五音乐曲对精神分裂症脑电活动率的影响

目的 :观察五音乐曲刺激对精神分裂症患者脑电活动产生的影响。方法 :选取 2 0例精神分裂症患者和 10名正常对照 ,分别记录安静时段及聆听五音乐曲时段的脑电图 ,将脑电信号转化为功率数值 ,将 β/α定义为脑电活动率。 结果 :1、正常人与精神分裂症患者的脑电活动率在安静状态差异无显著性 (P >0 0 5 )。在听乐曲时患者的脑电活动率在C3、T3、T4、T5导联中 ,明显高于正常人 (P <0 0 5 )。 2、正常人在安静状态和听乐曲时其左右脑脑电活动率差异无显著性 (P >0 0 5 )。精神分裂症患者在安静状态左右脑脑电活动率在O1、O2及T5、T6导联间差异有显著意义 (P <0 0 5 ) ,并且听乐曲时在P3、P4和C3、C4以及F7、F8导联间差异有显著意义 (P <0 0 5 )。结论 :在五音乐曲的刺激下 ,精神分裂症患者的脑电反应与正常人不同。     

Correlations of Soluble Interleukin-2 and Tumor Necrosis Factor Type II Receptors with Immunologic and Virologic Responses Under HAART

We assessed the correlations between some plasma markers of immune activation (soluble receptors of interleukin 2 (sIL2-R) and TNFp75 (sTNFII-R) and usual markers of HIV infection in patients treated with protease-inhibitors (PI). Forty-six PI-naive HIV-1-infected adults were included in a 1-year prospective cohort from the initiation of a PI-containing regimen (M0). Measurements of CD4+cell count, plasma HIV-RNA, sIL2-R and sTNFII-R were performed at M0, M6, and M12. The evolution of sIL2-R from baseline to M12 was significantly different between immunological responders (IR) (CD4+count above 200/mm³ for subject having less than 200 CD4 +/mm³ at inclusion, or increase of at least 50 CD4+/mm³ for others) (58 UI/ml) and non-IR (+28 UI/ml) (P =0.01). The evolution of sTNFII-R between M0 and M12 was significantly different between virological responders (VR) (plasma HIV-1 RNA less than 500 copies/ml at M12) (–2.5 ng/ml) and non-VR (+0.2 ng/ml) (P =0.02). Our study shows significative correlations between the evolutions of soluble interleukin-2 and TNFR-II receptors and those of CD4+T-lymphocytes or HIV-RNA responses in patients under HAART.     

Loss of CD8 and TCR binding to Class I MHC ligands following T cell activation

The capacity of T cells to bind peptide/MHC ligands changes with T cell development and differentiation. Here we study changes in peptide/MHC multimer binding following T cell activation. Surprisingly, T cell activation caused a marked reduction in specific peptide/MHC Class I multimer binding, which was distinct from transient TCR down-regulation, and was especially dramatic for engagement with low-affinity peptide/MHC ligands. Direct CD8-Class I interactions were also profoundly and rapidly impaired following T cell stimulation, even though surface CD8alpha and CD8beta levels were unchanged after activation, suggesting that decreased CD8 co-receptor binding contributes to this effect. Finally, we show that enzymatic desialylation restores much of the multimer binding on activated T cells, suggesting that altered glycosylation may inhibit TCR/CD8 binding to peptide/MHC ligands. These radical changes in activated T cells' ability to perceive peptide/MHC ligands may contribute to selective outgrowth of clones with high affinity for the stimulatory ligand.     

CD45RA antibodies split the CD3bright T cell subset.

Thymocyte subsets have been well characterized on the basis of CD4 and CD8 antigen expression. Recently, the use of anti-CD3 antibodies has allowed more precise phenotyping of these subsets. The most immature T cell precursors are largely CD3-CD4-CD8-, while the most mature are CD3brightCD4+CD8- or CD3brightCD4-CD8+. Moreover, the expression of CD45RA on thymocytes appears to define a progenitor population and may define a continuous lineage of cells. Using a panel of CD45RA antibodies, we have further characterized the CD45RA+ thymocyte population in the murine system. The size of this subset is greatly enhanced in cortisone-treated mice and in sublethally irradiated mice. Moreover, the CD45RA+ population is present early in foetal life and is maintained thereafter. Using three-colour immunofluorescence, we show that (i) while most CD45RA+ cells are present amongst the CD4-CD8- thymocyte subset in the normal thymus, after cortisone treatment or irradiation, all four thymocyte subsets co-express significant amounts of CD45RA. This suggests that not only progenitor cells but also the mature population which can survive such manipulation are CD45RA+; and (ii) a large proportion of CD45RA+ cells are CD3bright and this subset is represented in the thymus at all stages of maturation tested. These data suggest that a proportion of TCR-gamma delta + CD3+ cells in the fetus as well as of TCR-alpha beta+ CD3+ cells in the adult co-express CD45RA.     

Activation induces apoptosis in Herpesvirus saimiri-transformed T cells independent of CD95 (Fas,APO-1)

Signaling via the T cell receptor (TCR)/CD3 complex of pre-activated T cells induces apoptosis. Such an activation-induced cell death (AICD) is thought to play an important role in the regulation of cellular immune responses. In this study we analyzed pathways of AICD by using human T cells transformed by Herpesvirus saimiri. These growth-transformed T cells show the phenotype of activated mature T cells and continue to express a functionally intact TCR. We show that human H. saimiri-transformed T cell clones readily undergo cell death upon signaling via the TCR/CD3 complex or via phorbol 12-myristate 13-acetate (PMA) + ionomycin. The AICD in H. saimiri-transformed T cells was detectable a few hours after activation and it was not affected by the presence of interleukin (IL)-2 or by anti-CD4 cross-linking. However, AICD required tyrosine phosphorylation, since it could be blocked by herbimycin A. Cyclosporin A (CsA) did not block the development of AICD, but other consequences of activation in H. saimiri-transformed T cells like the production of interferon-γ. Surprisingly, the development of AICD was not reduced by neutralizing antibodies to tumor necrosis factor (TNF)-α or blocking antibodies directed to CD95 (Fas, APO-1), although H. saimiri-transformed T cells were sensitive to CD95 ligation. To confirm that this form of AICD is really independent of CD95, we have established an H. saimiri-transformed T cell line from a patient with a homozygous deletion in the CD95 gene. This CD95-deficient T cell line was as sensitive to AICD as other CD95-expressing H. saimiri-transformed T cells. In conclusion, we describe here a type of AICD in H. saimiri-transformed T cells that is independent of CD95 and TNF-α, not sensitive to CsA, but requires tyrosine phosphorylation. This system should be useful for the investigation of CD95-independent forms of AICD.     

Elevation of activated gamma delta T cell receptor bearing T lymphocytes in patients with autoimmune chronic liver disease.

To study the possible role of T cells bearing the gamma delta T cell receptor (TCR) heterodimer in the pathogenesis of autoimmune chronic active hepatitis (AI-CAH) and primary sclerosing cholangitis (PSC) in children, we measured levels of gamma delta+ T cells in the peripheral blood, assessed the proportion of cells bearing the disulphide-linked (BB3+) and non-disulphide-linked (A13+) subtypes of the receptor, and studied the co-expression of TCR-gamma delta and the activation markers HLA-DR and IL-2 receptor (IL-2R), and the memory cell marker CD45RO. Percentage levels and absolute numbers of gamma delta +T cells were higher in both groups of patients than in controls (P less than 0.01), mainly as a result of an increase in both percentage levels and absolute numbers of the A13+ subtype (P less than 0.001). Co-expression of IL-2R and TCR-gamma delta was not found in controls but was present in some patients with AI-CAH (four out of 17) and PSC (six out of 12) at low levels (median 2.3%, range 1.7-5.0%). Expression of HLA-DR on gamma delta+ T cells was similar in both groups of patients and controls. The majority of gamma delta+ T cells in children with AI-CAH and PSC also expressed CD45RO (74.7 +/- 18.4% and 79.8 +/- 24.3%, respectively) at levels significantly higher than in controls (53.3 +/- 17.2%, P less than 0.01). These results suggest that autoimmune liver diseases in children are associated with an expansion and activation of gamma delta+ T cells in the peripheral blood, which may be important in the pathogenesis of these disorders.     

Vortex Shedding in Steady Flow Through a Model of an Arterial Stenosis and Its Relevance to Mural Platelet Deposition

In this study, the development of unsteady vortical formations in the separated flow region distal to a stenosis throat is presented and compared with the platelet deposition measurements, to enhance our understanding of the mechanisms involved in platelet kinetics in flowing blood. Qualitative and quantitative flow visualization and numerical simulations were performed in a model of a streamlined axisymmetric stenosis with an area reduction of 84% at the throat of the stenosis. Measurements were performed at Reynolds numbers (Re), based on upstream diameter and average velocity, ranging from 300 to 1800. Both the digital particle image visualization method employed and the numerical simulations were able to capture the motion of the vortices through the separated flow region. Periodic shedding of vortices began at approximately Re=375 and continued for the full range of Re studied. The locales at which these vortices are initiated, their size, and their life span, were a function of Re. The numerical simulations of turbulent flow through the stenosis model entailed a detailed depiction of the process of vortex shedding in the separated flow region downstream of the stenosis. These flow patterns were used to elucidate the mechanisms involved in blood platelet kinetics and deposition in the area in and around an arterial stenosis. The unsteady flow development in the recirculation region is hypothesized as the mechanism for observed changes in the distribution of mural platelet deposition between Re=300, 900, and 1800, despite only a marginal variation in the size and shape of the recirculation zone under these flow conditions. © 1999 Biomedical Engineering Society. PAC99: 8719Uv, 8710+e     

淋巴细胞经TCR－CD3活化增殖作用的分析

本文探讨了抗ＣＤ３单抗诱导的淋巴细胞活化增殖及有关影响因素。实验结果表明：①淋巴细胞内钙升高是淋巴细胞活化增殖的重要条件，ＣＤ３ＭｃＡｂ引起的早期胞浆游离钙迅速升高主要由内质网释放钙离子所致，而淋巴细胞增殖不仅需要细胞内钙释放，还需要细胞外钙内流；②ＧＴＰ结合蛋白是淋巴细胞激活过程的一重要环节，经Ｇ蛋白作用物霍乱毒素作用后，淋巴细胞ＤＮＡ合成显著降低；③新霉素和ＰＳＳ可抑制ＰＬＣ和ＰｋＣ的活性，对淋巴细胞ＮＤＡ合成造成剂量依赖性抑制作用。此外，抗ＣＤ３ＭｃＡｂ诱导的淋巴细胞ＤＮＡ合成需要辅佐细胞的存在，高度纯化的Ｔ细胞对ＣＤ３ＭｃＡｂ的刺激不发生增殖反应。     

Preferential expansion of Ly-1 B and CD4 CD8 T cells in the polyclonal lymphocyte responses to murine T.cruzi infection

Acute murine infection with T.cruzi results in polyclonal lymphocyteresponses manifested by blast transformation of a large fractionof B, CD4+, and CD8+ cells. We describe here the finding ofsignificant increases in the splenic representation of minorpopulations, Ly-1+ B cells and CD4-CD8- T cells. These lymphocytepopulations might play an important role in the host response,as shown by T.cruzi infection of hosts that had been lethallyirradiated and reconstituted with autologous bone marrow. Underthese conditions, the splenic polyclonal PFC responses are nearlyabrogated, and not restored by the transfer of syngeneic peritonealcells which, however, reconstitute T15 idiotype production inthe same hosts. Control levels of PFC responses, however, arereconstituted by transfer of syngeneic splenic T cells. Sincebone marrow-reconstituted animals contain normal numbers ofCD4+ and CD8+ T cells which are actually activated by infection,these results suggest the participation of other T cell populationsin the host response to infection, as also suggested by themarked increases in T cell receptor and messages detectedin the spleen of infected animals. The implications of thesefindings in immunopathology of Chagas' disease are discussed.     

一个新的人B细胞活化抗原—5C5

用活化人B细胞株3D5细胞免疫小鼠和作为筛选的靶细胞,我们建立了产生单克隆抗体5C5的杂交瘤细胞株。此单抗识别的抗原5C5在25μg/ml anti-μ刺激的B细胞,于第10小时开始表达,亦即于G_1期开始表达。5C5细胞百分率随培养时间而增多。在PWM诱导下.外周血单一核细胞中5C5~ 细胞随培养时间而增加,至第3～4天达最高峰,然后减少,至第7天降至本底水平。5C5~ 细胞在不能为BCDF诱导分化至免疫球蛋白分泌细胞(ISC)的B细胞株3D5,Raji和Daudi阳性,但在能为BCDF诱导分化至ISC的CESS和SKW6细胞却不表达。这均表明5C5抗原表达于B细胞活化的早期和中期,但在B细胞终末分化阶段消失。在休止期B细胞、休止期T细胞、PHA激活的T细胞、单核细胞和中性粒细胞,以及在所检测的T细胞株和髓细胞株,5C5抗原均为阴性。~(125)I标记后用单抗5C5免疫沉淀提取的抗原,在还原与非还原条件下电泳,均只有分子量为52000的一条带,表明5C5是一个单链细胞表面蛋白。鉴于5C5抗原的分子量与文献中已报道的B细胞活化抗原分子量不同,以及5C5在细胞株表达的特点,它可能是一个新的人B细胞活化抗原。