Browsing by Author "Ju, Young H."

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    Anti-Diabetic Potentials of Bitter Melon
    Ju, Young H.; Kim, Morgan (Virginia Cooperative Extension, 2018-05-17)
    Discusses the pros and cons of bitter melon as an anti-diabetic food.
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    Anti-Diabetic Potentials of White Mulberry
    Ju, Young H.; Kim, Morgan (Virginia Cooperative Extension, 2018-08-30)
    Discusses the pros and cons of white mulberries as an anti-diabetic food. Summaries recent research on white mulberry foods and extracts which may help prevent or treat impaired glycemic control.
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    Caffeinated Energy Drinks/Energy Shots Among Young Adults
    Ju, Young H. (Virginia Cooperative Extension, 2015-12-09)
    Discusses the caffeinated energy drinks and shots and the impacts on young adults when they are mixed with alcohol.
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    Can flaxseed lower cholesterol levels?
    Ju, Young H. (Virginia Cooperative Extension, 2017-10-13)
    Provides information about flaxseed and how it might help with lowering cholesterol.
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    The effect of spindle geometry on the establishment of merotelic kinetochore attachment and chromosome mis-segregation
    Silkworth, William Thomas (Virginia Tech, 2012-06-26)
    At any given time there are on the order of one hundred million cells undergoing mitosis in the human body. To accurately segregate chromosomes, the cell forms the bipolar mitotic spindle, a molecular machine that distributes chromosomes equally to the daughter cells. To this end, microtubules of the mitotic spindle must appropriately attach the kinetochores: protein structures that form on each chromatid of each mitotic chromosome. The majority of the time correct kinetochore microtubule attachments are formed. However, mis-attachments can and do form. Mis-attachments that are not corrected before chromosome segregation can give rise to aneuploidy, an incorrect number of chromosomes. Aneuploidy occurring in the germ line can cause both miscarriage and genetic diseases. Furthermore, aneuploidy is a major characteristic of cancer cells, and aneuploid cancer cells frequently mis-segregate chromosomes at high rates, a phenotype termed chromosomal instability (CIN). CIN has been correlated with both advanced tumorigenesis and poor patient prognosis and over the years there have been many hypotheses for what causes CIN. In this study, we identified two distinct mechanisms that are responsible for CIN. Both of these mechanisms cause a transient, abnormal geometric arrangement of the mitotic spindle. Specifically, cancer cells possess supernumerary centrosomes, which lead to the assembly of multipolar spindles during early mitosis when attachments between kinetochores and microtubules are forming. Supernumerary centrosomes facilitate the formation of merotelic attachments, in which a single kinetochore binds microtubules from more than one centrosome. As mitosis progresses the supernumerary centrosomes cluster, giving rise to a bipolar spindle by the time of chromosome segregation. However, the high rates of merotelic attachments formed during the transient multipolar stage result in high rates of chromosome mis-segregation. The second geometric defect characterized is caused by failure of centrosomes to separate before kinetochore-microtubule attachments begin to form. This mechanism, too, leads to high rates of kinetochore mis-attachment formation and high rates of chromosome mis-segregation. Finally, this study shows that the mechanisms characterized here are prevalent in human cancer cells from multiple organ sites, thus revealing that both mechanisms are a common cause of CIN.
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    Effects of low linolenic soy oil on pre-malignant human mammary epithelial cell progression
    McCall, Elaine Teresa (Virginia Tech, 2008-12-10)
    Beginning January 1, 2006 the U.S. Food and Drug Administration mandated that the amount of trans fats per serving be listed on the Nutrition Facts panel. Consequently new soybean breeds that would no longer be subject to the hydrogenation process, thus reducing trans fats, were developed. By traditional plant breeding techniques, plant breeders have developed a low linolenic soybean with 83.36% less alpha-linolenic acid (ALA; omega-3) than conventional soybean. A number of studies have demonstrated that the influence of dietary fats on cancer depends on the quantity as well as the type of lipids and diets with a disproportionately high omega-6 (n-6)/omega-3 (n-3) ratio are thought to contribute to cardiovascular disease, inflammation and cancer. Conventional soybean oil (SO) has an n-6/n-3 ratio of 8/1 while the new low linolenic soy bean oil (LLSO) has an n-6/n-3 ratio of 56/1. In this study, we evaluated the effects of dietary LLSO, SO and lard on the progression of breast cancer (BC). Thirty-five, 6-wk old, ovariectomized, athymic mice received human pre-malignant breast cells (MCF-10AT1 1 x 105 cells/40μl/ Matrigel/spot, 4 spots/mouse). Mice were divided into three groups and then fed isocaloric and isonitrogenous diets with disparate fat sources: LLSO (20% of total energy intake), SO (20%) and lard (20%). The dietary treatment lasted 24 weeks upon which the study was terminated and tumors, tissues and blood samples were analyzed. Average tumor surface area at termination for the LLSO group was 45.11 ± 4.46 mm2, 40.08 ± 4.2 mm2 for lard and 56.63 ± 5.42 mm2 for SO. Messenger RNA (mRNA) expression of HER2/neu, epidermal growth factor receptor (EGFR), H-ras, Bcl-2, cyclooxygenase-2 (COX-2), vascular epidermal growth factor (VEGF), and fatty acid synthase (FAS) in tumors were analyzed using quantitative real time-polymerase chain reaction (qRT-PCR). We found that dietary LLSO supplementation significantly (p < 0.05, Tukey's test) increased tumor expression of oncogenes HER2/neu, EGFR, FAS, and H-ras, but not in the SO or lard supplemented groups. Relative mRNA expression was also significantly increased in both LLSO and SO groups, however, there was no marked difference in mRNA expression for Bcl-2 and COX-2. Removed tumors were evaluated microscopically for histologic lesion progression corresponding to human breast cancer progression. Tumors from the LLSO group showed more advanced lesions (grade 2) (p < 0.05, Chi Square test) with areas of four or more layers of epithelial cells and irregularly shaped lumens. These data suggest that dietary intake of LLSO may accelerate mammary tumor progression at a faster rate than conventional SO or lard.
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    The effects of Low α-Linolenic fatty acid Soybean Oil and Mid Oleic acid Soybean Oil on the growth of Her-2/neu and Fatty acid synthase over-expressing human breast cancer (SK-Br3) cells
    Bark, Jee Hyun (Virginia Tech, 2010-09-09)
    A variety of soybean oils (SOs) were developed with improved functional properties. Some of the modified SOs contain altered fatty acid (FA) composition by selective breeding methods. Currently, low α- linolenic acid soybean oil (LLSO) and low α- linolenic acid and mid oleic acid soybean oil (LLMOSO) are available FA modified SOs in the market. The consumption of FA modified SOs has been increased because the United States Food and Drug Administration required listing trans fat content in food products sold in U.S. as an effort to reduce possible health risks caused by trans fat beginning 2006. However, the effects of these FA modified SOs on human chronic diseases including breast cancer (BC) have not been studied. BC has become the most frequently diagnosed cancer and is the second leading cause of cancer death among American women. The type of dietary fat, FA composition, and n-6/n-3 ratio are known to influence BC development. Therefore, it is possible that the changed FA composition and n-6/n-3 ratio in the FA modified SOs may affect BC progression, and its critical health concern needs to be investigated. Increased human epithelial growth factor receptor 2 (Her-2/neu) and fatty acid synthase (FAS) are associated with BC progression. In fact, FAS activity and expression are affected by dietary FA composition and FA metabolism. Hypothesis of this research is that LLSO and LLMOSO may affect Her-2/neu and FAS expressing human BC (SK-Br3) cell growth in vitro and in vivo. To test our hypothesis, we investigated the potential adverse or beneficial effects of LLSO and LLMOSO in comparison with conventional SO and lard on human BC cells and then examined the possible mechanisms of action by evaluating the expression level of genes markers involved in growth factor mediated signal transduction pathway, specifically Her-2/neu PI 3-kinase (phophoinositide 3- kinase)-FAS signal transduction pathway. In vitro study demonstrated that all the tested oils at 0-2 μl/ml level have cytotoxic effects. LLMOSO had less cytotoxic effects on the growth of SK-Br3 cells compared to SO. However, there was no difference in SK-Br3 cell growth between LLSO and SO. The apoptotic protein markers (mutant p53 and caspase-3) analysis revealed that the cell growth inhibition by oil treatments was cytotoxic by triggering apoptosis. Western blot analysis demonstrated that LLSO- and LLMOSO- induced changes on cell growth involve Her-2/neu and FAS signaling transduction pathway and sterol regulatory element binding protein-1 (SREBP-1), mitogen activated protein kinase (MAPK), and phosphatidylinositol 3-kinase (PI 3-kinase) are possible down-stream effectors of Her-2/neu signaling pathway. We also evaluated the dietary effects of LLSO (20% fat of total calorie), SO (20%), and lard (20%) on the growth of SK-Br3 tumors implanted in athymic mice. Changes in tumor surface area, body weight, and food intake were monitored during the 6 months feeding study. After termination, tumor net weight, Her-2/neu and FAS mRNA expression in tumors, FAS protein expression in liver, lipid composition in diets, abdominal fat, and serum, as well as plasma total cholesterol and triglyceride levels were analyzed. In vivo study showed that there were no statistical differences in tumor size and tumor net weight among SO, LLSO, and lard groups. No differences in FAS mRNA and protein expression levels between the LLSO and SO groups were observed. Tumors from the lard group expressed higher Her-2/neu and FAS mRNA than those from the LLSO and SO group. The lipid analysis demonstrated that LLSO was not significantly distinct from SO in trans fat concentration after metabolism. Serum cholesterol and triglyceride levels were unchanged in LLSO fed compared to SO fed mice. In summary, LLSO which contained modification in αLA concentration showed similar effects on SK-Br3 as SO in both in vitro and in vivo. However, LLMOSO which contained more drastic modifications on FA composition exhibited less cytotoxicity compared to SO in vitro.
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    Green tea extract and epigallocatechin gallate decrease muscle pathology and NF-κB immunostaining in regenerating muscle fibers of mdx mice
    Evans, Nicholas Paul (Virginia Tech, 2009-09-25)
    Duchenne muscular dystrophy is a debilitating genetic disorder characterized by severe muscle wasting and early death in affected boys. The primary cause of this disease is mutations in the dystrophin gene resulting in the loss of the dystrophin protein from the plasma membrane of muscle fibers. In the absence of dystrophin, muscles undergo massive muscle degeneration and inflammation. Inflammation is believed to contribute substantially to dystrophic muscle pathology. The transcription factor NF-κB regulates inflammatory gene expression and provides a logical target for therapeutic treatments. Green tea extract and its primary polyphenol, epigallocatechin gallate, have been shown to have anti-inflammatory properties and to improve dystrophic muscle pathology. The purpose of these studies was to determine if dietary treatment with green tea extract or epigallocatechin gallate administered prior to disease onset could reduce dystrophic muscle pathology during the early disease time course and identify potential mechanisms through which NF-κB may be involved. Green tea extract has been shown to decrease muscle pathology and increase muscle function in mdx mice, a dystrophic mouse model. These changes have been attributed to the antioxidant potential of epigallocatechin gallate; however, other mechanisms such as suppression of the inflammatory response have not been evaluated. In the studies reported herein, both green tea extract and epigallocatechin gallate significantly decreased muscle pathology in mdx mice when provided in their diets prior to disease onset. In green tea extract (0.25% and 0.5%) treated mdx mice, serum creatine kinase, a systemic marker of muscle damage, was decreased by 85% at age 42 days. Normal fiber morphology in the tibialis anterior muscle was increased by 32% at this age (P≤0.05). The primary histopathological change was a 21% decrease in regenerating fibers (P≤0.05). NF-κB staining in central nuclei of regenerating fibers was decreased by 34% (P≤0.05). In epigallocatechin gallate (0.1%) treated mdx mice, serum creatine kinase was unchanged; however, normal fiber morphology in the tibialis anterior was increased by 20% at ages 28 and 42 days (P≤0.05). At age 42 days, the primary histopathological change was a 21% decrease in regenerating fibers (P≤0.05). NF-κB staining in central nuclei of regenerating muscle fibers was decreased by 21% at this age (P≤0.05). Epigallocatechin gallate appears to be the primary polyphenol of green tea extract responsible for many of the beneficial changes in dystrophic muscle. These data suggest that both green tea extract and epigallocatechin gallate decrease NF-κB activity in regenerating fibers resulting in reduced muscle pathology. Complimentary and alternative medicine approaches, including the use of green tea, provide important therapeutic options for ameliorating Duchenne muscular dystrophy. Green tea extract and epigallocatechin gallate are effective at decreasing muscle pathology potentially by reducing NF-κB activity in regenerating fibers in mdx mice. Use of these botanicals appears to elicit a beneficial response in dystrophic muscle that may ultimately lead to effective therapies for patients with this incurable disease.
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    The growth of murine breast cancer cells in dystrophic mice
    Meaney, Mary Patricia (Virginia Tech, 2011-09-26)
    The American Cancer Society predicted that 230,480 women would be diagnosed with, and 39,520 women would die from breast cancer (BC) in the United States in 2011. While the incidence of female BC has been decreasing, BC remains the second leading cause of cancer death among women in the United States. Cancer cachexia, the cancer-related loss of muscle, affects up to 25% of BC patients and is associated with poor prognosis and decreased quality of life. Alterations to the dystrophin glycoprotein complex (DGC), a transmembrane, multi-subunit protein complex with structural and signaling roles, have been reported in mammary tumors of BC patients and skeletal muscles of cachectic cancer patients. However, this complex is most frequently studied for its role in Duchenne muscular dystrophy (DMD), a severe, progressive muscle wasting disease. Despite the similar alterations reported in these diseases, it is unclear whether alterations in the DGC in one tissue can impact the progression of disease in another. Purpose: The purpose of the studies described in this dissertation was to identify differences in body composition, energy expenditure and plasma cytokine content between the C57BL/10ScSn-Dmdmdx/J (mdx) mouse model of DMD and C57BL/10ScSnJ (BL/10) control mice and to determine whether systemic alteration of the DGC (as observed in the mdx mouse) alters the growth of E0771 murine mammary tumors. Results: There were differences in body composition and plasma cytokine profiles between mdx and BL/10 mice. We also found that, relative to controls, the tumor–induced increase in cytokines that promote invasion and metastasis was not as severe in mdx mice. Conclusions: This study revealed several differences between mdx and BL/10 mice and provides support for the suggestion that the mdx mouse may not be an accurate model of DMD. In addition, the improved cytokine profile of tumor-bearing mdx mice suggests that the acute phase of DMD may be protective against BC invasion and metastasis. Further research should confirm this effect and determine whether alterations in the DGC of the mdx mouse are directly or indirectly responsible.
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    Is a Gluten-Free Diet Healthy for People Without Celiac Disease?
    Ju, Young H. (Virginia Cooperative Extension, 2016-04-15)
    Discusses gluten free diets in relation to celiac disease. Notes health benefits, and offers nutrition advice, and concerns.
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    Mechanisms of soy isoflavones in the regulation of vascular function
    Si, Hongwei (Virginia Tech, 2007-12-18)
    Cardiovascular diseases (CVD) are the leading cause of morbidity and mortality in the United States. It is also well recognized that the incidence of CVD is substantially increased in postmenopausal women due to the loss of estrogen. Experimental and clinical data support vascular protective effects of estrogen by various mechanisms. However, administration of estrogen is also associated with an increased incidence of heart disease which limits its therapeutic potential. Given the demonstrated risks of conventional estrogen therapy, a search for novel, cost-effective, alternative vasoactive agents for prevention of CVD is of major importance in the effort to decrease the burden of CVD morbidity. Genistein, a major soy isoflavone, may be one of those alternative agents because of its selective affinity to estrogen receptor-beta and various beneficial effects on CVD. However, the mechanism of the cardioprotective effects of genistein is still unclear. The objectives of this study were (1) to investigate the effect of genistein on the expression of endothelial nitric oxide synthase (eNOS) both in vitro and in vivo; (2) to define the mechanism by which genistein regulates eNOS expression; and, (3) to examine whether genistein protects against tumor necrosis factor-alpha (TNF-α)-induced apoptosis in human aortic endothelial cells (HAECs). The results demonstrated that genistein, at physiologically achievable concentrations (1-10 μM) in individuals consuming soy products, enhanced the expression of eNOS protein and subsequently elevated nitric oxie (NO) synthesis in both HAECs and human umbilical vein endothelial cells, concomitant with the increased eNOS mRNA expression (2.6-fold of control) and eNOS promoter activity, suggesting that genistein activates eNOS transcription. Furthermore, dietary supplementation of genistein to spontaneously hypertensive rats restored aortic eNOS levels, improved aortic wall thickness, and alleviated hypertension, confirming the biological relevance of the in vitro findings. However, the effects of genistein on eNOS and NO were not mediated by activation of estrogen signaling, mitogen-activated protein kinase, phosphatidylinositol 3-kinase/Akt kinase, protein kinase C or inhibition of typrosine kinases, but possibly through activating the cAMP/protein kinase A/cAMP responsive elemant binding protein pathway. These data suggest that genistein has direct genomic effects on the vascular wall that are unrelated to its known actions, leading to increase in eNOS expression and NO synthesis, thereby improving vascular homeostasis. We also found that genistein (5-10 μM) significantly inhibited TNF-α-induced apoptosis in HAECs as determined by caspase-3 activation, apoptotic cell detection and DNA laddering. The anti-apoptotic effect of genistein was associated with an enhanced expression of anti-apoptotic Bcl-2 protein and its promoter activity that was ablated by TNF-α. Moreover, this anti-apoptotic effect of genistein was not mediated by extracellular signal-regulated kinase 1/2, protein kinase A, or estrogen receptor. However, inhibition of p38 mitogen-activated protein kinase (p38) by SB203580 completely abolished the cytoprotective effect of genistein, suggesting that genistein acted through the p38-dependent pathway. Accordingly, stimulation of HAECs with genistein resulted in rapid and dose-dependent activation of p38. Unlike TNF-α which specifically activated p38α, genistein selectively induced phosphorylation of p38β, suggesting that p38β, but not p38α, is essential for the cytoprotective effect of genistein. These findings provide the evidence that genistein acts as a survival factor for vascular ECs to protect cells against apoptosis via activation of p38β. Taken together, the resuls of the present study suggest that genistein can act directly on vascular ECs, improves endothelium homeostasis by promoting eNOS expression and endothelial-derived NO synthesis through activating the cAMP/PKA/CREB cascade, and protects against TNF-α-induced apoptosis via activation of p38 β. These data potentially provide a basic mechanism underlying the physiological effects of genistein in the vasculature.
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    To Soy or Not to Soy: Effects of Soybeans on Breast Cancer, Menopause and Heart Disease
    Ju, Young H. (Virginia Cooperative Extension, 2016-03-29)
    Provides information about the potential health benefits of soybeans, focusing on those benefits that may lower the likelihood of breast cancer, and heart disease, and those benefits that may relieve hot flashes and other menopausal symptoms.
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    Understanding Cancer: What we know about breast cancer
    Rafie, Carlin; Zarghami, Fatemeh; Ju, Young H. (Virginia Cooperative Extension, 2017-01-04)
    Provides basic facts about breast cancer, including statistics, survival rate, types, symptoms, risks, treatment strategies, and prevention.
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    Understanding Cancer: What We Know About Colorectal Cancer
    Rafie, Carlin; Anderson, Cody; Zarghami, Fatemeh; Ju, Young H. (Virginia Cooperative Extension, 2016-05-19)
    Offers basic facts about colorectal cancer, including statistics on number of cases, number of deaths, chances of survival, symptoms, early detection, risk factors, high risk populations, and treatment strategies.
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    Understanding Cancer: What We Know About Lung Cancer
    Rafie, Carlin; Zarghami, Fatemeh; Ju, Young H. (Virginia Cooperative Extension, 2015-12-14)
    Provides information about lung cancer, including statistics, survival rate, types, symptoms, treatment, risks, and prevention.