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Biomedical subjects

B A Watkins

Publications and source records attributed to B A Watkins.

At least 91 records · Page 5Linked to original sources
PubMed1989

Eicosanoic fatty acid reduction in the tibiotarsus of biotin-deficient chicks.

Day-old male broiler chicks (Hubbard x Hubbard) were fed a purified diet containing biotin at 0 microgram/kg of diet (biotin-deficient) or 500 micrograms/kg of diet (biotin-adequate). Biotin-deficient (BD) chicks had decreased growth and feed efficiency and greater twisted leg and dermatitis symptoms than biotin-adequate (BA) chicks. Lipids in cortical bone of the tibiotarsi in BD chicks contained higher levels of linoleate, gamma-linolenate, and alpha-linolenate. Prostaglandin precursors, dihomo-gamma-linolenate (20:3 omega 6), arachidonate (20:4 omega 6), and eicosapentaenoate (20:5 omega 3) were all lower in BD chicks compared with BA chicks. Periosteal bone appositional and bone formation rates, and percent new bone formation were reduced in the tibiotarsi of BD chicks. Anatomically there were two different bone modeling patters at the mid-diaphysis. The cortex was thickest laterally in chicks fed the BA diet and thickest medially in chicks fed the BD diet. The quantitative differences in bone growth and the distinct bone modeling patterns, coupled with corresponding decreases in PG precursors, suggest that biotin deficiency may alter bone growth and modeling via a PG-dependent mechanism.

Animals↗
PubMed1989

Growth of epithelium from a preneoplastic mammary outgrowth in response to mammary adipose tissue.

We investigated the effects of conditioned media derived from mouse mammary fat pads on the proliferation of CL-S1 cells, an epithelial cell line originally isolated from a preneoplastic mammary outgrowth line. Cell proliferation in vitro in serum-free defined medium was compared to that in this medium conditioned using intact mammary fat pad pieces or isolated fat pad adipocytes. Culture medium was conditioned by incubating the conditioning material in defined culture medium for 24 h at 37 degrees C. Conditioned medium induced CL-S1 proliferation as much as 10- to 20-fold above the minimal levels of growth in control cultures after 13 d of culture. The growth-stimulatory factor(s) had an apparent molecular weight of greater than 10 kDa. This growth-stimulatory activity was both heat and trypsin stable. Because the role of adipose tissue is to store and release lipids, we next tested whether lipids are released during medium conditioning. The lipid composition of the fat pad conditioned medium was characterized using both thin layer and gas liquid chromatography. These lipid analyses indicated that the fat pad pieces released significant amounts of fatty acids and phospholipids into the medium during the conditioning period. The free fatty acid composition included both saturated and unsaturated molecules, and about 80% of the total fatty acids consisted of palmitate, stearate, oleate, and linoleate. These same fatty acids were a structural component of the majority of phospholipid found in the medium. The addition of palmitate or stearate to defined medium had no effect or was inhibitory for CL-S1 proliferation, depending on the concentration used. Defined medium supplemented with oleate, arachidonate, or linoleate induced CL-S1 proliferation, and the inhibitory effects of palmitate and stearate were overcome by addition of oleate and linoleate. These data indicate that both unsaturated and saturated fatty acids are released from intact adipose cells of the mouse mammary fat pad and that fatty acids can influence the growth of preneoplastic mouse mammary epithelium. Thus, unsaturated fatty acids, perhaps in conjunction with other substances released simultaneously, are candidate molecules for the substances that mediate the effect of adipose tissue on growth of epithelium.

Adipose Tissue↗
PubMed1989

Influences of biotin deficiency and dietary trans-fatty acids on tissue lipids in chickens.

1. The combined effects of feeding hydrogenated fats and varying the levels of biotin and linoleate (18:2 omega 6) on polyunsaturated fatty acids were studied in the chicken. 2. Biotin deficiency signs were not exacerbated by feeding hydrogenated fats or by diets low in linoleate for 21 d. 3. Biotin deficiency resulted in proportionately higher levels of 18:2 omega 6 and gamma-linolenate (18:3 omega 6) in liver triglycerides, and lower levels of dihomo-gamma-linolenate (20:3 omega 6) in liver and heart phospholipids irrespective of the 18:2 omega 6 level in the diet. 4. Biotin deficiency did not alter arachidonate (20:4 omega 6) levels in tissue lipids at 21 d. 5. Feeding high levels of trans-18:1 isomers with adequate biotin led to reduced 20:3 omega 6 and 20:4 omega 6 levels in liver and heart phospholipids with compensatory increases in omega 3 fatty acids. 6. The trans-isomers of 18:1 were incorporated into several tissues of the chick. Incorporation was dependent on the levels fed. Very small amounts were incorporated into brain compared with other tissues when dietary trans-isomer levels were high, but were similar when dietary trans-isomer levels were low. The trans-18:1 isomers appear to be preferentially incorporated into phospholipids as opposed to triglycerides in heart and liver.

Animals↗
PubMed1989

Linoleic acid and linolenic acid: effect on permeability properties of cultured endothelial cell monolayers.

High circulating plasma levels of free fatty acids may injure endothelial cells, resulting in decreased barrier function of the vascular endothelium. The effect of media supplementation with varying concentrations of either linoleic (C18:2 omega 6) or linolenic acid (C18:3 omega 3) on albumin transfer across cultured endothelial monolayers was studied. A 24-h cell exposure to linoleic but not linolenic acid resulted in a concentration dependent and largely reversible increase in albumin transfer. Both fatty acids and in particular linolenic acid incorporated into cellular phospholipids. In contrast, only supplementation with linoleic but not linolenic acid resulted in an increased incorporation of this fatty acid into cell triglycerides. Similarly, only total cell triglyceride content increased after incubation with linoleic- but not with linolenic-enriched media. These results indicate that cellular enrichment with linoleic but not linolenic acid causes cellular perturbations that may be implicated in atherosclerosis.

Animals↗
PubMed1989

Levels of dihomo-gamma-linolenate are depressed in heart phosphatidylcholine and phosphatidylethanolamine in the biotin-deficient chick.

Male broiler chicks were fed a purified diet with 0 or 500 micrograms/kg of added biotin for 21 days posthatch. Fatty acid composition of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were determined in erythrocytes and in heart mitochondria and microsomes of chicks at 12 and 21 days of age. The biotin-deficient (BD, 0 microgram biotin) chicks had lower body weights, lower feed efficiencies, and higher scores for dermatitis and twisted leg than the biotin-adequate (BA, 500 micrograms biotin) chicks. The erythrocyte arachidonate level in PC was higher in BD chicks compared to the BA controls, and the level increased with age in PC and PE in the erythrocytes. The level of dihomo-gamma-linolenate (20:3 omega 6) in PC and PE in heart mitochondria and microsomes was consistently decreased in BD chicks compared with that in BA chicks. In heart subcellular organelles, the level of arachidonate in PC increased, but the level of dihomo-gamma-linolenate in PE decreased with age. These data demonstrate that biotin deficiency results in dramatic changes in the fatty acid composition of specific phospholipids in chick erythrocytes and heart subcellular organelles.

Age Factors↗
PubMed1988

Chromatographic analysis of 18:1 isomers in blended feed-grade fats used in poultry diets.

The presence of trans and cis 18:1 isomers was determined in samples of commercially available blended feed-grade fats (BFF) used in poultry diets. Total lipids (TL) were extracted with chloroform:methanol (2:1, v/v); triglycerides (TG) and free fatty acids (FFA) were separated by thin-layer chromatography (TLC). The trans and cis isomers of 18:1 in TL, TG, and FFA were separated by argentation TLC and quantified by gas-liquid chromatography (GLC). The trans isomers of 18:2 were directly separated by GLC. The BFF contained many trans and cis 18:1 isomers. Total trans 18:1 ranged from 0 to 11.7% in the BFF sources and up to 31.3% of the total 18:1 isomers. The trans isomers of 18:2 were found in lesser amounts (.1 to .7%). Levels of essential fatty acids linoleate and linolenate ranged from 11.5 to 50.3 and .7 to 2.8%, respectively. Ratios of saturated:unsaturated fatty acids ranged from .17 to .68. These data indicate that trans and cis isomers of 18:1 are present in varying amounts in BFF.

Animal Feed↗
PubMed1988

Biotin deficiency may alter tibiotarsal bone growth and modeling in broiler chicks.

Forty-eight, day-old male broiler chicks (Hubbard x Hubbard strain) were fed purified diets with two levels of biotin (0 and 400 micrograms/kg) and two levels of linoleate (26.5 and 1.5 g/kg) in a factorially designed experiment to determine the effects of these nutrients on tibiotarsal bone growth and modeling. Chicks fed biotin-deficient diets (0 microgram/kg diet) exhibited varus deformities, footpad dermatitis, shortened tibiotarsi, and significantly higher bone densities and percentage bone ash. Anatomically there were two different bone modeling patterns. The mid-diaphyseal cortex was thickest laterally in chicks fed adequate biotin and thickest medially in biotin-deficient chicks. Periosteal bone appositional and bone formation rates, osteoid perimeter, and osteoid area of perimeter were reduced in tibiotarsi of chicks fed diets deficient in biotin compared with effects in chicks fed adequate biotin. Altered bone modeling patterns and quantitative differences in bone histomorphometry suggest a relationship between the effects of biotin on bone growth and the development of varus limb deformities.

Animals↗
PubMed1988

Distribution of trans and cis 18:1 fatty acid isomers in chicks fed different fats.

The effects of dietary trans isomers of 18:1 (t-18:1) were studied in chicks by feeding purified diets containing soybean oil (SBO) as the control lipid source, saturated fat (SF), hydrogenated soybean oil (HSBO), or spent restaurant grease (SRG) for three weeks. Argentation thin-layer chromatography and gas-liquid chromatography were used to separate trans and cis (c) isomers of 18:1 and to determine the fatty acid composition in chick tissues. Chicks fed HSBO (34% t-18:1 of total 18:1) had weight gains similar to those of chicks fed SF but significantly (P less than .05) lower gains than those of chicks fed SBO or SRG. No differences were observed in feed conversion ratios (total feed:total gain) across treatments. Trans-18:1 was incorporated into liver, heart, lung, and abdominal fat pad of chicks fed HSBO. Chicks fed HSBO had higher levels of c-16:1 omega 7 and 18:1 and lower levels of linoleate and arachidonate in tissue lipids. Similar changes were observed in liver microsomal fatty acids of chicks fed SRG that was adequate in linoleate, but which contained low levels of t-18:1 (4% of total 18:1). Positional and geometrical isomers of 18:1 appear to impair essential fatty acid metabolism in the chick.

Adipose Tissue↗
PubMed1987

A cultured human oligodendroglioma cell line and herpes simplex virus-infected cells share antigenic determinants.

Cell cultures derived from 60 different human brain tumors were screened for the presence of HSV infected cell antigens by indirect immunofluorescence using a polyclonal rabbit antiserum reacting with herpes simplex virus (HSV), 3 monoclonal antibodies recognising different HSV-specified proteins, and one monoclonal antibody T181 reacting with a DNA binding protein present in HSV-infected cells. Only one tumor (IN/157), derived from an oligodendroglioma, stained with the polyclonal antiserum. T181 but none of the other monoclonal antibodies used also specifically reacted with IN/157 cells. High levels of the T181-defined protein were detected using immunoblotting in HSV-1 infected BHK/21 cells but not in IN/157 cells. T181 may react with either an epitope shared between two different molecules in HSV-1 infected and IN/157 cells or a cell-specified polypeptide that is upregulated after HSV-1 infection.

Antigens, Viral↗
PubMed1987

Liver subcellular fatty acid profiles of chicks fed diets containing hydrogenated fats and varying linoleate levels.

Day-old male broiler chickens were fed semipurified diets containing 5% lipid from one of four different lipid sources: corn oil (CO), partially hydrogenated soybean oil (HSBO), a spent restaurant grease (SRG) and a purified mixture of triolein, tripalmitin and tristearin (OPS). Diets CO and HSBO contained adequate amounts of linoleic acid, but diets SRG and OPS were deficient in linoleate. In addition, SRG and HSBO contained trans isomers of 16:1 and 18:1. The diets were fed for 3 wk to determine the effects of low linoleate levels and trans isomers on fatty acid profiles in liver microsomes, mitochondria and cytosol. Chicks fed HSBO had the highest body weights, while those fed SRG and OPS had the lowest. The incidence and severity of dermatitis were similar for all treatments. The proportions of linoleate and arachidonate in lipids from liver subcellular fractions were reduced significantly in chicks fed OPS and SRG; however, levels of 20:3 omega 9 were not increased. Feeding HSBO, which is high in both linoleate and linolenate, resulted in higher levels of 18:3 omega 3 and 20:5 omega 3 in liver subcellular fractions and lower levels of 20:4 omega 6 than those seen in chicks fed CO. The isomeric forms of 18:1 present in the partially hydrogenated fats (HSBO and SRG) appeared to be incorporated into the lipids of liver fractions. The results of this study show that dietary lipids influence fatty acid profiles of chick liver microsomes, mitochondria and cytosol. Decreases in linoleate and arachidonate in these organelles occur before overt essential fatty acid (EFA), deficiency signs in chicks fed EFA-deficient diets.

Animals↗
PubMed1987

Tissue lipid fatty acid composition of biotin-adequate and biotin-deficient chicks.

Male broiler chicks were fed a purified ingredient diet containing various levels of added biotin to study dietary biotin effects on polyunsaturated fatty acids in selected tissues. Chicks were fed a basal diet containing adequate or deficient levels of added biotin and an additional group was fed a natural ingredient practical diet as a control. No significant differences in average body weights were found in chicks at 21 days fed 200 micrograms or more of biotin or the stock mash diet. Liver and heart biotin levels were lower in chicks fed less than 200 micrograms of biotin (P less than .01). At 21 days of age, the liver fatty acids of biotin-deficient chicks contained greatly (P less than .05) elevated c16:l, 18:ln9, 18:2n6, 18:3n6, and 18:3n3, whereas 20:3n6 and 20:4n6 were significantly lowered (P less than .05). Heart fatty acids c16:l and 18:2n6 of 21-day-old biotin-deficient chicks were elevated (P less than .05) and 18:3n3, 20:3n6, and 20:5n3 were lowered (P less than .05). It appears that the impaired conversion of 18:2n6 to 20:4n6 in liver tissue from biotin-deficient chicks at 3 weeks can result in lowered prostaglandin precursors not only in the liver but in the heart and muscle lipids as well. Changes in the brain and lung lipids are less marked.

Animals↗
PubMed1987

White lupin as a protein source for layers.

Three feeding experiments were conducted with Single Comb White Leghorn hens to determine the effects of Lupinus albus cv. Ultra on performance. Raw, autoclaved, and extruded lupins were fed at 10 and 20% of the diet for 12 wk in Experiment 1. In Experiment 2 raw and extruded lupins were fed at 10, 15, 20, and 25% of the diet for 16 wk. Raw lupin was fed for 32 wk at 10, 15, 20, 25, and 30% of the diet in Experiment 3. Average egg weight, egg production (percent hen-day basis), and feed consumption of hens fed lupins were not significantly different (P greater than .05) from those of hens fed no lupin (basal diet) in Experiments 1 and 2. Haugh unit measurements of eggs from hens fed lupins (Experiment 2) were not significantly different (P greater than .05) from those of hens fed the basal diet (control). Egg production was depressed (P less than .01) in hens fed 30% lupin compared to production of hens fed lower levels of lupin or the basal diet in Experiment 3. Lupin fed at the 15% level or higher in the diet increased (P less than .01) feed consumption of hens in Experiment 3. In all three experiments the average yolk color of eggs from hens fed lupins was significantly higher than that of hens fed the basal diets. Our data indicate that Ultra can serve as a primary protein source when fed to productive hens.

Animals↗
PubMed1987

Dietary biotin effects on polyunsaturated fatty acids in chick tissue lipids and prostaglandin E2 levels in freeze-clamped hearts.

Chicks were fed a purified diet with 0, 100, 200, 300, 400, or 500 micrograms/kg diet of added biotin to determine the effects of biotin deficiency on polyunsaturated fatty acids in tissue lipids. Body weight was reduced by biotin deficiency and liver and heart biotin levels varied with the biotin in the diet. Fatty acids in liver and lung from biotin-deficient chicks at 15 days contained elevated (P less than .03) 18:3 omega 3 and 18:2 omega 6 but prostaglandin precursors 20:3 omega 6 and 20:4 omega 6 were reduced (P less than .03) in liver lipids. Heart tissues from 15-day-old chicks fed the biotin-deficient diet were low (P less than .03) in 20:3 omega 6. Feeding acetylsalicylic acid in diets containing added biotin (0, 100, 400, and 500 micrograms/kg) did not significantly alter fatty acid levels in chick tissue lipids but significantly reduced plasma prostaglandin E2 (PGE2). Biotin deficiency reduced heart PGE2 levels in 22-day-old chicks. An 8-h fast reduced (P less than .04) 20:4 omega 6 in chick heart total fatty acids.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Effects of dietary biotin and linoleate on polyunsaturated fatty acids in tissue phospholipids.

Two experiments with factorial designs were conducted to study the interaction between dietary biotin and linoleate in male broiler chicks. Chicks were fed a purified basal diet containing varying levels of d-biotin (0, 200, or 400 micrograms/kg diet) and linoleate. In Experiment 1, chicks were fed the basal diet containing three levels of added linoleate (.5, 3.1, or 4.1% of diet) for each biotin level and in Experiment 2, four levels of linoleate were fed (.27, .98, 2.00, or 2.20% of diet). The average body weights of chicks fed biotin at 200 micrograms/kg of diet and .27 or .5% added linoleate were not different (P greater than .05) from those of chicks fed higher levels of biotin or linoleate supplements to the basal diets. Linoleate deficiency resulted in elevated omega-9 fatty acids (18:1 omega 9 and 20:3 omega 9) in liver and heart phospholipids. For liver phospholipids, linoleate deficiency led to reduced 18:2 omega 6, 20:3 omega 6, and 20:4 omega 6 but for heart phospholipids only 20:4 omega 6 was lowered. Biotin deficiency resulted in elevated 18:3 omega 6 in liver and heart lipids and decreased 20:3 omega 6 in liver phospholipids. Liver microsomes from biotin-deficient chicks contained increased 18:2 omega 6 and reduced 20:3 omega 6 compared with those of biotin-adequate chicks.

Animals↗
PubMed1984

Drinking water treatment with a commercial preparation of a concentrated Lactobacillus culture for broiler chickens.

Three hundred male broiler chicks were used to determine the effects of supplying Lactobacillus in the drinking water. The product used, Biomax 40TM, was a fresh-frozen, pure culture of Lactobacillus containing 40 X 10(9) cfu/ml. Water treatments consisted of continuous lactobacilli dosing (CD) and skip-a-day lactobacilli dosing (SAD). A control group (C) received no lactobacilli. Each treatment and control contained two pens of 50 chicks each and were fed for a duration of 7 weeks. At the termination of the experiment, weights of the wet viscera, and wet and dry small intestines of the broilers revealed no significant differences between treatments and control. Surface pH readings taken from crop and duodenum showed that there was no significant difference (P greater than .05). Microbiology performed on duodenal contents revealed higher numbers of lactobacilli for CD and SAD broilers than for C broilers. The liver biotin contents of the lactobacilli-treated broilers were not significantly different from those of the controls. Body weights were not changed by either treatment, although they were greater for the CD broilers than for the SAD broilers. No difference was observed in feed conversion (feed/gain).

Animals↗
PubMed1983

Competitive gut exclusion of avian pathogens by Lactobacillus acidophilus in gnotobiotic chicks.

A total of 205 Grey Leghorn chicks were hatched germfree for separate trials to determine the effects of Lactobacillus acidophilus treatment on pathogenic Salmonella typhimurium and Staphlococcus aureus. Prophylactic and therapeutic treatments with L. acidophilus were administered either before or after the pathogens were introduced. Prophylactic treatments significantly reduced chick mortality (P less than .01) and shedding of the pathogens (P less than .05). The L. acidophilus prophylactic treatments were also effective qualitatively in reducing the isolation of S. typhimurium and Staph. aureus from crop contents but not, to a great extent, from cecal or rectal contents of gnotobiotic chicks at postmortem. The average surface pH values for the crop, proventriculus, duodenum, cecum, and rectum for gnotobiotic chicks were 5.43, 5.02, 6.18, 6.56, and 6.71, respectively. The L. acidophilus treatments did not significantly affect surface pH of the various segments of the intestinal tract.

Animals↗
PubMed1983

Effect of oral dosing of Lactobacillus strains on gut colonization and liver biotin in broiler chicks.

Strains of host specific (KTM, 74/1, and 59) and nonhost specific (40) lactobacilli were orally dosed to day-old broiler chicks. Dose levels consisted of: 5.0, 7.0, and 9.0 log10 cfu/day for 21 days. Each treatment and control group (placebo, no culture) contained three replications of 6 chicks in Experiment 1 (strains 40 and KTM) and 7 chicks in Experiment 2 (strains 74/1 and 59). Dosing of 7.0 log10 cfu and above tended to depress chick growth. Fecal shedding of lactobacilli were the same (8.8 log10 cfu) for all dose levels on Day 5 but decreased on Day 14 for strains KTM and 40. For strains 74/1 and 59 at all dose levels, the fecal shedding of lactobacilli was 9.9 log10 cfu for Day 5 and 8.5 log10 cfu for Day 14. Microbiology was performed on contents of the crop and ileum and on the tissue macerates from the crop, ileum, and ceca from chicks killed on Days 7 and 21 of the experiments. Chicks dosed with strains 59 and KTM had lower numbers of coliforms in cecal macerates than the control and chicks dosed with strains 40 and 74/1. No significant differences were observed in lactobacilli found in contents and tissues between 5.0 and 9.0 log10 cfu for all lactobacilli strains dosed. There was a trend for the liver biotin to be higher in chicks dosed with 7.0 log10 cfu than chicks dosed with 5.0 or 9.0 log10 cfu or no culture, but the difference was not significant (P greater than .05).

Animals↗