Spanish for Veterinarians Part 1: An Approach to Weaving Spanish Language Education into DVM Curricula.

The authors describe the need for discipline-specific Spanish language training in veterinary programs and elaborate on student interest in veterinary Spanish offerings. They outline their interdisciplinary approach to field-specific Spanish curriculum development that evolved from a single third-year practicum offering into a 7-credit Spanish language program while summarizing curriculum content, assessments, and student feedback. The challenges and approaches to weaving the language program into a demanding veterinary curriculum are addressed and program limitations are discussed. The paper ends with an outline of exciting future directions currently underway that hold achieving the necessary level of Spanish language proficiency for successful communication about animal health and wellbeing as a primary goal. The intent of this publication is to shed light on unique aspects associated with designing and delivering a Spanish language program within veterinary education, including the importance of interdisciplinary collaboration with language teaching professionals for curriculum development and delivery.

Characterizing the use of class rank in evaluating applicants for veterinary internship and residency positions.

OBJECTIVE: To characterize how class rank and other criteria are used to evaluate applicants for veterinary internship and residency positions. SAMPLE: Program directors for 572 internship and residency programs. PROCEDURES: A survey was sent to program directors asking them to score the importance of 7 items (cover letter, letters of reference, curriculum vitae, veterinary class rank, grade point average, grades for classes specifically related to the internship or residency specialty area, and interview) they could use in evaluating applicants for an internship or residency and to rank those 7 items, along with an open item asking participants to list other criteria they used, from most to least important. RESULTS: Responses were obtained for 195 internship and 222 residency programs. For both internship programs and residency programs, mean importance scores assigned to the 7 items resulted in the same ordering from most to least important, with letters of reference, interview, curriculum vitae, and cover letter most important. Rankings of the importance of the 7 items, along with an "other" item, were similar for internship and residency programs; the most important item was a candidate's letters of reference, followed by the interview, cover letter, and curriculum vitae. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that although most veterinary internship and residency programs consider class rank and overall grade point average when evaluating applicants, these 2 items were not the most important. For both internship and residency programs, the most important items were an applicant's letters of reference, followed by the interview, cover letter, and curriculum vitae. (J Am Vet Med Assoc 2021;258:776-785).

Integrating Individual Student Advising into Financial Education to Optimize Financial Literacy in Veterinary Students.

The debt-to-income ratio (DIR) of Doctor of Veterinary Medicine (DVM) students has exceeded the recommended 1.4 and it is predicted that the DIR will approach 2.18 by 2026. The associated stressors negatively impact professional satisfaction and well-being. In conventional approaches to financial education, content is delivered to groups of students as part of the curriculum, but with little opportunity for application. Research in medical and financial education suggests that convenient timing, relevant subject matter and individualization are key characteristics of a successful program that promotes retention and application of knowledge. In this article, we describe an integrative approach to financial education developed by the Colorado State University (CSU) Financial Education Specialist (FES). The FES position requires that the individual be qualified to provide one-on-one financial advising to DVM students as well as develop targeted curricular interventions and optional workshops. Data from student and alumni surveys suggest that this integrative approach to financial education both improves knowledge and alters behaviors surrounding financial management. Interest from academic and professional entities across the United States reflects recognition of the program as an emerging best practice. We describe lessons learned through program implementation, including demands for FES services throughout the academic year, and topics relevant to each student cohort. We propose that providing one-on-one financial advice to DVM students is a critical component of a broader financial education program. Actualizing timing, relevance, and individualization, this integrated approach optimizes opportunities for knowledge application and ultimately behavioral change.

Knowledge and Opinions of Third Year Veterinary Students Relevant to Animal Welfare Before and After Implementation of a Core Welfare Course.

Although leading veterinary organizations emphasize the importance of animal welfare knowledge, there exists a gap in current veterinary student animal welfare education and training. A survey instrument was created to assess third-year Doctor of Veterinary Medicine (DVM) student knowledge of key animal welfare topics, opinions regarding the inclusion of welfare education in the veterinary curriculum, and views on veterinarian responsibilities as advocates. In Spring 2018, Colorado State University added a required animal welfare course to the DVM curriculum. Pre- and post-course paper surveys were distributed to the third-year students enrolled in the animal welfare course. One hundred thirty one completed pre-course surveys were collected and 125 completed post-course surveys were collected. Of the pre and post-course surveys collected, 61 were paired with identification codes and utilized for statistical comparison. Results indicated that the course led students to view the inclusion of an animal welfare course in the veterinary curriculum more favorably (p = 0.009) and improved their confidence in conducting research on animal welfare topics (p < 0.001). The course did not change students' sense of responsibility toward welfare advocacy. Associations were not found between attitudes toward these issues and demographic variables of home community, respondent gender, and track selection (p > 0.06). Veterinarians were consistently ranked by students as the most influential member of a community in matters of animal welfare. Future research on the lack of veterinary student knowledge of animal welfare should be done on a national scale to facilitate strategic development of mandatory animal welfare courses in veterinary curricula. Future research should be designed to gain knowledge regarding DVM students' opinions and attitudes regarding effective methods of incorporating animal welfare education into their professional training.

Hypoxia mediated pulmonary edema: potential influence of oxidative stress, sympathetic activation and cerebral blood flow.

BACKGROUND: Neurogenic pulmonary edema (NPE) is a non-cardiogenic form of pulmonary edema that can occur consequent to central neurologic insults including stroke, traumatic brain injury, and seizure. NPE is a public health concern due to high morbidity and mortality, yet the mechanism(s) are unknown. We hypothesized that NPE, evoked by cerebral hypoxia in the presence of systemic normoxia, would be accompanied by sympathetic activation, oxidative stress, and compensatory antioxidant mechanisms. METHODS: Thirteen Walker hounds were assigned to cerebral hypoxia (SaO2 ~ 55 %) with systemic normoxia (SaO2 ~ 90 %) (CH; n = 6), cerebral and systemic (global) hypoxia (SaO2 ~ 60 %) (GH; n = 4), or cerebral and systemic normoxia (SaO2 ~ 90 %) (CON; n = 3). Femoral venous (CH and CON) perfusate was delivered via cardiopulmonary bypass to the brain and GH was induced by FiO2 = 10 % to maintain the SaO2 at ~60 %. Lung wet to lung dry weight ratios (LWW/LDW) were assessed as an index of pulmonary edema in addition to hemodynamic measurements. Plasma catecholamines were measured as markers of sympathetic nervous system (SNS) activity. Total glutathione, protein carbonyls, and malondialdehyde were assessed as indicators of oxidative stress. Brain and lung compensatory antioxidants were measured with immunoblotting. RESULTS: Compared to CON, LWW/LDW and pulmonary artery pressure were greater in CH and GH. Expression of hemeoxygenase-1 in brain was higher in CH compared to GH and CON, despite no group differences in oxidative damage in any tissue. Catecholamines tended to be higher in CH and GH. CONCLUSION: Cerebral hypoxia, with systemic normoxia, is not systematically associated with an increase in oxidative stress and compensatory antioxidant enzymes in lung, suggesting oxidative stress did not contribute to NPE in lung. However, increased SNS activity may play a role in the induction of NPE during hypoxia.

Dietary fatty acids alter left ventricular myocardial gene expression in Wistar rats.

Obesity increases the risk for cardiomyopathy in the absence of comorbidities. Myocardial structure is modified by dietary fatty acids. Left ventricular hypertrophy is associated with Western (WES) diet consumption, whereas intake of n-3 polyunsaturated fatty acids is associated with antihypertrophic effects. We previously observed no attenuation of left ventricular thickening after 3 months of docosahexaenoic acid (DHA) supplementation of a WES diet, compared with WES diet intake alone, in rats that had similar weight, adiposity, and insulin sensitivity to control animals. The objective of this study was to define left ventricular gene expression in these animals to determine whether diet alone was associated with a physiologic or pathologic hypertrophic response. We hypothesized that WES diet consumption would favor a pathologic or maladaptive myocardial gene expression pattern and that DHA supplementation would favor a physiologic or adaptive response. Microarray analysis identified 64 transcripts that were differentially expressed (P ≤ .001) within one or more treatment comparisons. Using quantitative real-time polymerase chain reaction, 29 genes with fold change at least 1.74 were successfully validated; all but 3 had similar directionality to that observed using microarray, and 2 genes, connective tissue growth factor and cathepsin M, were differentially expressed according to diet. WES blot analysis was performed on 4 proteins relevant to myocardial hypertrophy and metabolism. Acyl-CoA thioesterase 1, B-cell translocation gene 2, and carbonic anhydrase III showed directional change consistent with gene expression. Retinol saturase (all-trans-retinol 13,14-reductase), although not consistent with gene expression, was different according to diet, with increased concentrations in WES-fed rats compared with control and DHA-supplemented animals. Diet did not distinguish a transcriptome reflecting physiologic or pathologic myocardial hypertrophy; furthermore, the modest changes observed suggest that obesity and associated comorbidities may play a larger role than mere dietary fatty acid composition in development of cardiomyopathy.

Changing the paradigm for myoglobin: a novel link between lipids and myoglobin.

Myoglobin (Mb) is an oxygen-binding muscular hemeprotein regulated via Ca(2+)-signaling pathways involving calcineurin (CN), with Mb increases attributed to hypoxia, exercise, and nitric oxide. Here, we show a link between lipid supplementation and increased Mb in skeletal muscle. C2C12 cells were cultured in normoxia or hypoxia with glucose or 5% lipid. Mb assays revealed that lipid cohorts had higher Mb than control cohorts in both normoxia and hypoxia, whereas Mb Western blots showed lipid cohorts having higher Mb than control cohorts exclusively under hypoxia. Normoxic cells were compared with soleus tissue from normoxic rats fed high-fat diets; whereas tissue sample cohorts showed no difference in CO-binding Mb, fat-fed rats showed increases in total Mb protein (similar to hypoxic cells), suggesting increases in modified Mb. Moreover, Mb increases did not parallel CN increases but did, however, parallel oxidative stress marker augmentation. Addition of antioxidant prevented Mb increases in lipid-supplemented normoxic cells and mitigated Mb increases in lipid-supplemented hypoxic cells, suggesting a pathway for Mb regulation through redox signaling independent of CN.

Pro-inflammatory mediation of myoblast proliferation.

Skeletal muscle satellite cell function is largely dictated by the surrounding environment following injury. Immune cell infiltration dominates the extracellular space in the injured area, resulting in increased cytokine concentrations. While increased pro-inflammatory cytokine expression has been previously established in the first 3 days following injury, less is known about the time course of cytokine expression and the specific mechanisms of cytokine induced myoblast function. Therefore, the expression of IL-1ß and IL-6 at several time points following injury, and their effects on myoblast proliferation, were examined. In order to do this, skeletal muscle was injured using barium chloride in mice and tissue was collected 1, 5, 10, and 28 days following injury. Mechanisms of cytokine induced proliferation were determined in cell culture using both primary and C2C12 myoblasts. It was found that there is a ∼20-fold increase in IL-1ß (p≤0.05) and IL-6 (p = 0.06) expression 5 days following injury. IL-1ß increased proliferation of both primary and C2C12 cells ∼25%. IL-1ß stimulation also resulted in increased NF-κB activity, likely contributing to the increased proliferation. These data demonstrate for the first time that IL-1ß alone can increase the mitogenic activity of primary skeletal muscle satellite cells and offer insight into the mechanisms dictating satellite cell function following injury.

Delta-6-desaturase links polyunsaturated fatty acid metabolism with phospholipid remodeling and disease progression in heart failure.

BACKGROUND: Remodeling of myocardial phospholipids has been reported in various forms of heart failure for decades, but the mechanism and pathophysiological relevance of this phenomenon have remained unclear. We examined the hypothesis that δ-6 desaturase (D6D), the rate-limiting enzyme in long-chain polyunsaturated fatty acid biosynthesis, mediates the signature pattern of fatty acid redistribution observed in myocardial phospholipids after chronic pressure overload and explored plausible links between this process and disease pathogenesis. METHODS AND RESULTS: Compositional analysis of phospholipids from hearts explanted from patients with dilated cardiomyopathy revealed elevated polyunsaturated fatty acid product/precursor ratios reflective of D6D hyperactivity, manifesting primarily as lower levels of linoleic acid with reciprocally higher levels of arachidonic and docosahexaenoic acids. This pattern of remodeling was attenuated in failing hearts chronically unloaded with a left ventricular assist device. Chronic inhibition of D6D in vivo reversed similar patterns of myocardial polyunsaturated fatty acid redistribution in rat models of pressure overload and hypertensive heart disease and significantly attenuated cardiac hypertrophy, fibrosis, and contractile dysfunction in both models. D6D inhibition also attenuated myocardial elevations in pathogenic eicosanoid species, lipid peroxidation, and extracellular receptor kinase 1/2 activation; normalized cardiolipin composition in mitochondria; reduced circulating levels of inflammatory cytokines; and elicited model-specific effects on cardiac mitochondrial respiratory efficiency, nuclear factor κ B activation, and caspase activities. CONCLUSIONS: These studies demonstrate a pivotal role of essential fatty acid metabolism in myocardial phospholipid remodeling induced by hemodynamic stress and reveal novel links between this phenomenon and the propagation of multiple pathogenic systems involved in maladaptive cardiac remodeling and contractile dysfunction [corrected].

Saturated Fatty Acid-induced cytotoxicity in liver cells does not involve phosphatase and tensin homologue deleted on chromosome 10.

Liver specific deletion of the tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) induces steatosis and hypersensitivity to insulin. Saturated fatty acids, which induce endoplasmic reticulum stress and cell death, appear to increase PTEN, whereas unsaturated fatty acids which do not induce endoplasmic reticulum stress or cell death reduce this protein. In the present study, the role of PTEN in saturated fatty acid-induced cytotoxicity was examined in H4IIE and HepG2 liver cells. Palmitate and stearate increased the expression of PTEN, whereas the unsaturated fatty acids, oleate and linoleate, reduced PTEN expression in both cell types. SiRNA-mediated knockdown of PTEN did not increase liver cell triglyceride stores or reduce palmitate- or stearate-mediated ER stress or apoptosis. These results suggest that PTEN does not play a significant role in saturated fatty acid-induced cytotoxicity in these liver cell models and in the absence of insulin.

The impact of an educational intervention on college athletes' knowledge of concussions.

OBJECTIVE: The purpose of this study was to determine college athletes' knowledge regarding concussions and to determine if an educational lecture before their sport season would improve their knowledge and reporting of concussions. DESIGN: Cross-sectional study. SETTING: University classroom. PARTICIPANTS: Seventy National College Athletic Association Division II men's/women's soccer players and men's/women's basketball players. INTERVENTIONS: Educational lecture regarding the basics of concussions. MAIN OUTCOME MEASURES: Descriptive statistics, ANOVAs, and a paired sample t test determined the athletes' knowledge of concussion before and after the season and the impact of the educational intervention. RESULTS: A paired sample t test indicated that the athletes scored better on the postseason concussion knowledge assessment [t(49) = 10.34, P < 0.000, d = 1.47]. CONCLUSIONS: After an educational intervention, athletes demonstrated an improvement in their knowledge on concussions.

Fatty acid-mediated endoplasmic reticulum stress in vivo: differential response to the infusion of Soybean and Lard Oil in rats.

BACKGROUND: In cell systems, saturated fatty acids, compared to unsaturated fatty acids, induce a greater degree of ER stress and inflammatory signaling in a number of cell types, including hepatocytes and adipocytes. The aim of the present study was to determine the effects of infusions of lard oil (enriched in saturated fatty acids) and soybean oil (enriched in unsaturated fatty acids) on liver and adipose tissue ER stress and inflammatory signaling in vivo. METHODS: Lipid emulsions containing glycerol, phosphatidylcholine, antibiotics (Control, n=7) and either soybean oil (Soybean, n=7) or lard oil (Lard, n=7) were infused intravenously into rats over a 4 h period. RESULTS: Plasma free fatty acid levels were 0.5±0.1 mmol/L (mean±SD) in Control and were increased to 1.0±0.3 mmol/L and 1.1±0.3 mmol/L in Soybean and Lard, respectively. Glucose and insulin levels were not different among groups. Markers of endoplasmic reticulum (ER) stress and activation of inflammatory pathway signaling were increased in liver and adipose tissue from Soybean and Lard compared to Control, but were increased to a greater extent in Lard compared to Soybean. CONCLUSIONS: These data suggest that elevated plasma free fatty acids can induce hepatic and adipose tissue ER stress and inflammation in vivo. In addition, saturated fatty acids appear to be more cytotoxic than unsaturated fatty acids in vivo.

Docosahexaenoic acid supplementation does not improve Western diet-induced cardiomyopathy in rats.

Obesity increases risk for cardiomyopathy in the absence of hypertension, diabetes or ischemia. The fatty acid milieu, modulated by diet, may modify myocardial structure and function, lending partial explanation for the array of cardiomyopathic phenotypy. We sought to identify gross, cellular and ultrastructural myocardial changes associated with Western diet intake, and subsequent modification with docosahexaenoic acid (DHA) supplementation. Wistar and Sprague-Dawley (SD) rats received 1 of 3 diets: control (CON); Western (WES); Western + DHA (WES+DHA). After 12 weeks of treatment, echocardiography was performed and myocardial adiponectin, fatty acids, collagen, area occupied by lipid and myocytes, and ultrastructure were determined. Strain effects included higher serum adiponectin in Wistar rats, and differences in myocardial fatty acid composition. Diet effects were evident in that both WES and WES+DHA feeding were associated with similarly increased left ventricular (LV) diastolic cranial wall thickness (LVW(cr/d)) and decreased diastolic internal diameter (LVID(d)), compared to CON. Unexpectedly, WES+DHA feeding was associated additionally with increased thickness of the LV cranial wall during systole (LVW(cr/s)) and the caudal wall during diastole (LVW(ca/d)) compared to CON; this was observed concomitantly with increased serum and myocardial adiponectin. Diastolic dysfunction was present in WES+DHA rats compared to both WES and CON. Myocyte cross sectional area (CSA) was greater in WES compared to CON rats. In both fat-fed groups, transmission electron microscopy (TEM) revealed myofibril degeneration, disorganized mitochondrial cristae, lipid inclusions and vacuolation. In the absence of hypertension and whole body insulin resistance, WES+DHA intake was associated with more global LV thickening and with diastolic dysfunction, compared to WES feeding alone. Myocyte hypertrophy, possibly related to subcellular injury, is an early change that may contribute to gross hypertrophy. Strain differences in adipokines and myocardial fatty acid accretion may underlie heterogeneous data from rodent studies.

The role of dietary fatty acids in predicting myocardial structure in fat-fed rats.

BACKGROUND: Obesity increases the risk for development of cardiomyopathy in the absence of hypertension, diabetes or myocardial ischemia. Not all obese individuals, however, progress to heart failure. Indeed, obesity may provide protection from cardiovascular mortality in some populations. The fatty acid milieu, modulated by diet, may modify obesity-induced myocardial structure and function, lending partial explanation for the array of cardiomyopathic phenotype in obese individuals. METHODS: Adult male Sprague-Dawley rats were fed 1 of the following 4 diets for 32 weeks: control (CON); 50% saturated fat (SAT); 40% saturated fat + 10% linoleic acid (SAT+LA); 40% saturated fat + 10% α-linolenic acid (SAT+ALA). Serum leptin, insulin, glucose, free fatty acids and triglycerides were quantitated. In vivo cardiovascular outcomes included blood pressure, heart rate and echocardiographic measurements of structure and function. The rats were sacrificed and myocardium was processed for fatty acid analysis (TLC-GC), and evaluation of potential modifiers of myocardial structure including collagen (Masson's trichrome, hydroxyproline quantitation), lipid (Oil Red O, triglyceride quantitation) and myocyte cross sectional area. RESULTS: Rats fed SAT+LA and SAT+ALA diets had greater cranial LV wall thickness compared to rats fed CON and SAT diets, in the absence of hypertension or apparent insulin resistance. Treatment was not associated with changes in myocardial function. Myocardial collagen and triglycerides were similar among treatment groups; however, rats fed the high-fat diets, regardless of composition, demonstrated increased myocyte cross sectional area. CONCLUSIONS: Under conditions of high-fat feeding, replacement of 10% saturated fat with either LA or ALA is associated with thickening of the cranial LV wall, but without concomitant functional changes. Increased myocyte size appears to be a more likely contributor to early LV thickening in response to high-fat feeding. These findings suggest that myocyte hypertrophy may be an early change leading to gross LV hypertrophy in the hearts of "healthy" obese rats, in the absence of hypertension, diabetes and myocardial ischemia.

Fatty acids and the endoplasmic reticulum in nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease (NAFLD) represents a burgeoning public health concern in westernized nations. The obesity-related disorder is associated with an increased risk of cardiovascular disease, type 2 diabetes and liver failure. Although the underlying pathogenesis of NAFLD is unclear, increasing evidence suggests that excess saturated fatty acids presented to or stored within the liver may play a role in both the development and progression of the disorder. A putative mechanism linking saturated fatty acids to NAFLD may be endoplasmic reticulum (ER) stress. Specifically, excess saturated fatty acids may induce an ER stress response that, if left unabated, can activate stress signaling pathways, cause hepatocyte cell death, and eventually lead to liver dysfunction. In the current review we discuss the involvement of saturated fatty acids in the pathogenesis of NAFLD with particular emphasis on the role of ER stress.

Endoplasmic reticulum stress and the unfolded protein response in nonalcoholic fatty liver disease.

The underlying causes of nonalcoholic fatty liver disease (NAFLD) are unclear, although recent evidence has implicated the endoplasmic reticulum (ER) in both the development of steatosis and progression to nonalcoholic steatohepatitis. Disruption of ER homeostasis, often termed "ER stress," has been observed in liver and adipose tissue of humans with NAFLD and/or obesity. Importantly, the signaling pathway activated by disruption of ER homeostasis, the unfolded protein response, has been linked to lipid biosynthesis, insulin action, inflammation, and apoptosis. Therefore, understanding the mechanisms that disrupt ER homeostasis in NAFLD and the role of ER-mediated signaling have become topics of intense investigation. The present review will examine the ER and the unfolded protein response in the context of NAFLD.

Use of fat-fed rats to study the metabolic and vascular sequelae of obesity and beta-adrenergic antagonism.

Obesity-associated cardiovascular disease exerts profound human and monetary costs, creating a mounting need for cost-effective and relevant in vivo models of the complex metabolic and vascular interrelationships of obesity. Obesity is associated with endothelial dysfunction and inflammation. Free fatty acids (FFA), generated partly through beta-adrenergic receptor-mediated lipolysis, may impair endothelium-dependent vasodilation (EDV) by proinflammatory mechanisms. beta-Adrenergic antagonists protect against cardiovascular events by mechanisms not fully defined. We hypothesized that beta antagonists may exert beneficial effects, in part, by inhibiting lipolysis and reducing FFA. Further, we sought to evaluate the fat-fed rat as an in vivo model of obesity-induced inflammation and EDV. Control and fat-fed rats were given vehicle or beta antagonist for 28 d. Serum FFA were measured to determine the association to serum IL6, TNFalpha, and C-reactive protein and to femoral artery EDV. Compared with controls, fat-fed rats weighed more and had higher FFA, triglyceride, leptin, and insulin levels. Unexpectedly, in control and fat-fed rats, beta antagonism increased FFA, yet inflammatory cytokines were reduced and EDV was preserved. Therefore, reduction of FFA is unlikely to be the mechanism by which beta antagonists protect the endothelium. These results reflect the need for validation of ex vivo models of obesity-induced inflammation and endothelial dysfunction, concurrent with careful control of dietary fat composition and treatment duration.