Experimental evaluation of the threshold limit of cristobalite--calcined diatomaceous earth.
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Animals↗
Biomedical subjects
W D Wagner
Publications and source records attributed to W D Wagner.
Aortic glycosaminoglycans in genetically selected WC-2 pigeons with increased atherosclerosis susceptibility.
A genetically selected line of White Carneau pigeons (WC-2) was studied in an attempt to relate changes in composition and content of aortic glycosaminoglycan (GAG) to increased atherosclerosis susceptibility. The WC-2 pigeons were fed an atherogenic diet for 3 months and, when compared to randomly bred White Carneau (RBWC) controls, they showed similar plasma cholesterol concentrations but significantly greater aortic atherosclerosis. In the WC-2 pigeons, 35% of the aortic surface was covered with plaque compared with only 12% in RBWC pigeons; WC-2 birds showed cholesterol contents of 3.3 mg/aorta/500 g body weight, while the RBWC birds had only 0.9 mg/aorta/500 g body weight. After papain treatment of delipidated dried artery, the aortic GAG were isolated, purified using cetylpyridinium chloride, and identified and quantitated by a combination of procedure including selective enzymatic digestion and electrophoresis. In both pigeon groups, aortic GAG included 8% hyaluronic acid, 11% dermatan sulfate, 15% heparan sulfate, and 66% chondroitin sulfate. For the entire group, total aortic GAG content was 35% greater in WC-2 pigeons. Since we did not know if this increase in GAG was simply due to increased atherosclerosis in the WC-2 birds, we sorted the pigeons into matched groups representing minimal, moderate, and severe atherosclerosis on the basis of aortic cholesterol content. At all levels of cholesterol, all GAG contents were greater in the aortas of WC-2 pigeons. The accumulation of dermatan sulfate was 30% higher than in RBWC birds in the minimal arteriosclerosis group, 101% higher in the moderate group, and 53% higher in the severe group. Hyaluronic acid tended to decrease as aortic cholesterol contents increased in WC-2 pigeons. Reduced hyaluronic acid and increase dermatan sulfate may suggest the presence of an altered hyaluronic acid-dermatan sulfate-containing proteoglycan aggregate in the intercellular matrix of the WC-2 pigeon aorta. Possible consequences include increased artery permeability and a binding and retention of lipoproteins in the artery wall. These factors may explain why atherosclerosis develops at an increased rate in the WC-2 pigeon.
Animals↗
Metabolism and turnover of cell surface-associated heparan sulfate proteoglycan and chondroitin sulfate proteoglycan in normal and cholesterol-enriched macrophages.
Analysis of sulfur-35-labeled proteoglycans indicated that cholesterol-enriched pigeon peritoneal macrophages synthesized 42% more 35S-labeled proteoglycan when compared with control macrophages during a 24-hour incubation. Proteoglycan turnover was subsequently studied in radiolabeled macrophage cultures after a 1-, 3-, 6-, 12-, or 24-hour chase with fresh media. During the chase, intracellular proteoglycan disappeared rapidly, whereas there was a small accumulation of 35S-labeled proteoglycan in the media that plateaued at about 6 hours and remained relatively constant thereafter. Pericellular heparan sulfate proteoglycan and chondroitin sulfate proteoglycan disappeared throughout the chase and did not appear to accumulate in the media or in the intracellular compartment. The rapid disappearance of intracellular proteoglycans along with the relative lack in metabolism of media proteoglycans indicated that the majority of pericellular proteoglycans were metabolized via an intracellular degradative pathway. Kinetic analysis of pericellular proteoglycans revealed the presence of a single pool of heparan sulfate proteoglycan (half-life [t1/2] = 6.9 hours) and a single pool of chondroitin sulfate proteoglycan (t1/2 = 11.5 hours) in control macrophage cultures. Cholesterol-enriched macrophage cultures also contained a single pool of pericellular heparan sulfate proteoglycan (t1/2 = 7.3 hours) but contained two pools of chondroitin sulfate proteoglycan (t1/2 = 0.8 hour and 25.9 hours).
Animals↗
Reduced proteoglycan binding of low density lipoproteins from monkeys (Macaca fascicularis) fed a fish oil versus lard diet.
We examined the effect of isocaloric substitution of dietary fish oil for lard on the properties of low density lipoproteins (LDL) important in binding to arterial proteoglycans (PG). Cynomolgus monkeys (n = 10) were fed atherogenic diets enriched in fish oil or lard in a crossover study consisting of two 15-week phases of atherogenic diet separated by a 6-week monkey chow "wash-out period." LDL were isolated from plasma during each dietary phase, characterized for chemical and physical properties, and assessed for their ability to interact in vitro with arterial PG. Plasma LDL cholesterol was similar during fish oil and lard consumption (356 +/- 34 and 331 +/- 17 mg/dl, mean +/- SEM), but during fish-oil feeding relative to that of lard, LDL size was smaller (4.2 +/- 0.1 versus 4.9 +/- 0.1 g/mumol) and LDL particles differed in chemical composition. When animals were fed fish oil, significantly fewer (p less than 0.05) LDL particles bound to PG in both dietary phases: 1.00 +/- 0.27 (x10(12)) versus 5.31 +/- 0.83 (x10(12)) particles/micrograms PG in phase 1 and 3.56 +/- 0.67 (x10(12)) versus 6.00 +/- 0.52 (x10(12)) in phase 2 for LDL from animals fed fish oil and lard, respectively. These studies indicate that dietary fat-induced changes in LDL particles lead to altered in vitro interactions with artery wall PG and suggest a novel mechanism for the protective effect of fish oil against atherosclerosis.
Animals↗
Arterial dermatan sulfate proteoglycan structure in pigeons susceptible to atherosclerosis.
Arterial dermatan sulfate proteoglycans (DS-PG) were isolated from randomly bred White Carneau (RBWC) pigeons and a line of White Carneau pigeons (WC-2) genetically selected for increased atherosclerosis susceptibility. To characterize the basic proteoglycan (PG) structure and to identify structural differences that may relate to a specific arterial phenotype, embryos were labeled with radioactive sulfate in ovo and PG were isolated from aortas with 4.0 M GdnHCl. DS-PG were separated from chondroitin sulfate PG by gel chromatography and further purified by CsCl buoyant density ultracentrifugation and ion-exchange of chromatography. The DS-PG monomers from the two genetic lines of pigeons eluted at different positions on two high pressure liquid chromatography (HPLC) gel permeation systems, which suggested a structural difference between the two monomers. Analysis of the monomer components showed a similar protein core molecular weight of 50,000 for each and a similar amino acid composition. Glycosaminoglycans (GAG) molecular weights were estimated to be 15,000 for WC-2 and 18,000 for RBWC. The findings suggest a basic difference in post-translational processing of PG in the two pigeon types which may reflect distinct functional properties associated with resistance or susceptibility to atherosclerosis.
Amino Acids↗
A proposed structure of chondroitin 6-sulfate proteoglycan of human normal and adjacent atherosclerotic plaque.
Chondroitin sulfate proteoglycan monomers were prepared from intima media minces of grossly normal human aorta and adjacent fatty fibrous atherosclerotic plaques. Glycosaminoglycan chains prepared from monomer from normal aorta displayed a normal distribution profile on Ultrogel ACA 54 with a Kav of 0.48, whereas those of atherosclerotic aorta displayed a bimodal distribution (major peak, Kav 0.35; minor peak, Kav 0.70). The Mr of glycosaminoglycans from normal aorta was estimated to be 1.5 X 10(4). For atherosclerotic aorta, the majority of chains were 2.0 X 10(4) while the smaller population was 1.2 X 10(4). All glycosaminoglycans were identified as chondroitin sulfate sulfated at the C-6 position. The amino acid compositions of both core proteins were similar with Mr of about 1.6 X 10(5). After beta-elimination in the presence of sodium borohydride prior to acid hydrolysis, chondroitin sulfate proteoglycan from normal aorta had reductions in serine from 109 to 68 and in threonine from 117 to 55. For the monomer from atherosclerotic plaque, reductions in serine and threonine, respectively, were from 103 to 81 and from 107 to 77 residues per 1000. The results suggested fewer chondroitin sulfate chains and oligosaccharides on the core protein in the proteoglycan of atherosclerotic plaque. Compared to normal aorta, substituted serines and threonines in the proteoglycan of atherosclerotic plaque were about half, respectively, 38% vs 21% for serine, 53% vs 28% for threonine. It is estimated that in atherosclerotic plaque there are fewer, but longer, chondroitin sulfate chains per core protein, translating into a smaller overall monomer size in atherosclerotic plaque.
Adult↗
Effect of disulfiram pretreatment on the tissue distribution, macromolecular binding, and excretion of [U-1,2-14C]dichloroethane in the rat.
The effect of disulfiram (DSF) pretreatment on the distribution of [14C]ethylene dichloride (EDC) in selected organs and/or tissues of control and EDC-pretreated rats was studied. The presence of EDC metabolites and their binding to an acid-insoluble extract of the tissues, as well as purified protein and DNA, were evaluated. Dietary DSF was found to modulate the distribution, excretion, and macromolecular binding of EDC and/or its metabolites at 4 and 24 hr following ip administration. The urinary excretion of [14C]EDC metabolites was not affected by subchronic inhalation exposure to nonradiolabeled EDC. However, DSF pretreatment increased the fat deposition of EDC and decreased the urinary excretion of its metabolites. DSF also increased the binding of EDC metabolites to DNA and decreased the binding to protein in the liver, kidneys, spleen, and testes. However, prior exposure to EDC alone increased the binding of its metabolites to DNA in the kidneys only.
Animals↗
Survey of the pathologic findings in a large production colony of pigeons, with special reference to pseudomembranous stomatitis and nephritis.
Pathologic evaluations of pigeons dying between September 1984 and August 1985 are reported for a production colony of 1200-1800 White Carneau and Show Racer pigeons ranging in age from hatchlings to 12 years. Infectious diseases were the common causes of death in pigeons younger than 1 year; salmonellosis and nephritis were the common causes in pigeons 1-3 years old; and neoplasia and reproductive organ disorders were the common causes in pigeons older than 3 years. Monthly mortality was 2-4% in pigeons fed a cholesterol-containing diet and 0.9% in those fed noncholesterol-containing pellet diets. The increased deaths in the cholesterol-fed birds were attributed primarily to end-stage renal disease and atherosclerosis with secondary complications. The most frequently observed clinical entity in pigeons younger than 6 months was pseudomembrane formation on the oral and pharyngeal mucosa, termed pseudomembranous stomatitis. The definitive etiologic factor was not determined. Although all affected pigeons had similar gross lesions, the cases fell into one of three subsets, suggestive of bacterial, fungal, or viral etiologies. Chronic nephritis occurring as end-stage renal disease was more severe in pigeons fed a cholesterol-containing diet.
Animals↗
What providers should know about community cancer control.
PURPOSE: The authors describe a framework for developing an effective, community-focused cancer control program. OVERVIEW: Progress in the application of cancer control interventions has proven to be quite variable across different populations and communities. The Kentucky Cancer Program, developed under joint sponsorship of cancer centers at two state universities, has been using a model that appears to provide a high degree of sensitivity to community-specific problems and solutions. The Kentucky four-step model includes 1) using data from a population-based cancer registry and other sources to identify problems; 2) ensuring community involvement with providers in selecting the target population and developing the intervention strategy; 3) implementing the intervention plan; and 4) using cancer registry and other data to evaluate the impact of this intervention. CLINICAL IMPLICATIONS: This framework may be useful to providers as they try to balance the goals of their clinical practice and the goals of community cancer control. Developing an effective, community-focused cancer control program requires that providers gain a solid knowledge about their community. The depth and richness of that knowledge base is enhanced by the active participation of community members as they collaborate with the providers on planning and implementing cancer control activities.
Breast Neoplasms↗