PubMed Health⌕ Search

Biomedical subjects

F L Tucker

Publications and source records attributed to F L Tucker.

9 recordsLinked to original sources
PubMed1988

Erythrocyte sedimentation rate in glomerular disease: association with urinary protein.

The erythrocyte sedimentation rate (ESR) correlated significantly with the total urinary protein (TUP) in 24-hour urine collections in patients with glomerular disease (p less than 0.05 to p less than 0.001). The relationship was linear for all patients with a glomerular process but no longer held true once the patients were treated with immunosuppressives, or when the underlying disease excluded the glomerulus. The association between ESR and TUP was generally of the magnitude ESR = TUP X 10. ESR was not correlated with creatinine clearance. Multiple factors cause an increased ESR. To our knowledge, this is the first demonstration of an association between ESR and proteinuria.

Adult↗
PubMed1987

Hepatitis B virus serology. Loss of antibody to surface antigen.

A retrospective review of hepatitis B serologies from 6,686 patients was conducted to determine the incidence of loss of antibody to hepatitis B surface antigen (anti-HBs) with retention of antibody to the core antigen of hepatitis B virus (anti-HBc) activity. In a subgroup of 48 multiply tested patients who were presumed to have resolved their acute or subacute hepatitis B virus infection, 9 (19%) were found to have lost anti-HBs while retaining anti-HBc activity.

Hepatitis B Antibodies↗
PubMed1987

Immunoglobulin light chain nephropathies.

Excessive monoclonal light chain production and excretion may result in a variety of renal diseases which may collectively or individually be referred to as light chain nephropathy. Kappa light chains are more likely to produce tubular dysfunction and nodular nonamyloidotic glomerulosclerosis, while lambda light chains are more likely to be involved in the development of amyloidosis. The physicochemical reasons for this segregation are poorly understood. Affected patients may present with minor tubular dysfunctions, acute or chronic renal failure, mild proteinuria, or severe nephrotic syndrome. Underlying each is a dyscrasia of plasma cells or frank multiple myeloma with excessive production of monoclonal light chains. Electron microscopy and immunofluorescence studies of renal biopsies have been critical in defining these nephropathies and continue to be essential in establishing the diagnosis.

Amyloidosis↗
PubMed1985

Ultrastructural studies of experimental autoimmune glomerulonephritis in normal and bursectomized chickens.

Immunizations of chickens with bovine glomerular basement membrane (GBM) results in the development of experimental autoimmune glomerulonephritis (EAG). Animals lacking antibody to GBM develop nephritis comparable to those with antibody. The present study examined the ultrastructural lesions of EAG. Normal and bursectomized (Bsx) chickens were immunized with complete Freund's adjuvant (CFA) or CFA-GBM. We studied 3 CFA controls, 5 CFA-Bsx controls, 5 GBM immunized, 4 Bsx-GBM immunized antibody positive birds, and 6 Bsx-GBM immunized birds with no antibody. Ultrastructure of control animals was consistent with previous descriptions in chickens. In nephritic GBM-immunized animals the proliferative glomerulonephritis was associated with an increase in resident mesangial (type I) cells identified by small regularly shaped nuclei with coarsely clumped chromatin and scanty cytoplasm. (p less than 0.05). Glomerulonephritis was also associated with the occurrence of type II cells characterized by an irregular folded lobulated nucleus, finely granular chromatin, abundant cytoplasm, and dense granules and vacuoles in the cytoplasm with an appearance similar to macrophages. The presence of type II cells was highly associated with the development of glomerulonephritis, p less than 0.05. The increase in type II cells was observed in animals with and without antibody along the GBM. A third type of cell was also observed in intimate contact with type II cells and had the morphology of a lymphocyte. The lymphocytoid cells were only seen in nephritic animals. Bsx was associated with trabeculation and lucencies of the GBM not found in normal birds, p less than 0.05. EAG in chickens occurs regardless of the presence or absence of GBM-bound anti-GBM antibody. Other studies have shown that the disease can be transferred by specifically sensitized lymphocytes, but not by antibody. The present ultrastructural findings provide further evidence for the role of cell mediated immunity in the pathogenesis of this model of EAG in chickens.

Animals↗
PubMed1984

Bladder polyp and heavy proteinuria in a patient with Hodgkin's disease in remission.

A 21-year-old man who developed heavy proteinuria 8 years after remission of Hodgkin's disease treated with MOPP chemotherapy and radiation therapy is reported. Evidence of Hodgkin's disease could not be documented, and minimal changes were revealed by renal biopsy. Proteinuria persisted for 20 months and was followed by dysuria and the discovery of an inflammatory polyp of the bladder. The proteinuria decreased 1 month after excision of the polyp, and disappeared during the following year. Rather than indicating relapse of lymphoma, proteinuria in this patient resulted from a lesion not previously associated with Hodgkin's disease, but possibly resulting from long-term effects of therapy.

Adult↗
PubMed1984

New avian model of experimental glomerulonephritis consistent with mediation by cellular immunity. Nonhumorally mediated glomerulonephritis in chickens.

The present study examined the role of cell-mediated immunity (CMI) in the production of experimental autoimmune glomerulonephritis (EAG) in chickens deficient in humorally mediated immunity (HMI). Cyclophosphamide bursectomized (Bsx) and normal control chickens were used. Bsx chickens were used only if they had severe depression of HMI, which was evidenced by marked reduction in bursal weights (0.89 +/- 0.23 vs. 2.92 +/- 0.9 g), decreased serum IgG to less than or equal to 10% of normal, and total lack of HMI to immunization with sheep red blood cells. EAG was produced by immunizing chickens with bovine glomerular basement membrane (GBM) in complete Freund's adjuvant. CMI manifested by wattle thickness increments to PPD was not different, 3.89 +/- 0.45 mm for Bsx compared with 3.73 +/- 0.75 mm for controls. No circulating antibodies to GBM developed in 68% of Bsx chickens, and the anti-GBM titers were less than 1:312 in those Bsx chickens positive for antibody compared with greater than 2,000 for controls. GBM deposits of IgG by fluorescence were much decreased, 0.53 +/- 0.16 compared with 2.19 +/- 0.32 for controls, and were absent in 64% of Bsx chickens. Nonetheless, proliferative nephritis with crescents was present and was even more severe in Bsx chickens than in controls, with glomerular sizes of 20.8 +/- 0.6 U for Bsx-GBM, 19.8 +/- 1.2 for control-GBM, 14.9 +/- 1.5 for Bsx, and 13.6 +/- 0.8 for normal chickens. Nephritic eluates did not produce disease in normal chickens, while administration of sensitized cells with [H3]thymidine to naive birds was associated with increased mesangial grain counts by autoradiography. These findings suggest that CMI plays a major role in the pathogenesis of EAG in chickens in the absence of HMI. By implication, CMI may be crucial in the development of other types of glomerulonephritis as well.

Animals↗
PubMed1980

Experimental autoimmune glomerulonephritis in chickens.

A definite role of the humoral immune system in experimental autoimmune glomerulonephritis (EAG) has been shown. However, the role of the cellular immune system is less clear. Difficulty in separating these two systems has previously precluded examination of their isolated roles in the pathogenesis of EAG. The development of a chicken model of EAG would obviate these difficulties. We immunized chickens with bovine glomerular basement membrane (GBM) in complete Freund's adjuvant. The resultant disease is associated with circulating antibody to both chicken and bovine GBM and in vivo deposition of chicken IgG along the GBM in a linear pattern with minimal fixation of chicken complement. The lesion consists of proliferative glomerulonephritis as indicated by an increase in glomerular size and a decrease in the ratio of tuft size to the number of nuclei present. The proliferative component involves mainly the mesangium with little alteration of the capillary loops. In addition to proliferation of the glomerular tuft, there are associated adhesions and small crescents. No abnormal proteinuria developed in test animals compared to controls through 22 weeks of observation, although animals did develop proteinuria after intravenous colloidal carbon. Renal function remained normal throughout the period of our observations. The present study demonstrates that EAG can be successfully produced in chickens. This model affords the opportunity to examine the isolated roles of the humoral and cellular immune systems in the pathogenesis of EAG.

Animals↗
PubMed1966

X-ray diffraction studies on metal deposition in group D streptococci.

Tucker, Fayne L. (University of Southern California, Los Angeles), John W. Thomas, Milo D. Appleman, Stewart H. Goodman, and Jerry Donohue. X-ray diffraction studies on metal deposition in group D streptococci. J. Bacteriol. 92:1311-1314. 1966.-Streptococcus faecalis N83 and S. faecium K6A reduced several compounds of Group VI elements to the elemental form, but reduced none of several compounds tested containing elements of other groups. The elemental tellurium deposited by S. faecium K6A was in general of a larger particle size than that deposited by S. faecalis N83 as judged from X-ray diffraction analysis. The particle size of the deposited tellurium was correlated with the blackness of the precipitate produced by cells growing in the presence of tellurite. A black and gray variation was observed in S. faecium K6A which was considered to be due to particle size, the amount of tellurium present, and the location of the deposited tellurium. The gray color of S. faecium K6A was not due to the presence of any oxidized tellurium products.

Enterococcus faecalis↗