子宫内膜组织ER、PR及PCNA表达与子宫内膜增生过长的关系

目的：探讨子宫内膜增生过长的发病机理，为临床内分泌治疗提供理论基础。方法：应用免疫组织化学Ｓ－Ｐ法，对手术切除和诊刮的６７例不同时期子宫内膜和不同类型增生过长子宫内膜标本进行ＥＲ、ＰＲ和ＰＣＮＡ含量检测分析。结果：ＥＲ、ＰＲ在正常增生期子宫内膜中的含量显著高于分泌期（Ｐ＜０．０１），在单纯性增生过长和复杂性增生过长子宫内膜中ＥＲ、ＰＲ的含量也有显著差异（Ｐ＜０．０１）。各组增生过长子宫内膜中ＥＲ的含量高于ＰＲ（Ｐ＜０．０１）。ＰＣＮＡ在内膜分泌期和伴有非典型增生的子宫内膜中含量高（Ｐ＜０．０１）。结论：ＥＲ主要与子宫内膜增生过长有关，ＰＣＮＡ在非典型增生子宫内膜中过表达可能与宫内膜异常生长有关。     

癫痫患者免疫状态的探讨

本文观察了７０例癫痫（ＥＰ）患者的免疫状态，首次检测了Ｂ淋巴细胞亚群，ｓＩＬ－２Ｒ及ＴＮＦ，对各项免疫学指标进行了对比研究，发现ＩｇＡ，ＩｇＭ含量明显降低，ＣＩＣ含量明显增高（Ｐ＜０．０１），Ｃ３明显降低（Ｐ＜０．０５），显示患者体液免疫功能低下；淋巴细胞亚群测定发现ＣＤ３＾＋，ＣＤ４＾＋明显降低，ＣＤ８＾＋明显增高，ＣＤ４＾＋／ＣＤ８＾＋比值明显低于对照组（Ｐ＜０．０１），表明细胞免疫功能低下；     

绞股蓝总皂甙抗大鼠海马结构缺血再灌注损伤的实验研究

探讨大鼠海马结构缺轿再灌注损伤机理及绞股蓝总皂甙抗缺血再灌注损伤的作用，结果：ＩＲ组海马组织中ＭＤＡ含量高于组（Ｐ〈０．０１），而ＳＯＤ含量低于ＳＯＣ组（Ｐ〈０．０１），差异非常显著：ＩＲ＋ＧＰ组海马组织中ＭＤＡ含量明显低于ＩＲ组（Ｐ〈０．０１），而ＳＯＣ含量明显高于ＩＲ组（Ｐ〈０．０１），ＩＲ组海马组织Ｎａ＾＋－Ｋ＾＋－ＡＴＰａｓｅ，Ｃａ＾２＋－ＡＴＰａｓｅ的活性明显低于ＳＯＣ组（Ｐ〈０．０１）     

子宫肌瘤ER,PR与其细胞核体定量关系的探讨

应用ＡＢＣ法和计算机图象分析系统（ＩＡＳ）定量分析３９例子宫肌瘤患者子宫组织雌、孕激素受体（ＥＲ．ＰＲ）含量，对其中８例子宦肌瘤及肌层细胞核体作定量分析，并探讨它们之间的关系。结果为子宫肌瘤ＥＲ、ＰＲ含量显著高于同一子宫肌层的含量（Ｐ＜０．０１）：子宫肌瘤细胞核体数密度、体密度亦显著高于相应子宫肌层的对应值（Ｐ＜０．０５，Ｐ＜０．０１）：子宫肌瘤ＥＲ与其细胞核体数密度呈正相关（ｒ＝０．８３，Ｐ＜０．０５）。提示子宫肌瘤的发生，发展与雌、孕激素及其受体含量有关。     

外周血CD3^＋CD56^＋T细胞在恶性肿瘤患者中的表现及临床意义

目的 了解ＣＤ３＾＋ＣＤ５６＾＋Ｔ细胞与ＣＤ３＾－ＣＤ５６＾＋、ＣＤ３＾＋ＣＤ５６＾－的关系及其在参与恶性肿瘤患者抗肿瘤免疫中的作用。方法 采用流式细胞术对１００例恶性肿瘤患者（５５例实体瘤患者和４５例非实体瘤患者）及４６例健康对照组外周血中的ＣＤ３＾＋ＣＤ５６＾＋、ＣＤ３＾－ＣＤ５６＾＋、ＣＤ３＾＋ＣＤ５６＾－３类淋巴细胞进行标记分析。结果 在实体瘤和非实体瘤患者组中：ＣＤ３＾＋ＣＤ５６＾＋Ｔ细胞均有高表达,２组患者与健康对照组比较均有显著性差异（Ｐ〈０．０１）。ＣＤ３＾＋ＣＤ５６＾－Ｔ细胞在实体瘤组的表达都显著低于非实体瘤组和健康对照组,２组间比较均有显著性差异（Ｐ〈０．００１）;而ＣＤ３＾－ＣＤ５６＾＋ＮＫ细胞在２患者组中的表达与健康对照组比较均无显著性差异（Ｐ〉０．０５）。结论 ＣＤ３＾＋ＣＤ５６＾＋Ｔ     

肾病综合征可溶性白细胞介素2受体改变的研究

采用ＥＬＩＳＡ法检测３２例ＮＳ患儿及２４例健康对照儿童血清和尿液ｓＩＬ－２Ｒ浓度并采用单克隆抗体间持免疫荧光法检测Ｔ细胞亚群，结果；（１）ＮＳ活动期组患儿血清及尿液ｓＩＬ－２Ｒ浓度明显高于ＮＳ缓解期组（Ｐ〈０．０１）和健康对照组（Ｐ〈０．０１），而ＮＳ缓解期组血清及尿液ｓＩＬ－２Ｒ浓度与健康对照组间无显著性差异（Ｐ〉０．０５）；（２）ＮＳ活动患儿尿液ｓＩＬ－２Ｒ与血清ｓＩＬ－２Ｒ浓度呈正相关（Ｒ＝     

EGR-1、c-erbB-2、ER、PR在乳腺癌中的表达及其相互关系

目的：探讨早期生长反应基因（ＥＧＲ－１）在乳腺癌的表达及其与癌基因ｃ－ｅｒｂＢ－２和ＥＲ、ＰＲ的关系。方法：应用免疫组织化学ＳＡＢＣ法,以ＥＧＲ－１、ｃ－ｅｒｂＢ－２、ＥＲ、ＰＲ抗体标记７５例不同病变的乳腺组织。结果：乳奶性病变可见相对高水平的ＥＧＲ－１表达而乳腺癌ＥＧＲ－１阳性仅１９例（４２．２％）,ＥＧＲ－１表达与乳腺癌淋巴结转移和ＥＲ、ＰＲ表达有关（Ｐ〈０．０５,Ｐ〈０．０１）,与ｃ－ｅｒｂ     

IL—4对多发性骨髓瘤患者外周血细胞CD20及HLA—DR表达…

本文报道用流式细胞分析技术，检测了２８例多发性骨髓瘤（Ｍ Ｍ）患者和２０名健康对照者外周血Ｂ细胞（ＣＤ＾＋２０）以及Ｂ、Ｔ和单核细胞中ＨＬＡ－ＤＲ＾＋细胞比率。结果发现，ＭＭ患者ＣＤ＾＋２０以及Ｂ、Ｔ及单核细胞中ＨＬＡ－ＤＲ＾＋细胞比率与正常对照组差异非常显著（Ｐ＜０．０１）。加入重组ＩＬ－４，可使８名ＭＭ患者ＣＤ＾＋２０、ＨＬＡ－ＤＲ＾＋ＣＤ＾＋２０、ＨＬＡ－ＤＲ＾＋单核细胞比率提高非常显著（Ｐ     

高频心电图对小儿川崎病心脏损害的敏感性研究

应用高频心电图（ＨＦＥＣＧ）技术对４８例川崎病患儿和１２１例正常儿童作对照检测，进行川崎病致心脏损害的敏感性研究。结果表明川崎病组６导联组合切迹计数的阳性率（７９．１６％）与正常组相比，有非常显著性差异（Ｐ＜０．０１）；川崎病组在病程不同时期内高频心电图均表现出不同程度的异常，尤以１－８周内比较，有非常显著性差异（Ｐ＜０．０１）；ＨＦＥＣＧ检测阳性率高于二维超声心电图（２ＤＥ），尤在患病１－８周九两组比较有显著性差异（Ｐ＜０．０１）；两对照组ＨＦＥＣＧ切迹数分布规律均为中间部＞终末部＞起始部，而以起始部具有显著性差异（Ｐ＜０．０１）。     

食管癌患者五项细胞免疫学指标的测定及其意义

对３５例食管癌（ＥＣ）患者和３０例正常人（ＮＣ）的外周血自然杀伤（ＮＫ）细胞活性、Ｔ细胞亚群、血浆可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）、肿瘤坏死因子α（ＴＮＦ－α）以及外周血诱生γ干扰素（ＩＦＮ－γ）的水平进行了检测。结果显示，ＥＣ患者ＮＫ细胞活性明显降低（Ｐ＜０．０１）；ＣＤ８＋细胞增多（Ｐ＜０．０６），ＣＤ４＋／ＣＤ８＋细胞比值降低（Ｐ＜０．０５）；ｓＩＬ－２Ｒ明显增高（Ｐ＜０．０１）；外周血诱生ＩＦＮ－γ降低（Ｐ＜０．０５）；血浆ＴＮＦ－α升高。表明，上述指标对判断、分析ＥＣ患者细胞免疫功能状况及病变程度有较大的意义。     

Cellular receptor for pixuna virus in chicken embryonic fibroblasts

In this study, we describe the isolation and partial characterization of a Pixuna virus receptor, which is a component of a plasma membrane fraction of chicken embryo fibroblast (CEF). Polyclonal antiserum was prepared from rabbits immunized with the membrane fraction. Said polyclonal antiserum reacted in a similar way as monoclonal antibodies raised against the membrane fraction. Both antisera were able to prevent CEF and Vero cells from infection with Pixuna virus. Immunofluorescence studies suggested that the receptors found in the fibroblasts and in the Vero cells shared at least some epitopes. The Western blot analysis of the purified membrane fraction antigens, which reacted with the monoclonal and polyclonal antibodies, detected a double band with a molecular mass of approximately 60 kDa. Not only immunofluorescence staining but also electron and immunoelectron microscopy studies evidenced the receptor localization in the plasma membrane. In this manner, we reported the isolation and partial characterization of a new Pixuna virus receptor in the plasma membrane of chicken embryo fibroblasts in culture. The data obtained demonstrated the receptor significance for the penetration of Pixuna virus into fibroblasts and mammalian cell and the related importance of designing new antiviral drugs by blocking the mechanism of receptor penetration of the virus into the cells.     

Ammonia-induced alterations in glutamate and muscimol binding to cerebellar synaptic membranes

Binding of glutamate and muscimol (an agonist for GABA_A receptors) to their respective receptors has been studied in the cerebellum of normal and hyperammonemic rats. There was a decrease in both high- and low-affinity binding of glutamate in the cerebellum during hyperammonemia. Kinetic studies revealed that the decrease is due to a reduction in the number of binding sites, but not due to changes in the binding affinities. Further studies also revealed that the decrease was only in the (NMDA)-specific binding sites without any alterations in the binding to non-NMDA sites represented by kianic acid (KA)- and quisqualic acid (QQ)-sensitive receptor sites. These effects were also mimicked when the membrane preparations from the cerebellum of normal animals were incubated with ammonium acetate. Enhancement of muscimol binding was observed in animals injected with ammonium acetate. It is concluded that hyperammonemic states, even in the presence of a functional liver, are capable of altering amino acid neurotransmission and this might play an important role in cerebral dysfunction under these conditions.     

IL-4 down-regulates IL-2 receptor p75 by accelerating its endocytosis

We examined the effects of interleukin 4 (IL-4) on the expressionof IL-2 receptor p75 (IL-2R p75) or ß chain on varioushuman T cells. IL-4 promptly down-regulated surface IL-2 receptor(IL-2R) p75 In these cells. Although IL-2-lnduced IL-2R p75down-regulation was seen more quickly, IL-2 did not contributeto the process of the IL-4-induced decrease of IL-2R p75. Northernblotting revealed that IL-4 did not reduce the expression ofIL-2R p75 mRNA. Studies using Pronase E, which digests cellsurface IL-2R p75, or brefeldin A, which blocks Intracytoplasmicprotein transport from endoplasmicretculum to the Golgi apparatus,suggest that IL-4-lnduced IL-2R p75 down-reguation is controlledafter IL-2R p75 is expressed on the cell surface. We found thatIL-4 accelerated the endocytosis of IL-2R p75, which was monitoredby (¹²⁵)||M||k-ß3 monocional antibody that recognizesnon-IL-2-bindlng epitope on IL-2R p75. These findings demonstratethat IL-4 down-regulates IL-2R p75 mainly by accelerating Itsendocytosis.     

Use of monoclonal antibody for assessment of estrogen and progesterone receptors in malignant effusions.

An immunocytochemical assay utilizing specific monoclonal antibodies against estrogen receptor (ER) and progesterone receptor (PgR) has been shown to be highly reliable for the detection of hormone receptors in hormone sensitive tumors. To assess the usefulness of this technique in malignant effusions, CytospinR (Shandon, Inc., Pittsburgh, PA 15275), preparations of 41 pleural and ascitic fluid were studied. The findings from the malignant cells employing estrogen and progesterone receptor immunocytochemical assay were compared with the results obtained from primary tumors by biochemical (dextran-coated charcoal) assay. The results agreed in 88% for ER and 83% for PgR. This study supports the potential value of cytochemical technique in detection of hormone receptors in malignant effusions. Assessment of hormone receptors in malignant effusions may be of clinical significance, particularly in situations where the hormone receptor status of the original tumor is not known. This information may also have some diagnostic and therapeutic importance in assessment of patients presenting with metastatic tumors of unknown origin.     

Identification of C-terminal domain residues involved in protein kinase A-mediated potentiation of kainate receptor subtype 6

Glutamate receptors are the major excitatory receptors in the vertebrate CNS and have been implicated in a number of physiological and pathological processes. Previous work has shown that glutamate receptor function may be modulated by protein kinase A (PKA)-mediated phosphorylation, although the molecular mechanism of this potentiation has remained unclear. We have investigated the phosphorylation of specific amino acid residues in the C-terminal cytoplasmic domain of the rat kainate receptor subtype 6 (GluR6) as a possible mechanism for regulation of receptor function. The C-terminal tail of rat GluR6 can be phosphorylated by PKA on serine residues as demonstrated using [gamma-32P]ATP kinase assays. Whole cell recordings of transiently transfected human embryonic kidney (HEK) 293 cells showed that phosphorylation by PKA potentiates whole cell currents in wildtype GluR6 and that removal of the cytoplasmic C-terminal domain abolishes this potentiation. This suggested that the C-terminal domain may contain residue(s) involved in the PKA-mediated potentiation. Single mutations of each serine residue in the C-terminal domain (S815A, S825A, S828A, and S837A) and a truncation after position 855, which removes all threonines (T856, T864, and T875) from the domain, do not abolish PKA potentiation. However, the S825A/S837A mutation, but no other double mutation, abolishes potentiation. These results demonstrate that phosphorylation of the C-terminal tail of GluR6 by PKA leads to potentiation of whole cell response, and the combination of S825 and S837 in the C-terminal domain is a vital component of the mechanism of GluR6 potentiation by PKA.     

Role of alpha chain-IL-2 complex in the formation of the ternary complex of IL-2 and high-affinity IL-2 receptor

Using anti-Tac (anti-alpha chain) and 2R-B (anti-beta chain) antibodies, we studied the roles of IL-2 receptor subunits (alpha and beta chains) in the formation of IL-2 and high-affinity IL-2 receptor complex, which is the initial event of IL-2 induced T cell growth. High-affinity IL-2 binding which was undetectable in the presence of 2R-B antibody at 4 degrees C became fully detectable when examined at 37 degrees C, which explained the lack of inhibition by 2R-B antibody of IL-2-induced proliferation of the cells expressing high-affinity IL-2 receptor. We further studied the mechanism of the 'reappearance' of high-affinity IL-2 binding in the presence of 2R-B antibody. The addition of IL-2 to the cells preincubated with radiolabeled or fluorescence-labeled 2R-B antibody resulted in a marked decrease in the antibody bound to the cells expressing high-affinity IL-2 receptor at 37 degrees C. This decrease was blocked by the presence of anti-Tac antibody, which inhibited IL-2 binding to alpha chain, but not by 7G7/B6 antibody, which recognized a non-IL-2 binding site of its chain. Furthermore, the decrease in cell-bound 2R-B antibody was not due to the internalization of beta chain-2R-B antibody complex, because the amount of cell-bound Mik-beta3 antibody recognizing a non-IL-2 binding epitope of beta chain remained unchanged, nor to the inhibition by simple competitive binding of IL-2 molecules to beta chain as judged from comparative studies of competitive binding inhibition. Taking these data together, the reappearance of high-affinity IL-2 binding was considered to be caused by the replacement of 2R-B antibody at the IL-2 binding site of beta chain by alpha chain-mediated IL-2, and it was strongly suggested that alpha chain-IL-2 complex has a key role in the formation of the ternary complex of IL-2 and high-affinity IL-2 receptor. alpha chain may function as a dimension converter of IL-2 to effectively deliver IL-2 molecules to a relatively small number of beta chains in the dynamics of the formation of high-affinity IL-2 binding in T cells.     

IL-1 up-regulates the expression of cytokine receptors on a factor-dependent human hemopoietic cell line, TF-1

A factor-dependent human hemopoietic cell line, TF-1, requiresinterleukln 3 (IL-3) or granulocyte/acrophage colony-stimulatingfactor (GM-CSF) for its long-term growth. We have found thatIL-4, IL-5, and IL-6 also support the growth of TF-1 and thatIL-1 enhances the proliferative effect of these cytoklnes. Augmentationby IL-1 is associated with up-regulatlon of the receptors forIL-3, IL-5, GM-CSF, and erythropoietln (Epo). IL-1 increasedthe number of binding sites forIL-3 and Epo without changingtheir affinities. In contrast, IL-1 Increased the number ofhigh affinity binding sites forGM-CSF and IL-5, whereas thetotal number of binding sites was unchanged. Chemical crossllnkingexperiments Indicated that the receptors for IL-3, IL-5, andGM-CSF were composed of two components and that the molecularmasses of the larger components of these cytokine receptorswere quite similar (120 kd). The enhanced expression of thelarger components of theIL-3, IL-5, and GM-CSF receptors byIL-1 may be responsible for IL-1-induced up-regulation of thesereceptors. These observations are consistent with the modelthat the receptors for IL-3 and GM-CSF share a common component.     

Human olfactory epithelial cells generated in vitro express diverse neuronal characteristics

The olfactory epithelium constitutes the sole source of regenerating neural cells that can be obtained from a living human. As such, primary cultures derived from human olfactory epithelial biopsies can be utilized to study neurobiological characteristics of individuals under different conditions and disease states. Here, using such human cultures, we report in vitro generation of cells that exhibit a complex neuronal phenotype, encompassing receptors and signaling pathways pertinent to both olfaction and other aspects of CNS function. Using in situ hybridization, we demonstrate for the first time the native expression of olfactory receptors in cultured cells derived from human olfactory epithelial tissue. We further establish the presence and function of olfactory transduction molecules in these cells using immunocytochemistry, calcium imaging and molecular methods. Western blot analysis revealed the expression of neurotransmitter receptors for dopamine (D2R), 5-HT (5HT2C) and NMDA subtypes 1 and 2A/2B. Stimulation with dopamine or 5-HT enhanced receptor G protein activation in a subtype specific manner, based on 35S-guanosine triphosphate incorporation assay. Functional characteristics of the cultured cells are demonstrated through enhanced tyrosine phosphorylation of NMDAR 2A/2B and recruitment of signaling partners in response to NMDA stimulation. The array of neuronal characteristics observed here establishes that proliferating cells derived from the human olfactory epithelium differentiate in vitro to express functional and molecular attributes of mature olfactory neurons. These cultured neural cells exhibit neurotransmitter pathways important in a number of neuropsychiatric disorders. Their ready availability from living humans thus provides a new tool to link functional and molecular features of neural cells with clinical characteristics of individual living patients.     

Toll-like receptors (TLRs) and Nod-like receptors (NLRs) in inflammatory disorders

Toll-like receptors (TLRs) and Nod-like receptors (NLRs) are two major forms of innate immune sensors, which provide immediate responses against pathogenic invasion or tissue injury. Activation of these sensors induces the recruitment of innate immune cells such as macrophages and neutrophils, initiates tissue repair processes, and results in adaptive immune activation. Abnormalities in any of these innate sensor-mediated processes may cause excessive inflammation due to either hyper responsive innate immune signaling or sustained compensatory adaptive immune activation. Recent gene association studies appear to reveal strong associations of NLR gene mutations and development of several idiopathic inflammatory disorders. In contrast, TLR polymorphisms are less often associated with inflammatory disorders. Nevertheless, TLRs are up-regulated in the affected tissue of most inflammatory disorders, suggesting TLR signaling is involved in the pathogenesis of chronic and/or idiopathic inflammatory disorders. NLR signaling results in the formation of a molecular scaffold complex (termed an inflammasome) and orchestrates with TLRs to induce IL-1β and IL-18, both of which are important mediators in the majority of inflammatory disorders. Therefore, understanding the roles of TLRs and NLRs in the pathogenesis of chronic and idiopathic inflammatory disorders may provide novel targets for the prevention and/or treatment of many common and uncommon diseases involving inflammation.