α1b干扰素治疗小儿乙型肝炎病毒相关性肾炎的远期疗效

鉴于皮质醇激素治疗小儿乙型肝炎病毒相关性肾炎（ＨＢＶ－ＧＮ）的各种不良反应，现应用国产人α１ｂ基因工程干扰素治疗８例小儿ＨＢＶ－ＧＮ，剂量为３００万Ｕ／ｍ＾２体表面积隔天肌注，４个月后改为每周肌注２次持续２个月，总疗程６个月，用药期间无严重副反应，结果是５例尿蛋白消失，肾病缓解，２例尿蛋白减少，１例无进步，６例血清总蛋白，白蛋白上升，有３例血清ＨＢＶ抗原转阴（其中２例ＨＢｅＡｇ，ＨＢｓＡｇ均转阴，     

干扰素联合胸腺肽治疗慢性乙型肝炎62例

目的：观察干扰素α（ＩＮＦ－α）联合胸腺肽治疗慢性乙型肝炎（Ｃｈｒｏｎｉｃ Ｈｅｐａｔｉｔｉｓ Ｂ，ＣＨＢ）的疗效。方法：１２６例患者随机分为治疗组６２例，给ＩＦＮ－α３００万ＩＵ＋胸腺肽２０ｍｇ，均隔日１次；对照组６４例，单用ＩＮＦ－α３００万ＩＵ，隔日１次，疗程均为６个月。主要观察患者治疗前后症状、体征、病毒复制指标、肝功能指标的变化。结果：①两组患者在主要症状、体征方面改善明显（ｘ＾２＝７．４５，Ｐ〈０．０５）。②疗程结束时及１年后，治疗组患者ＨＢｅＡｇ及ＨＢＶ－ＤＮＡ的阴转率均显著高于对照组（ｘ＾２＝５．４７、ｘ＾２＝８．６１，Ｐ〈０．０５、Ｐ〈０．０１）。结论：两药联用能明显抑制ＨＢＶ复制，降低其反跳和病情复发。     

肝胆管癌丙型肝炎病毒感染与p53和p21WAFD/CIP1异常表达的关系

为探讨丙型肝炎病毒（ＨＣＶ）感染与Ｐ５３和Ｐ２１ＴＷＡＦ－／ＣＩＰ１基因的关系。采用 化技术对２９例原发性肝胆管癌中ＨＣＶ抗原（ＮＳ５－Ａｇ）、ｐ５３和ｐ２１＾ＷＡＦＩ＝／ＣＩＰ１蛋白表达进行研究。结果：２９例胆管癌中ＮＳ５－Ａｇ、ｐ５３及Ｐ２１ＴＷＡＦＩ／ＣＩＰＩ蛋白表达进行研究。结果：２９例胆管癌中ＮＳ５－Ａｇ、Ｐ５３display structure     

肝癌组织IGF－II、IGF－IIR、HBxAg的表达与细胞DNA倍体和S期的关系

为了探讨胰岛素样生长因子ＩＩ（ＩＧＦ－ＩＩ）在肝癌发生发展中的作用，采用免疫组织化学ＰＡＰ法检测了肝癌组织ＩＧＦ－ＩＩ及其受体（ＩＧＦ－ＩＩＲ）、乙型肝炎病毒Ｘ抗原（ＨＢｘＡｇ）的表达，并用流式细胞术分析了ＩＧＦ－ＩＩ表达与细胞ＤＮＡ倍体、Ｓ期的关系。结果显示：（１）ＩＧＦ－ＩＩ、ＩＧＦ－ＩＩＲ、ＨＢｘＡｇ在血清乙型肝炎病毒（ＨＢＶ）标记阳性的癌组织阳性率均为９３％（ｎ＝１５），高于ＨＢＶ标记阴性的癌组织（１／５）（Ｐ＜０．０５）；（２）ＩＧＦ－ＩＩ阳性的癌组织ＤＮＡ异倍体出现率为１００％、Ｓ期比例为２８．８±６．４％，高于ＩＧＦ－ＩＩ阴性的癌组织ＤＮＡ异倍体出现率（６０％）和Ｓ期比例（１２．８±２．４％）（Ｐ＜０．０５）；（３）肝癌组织ＩＧＦ－ＩＩ、ＩＧＦ－ＩＩＲ的表达与ＨＢｘＡｇ表达一致。研究结果提示ＩＧＦ－ＩＩ可能在乙型肝炎病毒标志物（ＨＢＶ－Ｍ）阳性的肝细胞癌发生发展中有某种作用，ＨＢｘＡｇ可能是ＩＧＦ－ＩＩ基因的一种激活因子。     

α1b干扰素治疗慢性乙型病毒性肝炎随访研究

现报道５２例α１ｂ干扰素治疗慢性乙型肝炎患者１２月的随访结果。 １．研究对象：（１）病例均为１９９８年１月～２０００年４月四川大学传染科门诊或住院患者。诊断符合第五次全国传染病寄生虫病学术会议（北京）修订的标准。治疗组，男３７例，女１５例，平均年龄２８．６岁；ＩＦＮ－α１ｂ：３ＭＵ ３１例，５ＭＵ ２１例。对照组男２９例，女１１例，平均年龄２７．５岁，具有可比性（Ｐ＞０．０５）。（２）纳入标准：ＨＢｓＡｇ（＋），ＨＢｅＡｇ（＋），ＨＢＶＤＮＡ（＋）；７０Ｕ／Ｌ≤ＡＬＴ≤６００Ｕ／Ｌ的慢性乙型肝炎患…     

G—CSF配合大剂量CTX和VCR动员自体外周血干细胞的研究

本研究对１２例拟行ＡＰＢＳＣＴ的患者予ＶＣＲ１－２ｍｇ／ｍ２，体表面静注及ＣＴＸ７ｇ／＾２体表面积静滴，５－７天后予Ｇ－ＣＳＦ１００μｇ／ｍ＾２体表面积静注５－７天，白细胞升至３．０×１０＾９／Ｌ以上时，用ＣＳ３０００血细胞分离机单次收集单个核细胞ＭＮＣ〉２．８×１０＾８／ｋｇ，ＣＤ＾＋３４〉．６×１０＾６／ｋｇ，ＣＦＵ－ＧＭ〉３．９×１－０＾４／ｋｇ，ＡＰＢＳＣＴ后，全部患者于＋５天－＋１０天白     

华蟾素治疗慢性HBV携带者及慢性乙型肝炎的疗效观察

为了观察华蟾素治疗慢性ＨＢＶ携带者及慢性乙型肝为使乙肝病毒复制指标转阴的作用。我们选择ＨＢＶ携带者及慢性乙型肝炎６０例。治疗组用华蟾素４ｍｌ肌注,日一次,连用３个月,对照组不同华蟾素治疗,结果治疗组ＨＢｓＡｇ阳性者３０例中转阴１例,对照组无转阴者。ＨＢｅＡｇ阳性１６例中转阴８例,占（５０％）与对照组比Ｐ〈０．０２５,Ｐｒｅ－Ｓ２阳性者２３例中转阴１１例占（４７．８２％）与对照组比Ｐ〈０．０２５。结     

乳梨醇对亚临床性肝性脑病的疗效观察—随机双盲临床试验

目的：评估乳梨醇（Ｌａｃｔｉｔｏｌ）治疗亚临床性肝性脑病的疗效和安全性。方法：３１例亚临床性肝性脑病病人随机分为两组，治疗组１６例，对照组１５例。双盲法分别给予４０％乳梨醇溶液０．５５－１．７５ｍｌ·ｋｇ￣（－１）·ｄ￣（－１），平均１．０５ｍｌ·ｋｇ￣（－１）·ｄ￣（－１）１日３次，以获得每天１－２次软便，及安慰剂５％葡萄糖１０ｍｌ，１日３次，均连续服用２周。服药前后分别行数字连按试验（ＮＣＴ）、数字符号试验（ＤＳ），体表感觉诱发电位（ＳＳＥＰ）及血氨检查，并随访有无临床肝性脑病发生。结果：乳梨醇能有效降低血氨，改善ＮＣＴ、ＤＳ，缩短ＳＳＥＰ的Ｎ２、Ｐ２、Ｎ３、Ｐ３潜伏期。Ｎ１－Ｐ３、Ｎ１－Ｎ３峰间潜伏期，且副反应小。结论：乳梨醇是一种安全，有效的亚临床性肝性脑病的治疗药物。     

乙型肝炎病毒前C／C基因区硫代和脂肪链—硫代反义寡核苷酸的体外抗…

为了研究修饰的反义寡核苷酸（ＡＳＯＮ）的抗乙型肝炎病毒（ＨＢＶ）作用。以２．２．１５细胞为靶细胞，在ＨＢＶ前Ｃ／Ｃ基因区设计合成了１６聚硫代和脂肪链－硫代两种修饰的ＡＳＯＮ，用酶联免疫吸附和斑点杂交技术分别检测作用细胞的乙型肝炎病毒表面抗原（ＨＢｓＡｇ）和ｅ抗原（ＨＢｅＡｇ）以及ＨＢＶ ＤＮＡ的分泌情况。结果显示，ＡＳＯＮ在浓度为１０μｍｏｌ／Ｌ时能特异性抑制细胞９２％￣９５％ＨＢｓＡｇ和８４％￣     

慢性HCV感染者IFN治疗前后血清HCV RNA水平

目的评价ＩＦＮ对丙肝患者病毒血症水平的作用．方法竞争性逆转录聚合酶链反应（ＣＲＴＰＣＲ）法定量检测１２例慢性ＨＣＶ感染者（男８例，女４例，ＨＣＶＲＮＡ阳性，ＡＬＴ异常持续６个月以上）ＩＦＮ治疗（ＩＦＮａ２ｂ３ＭＵ，肌注，３次／周，疗程３个月）前后（随访６个月）血清ＨＣＶＲＮＡ水平．结果慢性ＨＣＶ感染者１２例，３例呈完全反应，６例呈部分反应，另外３例无反应．９例有反应者中４例复发，有反应者治疗结束时血清ＨＣＶＲＮＡ水平明显下降（５１７±０４０８ｖｓ２０６±１５５，１０ｃｏｐｉｅｓ／５０μｌｓｅｒｕｍ，ｘ±ｓ，Ｐ＜００５），无反应者血清ＨＣＶＲＮＡ水平未见明显下降（５６７±０５８ｖｓ４５±０８７，ｘ±ｓ，Ｐ＞００５）．３例完全反应者仅１例血清ＨＣＶＲＮＡ持续阴性，３例无反应者２例血清ＨＣＶＲＮＡ水平略有下降．结论ＩＦＮ治疗丙肝有效，但ＩＦＮ不能有效清除病毒，仅抑制病毒复制，未见治疗前血清ＨＣＶＲＮＡ水平与复发与否有关．     

脂蛋白（a）和载脂蛋白（a）多态性与女性冠心病的相关性研究

冠心病（ＣＨＤ）在病因、发病年龄等诸多方面存在性别差异。载脂蛋白（ａ）［ａｐｏ（ａ）］多态性与脂蛋白（ａ）［Ｌｐ（ａ）］血浆水平对女性ＣＨＤ影响的资料甚少。我们通过检测３５例女性ＣＨＤ患者和４５例女性正常对照者的ａｐｏ（ａ）多态表型及Ｌｐ（ａ）水平，并与相应的男性组对比分析，发现含有等位基因Ｓ１、Ｓ２、Ｂ的ａｐｏ（ａ）低分子量表型的ＣＨＤ患者，女性占３７．１４％，显著高于对照组，而男性仅占２５．７１％，与对照组比较差异无显著性。在女性中低分子量表型发生ＣＨＤ危险度为对照组的４．７倍，在男性中仅为１．４倍。提示：低分子量表型对女性ＣＨＤ的影响大于男性。Ｌｐ（ａ）水平在两性ＣＨＤ组均明显高于对照组，而两性之间则差异无显著性。     

Fibrodysplasia (myositis) ossificans progressiva (FOP)

Clinical Rheumatology -     

Erythropoiesis Inhibiting Factor(s) (EIF)

The specificity and toxicity of the urinary erythropoiesis inhibiting factor (EIF) has been tested both in vivo and in vitro. When EIF was given to ESF stimulated erythropoietically suppressed polycythaemic mice and to mice at maximal endogenous erythropoietic stimulation, a reduction of the erythroid bone marrow cells, the erythropoietic ³H-TdR L.I. and the total number of bone marrow cells were observed. No effect was seen on the myelopoietic bone marrow cells. An unspecific toxic effect was unlikely, since addition of EIF did not alter the proliferation of lymphoblastic cells nor change the glucose utilization of bone marrow cells in vitro. Neither did the amount of dead bone marrow cells increase after being incubated with EIF for 72 h. The results indicate that the urinary EIF is a non-toxic, cell specific inhibitor on erythropoiesis.     

Compound heterozygosity of Hb D(Iran) (beta(22) Glu-->Gln) and beta(0)-thalassemia (619 bp-deletion) in India

The present report describes the hematologic and molecular study of the second case of Hb D(Iran) associated with beta(0)-thalassemia (619 bp-deletion) found in India and the first case in which the mutations have been identified at molecular level. The patient showed hypochromic, microcytic red cell picture with reduced red cell indices. The characterization of the hemoglobinopathy was made by electrophoretic and chromatographic techniques and confirmed by sequencing of the beta-globin gene. Both the propositus and her father were found to be carriers of the gene for beta(0)-thalassemia owing to the 619 bp-deletion mutation as seen by the polymerase chain reaction (PCR). Single base substitution GAA > CAA (indicative of Hb D(Iran)) in the heterozygous form was seen in the propositus as well as the mother by sequencing.     

Platelet HDL(3) binding sites are not related to integrin alpha(IIb)beta(3) (GPIIb-IIIa)

Early studies considered that fibrinogen receptor (glycoprotein [GP] IIb-IIIa or platelet integrin alpha(IIb)beta(3)) is the binding site for low-density lipoprotein (LDL) and high-density lipoprotein type 3 (HDL(3)). Recent data, however, do not support the hypothesis that the binding of LDL to human intact resting platelets is related to integrin alpha(IIb)beta(3). In this study we present evidence that platelet integrin alpha(IIb)beta(3) is also not involved in the interaction of HDL(3) and human intact resting platelets. Firstly, specific ligands for platelet integrin alpha(IIb)beta(3), such as fibrinogen, vitronectin, von Willebrand factor and fibronectin, were unable to inhibit the binding of HDL(3) to intact resting platelets. Secondly, the HDL(3) binding characteristics (K(d) and B(max) values), the activation of protein kinase C (PKC) and the inhibition of thrombin-induced inositoltriphosphate (IP(3)) formation and calcium (Ca(2+)) mobilization mediated by HDL(3) particles were similar in platelets from control subjects and patients with type I and type II Glanzmann's thrombasthenia, which are characterized by total and partial lack of GPIIb-IIIa and fibrinogen, respectively. In contrast, nitrosylation of tyrosine residues of HDL(3) by tetranitromethane fully abolished both the ability of particles to interact with its specific binding sites and the functional effects. Thirdly, polyclonal antibodies against the GPIIb-IIIa complex (edu-3 and 5B12), human antiserums against platelet alloantigens (anti-Bak(a/B) and anti-PL(A1/2)), anti-integrin subunits (anti-alpha(V) and anti-beta(3)), and a wide panel of monoclonal antibodies (mAbs) against well-known epitopes of GPIIb (M3, M4, M5, M6, M8 and M95-2b) and GPIIIa (P23-7, P33, P37, P40, and P97) did not affect the binding of HDL(3) particles to human intact resting platelets. Overall results show that neither the GPIIb-IIIa complex nor GPIIb or GPIIIa individually are the membrane binding proteins for HDL(3)on intact resting platelets.