98,025 research outputs found
Joshua Davis: Author of Spare Parts
No full textCitation: K-State First (2016). Joshua Davis: Author of Spare Parts [Flier]. Manhattan, Kansas: K-State First.Flyer advertising Joshua Davis's author talk at Kansas State University
Steven Johnson Author Talk Poster
No full textK-State Book NetworkA poster advertising an author talk by Steven Johnson at Kansas State University on September 3, 2014. Steven Johnson's book "The Ghost Map" was the 2014-2015 common book
The potential of maternal and child health service data in Australia: how lessons from the COVID-19 pandemic can accelerate data-informed decision making
No full textPerspectiveAshleigh Shipton, Meredith O, Connor, Melissa Wake, Sharon Goldfeld, Helen Lees, Catina Adams, Kristina Edvardsson, Leesa Hooker, Jatender Mohal, Rhiannon M Pilkington, Fiona K Mensa
Going Beyond Counting First Authors in Author Co-citation Analysis
No full textThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Exploring the genome-wide impact of estrogen receptor alpha and estrogen receptor beta in breast and colon cancer cells
No full textEstrogen signaling is involved in the development and progression of breast cancer and is implicated to be protective in colon cancer. Estrogenic actions are conveyed through transcriptional regulation by ligand stimulated estrogen receptors (ERα and ERβ). ERα is upregulated in most breast cancers and is responsible for the proliferative effect of estrogen. ERβ on the other hand is usually downregulated, and studies indicate an antiproliferative function. Therapies targeting ERα are available and commonly used in the treatment of breast cancer. In the normal colonic epithelia, however, ERβ is the most abundant estrogen receptor and the suggested mediator of the protective effects of estrogen in colon cancer. The role of ERβ in breast cancer and colon cancer is not well understood. Thus, exploring the genome-wide impact and contribution of both receptors in estrogen responsive cancers would substantially help to identify novel therapeutic and preventive strategies for these cancers.In Paper I, we examined differences in transcriptional regulation between ERα and ERβ in the breast cancer cell line T47D. We could show that ERβ often exhibited an opposing effect on ERα-regulated genes within proliferation and regulation of cell cycle. We also demonstrated a set of genes only regulated by ERβ, indicating that, despite the high homology between the two receptors, there are differences in their transcriptional targets. The fact that ERβ opposed ERα indicates that ERβ activation may be of value in the treatment of breast cancer. To further explore the transcriptional role of ERα in breast cancer, we performed large-scale analyses of microRNA in 24 hours estrogen treated ERα-expressing T47D cells, Paper II. However, we found no evidence of direct and rapid regulation of mature miRNAs by ERα.In Paper III, we studied ERβ gene regulation in colon cancer cells. We could show that ERβ-expressing xenografts grew significantly slower than those lacking ERβ. Further we demonstrated that ERβ induced a transcriptional response independently of ERα and induced inhibition of the proto-oncogene MYC and other G1-phase cell cycle genes.In Paper IV, we dissected the regulatory networks of ERβ-induced transcriptional changes in human colon cancer cells. The set of genes changed by ERβ varied in different colon cancer cell lines, however, corresponded to the same biological processes such as cell cycle regulation and kinase activity. In addition, we identified the ERβ-driven downregulation of the transcription factor PROX1 as a key mechanism behind a large proportion of the transcriptional changes.In Paper V, we studied the effect of long term expression of ERβ on the miRNA pool in SW480 colon cancer cells. While we could not show a direct and rapid effect of ERα on the miRNome, we showed that long term expression of ERβ did induce large changes in the miRNA pool in colon cancer cells. In particular, we found the oncogenic miR-17-92 cluster to be downregulated and proposed this to be a consequence of the ERβ-induced downregulation of MYC.In conclusion, we have shown that ERβ is antiproliferative in breast and colon cancer cells, both when co-expressed with ERα and alone, as well as identified key signaling pathways. We suggest that activation of ERβ will have a beneficial effect for treatment or prevention of estrogen dependent cancers.List of scientific papersI. Williams C, Edvardsson K, Lewandowski S, Ström A, Gustafsson JÅ. A genome-wide study of the repressive effects of estrogen receptor beta on estrogen receptor alpha signaling in breast cancer cells. Oncogene. (2008), 27, 1019-1032. https://doi.org/10.1038/sj.onc.1210712 II. Katchy A, Edvardsson K, Aydogdu E, Williams C. Estradiol-activated estrogen receptor α does not regulate mature microRNAs in T47D breast cancer cells. The Journal of Steroid Biochemistry and Molecular Biology. (2011). https://doi.org/10.1016/j.jsbmb.2011.10.008 III. Hartman J, Edvardsson K, Lindberg K, Zhao C, Williams C, Ström A, Gustafsson JÅ. Tumor Repressive Functions of Estrogen Receptor β in SW480 Colon Cancer Cells. Cancer research. (2009), 69, 6100-5106. https://doi.org/10.1158/0008-5472.CAN-09-0506 IV. Edvardsson K, Ström A, Jonsson P, Gustafsson JÅ, Williams C. Estrogen Receptor β Induces Antiinflammatory and Antitumorigenic Networks in Colon Cancer Cells. Molecular endocrinology. (2011), 25, 969-979.V. https://doi.org/10.1210/me.2010-0452 V. Edvardsson K, Vu HT, Kalasekar SM, Ponten F, Gustafsson JÅ, Williams C. Estrogen receptor beta expression induces changes in the microRNA pool in human colon cancer cells. [Manuscript]</p
Appropriate Similarity Measures for Author Cocitation Analysis
No full textWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Expanding “Communities and Collections” in the K-State Research Exchange (K-REx) to benefit the K-State Community and Beyond
No full textKansas State University has used its institutional repository, the K-State Research Exchange (K-REx), to store and share its first year experience program, K-State First, and notably its common reading program, K-State First Book. We have done so with the aim that the accessibility and preservation of these documents ensures program stability, promotes engagement with first year programming, and provides the ability to foster growth,educational opportunities, and community building outside of K-State. Moving away from research concentrated repositories and taking a more holistic approach to scholarship, especially when realizing the pedagogical significance of collaborative campus programming, institutions can showcase, discover, preserve, and grow programs that shape campus communities and engagement.
This session will provide an overview of K-REx and spotlight the digital archive of the university’s first year experience program and common reading program, K-State First Book. We will discuss the benefits and challenges to expanding the purview of your repositories. We talkthrough the types of materials we decide to host in our repository and why we share what we do. We will also provide recommendations on new ways to evaluate what belongs in institutional repositories and how this diversity can benefit your program, your institution, the community, and others
Ready Player One Program Event Poster
No full textK-State Book NetworkA poster advertising an author talk by Ernest Cline at Kansas State University on October 10, 2013. Ernest Cline's book "Ready Player One" was selected as the 2013-2014 common book
Depolarization and decreased surface expression of K+ channels contribute to NSAID-inhibition of intestinal restitution
No full textNon-steroidal anti-inflammatory drugs (NSAIDs) contribute to gastrointestinal ulcer formation by inhibiting epithelial cell migration and mucosal restitution; however, the drug-affected signaling pathways are poorly defined. We investigated whether NSAID inhibition of intestinal epithelial migration is associated with depletion of intracellular polyamines, depolarization of membrane potential (Em) and altered surface expression of K+ channels. Epithelial cell migration in response to the wounding of confluent IEC-6 and IEC-Cdx2 monolayers was reduced by indomethacin (100μM), phenylbutazone (100μM) and NS-398 (100μM) but not by SC-560 (1μM). NSAID-inhibition of intestinal cell migration was not associated with depletion of intracellular polyamines. Treatment of IEC-6 and IEC-Cdx2 cells with indomethacin, phenylbutazone and NS-398 induced significant depolarization of Em, whereas treatment with SC-560 had no effect on Em. The Em of IEC-Cdx2 cells was: −38.5±1.8mV under control conditions; −35.9±1.6mV after treatment with SC-560; −18.8±1.2mV after treatment with indomethacin; and −23.7±1.4mV after treatment with NS-398. Whereas SC-560 had no significant effects on the total cellular expression of Kv1.4 channel protein, indomethacin and NS-398 decreased not only the total cellular expression of Kv1.4, but also the cell surface expression of both Kv1.4 and Kv1.6 channel subunits in IEC-Cdx2. Both Kv1.4 and Kv1.6 channel proteins were immunoprecipitated by Kv1.4 antibody from IEC-Cdx2 lysates, indicating that these subunits co-assemble to form heteromeric Kv channels. These results suggest that NSAID inhibition of epithelial cell migration is independent of polyamine-depletion, and is associated with depolarization of Em and decreased surface expression of heteromeric Kv1 channels.ID: S0006295207001931; M3: Article; Accession Number: S0006295207001931; Author: L.C. Freeman (b); Author: D.F. Narvaez (a); Author: A. McCoy (a); Author: F.B. von Stein (c); Author: S. Young (b); Author: K. Silver (a); Author: S. Ganta (b); Author: D. Koch (b); Author: R. Hunter (b); Author: R.F. Gilmour (c); Author: J.D. Lillich (a, ⁎); Affiliation: Department of Clinical Sciences, Kansas State University, Manhattan, KS 66506, United States; Affiliation: Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, United States; Affiliation: Department of Biomedical Sciences, Cornell University, Ithaca, NY 14853, United States; Keyword: Non-steroidal anti-inflammatory drugs; Keyword: Intestinal epithelial cells; Keyword: Membrane potential; Keyword: Potassium channels; Number of Pages: 12; Language: English;Source type: Electronic(1)http://search.ebscohost.com/login.aspx?direct=true&db=edselp&AN=S0006295207001931&site=eds-live&scope=sit
Dispelling the Myths Behind First-author Citation Counts
No full textWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
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