57 research outputs found
Rising Seas: Representations of Antarctica, Climate Change, and Sea Level Rise in U.S. Newspaper Coverage
No full textData are stored in separate .csv/Excel files. All information identifying the coders of this data has been removed.A changing Antarctica carries large implications for global climate systems and sea level rise. However, how climate change is altering Antarctica and how these changes and their relevance are communicated in news media remains unclear. This study explores how Antarctica, climate change, and sea level rise are reported in news media by conducting a content analysis of Antarctic climate coverage in seven U.S. newspapers between March 2007 and December 2022. Findings suggest that newspaper reporting of Antarctica’s changing climate is limited, and that framed coverage about Antarctica, climate change, and sea level rise primarily emphasizes scientific and ecological implications.
Data used to conduct this study include:
1) A spreadsheet detailing article metadata for the 987 texts analyzed in this study. Details include the headline, outlet, author, data of publication, and ID number assigned to each article.
2) A spreadsheet containing the results of a content analysis of the 987 texts examined in this study. Analytical reliability was statistically assessed using a two-person inter-coder reliability process.Bruns, C.J.; Huffman, D.R.; Neff, P.D.; Timm, K.M.F.; Roop, H.A.. (2024). Rising Seas: Representations of Antarctica, Climate Change, and Sea Level Rise in U.S. Newspaper Coverage. Retrieved from the University Digital Conservancy, https://hdl.handle.net/11299/265195
Delta Np63 Knockdown Mice: A Mouse Model for AEC Syndrome
No full textDominant mutations in TP63 cause ankyloblepharon ectodermal dysplasia. and clefting (AEC), an ectodermal dysplasia characterized by skin fragility. Since Delta Np63 alpha is the predominantly expressed TP63 isoform, in postnatal skin, we hypothesized that mutant Delta Np63 alpha proteins are primarily responsible for skin fragility in AEC patients. We found that mutant Delta Np63 alpha proteins expressed in AEC patients function as dominant-negative molecules, suggesting that the human AEC skin phenotype could be mimicked in mouse skin by downregulating Delta Np63 alpha. Indeed, downregulating Delta Np63 expression in mouse epidermis caused severe skin erosions, which resembled lesions that develop in AEC patients. In both cases, lesions were characterized by suprabasal epidermal proliferation, delayed terminal differentiation, and basement membrane abnormalities. By failing to provide structural stability to the epidermis, these defects likely contribute to the observed skin fragility. The development of a mouse model for AEC will allow us to further unravel the genetic pathways that are normally regulated by Delta Np63 and that may be perturbed in AEC patients. Ultimately, these studies will not only contribute to our understanding of the molecular mechanisms that cause skin fragility in AEC patients, but may also result in the identification of targets for novel therapeutic approaches aimed at treating skin erosions. (C) 2009 Wiley-Liss, Inc
219 A skin cancer nursery: Hair follicles harbor epidermal neoplasms from immune surveillance
No full text128 Merging mass cytometry and flow-assisted cell sorting to simultaneously characterize a tumor and its microenvironment
No full textGender and Identity in Anita Desai's Postmodernist Narratives
No full textAnita Desai, a prominent Indian author, is known for her thought-provoking literary works that explore themes of identity, gender, and cultural conflicts. This research article examines Desai's postmodernist narratives through the lens of gender and identity. By analyzing selected works, including "Clear Light of Day," "Fasting, Feasting," and "In Custody," this study explores how Desai's characters navigate societal expectations, cultural traditions, and personal desires, offering a critique of traditional gender roles and highlighting the complexities of individual identity construction. The analysis reveals Desai's nuanced portrayal of gender dynamics and the challenges individuals face in negotiating their identities in a rapidly changing world
Withdrawn: Climate risk assessments and management options for redevelopment of the Parliamentary Complex in Samoa, South Pacific
No full textThis article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause.The full Elsevier Policy on Article Withdrawal can be found at http://www.elsevier.com/locate/withdrawalpolicy
Integration of Notch1 and calcineurin/NFAT signaling pathway in keratinocyte growth and differentiation control.
No full textNoThe Notch and Calcineurin/NFAT pathways have both been implicated in control of keratinocyte differentiation. Induction of the p21WAF1/Cip1 gene by Notch 1 activation in differentiating keratinocytes is associated with direct targeting of the RBP-J¿ protein to the p21 promoter. We show here that Notch 1 activation functions also through a second Calcineurin-dependent mechanism acting on the p21 TATA box-proximal region. Increased Calcineurin/NFAT activity by Notch signaling involves downregulation of Calcipressin, an endogenous Calcineurin inhibitor, through a HES-1-dependent mechanism. Besides control of the p21 gene, Calcineurin contributes significantly to the transcriptional response of keratinocytes to Notch 1 activation, both in vitro and in vivo. In fact, deletion of the Calcineurin B1 gene in the skin results in a cyclic alopecia phenotype, associated with altered expression of Notch-responsive genes involved in hair follicle structure and/or adhesion to the surrounding mesenchyme. Thus, an important interconnection exists between Notch 1 and Calcineurin-NFAT pathways in keratinocyte growth/differentiation control
Fos co-operation with PTEN loss elicits keratoacanthoma not carcinoma due to p53/p21<sup>WAF</sup>-induced differentiation triggered by GSK3b inactivation and reduced AKT activity
No full textTo investigate gene synergism in multistage skin carcinogenesis, the RU486-inducible cre/lox system was employed to ablate PTEN function [K14.cre/D5PTENflx] in mouse epidermis expressing activated v-fos [HK1.fos]. RU486-treated HK1.fos/D5PTENflx mice exhibited hyperplasia, hyperkeratosis and tumours that progressed to highly differentiated keratoacanthomas rather than carcinomas, due to re-expression of high p53 and p21WAF levels. Despite elevated MAP kinase activity, cyclin D1/E2 over expression and increased AKT activity forming areas of highly proliferative, papillomatous keratinocytes, increasing levels of GSK3b inactivation exceeded a threshold that induced p53/p21WAF expression to halt proliferation and accelerate differentiation, giving the hallmark keratosis of keratoacanthomas. A pivotal facet to this GSK3b-triggered mechanism centred on increasing p53 expression in basal layer keratinocytes. This reduced activated AKT expression and released inhibition of p21WAF, which accelerated keratinocyte differentiation, as indicated by unique basal layer expression of differentiation-specific keratin K1, alongside premature filaggrin and loricrin expression. Thus, fos synergism with PTEN loss elicited a benign tumour context where GSK3b-induced, p53/p21WAF expression continually switched AKT-associated proliferation into one of differentiation, preventing further progression. This putative compensatory mechanism required the critical availability of normal p53 and/or p21WAF otherwise deregulated fos, Akt and GSK3b associate with malignant progression
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