Vegetation Canopy Cover Effects on Sediment and Salinity Loading in the Upper Colorado River Basin Mancos Shale Formation, Price, Utah

With future climate change and increased water demand and scarcity in the Colorado River Basin, the Bureau of Reclamation estimates that the costs of salinity damage will increase for Colorado River users and will exacerbate the current salinity challenges. This study focuses on saline and sodic soils associated with the Mancos Shale formation in order to investigate the mechanisms driving sediment and salinity loads in the Price-San Rafael River Basin of the upper Colorado River. A Walnut Gulch rainfall simulator was operated with a variety of slope angles and rainfall intensities at two field sites (Price, Dry-X) near Price, Utah in order to evaluate how the amount and spatial distribution of vegetation affects salinity in runoff. For each simulated rainfall event, the time-varying concentrations of major cations, anions, and sediment in runoff were measured. Principal component analysis revealed that the two field sites are generally different in runoff water chemistry and soil chemistry, likely due to the difference in parent material and soil indicative of their location on different geologic members. The Dry-X site also has substantially greater total dissolved solids (TDS) and sediment in runoff, soil sodium absorption ratio (SAR), and soil cation exchange capacity (CEC) than the Price site. Despite these differences, a consistent positive linear relationship between the plot-averaged sediment and TDS concentration was found across both sites. The Rangeland Hydrology Erosion Model (RHEM) was calibrated to provide unbiased estimates of sediment in runoff from 23 runs of the rainfall simulator. RHEM simulated the plot-plot variability best at Dry-X compared to Price. Sensitivity analysis of the RHEM input parameters showed that the splash and sheet erodibility coefficient (Kss) and the effective saturated conductivity coefficient (Ke) had the largest influence on the model’s sediment and discharge outputs, respectively. The regression that predicted TDS concentration from sediment was applied to RHEM outputs to show that the model could be used to provide salinity estimates for different storm intensities on this part of the Mancos Shale. The potential influence of vegetation canopy cover on sediment production from these two sites was inferred by running RHEM with canopy cover values ranging from 0% to 100%. This changed sediment output by 111% to -91% relative to the present vegetation cover. Measures of the geometry of soil and vegetation patches at Dry-X, such as fractal dimension index and proximity index, showed a relationship to error residuals from RHEM. As the vegetation becomes less isolated, more uniform, and the tortuosity of the bare soil area increases, observed sediment decreases relative to RHEM predictions. The results of this study will help land management agencies assess the feasibility of mitigation strategies for reducing sediment and salinity loads from the saline and sodic soils of the Mancos Shale formation and indicate a possible benefit to incorporating the parameters that describe the spatial pattern of vegetation in RHEM

Dismantling Ideology: Structural Violence and the Role of Counseling Psychology

Forms of oppression and their impact on physical and mental health have been well documented in study. While the scope of psychology has traditionally been conceptualized as intervention at the individual level, the movements toward multicultural, cross-cultural, and critical views of psychology have expanded psychologists’ conceptualization of mental health practice and research. While social justice has gained greater attention, the translation of this perspective with traditional psychology has proved difficult. The proposed symposium offers the framework of structural violence as an organizing theory for exploration of violence (e.g. physical violence, oppression, discrimination, & injustice) within psychology. First introduced by sociologist Johan Galtung (1969) and echoed in the work of social medicine (Farmer, 2006) and the psychopathology of colonization (Bulhan, 1985), structural violence directly explores oppressive forces and their relationship to justice. The purpose of this symposium is to introduce the usefulness of structural violence as a construct in psychology and then demonstrate two contemporary applications of this construct to the work of counseling psychologists. First, this presentation uses the framework of structural violence as it operates in global and national labor markets. Focusing specifically on recent examples in labor practices that can be understood as structural violence and offering suggestions for research, advocacy, and policy for vocational psychology. Second, this presentation will explore counseling psychologists ethical role in the prediction and prevention of violence and make an argument for expanding current definitions of this role to include structural violence. This argument is made through the context of psychologists’ prediction and prevention of mass shootings, which call for practitioners to use societal-level risk factors (i.e. oppression, structural violence) in prediction strategies and engage in culturally-transformative prevention efforts. Overall, this symposium will present implications of structural violence for the work of clinicians, researchers and advocates

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

Body composition estimated by bioelectrical impedance analyses is diminished by prenatal stress in neonatal lambs and by heat stress in feedlot wethers

Body composition correlates to carcass value in livestock, which makes the ability to accurately estimate body composition in the live animal beneficial (Berg and Marchello, 1994). Bioelectrical impedance analysis (BIA) is a clinical tool used to assess body composition in humans (Lukaski et al., 1985), but its use in livestock has been minimal. Lean and fat content contribute to profitability for livestock producers, and poor body composition can be caused by stress that occurs either during in utero development (De Blasio et al., 2007) or during postnatal growth (Boyd et al., 2015). Maternal hyperthermia-induced placental insufficiency (Brown et al., 2015) and sustained maternal inflammation (Cadaret et al., 2018) are two established causes of intrauterine growth restriction (IUGR). IUGR-born animals are characterized by asymmetrical growth restriction that alters lifelong body composition due to impaired muscle growth capacity (Yates et al., 2018). In addition, acute heat stress during periods of peak postnatal growth can alter body composition in livestock (Boyd et al., 2015). We postulate that BIA can detect these changes in the live animal. Thus, the objective of this study was to determine whether BIA measurements can predict changes to body composition in live neonatal lambs exposed to intrauterine stress and in heat-stressed feedlot lambs

Acute exposure of primary rat soleus muscle to zilpaterol HCl (β2 adrenergic agonist), TNFα, or IL-6 in culture increases glucose oxidation rates independent of the impact on insulin signaling or glucose uptake

Recent studies show that adrenergic agonists and inflammatory cytokines can stimulate skeletal muscle glucose uptake, but it is unclear if glucose oxidation is similarly increased. Thus, the objective of this study was to determine the effects of ractopamine HCl (β1 agonist), zilpaterol HCl (β2 agonist), TNFα, and IL-6 on glucose uptake and oxidation rates in unstimulated and insulin-stimulated soleus muscle strips from adult Sprague-Dawley rats. Effects on phosphorylation of Akt (phospho-Akt), p38 MAPK (phospho-p38), and p44/42 MAPK (phospho-p44/42) was also determined. Incubation with insulin increased (P \u3c 0.05) glucose uptake by ~47%, glucose oxidation by ~32%, and phospho-Akt by ~238%. Insulin also increased (P \u3c 0.05) phospho-p38, but only after 2 hours in incubation. Muscle incubated with β2 agonist alone exhibited ~20% less (P \u3c 0.05) glucose uptake but ~32% greater (P \u3c 0.05) glucose oxidation than unstimulated muscle. Moreover, co-incubation with insulin + β2 agonist increased (P \u3c 0.05) glucose oxidation and phospho-Akt compared to insulin alone. Conversely, β1 agonist did not appear to affect basal or insulin-stimulated glucose metabolism, and neither β agonist affected phospho-p44/42. TNFα and IL-6 increased (P \u3c 0.05) glucose oxidation by ~23% and ~33%, respectively, in the absence of insulin. This coincided with increased (P \u3c 0.05) phospho-p38 and phospho-p44/42 but not phospho-Akt. Furthermore, co-incubation of muscle with insulin + either cytokine yielded glucose oxidation rates that were similar to insulin alone, despite lower (P \u3c 0.05) phospho-Akt. Importantly, cytokine-mediated increases in glucose oxidation rates were not concomitant with greater glucose uptake. These results show that acute β2 adrenergic stimulation, but not β1 stimulation, directly increases fractional glucose oxidation in the absence of insulin and synergistically increases glucose oxidation when combined with insulin. The cytokines, TNFα and IL-6, likewise directly increased glucose oxidation in the absence of insulin, but were not additive in combination with insulin and in fact appeared to disrupt Akt-mediated insulin signaling. Rather, cytokines appear to be acting through MAPKs to elicit effects on glucose oxidation. Regardless, stimulation of glucose oxidation by these key stress factors did not rely upon greater glucose uptake, which may promote metabolic efficiency during acute stress by increasing fractional glucose oxidation without increasing total glucose consumption by muscle

Maternal inflammation at 0.7 gestation in ewes leads to intrauterine growth restriction and impaired glucose metabolism in offspring at 30 d of age

Fetal programming associated with intrauterine growth restriction (IUGR) leads to lifelong deficits in growth and metabolic function (Hales and Barker, 2013). IUGR arises when fetuses respond to poor in utero conditions by developing adaptations that repartition nutrients to critical tissues and away from skeletal muscle (Yates et al., 2012, 2018). This fetal programming is beneficial in utero but leads to persistent reductions in muscle mass and glucose homeostasis in offspring (DeFronzo et al., 1981). Recent studies by our laboratory in sheep and rats demonstrate that maternal inflammation during gestation induces fetal inflammatory adaptations that impair growth and disrupt muscle glucose metabolism (Cadaret et al., 2017, 2018). IUGR fetal skeletal muscle exhibits indicators of enhanced inflammatory sensitivity, which could disrupt glucose uptake and oxidation (Yates et al., 2016; Cadaret et al., 2018). Enhanced inflammatory responsiveness would help explain growth and metabolic deficits observed in IUGR offspring. We hypothesize that fetal programming induced by maternal inflammation persists in offspring and contributes to impaired growth and glucose metabolism at 30 d. Therefore, the objective of this study was to determine whether sustained maternal inflammation induced by bacterial endotoxin at 0.7 gestation leads to fetal programming that contributes to deficits in growth and glucose metabolism in offspring

A potential role for mTORC1/2 in β2 adrenergic regulation of skeletal muscle glucose oxidation in models of intrauterine growth restriction.

The epidemic of intrauterine growth restriction (IUGR) continues to be a leading cause of perinatal morbidity and mortality throughout the world. This condition has been linked to the development of metabolic health problems such as obesity, hypertension, glucose intolerance, and type 2 diabetes at all ages. Previous studies have demonstrated that IUGR fetal adaptations impair proper glucose homeostasis in part via changes in insulin responsiveness in key tissues including skeletal muscle and liver, and that these deficits persists into adulthood. Many components of insulin signaling pathways associated with glucose metabolic regulation have been evaluated in IUGR tissues for adaptive changes. Among these are mammalian target of rapamycin complexes 1 and 2 (mTORC1/2) and their associated pathways, which function in mitochondrial control and maintenance. However, recent findings demonstrate that β2 adrenoceptors (β2AR) appear to activate an insulin-independent pathway or pathways that modify glucose metabolism via mTORC1/2 complexes. These findings represent a novel potential target for interventions that could improve the treatment and prevention of IUGR-induced metabolic disorders. This review will focus on mechanistic components of β2AR-mTORC1/2 signaling as well as their role in regulating glucose oxidative metabolism within skeletal muscle

Maternal inflammation at midgestation impairs subsequent fetal myoblast function and skeletal muscle growth in rats, resulting in intrauterine growth restriction at term

Maternal inflammation induces intrauterine growth restriction (MI-IUGR) of the fetus, which compromises metabolic health in human offspring and reduces value in livestock. The objective of this study was to determine the effect of maternal inflammation at midgestation on fetal skeletal muscle growth and myoblast profiles at term. Pregnant Sprague-Dawley rats were injected daily with bacterial endotoxin (MI-IUGR) or saline (controls) from the 9th to the 11th day of gestational age (dGA; term = 21 dGA). At necropsy on dGA 20, average fetal mass and upper hindlimb cross-sectional areas were reduced (P \u3c 0.05) in MI-IUGR fetuses compared with controls. MyoD+ and myf5+ myoblasts were less abundant (P \u3c 0.05), and myogenin+ myoblasts were more abundant (P \u3c 0.05) in MI-IUGR hindlimb skeletal muscle compared with controls, indicating precocious myoblast differentiation. Type I and Type II hindlimb muscle fibers were smaller (P \u3c 0.05) in MI-IUGR fetuses than in controls, but fiber type proportions did not differ between experimental groups. Fetal blood plasma TNFα concentrations were below detectable amounts in both experimental groups, but skeletal muscle gene expression for the cytokine receptors TNFR1, IL6R, and FN14 was greater (P \u3c 0.05) in MI-IUGR fetuses than controls, perhaps indicating enhanced sensitivity to these cytokines. Maternal blood glucose concentrations at term did not differ between experimental groups, but MI-IUGR fetal blood contained less (P \u3c 0.05) glucose, cholesterol, and triglycerides. Fetal-to-maternal blood glucose ratios were also reduced (P \u3c 0.05), which is indicative of placental insufficiency. Indicators of protein catabolism, including blood plasma urea nitrogen and creatine kinase, were greater (P \u3c 0.05) in MI-IUGR fetuses than in controls. From these findings, we conclude that maternal inflammation at midgestation causes muscle-centric fetal programming that impairs myoblast function, increases protein catabolism, and reduces skeletal muscle growth near term. Fetal muscle sensitivity to inflammatory cytokines appeared to be enhanced after maternal inflammation, which may represent a mechanistic target for improving these outcomes in MI-IUGR fetuses

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

Impaired muscle stem cell function in cows with high concentrations of androstenedione in their follicular fluid

It is unclear whether androstenedione (A4) increases muscle mass and strength similar to testosterone or whether it produces primarily catabolic effects on muscle-like estrogen (Rasmussen et al., 2000). Summers et al. (2014) observed two populations of cows that exhibit either high (\u3e40 ng/mL; High A4) or low (\u3c20 ng/mL; Low A4) concentrations of A4 within the fluid of the dominant follicle just prior to ovulation. High A4 cows had decreased reproductive rates and shorter times before falling out of the herd, but those that did produce calves weaned them ~10-kg heavier than their low A4 counterparts (Summers et al., 2014). It appears that the difference in weights is due to faster growing and more efficient skeletal muscle. High A4 cows share many characteristics with women suffering from polycystic ovary syndrome (PCOS), whose high levels of circulating androgens are associated with changes in body composition (Kirchengast and Huber, 2001)