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Author Monge-Rojas, R.; Fuster-Baraona, T.; Garita-Arce, C.; Sanchez-Lopez, M.; Colon-Ramos, U.; Smith-Castro, V.
Title How Self-Objectification Impacts Physical Activity Among Adolescent Girls in Costa Rica Type Journal Article
Year 2017 Publication Journal of Physical Activity & Health Abbreviated Journal J Phys Act Health
Volume 14 Issue (down) 2 Pages 123-129
Keywords Adolescent; *Adolescent Behavior; Body Image/*psychology; Costa Rica; Cultural Characteristics; *Exercise; Female; Focus Groups; Humans; Male; Women's Health; Latin America; female identity; machismo; sexual harassment
Abstract BACKGROUND: In Latin America, more than 80% of adolescent girls are physically inactive. Inactivity may be reinforced by female stereotypes and objectification in the Latin American sociocultural context. METHODS: We examined the influence of objectification on the adoption of an active lifestyle among 192 adolescents (14 and 17 years old) from urban and rural areas in Costa Rica. Analyses of 48 focus-groups sessions were grounded in Objectification Theory. RESULTS: Vigorous exercises were gender-typed as masculine while girls had to maintain an aesthetic appearance at all times. Adolescents described how girls were anxious around the prospect of being shamed and sexually objectified during exercises. This contributed to a decrease in girls' desire to engage in physical activities. Among males, there is also a budding tolerance of female participation in vigorous sports, as long as girls maintained a feminine stereotype outside their participation. CONCLUSION: Self-objectification influenced Costa Rican adolescent girls' decisions to participate in physical activities. Interventions may include: procuring safe environments for physical activity where girls are protected from fear of ridicule and objectification; sensitizing boys about girl objectification and fostering the adoption of a modern positive masculine and female identities to encourage girls' participation in sports.
Address
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1543-3080 ISBN Medium
Area Expedition Conference
Notes PMID:27775480 Approved no
Call Number ref @ user @ Serial 98041
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Author Brodie, S.; Lee, H.K.; Jiang, W.; Cazacu, S.; Xiang, C.; Poisson, L.M.; Datta, I.; Kalkanis, S.; Ginsberg, D.; Brodie, C.
Title The novel long non-coding RNA TALNEC2, regulates tumor cell growth and the stemness and radiation response of glioma stem cells Type Journal Article
Year 2017 Publication Oncotarget Abbreviated Journal Oncotarget
Volume 8 Issue (down) 19 Pages 31785-31801
Keywords Talnec2; glioblastoma; glioma stem cells; long non-cording RNAs; mesenchymal transformation
Abstract Despite advances in novel therapeutic approaches for the treatment of glioblastoma (GBM), the median survival of 12-14 months has not changed significantly. Therefore, there is an imperative need to identify molecular mechanisms that play a role in patient survival. Here, we analyzed the expression and functions of a novel lncRNA, TALNEC2 that was identified using RNA seq of E2F1-regulated lncRNAs. TALNEC2 was localized to the cytosol and its expression was E2F1-regulated and cell-cycle dependent. TALNEC2 was highly expressed in GBM with poor prognosis, in GBM specimens derived from short-term survivors and in glioma cells and glioma stem cells (GSCs). Silencing of TALNEC2 inhibited cell proliferation and arrested the cells in the G1\S phase of the cell cycle in various cancer cell lines. In addition, silencing of TALNEC2 decreased the self-renewal and mesenchymal transformation of GSCs, increased sensitivity of these cells to radiation and prolonged survival of mice bearing GSC-derived xenografts. Using miRNA array analysis, we identified specific miRNAs that were altered in the silenced cells that were associated with cell-cycle progression, proliferation and mesenchymal transformation. Two of the downregulated miRNAs, miR-21 and miR-191, mediated some of TALNEC2 effects on the stemness and mesenchymal transformation of GSCs. In conclusion, we identified a novel E2F1-regulated lncRNA that is highly expressed in GBM and in tumors from patients of short-term survival. The expression of TALNEC2 is associated with the increased tumorigenic potential of GSCs and their resistance to radiation. We conclude that TALNEC2 is an attractive therapeutic target for the treatment of GBM.
Address Davidson Laboratory of Cell Signaling and Tumorigenesis, Hermelin Brain Tumor Center, Department of Neurosurgery, Detroit, MI, USA
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1949-2553 ISBN Medium
Area Expedition Conference
Notes PMID:28423669 Approved no
Call Number ref @ user @ Serial 96594
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Author Yin, J.; Oh, Y.T.; Kim, J.-Y.; Kim, S.S.; Choi, E.; Kim, T.H.; Hong, J.H.; Chang, N.; Cho, H.J.; Sa, J.K.; Kim, J.C.; Kwon, H.J.; Park, S.; Lin, W.; Nakano, I.; Gwak, H.-S.; Yoo, H.; Lee, S.-H.; Lee, J.; Kim, J.H.; Kim, S.-Y.; Nam, D.-H.; Park, M.-J.; Park, J.B.
Title Transglutaminase 2 Inhibition Reverses Mesenchymal Transdifferentiation of Glioma Stem Cells by Regulating C/EBPbeta Signaling Type Journal Article
Year 2017 Publication Cancer Research Abbreviated Journal Cancer Res
Volume 77 Issue (down) 18 Pages 4973-4984
Keywords
Abstract Necrosis is a hallmark of glioblastoma (GBM) and is responsible for poor prognosis and resistance to conventional therapies. However, the molecular mechanisms underlying necrotic microenvironment-induced malignancy of GBM have not been elucidated. Here, we report that transglutaminase 2 (TGM2) is upregulated in the perinecrotic region of GBM and triggered mesenchymal (MES) transdifferentiation of glioma stem cells (GSC) by regulating master transcription factors (TF), such as C/EBPbeta, TAZ, and STAT3. TGM2 expression was induced by macrophages/microglia-derived cytokines via NF-kappaB activation and further degraded DNA damage-inducible transcript 3 (GADD153) to induce C/EBPbeta expression, resulting in expression of the MES transcriptome. Downregulation of TGM2 decreased sphere-forming ability, tumor size, and radioresistance and survival in a xenograft mouse model through a loss of the MES signature. A TGM2-specific inhibitor GK921 blocked MES transdifferentiation and showed significant therapeutic efficacy in mouse models of GSC. Moreover, TGM2 expression was significantly increased in recurrent MES patients and inversely correlated with patient prognosis. Collectively, our results indicate that TGM2 is a key molecular switch of necrosis-induced MES transdifferentiation and an important therapeutic target for MES GBM. Cancer Res; 77(18); 4973-84. (c)2017 AACR.
Address Specific Organs Cancer Branch, Research Institute and Hospital, National Cancer Center, Goyang, Korea
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0008-5472 ISBN Medium
Area Expedition Conference
Notes PMID:28754668 Approved no
Call Number ref @ user @ Serial 96575
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Author Sareddy, G.R.; Viswanadhapalli, S.; Surapaneni, P.; Suzuki, T.; Brenner, A.; Vadlamudi, R.K.
Title Novel KDM1A inhibitors induce differentiation and apoptosis of glioma stem cells via unfolded protein response pathway Type Journal Article
Year 2017 Publication Oncogene Abbreviated Journal Oncogene
Volume 36 Issue (down) 17 Pages 2423-2434
Keywords Animals; Apoptosis/*drug effects; Cell Differentiation/*drug effects; Cell Line, Tumor; Cell Survival/drug effects; Cell Transformation, Neoplastic; Disease Progression; Enzyme Inhibitors/*pharmacology; Gene Expression Regulation, Neoplastic/drug effects; Glioma/*pathology; Histone Demethylases/*antagonists & inhibitors; Mice; Neoplastic Stem Cells/*drug effects/metabolism/pathology; Signal Transduction/drug effects; Survival Analysis; Transcription, Genetic/drug effects; Unfolded Protein Response/*drug effects
Abstract Glioma stem cells (GSCs) have a central role in glioblastoma (GBM) development and chemo/radiation resistance, and their elimination is critical for the development of efficient therapeutic strategies. Recently, we showed that lysine demethylase KDM1A is overexpressed in GBM. In the present study, we determined whether KDM1A modulates GSCs stemness and differentiation and tested the utility of two novel KDM1A-specific inhibitors (NCL-1 and NCD-38) to promote differentiation and apoptosis of GSCs. The efficacy of KDM1A targeting drugs was tested on purified GSCs isolated from established and patient-derived GBMs using both in vitro assays and in vivo orthotopic preclinical models. Our results suggested that KDM1A is highly expressed in GSCs and knockdown of KDM1A using shRNA-reduced GSCs stemness and induced the differentiation. Pharmacological inhibition of KDM1A using NCL-1 and NCD-38 significantly reduced the cell viability, neurosphere formation and induced apoptosis of GSCs with little effect on differentiated cells. In preclinical studies using orthotopic models, NCL-1 and NCD-38 significantly reduced GSCs-driven tumor progression and improved mice survival. RNA-sequencing analysis showed that KDM1A inhibitors modulate several pathways related to stemness, differentiation and apoptosis. Mechanistic studies showed that KDM1A inhibitors induce activation of the unfolded protein response (UPR) pathway. These results strongly suggest that selective targeting of KDM1A using NCL-1 and NCD-38 is a promising therapeutic strategy for elimination of GSCs.
Address Cancer Therapy and Research Center, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0950-9232 ISBN Medium
Area Expedition Conference
Notes PMID:27893719 Approved no
Call Number ref @ user @ Serial 96621
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Author Godin, K.M.; Chacon, V.; Barnoya, J.; Leatherdale, S.T.
Title The school environment and sugar-sweetened beverage consumption among Guatemalan adolescents Type Journal Article
Year 2017 Publication Public Health Nutrition Abbreviated Journal Public Health Nutr
Volume 20 Issue (down) 16 Pages 2980-2987
Keywords Latin America; Nutrition policy; School health; Sugar-sweetened beverages
Abstract OBJECTIVE: The current study sought to examine Guatemalan adolescents' consumption of sugar-sweetened beverages (SSB), identify which individual-level characteristics are associated with SSB consumption and describe school characteristics that may influence students' SSB consumption. DESIGN: Within this observational pilot study, a questionnaire was used to assess students' consumption of three varieties of SSB (soft drinks, energy drinks, sweetened coffees/teas), as well as a variety of sociodemographic and behavioural characteristics. We collected built environment data to examine aspects of the school food environment. We developed Poisson regression models for each SSB variety and used descriptive analyses to characterize the sample. SETTING: Guatemala City, Guatemala. SUBJECTS: Guatemalan adolescents (n 1042) from four (two public, two private) secondary schools. RESULTS: Built environment data revealed that students from the two public schools lacked access to water fountains/coolers. The SSB industry had a presence in the schools through advertisements, sponsored food kiosks and products available for sale. Common correlates of SSB consumption included school type, sedentary behaviour, frequency of purchasing lunch in the cafeteria, and frequency of purchasing snacks from vending machines in school and off school property. CONCLUSIONS: Guatemalan adolescents frequently consume SSB, which may be encouraged by aspects of the school environment. Schools represent a viable setting for equitable population health interventions designed to reduce SSB consumption, including increasing access to clean drinking-water, reducing access to SSB, restricting SSB marketing and greater enforcement of existing food policies.
Address 1School of Public Health and Health Systems,University of Waterloo, 200 University Avenue West,Waterloo,ON,Canada,N2L 3G1
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1368-9800 ISBN Medium
Area Expedition Conference
Notes PMID:28803573 Approved no
Call Number ref @ user @ Serial 97159
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