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Biomedical subjects

R Bluestone

Publications and source records attributed to R Bluestone.

At least 91 records · Page 5Linked to original sources
PubMed1975

Macrophage-lymphocyte clustering in rheumatoid arthritis.

The cells in synovial fluid from patients with rheumatoid arthritis contain a small percentage of macrophages. Such macrophages were isolated and cultured alone and with homologous and heterologous lymphocytes for 24 hours, in an attempt to identify possible contact between living lymphocytes and macrophages. Such contact was found, with clustering of lymphocytes around macrophages, and was particularly well shown by scanning electron microscopy.

Arthritis, Rheumatoid↗
PubMed1975

Lacrimal immunoglobulins and complement quantified by counter-immunoelectrophoresis.

Immunoglobulin and complement concentrations of tears were measured using a sensitive electroimmunodiffusion assay. In the 13 subjects tested, the predominant immunoglobulin was secretory IgA (mean concentration 107 mug/mg protein; standard error of mean 15; n equal 17). The B1C component of complement was measurable in half of the subjects studied. The data illustrate that it is possible to quantify exactly certain humoral indices which may be important in the host defense of the eye.

Complement System Proteins↗
PubMed1975

Hyperuricemic nephropathy: pathologic features and factors influencing urate deposition.

The three general types of renal pathology associated with hyperuricemia are reviewed. Factors influencing urate solubility are discussed, as well as the effect of uricosuric drugs on renal urate handling, with particular emphasis upon their efficacy in competing with urate for protein binding sites. In addition, a new experimental model of hyperuricemic nephropathy is described which could yield valuable data concerning the complex relationships between hyperuricemia, urate deposition and renal function.

Acute Kidney Injury↗
PubMed1975

UCLA Conference. Diagnosis and treatment of erosive rheumatoid arthritis and other forms of joint destruction.

Single or multiple destruction of joints arises from many causes, ranging from the acute destructive process (usually monarticular) in septic joint disease to the chronic, slowly evolving destruction of cartilage and adjacent bone that occurs in osteoarthritis. Medical treatment of a few of these conditions (including rheumatoid arthritis) is reasonably satisfactory if it is initiated early. On the other hand, surgical procedures are indicated if physical and X-ray examination of the involved joints discloses the presence of a significant destructive process involving both articular cartilage and bone. Several very satisfactory such operative techniques, including synovectomy (in the relatively early phases) and prosthetic joint replacement, have been recently developed. These are especially favorable in destructive disease of the hip, knee, or small joints of the hand. The various differential diagnostic, radiographic medical, and surgical procedures are discussed in some detail in this conference.

Anti-Bacterial Agents↗
PubMed1975

Cellular immunity to intrinsic factor in pernicious anemia.

Cellular immunity to hog intrinsic factor was detected by a modified agarose-leukocyte migration test in 18 patients with pernicious amemia. Lymphocytes from 17 out of 18 patients with pernicious anemia gave positive responses to a concentrate of hog intrinsic factor; the intrinsic factor present in 1 mg. of this concentrate bound 128 ng. of vatamin B12. Six patients with atrophic gastritis, 7 with regional enteritis, and 9 out of 10 healthy adults did not respond to this preparation. No correlation existed between the presence of serum autoantibodies to intrinsic factor and in vitro lymphocyte responsiveness to intrinsic factor. The results demonstrate that cellular immunity to intrinsic factor concentrates is present in the majority of patients with pernicious anemia.

Adult↗
PubMed1975

Chronic experimental hyperuricemic nephropathy.

Sustained, moderately severe hyperuricemia and severe uricosuria were produced in male Wistar rats by feeding dietary supplements of oxonic acid (0.4 gm. per day) and uric acid (0.6 gm per day). After 1 month, the kidneys showed the previously described histologic features of urate-blockade nephropathy characterized by intratubular deposits, tubular injury, and an exudative response consisting of neutrophilic granulocytes with early tophus formation. After 36 and 52 weeks of hyperuricemia, and with no gross evidence of renal failure, the kidneys showed a predominantly interstitial mononuclear cell infiltrate around regenerated tubules, an increase in interstitial fibrous tissue, infrequent renal tophi, and renal stones. The glomeruli and blood vessels appeared completely normal. There was no evidence of arthritis and no other target organ damage was detected. The chronic renal changes present in this animal model of induced hyperuricemia resemble those seen in human gouty nephropathy. The evolution of the experimental urate nephropathy observed during 1 year suggests that a primary acute inflammatory tubular injury is followed by a diffuse chronic interstitial nephritis and that the glomeruli and blood vessels are not primarily involved in the renal disease. This animal model may provide the opportunity to study factors influencing the renal sequelae of sustained hyperuricemia.

Animals↗
PubMed1975

Acute hyperuricemic nephropathy in rats. An electron microscopic study.

Hyperuricemia and uricosuria were induced in rats fed uric acid and oxonic acid. Kidneys then were studied by light and electron microscopy. After 1 day of hyperuricemia, animals had deposits of uric acid and urate crystals within collecting tubules of the renal papillae, and tubular cells were altered. By 10 days, there was an exudative response with further injury to epithelium. Clear spaces within lumens, epithelium, and neutrophils suggested the presence of crystals; however, there was no direct ultrastructural evidence that neutrophils or epithelial cells ingested crystals and suffered injury. Presumably, crystals readily seen in frozen, unfixed tissue were lost during preparation for electron microscopy. Nonetheless, the ultrastructural findings indicated that hyperuricemic nephropathy was initiated in a fashion analogous to urate arthropathy. Urate crystals formed within collecting tubules, epithelial cells were altered, and most likely there was chemotaxis of neutrophils which underwent degranulation and vacuolation followed by lysis freeing any ingested urate. Release of ingested crystals plus precipitation of new crystals both might serve to sustain the nephritis.

Animals↗
PubMed1975

Human polymorphonuclear leucocyte migration inhibitory factor. Evidence for antigen dependency.

Sudies were performed on human polymorphonuclear leucocyte migration inhibitory factor (PMN-MIF) to determine its antigen dependence. PMN-MIF produced by lymphocytes in response to purified protein derivative or coccidiodin was measured in an agarose gel system with buffy coat leucocytes as indicator cells. PMN-MIF activity contained in the lymphocyte supernatants uniformly disappeared when the supernatants were diluted 1:50 with medium; the inhibitory activity was only restored when the diluted supernatants were reconstituted with specific antigen. PMN-MIF isolated by polyacrylamide gel electrophoresis showed the same properties as PMN-MIF present in whole supernatants. This factor consistently migrated in the albumin region on gel electrophoresis. These data indicate that human PMN-MIF is antigen-dependent.

Antigens↗
PubMed1974

Migration enhancement factor: a new lymphokine.

Production of human migration inhibitory factor by lymphocytes exposed to antigen was studied at intervals over a 7-day period. Migration inhibitory factor was measured by an agarose gel method, with buffycoat leukocytes as indicator cells. Lymphocyte supernatants from 7-day cultures consistently showed migration inhibitory factor activity; by contrast, enhancement of migration was frequently noted when effector cells were exposed to supernatants from 2- to 5-day cultures. Enhancement activity was manifested either by enhanced migration or by a sequential reduction in inhibitory activity consistent with a factor opposing the action of migration inhibitory factor. When supernatants were subjected to polyacrylamide gel electrophoresis, enhancement activity was regularly found in the beta-globulin region and migration inhibitory factor in the albumin fraction of the gel. The enhancement activity was heat-stable and nondialyzable. These findings characterize a hitherto unreported lymphokine, migration enhancement factor.

Cell Migration Inhibition↗