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An application of finite-element analysis with an optimisation technique to assess the myocardial material properties in diastasis in vivo is described. Using the data collected from an animal model, the three-dimensional geometry of the left ventricular chamber, at several times in diastole, was reconstructed. From the measurement of the ventricular chamber pressure during image acquisition, finite-element analysis was performed to predict the expansion during diastasis. Initially, by restricting the motion of the epicardial nodes and computing the reaction forces, an 'equivalent pericardial pressure' was determined and applied in subsequent analysis. The duration of diastasis was divided into three or four intervals and the analysis was performed at each interval to assess the material properties of the myocardium. Using such a step-wise linear approach, the non-linear material properties of the myocardium during passive expansion was determined. Our results demonstrated that the computed 'equivalent pericardial pressure' increased with and was smaller than the corresponding left ventricular chamber pressure. The passive myocardium exhibited a linear tangent modulus against chamber pressure relationship which is equivalent to an exponential stress/strain relationship, similar to those suggested by in vitro studies.

In this study, the sensitivity of a novel fibrin-targeted contrast agent for fibrin detection was defined in vitro on human thrombus. The contrast agent was a lipid-encapsulated perfluorocarbon nanoparticle with numerous Gd-DTPA complexes incorporated into the outer surface. After binding to fibrin clots, scanning electron microscopy of treated clots revealed dense accumulation of nanoparticles on the clot surfaces. Fibrin clots with sizes ranging from 0.5-7.0 mm were imaged at 4.7 T with or without treatment with the targeted contrast agent. Regardless of sizes, untreated clots were not detectable by T(1)-weighted MRI, while targeted contrast agent dramatically improved the detectability of all clots. Decreases in T(1) and T(2) relaxation times (20-40%) were measured relative to the surrounding media and the control clots. These results suggest the potential for sensitive and specific detection of microthrombi that form on the intimal surfaces of unstable atherosclerotic plaque.

Site-directed contrast enhancement of angiogenic vessels in vivo was demonstrated using antibody targeting of an MRI contrast agent to the alpha(v)beta(3) integrin, a molecular marker characteristic of angiogenic endothelium. The agent was tested in a rabbit corneal micropocket model, in which neovasculature is induced in the cornea using basic fibroblast growth factor. The targeted contrast agent consists of Gd-perfluorocarbon nanoparticles linked to alpha(v)beta(3) integrin antibody DM101. The animal group receiving the targeted contrast agent displayed a 25% increase in the average MR signal intensity after 90 min. Control groups in which the nanoparticles are either used alone, linked to an isotype-matched antibody, or linked to DM101 and administered following receptor blocking did not display MR contrast enhancement at similar dose levels. These findings indicate that the antibody-targeted agent enhances MR signal intensity in the capillary bed in a corneal micropocket model of angiogenesis, and is selectively retained within the angiogenic region via specific interaction with the alpha(v)beta(3) epitope.

This study delineates the role of angiotensin II type I (AT1) receptor in the remodeling of Syrian cardiomyopathic hamsters. Twelve cardiomyopathic (T0-2) hamsters received L-158,809 treatment and libitum in their drinking water (27 micrograms/ml) and 9 cardiomyopathic and 9 normal FL-B hamsters received tap water from 1 to 4 months of age. Although pharmacologically effective with regard to complete suppression of the blood pressure response to angiotensin II infusion, L-158,809 did not diminish the progression or severity of cardiomyopathy. Heart weight/100 g body weight and left ventricular wall thickness adjusted for body weight of both L-158,809 and cardiomyopathic control hamsters did not differ and exceeded those of F1-B controls (p0.05). Myocardial material properties (e.g., stiffness and density) of cardiomyopathic hamsters treated with L-158,809 were not affected. Thus, the progression of fibrosis, calcification, and necrosis in T0-2 cardiomyopathic hamsters was not sensitive to AT1 receptor blockade.

This study investigated the effects on growth and composition of the blood of dietary aflatoxin fed at levels of 0, 2.5, or 5.0 microgram/g of diet for a three week period beginning at 1, 7, 14, and 21 days of age in commercial broilers. Packed cell volume (PCV), erythrocyte counts, mean corpuscular volume, hemoglobin content and mean corpuscular hemoglobin concentration, body weight, and mortality were measured weekly. Plasma cholesterol and total plasma protein levels were determined weekly. Dietary aflatoxin at levels of 2.5 and 5.0 microgram of aflatoxin per gram of diet when fed to young chicks for three weeks, beginning at either one or seven days, depressed body weight and PCV in a dose related fashion. Body weight and PCV continued to be depressed by the 5.0 microgram/g diets in chicks treated from 2 to 5 weeks of age but not at the lower dosages. The feeding of aflatoxin at levels of up to 5.0 microgram aflatoxin per gram of diet from 3 to 6 weeks of age did not significantly depress body weight or PCV from control levels. Plasma cholesterol and total protein were found to be more sensitive to aflatoxin treatment at the later ages than body weight and other blood values. Plasma cholesterol was significantly depressed by the 5.0 microgram/g level of aflatoxin in all treatment periods, but the 2.5 mirogram/g level of aflatoxin did not significantly reduce cholesterol during the 3 to 6 week treatment period. Plasma proteins were found to be the most sensitive criteria for detecting broiler susceptibility to aflatoxin, being depressed by all levels of aflatoxin for all age groups.

The effects of dietary gentian violet upon certain physiological parameters of broiler chickens were studied. Gentian violet exhibited no effect upon growth rates or feed conversion ratios at dietary levels of 16, 32, or 64 micrograms/g. In vitro intestinal absorption of methionine and glucose was also unaltered. Dietary gentian violet significantly increased hemoglobin concentration without an effect on packed cell volume. Furthermore, commercial gentian violet containing preparations, when incorporated into the diet, resulted in increased intestinal absorption of Fe59 but this increase was dependent upon type of inert carrier used. Dietary gentian violet alleviated some of the growth suppression caused by dietary aflatoxin; however, no effect was observed on plasma pigmentation. These data suggest that dietary gentian violet possesses effects other than those for which it has been traditionally employed.

Changes in shell strength and relative size of the egg components associated with feeding dietary aflatoxin to hens differing in shell strength were determined. Shell strength was increased in groups fed aflatoxin because the shell weight of these groups was not decreased in proportion to the decrease in total egg weight. This resulted in a greater percentage shell. The effects of aflatoxin on percentage shell was greater for hens whose initial shell strength was poorer. A consistent relationship was observed between shell strength and percentage shell of groups differing in shell strength.

This study investigated the relationship between 59 Fe absorption and the anemia associated with aflatoxicosis in commercial broilers. A level of 0 or 5 micrograms of aflatoxin per gram of diet was fed for a 21 day period beginning at 1, 7, 14, or 21 days of age in each of two trials. Packed cell volume (PCV) and percent retention of an oral dose of 59 Fe were determined. The feeding of aflatoxin resulted in an anemia when fed from 0 to 3 or 1 to 4 weeks of age. At the conclusion of these treatment periods, percent 59 Fe retention was significantly reduced from the controls. Aflatoxin when fed from 2 to 5 weeks of age resulted in a slight but significant depression in PCV (P less than .05) with a slight but nonsignificant depression in percent 59 Fe retention. At the conclusion of the 3 to 6 week treatment period both percent iron retention and PCV were greater than controls but not significantly so. The iron retentions of birds separated into high and low PCV groups within each treatment combination were compared. Although the iron retentions of the low PCV groups were lower than those of the high PCV groups, none of the differences were statistically significant. However, Pearson correlations of PCV with percent 59 Fe retention were - .28 (P less than or equal to .02, n = 69) for control birds and - .19 (P less than or equal to .14, n = 58) for birds fed aflatoxin, suggesting a relationship between PCV and iron absorption.

Distributions of egg weight and egg deformation values of 10,548 eggs, obtained from 530 pullets, were examined. The deviations from normality based on mean values of all eggs from individual pullets over the experimental period were small relative to the estimates obtained when all 10,548 values were used. The effect of these deviations from normality on selection intensities was studied when 5 to 95% of the pullets were hypothetically retained for reproduction. Distribution of both egg weight and deformation using individual data showed considerable departure from presumed normal distribution in the form of positive skewness and positive kurtosis. The nonnormality of distribution tended to over- or underestimate the selection intensities, depending upon the fraction saved and type and extent of deviations from normality.

Strain variation of iron absorption in response to dietary aflatoxin was studied using two commercial broiler strains and a nonselected randombred strain. Aflatoxin depressed chick body weights and increased mortalities in each strain. Hematocrits were significantly reduced in the commercial broilers receiving the toxin, but not in the randombreds. Aflatoxin reduced iron absorption in each strain regardless of the presence of anemia.

The effect of graded levels of dietary aflatoxin on the assessment of genetic variability of body weight and gain and plasma protein response was tested utilizing the Athens-Canadian randombred population of chickens. Dietary aflatoxin was administered at levels of either 0, 1.25, 2.50 or 5.0 µg/g of diet ad libitum from 7 to 21 days of age to progeny from 58 sire families. Twenty-one-day body weights, gain and plasma protein concentration were used to assess the variation in response.—The administration of increasing levels of aflatoxin resulted in a dose-related decrease of gains and plasma protein concentrations. Plasma protein concentrations were significantly higher among males than females within the control group; however, this difference was reversed as the severity of the aflatoxin challenge increased. Heritability estimates for all responses increased as the level of aflatoxin administered increased. This change was most notable for total plasma protein concentration. Phenotypic correlations for plasma protein concentration and growth measurements tended to diminish with increasing levels of aflatoxin. A similar trend was noted for the genetic correlations; however, a moderate correlation between growth responses and plasma protein response was detected in the 5.0-µg/g aflatoxin treatment group. Genetic correlations were calculated for the same characters between the different levels of aflatoxin. Regardless of which aflatoxin challenges were compared, a very high genetic correlation for 21-day body weight and 7- to 21-day gain was estimated. This variation in growth potential in the toxic environment paralleled that observed in the control environment but at a lower plane. Genetic correlations for plasma protein response across aflatoxin levels diminished as the difference between the levels of aflatoxin administered increased. Plasma protein concentration in the control environment was positively correlated with plasma protein response in groups fed a low level of aflatoxin, but negatively correlated when an aflatoxin challenge of 2.5 µg/g or more was given, suggesting that selection for aflatoxin resistance using plasma protein response as a selection criterion should be made under an aflatoxin stress environment.

Summary Polymorphism in plasma amylase, plasma alkaline phosphatase, non-specific esterase and red cell esterase-D of the Athens-Canadian randombred (ACRB) population of chickens was determined by polyacrylamide and starch gel electrophoresis. Amylase alleles Amy-1A and Amy-1B were segregating in the ACRB population with frequencies of 0.45 and 0.55 respectively. For the plasma alkaline phosphatase the F and S bands, the B band and a new isozyme migrating at a faster rate than the previously reported F band were detected. A genetic nomenclature for plasma alkaline phosphatase is suggested which considers the difference between the F and S bands as the presence or absence of sialic acid attached to a primary protein. Plasma esterase activity was observed in all four of the regions previously reported, but there was no polymorphism found in any of the loci. All birds in this population showed the same red-cell esterase-D phenotype which consisted of a main band with sub-bands on each side.

The response of clinical blood values to graded levels of dietary aflatoxin was studied in three populations of chickens. Male chicks of two commercial broiler strains, one color-sexed and the other feather-sexed, and a randombred strain were fed dietary aflatoxin at levels of 0, 1.25, 2.50 or 5.0 μg/g of diet from 1 to 21 days of age. At the conclusion of the 21-day treatment period, all remaining birds were bled by cardiac puncture and packed cell volume (PCV), erythrocyte counts (RBC), hemoglobin concentration (Hb), mean corpuscular volume (MCV), mean corpuscular hemoglobin concentration (MCHC), total plasma protein, and total plasma cholesterol were determined. All strains of broilers were susceptible to aflatoxicosis as detected by total plasma protein and cholesterol. Anemia associated with aflatoxicosis was induced in the two commercial broiler lines, but not in the randombred line. The PCV, RBC, and Hb were diminished from control values in a dose-related fashion by graded levels of aflatoxin in the commercial broilers, but not in the randombred line. Decreases in MCV with no significant changes in MCHC were observed in all strains.

A pedigreed, commercial broiler population of 31 sire families was administered dietary aflatoxin at levels of either 0.0 or 5.0 μg of aflatoxin per g of diet from 7 to 21 days of age and their response assessed by various physiological parameters.Body weight, gain, packed red blood cell volume (PCV). plasma albumin, plasma protein and cholesterol responses were significantly reduced from control values by the 5.0 μg/g aflatoxin diet. Males had greater body weights and gains in both dietary regimes than females. Females had significantly higher PCV, protein, albumin and cholesterol values in the 5.0 μg/g aflatoxin group than their male counterparts. These differences resulted in significant sex × aflatoxin level interactions for these parameters. Coefficients of variation were increased for all parameters measured in the 5.0 μg/g aflatoxin treatment compared to values for the control group. This increase was greatest for plasma protein, albumin, and cholesterol responses. Heritabilities were calculated for all responses within both treatment groups and were found to be increased in all cases by the 5.0 μg/g aflatoxin diet. Highly significant phenotypic correlations were determined between body weight and gain and between plasma albumin and total plasma protein in both treatment groups. High phenotypic correlations among PCV, plasma cholesterol, plasma protein, and plasma albumin were noted in the 5.0 μg/g aflatoxin group. Significant genetic correlations were determined between body weight and gain and between plasma albumin and plasma protein in the control group. Body weight and gain and plasma protein, albumin, cholesterol and PCV were genetically correlated in the 5.0 μg/g aflatoxin group. Genetic correlations calculated across environments for the same traits were high for PCV, body weight and gain and much lower for plasma albumin, plasma protein, and plasma cholesterol.The results of this study demonstrate that genetic variability for resistance to aflatoxin exists in commercial broiler populations. Strong genetic and phenotypic relationships, and high heritabilities associated with plasma albumin and protein suggest their applicability as selection criteria for aflatoxin resistance. Genetic correlation for these traits across dietary environments indicate that responses for aflatoxin resistance should be measured during aflatoxin challenge and suggest that selection for growth and selection for aflatoxin resistance are not antagonistic.

Body weights, packed cell volumes and plasma protein concentrations among nonsurviving chicks receiving 5·0 μg of aflatoxin per g of diet were significantly less than in surviving chicks. Over the last 14 days of life, changes in plasma protein concentrations among nonsurvivors were significantly greater than among surviving chicks.

Genetic variability in adaptation to brooding at a reduced temperature was examined by comparing 1 to 14-day body weight gains of progeny from 28 sire families of the Athens-Canadian randombred population brooded at 32.2 C and at 26.7 C. The 1 to 7-day gain of the chicks brooded at 26.7 C was significantly depressed, but 7 to 14-day gain was not significantly depressed by brooding at the reduced temperature. Heritability estimates averaged over the two trials were .31, .23, and .35 for the 1 to 7-, 7 to 14-, and 1 to 14-day weight gains of groups brooded at 32.2 C and .55, .59, and .67 for the gain of groups brooded at 26.7 C. The heritability estimates for the difference in weight gain of families brooded at the two temperatures was .78.