26 research outputs found

    The Effects of Non-Nutritive Sweeteners on the Health of Youth in United States

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    Obesity results from a multitude of problems from depression, an imbalance in hormones, genetics, environmental factors, and can also result from a poor diet, where we are focusing our attention. A strong correlation is made with low income and obesity in children. In 2014, 14.5% of patients ages 2-4 were obese. From 2011 to 2014 17% of adolescents experienced obesity and this affects around 12.7 million people. Statistics have shown the as the age increases in adolescents, so does the prevalence of obesity

    Effects of Excessive Sugar Consumption in Adolescents

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    With sugar consumption in the youth on the rise, many people have turned their heads towards this epidemic in response to the many side effects associated with excess sugar in the diet. Roughly 75% of all foods and beverages have some form of added sugar. It’s difficult to find a safe product for your child to eat without running into something like high fructose corn syrup (HFCS). Sugar-sweetened beverage intake has increased nearly 500% since 1950. This excessive sugar intake is very taxing on the body and may lead to long term impairments if not properly regulated. A study documented that drinking two 16-oz sugar-sweetened beverages every day over a time span of 6 months induced features of metabolic syndrome and fatty liver. Chronic conditions such as diabetes and CVD may occur if the consumption of sugar remains too high

    Case Report Asparaginase-Induced Hypertriglyceridemia Presenting as Pseudohyponatremia during Leukemia Treatment

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    Asparaginase is a chemotherapeutic agent used to induce disease remission in children with acute lymphoblastic leukemia (ALL). We describe the cases of two females with ALL who developed pseudohyponatremia as a presentation of hypertriglyceridemia following asparaginase treatment. Nine similar published cases of asparaginase-induced hypertriglyceridemia and its complications are also discussed. Possible mechanisms of action include inhibition of lipoprotein lipase, decreased hepatic synthesis of lipoprotein, and increased synthesis of VLDL. Effects of asparaginase-induced hypertriglyceridemia range from asymptomatic to transaminasemia, pancreatitis, and life-threatening thrombosis or hyperviscosity syndrome. All cases of hypertriglyceridemia described resolved following cessation of asparaginase treatment ± further treatments

    Germ cells are not required to establish the female pathway in mouse fetal gonads.

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    The fetal gonad is composed of a mixture of somatic cell lineages and germ cells. The fate of the gonad, male or female, is determined by a population of somatic cells that differentiate into Sertoli or granulosa cells and direct testis or ovary development. It is well established that germ cells are not required for the establishment or maintenance of Sertoli cells or testis cords in the male gonad. However, in the agametic ovary, follicles do not form suggesting that germ cells may influence granulosa cell development. Prior investigations of ovaries in which pre-meiotic germ cells were ablated during fetal life reported no histological changes during stages prior to birth. However, whether granulosa cells underwent normal molecular differentiation was not investigated. In cases where germ cell loss occurred secondary to other mutations, transdifferentiation of granulosa cells towards a Sertoli cell fate was observed, raising questions about whether germ cells play an active role in establishing or maintaining the fate of granulosa cells. We developed a group of molecular markers associated with ovarian development, and show here that the loss of pre-meiotic germ cells does not disrupt the somatic ovarian differentiation program during fetal life, or cause transdifferentiation as defined by expression of Sertoli markers. Since we do not find defects in the ovarian somatic program, the subsequent failure to form follicles at perinatal stages is likely attributable to the absence of germ cells rather than to defects in the somatic cells

    Characterization of ovarian cell lineages.

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    <p>(A–D) Ovaries were dissected from 14.5 dpc embryos expressing <i>αSma-EYFP</i> (red) and were immunostained for PECAM1 to label germ cells and vasculature (blue) and an additional somatic marker (green). (A) Laminin (green) is observed in the coelomic domain and around <i>αSma-EYFP</i>-expressing cells and vasculature (blue). (B) MAFB (green) marks both the nuclei of <i>αSma-EYFP-</i>expressing cells and non-<i>αSma-EYFP</i> expressing cells. Both cell types are closely associated with vasculature. (C) WT1 (green) is expressed in all non-endothelial somatic cells of the ovary, including <i>αSma-EYFP-</i>positive cells (C, yellow nuclei, inset in right panel). (D) FOXL2 (green), a marker of the pregranulosa cell lineage, is expressed in <i>αSma-EYFP-</i>negative somatic cells. <i>αSma-EYFP</i>/FOXL2 double-positive cells were occasionally observed (D, inset in right panel). (E–F) Gonads were collected from 12.5 dpc <i>Wnt4<sup>GC</sup></i> embryos. <i>Wnt4</i>-expressing cells, only detectable using an antibody to GFP (green), were present throughout the mesonephros of both XX (E) and XY samples (inset in E). <i>Wnt4</i>-expressing cells were present in the gonad only in XX samples (E) and <i>Wnt4</i> expression overlapped with FOXL2 in many cells (F and F′). Whole mount immunostaining was performed on all samples. The scale bar in panel (A) represents 50 µm in panels A–F, 18.5 µm in all insets except E (20.8 µm) and 16.5 µm in panel G′.</p

    Ovaries lacking germ cells do not transdifferentiate towards a Sertoli cell fate.

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    <p>(A–C) SOX9 (red) and FOXL2 (green) immunostaining of cryosectioned 17.5 dpc gonads. (A) XY <i>Kit<sup>+/+</sup></i> testes express SOX9, but not FOXL2 (XY germ cells exhibit high background staining). (B–C) XX <i>Kit<sup>+/+</sup></i> and <i>Kit<sup>Wv/Wv</sup></i> ovaries express only FOXL2 and show no evidence of transdifferentiation. (D–F) AMH (red) and SCP3 (green) immunostaining of the same samples as in A–C. (D) As expected, XY <i>Kit<sup>+/+</sup></i> testes express AMH, but not the meiotic germ cell marker SCP3. (E–F) XX <i>Kit<sup>+/+</sup></i> and <i>Kit<sup>Wv/Wv</sup></i> ovaries do not express AMH. SCP3 immunostaining confirms significant germ cell loss in <i>Kit<sup>Wv/Wv</sup></i> ovaries (E,F). All samples were cryosectioned then immunostained. The scale bar represents 50 µm in all panels. The dotted line demarcates the boundary of the ovary.</p
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