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Biomedical subjects

C B Wilson

Publications and source records attributed to C B Wilson.

At least 649 records · Page 36Linked to original sources
PubMed1974

Increased polyamine concentrations in the cerebrospinal fluid of patients with brain tumors.

An automated method for the quantitative analysis of the polyamines putrescine, spermidine and spermine in cerebrospinal fluid (CSF) was used to analyze CSF samples from 37 patients with central nervous system (CNS) tumors and from 13 patients without tumors. The putrescine and spermidine concentrations in the CSF of most patients in tumors, particularly those with glioblastomas or medulloblastomas, were elevated when compared with those of non-tumor-bearing patients.

Adenoma, Acidophil↗
PubMed1974

Interstitial immune complex thyroiditis in mice: the role of autoantibody to thyroglobulin.

Mice immunized with soluble heterologous thyroglobulins developed autoantibody that cross-reacted with autologous thyroglobulin. There was a direct correlation between the temporal appearance and quantity of serum autoantibody and the presumed in situ formation of immune complexes in the interstitium of the thyroid glands. Immediately after the formation of interstitial immune complexes containing antibody of the IgG complement-fixing type, the thyroids were invaded by a transient but intense neutrophil infiltrate which within 1 wk was replaced by chronic mononuclear elements. By the combination of fluorescence microscopy and autoradiography, thyroglobulin was demonstrated to be one, if not the sole, antigen in the interstitial immune complexes. The interstitial immune complexes were granular to lumpy in appearance and formed at the basal area of the follicular cells in intimate association with the follicular basement membrane. Electron microscopy revealed electron dense deposits, presumably immune complexes, between the follicular basement membrane and the plasma membrane. The presumed in situ formation of immune complexes in this model is similar to that which occurs in the Arthus reaction and is a different mechanism of immune complex injury than that caused by tissue deposition of circulating immune complexes as occurs in serum sickness.

Animals↗
PubMed1974

Binding of soluble immune complexes to human lymphoblastoid cells. II. Use of Raji cells to detect circulating immune complexes in animal and human sera.

Cells from a human lymphoblastoid cell line (Raji), with B-cell characteristics, and having receptors for human IgG Fc, C3b, and C3d, were used in an immunofluorescence test as in vitro detectors of immune complexes in animal and human sera. By this test, as little as 200-300 ng aggregated human gamma globulin or immune complexes per ml serum could be detected. The receptors for IgG Fc on the Raji cells were shown to be inefficient in detecting aggregated human gamma globulin and binding of aggregates to these receptors was inhibited by physiologic concentrations of 7S human IgG. Enhancement of aggregated human gamma globulin binding and binding of immune complexes formed in vitro to Raji cells was observed when the receptors for complement on these cells were used. By using the receptors for complement on Raji cells, circulating immune complexes were detected in rabbits with acute serum sickness, in mice with acute lymphocytic choriomeningitis virus infection, and in humans with immune complex type glomerulonephritis. The Raji cell test may be useful in detecting complement fixing immune complexes in different disease states, in monitoring circulating complexes in patients with immune complex diseases and in identifying the antigen(s) responsible for the induction of pathogenic immune complexes in humans and animals.

Animals↗
PubMed1974

Glomerular complement components in human glomerulonephritis.

154 of 255 individual human renal biopsies studied by immunofluorescence contained varying combinations of immunoglobulins (Ig), complement (C) components C1q, C3, C4, C5, C6, C8, C3 proactivator (C3PA), and/or properdin. 10 patients had linear deposits of Ig in glomeruli characteristic of antiglomerular basement membrane (GBM) antibodies; nine patients had C3 deposits (minimal in three) with generally lesser amounts of C1q, C4, C5, C6, and/or C8. 118 of the patients had granular deposits of Ig, suggesting immune complex glomerulonephritis; 114 of these had deposits of C3, usually accompanied by C1q, C4, C5, and/or C6. These observations indicate that the entire C sequence is deposited in glomeruli in most Ig-mediated glomerulonephritides. However, certain cases of anti-GBM glomerulonephritis with few or no C deposits may utilize pathways of injury independent of C.21 patients had granular C3 deposits without detectable Ig. C5, C6, and C8 were present in the majority of these patients while C1q was absent and scant C4 was observed in only two patients. The presence of only late-acting C components in the absence of Ig, C1q, and C4 suggests selective, possible nonimmune activation of the alternate C pathway. Finally, five patients had granular deposits of C3, C5, C6, and/or C8 diffusely in all or most glomeruli with a lesser number of glomeruli having additional focal granular deposits of Ig, C1q, and C4. This observation suggests that at least two patterns of C activation can occur simulatenously, possibly triggered by antecedent immune complex deposition and then perpetuated by an as yet undetermined mechanism.

Adult↗
PubMed1974

Pathophysiology of experimental glomerulonephritis in rats.

Micropuncture, clearance, immunofluorescence and light microscopy techniques were used to study kidney structure and single nephron function in rats with autologous immune complex nephritis (AICN), a membranous glomerulonephritis developing over 5 to 20 mo, in the more acute and proliferative glomerular basement membrane (GBM) nephritis and in controls. Both models are known to have clinical counterparts in human disease. Kidney functional abnormalities correlated with the degree of architectural derangement. In both AICN and anti-GBM nephritis filtration fraction fell in direct proportion to the fall in glomerular filtration rate (GFR), renal plasma flow being unchanged. Fractional electrolyte excretion increased as the GFR fell. Despite marked heterogeneity of single nephron filtration rate (SNGFR) (AICN, 5-93 nl/min; anti-GBM, 0-50 nl/min) and of proximal tubular hydrostatic pressure (4-48 mm Hg), each nephron showed almost complete glomerulotubular balance, absolute reabsorption to the late proximal convolution varying directly with filtration rate. In addition SNGFR could be related both to proximal intratubular hydrostatic pressure and to calculated glomerular capillary pressure (Pg), being lowest in those nephrons with the highest intratubular pressure. Nephrons with very high filtration rates did not apparently reach filtration equilibrium. Mean SNGFR was significantly lower in the anti-GBM group, while calculated Pg was the same in both. This probably reflects the acute and diffuse involvement of the anti-GBM lesion with different filtration characteristics from the more chronic AICN disease. Tubular damage was more marked in AICN, and extraction of p-aminohippurate was reduced in this group.

Blood Proteins↗