Naltrexone in federal probationers.
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Follow-Up Studies↗
Biomedical subjects
J Cornish
Publications and source records attributed to J Cornish.
Immunoregulation in Heymann nephritis. II. Functional studies.
In this study, the functional properties of the cells involved in the immunoregulation of Heymann nephritis (HN) have been investigated. HN is a disease model in the rat where the pathology closely resembles membranous glomerulonephropathy (MGN) in man. This autoimmune model is induced by injection of renal tubular antigen (RTA) incorporated in Freund's complete adjuvant (FCA). The strong B cell and plasma cell response in the chronic phase of HN, as determined by cell marker analyses, is predominantly antigen-non-specific. The secondary response pattern found was not only to RTA upon repeated immunization, but also to non-related antigen (SRBC). Although cell marker studies have indicated no major quantitative changes in the T cell population throughout the development of HN, a severe deregulation of the cellular immune response is observed especially during the induction period of HN. This was shown by a strong decrease of the mitogen-induced proliferative response and IL-2 production. This phenomenon is caused by both defective cellular components and inhibitory serological factors. Finally, in the chronic phase, these aberrations gradually return to normal.
Animals↗
Reliable diagnosis of Trichosomoides crassicauda in the urinary bladder of the rat.
Two reliable methods are described for identifying infection of laboratory rats with the nematode Trichosomoides crassicauda. The first is a rapid method where cryostat sections of the rat urinary bladder are stained with acridine orange and viewed under a fluorescence microscope. The second involves the stabilization of the bladder surface prior to examination using scanning electron microscopy (SEM).
Animals↗
Host defence mechanisms in the bladder. II. Disruption of the layer of mucus.
The urinary bladder wall is lined by a layer of mucus which is believed to provide an important barrier to bacterial invasion of the urinary tract. Abnormal function of this protective layer could therefore be a factor predisposing the host to urinary tract infection (UTI). This study investigated the contribution of the bladder mucus to host defence in both acute and chronic lower UTI, using a non-obstructive animal model of infection which reproduces many features of the disease in man. The ultrastructural appearance of the infected bladder mucosa was assessed in tissue in which both the layer of mucus and bacterial glycocalyces were stabilized prior to examination by scanning and transmission electron microscopy. The protective role of the mucus layer was determined by disrupting the layer immediately prior to bacterial challenge. Both ultrastructural and bacteriological analyses have shown that infection was increased in those animals where the mucus barrier was disrupted.
Animals↗
Significance of cyclosporin-A-associated renal surface irregularities.
The purpose of this study was to investigate unusual irregularities observed on the surface of kidneys from rats which had been treated with seven 'clinically effective doses' (25 or 50 mg/kg) of cyclosporin A (CsA). Surface corrugations were obvious on gross examination and were a universal finding in our study which involved greater than 50 rats. Examination by scanning electron microscopy (SEM) showed that the surface irregularities resulted from swollen peritubular capillaries adjacent to vacuolized and partially collapsed tubules at the cortical surface. The enlarged capillaries were associated with vascular congestion, and although peritubular capillary congestion has been recognized in CsA-treated patients, it has been difficult to determine whether this reaction is associated with drug toxicity or graft rejection. Our findings, indicating that peritubular capillary congestion in addition to vacuolization and collapse of subcapsular tubules is a drug-associated phenomenon, may help give a more accurate assessment of biopsy and autopsy material from CsA-treated patients and laboratory animals.
Animals↗
Host defence mechanisms in the bladder. I. Role of mechanical factors.
This study evaluated the contribution of host defence mechanisms to bacterial clearance from the urinary bladder using an animal model in which rats were infected with Escherichia coli. Factors studied included the effect of hydration status, induced ultrastructural changes to the surface of the bladder mucosa, and the relevance of bacterial replication. Clearance was divided into two phases, primary (0-4 h), and secondary (4-24 h). Ninety-nine per cent of Escherichia coli 075 was cleared during the primary phase from normal, dehydrated and polyuric animals and 93% from anuric animals. Clearance was shown to be dependent on the presence of viable tissue. Bacterial numbers continued to decrease during the secondary phase in normal and dehydrated animals but increased in polyuric and anuric groups. No such rise occurred when rats were inoculated with Escherichia coli E/2/64, a non-replicating mutant. Evidence of ultrastructural changes to the bladder associated with impaired antibacterial properties was found in polyuric and anuric animals. Clearance of particulate matter (killed Candida albicans) however was unaffected by mucus disruption. The study has shown that the clearance of microorganisms from the bladder was unrelated to the voided volume, but is closely associated with the antibacterial activity of the mucosal surface.
Animals↗
An animal model for chronic infection of the unobstructed urinary tract.
Chronic cystitis due to Escherichia coli is frequently associated with anatomical or functional abnormalities of the lower urinary tract, but there is no satisfactory animal model available to help resolve biological and management problems. We have induced chronic infection of the unobstructed urinary tract in the rat by implanting a small polyurethane sponge into the dome of the bladder, 14 days before bacterial challenge. This manipulation provides a focus of infected urine and leads to the establishment of a chronic cystitis. Both the predisposing factor and the pathological details mimic important features of the disease in man.
Animals↗
Mucus stabilization in the urinary bladder.
Mucus in the urinary bladder may act as an important intrinsic defence mechanism by shielding the epithelial layer from pathogens. Visualization of any such layer of mucus using electron microscopy has not been possible, as preparative procedures in current use result in the loss or distortion of mucus. We evaluated methods reported to stabilize polysaccharide layers and demonstrated that pretreatment of rat bladder tissue with anti-mucus antiserum, minimized the collapse of the mucus that normally occurred during dehydration of the tissue for electron microscopic examination. Under these conditions, mucus was stabilized as a layer closely adherent to the epithelium.
Animals↗
Mucosal mast cells as a component of the inflammatory response to lower-urinary tract infection.
Globule cells have been observed in mucosae for many years. Recently, a subpopulation of these globule cells in the intestinal mucosa of man and rodents have been identified as unique mast cells. In this communication, intraepithelial globule cells and some lamina-propria mast cells found in the normal rat urinary-bladder wall have been characterized as mucosal mast cells, similar to intestinal mast cells, and differentiated morphologically and histochemically from rat peritoneal mast cells. The number of mast cells in the bladder wall increased significantly during various bladder manipulations, including mechanical trauma, parasitic infestation and bacterial infection. The origin and function of the mucosal mast cells remains unknown.
Animals↗
Suicide and attempted suicide: legal issues.
Canadian Federal and Ontario Provincial statutes are reviewed as they relate to suicide and attempted suicide. Issues addressed include involuntary committal to psychiatric facilities, death by suicide as a legal cause of action, insurance exclusionary clauses and coroner's inquests.
Adult↗
Stimulation of circulating autoantibody levels in the rat with established progressive passive Heymann nephritis.
Rats with established progressive passive Heymann nephritis (PPHN) were stimulated with tubular nephritogenic antigen derived from rat kidney fraction 3 (rKF3) or heterologous antibody to the eKF3 antigen. Rats stimulated with antigen had elevated levels of circulating autoantibody and increased amounts of rat IgG in a beaded pattern around the glomerular capillaries. The brush border (BB) region of the proximal convoluted tubules also stained for rat IgG. Rats stimulated with antibody had similar changes, but in addition the injected antibody was demonstrated in the glomerular deposits and in the BB region of the proximal convoluted tubules. Proteinuria was markedly increased in the antibody injected rats. This study indicates that the cells of the 'primed' immune system of rats with PPHN can be stimulated by 'additional' rKF3 antigen or antibody to it, to produce increased levels of circulating autoantibody. It is suggested that the progression of PPHN is dependent on the availability and access of the nephritogenic autoantigen to the immune system and that autoantigen may be released by autoantibody.
Animals↗
Passive Heymann nephritis in pre- and post-natal rats.
Passive Heymann nephritis (PHN) was induced in pre- and post-natal rats by a single intra-peritoneal injection of 0.2 ml of a rabbit anti-rat kidney fraction 3 (rKF3) antibody. Immune complex formation occurred only in those glomeruli or parts of glomeruli which were open to the circulation. Double staining of kidney sections for the glomerular nephritogenic antigen and rabbit IgG, 2 days after the injection of the antibody showed an identical distribution of both components in the glomeruli. In rats killed more than 4 days after the injection of the anti-rKF3 antibody, the nephritogenic antigen could be demonstrated in the subcapsular glomeruli, in the absence of rabbit IgG; and the same applied when the kidneys had reached maturity. When the injected antibody was expected to be present in the circulation, no nephritogenic antigen was demonstrated in the glomeruli in the absence of the heterologous IgG. These observations indicate that the nephritogenic antigen appears in the glomerulus at the same time as the glomerular capillary loops open to the circulation. Unlike PHN in the adult rat, the immune complexes in the glomeruli of neonatal rats do not persist longer than 84 days.
Aging↗
Passive Heymann-like nephritis in the rabbit.
Rabbits injected with a guinea-pig anti-rabbit kidney fraction 3 antiserum developed immune complex deposition in the glomerulus which disappeared by the sixth day. The distribution of the glomerular deposits was similar to those of passive Heymann nephritis in the rat. A glomerular fixed antigen was not demonstrated in normal rabbit kidneys after perfusion with the guinea-pig anti-tubular antiserum. When tubular antigen was injected intraperitoneally in saline it could be detected in the glomeruli and after injection of the anti-tubular antiserum the deposits stained with increased intensity. Addition of a small amount of anti-GBM antiserum to the anti-tubular antiserum enhanced the size and number of glomerular deposits and increased their survival time. It is concluded that there is no pre-existing tubular antigen in the rabbit glomerulus and that the injected heterologous anti-tubular antiserum releases antigen from an extraglomerular source, probably the proximal tubules, and this released antigen becomes trapped in the glomerulus.
Animals↗
Progressive passive Heymann nephritis: induction of autologous antibodies to rat brush border by multiple injections of heterologous antiserum.
Multiple i.v. injection of a heterologous anti-rat kidney fraction 3 antiserum and guinea pig anti-rabbit F3 into rats produced a progressive immune complex glomerulonephritis. The kidney disease was characterized by diffuse beaded deposition of rat gammaglobulin along the glomerular capillaries and proteinuria. Gammaglobulin eluted from the kidneys reacted with the brush border region of normal rat kidney frozen sections. Control animals did not develop the progressive disease. It appears that multiple i.v. injections of the heterologous antisera are capable of inducing an autoimmune kidney disease which is similar to Heymann nephritis.
Animals↗
Modified immunofluorescent antibody test: demonstration of nephritogenic antigen in glomeruli of rats.
This article describes a modified immunofluorescent antibody technique for the detection of a glomerular fixed tubular nephritogenic antigen in the rat. The presence of the nephritogenic antigen in the glomeruli of rats can be detected by this modified technique, while the conventional method gives negative results.
Animals↗
The effect of pre-injection of rat kidney F3 antigen on the development of passive Heymann nephritis.
The effect of repeated i.p. injections of a small dose of rat kidney F3 antigen, in an aqueous solution, on the development of passive Heymann nephritis in the rat has been investigated. The test animals receiving the antigen before the i.v. injection of the heterologous antibody developed more numerous and larger immune complexes on the epithelial side of the glomerular basement membrane than the control rats. It is suggested that the injected antigen is trapped in the glomerular basement membrane at sites where the pre-existing nephritogenic antigen is present making it possible for the more numerous and larger deposits to form.
Animals↗
Progressive passive Heymann nephritis in the rat.
Progressive passive Heymann nephritis was produced in rats by simultaneous intravenous injections of heterologous antirat glomerular basement membrane antiserum and heterologous antirat kidney tubular fraction 3 antibody. The animals were killed at 16 weeks by which time approximately one-half of them were severely proteinuric. The glomeruli showed beaded immune deposits around the capillaries by immunofluorescence, and on electron microscopy osmiophilic deposits were noted in the subepithelial zones and within the glomerular basement membrane. The lesion resembled that of severe Heymann nephritis. gamma-Globulin eluted from the kidneys contained an autologous IgG that reacted with the brush border region of the renal proximal tubules of normal rats. This component was present in proteinuric and nonproteinuric animals. It is concluded that the progression results from the development of autoantibodies to the tubular nephritogenic antigen and the proteinuria is related to increasing deposition of immune complexes in the glomeruli.
Animals↗
Passive Heymann nephritis in the rat produced by a heterologous antibody to a heterologous kidney fraction 3 antigen.
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Animals↗