1,630 research outputs found

    A comparison of two methods for determining titanium dioxide marker content in broiler digestibility studies

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    The use of inert markers in broiler diets eliminates the need to quantitatively evaluate feed intake and excreta output to determine diet digestibility, and enables nutrient uptake at specific points along the gastrointestinal tract to be examined. Titanium dioxide (TiO2) is commonly used for this purpose and measured using a UV spectrophotometric assay. Two experiments were conducted to observe whether an inductively coupled plasma optical emission spectrophotometer (ICP-OES) assay is able to replace the UV-spectroscopy assay for rapid analysis of TiO2 in broiler feed and ileal digesta samples. In the first experiment, TiO2 was added at 5g/kg to 19 broiler diets. Ross 308, male broilers (n=452) fed these diets were involved in a series of digestion studies to determine ileal digesta recovery of TiO2. In the second experiment, defined amounts of TiO2 were added to ileal digesta samples from Ross 308, male broilers (n=176) and TiO2 recoveries were determined

    Use of Zn concentration in the gastrointestinal tract as a measure of phytate susceptibility to the effect of phytase supplementation in broilers

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    Zinc (Zn) is the most vulnerable cation to complexation with phytate. An experiment was conducted to evaluate the potential of measurements of Zn concentration in the gastrointestinal tract as a marker to assess the anti-nutritional impact of phytate and susceptibility of phytate to phytase in broilers. Ross 308 broilers (n = 180) were fed one of 5 experimental diets with differing phytase activity levels, analyzed at 605, 1150, 1804, 3954 and 5925 U/kg. Broiler performance and Zn concentration, pH and amount of phytate hydrolyzed in the gizzard, duodenum and ileum were analyzed at d21 post hatch. Phytate susceptibility to phytase degradation was determined in vivo and in vitro by measuring total phytate-P hydrolyzed in the tract or in conditions that mimicked the tract, respectively. Phytase activity level had a significant (P < 0.05) impact on Zn concentration and phytate hydrolyzed in the gizzard and ileum, but not in the duodenum. Strong relationships were observed between the amount of phytate hydrolyzed and Zn concentration in the gizzard in birds fed the diets with 1804 U/kg or higher levels of phytase. Phytate and phytase effects could therefore potentially be evaluated by measuring Zn concentration in the gizzard. Susceptible phytate levels measured in vivo and in vitro were almost identical in the diet with phytase activity of 5925 U/kg, but in the diets with lower phytase activity levels the in vitro assay overestimated the amount of P released. There were strong relationships between in vivo susceptible phytate level and pH and amount of phytate hydrolyzed in the gizzard, duodenum and ileum and Zn concentration in the gizzard and ileum. This illustrates that phytate susceptibility directly effects mineral availability in the gastrointestinal tract. Measurements of Zn concentration in the gastrointestinal tract, particularly in the gizzard, can potentially be used as a marker to assess the anti-nutritional impact of phytate and susceptibility of phytate to phytase in broilers

    Contribution of intestinal- and cereal-derived phytase activity on phytate degradation in young broilers

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    There is little consensus as to the capability of poultry to utilize dietary phytate without supplemental phytase. Therefore, an experiment was conducted to examine the extent to which endogenous phytase of intestinal and cereal origin contributes to phytate degradation in birds aged 0 to 14 d posthatch. Ross 308 broilers (n = 720) were fed one of 4 experimental diets with differing dietary ingredient combinations and approximate total phytate levels of 10 g/kg, dietary phytase activity analyzed at 460 U/kg, dietary calcium (Ca) levels of 11 g/kg, and nonphytate-phosphorus (P) levels of 4 g/kg. Broiler performance, gizzard, duodenum, jejunum and ileum pH, Ca and P digestibility and solubility, amount of dietary phytate hydrolyzed in the gizzard, jejunum, and ileal digesta phytase activity were analyzed at d 4, 6, 8, 10, 12, and 14 posthatch. Intestinal endogenous phytase activity increased significantly (P < 0.001) between d 4 and 6, resulting in increased phytate hydrolysis in the gizzard (P = 0.003), jejunum (P < 0.001), and ileum (P < 0.001). Phytase activity and phytate hydrolysis continued to increase with age, with a greater phytase activity and associated increase in phytate hydrolysis and mineral utilization between d 10 and 12. Gizzard and jejunum Ca and P solubility and ileal Ca and P digestibility increased significantly (P < 0.001), and gastrointestinal pH decreased significantly (P < 0.001) between d 4 and 6. By d 14, phytase activity recovered in the ileum was approximately 45 U/kg. There were strong correlations between phytase activity measured in the ileum and phytate hydrolyzed in the gizzard (r = 0.905, P < 0.001), jejunum (r = 0.901, P = 0.023), and ileum (r = 0.938, P = 0.042). This study shows intestinal- and dietary-derived endogenous phytase activity is responsible for phytate-P hydrolysis in broilers

    In vitro versus in situ evaluation of the effect of phytase supplementation on calcium and phosphorus solubility in soya bean and rapeseed meal broiler diets

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    1. In vitro assays provide a sensitive and economic tool to evaluate dietary effects, but have limitations. In this study, the effect of phytase supplementation on solubility, and presumed availability, of calcium (Ca) and phosphorus (P) in soybean meal (SBM) and rapeseed meal (RSM) based diets was evaluated both in situ and by a 2-step in vitro digestion assay that simulated the gastric and small intestine (SI) phases of digestion

    Flow cytometric characterization and clinical outcome of CD4+ T-cell lymphoma in dogs: 67 cases.

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    BackgroundCanine T-cell lymphoma (TCL) is conventionally considered an aggressive disease, but some forms are histologically and clinically indolent. CD4 TCL is reported to be the most common subtype of TCL. We assessed flow cytometric characteristics, histologic features when available, and clinical outcomes of CD4+ TCL to determine if flow cytometry can be used to subclassify this group of lymphomas.ObjectiveTo test the hypothesis that canine CD4+ T-cell lymphoma (TCL) is a homogeneous group of lymphomas with an aggressive clinical course.AnimalsSixty-seven dogs diagnosed with CD4+ TCL by flow cytometry and treated at 1 of 3 oncology referral clinics.MethodsRetrospective multivariable analysis of outcome in canine CD4+ TCL including patient characteristics, treatment, and flow cytometric features.ResultsThe majority of CD4+ TCL were CD45+, expressed low class II MHC, and exhibited an aggressive clinical course independent of treatment regimen (median survival, 159 days). Histologically, CD4+ TCL were classified as lymphoblastic or peripheral T cell. Size of the neoplastic lymphocytes had a modest effect on both PFI and survival in this group. A small number of CD4+ TCL were CD45- and class II MHC high, and exhibited an apparently more indolent clinical course (median survival not yet reached).Conclusions and clinical importanceAlthough the majority of CD4+ TCL in dogs had uniform clinical and flow cytometric features and an aggressive clinical course, a subset had a unique immunophenotype that predicts significantly longer survival. This finding strengthens the utility of flow cytometry to aid in the stratification of canine lymphoma

    Career and leadership development in the field of violence and abuse

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    PowerPoint PresentationConference Theme: Future Without Violencepostprin

    Lesion topography and microscopic white matter tract damage contribute to cognitive impairment in symptomatic carotid artery disease

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    Purpose: To investigate associations between neuroimaging markers of cerebrovascular disease, including lesion topography and extent and severity of strategic and global cerebral tissue injury, and cognition in carotid artery disease (CAD). Materials and Methods: All participants gave written informed consent to undergo brain magnetic resonance imaging and the Addenbrooke’s Cognitive Examination–Revised. One hundred eight patients with symptomatic CAD but no dementia were included, and a score less than 82 represented cognitive impairment. Group comparison and interrelations between global cognitive and fluency performance, lesion topography, and ultrastructural damage were assessed with voxel-based statistics. Associations between cognition, medial temporal lobe atrophy (MTA), lesion volumes, and global white matter ultrastructural damage indexed as increased mean diffusivity were tested with regression analysis by controlling for age. Diagnostic accuracy of imaging markers selected from a multivariate prediction model was tested with receiver operating characteristic analysis. Results: Cognitively impaired patients (n = 53 [49.1%], classified as having probable vascular cognitive disorder) were older than nonimpaired patients (P = .027) and had more frequent MTA (P<.001), more cortical infarctions (P = .016), and larger volumes of acute (P = .028) and chronic (P = .009) subcortical ischemic lesions. Lesion volumes did not correlate with global cognitive performance (lacunar infarctions, P = .060; acute lesions, P = .088; chronic subcortical ischemic lesions, P = .085). In contrast, cognitive performance correlated with presence of chronic ischemic lesions within the interhemispheric tracts and thalamic radiation (P< .05, false discovery rate corrected). Skeleton mean diffusivity showed the closest correlation with cognition (R2 = 0.311, P< .001) and promising diagnostic accuracy for vascular cognitive disorder (area under the curve, 0.82 [95% confidence interval: 0.75, 0.90]). Findings were confirmed in subjects with a low risk of preclinical Alzheimer disease indexed by the absence of MTA (n = 85). Conclusion: Subcortical white matter ischemic lesion locations and severity of ultrastructural tract damage contribute to cognitive impairment in symptomatic CAD, which suggests that subcortical disconnection within large-scale cognitive neural networks is a key mechanism of vascular cognitive disorder
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