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Biomedical subjects

H B Lindsley

Publications and source records attributed to H B Lindsley.

At least 37 records · Page 2Linked to original sources
PubMed1984

Elevated sacroiliac joint uptake ratios in systemic lupus erythematosus.

Sacroiliac joint radiographs and radionuclide sacroiliac joint uptake ratios were obtained on 14 patients with active systemic lupus erythematosus. Elevated joint ratios were found unilaterally in two patients and bilaterally in seven patients when their lupus was active. In patients whose disease became quiescent, the uptake ratios returned to normal. Two patients had persistently elevated ratios with continued clinical and laboratory evidence of active lupus. Mild sacroiliac joint sclerosis and erosions were detected on pelvic radiographs in these same two patients. There was no association between low back pain or HLA-B27 positivity and the radiographic or scintigraphic abnormalities. Elevated quantitative sacroiliac joint uptake ratios may occur as a manifestation of active systemic lupus erythematosus.

Adult↗
PubMed1982

Tomography for evaluation of sacroiliitis.

The radiographs and charts of 18 patients were reviewed to determine if sacroiliac joint tomography clarified the equivocal or clinically inconsistent findings of other imaging procedures. In six of eight patients with proven sacroiliitis, tomography detected joint erosions or sclerosis that were not detected on routine pelvis radiographs. In the other 10 patients, tomography excluded sacroiliitis which had been initially suggested by plain radiographs (four patients), quantitative sacroiliac scintigraphy (three patients), or clinical findings (three patients). The estimated average skin radiation exposure was 1.27 R (0.33 mC/kg) per tomographic section. The authors conclude that tomography improves delineation of sacroiliac joint abnormalities, but its use should be restricted to problem cases because of the high radiation exposure.

Adolescent↗
PubMed1982

Glomerular accumulation of monocytes and macrophages in experimental glomerulonephritis associated with Trypanosoma rhodesiense infection.

Experimental infection in rabbits with a human isolate of Trypanosoma rhodesiense led to the formation of circulating immune complexes and glomerulonephritis. Granular deposits of C3 and lesser amounts of IgM and IgG were seen deposited in the glomeruli in a primarily mesangial pattern. The glomeruli became hypercellular beginning on day 7. This was associated with diffuse swelling and vacuolation of endothelial cells with focal loss of fenestrae, as well as vacuolation of mesangial cells processes protruding into the capillary lumina. The hypercellularity became maximal on day 21 and was accompanied by proteinuria and increased tubular hyaline droplets. The hypercellularity was in large part due to the accumulation of monocytes as demonstrated by nonspecific cytoplasmic esterase stains. Counts of the number of monocytic cellular profiles per glomerulus showed that maximal numbers were reached on the 21st day of the infection. Ultrastructural examination confirmed the presence of monocytes within capillary lumina and macrophages within mesangial regions. Electron-dense deposits were rarely seen by transmission electron microscopy, and the heavy granular deposits of IgM and C3 observed by immunofluorescence were attributed to ingested proteins within macrophages. This study implies an active role for monocytes and macrophages in immune complex-mediated glomerulonephritis.

Animals↗
PubMed1981

Detection and composition of immune complexes in experimental African trypanosomiasis.

Humoral immune responses in experimental African trypanosomiasis were assessed in rabbits infected with Trypanosoma rhodesiense. Immune complexes as measured by a Clq binding assay or a Clq solid-phase assay were detected by day 10 and increased progressively through day 28. Immune complexes analyzed by double diffusion in agar or enzyme immunoassay contained immunoglobulin M (IgM) and IgG consistently, and usually C3. In one serum, immune complexes contained trypanosomal antigens in addition to C3, IgG, and IgM. By sucrose density gradient ultracentrifugation Clq-binding immune complex-like materials were shown to contain IgG, IgM, and C3, sedimentating as intermediate (between 7S and 19S) or as higher-molecular-weight (greater than 19S) aggregates. Serum IgM and IgG antibodies to trypanosomes were measured by enzyme immunoassay. IgM antibodies were detected by day 7, rose to peak by day 14, and declined slowly thereafter. IgG antibodies were detected by day 14 and continued to rise through day 32. Total IgM and IgG measured by radial immunodiffusion paralleled the corresponding changes in antibody levels. Host immune responses, in part directed to trypanosomal antigens, produced circulating immune complexes containing bound C3; these may be deposited in tissue or may serve as a serological marker of immune complex-mediated tissue injury.

Animals↗
PubMed1981

Radiographic projections for the diagnosis of arthritis of the hands and wrists.

One hundred consecutive sets of radiographs with the hands halfway supinated (Nørgaard's view) were reviewed retrospectively without knowledge of the clinical diagnosis to determine the value of this view for diagnosis of rheumatoid arthritis. Indistinct cortex at specific sites, reported to be a sensitive indicator of rheumatoid arthritis, was seen in 81% of rheumatoid patients: however, it was not specific for rheumatoid arthritis, being present in both inflammatory and noninflammatory arthritides. These changes are apparently due to variations in cortical morphology and are not true erosions. Definite erosions, which were more specific for inflammatory arthritis, were seen at the same sites; however, erosions could be identified on postero-anterior radiographs in 14 of the 16 cases in which they were seen on the Nørgaard views.

Adolescent↗
PubMed1981

Network theory in autoimmunity. In vitro suppression of serum anti-DNA antibody binding to DNA by anti-idiotypic antibody in systemic lupus erythematosus.

Regulation of serum anti-DNA antibody in systemic lupus erythematosus (SLE) by an antiidiotypic antibody was evaluated. Various sera from SLE patients in active and inactive states of their disease, as well as sera from normal individuals, were first completely depleted of anti-DNA and of DNA by affinity chromatography. The suppressive capacity of equimolar concentrations of the various depleted sera (blocking sera) on target lupus sera were determined. The target sera were from lupus patients with known DNA-binding capacity. Blocking sera from inactive SLE suppressed the binding of autologous anti-DNA antibody to [(3)H]DNA (n = 19,P < 0.01). Blocking sera from active SLE (n = 19), as well as human serum albumin, did not suppress. Sera from normal donors who had no contact with lupus patients or with lupus sera did not suppress (n = 14, P > 0.5), whereas those from normal donors who had contact with lupus patients or sera did suppress the binding (n = 5,P < 0.02). The anti-anti-DNA antibody suppressive activity in the inactive lupus serum was shown to be localized within the F(ab')(2) portion of immunoglobulin (Ig)G and could not be removed upon adsorption by normal human gammaglobulin. Furthermore, immune complexes could be detected by a Clq binding assay when the inactive lupus blocking sera were incubated with the anti-DNA antibody containing target sera. The specificity of the suppressive serum factor was shown by its inability to block the binding of tetanus toxoid to antitetanus antibody and its ability to block the binding of DNA to F(ab')(2) fragments of active lupus IgG. Regulation of serum anti-DNA antibody levels by anti-antibodies could induce and maintain disease remission in lupus patients and prevent disease expression in normals.

Antibodies, Antinuclear↗
PubMed1980

Pathology of experimental African trypanosomiasis in rabbits infected with Trypanosoma rhodesiense.

The pathologic response of New Zealand White rabbits to experimental infection with Trypanosoma rhodesiense is described. Autopsies of 18 rabbits killed from 30-44 days after infection revealed focal perivascular inflammation of the ears, eyes and testes. Examination by electron microscopy revealed extravascular trypanosomes in the dermis of the ear and interstitium of testes. Deposits of IgG, IgM and C3 were in renal glomeruli associated with glomerular hypercellularity; proteinuria was present as evidenced by an increase in tubular hyaline droplets. There was marked hyperplasia of lymph nodes and spleen with generalized increase in the number of macrophage and plasma cells. In contrast there was thymic atrophy. The findings suggest an immunologic host response associated with severe localized vascular injury.

Animals↗
PubMed1980

Variable severity of glomerulonephritis in inbred rats infected with Trypanosoma rhodesiense. Correlation with immunoglobulin class-specific antibody responses to trypanosomal antigens and total IgM levels.

Five strains of inbred rats (ACI, BUF, F344, WF and WL) were infected with Trypanosoma rhodesiense and killed at 28 days for renal pathology and serological studies. The BUF strain demonstrated the most consistent and severe glomerulonephritis, accompanied by high titer IgM antibodies to trypanosomes and high total IgM levels. The WL strain demonstrated mild glomerulonephritis but prominent PAS (+) intracytoplasmic inclusions in proximal convoluted tubules, accompanied by low titer IgM antibodies and slightly elevated total IgM levels. All strains had low to medium titer IgG1 and IgGa antibodies to trypanosomes. Serial serologic studies in BUF rats showed peak titers of IgM, IgGa and IgG1 antibodies to trypanosomal antigens at 10 days. Immune complexes as measured by a C1q binding assay were elevated at 10 days, 3 days following the first detectable antibody responses, and remained so through the 30th day.

Animals↗
PubMed1980

Iron overload.

Explore the source record for details and available documents.

Bloodletting↗
PubMed1978

Proliferative glomerulonephritis, hypocomplementemia, and nucleic acid antibodies in rats infected with Trypanosoma rhodesiense.

Host immunologic responses were studied in Sprague-Dawley rats infected with a human isolate of Trypanosoma rhodesiense. Retro-orbital sinus bleedings were obtained on days 0 and 14 and at 21 or 28 days. Infected and control rats were sacrificed on day 21 or 28 of the infection. Mild glomerulitis, as assessed by increased cellcularity and/or widening of the mesangial region, was apparent in 6 of 7 infected animals. Finely granular deposits of IgM and IgGl were found in most glomeruli with less prominent deposits of IgGa and IgA. Focal cortical mononuclear interstitial infiltrates were present in 2 of 7 rats. Subepithelial or mesangial electron dense deposits were present in the glomeruli of infected rats. Hypocomplementemia was present by day 21 and involved both the classical and alternative pathways of complement activation. Antibodies to native DNA and single-stranded RNA were present by day 21. These studies indicate the feasibility of studying trypanosomal glomerulonephritis in rats and will provide a convenient model for detailed immunologic and morphologic investigation of host immune responses in African trypanosomiasis.

Animals↗