Calcitonin gene-related peptide immunoreactivity in the nucleus of the tractus solitarius and the carotid receptors of the cat originates from peripheral afferents.

The presence and distribution of the calcitonin gene-related peptide was studied, using immunohistochemical techniques, in carotid receptors, in the nodose and glossopharyngeal ganglia and in the nucleus tractus solitarii of the cat. Seventy-seven per cent of the 42% of the nodose ganglion cells were labeled. Fine, sparsely branched immunoreactive terminal axonal arborizations were found in the carotid body; they disappeared after petrosal ganglionectomy. The intense immunoreactivity present in fibers in the commissural, medial, interstitial, gelatinosus, dorsal, intermediate and rostral gustatory subnuclei of the nucleus tractus solitarius was drastically reduced after removal of the ipsilateral nodose and petrosal ganglia. The central distribution of the immunoreactive axons, the morphology of the terminals in the carotid receptors and their dependence on an intact peripheral innervation are consistent with the idea that in the cat the calcitonin gene-related peptide is present in a high proportion of the primary visceral afferents, most of them unmyelinated.     

Anatomical substrate for separate processing of ascending and descending visceral information in the nucleus of the solitary tract of the rat

We examined the possible existence of divergent visceral pathways arising from the nucleus of the solitary tract, by co-injecting axonal tracers into the parabrachial nucleus and into the ventrolateral medulla. We found that around 5% of NTS neurons projected to both sites, and that neurons projecting to VLM were larger. This parallel organization allows a differential control of the ascending versus descending visceral pathways at an early stage of processing.     

CD4(+) CD25(+) T cells prevent arthritis associated with Borrelia vaccination and infection

CD4(+) CD25(+) T cells are a population of regulatory T cells associated with control of arthritis in anti-interleukin-17 antibody-treated Borrelia-vaccinated and challenged gamma interferon-deficient mice. Here, we present direct evidence that adoptive transfer of enriched CD4(+) CD25(+) T cells from these mice can prevent the development of arthritis in Borrelia-vaccinated and challenged mice. These findings establish a major role for CD4(+) CD25(+) T cells in the prevention of arthritis in Borrelia-vaccinated and challenged animals.     

Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody

CD4+ CD25+ T cells are a population of regulatory T cells responsible for active suppression of autoimmunity. Specifically, CD4+ CD25+ T cells have been shown to prevent insulin-dependent diabetes mellitus, inflammatory bowel disease, and pancreatitis. Here, we present evidence that CD4+ CD25+ T cells also play a major role in controlling the severity of arthritis detected in Borrelia burgdorferi-vaccinated gamma interferon-deficient (IFN-gamma degrees ) C57BL/6 mice challenged with the Lyme spirochete. When B. burgdorferi-vaccinated and challenged IFN-gamma degrees mice were treated with anti-interleukin-17 (IL-17) antibody, the number of CD4+ CD25+ T cells increased in the local lymph nodes. Furthermore, histopathologic examination showed the mice to be free of destructive arthritis. When these anti-IL-17-treated B. burgdorferi-vaccinated and challenged mice were also administered anti-CD25 antibody, the number of CD4+ CD25+ T cells in the local lymph nodes decreased. More importantly, severe destructive arthropathy was induced. In addition, delayed administration of anti-CD25 antibody decreased the severity of the arthritis. These results suggest that CD4+ CD25+ T cells are involved in regulation of a severe destructive arthritis induced with an experimental model of vaccination and challenge with B. burgdorferi.     

Neurotoxic lesion of anteromedial/posterior parietal cortex disrupts spatial maze memory in blind rats

The primary visual cortex of rats is surrounded laterally (in Oc2L) and medially (in Oc2M) by several peristriate visual areas. Previous studies from our laboratory demonstrated that bilateral lesions in Oc2L result in visual pattern discrimination deficit, and in failure to solve a conditional discrimination which requires figure-background association. In contrast, neurotoxic lesions of the rostral part of Oc2M (which contains the anteromedial and anterior peristriate visual areas, collectively referred to as AM complex) result in deficits in visuospatial discrimination, and in disruptions in visual tasks involving spatial memory. The objective of this study was to behaviorally test the role of AM complex in a spatial memory task in absence of visual cues. For this purpose, we analyzed memory retention of Lashley III maze in blind rats after bilateral ibotenate lesions in AM complex, or in the primary visual cortex (V1, Oc1), to test the hypothesis that AM complex is essential for this cognitive task. The results showed a significant loss of memory retention of the maze in rats with lesions in AM complex, but not in rats with lesions in V1. Furthermore, the retention loss in rats with AM complex lesions was positively and significantly correlated with the size of the lesion. The results indicate a critical role of AM complex in spatial memory mechanisms independent on visual cues. A probable homology of rat AM complex with the posterior parietal cortex of primates is discussed.     

Banff Schema for Grading Pancreas Allograft Rejection: Working Proposal by a Multi-Disciplinary International Consensus Panel

Accurate diagnosis and grading of rejection and other pathological processes are of paramount importance to guide therapeutic interventions in patients with pancreas allograft dysfunction. A multi-disciplinary panel of pathologists, surgeons and nephrologists was convened for the purpose of developing a consensus document delineating the histopathological features for diagnosis and grading of rejection in pancreas transplant biopsies. Based on the available published data and the collective experience, criteria for the diagnosis of acute cell-mediated allograft rejection (ACMR) were established. Three severity grades (I/mild, II/moderate and III/severe) were defined based on lesions known to be more or less responsive to treatment and associated with better- or worse-graft outcomes, respectively. The features of chronic rejection/graft sclerosis were reassessed, and three histological stages were established. Tentative criteria for the diagnosis of antibody-mediated rejection were also characterized, in anticipation of future studies that ought to provide more information on this process. Criteria for needle core biopsy adequacy and guidelines for pathology reporting were also defined.
The availability of a simple, reproducible, clinically relevant and internationally accepted schema for grading rejection should improve the level of diagnostic accuracy and facilitate communication between all parties involved in the care of pancreas transplant recipients.