The location and distribution of type A and type B atrial endings in cats

Summary In the attempt to explain the difference in discharge pattern of atrial endings, 131 endings were localized by punctate stimulation, 44 were type A, 77 type B and 10 of an intermediate type. All were located on the dorsal wall of the atria with none on the ventral wall or in the appendage. On the right side, 74% of type A were located in the atria and 63% of type B in or near the veins. On the left side, 67% of type A and 94% of type B were located in or near the veins. Thus, there appeared to be some difference in the location of type A and type B endings on the right side, but on the left side both types of endings were for the most part confined to the venous region. Further, on both right and left sides, these endings were present both in the central part of the atria and in or adjacent to veins. This leads to the suggestion that the difference in discharge patterns is not caused by the location but may be due to some other reasons, e. g. difference of arrangement in the atrial wall with respect to the contractile elements.     

Astrocytes and intracerebral immune responses

The astrocyte is the most abundant cell within the central nervous system (CNS). This cell subserves a multiplicity of important functions that contribute to the process of neural development as well as to the integrity of normal brain function. Adding to the already exhaustive list of capabilities, the astrocyte has now been demonstrated to function as an intracerebral antigen presenting cell. These findings are serving to revise our view of the brain as an immunoprivileged site and perhaps will shed some light on the pathogenetic mechanisms involved in a number of CNS disorders of immune dysregulation. In this review we provide some perspective on the regulatory mechanisms that influence astrocyte immune functions. Specifically, we address the role played by the major histocompatibility complex (MHC) antigens as well as adhesion molecules in the initiation of brain immune responses.     

Subpopulations of human T lymphocytes. XVI. Maldistribution of T cell subsets associated with abnormal locomotion of T cells in untreated adult patients with Hodgkin's disease

Peripheral blood and splenic T cells from adult patients with Hodgkin's disease were examined for the proportions and numbers of T cells with receptors for IgM (Tμ) or IgG (Tγ) and their locomotor responses to chemotactic stimuli of casein and endotoxin-activated serum (EAS). Thirty per cent of patients had absolute lymphopenia in the peripheral blood. The proportion of Tμ cells was comparable but the proportion of Tγ cells was significantly increased (P<0·001) resulting in an abnormally low ratio of Tμ/Tγ cells when compared to those for age- and sex-matched controls. In the spleens, the proportions of T cells and Tμ cells were significantly increased (P<0·001) and Tγ cells significantly decreased (P<0·001) resulting in an abnormally high ratio of Tμ/Tγ cells when compared with normal spleens. In the peripheral blood both Tμ and Tγ cells were increased and T cells lacking either receptor (T) were significantly decreased in patients in whom spleens were involved by the tumour when compared to those in whom spleens were not involved by the tumour. Peripheral blood T cells from patients with Hodgkin's disease responded poorly to the chemotactic stimuli when compared to T cells from normal controls or T cells from the spleens of the same patients. Tμ cell proportions in patients with combined stages III and IV were significantly lower (P<0·025) than those in the peripheral blood of patients in combined stages I and II. No correlation was observed between the above parameters and histopathological types of Hodgkin's disease. This study demonstrates an abnormal distribution of T cell subsets and abnormality of locomotion of T cells between peripheral blood and spleens in patients with Hodgkin's disease. This might explain the cellular basis of at least certain immunodeficiencies so commonly associated with Hodgkin's disease.     

Sclerochoroidal calcification associated with Gitelman syndrome and calcium pyrophosphate dihydrate deposition

Sclerochoroidal calcification is an uncommon condition. Metabolic evaluation and clinical examination are important to exclude associated systemic conditions such as the Bartter and Gitelman syndromes. It has been suggested that the lesions seen in sclerochoroidal calcification are calcium pyrophosphate dihydrate crystals. This report describes the first documented case in the UK of sclerochoroidal calcification associated with Gitelman syndrome and calcium pyrophosphate dihydrate deposition.