Search PubMed⌕ Search

Biomedical subjects

J S Davis

Publications and source records attributed to J S Davis.

At least 145 records · Page 8Linked to original sources
PubMed1981

Interaction between rheumatoid factor and antibody/DNA complexes: enhancement of complement fixation.

The influence of rheumatoid factor (RF) on the complement mediated binding of antibody/double-stranded DNA immune complexes to red blood cells has been investigated. Our results indicate that RF enhances this binding reaction, apparently by fixing complement via its own Fc region. These findings suggest that under certain circumstances, RF may play an exacerbating role in the antibody/DNA induced glomerulonephritis of systemic lupus erythematosus.

Antigen-Antibody Complex↗
PubMed1981

Age influences the clinical and serologic expression of systemic lupus erythematosus.

The clinical and serologic characteristics of 17 patients with onset of systemic lupus erythematosus (SLE) after age 50 were compared with those of 49 younger patients. All patients were followed prospectively for a mean duration of 47 months. A clinical and serological data base was established for each patient, and information collected at each visit to a lupus clinic was analyzed by computer. The clinical featured distinguishing old-age SLE were a low incidence of significant renal disease and prominent pleuropericarditis and arthritis throughout the period of followup. Serologic abnormalities were milder in older patients. Thus, hypocomplementemia, anti-DNA antibodies, and C1q precipitins occurred less frequently, and rheumatoid factor was more often present than in younger patients with SLE. Regression analysis suggested linear change in disease expression with age rather than distinct age-related subgroups.

Adult↗
PubMed1981

Antibodies to Sm in patients with systemic lupus erythematosus. Correlation of Sm antibody titers with disease activity and other laboratory parameters.

Thirty patients with systemic lupus erythematosus (SLE) were studied over a 2.5-year period. The group was divided into 14 patients with antibodies to Sm and a control group that failed to exhibit antibodies to Sm over the study period. The titer of antibodies to Sm fluctuated in all 14. A rising titer of antibodies to Sm 1) predicted a flare disease in 50% an 2) correlated with an exacerbation of disease in 60%. Patients with antibodies to Sm had a comparable incidence of severe disease, renal disease, and central nervous system disease. They exhibited significantly more leukopenia and antibodies to non-Sm, non-RNP extractable nuclear antigen. In only 1 patient, a rise in titer of antibodies to Sm did not correlate with or predict a disease flare in contradistinction to other serologic markers of SLE, specifically antibodies to double-stranded DNA and cryoglobulins. Though infrequently detected, antibodies to Sm can help in the management of patients with SLE.

Adolescent↗
PubMed1981

Studies of artificial cryoprecipitates containing anti-DNA antibody activity.

Artificial cryoprecipitates have been prepared from SLE sera by incubation of anti-double stranded DNA with 3H-PM2 DNA. IgM rheumatoid factor, and complement to study further the relationships between natural cryoprecipitation and the DNA/anti-DNA system in this disorder. Addition of rheumatoid factor and/or complement to a mixture of SLE serum and 3H-DNA results in increased precipitation of the 3H-DNA following incubation at 4 degrees C. Precipitation formed with added complement or complement plus rheumatoid factor could be rapidly resolubilized or reprecipitated by warming to 37 degrees C or recooling to 4 degrees C, i.e., exhibited the behavior of natural cryoprecipitates. The resolubilized cryoprecipitates contained excess antibody, because they bound significant quantities of additional 3H-DNA in the Farr assay. Of special interest was the observation that DNA binding activity frequently could be recovered from solubilized cryoprecipitates even though 3H-DNA was not added during the original cryoprecipitate preparation. With certain cryoprecipitations prepared in this way, the DNA binding activity was further increased by deoxyribonuclease treatment, raising the possibility that endogenous DNA may be constituent of such cryoprecipitates. The implications of these findings with respect to the nature of antibody-DNA immune complexes in SLE are discussed.

Antibodies, Antinuclear↗
PubMed1981

Anti-inflammatory, antiproteolytic, and antihemolytic properties of pyrrole carboxylic acids.

Eight substituted pyrrole carboxylic acids were evaluated for their anti-inflammatory activity against carageenin-induced edema in rats. The protection afforded by seven of these compounds at a dose of 100 mg/kg i.p. ranged from 11 to 42%. Indomethacin (10 mg/kg i.p.), used as a reference drug, possessed 45% anti-inflammatory activity under similar experimental conditions. The ability of these compounds to exhibit in vitro antiproteolytic activity was reflected by their ability to inhibit trypsin-induced hydrolysis of bovine serum albumin. The inhibition of the activity of trypsin by these substituted pyrrole carboxylic acids (1 mM) ranged from 42 to 90% while such an inhibition with indomethacin (1 mM) was 95%. The in vitro membrane stabilizing property of these substituted pyrrole carboxylic acids was observed by their ability to provide protection against heat-induced dog erythrocyte hemolysis. The I50 value of these compounds, representing the concentration required to inhibit one-half of heat-induced erythrocyte hemolysis, ranged from 0.29 to 6.0 mM. Such an inhibition was concentration-dependent and biphasic in nature. The I50 value for indomethacin, showing greater antihemolytic activity was found to be 0.02 mM under similar experimental conditions. These results have provided some correlation of anti-inflammatory activity with antiproteolytic and membrane stabilizing properties for substituted pyrrole-3-carboxylic acids alone but not for pyrrole-2-carboxylic acids.

Animals↗
PubMed1981

The role of immune complexes in the pathogenesis of pleural effusions.

Thirty-two patients with pleural effusions (7 malignant, 5 with connective tissue disease, 5 with infections, 9 idiopathic, 6 miscellaneous) were studied to determine if immune complex formation might be involved in the pathogenesis of pleural fluid formation. Immune complexes were detected in serum, pleural fluid and in parietal pleural capillaries using direct immunofluorescence in the following groups: malignant disease (57%, 29%, 67%), connective tissue diseases (100%, 100%, 100%), infectious diseases (0%, 44%, 67%), idiopathic (67%, 44%, 75%), and miscellaneous (25%, 17%, 0%). Whereas the degree of immune complex was higher in serum than in pleural fluid in patients with malignant disease, the converse was true in patients with connective tissue diseases. Activation of C3 and properdin factor B was almost invariable in pleural fluid from patients with connective tissue disease and bacterial infections. These data suggested that pleural immune complexes are frequently associated with exudative pleural effusions. Immune complexes may lead to formation of pleural fluid by increasing capillary permeability. This may result from either a local Arthus-type reaction within the pleura, local immune complex formation within pleural fluid leading to release of inflammatory mediators, and/or deposition of circulating immune complexes in pleural vessels.

Adult↗
PubMed1981

Stimulation of phospholipid labeling and steroidogenesis by luteinizing hormone in isolated bovine luteal cells.

The present study was conducted to examine the effect of LH on phospholipid metabolism in corpora luteal tissue. Collagenase-dispersed cells obtained from bovine corpora lutea of early pregnancy were incubated with 32PO4 in the presence or absence of LH and examined for their ability to incorporate this label into phospholipids. LH (1 microgram/ml) significantly increased 32P incorporation into total lipid extracts, with a time course similar to that of progesterone synthesis. This stimulation of 32P incorporation was dependent on the concentrations of LH, and this dose-response relationship correlated well with the dose response of LH-induced progesterone production. Bovine serum albumin and ACTH had no apparent effect on 32P incorporation into phospholipids or progesterone production. Separation of luteal cell phospholipid extracts by thin layer chromatography revealed that LH stimulated the incorporation 32PO4, mainly into phosphatidic acid and phosphatidylinositol, with small increases occurring in the polyphosphoinositide fraction. The LH-induced labeling of these individual phospholipids also appeared to be temporally and dose-related to the LH-induced increases in progesterone synthesis. LH had no effect on the labeling of phosphatidylcholine, phosphatidylserine, sphingomyelin, or cardiolipin. These results indicate that LH has selective effects on phospholipid metabolism in bovine luteal cells which may be a part of the mechanism of action of LH on steroidogenesis.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1981

Demonstration of a C1q receptor on the surface of human endothelial cells.

A receptor for C1q on the surface of human endothelial cells has been demonstrated. This receptor is present on the surface of viable cultured endothelial cells derived from human umbilical veins, and C1q binding can also be demonstrated to the endothelial lining cells of human umbilical artery and vein on frozen tissue sections. Receptors for the complement components C3b and C3d were not detected on tissue sections or endothelial cells in suspension. Endothelial cell C1q receptors are discussed in relationship to possible immune complex localization in vivo.

Binding Sites↗
PubMed1980

Interactions of cytochrome c with mitochondrial membranes. Binding to succinate-cytochrome c reductase.

Methyl-4-azidobenzoimidate was reacted with horse heart cytochrome c to give a photoaffinity-labeled derivative of this heme protein. The modified cytochrome c bound to cytochrome c-depleted mitochondria with the same Kd as native cytochrome c and restored oxygen uptake to the same extent. Irradiation of cytochrome c-depleted mitochondrial membranes with 3- to 4-fold excess of photoaffinity-labeled cytochrome c over cytochrome c oxidase resulted in covalent binding of the derivative to the membranes. Fractionation of the irradiated mitochondria in the presence of detergents and salts followed by chromatography on an agarose Bio-Gel-A-5m showed that the labeled cytochrome c was bound covalently to succinate-cytochrome c reductase. The covalently bound cytochrome c was active in mediating electron transfer between its reductase and oxidase. Sodium dodecyl sulfate polyacrylamide gel electrophoresis of the succinate-cytochrome c reductase containing photoaffinity-labeled 125I-cytochrome c showed that the reductase contained a protein binding site for cytochrome c. It is suggested that cytochrome c1 is the most likely site for the cytochrome c binding in mitochondria in situ.

Affinity Labels↗
PubMed1980

Free plasma DNA in patients with pulmonary embolism.

Plasma samples from 46 patients with suspected pulmonary embolism and 25 patients with suspected acute myocardial infarction were analyzed for DNA by counterimmunoelectrophoresis (CIE). Anti-DNA serum was obtained from a patient with systemic lupus erythematosus who had a high titer of anti-DNA antibodies. Seven of eight patients (88%) with high probability of pulmonary embolism by lung scan criteria had free DNA in their plasma. Six of 21 patients (29%) with low probability scans for pulmonary embolism also had DNA in their plasma. None of the eight patients with normal scans and only one of 13 patients with myocardial infarction had DNA in their plasma. Detection of plasma DNA by CIE is a rapid and simple method of screening for pulmonary embolism.

Counterimmunoelectrophoresis↗
PubMed1980

Scleroderma: developments from Osler to the present.

The clinical entity of progressive systemic sclerosis (PSS, or scleroderma) has remained unchanged since Osler's first description in 1892. Several related or overlap syndromes have now been recognized, which may afford some insight into etiologic events in the development of PSS. As yet, the cause of PSS remains elusive. Abnormalities of collagen synthesis, the role of cellular and humoral immunity, and the relationship of these to vascular disease and hyperreactivity represent current areas of research. Few therapeutic advances of proven efficacy have been forthcoming over this period except for the use of vigorous antihypertensive therapy or early nephrectomy, dialysis, and transplantation in the control of malignant hypertension and progressive renal failure.

Adult↗
PubMed1980

Soluble immune complexes in human disease.

The great variety in biochemical properties of immune complexes occurring in human and animal disease states has made the detection of such complexes a difficult task. Variability in immune complex size, specificity, and interaction with humoral or cellular receptor systems, such as complement and phagocytes, suggests different pathogenic properties. The introduction of radioimmunoassays and the recently improved knowledge of the immune complex-receptor interactions have lead to the description of a large number of detection procedures, which in turn has widened the catalogue of diseases associated with immune complexes. This widespread occurrence of soluble immune complexes has lead many investigators to think that such complexes may occur either as a transient physiological phenomenon, important for fast clearance of the antigen, or as primary pathogenic factors triggering inflammatory reactions. Among the 50 procedures for immune complex detection known today, the article will select some pertinent tests, which will be discussed with respect to their specificity, sensitivity, and reproducibility. Furthermore, it is well known that when applied to the study of a patient group with one particular immune complex disease, various tests will result in different percentages of patients having complexes. This observation is due to differences in the underlying principle on which the various tests are based. Thus immune complexes must be further characterized with respect to their size, to the antibody class or specificity involved and, most difficult, to the antigenic specificity which participates in the complex. Recent advances in such experimental characterization of immune complexes in vitro and in the clinical evaluation of patients with complement activation associated to the presence of immune complexes will be discussed.

Animals↗