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Biomedical subjects

R W Strickland

Publications and source records attributed to R W Strickland.

8 recordsLinked to original sources
PubMed1993

Axillary lymphadenopathy due to Swanson implants.

We describe a case of unilateral axillary lymphadenopathy in an elderly woman with a long history of rheumatoid arthritis, 7 years status post placement of Swanson silastic elastomer implants in her right hand with good surgical outcome and with no outward reason for adenopathy. Though there was concern for malignancy, pathologic evaluation of the lymph node revealed foreign body giant cells reacting to silastic from her hand implants and no evidence of malignancy. This is only the 10th such case reported, despite the number of implants placed.

Adult↗
PubMed1991

Hemorrhagic subcutaneous bursitis.

Hemarthrosis is a well recognized complication of a number of conditions. Hemorrhagic subcutaneous bursitis is less understood. We encountered a patient with a myeloproliferative disease who developed hemorrhagic olecranon bursitis. Upon reviewing other patients with subcutaneous bursitis, we found that hemorrhagic bursitis also occurs in the setting of traumatic or idiopathic bursitis, rheumatoid arthritis, gout, and septic bursitis.

Bursitis↗
PubMed1988

Hairy cell leukemia presenting as a lupus-like illness.

We describe a young Hispanic man who presented with features suggestive of a diagnosis of systemic lupus erythematosus. Eventually, a bone marrow biopsy was performed, and it revealed the presence of hairy cell leukemia. This case of a lupus-like syndrome should be added to the list of reported rheumatic syndromes that are associated with hairy cell leukemia.

Adult↗
PubMed1988

Dimers of human immunoglobulin G1 provide an insufficient signal for their degradation by human monocytes.

In order to better define the processing of small soluble immune complexes by normal human monocytes, we have characterized the binding and degradation of human IgG1 monomers and covalently crosslinked dimers and heavier oligomers (composed predominantly of trimers, tetramers, and pentamers) by these cells. Whereas 15,000 molecules of monomeric IgG1 bound, about 110,000 and 65,000 IgG1 protomers of the oligomers and dimers, respectively, bound to the monocytes. Dimers bound dimerically to the cells as demonstrated by their enhanced rate of dissociation in the presence of excess heat-aggregated gamma-globulin. Despite occupying two Fc receptors, the intracellular fate of dimers was essentially that of the monomers; only 5-10% of the bound protomers were degraded. In contrast, approximately 40,000 IgG protomers of the heavy oligomers (30% of total bound) were degraded over a 5-hr incubation period. Since binding of a heavier complex, is required for degradation by the monocyte, dimeric immune complexes can generally escape the normal clearance mechanisms of the host.

Antigen-Antibody Complex↗
PubMed1987

The frequency of sicca syndrome in an elderly female population.

In a population of 103 elderly Caucasian women, 39% had sicca symptoms and 24% had abnormal Schirmer's tear tests. Two (2%) satisfied criteria for Sjögren's syndrome and 12 (12%) were felt to have possible Sjögren's syndrome. Fifty percent of those with sicca were taking medications that might induce mucosal dryness. Fibrosis was noted on all 23 labial minor salivary gland biopsy specimens obtained. Mucosal drying medications and senile salivary gland atrophy seemed to contribute to the high frequency of sicca in this population with a lesser proportion of the subjects demonstrating previously undiagnosed Sjögren's and possible Sjögren's syndrome.

Aged↗
PubMed1986

Corticosteroids enhance the binding of recombinant interferon-gamma to cultured human monocytes.

Human peripheral blood monocytes possess receptors on their surface for human interferon-gamma (IFN-gamma). Inasmuch as the biologic effects of IFN-gamma are thought to be mediated through binding of the molecule to this receptor, modulation of receptor number may be a means for enhancing the effect of IFN-gamma. We examined this possibility by treating human monocytes in culture with dexamethasone. At a dexamethasone concentration of 200 nM, there was a twofold increase in the number of 125I-recombinant IFN-gamma molecules bound to the cell. An effect was noted at concentrations of dexamethasone greater than 50 nM, and was observed as early as after 18 hr of treatment. The observed effect was the result of both a 50% decrease in receptor number in untreated cells and an increase to pretreatment levels or greater in cells incubated with dexamethasone. These results suggest that dexamethasone may modulate the effects of IFN-gamma on monocytes by changes in receptor number.

Cells, Cultured↗