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  • 1
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In a series of 316 surgically removed spleens, a histological and supportive immunohistological study was performed on methylmethacrylate sections. The structure of the human white and red pulp differs from the rat spleen in many respects, e.g. the human lacks the marginal sinus and the architecture of the periarteriolar lymph sheath seen in the rat. In man, the lymphoid compartment is in both white and red pulps. In the white pulp separate periarteriolar T-cell areas contain a large lymph-vessel plexus, which was reconstructed in serial sections. The circulation in the red pulp is discussed. The area between the red and white pulp, the perifollicular zone, is not the equivalent of the marginal sinus in the rat. Its anatomy in man suggests that it is an area formed from red pulp during the expansion of new follicles. The micro-anatomy was analysed in 119 controls. In cases of traumatic rupture the white pulp showed evidence of stimulation. A pathognomonic histological picture was not found in idiopathic thrombocytopenic purpura. In haemolytic anaemia the pulp cords were engorged by erythrocytes accompanied by a decreased B/T cell ratio in autoimmune haemolytic anaemia and by an increased B/T cell ratio in congenital spherocytosis.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1619-7089
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Bone radiotracer uptake in renal osteodystrophy was investigated in 35 dialysis patients by correlating the results of quantitative bone scintigraphy with those of biochemical and bone morphometric studies. There were highly significant correlations (P〈0.001) between the total skeletal activity and the biochemical (iPTH and alkaline phosphatase), and histologic parameters of hypeparathyroidism. These clinical results strongly suggest that increased bone turnover i.e. hyperparathyroidism, rather than osteomalacia is the major cause of increased skeletal uptake in renal osteodystrophy.
    Type of Medium: Electronic Resource
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