41 research outputs found

    Cruising The Borderlands: Queer Latinx Creating Space in Lowrider Culture

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    This ethnographic and interview-based study explores how queer Latinx lowriders create community through art, such as The Q Sides, an exhibition of photographs by Vero Majano, Kari Orvik, and DJ Brown Amy. Both lowrider culture and the queer Latinx community are marginalized communities that are often silenced, ignored, and not included in historical preservation or well documented. Lowrider culture and the queer Latinx community have largely been explored separately, such as ethnographer Ben Chappell and interdisciplinary scholar Michael Hames-García. My Senior Independent Study project examines the unique intersection of the queer Latinx experience in lowrider culture in the context of women of color feminist theory. My study employs activist scholarship and collaborative ethnographic methods to document the experience of the queer Latinx lowrider participants in The Q-Sides. My study highlights the ways that queer Latinx lowriders create space for their narrative through community dialogues and claiming their narrative in lowrider culture through The Q-Sides photography series

    The human DEK oncogene regulates DNA damage response signaling and repair

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    The human DEK gene is frequently overexpressed and sometimes amplified in human cancer. Consistent with oncogenic functions, Dek knockout mice are partially resistant to chemically induced papilloma formation. Additionally, DEK knockdown in vitro sensitizes cancer cells to DNA damaging agents and induces cell death via p53-dependent and -independent mechanisms. Here we report that DEK is important for DNA double-strand break repair. DEK depletion in human cancer cell lines and xenografts was sufficient to induce a DNA damage response as assessed by detection of γH2AX and FANCD2. Phosphorylation of H2AX was accompanied by contrasting activation and suppression, respectively, of the ATM and DNA-PK pathways. Similar DNA damage responses were observed in primary Dek knockout mouse embryonic fibroblasts (MEFs), along with increased levels of DNA damage and exaggerated induction of senescence in response to genotoxic stress. Importantly, Dek knockout MEFs exhibited distinct defects in non-homologous end joining (NHEJ) when compared to their wild-type counterparts. Taken together, the data demonstrate new molecular links between DEK and DNA damage response signaling pathways, and suggest that DEK contributes to DNA repair

    Antioxidant assessment of an anthocyanin-enriched blackberry extract

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    10.1016/j.foodchem.2006.02.060Food Chemistry10131052-1058FOCH

    Tryptophan from human milk induces oxidative stress and upregulates the Nrf-2-mediated stress response in human intestinal cell lines

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    Chemical screening of digested human milk protein using the oxygen radical absorbance capacity (ORAC FL) antioxidant assay confirmed the presence of a peptide fraction (PF23) with high antioxidant activity [5.53 mmol Trolox equivalents (TE)/g] that contained tryptophan as a main component. We evaluated the effects of both PF23 and tryptophan alone on the modulation of oxidative stress in cultured intestinal cells using a dichlorofluorescein diacetate probe. Despite the high ORAC FL value, PF23 enhanced (P< 0.05) 2, 2'-azobis (2-amidinopropane) dihydrochloride (peroxyl radical generator)-induced intracellular oxidation in the Caco-2 human adenocarcinoma cell line, suggesting prooxidant activity. Compared to selected peptide fractions with relatively lower ORAC FL values, PF23 induced oxidative stress more than all other peptide fractions tested (P< 0.05) and contained more tryptophan than the others (P< 0.05). Similar prooxidant activity was observed for tryptophan when it was added to culture medium for both the Caco-2 cells and FHs 74 Int primary fetal enterocytes, while also exhibiting a high ORAC FL value (9.69 mmol TE/g). The effect of tryptophan that involves activation of the Nrf-2 pathway and transcription of antioxidant enzymes was therefore investigated in FHs 74 Int cells. Exposure of infant intestinal cells to tryptophan resulted in Nrf-2 activation and an increase in the gene transcript level of glutathione peroxidase 2. We conclude that tryptophan-induced oxidative stress associated with tryptophan-containing milk peptides induces an adaptive response that involves the activation of the antioxidant responsive signaling pathway in intestinal cells

    Tryptophan released from mother's milk has antioxidant properties

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    Bioactive factors in human milk (HM) are crucial to the health of newborns, especially preterm infants. These compounds assist in reducing the oxidative stress that may occur as a result of combined exposure to supplemental oxygen and immature physiologic defenses. To identify the components in HM that contribute to its greater resistance to oxidative stress compared with infant formulae, enzymatic hydrolysates of HM were prepared, ultrafiltered, separated, and analyzed for antioxidant potential. The antioxidant activity [μM Trolox equivalent (TE/g)] of nondigested milk, whole digested milk, and derived ultrafiltrates were 80.4 ± 13.3, 159.0 ± 5.6, and 127.4 ± 3.1, respectively. An HPLC fraction denoted as fraction 23 (5274 ± 630 μM TE/g) was obtained and its constituents identified as tryptophan (Trp), peptides HNPI, and PLAPQA. Scavenging activity was not observed for PLAPQA, whereas moderate activity was associated with HNPI (144 ± 10.7 μM TE/g) and very high activity to Trp (7986 ± 468 μM TE/g). Trp addition to HM and two infant formulas significantly increased formulae antioxidant properties. Trp appeared to be a powerful free radical scavenger naturally present in HM. Its antioxidant effects and potential application in the diets of infants, particularly preterm, must be examined further
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