Endothelial dysfunction occurs early in the development of vascular disease in diabetes. Total plasma homocyst(e)ine (tHcy) is associated with endothelial dysfunction. We therefore aimed to assess endothelial function in children with type 1 diabetes in relation to tHcy and its determinants. Endothelial function was assessed in 36 children with type 1 diabetes aged 13.7 ؎ 2.2 years and 20 age-and sex-matched control subjects using ultrasound assessment of flow-mediated dilatation (FMD) and glyceryl trinitrate (

In studies of immune cell defects in autoimmune diabetes mellitus, we observed that complete Freund's adjuvant (CFA) prevented the onset of diabetes when injected into 8- to 10-wk-old prediabetic nonobese diabetic (NOD) mice. The prevalence of the onset of diabetes in the CFA-injected versus uninjected NOD mice was 2 of 81 (2.5%) vs. 231 of 379 (61%) among females and 2 of 44 (4.5%) vs. 83 of 336 (25%) among males, respectively. The incidence of histologically identifiable insulitis was significantly reduced in CFA-treated prediabetic female NOD mice (18%) compared with the incidence in female age-matched controls (70%). Splenocytes or Mac-(1+)-enriched splenocytes from CFA-treated NOD mice, when cotransferred with splenocytes from diabetic mice, reduced the incidence of diabetes provoked by diabetic splenocytes in vivo. In the spleen, CFA injection induced sustained increases in cell proliferation and an associated major increase in the numbers of an immature cell type that expressed the Mac-1 surface antigen. In CFA-treated NOD mice, lymphocytes derived from the spleen failed to respond in vitro to stimulation by the mitogen concanavalin A or by anti-CD3. When cocultured, Mac-1+ cells, enriched from the splenocytes of CFA-treated mice, suppressed concanavalin A- or anti-CD3-induced proliferation of T lymphocytes derived from either the spleen or thymus of untreated NOD mice. Therefore, treatment with CFA prevents the development of diabetes, and concomitantly, insulitis while stimulating the generation of splenic suppressor cells that are capable of suppressing diabetogenic T-lymphocyte function in vivo and in vitro.

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This paper introduces a method for the substantial reduction of heading errors in inertial navigation systems used under GPS-denied conditions. Presumably, the method is applicable for both vehicle-based and personal navigation systems, but experiments were performed only with a personal navigation system called "Personal Dead Reckoning" (PDR). In order to work under GPS-denied conditions, the PDR system uses a foot-mounted Inertial Measurement Unit (IMU). However, gyro drift in this IMU can cause large heading errors after just a few minutes of walking. To reduce these errors, the Map-matched Heuristic Drift Elimination (MAPHDE) method was developed, which estimates gyro drift errors by comparing IMU-derived heading to the direction of the nearest street segment in a database of street maps. A heuristic component in this method provides tolerance to short deviations from walking along the street, such as when crossing streets or intersections. MAPHDE keeps heading errors almost at zero, and, as a result, position errors are dramatically reduced. In this paper, MAPHDE was used in a variety of outdoor walks, without any use of GPS. This paper explains the MAPHDE method in details and presents experimental results.

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In this report we examined the antigen-presenting cell (APC) requirements for activation of T-cell hybridomas specific for the protein antigen PPD (purified protein derivative of tuberculin). During the course of these studies we observed that glutaraldehyde fixation of Ia-positive A20.2JAD (A20) and P388D1 stimulator cells had different effects on T-cell activation. A20 cells fixed with glutaraldehyde stimulated the T cells in the presence of PPD as efficiently as nonfixed A20 cells. By contrast, glutaraldehyde treatment of Ia-positive P388D1 cells dramatically inhibited their ability to process and/or present PPD to T cells. This was not due to nonspecific effects on the P388D1 cells since cells prepulsed with PPD prior to glutaraldehyde treatment stimulated T cells as efficiently as non-glutaraldehyde-treated P388D1 cells. In addition, there was no apparent difference in "fixing" of the two cell types as determined by the uptake of radiolabeled thymidine. These observations suggested that P388D1, but not A20, cells required PPD internalization to form the relevant antigenic determinants. This was substantiated by showing that treatment of P388D1 cells with chloroquine prior to PPD pulsing eliminated their stimulatory capacity, but had no effect on P388D1 cells previously pulsed with PPD. Chloroquine treatment had no effect on stimulation by A20 cells. Since PPD internalization appeared not to be required for presentation by A20 cells, we next determined if isolated A20 plasma membranes would substitute for the intact cell. We observed that the isolated plasma membranes from PPD-pulsed A20 cells stimulated the T hybridoma cells, and that this stimulation was antigen-specific and was inhibited by anti-Ia monoclonal antibodies. Taken together, the results presented here suggest that for the PPD-specific T-cell responses examined here, different APC utilize distinct pathways to present the same antigenic determinant for T-cell recognition.