Different RBC aggregating properties of the Aalpha2Bbeta2gammaA2 and Aalpha2Bbeta2gammaAgamma' subpopulations of human fibrinogen

Human fibrinogen (TF) has been separated into two fractions: F1 - homodimers with respect to the gamma chain, and F2 - heterodimers composed of gammaA and gamma' polypeptides. Their rouleaux-inducing properties were as follows: (1) both, at the same concentration of 0.8%, were less effective than TF; (2) F1 produced larger rouleaux even under static conditions of a hemocytometer where F2 was silent; (3) F2 induced the process when a suspension was gently sheared between microscopic slides. Since the synthetic peptide gamma'(414-427) inhibited the rouleau formation in a mixture with F2, the C-terminal amino acids of the gamma' polypeptide probably bind the molecule to the cell. The inhibition was feebly visible in the native ratio of F1/F2, implicating a compensatory effect of F1.     

Structure-function of Hb Marseille-Long Island [alpha 2 beta 2 N-methionyl-2(NA2) His----Pro

Suspensions of red cells containing Hb Marseille-Long Island showed decreased oxygen affinity and low interaction with 2,3-diphosphoglycerate. Oxygen equilibrium studies of the purified component confirmed these abnormalities. Oxidation rate measurements of carbonmonoxy-Hb Marseille and carbonmonoxy-Hb A by ferricyanide showed an increased rate for the former, suggesting an increased dissociation constant for carbon monoxide. Nuclear Magnetic Resonance spectra in the high field region revealed small changes in the proximal region of the heme pocket. These results indicated that the mutation causes a perturbation at a distance from the mutation site.     

Identification of SH2B2beta as an inhibitor for SH2B1- and SH2B2alpha-promoted Janus kinase-2 activation and insulin signaling

The SH2B family has three members (SH2B1, SH2B2, and SH2B3) that contain conserved dimerization (DD), pleckstrin homology, and SH2 domains. The DD domain mediates the formation of homo- and heterodimers between members of the SH2B family. The SH2 domain of SH2B1 (previously named SH2-B) or SH2B2 (previously named APS) binds to phosphorylated tyrosines in a variety of tyrosine kinases, including Janus kinase-2 (JAK2) and the insulin receptor, thereby promoting the activation of JAK2 or the insulin receptor, respectively. JAK2 binds to various members of the cytokine receptor family, including receptors for GH and leptin, to mediate cytokine responses. In mice, SH2B1 regulates energy and glucose homeostasis by enhancing leptin and insulin sensitivity. In this work, we identify SH2B2beta as a new isoform of SH2B2 (designated as SH2B2alpha) derived from the SH2B2 gene by alternative mRNA splicing. SH2B2beta has a DD and pleckstrin homology domain but lacks a SH2 domain. SH2B2beta bound to both SH2B1 and SH2B2alpha, as demonstrated by both the interaction of glutathione S-transferase-SH2B2beta fusion protein with SH2B1 or SH2B2alpha in vitro and coimmunoprecipitation of SH2B2beta with SH2B1 or SH2B2alpha in intact cells. SH2B2beta markedly attenuated the ability of SH2B1 to promote JAK2 activation and subsequent tyrosine phosphorylation of insulin receptor substrate-1 by JAK2. SH2B2beta also significantly inhibited SH2B1- or SH2B2alpha-promoted insulin signaling, including insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1. These data suggest that SH2B2beta is an endogenous inhibitor of SH2B1 and/or SH2B2alpha, negatively regulating insulin signaling and/or JAK2-mediated cellular responses.     

Influence of Mixed Na2O/K2O on Chemical Durability and Spectral Properties of P2O5-Al2O3-BaO-K2O-Na2O-Nd2O3 Phosphate Glasses

A series of 56P₂O₅-7.5Al₂O₃-5.9BaO-(28.56-x)K₂O-xNa₂O-1.51Nd₂O₃ phosphate glasses with different Na/(Na+K) ratios, which were specially designed for high-power laser application, were prepared by a high-temperature melting method. Except for the density, refractive index, glass transition temperature, and DC conductivity, the chemical durability and spectral properties, as emphasized by high-power and high-energy laser material, were further measured and analyzed. Regarding the chemical durability, the dissolution rates of these glasses do not show an evident mixed alkali effect with increasing the Na/(Na+K) ratio, although the effect is obvious for the glass transition temperature and DC conductivity. To better understand the nature of the dissolution mechanism, the ionic release concentrations of every element are determined. Both Na and K undergo ion exchange, but the ion exchange rate of K is much larger than that of Na. In terms of the spectral properties, the J–O parameters, emission cross-section, radiation lifetime, fluorescence lifetime, effective bandwidth, fluorescence branching ratio, and quantum efficiency are determined from absorption and emission spectra. The trend of Ω₂ deviating from linearity indicates that the coordination environment symmetry of Nd³⁺ ions and the covalence of Nd-O also present an evident mixed alkali effect. The most important finding is that the emission cross-section and fluorescence lifetime of Nd³⁺ ions at 1053 nm were not affected by the change in the Na/K ratio. According to the above experimental results, the optimized value of the Na/K ratio was determined, based on which the 56P₂O₅-7.5Al₂O₃-5.9BaO-(28.56-x)K₂O-xNa₂O-1.51Nd₂O₃ glass maintains a high emission cross-section with good chemical durability.