148 research outputs found

    The interactive effects of high-fiber diets and Ractopamine HCl on finishing pig growth performance, carcass characteristics, carcass fat quality, and intestinal weights

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    In previous research, feeding pigs high amounts of dried distillers grains with solubles (DDGS) and wheat middlings (midds) has been shown to reduce carcass yield and negatively affect iodine value (IV). The influence of Ractopamine HCl (RAC; Paylean, Elanco Animal Health, Greenfield, IN) on this response is not known; therefore, a total of 575 finishing pigs (PIC 327 × 1050, initially 123 lb) were used in two consecutive 73-d trials to determine the effects of DDGS and midds (high fiber) withdrawal 24 d before harvest in diets with or without RAC on finishing pig growth performance, carcass characteristics, and fat quality. From d 0 to 49, pigs were allotted to 1 of 2 dietary treatments in a completely randomized design based on initial pen weight. The dietary treatments included a corn-soybean meal–based control diet or diets with 30% DDGS and 19% wheat midds. Twelve pens of pigs were fed the corn-soybean meal control diet, and 24 pens were fed the high-fiber diet. During this 49 d period, pigs fed the corn-soybean meal diets had improved (P < 0.0001) ADG and F/G compared with those fed the high-fiber diets. On d 49, pens of pigs were re-allotted to 1 of 6 dietary treatments; pigs remained on the corn-soybean meal diets, switched from the high-fiber diet to corn-soybean meal (withdrawal diet), or were maintained on the high-fiber diet. These 3 regimens were fed with or without 9 g/ton RAC

    Meta-analyses describing the variables that influence the backfat, belly fat, and jowl fat iodine value of pork carcasses

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    Concern about the quality of pork fat has increased in the United States over the last decade, largely because of the increased availability and use of dried distillers grains with solubles (DDGS) in swine diets. The iodine value (IV) of pork fat is commonly used as an indicator of quality. To identify the factors associated with carcass fat IV, meta-analyses were conducted to describe the relevant variables and to develop prediction equations to assist swine nutritionists and producers in producing pork fat with an acceptable IV. Data from 21 experiments were used to develop prediction equations for carcass fat IV of pigs fed a relatively constant dietary iodine value product (IVP) throughout the feeding period, and 6 experiments were used to develop prediction equations for carcass fat IV of pigs fed a dietary IVP-reduction strategy before marketing. Backfat, belly fat, and jowl fat IV were all highly correlated among the experiments that measured the IV of the multiple fat depots (r ≥ 0.880; P < 0.001). As expected, the dietary concentrations of unsaturated (primarily polyunsaturated) fatty acids were the most important in predicting carcass fat IV. However, improved prediction models were achieved by including variables to describe the pigs’ initial and final BW, ADG, and carcass leanness. Increased ADG, final BW, BW range over course of the diet, and backfat depth resulted in reduced backfat IV (P < 0.02). Belly fat IV was also reduced with increasing final BW, BW range over course of the diet, and backfat depth (P < 0.03). A reduced jowl fat IV was associated with an increase in backfat depth and a lower fat-free lean index (FFLI, P < 0.02). Data analyzed to develop equations for predicting carcass fat IV using a dietary IVP-reduction strategy indicated that the concentrations of dietary polyunsaturated fatty acids in the initial diet were the most important. The concentrations of dietary polyunsaturated fatty acids in the reduced- IVP diet fed before marketing were also important in predicting the IV of carcass fat. However, the IV of backfat was the most amenable to change using an IVP-reduction strategy. Feeding the pigs for a longer period and to a heavier final BW resulted in a reduced backfat IV (P ≤ 0.05). These results indicate that, although primarily determined by dietary factors, an understanding of the other variables that influence the IV of pork fat is necessary to reduce the likelihood of concerns with pork fat quality

    Hyperphosphorylation of the cardiac ryanodine receptor at serine 2808 is not involved in cardiac dysfunction after myocardial infarction.

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    RATIONALE: Abnormal behavior of the cardiac ryanodine receptor (RyR2) has been linked to cardiac arrhythmias and heart failure (HF) after myocardial infarction (MI). It has been proposed that protein kinase A (PKA) hyperphosphorylation of the RyR2 at a single residue, Ser-2808, is a critical mediator of RyR dysfunction, depressed cardiac performance, and HF after MI. OBJECTIVE: We used a mouse model (RyRS2808A) in which PKA hyperphosphorylation of the RyR2 at Ser-2808 is prevented to determine whether loss of PKA phosphorylation at this site averts post MI cardiac pump dysfunction. METHODS AND RESULTS: MI was induced in wild-type (WT) and S2808A mice. Myocyte and cardiac function were compared in WT and S2808A animals before and after MI. The effects of the PKA activator Isoproterenol (Iso) on L-type Ca(2+) current (I(CaL)), contractions, and [Ca(2+)](I) transients were also measured. Both WT and S2808A mice had depressed pump function after MI, and there were no differences between groups. MI size was also identical in both groups. L type Ca(2+) current, contractions, Ca(2+) transients, and SR Ca(2+) load were also not significantly different in WT versus S2808A myocytes either before or after MI. Iso effects on Ca(2+) current, contraction, Ca(2+) transients, and SR Ca(2+) load were identical in WT and S2808A myocytes before and after MI at both low and high concentrations. CONCLUSIONS: These results strongly support the idea that PKA phosphorylation of RyR-S2808 is irrelevant to the development of cardiac dysfunction after MI, at least in the mice used in this study

    Diabetic Cardiomyopathy: Current and Future Therapies. Beyond Glycemic Control

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    Diabetes mellitus and the associated complications represent a global burden on human health and economics. Cardiovascular diseases are the leading cause of death in diabetic patients, who have a 2–5 times higher risk of developing heart failure than age-matched non-diabetic patients, independent of other comorbidities. Diabetic cardiomyopathy is defined as the presence of abnormal cardiac structure and performance in the absence of other cardiac risk factors, such coronary artery disease, hypertension, and significant valvular disease. Hyperglycemia, hyperinsulinemia, and insulin resistance mediate the pathological remodeling of the heart, characterized by left ventricle concentric hypertrophy and perivascular and interstitial fibrosis leading to diastolic dysfunction. A change in the metabolic status, impaired calcium homeostasis and energy production, increased inflammation and oxidative stress, as well as an accumulation of advanced glycation end products are among the mechanisms implicated in the pathogenesis of diabetic cardiomyopathy. Despite a growing interest in the pathophysiology of diabetic cardiomyopathy, there are no specific guidelines for diagnosing patients or structuring a treatment strategy in clinical practice. Anti-hyperglycemic drugs are crucial in the management of diabetes by effectively reducing microvascular complications, preventing renal failure, retinopathy, and nerve damage. Interestingly, several drugs currently in use can improve cardiac health beyond their ability to control glycemia. GLP-1 receptor agonists and sodium-glucose co-transporter 2 inhibitors have been shown to have a beneficial effect on the cardiovascular system through a direct effect on myocardium, beyond their ability to lower blood glucose levels. In recent years, great improvements have been made toward the possibility of modulating the expression of specific cardiac genes or non-coding RNAs in vivo for therapeutic purpose, opening up the possibility to regulate the expression of key players in the development/progression of diabetic cardiomyopathy. This review summarizes the pathogenesis of diabetic cardiomyopathy, with particular focus on structural and molecular abnormalities occurring during its progression, as well as both current and potential future therapies

    Effects of dried distillers grains with solubles on sow carcass fat quality

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    A pilot experiment was conducted to determine the effects of feeding nonpregnant (open) sows a diet containing 50% dried distillers grains with solubles (DDGS) on growth and carcass fat quality. A total of 8 open sows were allotted to 1 of 2 diets by parity and BW. One diet was a standard corn-soybean meal-based gestation diet; the second diet was a corn-soybean meal-based diet that contained 50% DDGS. All sows were fed 5 lb/d of feed in a single feeding for 92 d. All sows were harvested on d 92 at the Kansas State University Meat Laboratory for determination of carcass fat quality. As expected, no differences in BW or backfat change were found (P \u3e 0.62) for the feeding period. Additionally, no differences (P \u3e 0.23) in lipid oxidation as measured by 2-thiobarbituric acid reactive substances (TBARS) assay were reported either initially or after 5 d of retail display for sows fed 50% DDGS compared with controls. Lipid oxidation increased (P \u3c 0.003) as measured by TBARS assay for both treatments from d 1 to 5 as expected. Jowl fatty acid analysis revealed an increase in linoleic acid (P \u3c 0.01), total polyunsaturated fatty acids (P \u3c 0.01), and the ratio of polyunsaturated fatty acids to saturated fatty acids (P \u3c 0.03). Also, there was a trend for increased jowl iodine value (P \u3c 0.08) for sows fed 50% DDGS compared with the controls. In summary, feeding 50% DDGS to open sows for 92 d did not significantly affect BW, backfat, and lipid oxidation compared with controls. However, feeding 50% DDGS increased the concentration of linoleic acid and total polyunsaturated fatty acids and tended to increase jowl iodine value compared with controls.; Swine Day, 2008, Kansas State University, Manhattan, KS, 200

    Challenges facing early career academic cardiologists

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    Early career academic cardiologists currently face unprecedented challenges that threaten a highly valued career path. A team consisting of early career professionals and senior leadership members of American College of Cardiology completed this white paper to inform the cardiovascular medicine profession regarding the plight of early career cardiologists and to suggest possible solutions. This paper includes: 1) definition of categories of early career academic cardiologists; 2) general challenges to all categories and specific challenges to each category; 3) obstacles as identified by a survey of current early career members of the American College of Cardiology; 4) major reasons for the failure of physician-scientists to receive funding from National Institute of Health/National Heart Lung and Blood Institute career development grants; 5) potential solutions; and 6) a call to action with specific recommendations

    Research priorities in hypertrophic cardiomyopathy: report of a Working Group of the National Heart, Lung, and Blood Institute.

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    Hypertrophic cardiomyopathy (HCM) is a myocardial disorder characterized by left ventricular (LV) hypertrophy without dilatation and without apparent cause (ie, it occurs in the absence of severe hypertension, aortic stenosis, or other cardiac or systemic diseases that might cause LV hypertrophy). Numerous excellent reviews and consensus documents provide a wealth of additional background.1–8 HCM is the leading cause of sudden death in young people and leads to significant disability in survivors. It is caused by mutations in genes that encode components of the sarcomere. Cardiomyocyte and cardiac hypertrophy, myocyte disarray, interstitial and replacement fibrosis, and dysplastic intramyocardial arterioles characterize the pathology of HCM. Clinical manifestations include impaired diastolic function, heart failure, tachyarrhythmia (both atrial and ventricular), and sudden death. At present, there is a lack of understanding of how the mutations in genes encoding sarcomere proteins lead to the phenotypes described above. Current therapeutic approaches have focused on the prevention of sudden death, with implantable cardioverter defibrillator placement in high-risk patients. But medical therapies have largely focused on alleviating symptoms of the disease, not on altering its natural history. The present Working Group of the National Heart, Lung, and Blood Institute brought together clinical, translational, and basic scientists with the overarching goal of identifying novel strategies to prevent the phenotypic expression of disease. Herein, we identify research initiatives that we hope will lead to novel therapeutic approaches for patients with HCM

    Method for Quantitative Study of Airway Functional Microanatomy Using Micro-Optical Coherence Tomography

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    We demonstrate the use of a high resolution form of optical coherence tomography, termed micro-OCT (μOCT), for investigating the functional microanatomy of airway epithelia. μOCT captures several key parameters governing the function of the airway surface (airway surface liquid depth, periciliary liquid depth, ciliary function including beat frequency, and mucociliary transport rate) from the same series of images and without exogenous particles or labels, enabling non-invasive study of dynamic phenomena. Additionally, the high resolution of μOCT reveals distinguishable phases of the ciliary stroke pattern and glandular extrusion. Images and functional measurements from primary human bronchial epithelial cell cultures and excised tissue are presented and compared with measurements using existing gold standard methods. Active secretion from mucus glands in tissue, a key parameter of epithelial function, was also observed and quantified
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