Supplementation of Laying-Hen Feed with Palm Tocos and Algae Astaxanthin for Egg Yolk Nutrient Enrichment

Adding supplements to hen feed can increase egg nutritional value. Astaxanthin, tocotrienols, and tocopherols are potent antioxidants that provide health benefits to humans. We hypothesized that the addition of these nutrients to hen feed would result in an increased nutrient content in egg yolk with minimum changes in functional properties. Laying hens (Hy-Line W-36 breed) were fed four diets with different supplementation levels of palm toco concentrate and algae biomass containing astaxanthin for 8 weeks. Egg yolks were analyzed for physical, chemical, and functional properties. The feed with the highest nutrient concentration was also studied for stability of these antioxidants using the Arrhenius approach. No significant differences were observed in functional properties except for emulsification capacity and sensory characteristics among eggs from different diet treatments. Changes in egg yolk color reached the maximum values at day 8. Incorporation of tocopherols and tocotrienols increased until day 8, astaxanthin incorporation increased until day 10, and all decreased thereafter. Feed nutrients resulted in a dose–response relationship of these compounds in the egg yolk. The transfer efficiency ranged from 0 to 9.9% for tocotrienols and tocopherols and from 7.6 to 14.9% for astaxanthin at their peak values. Results of the Arrhenius accelerated stability study showed significant differences in the shelf life of various nutrients, and these results can be used to properly formulate and store the feed materials

Oxidative stability of corn oil with elevated tocotrienols

Oxidation of tocotrienol enriched corn oil was measured for primary oxidative products, lipid hydroperoxides and quantified by peroxide value (PV). Oxidative Stability Index (OSI) was used to determine the induction period (hrs) by indirect measurement of volatile secondary oxidation products, mainly formic acid. Vitamin E stripped corn oil samples were spiked with individual tocotrienols or tocopherols (collectively, tocols) at concentrations between 100 and 5,000 ppm. A positive relationship was observed between the concentration of all tocols and inhibition of the formation of secondary products. Gamma tocotrienol (γ-T3) provided the most protection, with delta tocopherol (δ-T) and delta tocotrienol (δ-T3) providing similar protection. Alpha tocotrienol (α-T3) and alpha tocopherol (α-T) followed a similar trend but with diminishing capacity at concentrations higher than 700 ppm. The change in mean daily peroxide value increased as α- tocopherol and α- tocotrienol concentrations increased. When compared against the non-spiked, stripped control oil, both α- tocopherol and α- tocotrienol demonstrated better antioxidant effects at lower concentrations and actually promoted oxidation at concentrations at 700 ppm and above. These effects were not observed with the γ- and δ- tocols. Crude oils from corn kernels, both control and that expressing a homogentisate geranylgeranyl transferase (HGGT) gene, were tested for oxidative stability. No pro-oxidant effects were observed in the modified crude corn oil containing up to 5,000 ppm tocotrienols (6,200 ppm total tocotrienols and tocopherols) when compared to the control crude corn oil containing 300 ppm tocotrienols (1,500 ppm total tocols)

Impact of ADC non-linearities on the sensitivity to sterile keV neutrinos with a KATRIN-like experiment

International audienceADC non-linearities are a major systematic effect in the search for keV-scale sterile neutrinos with tritium β -decay experiments like KATRIN. They can significantly distort the spectral shape and thereby obscure the tiny kink-like signature of a sterile neutrino. In this work we demonstrate various mitigation techniques to reduce the impact of ADC non-linearities on the tritium β -decay spectrum to a level of <ppm . The best results are achieved with a multi-pixel ( ≥104 pixels) detector using full waveform digitization. In this case, active-to-sterile mixing angles of the order of sin2θ=10−7 would be accessible from the viewpoint of ADC non-linearities. With purely peak-sensing ADCs a comparable sensitivity could be reached with highly linear ADCs, sufficient non-linearity corrections or by increasing the number of pixels to ≥105

HMGA1 Induces Intestinal Polyposis in Transgenic Mice and Drives Tumor Progression and Stem Cell Properties in Colon Cancer Cells

Although metastatic colon cancer is a leading cause of cancer death worldwide, the molecular mechanisms that enable colon cancer cells to metastasize remain unclear. Emerging evidence suggests that metastatic cells develop by usurping transcriptional networks from embryonic stem (ES) cells to facilitate an epithelial-mesenchymal transition (EMT), invasion, and metastatic progression. Previous studies identified HMGA1 as a key transcription factor enriched in ES cells, colon cancer, and other aggressive tumors, although its role in these settings is poorly understood.To determine how HMGA1 functions in metastatic colon cancer, we manipulated HMGA1 expression in transgenic mice and colon cancer cells. We discovered that HMGA1 drives proliferative changes, aberrant crypt formation, and intestinal polyposis in transgenic mice. In colon cancer cell lines from poorly differentiated, metastatic tumors, knock-down of HMGA1 blocks anchorage-independent cell growth, migration, invasion, xenograft tumorigenesis and three-dimensional colonosphere formation. Inhibiting HMGA1 expression blocks tumorigenesis at limiting dilutions, consistent with depletion of tumor-initiator cells in the knock-down cells. Knock-down of HMGA1 also inhibits metastatic progression to the liver in vivo. In metastatic colon cancer cells, HMGA1 induces expression of Twist1, a gene involved in embryogenesis, EMT, and tumor progression, while HMGA1 represses E-cadherin, a gene that is down-regulated during EMT and metastatic progression. In addition, HMGA1 is among the most enriched genes in colon cancer compared to normal mucosa.Our findings demonstrate for the first time that HMGA1 drives proliferative changes and polyp formation in the intestines of transgenic mice and induces metastatic progression and stem-like properties in colon cancer cells. These findings indicate that HMGA1 is a key regulator, both in metastatic progression and in the maintenance of a stem-like state. Our results also suggest that HMGA1 or downstream pathways could be rational therapeutic targets in metastatic, poorly differentiated colon cancer

HMGA1 drives stem cell, inflammatory pathway, and cell cycle progression genes during lymphoid tumorigenesis

<p>Abstract</p> <p>Background</p> <p>Although the <it>high mobility group A1 </it>(<it>HMGA1</it>) gene is widely overexpressed in diverse cancers and portends a poor prognosis in some tumors, the molecular mechanisms that mediate its role in transformation have remained elusive. <it>HMGA1 </it>functions as a potent oncogene in cultured cells and induces aggressive lymphoid tumors in transgenic mice. Because HMGA1 chromatin remodeling proteins regulate transcription, <it>HMGA1 </it>is thought to drive malignant transformation by modulating expression of specific genes. Genome-wide studies to define HMGA1 transcriptional networks during tumorigenesis, however, are lacking. To define the HMGA1 transcriptome, we analyzed gene expression profiles in lymphoid cells from <it>HMGA1a </it>transgenic mice at different stages in tumorigenesis.</p> <p>Results</p> <p>RNA from lymphoid samples at 2 months (before tumors develop) and 12 months (after tumors are well-established) was screened for differential expression of > 20,000 unique genes by microarray analysis (Affymetrix) using a parametric and nonparametric approach. Differential expression was confirmed by quantitative RT-PCR in a subset of genes. Differentially expressed genes were analyzed for cellular pathways and functions using Ingenuity Pathway Analysis. Early in tumorigenesis, HMGA1 induced inflammatory pathways with NFkappaB identified as a major node. In established tumors, HMGA1 induced pathways involved in cell cycle progression, cell-mediated immune response, and cancer. At both stages in tumorigenesis, HMGA1 induced pathways involved in cellular development, hematopoiesis, and hematologic development. Gene set enrichment analysis showed that stem cell and immature T cell genes are enriched in the established tumors. To determine if these results are relevant to human tumors, we knocked-down HMGA1 in human T-cell leukemia cells and identified a subset of genes dysregulated in both the transgenic and human lymphoid tumors.</p> <p>Conclusions</p> <p>We found that <it>HMGA1 </it>induces inflammatory pathways early in lymphoid tumorigenesis and pathways involved in stem cells, cell cycle progression, and cancer in established tumors. <it>HMGA1 </it>also dyregulates genes and pathways involved in stem cells, cellular development and hematopoiesis at both early and late stages of tumorigenesis. These results provide insight into <it>HMGA1 </it>function during tumor development and point to cellular pathways that could serve as therapeutic targets in lymphoid and other human cancers with aberrant <it>HMGA1 </it>expression.</p

HMGA1 Reprograms Somatic Cells into Pluripotent Stem Cells by Inducing Stem Cell Transcriptional Networks

PMC3499526BACKGROUND: Although recent studies have identified genes expressed in human embryonic stem cells (hESCs) that induce pluripotency, the molecular underpinnings of normal stem cell function remain poorly understood. The high mobility group A1 (HMGA1) gene is highly expressed in hESCs and poorly differentiated, stem-like cancers; however, its role in these settings has been unclear. METHODS/PRINCIPAL FINDINGS: We show that HMGA1 is highly expressed in fully reprogrammed iPSCs and hESCs, with intermediate levels in ECCs and low levels in fibroblasts. When hESCs are induced to differentiate, HMGA1 decreases and parallels that of other pluripotency factors. Conversely, forced expression of HMGA1 blocks differentiation of hESCs. We also discovered that HMGA1 enhances cellular reprogramming of somatic cells to iPSCs together with the Yamanaka factors (OCT4, SOX2, KLF4, cMYC - OSKM). HMGA1 increases the number and size of iPSC colonies compared to OSKM controls. Surprisingly, there was normal differentiation in vitro and benign teratoma formation in vivo of the HMGA1-derived iPSCs. During the reprogramming process, HMGA1 induces the expression of pluripotency genes, including SOX2, LIN28, and cMYC, while knockdown of HMGA1 in hESCs results in the repression of these genes. Chromatin immunoprecipitation shows that HMGA1 binds to the promoters of these pluripotency genes in vivo. In addition, interfering with HMGA1 function using a short hairpin RNA or a dominant-negative construct blocks cellular reprogramming to a pluripotent state. CONCLUSIONS: Our findings demonstrate for the first time that HMGA1 enhances cellular reprogramming from a somatic cell to a fully pluripotent stem cell. These findings identify a novel role for HMGA1 as a key regulator of the stem cell state by inducing transcriptional networks that drive pluripotency. Although further studies are needed, these HMGA1 pathways could be exploited in regenerative medicine or as novel therapeutic targets for poorly differentiated, stem-like cancers.JH Libraries Open Access Fun

Oxidative stability of corn oil with elevated tocotrienols

Oxidation of tocotrienol enriched corn oil was measured for primary oxidative products, lipid hydroperoxides and quantified by peroxide value (PV). Oxidative Stability Index (OSI) was used to determine the induction period (hrs) by indirect measurement of volatile secondary oxidation products, mainly formic acid. Vitamin E stripped corn oil samples were spiked with individual tocotrienols or tocopherols (collectively, tocols) at concentrations between 100 and 5,000 ppm. A positive relationship was observed between the concentration of all tocols and inhibition of the formation of secondary products. Gamma tocotrienol (γ-T3) provided the most protection, with delta tocopherol (δ-T) and delta tocotrienol (δ-T3) providing similar protection. Alpha tocotrienol (α-T3) and alpha tocopherol (α-T) followed a similar trend but with diminishing capacity at concentrations higher than 700 ppm. The change in mean daily peroxide value increased as α- tocopherol and α- tocotrienol concentrations increased. When compared against the non-spiked, stripped control oil, both α- tocopherol and α- tocotrienol demonstrated better antioxidant effects at lower concentrations and actually promoted oxidation at concentrations at 700 ppm and above. These effects were not observed with the γ- and δ- tocols. Crude oils from corn kernels, both control and that expressing a homogentisate geranylgeranyl transferase (HGGT) gene, were tested for oxidative stability. No pro-oxidant effects were observed in the modified crude corn oil containing up to 5,000 ppm tocotrienols (6,200 ppm total tocotrienols and tocopherols) when compared to the control crude corn oil containing 300 ppm tocotrienols (1,500 ppm total tocols).</p

Supplementation of Laying-Hen Feed with Palm Tocos and Algae Astaxanthin for Egg Yolk Nutrient Enrichment

Adding supplements to hen feed can increase egg nutritional value. Astaxanthin, tocotrienols, and tocopherols are potent antioxidants that provide health benefits to humans. We hypothesized that the addition of these nutrients to hen feed would result in an increased nutrient content in egg yolk with minimum changes in functional properties. Laying hens (Hy-Line W-36 breed) were fed four diets with different supplementation levels of palm toco concentrate and algae biomass containing astaxanthin for 8 weeks. Egg yolks were analyzed for physical, chemical, and functional properties. The feed with the highest nutrient concentration was also studied for stability of these antioxidants using the Arrhenius approach. No significant differences were observed in functional properties except for emulsification capacity and sensory characteristics among eggs from different diet treatments. Changes in egg yolk color reached the maximum values at day 8. Incorporation of tocopherols and tocotrienols increased until day 8, astaxanthin incorporation increased until day 10, and all decreased thereafter. Feed nutrients resulted in a dose–response relationship of these compounds in the egg yolk. The transfer efficiency ranged from 0 to 9.9% for tocotrienols and tocopherols and from 7.6 to 14.9% for astaxanthin at their peak values. Results of the Arrhenius accelerated stability study showed significant differences in the shelf life of various nutrients, and these results can be used to properly formulate and store the feed materials.Posted with permission from Journal of Agricultural and Food Chemistry, 60, no. 8 (2012): 1989–1999, doi: 10.1021/jf204763f. Copyright 2012 American Chemical Society.</p