98,008 research outputs found
Joshua Davis: Author of Spare Parts
Get PDFCitation: 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
사람의 침윤성 암세포에서 후성학적 BTG2/TIS21/PC3 발현 조절과 암 억제 기전 연구
No full textB cell translocation gene 2 (BTG2/TIS21/PC3) belongs to the family of antiproliferative (APRO) genes and reported as a tumor suppressor by our group and others. Expression of BTG2 is significantly reduced in cancers developed in various organs and tissues. EJ (bladder carcinoma cells), MKN-1 (gastric cancer cells) are highly invasive and metastatic cells with very less endogenous BTG2 expression due to epigenetic regulation. Significantly lower endogenous expression of BTG2 was observed in human muscle-invasive bladder cancers (MIBC) than matched normal tissues and non-muscle invasive bladder cancers (NMIBC). BTG2 expression was inversely correlated with increased expression of the DNA methyltransferases DNMT1 and DNMT3a in MIBC, but not NMIBC, suggesting a potential role for BTG2 expression in muscle invasion of bladder cancer. Over 90% of tumor tissues revealed strong methylation at CpG islands of the BTG2 gene, compared with no methylation in the normal tissues, implying epigenetic regulation of BTG2 expression in bladder carcinogenesis. BTG2 is constitutively expressed in mucous epithelium and parietal cells of gastric glands in stomach, and the expression was increased in mucous epithelium with H. pylori infection as opposed to loss in human gastric adenocarcinoma. Indeed, adenoviral transduction of BTG2 significantly inhibited Tipα activity in MKN-1 and MGT-40, human and mouse gastric cancer cells, respectively, thereby downregulated TNFα expression and Erk1/2 phosphorylation via reducing nucleolin, Tipα receptor, expression. Chromatin immunoprecipitation proved that BTG2 inhibited Sp1 expression and it’s binding to the promoter of nucleolin gene. In addition, BTG2 expression significantly reduced membrane localized nucleolin expression in cancer cells and the loss of BTG2/TIS21 expression rather induced cytoplasmic nucleolin availability in gastric cancer tissues, evidenced by immunoblot and immunohistochemistry. The higher expression of BTG2 and the lower nucleolin expression accompanied with the better overall survival of the poorly differentiated gastric cancer patients.B cell translocation gene 2(BTG2/TIS21/PC3)는 antiproliferative gene(APRO) 계열에 속하며 본 연구팀을 포함한 많은 연구자들에 의해 BTG2 의 암억제 기능이 연구되어 왔다. BTG2 는 여러 조직과 기관에서 발생한 암에서 그 발현이 감소되어 있고, 특히 침윤(invasion)과 전이(metastasis)를 잘하는 암세포인 EJ (bladder carcinoma cells)와 MKN-1 (gastric cancer cells)에서도 후성유전학적(epigenetic regulation)으로 BTG2 발현이 매우 감소되어 있다. 최근 사람에서, 이런 침윤성과 전이성이 높은 암에서 BTG2 가 침윤을 억제하고 침윤을 조장하는 단백질과 mRNA 발현과는 음의 상관도를 보인다는 보고가 많기에, 본 저자는 BTG2 가 어떤 기전으로 침윤성 암을 조절하는지를 중점적으로 연구하였다. 사람의 근육침범 방광암(muscleinvasive bladder cancers, MIBC)에서 비-근육침범 방광암(non-muscle invasive bladder cancers, NMIBC)보다 BTG2 의 발현이 현저히 감소되어 있다는 것을 발견하였다. 이런 MIBC 에서의 BTG2 의 감소는 반대로 DNA 메틸기전달효소 DNMT1 과 DNMT3a 의 증가와 연관이 있었고, 이런 음의 상관관계는 NMIBC 에서는 발견되지 않음으로써 BTG2 이 방광암의 근육 침범에 분명한 역할을 하고 있다는 가능성을 보였다. 방광암 조직들의 90%에서 BTG2 유전자의 CpG 섬에 강한 메틸화를 보였고, 반대로 정상 방광조직에서는 메틸화가 발견되지 않음으로써, 방광암발생과정에서 BTG2 이 후성학적 조절을 받는다는 사실도 증명했다. 한편, BTG2 는 위 점막의 상피세포와 위샘의 벽세포(Parietal cell)에서 기본적으로 발현되고 있으며, 이 유전자의 발현은 H. pylori 감염시 위 점막 상피세포에서 증가되고, 반대로 위선암(gastric adenocarcinoma)에서는 감소됨을 발견했다. 사람 암세포 MKN-1 과 쥐 암세포 MGT-40 에서 BTG2 를 adenoviral transduction 을 통해 발현시키면 Tumor necrosis factor- α inducing protein (Tip α ) 활성이 억제되었고, 이는 Tip α receptor 인 nucleolin 을 감소시킴으로 TNFα의 발현과 Erk1/2 의 인산화를 억제시켰다. BTG2 는 Sp1 의 발현과 또한 염색질 면역침전(Chromatin immunoprecipitation) 실험을 통해 nucleolin 의 promoter 에 결합하는 Sp1 도 감소시킴을 확인했다. 또한 암세포에서 BTG2 를 발현시키면 세포막에 위치한 nucleolin 의 발현이 감소되었고, 반대로 BTG2 발현을 감소시키면 세포질 내에 nucleolin 의 발현이 증가함을 면역조직화학법과 면역블롯검사를 통해 위암조직에서 밝혔다. 이런 BTG2 의 강한 발현과 nuclolin 의 발현 저하는 저분화 위암 환자에서의 높은 생존율(overall survival)과 연관이 있었다. 더욱이 이런 BTG2 의 발현증가는 침윤성 암세포에서도 암 진행과 성장을 억제했다. 따라서, 본 저자는 본 연구를 통해 BTG2 유전자가 침윤성 암 환자를 위한 강력한 치료로 사용될 수 있으리라 제안한다.ABSTRACT i
TABLE OF CONTENTS iii
LIST OF FIGURES vi
ABBREVIATIONS viii
I. INTRODUCTION 1
II. EXPERIMENTAL METHODS 7
A. Tissues and cell cultures 7
B. RNA isolation and reverse transcription 8
C. Real-time and RT-PCR analyses 8
D. Methylation-specific PCR (MSP) and unmethylation-specific PCR (USP) analyses 9
E. Western blotting 9
F. DNMT activity assay 10
G. Chromatin immunoprecipitation (ChIP) analysis 10
H. Cloning of CpG islands and sequencing analyses 10
I. Immunoprecipitation/immunoblot analysis 11
J. Regulation of gene expression 11
K. Tumorigenesis study 12
L. Invasion assay 13
M. Immunohistochemistry analysis 14
N. Preparation of recombinant Tipα protein 15
O. Subcellular fractionation 15
P. Statistical analysis 15
III. RESULTS 16
A. Downregulation of BTG2 expression in human MIBC by DNA methylation of BTG2 gene 16
B. Inverse correlations between the expressions of BTG2 vs DNMT1 and DNMT3a in MIBC 18
C. Upregulation of BTG2 expression in EJ bladder cancer cells upon Decitabine treatment 22
D. Chromatin remodeling at the promoter and intron of BTG2 gene after decitabine treatment 27
E. Sp1, the transcription factor, for BTG2 gene upon decitabine treatment 28
F. Induction of BTG2 expression by knockdown of DNMT1 in EJ cells 32
G. Downregulation of tumorigenesis and cell cycle arrest by BTG2 overexpression 35
H. Inhibition of tumor invasion by BTG2 via downregulation of DNMT1
expression 38
I. Direct effect of BTG2/TIS21 expression on the inhibition of cancer invasiveness 41
J. Immunohistochemical findings 44
K. Induction of BTG2 expression by decitabine treatment in various cancer cell lines in addition to APRO gene expression analyses 46
L. Expression of BTG2/TIS21 is increased in mucous epithelium infected with H. pylori, but lost in human gastric adenocarcinoma 48
M. Absence of endogenous BTG2/TIS21 expression in the gastric cancer cells 51
N. Expression of BTG2/TIS21 is epigenetically regulated in gastric adenocarcinoma 52
O. Inhibition of cancer cell proliferation by BTG2/TIS21 gene 54
P. Inhibition of Tipα activity by BTG2/TIS21 in human gastric cancer cells 55
Q. Inhibition of Tipα activity by downregulation p-ERK1/2 in human gastric cancer cells 57
R. Downregulation of nucleolin expression by BTG2/TIS21 59
S. Expression of nucleolin, Tipα receptor, was reduced by BTG2 expression via inhibiting Sp1binding to the nucleolin promoter 61
T. Inverse regulation of Tipα -induced TNFα expression by NCL and BTG2 64
U. Reciprocal expression of BTG2/TIS21 and nucleolin expressions in normal and cancer regions 68
V. Inverse regulation of overall survival of gastric cancer patients by BTG2/TIS21 and NCL genes 71
IV. DISCUSSION 74
V. SUMMARY 80
VI. CONCLUSIONS 82
VII. REFERENCES 83
국문요약 95Docto
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe 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
Physiological roles and regulation of the cryptic prophage-encoded small protein DicB and small RNA DicF in Escherichia coli
Get PDFBacterial adaptation to stress conditions is vital for their survival in different environments. In the past decade, the important roles that small RNAs (sRNAs) and small proteins perform in regulating the stress response in bacteria has become evident. While the roles of numerous sRNAs and small proteins encoded on the bacterial core genome have been characterized, very few that are phage or prophage-encoded have been studied. This dissertation describes the roles and regulation of the sRNA DicF and small protein DicB encoded on the Qin cryptic prophage of Escherichia coli K12. Bacterial genomes harbor cryptic prophages that have lost genes required for induction, excision from host chromosomes, or production of phage progeny. DicB and DicF are encoded on the dicBF operon, which is located in the immunity region of the cryptic prophage Qin. DicB and DicF have previously been implicated in inhibiting cell division of the host bacterium. In this study, we show that the small protein DicB protects the host cells from phage infection. DicB specifically inhibits infection by λ and other phages that use ManYZ inner membrane proteins to inject their DNA into the host cell. DicB also inhibits the canonical function of ManYZ, which is mannose sugar transport. We demonstrated that the previously known interaction between DicB and MinC, a host protein involved in proper positioning of the Z ring during cell division, is necessary for the DicB-dependent phenotypes involving ManYZ identified in this study. The sRNA DicF is widely conserved is many E. coli strains and inhibits ftsZ mRNA translation in E. coli. In this study, we establish the mechanism of this regulation by characterizing the base pairing interaction between DicF and ftsZ, and delineate the roles of other host factors involved in this regulation. Additionally, we identify new mRNA targets of the sRNA DicF, that are primarily involved in host cell metabolism. The final part of this thesis work describes the genetic mechanisms defining the regulation of the dicBF operon. The dicBF operon is constantly repressed under laboratory conditions by the repressor DicA. In this work, we identified that the protein Rem impairs DicA repression of the dicBF operon and is the antirepressor of DicA. We show that Rem induces expression of dicB and dicF, which leads to the concomitant cell filamentation phenotype as DicB and DicF are cell division inhibitors. In the absence of the dicBF gene products, the promoter of the dicBF operon was found to undergo spontaneous induction in a subset of cells, reminiscent of the λ phage bistable genetic switch. Lastly, urea and high temperature were identified as strong inducers of the dicBF promoter in strains deleted for the dicBF operon. Our results suggest that expression of the dicBF operon is regulated in multiple ways in E. coli K12, indicative of the complex relationship that exists between the host cell and cryptic prophages.Submission published under a 24 month embargo labeled 'U of I Access', the embargo will last until 2023-05-01The student, Preethi Narayani Thattai Ragunathan, accepted the attached license on 2020-12-22 at 15:01.The student, Preethi Narayani Thattai Ragunathan, submitted this Dissertation for approval on 2020-12-22 at 16:38.This Dissertation was approved for publication on 2020-12-23 at 13:10.DSpace SAF Submission Ingestion Package generated from Vireo submission #16136 on 2021-09-16 at 17:01:29Made available in DSpace on 2021-09-17T02:34:10Z (GMT). No. of bitstreams: 2
THATTAIRAGUNATHAN-DISSERTATION-2021.pdf: 22774621 bytes, checksum: ce6861aa0e51fd8410a2de050f497792 (MD5)
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Previous issue date: 2020-12-23Embargo set by: Seth Robbins for item 118462
Lift date: 2023-09-17T02:34:57Z
Reason: Author requested U of Illinois access only (OA after 2yrs) in Vireo ETD systemAuthor requested U of Illinois access only (OA after 2yrs) in Vireo ETD systemU of I Onl
Appropriate Similarity Measures for Author Cocitation Analysis
Get PDFWe 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
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