PubMed Health⌕ Search

Biomedical subjects

J T Boyer

Publications and source records attributed to J T Boyer.

12 recordsLinked to original sources
PubMed1992

Arthritis and aging.

Thirty-seven million Americans suffer from some form of arthritis and the prevalence of arthritis among the elderly is particularly high. Therefore it is not surprising that there is a large new literature directed toward the epidemiology and health services for the older individual with arthritis. Many studies in osteoarthritis have refined the minutia or confirmed earlier work. Osteoarthritis increases with age and accounts for 46 million patient visits each year, with knee arthritis accounting for the most common complaint initiating such visits. Late stage rheumatoid arthritis has again been strongly associated with shortened life span, and factors predicting early death have been identified. Meanwhile, the "pyramid model" of rheumatoid arthritis treatment has been challenged. Of interest is the identification of obesity as a major risk factor for disability in elderly patients with arthritis and the fact that the incidence of hip fracture in the elderly, already known to be high, may be increasing. A provocative report suggests that mass screening for osteoporosis followed by selective treatment may be more cost effective than empirical treatment of all postmenopausal women.

Aged↗
PubMed1991

The incidence of attempted CPR in nursing homes.

We studied the frequency with which cardiopulmonary resuscitation (CPR) is attempted on residents of American nursing homes. Each author (all members of the Clinical Practice Committee of the American Geriatrics Society) completed a questionnaire in 1989 about policy and practice regarding CPR during 1988 in each of three to seven nursing homes, by questioning the medical or nursing director or the administrator. Because of the vagaries of nursing home record-keeping, data from some homes were allowed when they were "accurate to within 10%." Data from 58 nursing homes, totalling 10,836 bed-years were available. In 33 of these homes, accounting for 5,425 bed-years, CPR was never attempted. CPR was more likely to be foregone in nursing homes with religious affiliation than in nursing homes without (13 of 17 vs 18 of 38; chi 2 = 4.0; P less than 0.05). Religious affiliation was unknown for three nursing homes. Academic affiliation (10 of 16 vs 20 of 37 in non-affiliated nursing homes) and non-profit status (14 of 19 vs 16 of 23 in for-profit nursing homes) did not significantly affect the likelihood that CPR would never be used. In 31 of 54 nursing homes with explicit do not resuscitate (DNR) policies, CPR was never performed, compared to 2 of 4 homes without such policies. For nursing homes with complete data, there were 1,196 deaths in 32 facilities where CPR was never attempted compared to 1,294 deaths for 24 nursing homes with CPR. For 22 nursing homes without CPR, there were 2,172 emergency room transfers compared to 1,363 emergency room transfers in 18 nursing homes where CPR was attempted.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1979

Autosensitization to DNA: evidence for an immunologic basis.

A 59-year-old female with spontaneous painful ecchymoses developed ecchymoses after intracutaneous injection of washed autologous whole blood cells and calf thymus DNA. Immunofluorescent studies of the spontaneous lesions revealed granular deposits of IgM, C3, factor B and properdin at the dermal-epidermal junction but no deposits in her normal skin. T cells were decreased in number but responded normally to polyclonal mitogens and did not transform in response to DNA containing antigens. Repair of UV-damaged DNA by her lymphocytes appeared to be depressed. The findings presented here are the first immunologic abnormalities uncovered in this disorder and may help in understanding the pathogenesis of the inflammatory lesions seen in autosensitization to DNA.

Autoantibodies↗
PubMed1975

Consumption of classical complement components by heart subcellular membranes in vitro and in patients after acute myocardial infarction.

Experiments were conducted to characterize the antibody-independent activation of complement in human serum by isolated human heart mitochondrial membranes in vitro and to determine whether similar patterns of complement consumption occurred in patients after acute myocardial infarction. Direct evidence for the interaction of C1 and heart mitochondrial membranes was obtained by mitochondria-C1 binding and elution experiments. Exposure of normal human sera to isolated human heart mitochondria at 37 degrees C resulted in the consumption of C1, C4, C2, and C3 without significant consumption of the terminal components of the complement system (C6 through C9). The consumption occurred in the absence of detectable anti-heart mitochondria autoantibody, was demonstrated to be calcium dependent, and was inhibited by either 0.01 M EDTA or ethylene glycol bis(bets-aminoethyl ether) N,N,N',N',-tetraacetic acid (EDTA). Although specific absorption of C1q from human sera inhibited the mitochondria-dependent activation of C4, C3 donsumption was not affected. These data indicate that the consumption of C4 and C2 likely occurred due to the mitochondrial membrane-mediated activation of C1, but that the consumption of the C3 did not necessarily involve either the classical or alternative complement pathways. After the in vitro characterization of the mitochondria-dependent activation of the complement system, additional studies were performed to determine whether similar consumption occurred in patients after acute myocaridal infarction. During a 72-h period after hospital admission significant decreases in C1, C4, and C3 occurred in six patients with recent chest pain but no evidence of acute myocardial infarction. These studies suggest that myocardial cell necrosis results in the release of subcellular membrane constituents capable of activating the complement system in the absence of detectable anti-heart autoantibodies; such activation may be responsible in part for the development of acute inflammation and evolution of the infarct size following coronary artery occulusion.

Autoantibodies↗
PubMed1975

Hereditary deficiency of the seventh component of complement.

Deficiency of the seventh component of complement has been found in the serum of a 42-yr-old Caucasian woman who has Raynaud's phenomenon, sclerodactyly, and telangiectasia. Partial deficiency was found in the serum of the patient's parents and children, indicating a pattern of inheritance of autosomal codominance. Transfusion experiments indicated that exogenous C7 had a 91-h halk-life in the patient. There was no evidence for C7 synthesis after transfusion. No C7 inhibitors were detected in the patient's serum. The patient's serum was found to support the activation of complement by both the classical and properdin pathways to the C7 stage. The addition of C7 to the patient's serum permitted it to support hemolytic reactions initiated by either pathway. No defects could be detected in plasma or whole blood coagulation. The patient's serum was deficient in opsonizing unsensitized yeast particles in serum and in the generation of chemotactic factor by antigen-antibody complexes and endotoxin. Both deficiencies were corrected by the addition of C7. These observations suggest a key role for C7 for in vitro yeast phagocytosis and chemotaxis generation. However, the patient's lack of infections indicates a relatively minor role for C7 in human resistance to infection.

Adult↗
PubMed1975

Hypochlorite-induced alterations to canine serum complement.

Changes in the concentration of the components of complement produced by NaOC1 both in vitro and in vivo are recorded. C1, C4 and C7 are particularly sensitive to this oxidizing agent, although all components decrease at high concentrations of NaOC1. Following oxidation, complement componenets return rapidly to normal. Data are presented to indicate that part of this repair mechanism is due to the action of reducing agents such as ascorbic acid and part is due to the synthesis of the individual components. The unique sensitivity of complement components to oxidation make this treatment of potential value in suppressing the inflammatory response.

Animals↗