Spatial and Visual Reasoning: Do These Abilities Improve in First-Year Veterinary Medical Students Exposed to an Integrated Curriculum?

Spatial visualization ability refers to the human cognitive ability to form, retrieve, and manipulate mental models of spatial nature. Visual reasoning ability has been linked to spatial ability. There is currently limited information about how entry-level spatial and visual reasoning abilities may predict veterinary anatomy performance or may be enhanced with progression through the veterinary anatomy content in an integrated curriculum. The present study made use of two tests that measure spatial ability and one test that measures visual reasoning ability in veterinary students: Guay's Visualization of Views Test, adapted version (GVVT), the Mental Rotations Test (MRT), and Raven's Advanced Progressive Matrices Test, short form (RavenT). The tests were given to the entering class of veterinary students during their orientation week and at week 32 in the veterinary medical curriculum. Mean score on the MRT significantly increased from 15.2 to 20.1, and on the RavenT significantly increased from 7.5 to 8.8. When females only were evaluated, results were similar to the total class outcome; however, all three tests showed significant increases in mean scores. A positive correlation between the pre- and post-test scores was found for all three tests. The present results should be considered preliminary at best for associating anatomic learning in an integrated curriculum with spatial and visual reasoning abilities. Other components of the curriculum, for instance histology or physiology, could also influence the improved spatial visualization and visual reasoning test scores at week 32.

Production of a type 2 maternal diabetes rodent model using the combination of high-fat diet and moderate dose of streptozocin.

INTRODUCTION: Pregnancy may be complicated by maternal diabetes. The following experiments were performed in an attempt to produce mouse models of insulin-resistant maternal diabetes. METHODS: CD1 females received 200 mg/kg streptozocin (STZ) to model insulin-dependent diabetes (T1 group). Another group of females (T2 group) was put on a HFD 4 weeks before receiving 100 mg/kg STZ. After 4 additional weeks of HFD, hyperglycemic females were separated and bred. In another experiement, CD1 females were fed a HFD for 4 weeks before receiving an intravenous (GDM1 group) or intraperitoneal (GDM2 group) injection of 100 mg/kg STZ. Females from GDM2 group were bred at the same day of the STZ injection. Females from GDM1 group were bred 4 weeks after the STZ injection. RESULTS AND CONCLUSION: About 25% of the females from T2 group became hyperglycemic after 4 weeks of the injection of STZ. Fifty percent of the females from GDM1 group reached hyperglycemic levels greater than 250 mg/dl during pregnancy. The combination of HFD and moderate STZ in CD1 mice therefore produced hyperglycemic females; however numbers of these mice were somewhat low.

Late-gestation ventricular myocardial reduction in fetuses of hyperglycemic CD1 mice is associated with increased apoptosis.

BACKGROUND: Previous work in our laboratory showed reduced myocardium and dilated ventricular chambers in gestation day (GD) 17 hearts that were collected from hyperglycemic CD1 mouse dams. Pre-breeding maternal immune stimulation, using Freund's complete adjuvant (FCA), diminished the severity of these fetal heart lesions. The following experiments were performed to detect possible changes in fetal heart apoptotic cell death, under hyperglycemic conditions and with or without maternal immune stimulation. METHODS: Female CD1 mice were injected with 200 mg/kg of streptozocin (STZ) to induce insulin-dependent diabetes mellitus. Half of these mice received prior FCA injection. Fetal hearts were collected on GD 17 and myocardial apoptotic cells were quantified using flow cytometry. A panel of apoptosis regulatory genes (Bcl2, p53, Casp3, Casp9, PkCe) was then examined in the fetal myocardium using RT-PCR. RESULTS: Early apoptotic cells and late apoptotic/necrotic cells were significantly increased in fetal hearts from STZ or STZ+FCA dams. Pre-treatment with FCA reduced late apoptotic/necrotic cells to control level, suggesting some cell death protection was rendered by FCA. Paradoxically in the face of such increased cell death, the expression of pro-apoptotic genes Casp3 and Casp9 was decreased by diabetes, while the anti-apoptotic gene Bcl2 was increased. CONCLUSIONS: Maternal hyperglycemia causes dys-regulated apoptosis of fetal myocardial cells. Such effect may be prevented by maternal immune stimulation.

Current thoughts on maternal nutrition and fetal programming of the metabolic syndrome.

Chronic diseases such as type 2 diabetes and cardiovascular disease are the leading cause of death and disability worldwide. Although the metabolic syndrome has been defined in various ways, the ultimate importance of recognizing this combination of disorders is that it helps identify individuals at high risk for both type 2 diabetes and cardiovascular disease. Evidence from observational and experimental studies links adverse exposures in early life, particularly relating to nutrition, to chronic disease susceptibility in adulthood. Such studies provide the foundation and framework for the relatively new field of developmental origins of health and disease (DOHaD). Although great strides have been made in identifying the putative concepts and mechanisms relating specific exposures in early life to the risk of developing chronic diseases in adulthood, a complete picture remains obscure. To date, the main focus of the field has been on perinatal undernutrition and specific nutrient deficiencies; however, the current global health crisis of overweight and obesity demands that perinatal overnutrition and specific nutrient excesses be examined. This paper assembles current thoughts on the concepts and mechanisms behind the DOHaD as they relate to maternal nutrition, and highlights specific contributions made by macro- and micronutrients.

Aortic and ventricular dilation and myocardial reduction in gestation day 17 ICR mouse fetuses of diabetic mothers.

BACKGROUND: Maternal diabetes mellitus is associated with increased fetal teratogenesis, including cardiovascular defects. Information regarding cardiovascular changes in late-gestation fetal mice, related to maternal hyperglycemia, is not present in the literature. METHODS: Late-gestation fetal heart and great vessel morphology were analyzed in fetuses from control and diabetic mice. Female ICR mice were injected with streptozocin (200 mg/kg IP) prior to mating to induce diabetes (n = 8). Nonhyperglycemic females were used as controls (n = 8). At day 17 of gestation, females were euthanized and one fetus was arbitrarily selected per litter to analyze the heart and great vessels. Six additional fetuses from different litters, showing external malformations (spina bifida and/or exencephaly), were also evaluated from the diabetic group. Fetal thoraxes were processed using routine histopathologic techniques, and 7-mum transversal sections were stained with hematoxylin-eosin. Digital images of sections were made and analyzed using NIH Image J software to compare regional cardiac development. Student's t tests for means were performed to determine differences between groups (p < .05). RESULTS: Maternal hyperglycemia caused a dilation of late-gestation fetal ventricular chambers, a reduction of total ventricular myocardial area, and an increase in transversal ascending thoracic aortic area. Three of six fetuses that displayed external malformations showed an overt cardiac defect, beyond the ventricular and myocardial changes. CONCLUSIONS: Maternal hyperglycemia altered morphology of the late-gestation fetal mouse heart. Postnatal persistence or consequences of late-gestation heart chamber dilation and myocardial reduction are not yet known.