Scholarly Works, Human Nutrition, Foods, and Exercise
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- Preschoolers' Food Handling Skills - Motor DevelopmentHertzler, Ann A. (Virginia Cooperative Extension Service, 1984-04)Food activities provide the chance to learn many skills useful for a lifetime. For the preschooler , food handling skills need to be tailored to muscular development and coordination. The activities listed are for two to five-year-olds. The beginning level is for two-year-olds while the highest level is for five-year-olds.
- Food centsHertzler, Ann A.; Scott, Elaine D. (Virginia Cooperative Extension Service, 1987-08)Discusses how to plan and follow a food budget.
- Hurts and Hazards Kids, Kitchen Accidents, and SafetyHertzler, Ann A.; DeBord, Karen (Virginia Cooperative Extension, Virginia Tech and Virginia State University, 1993)
- Germ Squirm Kids and Safe Food HandlingHertzler, Ann A.; DeBord, Karen (Virginia Cooperative Extension, Virginia Tech and Virginia State University, 1993)
- Peptides Derived from Two Separate Domains of the Matrix Protein Thrombospondin-1 Have Anti-Angiogenlc ActivityTolsma, Sara S.; Volpert, Olga V.; Good, Deborah J.; Frazier, William A.; Polverini, Peter J.; Bouck, Noel (Rockefeller University Press, 1993-07-01)Thrombospondin-1 (TSP1) is a large modular matrix protein containing three identical disulfide-linked 180-kD chains that inhibits neovascularization in vivo (Good et al., 1990). To determine which of the structural motifs present in the 180-kD TSP1 polypeptide mediate the anti-angiogenic activity, a series of protease-generated fragments were tested using several in vitro and in vivo assays that reflect angiogenic activity. The majority of the anti-angiogenic activity of TSP1 resides in the central 70-kD stalk region which alone could block neovascularization induced by bFGF in the rat cornea in vivo and inhibit both migration in a modified Boyden chamber and [~H]thymidine incorporation stimulated by bFGF in cultured capillary endothelial cells. Although TSP1 has been shown to bind active TGF/31, this cytokine could not account for the inhibitory effects of the stalk region of TSP1 on cultured endothelial cells.
- Food CentsHertzler, Ann A.; Brochetti, Denise (Virginia Cooperative Extension, Virginia Tech and Virginia State University, 1995)
- Nourishing Children with BooksHertzler, Ann A. (Virginia Cooperative Extension, Virginia Tech and Virginia State University, 1999)
- The Nitty-Gritty of Food Safety. A Guide for Parents and Childcare ProvidersParra, Danielle Elizabeth; Nickols-Richardson, Sharon Michelle, 1965-; Serrano, Elena L.; Boyer, Renee R. (Virginia Cooperative Extension, 2002-12-02)This guide illustrates for you and the children you for care ways to prevent foodborne illnesses. Follow these principles to fight bacteria - clean, separate, cook and chill. Children are never too young to learn and establish healthy practices as the safe handling of food.
- Healthy weights for healthy kids : what should I do if my child is overweight?Serrano, Elena L.; Branstad, Kathryn Elizabeth (Virginia Cooperative Extension, 2003)
- Calcium : build strong bonesSerrano, Elena L.; Sablik, Anna (Virginia Cooperative Extension, 2003)
- The molecular mechanism linking muscle fat accumulation to insulin resistanceDohm, G. Lynis; Hulver, Matthew W. (The Nutrition Society, 2004)Skeletal muscle insulin resistance is a co-morbidity of obesity and a risk factor for the development of type 2 diabetes mellitus. Insulin resistance is associated with the accumulation of intramyocellular lipids. Intramyocellular triacylglycerols do not appear to be the cause of insulin resistance but are more likely to be a marker of other lipid intermediates such as fatty acyl-CoA, ceramides or diacylglycerols. Fatty acyl-CoA, ceramides and diacylglycerols are known to directly alter various aspects of the insulin signalling cascade. Insulin signalling is inhibited by the phosphorylation of serine and threonine residues at the levels of the insulin receptor and insulin receptor substrate 1. Protein kinase C is responsible for the phosphorylation of the serine and threonine residues. Fatty acyl-CoA and diacylglycerols are known to activate protein kinase C. The cause of the intramyocellular accumulation of fatty acyl-CoA and diacylglycerols is unclear at this time. Reduced fatty acid oxidation does not appear to be responsible, as fatty acyl-CoA accumulates in skeletal muscle with a normal fatty acid oxidative capacity. Other potential mechanisms include oversupply of lipids to muscle and/or up regulated fatty acid transport.
- Calcineurin activation influences muscle phenotype in a muscle-specific fashionTalmadge, Robert J.; Otis, Jeffrey S.; Rittler, Matthew R.; Garcia, Nicole D.; Spencer, Shelly R.; Lees, Simon J.; Naya, Francisco J. (2004-07-28)Background The calcium activated protein phosphatase 2B, also known as calcineurin, has been implicated as a cell signaling molecule involved with transduction of physiological signals (free cytosolic Ca2+) into molecular signals that influence the expression of phenotype-specific genes in skeletal muscle. In the present study we address the role of calcineurin in mediating adaptations in myosin heavy chain (MHC) isoform expression and muscle mass using 3-month old wild-type (WT) and transgenic mice displaying high-level expression of a constitutively active form of calcineurin (MCK-CN* mice). Results Slow muscles, e.g., soleus, were significantly larger (by ~24%), whereas fast muscles, e.g., medial gastrocnemius (MG) and tibialis anterior were significantly smaller (by ~26 and ~16%, respectively) in MCK-CN* mice compared to WT. The masses of mixed phenotype muscles, such as the plantaris and the extensor digitorum longus, were not significantly changed from WT. The soleus, plantaris, MG and diaphragm displayed shifts toward slower MHC isoforms, e.g., soleus from WT mice contained ~52% MHC-I, ~39% MHC-IIa, and ~9% MHC-IIx, whereas MCK-CN* mice had ~67% MHC-I, ~26% MHC-IIa, and ~7% MHC-IIx. The specific isoforms that were either up or down-regulated were muscle-specific. For instance, the proportion of MHC-IIa was decreased in the soleus and diaphragm, but increased in the plantaris and MG of MCK-CN* mice. Also, the proportion of MHC-IIx was unchanged in the soleus, decreased in the diaphragm and increased in the plantaris and MG of MCK-CN* relative to WT mice. Fast to slow shifts in fiber type proportions were evident for the plantaris, but not the soleus. Fast, but not slow, plantaris fibers of MCK-CN* mice had higher oxidative and lower glycolytic properties than WT. Conclusion These data suggest that calcineurin activation can influence muscle phenotype and that the specific influence of calcineurin activation on the phenotypic and mass characteristics of a muscle is dependent upon the original phenotypic state of the muscle.
- Jump rope rhymesSerrano, Elena L. (Virginia Cooperative Extension, 2005)
- Genistein activates the 3 ',5 '-cyclic adenosine monophosphate signaling pathway in vascular endothelial cells and protects endothelial barrier functionLiu, Dongmin; Jiang, Honglin; Grange, Robert W. (Endocrine Society, 2005-03)The soy phytoestrogen, genistein, has an array of biological actions, including weak estrogenic effects, inhibition of tyrosine kinase, and cellular antioxidant activity. Recent studies showed that genistein may improve vascular function, but the mechanism is unclear. We show that genistein stimulates intracellular cAMP accumulation in intact bovine aortic endothelial cells and human umbilical vein endothelial cells over an incubation period of 30 min. Increases in intracellular cAMP are evoked by as low as 10 nM genistein but not by estrogen. These increases in cAMP may result primarily from enhanced adenylate cyclase activity by a mechanism that does not involve genomic actions or estrogen receptors. The cAMP induced by genistein activates cAMP-dependent protein kinase (PKA) in bovine aortic endothelial cells. The activation of PKA phosphorylates and activates cAMP response element binding protein, leading to up-regulation of cAMP response element-containing gene expression. In addition, activation of PKA protects thrombin-induced endothelial monolayer permeability, a novel cardioprotective effect of genistein mediated by the cAMP/PKA cascade. These findings demonstrate that a nongenomic action of genistein leads to activation of the cAMP/PKA signaling system to protect the vascular barrier function and alter the expression of cAMP-regulated genes, thereby providing a novel mechanism underlying some of the cardiovascular protective effects proposed for soy phytoestrogens.
- Go Local, Virginia: A Consumer's Guide to Buying Healthful, Locally Produced Foods in VirginiaRose, Nick; Serrano, Elena L. (Virginia Cooperative Extension, 2005-09-01)A consumer's guide to buying healthful, locally produced foods in Virginia.
- Safe and Nutritious Seafood in VirginiaVillalba, Abigail; Serrano, Elena L.; Sarjahani, Andy; Schwarz, Michael H.; Jahncke, Michael L. (Virginia Cooperative Extension, 2005-09-01)This publication provides the information you need to help ensure that the seafood you buy and consume is safe and nutritious.
- Coronary Heart Disease (CHD) Risk Factors and Metabolic Syndrome in HIV-Positive Drug Users in MiamiBaum, Marianna K.; Rafie, Carlin; Lai, Shenghan; Xue, Lihua; Sales, Sabrina; Page, J. Bryan; Berkman, Ronald; Karas, Linden; Campa, Adriana (Science Publications, 2006-01)The frequency of coronary heart disease (CHD) is increasing among HIV seropositive persons. This phenomenon may be related to HIV disease itself, the use of antiretroviral medications and increased length of survival, or the synergism of these factors. In this study we have calculated the 10-year CHD risk estimate and the prevalence of metabolic syndrome in a cohort of 118 HIV seropositive chronic drug users, including those who are on HAART with or without protease inhibitors (PI). The results showed that the 10-year coronary heart disease risk among the HIV seropositive drug users was 4.8 ± 5.7, which is within the range of results published for other HIV infected cohorts. The 10-year CHD risk was significantly higher in men (5.9±6.1, p<0.001) than in women (1.7±2.4), due to their gender and the pre-menopausal mean age of the women (39.4±7.3 years of age), despite a significantly higher rate of abdominal obesity (54.8% in women vs. 8.1% in men, p<0.001) and lower HDL (61.3% in women vs. 40% in men, p=0.042). The rate of metabolic syndrome among our female HIV seropositive drug users was significantly higher (29% vs 10.3%, p=0.013) compared to men (10.3%). Participants with metabolic syndrome had a significantly higher 10-year CHD risk (27.8% vs. 10.2%, p=0.041) and higher mean BMI (28.6 ± 4.1 vs. 24.2±4, p<0.001) than those without the syndrome. The predominant proportion of the cohort had a high viral load, suggesting that their use of illicit drugs has an influence on either adherence or effectiveness of antiretroviral medication. Increased viral load was significantly associated with metabolic syndrome (OR=2.23, 95% CI:1.12, 4.47; p=0.023), high fasting glucose (OR=1.61, 95% CI: 1.02, 2.55; p=0.042) and low HDL levels (OR=1.41, 95% CI: 1.01, 1.98; p=0.046), after controlling for age gender, smoking, PI exposure, BMI and CD4. HAART with or without PI did not significantly impact the 10-year CHD risk estimate or metabolic syndrome in this cohort. The estimated effect of PI, however, was positively and significantly related to triglyceride levels (effect estimate=95.81; 95% CI:39.40, 152.21; p<0.01) after controlling for age, gender, smoking, viral load, CD4 cell count and BMI. Heavy use of cigarettes and crack/cocaine was inversely associated with obesity (OR=0.84, 95% CI:0.67, 0.99; p=0.049; OR=0.43, 95% CI:0.19, 0.98; p=0.044, respectively), while use of marijuana tended to be associated with increased central obesity (p=0.08). Heavy cigarette smoking was significantly associated with low HDL (OR=3.06, 95% CI:1.18; 7.95, p=0.02). The significant association of higher viral load with CHD risk indicates that controlling viral load may be important in reducing CHD risk in HIV infected drug users.
- Comparison of assessment techniques: plasma lipid and lipoproteins related to the metabolic syndromeDavy, Brenda M.; Davy, Kevin P. (Biomed Central, 2006-01-31)Background The purpose of this investigation was to determine the influence of analytical method on reported concentrations of plasma lipids and lipoproteins, and to determine if there are clinical implications of any potential differences on identification of the metabolic syndrome dyslipidemia, CVD risk stratification and classification of LDL subclass phenotype. Results Plasma triglyceride (TG) concentrations were 1.09 ± 0.06 and 1.17 ± 0.06 mmol/L and plasma high density lipoprotein cholesterol (HDL-C) concentrations were 1.09 ± 0.03 vs 1.19 ± 0.03 mmol/L (both p < 0.05) from 113 duplicate samples sent to two laboratories utilizing different lipid and lipoprotein analytical methods (LABS 1 and 2, respectively). Plasma total cholesterol and low-density lipoprotein cholesterol (LDL-C) concentrations were also significantly different between laboratories. Spearman rho correlations indicate excellent agreement of TG and HDL-C determined by the two laboratories (r = 0.96, TG; r = 0.91, HDL-C, both p < 0.001). Eleven vs. 14 individuals met the TG criteria and 70 vs. 48 met HDL-C metabolic syndrome criteria with LAB 1 and 2, respectively. Apoprotein B concentration (LAB 1) and LDL particle number (LAB 2) were highly correlated. (r = 0.92, P < 0.01). LAB 2 characterized more individuals as LDL pattern B phenotype, as compared to LAB 1 (30 vs. 14%, P < 0.05). Conclusion Different plasma lipid and lipoprotein analytical techniques yield results which are highly correlated, yet significantly different, which suggests a consistent measurement difference. This difference has clinical implications, in that the proportion of individuals identified as meeting the metabolic syndrome dyslipidemia criteria, "at risk" based upon apo B or LDL particle number, and the LDL pattern B phenotype will differ based upon choice of analytical method.
- Unsupervised clustering of gene expression data points at hypoxia as possible trigger for metabolic syndromePtitsyn, Andrey; Hulver, Matthew W.; Cefalu, William; York, David; Smith, Steven R. (2006-12-19)Background Classification of large volumes of data produced in a microarray experiment allows for the extraction of important clues as to the nature of a disease. Results Using multi-dimensional unsupervised FOREL (FORmal ELement) algorithm we have re-analyzed three public datasets of skeletal muscle gene expression in connection with insulin resistance and type 2 diabetes (DM2). Our analysis revealed the major line of variation between expression profiles of normal, insulin resistant, and diabetic skeletal muscle. A cluster of most "metabolically sound" samples occupied one end of this line. The distance along this line coincided with the classic markers of diabetes risk, namely obesity and insulin resistance, but did not follow the accepted clinical diagnosis of DM2 as defined by the presence or absence of hyperglycemia. Genes implicated in this expression pattern are those controlling skeletal muscle fiber type and glycolytic metabolism. Additionally myoglobin and hemoglobin were upregulated and ribosomal genes deregulated in insulin resistant patients. Conclusion Our findings are concordant with the changes seen in skeletal muscle with altitude hypoxia. This suggests that hypoxia and shift to glycolytic metabolism may also drive insulin resistance.
- Dehydroepiandrosterone protects vascular endothelial cells against apoptosis through a G alpha(i) protein-dependent activation of phosphatidylinositol 3-kinase/Akt and regulation of antiapoptotic Bcl-2 expressionLiu, D. M.; Si, H. W.; Reynolds, K. A.; Zhen, W.; Jia, Z. Q.; Dillon, J. S. (Endocrine Society, 2007-07)The adrenal steroid dehydroepiandrosterone (DHEA) may improve vascular function, but the mechanism is unclear. In the present study, we show that DHEA significantly increased cell viability, reduced caspase-3 activity, and protected both bovine and human vascular endothelial cells against serum deprivation-induced apoptosis. This effect was dose dependent and maximal at physiological concentrations (0.1-10 nM). DHEA stimulation of bovine aortic endothelial cells resulted in rapid and dose-dependent phosphorylation of Akt, which was blocked by LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K), the upstream kinase of Akt. Accordingly, inhibition of PI3K or transfection of the cells with dominant-negative Akt ablated the antiapoptotic effect of DHEA. The induced Akt phosphorylation and subsequent cytoprotective effect of DHEA were dependent on activation of G alpha(i) proteins, but were estrogen receptor independent, because these effects were blocked by pertussis toxin but not by the estrogen receptor inhibitor ICI182,780 or the aromatase inhibitor aminoglutethimide. Finally, DHEA enhanced antiapoptotic Bcl-2 protein expression, its promoter activity, and gene transcription attributable to the activation of the PI3K/Akt pathway. Neutralization of Bcl-2 by antibody transfection significantly decreased the antiapoptotic effect of DHEA. These findings provide the first evidence that DHEA acts as a survival factor for endothelial cells by triggering the G alpha(i)-PI3K/Akt-Bcl-2 pathway to protect cells against apoptosis. This may represent an important mechanism underlying the vascular protective effect of DHEA.