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Biomedical subjects

C B Wolf

Publications and source records attributed to C B Wolf.

9 recordsLinked to original sources
PubMed1989

Dyscoordinate expression of tumor necrosis factor-alpha by human blood monocytes and alveolar macrophages.

Previous studies have shown that human alveolar macrophages produce less interleukin-1 (IL-1) in response to lipopolysaccharide (LPS) than do their precursors, blood monocytes. The purpose of this study was to compare the capacities of alveolar macrophages and blood monocytes to synthesize tumor necrosis factor (TNF) in response to LPS. Alveolar macrophages were obtained by bronchoalveolar lavage of healthy nonsmoking subjects, and blood monocytes were obtained by adherence of mononuclear cells to plastic. TNF activity was measured in supernatants and cell lysates as cytotoxicity to L929 fibroblasts (uptake of neutral red at 570 nm). TNF activity of alveolar macrophages stimulated at 10(6) cells/ml with LPS (10 micrograms/ml) for 16 h was 596 +/- 367, and of blood monocytes it was 60 +/- 84 U/ml (mean +/- SD, p less than 0.005). At no concentration of LPS and at no period of stimulation did alveolar macrophages express less TNF activity than did blood monocytes. In concurrent experiments, supernatants of LPS-stimulated alveolar macrophages contained less IL-1 activity than did blood monocytes. Lysates of both cell types contained less than 20% of total TNF activity. The TNF activity of LPS-stimulated alveolar macrophages was neutralized greater than 99% by monoclonal antibody to TNF-alpha; control monoclonal antibody OKT3 had no effect. Next, alveolar macrophages and blood monocytes were biosynthetically labeled with [3H]leucine during incubation with LPS; supernatants were immunoprecipitated with anti-TNF, and precipitates were electrophoresed on polyacrylamide gels. Autoradiographs indicated that immunoreactive TNF was produced by both blood monocytes and alveolar macrophages and that the relative molecular weights were identical (17,000).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

AA amyloid-associated gastroenteropathy in a horse.

Systemic amyloidosis involving the digestive tract is described in an 11-year-old Morgan stallion. The disease was characterized clinically by weight loss, ptyalism, anaemia, persistent mature neutrophilia, hypoalbuminaemia and hypergammaglobulinaemia. The D-xylose absorption test indicated malabsorption. Necropsy revealed oral, oesophageal and gastric ulcers and reddened segments of small bowel mucosa with scant haemorrhages. Microscopically, amyloid deposits were found throughout all tissue layers of the digestive tract, except the serosa. Deposits of amyloid were most apparent in the small bowel mucosa and submucosal arteries. Amyloid was also present in the spleen and lymph nodes and to a lesser extent in the liver, kidneys, lungs, pancreas and bone marrow. All amyloid deposits gave the typical histochemical reaction for AA amyloid with the KMnO4-Congo red stain procedure and immunohistochemical cross-reactivity was demonstrated with antisera to both canine and bovine protein AA by the peroxidase-antiperoxidase technique. The cause of the amyloidosis was not identified, although the haematological and serological data were compatible with an underlying chronic inflammatory process.

Amyloidosis↗
PubMed1976

Evaluation of thyroid function during growth hormone therapy.

Decrease in the blood levels of PBI, in the thyroidal uptake of iodine, and diminished effect of TRH on TSH release have been reported to occur during growth hormone administration. We assessed thyroid function indices in two groups of growth hormone deficient children before and during long-term HGH therapy. Eight patients were given TSH prior and at 2, 4, and 6 mo of growth hormone treatment. In four other children, the disposal rates of simultaneously administered I125-T4 and I131-T3 were measured before and at 2 and 6 mo after initiation of HGH replacement. Blood levels of TSH, T3, T4, TBG capacity, and the T3 resin uptake were obtained at the time of each study. Growth hormone therapy did not affect the blood levels of T4, T3, TSH, TBG capacity, the T3 resin uptake, the thyroidal response to exogenous TSH, nor the disposal rates of thyroid hormones.

Adolescent↗