Ractopamine HCl improved cardiac hypertrophy but not poor growth, metabolic inefficiency, or greater white blood cells associated with heat stress in concentrate-fed lambs

Heat stress decreases livestock performance and well-being (Hahn, 1999; Nienaber and Hahn, 2007), causes metabolic dysfunction that decreases growth efficiency (O’Brien et al., 2010), and alters cardiovascular function (Crandall et al., 2008). Each year, heat stress costs the livestock industry up to $2.5 billion (St-Pierre et al., 2003). Ractopamine HCl acts as a nutrient repartitioning agent (Beermann, 2002); classified as a β adrenergic agonist (βAA), it shares pharmacological properties with adrenaline (Beermann, 2002). βAA increase muscle mass and decreases fat deposition through unknown mechanisms (Beermann, 2002). In feedlot cattle, they increase growth efficiency and improve carcass yield and merit (Scramlin et al., 2010; Buntyn et al., 2017), which increases profit and allows more meat to be produced from fewer animals. However, because βAA act via a stress system, it is unclear how the products affect animals under stress conditions. β1AA and β2AA can also cause tachycardia, heart palpitations, and arrhythmias (Sears, 2002). We hypothesize that β1AA combined with heat stress may overstimulate the adrenergic system, resulting is metabolic dysfunction and decreased performance. Sheep are a common model for cattle, and thus, the objective of this study was to determine the impact of ractopamine HCl on health and cardiovascular parameters, growth, and metabolic efficiency in feeder lambs

University of Texas bulletin

Two reports published in a scientific bulletin, describing the San Angelo Formation and the geology of Foard County

Gender differences in the Force Concept Inventory for different educational levels in the United Kingdom

The Force Concept Inventory (FCI) is widely used to investigate the effect of education level on conceptual understanding of Newtonian mechanics but has only recently been scrutinized for gender effects and retention. This study examines both the gender gap in first year physics undergraduates compared to the gap for nonphysicists and the FCI retention after three months. All participants were either studying or working at the University of Sheffield in the UK and had completed a similar compulsory level of secondary education. As expected the results show that a greater level of education in physics is associated with a larger average FCI score. However, further analysis shows that there exists a gender gap at all levels of education. The size of the effect of gender is quantified using Cohen’s d and ranges from 0.84 to 1.17 which indicates a large effect due to gender for all levels of education. Despite the FCI having been used as a tool to measure learning gains immediately following instruction in Newtonian mechanics there has been little work to investigate whether this increase in FCI score remains after some time has elapsed. Here the increase in FCI scores is found to remain increased after a three month absence of mechanics-related teaching, and that this retention of FCI scores is independent of gender. Despite this, the gender gap still remains large and statistically significant after the three month delay

Maternal Inflammation at Mid-gestation in Pregnant Rats Impairs Fetal Muscle Growth and Development at Term

Intrauterine growth restriction (IUGR) is a leading cause of perinatal morbidity and mortality. Low birth weight resulting from preterm birth and/or IUGR is an underlying factor in 60–80% of perinatal death worldwide, and is particularly common in developing countries (UNICEF, 2008). Furthermore, studies have linked IUGR and the associated fetal malnutrition to increased incidence of metabolic syndrome in adult life (Barker et al., 1993; Godfrey and Barker, 2000). The “thrifty phenotype hypothesis” developed by David Barker (Hales et al., 1991) states that IUGR-associated fetal malnutrition forces the fetus to spare nutrients by altering tissue-specific metabolism in order to survive. In utero, adaptive changes disproportionately impact skeletal muscle development, growth, and metabolism (Yates et al., 2016). Skeletal muscle is responsible for the majority of insulin-stimulated glucose utilization, and adaptive restriction in muscle growth capacity helps to spare glucose in the IUGR fetus but result in lifelong deficits in muscle mass and metabolic homeostasis (Brown and Hay, 2016). Skeletal muscle growth requires proliferation, differentiation, and fusion of myoblast into new muscle fibers early in gestation and fusion with existing fibers in the third trimester of pregnancy (Zhu et al., 2004). This process can be impaired by inflammation from resident macrophages within skeletal muscle. Classically activated M1 macrophages are pro-inflammatory but can polarize to an anti-inflammatory M2 phenotype that inhibits cytokine production and stimulates tissue repair by producing growth factors (Mantovani et al., 2004; Kharraz et al., 2013). The acute effects of inflammatory factors on myoblast function have been investigated in vitro (Frost et al., 1997; Guttridge et al., 2000), and we postulate that inflammatory stress may have similar effects on fetal myoblasts in utero. Impaired myoblast function and the resulting decrease in muscle growth capacity affect long-term metabolic health. Therefore, the objective of this study was to determine the effect of sustained maternal inflammation at mid-gestation on fetal mortality, muscle growth, and metabolic parameters at term

Ractopamine HCl improved cardiac hypertrophy but not poor growth, metabolic inefficiency, or greater white blood cells associated with heat stress in concentrate-fed lambs

Heat stress decreases livestock performance and well-being (Hahn, 1999; Nienaber and Hahn, 2007), causes metabolic dysfunction that decreases growth efficiency (O’Brien et al., 2010), and alters cardiovascular function (Crandall et al., 2008). Each year, heat stress costs the livestock industry up to $2.5 billion (St-Pierre et al., 2003). Ractopamine HCl acts as a nutrient repartitioning agent (Beermann, 2002); classified as a β adrenergic agonist (βAA), it shares pharmacological properties with adrenaline (Beermann, 2002). βAA increase muscle mass and decreases fat deposition through unknown mechanisms (Beermann, 2002). In feedlot cattle, they increase growth efficiency and improve carcass yield and merit (Scramlin et al., 2010; Buntyn et al., 2017), which increases profit and allows more meat to be produced from fewer animals. However, because βAA act via a stress system, it is unclear how the products affect animals under stress conditions. β1AA and β2AA can also cause tachycardia, heart palpitations, and arrhythmias (Sears, 2002). We hypothesize that β1AA combined with heat stress may overstimulate the adrenergic system, resulting is metabolic dysfunction and decreased performance. Sheep are a common model for cattle, and thus, the objective of this study was to determine the impact of ractopamine HCl on health and cardiovascular parameters, growth, and metabolic efficiency in feeder lambs

Chronic maternal inflammation during late gestation impairs subsequent β-cell function but not islet growth in fetal sheep

Intrauterine growth restriction (IUGR) greatly increases perinatal mortality and morbidity rates, and leads to much greater risk for metabolic complications later in life. One such complication is the development of glucose intolerance or diabetes, which typically develops concurrently with abhorrent patterns of insulin secretions due to diminished β-cell mass and impaired function as well as an overall reduction in pancreatic endocrine tissue. The mechanisms by which IUGR causes problems with health and function of the pancreatic islets are not well understood. Therefore, our goal for this study was to determine how materno-fetal inflammation (MI) affects β-cell growth and function. To do this, we compared the average islet areas, plasma insulin concentrations, and blood glucose concentrations between MI-IUGR fetal lambs (n = 7) and control fetal lambs (n = 7). Pregnant ewes were injected with saline (controls) or 0.1- μg/kg bacterial lipopolysaccharide (LPS) every 3 d from days 100 to 115 of gestation (term = 150 d). Throughout late gestation, arterial blood of the fetus was periodically drawn and analyzed for plasma insulin (ELISA) and blood glucose (ABL90 FLEX) levels. On day 125 of gestation, ewes were euthanized and fetal pancreas was extracted. Sections of the fetal pancreas were then fixed in 4% paraformaldehyde, sectioned (cryostat) at a thickness of 8 μm, stained for insulin- positive area, and imaged on 20x magnification for analysis of average islet area. Between MI-IUGR and control fetuses, there were no differences in average islet areas (1675 ± 286 and 1678 ± 287 μm2, respectively), which indicates that MI did not impair growth and physical development of fetal islets. In addition, blood glucose was similar in all fetuses. However, results showed less (P ≤ 0.05) plasma insulin concentration in MI-IUGR fetuses (0.39 ± 0.07 ng/mL) than in controls (0.70 ± 0.09 ng/mL). This indicates impaired β-cell functional capacity in MI-IUGR fetuses despite normal growth, which is quantified by a tendency (P = 0.08) for strong positive correlation (r = 0.91) between plasma insulin and islet area in control fetuses but an absence of correlation in MI-IUGR fetuses. From this study, we can conclude that MI-IUGR has no effect on the growth and physical development of β cells; however, it does greatly affect their function