Biomedical subjects

J L Schaeffer

Publications and source records attributed to J L Schaeffer.

11 recordsLinked to original sources

PubMed1995

Lined multifocal wearers prefer progressive addition lenses.

BACKGROUND: Despite reported successes with progressive addition lenses, lined multifocals remain the lens of choice for previous lined multifocal wearers. METHODS: To explore the feasibility of switching lined multifocal wearers to PALs, in a prospective clinical trial we interviewed 265 lined multifocal wearers, prescribed a new PAL (Varilux Comfort) and then interviewed them again to compare the lens types and patient preferences. RESULTS: PALs ranked significantly higher than lined multifocals for all questions and were preferred by 92 percent of the patients. CONCLUSIONS: PALs should be the lens of choice for previous bifocal wearers.

Adaptation, Ocular↗

PubMed1991

Measurement of malabsorption of carotenoids in chickens with pale-bird syndrome.

Because pale-bird syndrome (PBS), defined as the failure of birds to realize the color potential of their diet, has been demonstrated to be caused by malabsorption or by hyperexcretion of carotenoids, a method for measuring malabsorption of carotenoids would be useful. The absorption of dietary canthaxanthin, a red diketocarotenoid, into serum during aflatoxicosis was measured in an experiment with a 2 x 9 factorial arrangement of treatments (0 and 5 micrograms of aflatoxin/g of diet; serum collected at 0, 2, 4, 6, 8, 10, 12, 14, and 24 h after a standard meal fed to four groups of 10 3-wk-old birds). Serum canthaxanthin levels determined by HPLC attained plateau values between 8 and 14 h after the meal. The absorption of canthaxanthin was depressed significantly (P less than .05) in birds with aflatoxicosis from 4 to 24 h after feeding the standard meal. Four field flocks diagnosed as having PBS were tested for malabsorption by intubating 10 birds with a standard amount of canthaxanthin and measuring serum canthaxanthin 12 h later. One flock had about 85% normally pigmented birds and 15% extremely pale birds, the second flock had a coccidiosis history, the third had a Newcastle disease history, and the fourth had a history of both coccidiosis and Newcastle disease. The flocks were 5- to 6-wk-old, received feed of the same manufacture, and their disease outbreaks had occurred 2 wk earlier.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗

PubMed1990

Effect of dietary lipid on lutein metabolism during aflatoxicosis in young broiler chickens.

The effect of concentration of dietary fat on pigmentation of broiler chickens was investigated in diets containing: 1) 0 or 1.4 micrograms of aflatoxin and 35 micrograms of lutein/kcal of diet; and 2) different levels of dietary fat (0, 2, 4, 6, 8, or 10% cottonseed oil). Serum lutein and its metabolite, 3'-oxolutein, increased with increasing dietary fat until it reached a plateau at 6% fat. Aflatoxin significantly (P less than .05) lowered serum lutein and 3'-oxolutein at all levels of fat. Dietary fat and aflatoxin interacted significantly (P less than .05), with the effect of aflatoxin being greater at the low levels of fat than at the high fat levels. In the toe webs of the birds, the concentrations of lutein and its metabolites, lutein monoester, lutein diester, and 3'-oxolutein responded similarly to aflatoxin and to dietary fat, except that increasing the amount of dietary fat did not spare the effect of aflatoxin on 3'-oxolutein. The effect of chain length and the saturation of fatty acids on the absorption of lutein during aflatoxicosis was investigated in a factorial design for aflatoxin (0 and 4 micrograms/g of diet) and seven fatty acids at 5% of the diet. In control birds, lutein absorption was promoted by lauric = oleic greater than capric = linoleic greater than myristic greater than palmitic = stearic acids. Aflatoxin significantly (P less than .05) depressed the absorption of lutein regardless of the fatty acid present.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

PubMed1988

Carotenoid composition of serum and egg yolks of hens fed diets varying in carotenoid composition.

High performance liquid chromatography of yolks of hens fed a diet based on yellow corn, alfalfa, and soybeans revealed over 20 cartenoids. Lutein, lutein monester, lutein diester, 3'-oxolutein, cryptoxanthin, zeaxanthin, beta-carotene, and zeacarotene were identified by their retention times, visible absorption spectra, behavior on saponification, and their presence or absence when lutein was the primary carotenoid fed. Three weeks after placing the hens on a white corn-soy-based diet supplemented with lutein (20 micrograms/g diet), cryptoxanthin, zeaxanthin, and zeacarotene were undetectable in the yolk and lutein, lutein monoester, lutein diester, and 3'-oxolutein assumed new equilibrium concentrations. The data imply an esterification pathway and an oxidative pathway in laying hens for the metabolism of hydroxycarotenoids. Consideration of the concentrations and ratios of lutein and its metabolites in serum and yolk suggest a nonovarian site for the metabolism of lutein in laying hens.

Animals↗

PubMed1988

Aflatoxin-impaired ability to accumulate oxycarotenoid pigments during restoration in young chickens.

The mechanism by which aflatoxin causes paling in chickens was investigated by measuring its effect on the restoration of pigments in 3-wk-old birds made pale by feeding a white corn-soy diet. Pigment restoration was accomplished by feeding the same diet supplemented with lutein (70 micrograms/g of diet), which is the major oxycarotenoid pigment in chicken diets and tissues. The oxycarotenoids (free, monoester, and diester forms of lutein) in the toe web, liver, serum, and jejunal mucosa of control and aflatoxin-fed (2 micrograms/g of diet) birds were measured by HPLC at 0, 1, 2, 3, 6, and 9 days of repletion. Aflatoxin caused a significant (P less than .05) depression of all forms of lutein in the toe web. In the liver, aflatoxin decreased lutein significantly (P less than .05) but increased lutein monoester and lutein diester. Lutein accumulation in serum and mucosa were inhibited significantly (P less than .05) starting on Days 2 and 3, respectively. These data imply that the normal accumulation of lutein from the diet proceeded into and through the mucosa to the serum to depot sites in the liver and integument, where lutein was acylated to its monoester, which was acylated to its diester. Further, aflatoxin inhibited, apparently independently, the accumulation of lutein by the mucosa, serum, liver, and integument. Pharmacokinetic analysis of the data indicated that both acylation steps in the integument were sensitive to aflatoxin, but the passage of lutein from serum into the integument was not affected.

Aflatoxins↗

PubMed1988

Depletion of oxycarotenoid pigments in chickens and the failure of aflatoxin to alter it.

Aflatoxin, a demonstrated cause of pale bird syndrome in chickens, was investigated for its effects on the depigmentation of chickens placed on a diet low in carotenoids. Chickens were pigmented by feeding for 3 wk a white corn-soy diet supplemented with 50 micrograms free lutein and 0 or 4 micrograms aflatoxin/g diet. Then birds were switched to the same diets unsupplemented with lutein. At 0, 1, 2, 3, 6, and 9 days after switching, jejunal contents and mucosa, serum, liver, and toe web of 4 groups of 10 birds were removed for analysis of their carotenoids by high performance liquid chromatography. In control birds the order of decrease in total lutein was jejunal contents greater than jejunal mucosa greater than serum greater than liver greater than toe web. Aflatoxin did not alter the depletion process, except for minor retardation of lutein depletion in the mucosa and liver. Pharmacokinetic analysis of the data indicated that lutein depletion in the integument was accomplished through three sequential reactions (lutein diester----lutein monoester----lutein----serum lutein) and that aflatoxin had no effect on the reactions. These results imply that aflatoxin induces pale bird syndrome by interfering with the accumulation of pigment by chickens rather than by enhancing the depletion of pigment.

Aflatoxins↗

PubMed1987

Alterations in carotenoid metabolism during ochratoxicosis in young broiler chickens.

The mechanism by which ochratoxin impairs the ability of chickens to utilize dietary carotenoids for carcass pigmentation was investigated. Graded doses of pure ochratoxin A (0, .5, 1.0, 2.0, and 4.0 micrograms of toxin/g of feed) were incorporated into a white corn-soy diet supplemented with an efficiently used oxycarotenoid (110 micrograms free lutein/g) and fed to broiler chicks from day of hatch to 3 weeks of age. Concentrations of free lutein and its metabolites, lutein diester, lutein monoester, and oxolutein, in the jejunal contents, jejunal mucosa, serum, liver, and toe web from these birds were measured by high performance liquid chromatography. Based on the threshold level of ochratoxin required for an effect on the concentrations of carotenoids and on the severity of the effect, five separate loci for the action of ochratoxin on carotenoid metabolism were detected: dilution of carotenoids in intestinal contents, depressed uptake by intestinal mucosa, depressed transport in serum, altered accumulation in liver, and altered acylation steps in the integument.

Animals↗

PubMed1986

3'-Oxolutein, a metabolite of lutein in chickens.

3'-Oxolutein (3-hydroxy-3'-oxo-beta,epsilon-carotene) was isolated using high performance liquid chromatography (HPLC) from the tissues and egg yolks of chicken fed a diet high in lutein and free of detectable 3'-oxolutein. It was identified by HPLC retention time, absorption spectrum identical to lutein and its esters, disappearance under alkaline conditions without giving rise to lutein, formation of an alkali labile palmitate, formation of a 2,4-dinitrophenylhydrazone, and reduction to lutein from which the dipalmitate was prepared. In each instance the isolated compound behaved identically with authentic 3'-oxolutein prepared by nickel peroxide oxidation of lutein. The order of ratios of lutein to 3'-oxolutein in the various tissues from laboratory and field birds was, in general, intestinal contents greater than intestinal mucosa greater than serum greater than liver approximately toe web approximately egg yolk greater than bile. This order was consistent with the hypothesis that lutein was oxidized to 3'-oxolutein in the liver, which, at least in part, was excreted via the bile into the intestinal lumen where it was diluted with dietary lutein. The remainder of the 3'-oxolutein formed in the liver presumably went into the serum where it was transported to depot sites. The ratio of lutein to 3'-oxolutein in the toe webs of broilers varied with their diet and pigmentation status. Amounts of 3'-oxolutein were found in quail and turkey egg yolks. This previously unreported lutein oxidative capability of liver extends the previously known metabolic acylation and deacylation reactions in poultry.

Animals↗

PubMed1980

Measurement of antithrombin III in normal and pathologic states using chromogenic substrate S-2238. Comparison with immunoelectrophoretic and factor Xa inhibition assays.

Synthetic substrates have recently been developed for the assay of several of the proteolytic enzymes required for blood coagulation, One of these substrates, S-2238, is specific for thrombin and hence can also be used to measure antithrombin-heparin co-factor (AT-III). The thrombin remaining after neutralization by AT-III cleaves a chromophore, p-nitroaniline, from the substrate, which can then te quantified in a spectrophotometer. This new assay for AT-III inhibitory activity was evaluated for normal subjects and for patients who had certain pathologic conditions associated with reduced levels of AT-III. Results from this assay were compared with those from AT-III assays by Laurell immunoelectrophoresis (an immunologic method) and antithrombin inhibition of factor Xa (a biologic clotting method). The chromogenic assay using S-2238 was found to be sensitive, accurate, and easy to perform; its results for both normal subjects and patients correlated extremely well with those of the immunologic and factor Xa inhibition assays (r = 0.94-0.98). Measurement of AT-III using this synthetic substrate should be a valuable addition to routine assays in a clinical coagulation laboratory. These and future substrates may prove extremely useful for assays of factors involved in blood coagulation and fibrinolysis.

Antithrombin III↗

PubMed1978

Counseling sexual abuse victims.

Rape can cause tremendous physical, social and psychologic disruption which affects the victims, their families and friends, and the community. In the past, society has been quite remiss in its response to rape victims. Major attitudinal changes based on factual information must take place, because the attitudes and biases of those helping the victim can further victimize the sexually assaulted woman.

Child↗

PubMedDate not supplied

Inclusion-body hepatitis in day-old turkeys.

Inclusion-body hepatitis was diagnosed in 1-day-old turkeys experiencing above-average mortality. At necropsy, turkeys appeared anemic and had pale yellow livers. Histopathologic examination of affected livers revealed diffuse hepatic degeneration and multifocal necrosis, with approximately 70% of the hepatocytes containing large, basophilic, intranuclear inclusion bodies. An adenovirus was isolated from affected livers and identified as a group I avian adenovirus by indirect immunofluorescence.

Adenoviridae↗