Increase in the proportion of granulated CD56+ T cells in patients with malignancy.

Evidence is presented for the existence of a unique T cell population which expressed one of the natural killer (NK) markers, CD56 antigen, in humans. Although such CD56+ T cells were a minor population in the peripheral blood (< 10%), they were abundant in the liver (up to 50%), which was recently demonstrated to be a major organ for extrathymic T cell differentiation in mice. As in the case of extrathymic T cells in mice, these CD56+ T cells in humans contained a higher proportion of gamma delta T cells than did CD56- T cells, contained double-negative CD4-8- cells, and had the morphology of large granular lymphocytes. This unique population of CD56+ T cells tended to be elevated in the blood and among tumour-infiltrating lymphocytes in patients with colorectal cancer, especially in advanced cases. These results raise the possibility that, as in mice, CD56+ T cells with extrathymic T cell properties may also be associated with tumour immunity in humans.     

Subpopulations of CD4+ cells in lpr/lpr mice: differences in expression of T cell receptor/CD3 complex and proliferative responses.

CD4+ cells from autoimmune-prone C57BL/6 lpr/lpr mice contain two subpopulations, B220-CD4+ and B220+CD4+ cells. Highly purified B220-CD4+ cells from C57BL/6 +/+ and lpr/lpr mice were examined by comparing functional characteristics and expression of cell surface antigens and T cell receptor (TcR)/CD3 complex. Both lpr B220+CD4+ and B220+CD4-CD8- cells, most of which were PgP-1 positive, expressed TcR/CD3 complex on the cell surface at lower level as compared with B220-CD4+ cells of age-matched normal mice. In addition, the B2200-CD4+ cells were heterogeneous on the basis of surface expression of PgP-1 and CD3 antigens. Normal levels of TcR C alpha-, C beta- and V beta 8-specific mRNA were found in the B220-CD4+ cells and B220+CD4+ cells as compared with normal B220-CD4+ cells, while V beta 8-specific mRNA was preferentially expressed only by B220+CD4-CD8- cells. Either B220+CD4+ cells and B220+CD4-CD8- cells failed to respond to anti-CD3 monoclonal antibody (MoAb) as assessed by proliferative responses and production of interleukin-2 (IL-2). However, appreciable levels of reactivity to anti-CD3 MoAb were detected in the B220-CD4+ cells, although the responsiveness of this subset to such stimuli were reduced, compared with those of normal control. These results indicate that the B220-CD4+ cells in lpr mice are phenotypically and functionally distinct from normal B220-CD4+ cells.     

Human IgG anti-F(ab'')2 antibodies possess rheumatoid factor activity.

Individual preparations of affinity purified anti-F(ab')2 antibodies and anti-Fc antibodies isolated from the sera of patients with rheumatoid arthritis (RA), were examined for reactivity with the Fab and Fc fragments of human IgG. Western blot assays demonstrated specific interaction of affinity-purified anti-Fab antibodies with both Fab and Fc molecules. Approximately one-half of the anti-Fab antibody preparations studied contained IgG antibodies reactive with Fab and Fc fragments in ELISA, suggesting the existence of naturally occurring epibody-like autoantibodies in these patients. Thirteen of 14 affinity-purified anti-Fc antibody preparations contained IgG cross-reactive with Fab molecules in ELISA. Double-adsorption assays on affinity columns demonstrated that a minimum of 14%, and possibly as much as 50%, of the IgG anti-Fab antibodies reacted with the Fc of IgG. Conversely, a minimum of 12%, and possibly as much as 70%, of the IgG anti-Fc antibodies reacted with IgG Fab molecules. Anti-Fab antibodies isolated from non-RA individuals also exhibited anti-Fc reactivity in ELISA, demonstrating the presence of these dual-reactive antibodies in other autoimmune and normal individuals. These studies establish the presence of naturally occurring IgG autoantibodies reactive with both the Fab and Fc fragments of human IgG. Their existence emphasizes the potential of anti-immunoglobulin antibodies to recognize a multiplicity of antigens, possibly including other members of the immunoglobulin supergene family.     

Neuropeptides TRH and cyclo(His-Pro) share neuromodulatory,but not stimulatory,action on hypothalamic neurons in vitro: implication for the regulation of feeding

Summary Electrical activity of neurons in rat hypothalamic ventromedial nucleus was recorded in tissue slices, to investigate central neural mechanisms underlying reduction of food intake caused by TRH and its metabolite, cyclo(His-Pro) [cHP]. Application of TRH had two actions: stimulation of neuronal activity, which was desensitized on closely repeated applications; and modulation of neuronal responses to neurotransmitters, even in the absence of the stimulatory action. The neuromodulatory but not the direct stimulatory action could also be achieved by cHP. The neuromodulatory action is more likely to be a neural mechanism underlying the inhibition of feeding, while other biological functions, unique to TRH, may depend on direct stimulation. In this way, TRH could achieve different biological results through different modes of action on hypothalamic neurons.     

Effects of SITS on urate transport by isolated,perfused snake renal tubules

Effects of an inhibitor of membrane anion-exchange transport processes, 4-acetamido-4-isothiocyano-2,2-disulfonic stilbene (SITS), on urate transport by isolated, perfused snake (Thamnophis spp.) proximal renal tubules were studied. SITS (10^–4 mol/l) in the luminal perfusate had absolutely no effect on net urate secretion (J _urate ^net ) or on net fluid absorption (J _v). This observation is compatible with other data that give no support to the concept of a mediated transport step for urate from the cells to the lumen. SITS (10^–4 mol/l) in the bathing medium reversibly inhibitedJ _urate ^net without affectingJ _v. At the time of maximum inhibition ofJ _urate ^net , the concentration of urate in the cell water was increased and the apparent permeability of the luminal membrane to urate was decreased, but the urate efflux across the peritubular membrane and the apparent permeability of the peritubular membrane to urate were unchanged. There was no evidence of significant intracellular binding or trapping of urate. Although an increase in the initial rate of urate transport into the cells across the peritubular membrane could not be demonstrated conclusively in nonperfused tubules, the results still suggest that SITS in the bathing medium may inhibitJ _urate ^net by inhibiting urate movement from the cells to the lumen while actually enhancing transport from the bathing medium into the cells.     

Generation of the eosinophil chemotactic factor (ECF) from various cell types by melittin

The peptide melittin, the main constituent of bee venom is a potent stimulus for the generation of an eosinophil chemotactic factor (ECF) from human polymorphonuclear neutrophils, rat mast cells and rat peritoneal cells depleted in mast cells. Optimal EFC induction required a sublytic activation of the cells. With each cell type the kinetics of ECF generation were similar in that after an early rise in activity a steep fall off occurred at later times of incubation suggesting a mechanism of inactivation. The induction of ECF by melittin is increased in the presence of calcium. The polar portion of the melittin molecule (aminoacids 20–26) is responsible for the generation of the chemotactic activity. Other peptides of honey bee venom such as the mast cell degranulating peptide (MCD) or apamine do not initiate ECF release. It appears that melittin leads to ECF induction via the phospholipase A₂-arachidonic acid dependent pathway of cell activation. Our data suggests that the lipid mediator ECF can be obtained from phagocytes and mast cells thus indicating the interdependence of inflammatory reactions.     

Migration of Medical Image Data Archived Using Mini-PACS to Full-PACS

This study evaluated the migration to full-PACS of medical image data archived using mini-PACS at two hospitals of the Yonsei University Medical Center, Seoul, Korea. A major concern in the migration of medical data is to match the image data from the mini-PACS with the hospital OCS (Ordered Communication System). Prior to carrying out the actual migration process, the principles, methods, and anticipated results for the migration with respect to both cost and effectiveness were evaluated. Migration gateway workstations were established and a migration software tool was developed. The actual migration process was performed based on the results of several migration simulations. Our conclusions were that a migration plan should be carefully prepared and tailored to the individual hospital environment because the server system, archive media, network, OCS, and policy for data management may be unique.     

大鼠嗅球和鼻腔嗅粘膜成鞘细胞的形态学研究

目的：观察大鼠嗅神经成鞘细胞在嗅球和嗅粘膜的分布及其形态学结构特征，研究其与中枢神经再生的关系。方法：Luxol固蓝染色、Mallory染色和NGFRp75免疫组织化学染色结合透射电镜观察。结果：在嗅球纤维层的成鞘细胞随神经纤维呈纵向排列，在嗅小球层的成鞘细胞则围绕着嗅小球环行排列。在嗅粘膜的成鞘细胞位于柱状上皮深方，沿基底膜分布。成鞘细胞的胞体为细长梭形，有较长的突起，细胞核呈圆形或椭圆形。在嗅小球周围或嗅粘膜内的成鞘细胞呈NGFRp75免疫反应阳性。在电镜下，嗅球成鞘细胞的纵断面上可见其胞体呈长梭形，细胞核为不规则形，核仁清晰。在胞体的周围有大量的平行神经纤维纵向排列，在放大的横断面上，可见在1个成鞘细胞的细胞核周围有数根神经纤维被胞质包裹在一起。结论：嗅成鞘细胞是一种特殊的胶质细胞，分布于嗅球的纤维层、嗅小球层和嗅粘膜内。嗅神经成鞘细胞的胞体细长，有较长突起，其轴系膜紧密包裹成束的无髓神经纤维。     

CD4+CD56+ hematodermic neoplasms bear a plasmacytoid dendritic cell phenotype

CD4+CD56+ hematodermic neoplasms (HNs) with initial presentation in the skin are characterized by highly aggressive behavior and poor prognosis. Recent studies indicate that malignant cells, which are devoid of common T-, B-, NK-, and myeloid lineage markers, may be of plasmacytoid dendritic cell (pDC) origin. We undertook a study to assess the expression of several pDC-associated molecules on a series of 5 CD4+CD56+ HN cases. CD123 was expressed in all 5 cases, with some heterogeneity in individual cases. All but one case revealed fine membranous BDCA-2 staining of the dermal infiltrate. pDC-like phenotype of the malignant infiltrating cells was confirmed by costaining of BDCA-2+ cells with CD123 and CD4. MxA protein, representing the surrogate marker for lesional type I interferon activity, was expressed in 4 of 5 evaluated cases. Our findings further substantiate the putative pDC origin of CD4+CD56+ HNs.