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Biomedical subjects

R A Proctor

Publications and source records attributed to R A Proctor.

99 records · Page 6Linked to original sources
PubMed1978

Salicylate-induced enzymuria: comparison with other anti-inflammatory agents.

N-acetyl-beta glucosaminidase (NAG) enzymuria was used as a marker of renal injury in patients with rheumatic disease. An elevated NAG level was particularly common in patients receiving gold or aspirin therapy. The multiplicity of drugs received and the unknown role of underlying disease in these patients led to a study in healthy volunteers. Customary therapeutic doses of aspirin, choline salicylate, ibuprofen, indomethacin and acetaminophen did not produce enzymuria. Large single doses of salicylates equivalent to 6 tablets of aspirin consistently did produce enzymuria. The size of the individual dose in relation to body weight was more important than the total daily dose. NAG enzymuria appears to be a sensitive tool for identifying potentially nephrotoxic drugs.

Acetaminophen↗
PubMed1975

Phagocytosis of Francisella tularensis by Rhesus monkey peripheral leukocytes.

Phagocytosis of Francisella tularensis by rhesus monkey peripheral neutrophils (PMN, was assessed by autoradiography, electron microscopy, and biochemical techniques. PMN, in contrast to mononuclear phagocytes, were unable to phagocytize F. tularensis in vitro in the absence of immune serum. It is postulated that in the nonimmune host the innate inability of PMN to phagocytize F. tularensis deletes one of the possible mechanisms of host defense to bacterial infection and thus permits the early dissemination of F. tularensis to intracellular sites of specific target tissues.

Animals↗
PubMedDate not supplied

University of California/Davis Interdepartmental Conference on gram-negative septicemia.

Gram-negative septicemia remains one of the most serious forms of hospital-acquired infection. The most consistently virulent component of the gram-negative lipopolysaccharide (endotoxin) appears to be lipid A. Elucidation of the structure-function relationships of lipid A and the biochemical configurations required for endotoxicity makes possible the design of lipopolysaccharide antagonists and/or the production of poly- or monoclonal antibodies that may abrogate the biologic effects of endotoxin. The mechanisms of activity of lipopolysaccharide and the pathophysiologic events it triggers are now better understood than in the recent past. Lipid A triggers the release of mediators such as cachectin (tumor necrosis factor), thereby initiating a cascade of potentially lethal events. Although recent studies indicate no routine role for corticosteroids in gram-negative septic shock or acute respiratory distress syndrome, considerable progress has been made in the development of effective antibiotics. Recent studies of septicemia in neutropenic patients show survival rates significantly higher than those reported more than two decades ago.

Animals↗
PubMedDate not supplied

Fibronectin: a brief overview of its structure, function, and physiology.

Fibronectin is a large glycoprotein that is composed of blocks of three types of repeating, homologous peptide sequences. Several of the homologous blocks form functional domains that are organized in a linear array on two nearly identical subunit arms. Specific domains allow fibronectin to promote cell-to-cell adhesion, cell-to-basement-membrane attachment, clot stabilization, embryogenesis, nerve regeneration, fibroblast migration, macrophage function, and pathogen (virus, fungus, bacteria, and protozoa) binding to mammalian cells and extracellular matrix. Thus, this complex and multifunctional protein is involved in the pathogenesis of infections from the initiation of the infection through the final stages of wound healing.

Amino Acid Sequence↗
PubMedDate not supplied

The staphylococcal fibronectin receptor: evidence for its importance in invasive infections.

Fibronectin binds specifically and irreversibly to Staphylococcus aureus. The expression of fibronectin-binding sites correlates with the invasiveness of the isolate. It has been suggested that the fibronectin receptor of S. aureus is either a protein or a carbohydrate that localizes at the surface of the bacterium, permitting interactions of the bacteria with the fibronectin of the host. Sites at which S. aureus typically initiates infection are rich in fibronectin, e.g., blood clots and subendothelium; the cells of the luminal surface of intact endothelium are among the few cell types that are relatively devoid of fibronectin. Removal of fibronectin receptors from S. aureus by mechanical means or by growing the bacteria in an antibiotic-containing medium decreases their ability to adhere. Thus, the fibronectin receptor appears to play a role in the initiation of S. aureus infections. These findings offer hope for the development of a vaccine that will prevent invasive disease-if the S. aureus fibronectin receptor(s) can be purified, proves to be immunogenic, and inhibits bacterial adherence to host tissues.

Fibronectins↗
PubMedDate not supplied

Fibronectin: an enhancer of phagocyte function.

Although fibronectin does not act as a direct opsonin as originally described, it does mediate important interactions with phagocytes throughout the inflammatory process. Fragments of fibronectin released by neutrophil proteases are chemoattractants for monocytes. Moreover, subendothelial matrix fibronectin and "inflammatory" fibronectin released from phagocytes enhance phagocyte adherence to host tissues at an inflammatory site. Fibronectin also increases chemokinesis. Once the phagocyte enters tissues, fibronectin promotes C3- and Fc-receptor activation, allowing complement-coated bacteria to be ingested. Finally, fibronectin enhances the bactericidal activity of monocytes. Thus, fibronectin plays an important, but indirect role, in the activities of phagocytes.

Bacteria↗
PubMedDate not supplied

[Development of gentamicin-resistant Small Colony Variants of S. aureus after implantation of gentamicin chains in osteomyelitis as a possible cause of recurrence].

AIM: Recently, S. aureus small colony variants (SCVs) were reported to persist within cultured endothelial cells and to cause persistent and antibiotic resistant infections in humans. Because gentamicin can very reproducably select for electron transport deficient SCVs as shown in earlier in vitro experiments, we searched for SCVs in a patient with chronic osteomyelitis, who received gentamicin beads. METHOD: Special culture and identification procedures for determination of SCVs were used, including testing of the S. aureus specific nuc gene, pulsed field gel electrophoresis (PFGE) as a typing method and characterization of the auxotrophism of the SCVs. RESULTS: In a case of a 34-year-old patient with chronic osteomyelitis who had previously been treated with gentamicin beads, menadione auxotrophic S. aureus SCVs as well as wild type S. aureus were recovered in multiple bone specimen. All different colony types isolated from simultaneous or from sequential specimen were shown to be clonal by PFGE. CONCLUSION: Recovery of S. aureus SCVs from a patient treated with gentamicin beads suggests that the slow release of gentamicin into the local environment may be an efficient way to select for and/or induce SCVs. These data should alert physicians to also consider SCVs when a treatment failure occurs in a patient that has received gentamicin beads.

Adult↗