Exploring and Preventing Accidental Plagiarism in a Digital Age

In our online only college writing center, we often hear from students that they are not sure that they need citation or references in their papers because they did not use any research but instead only looked at a few web sites. Students sometimes present with plagiarism issues in their writing and attest that they did not borrow any outside wording when a quick Internet search confirms that they did, in fact, use text verbatim without directly quoting the words. These scenarios and others seem to be instances of accidental plagiarism, and helping students work through them raises the following key questions which will be addressed and explored in this poster session in order to promote a beneficial and engaging exchange of ideas among conference attendees: Does the use of the Internet to casually locate information (i.e. surf the web) cause students to be less careful researchers who are more prone to plagiarize in a more formal, academic setting? Do online students use Internet research differently than students who are attending classes in a more traditional campus setting? Does the ability to quickly copy and paste information from the Internet contribute to plagiarism in students’ writing? How can we best help students to cognitively switch from casually using the Internet to locate information to carefully using and documenting their use of outside sources in their academic writing? How can educators best assist students who complete online research and present with plagiarism issues in their writing in this digital age

Studio Recital: Students of Jana Young

Kennesaw State University School of Music presents Studio Recital: Students of Jana Young.https://digitalcommons.kennesaw.edu/musicprograms/1367/thumbnail.jp

Evaluation of recombinant influenza virus-simian immunodeficiency virus vaccines in macaques

There is an urgent need for human immunodeficiency virus (HIV) vaccines that induce robust mucosal immunity. Influenza A viruses (both H1N1 and H3N2) were engineered to express simian immunodeficiency virus (SIV) CD8 T-cell epitopes and evaluated following administration to the respiratory tracts of 11 pigtail macaques. Influenza virus was readily detected from respiratory tract secretions, although the infections were asymptomatic. Animals seroconverted to influenza virus and generated CD8 and CD4 T-cell responses to influenza virus proteins. SIV-specific CD8 T-cell responses bearing the mucosal homing marker 7 integrin were induced by vaccination of naïve animals. Further, SIV-specific CD8 T-cell responses could be boosted by recombinant influenza virus-SIV vaccination of animals with already-established SIV infection. Sequential vaccination with influenza virus-SIV recombinants of different subtypes (H1N1 followed by H3N2 or vice versa) produced only a limited boost in immunity, probably reflecting T-cell immunity to conserved internal proteins of influenza A virus. SIV challenge of macaques vaccinated with an influenza virus expressing a single SIV CD8 T cell resulted in a large anamnestic recall CD8 T-cell response, but immune escape rapidly ensued and there was no impact on chronic SIV viremia. Although our results suggest that influenza virus-HIV vaccines hold promise for the induction of mucosal immunity to HIV, broader antigen cover will be needed to limit cytotoxic T-lymphocyte escape

Expression von Parathormone-related Peptide in koronaren Endothelzellen und der glatten Gefäßmuskulatur

Das Parathormon related peptide (PTHrP) wird im gesamten Gefäßsystem einschließlich der koronaren Endothelzellen exprimiert. Im Gegensatz zu den benachbarten Glattmuskelzellen, welche bislang hinsichtlich PTHrP eingehend untersucht wurden, hat man die koronaren Endothelzellen nur als Produktionsstätte des Ventrikels angesehen. Aus diesem Grund blieben bisher die PTHrP-Expression und seine biologische Rolle in diesen Zellen ungeklärt. Deshalb habe ich mich dafür interessiert, ob eine Stimulation a-adrenerger bzw. AT-Rezeptoren die Expression in den koronaren Endothelzellen steigert und ob das endogen exprimierte PTHrP einen sogenannten intrakrinen Effekt in diesem Zelltyp ausübt. Besonders interessant ist diese Fragestellung vor dem Hintergrund, daß diese Zellen keine klassischen Zielzellen des Peptidhormones darstellen, da sie nicht den korrespondierenden PTHrP-Rezeptor besitzen, wie das z. B. bei den Glattmuskelzellen der Fall ist. Was anhand der Ergebnisse gezeigt werden konnte ist die Tatsache, daß durch Stimulation der Zellen mit der a-adrenergen Substanz Phenylephrin im Vergleich zur Stimulation mit Angiotensin II, eine deutliche Steigerung in der Expression des PTHrP hervorgerufen werden konnte. Dieser Effekt konnte jedoch nicht im Stadium der Konfluenz reproduziert werden. Im Gegensatz dazu erhielten wir in den Glattmuskelzellen ein genau umgekehrtes Bild, da hier nur Angiotensin II eine signifikante Expressionssteigerung hervorrief. Deshalb wollte ich mehr über die Lokalisation des endogenen PTHrP in den verschiedenen Proliferationsstadien mit Hilfe der Immunfluoreszenz in Erfahrung bringen. Die Ergebnisse zeigten, daß der Anteil an PTHrP, welcher in den Kern transloziert wird, umso größer ist, je mehr sich die Zellen dem Konfluenzstadium nähern. Diese Tatsache war für mich Anlaß zu vermuten, daß das Peptidhormon einen intrakrinen Effekt auf die koronaren Endothelzellen ausübt. Mit Hilfe der Transfektion der Zellen mit Antisense-Oligonukleotiden gegen PTHrP und der daraus sich ergebenden Herabregulierung seiner Expression untersuchte ich seinen möglichen Einfluß auf die Proliferation bzw. Apoptose. Im Bezug auf die Proliferation ergaben sich keine Hinweise auf eine Beeinflussung. Bei der Betrachtung der Endothelzellen in den unterschiedlichen Konfluenzstadien konnte mit Hilfe einer UV-Bestrahlung in Zellen, in denen der Anteil des nukleären PTHrP normalerweise erhöht wäre, eine stärkere Apoptoserate als unter Basalbedingungen hervorgerufen werden. Im Gegensatz dazu wurde durch eine erhöhte Expression des PTHrP - welche durch Phenylephrin vermittelte wurde -der Anteil der apoptotischen Zellen sowohl gegenüber Basalbedingungen als auch unter UV-Induktion deutlich vermindert. Zusammenfassend läßt sich anhand der Ergebnisse der vorliegenden Studie sagen, daß in koronaren Endothelzellen die PTHrP-Expression durch eine a-Adrenozeptor-Stimulation in einer Zellzyklus-abhängigen und Zelltyp-spezifischen Art und Weise reguliert wird. Diese Studie zeigt eine neue biologische Rolle des PTHrP im Gefäßbett auf, da über den nachgewiesenen intrakrinen Effekt das Peptidhormon einen Anteil am Schutzmechanismus der Endothelschicht vor Apoptose besitzt.Parathyroid hormone related peptide (PTHrP) is expressed throughout the vascular system including coronary endothelial cells. The regulation of endothelial PTHrP expression and the role of PTHrP expression in endothelial cells is not clear. The present study investigates the question whether stimulation of a-adrenergic or angiotensin II receptors increases endothelial expression of PTHrP and whether endogenously expressed PTHrP exerts intracrine effects in coronary endothelial cells. It was found that stimulation of alpha1A-adrenoceptors, but not that of angiotensin II, increases cellular expression of PTHrP in growing, but not in growth arrested, coronary endothelial cells. Angiotensin II increases the expression of PTHrP in smooth muscle cells, but not in endothelial cells. PTHrP enters the nucleus of endothelial cells at the stadium of confluence. This suggests an intracrine effect of PTHrP. It was further investigated whether downregulation of endogenous PTHrP expression by transfection with antisense oligonucleotides alters cell proliferation or apoptosis resistance in growing or non-growing endothelial cells. Downregulation of PTHrP did not modify cell proliferation but increased the amount of UV-induced apoptosis. An increased expression of PTHrP in cells pre-treated with an a-adrenoceptor agonist reduced basal rate of apoptosis and improved resistance against UV-induced apoptosis. These results indicate a novel intracrine effect of PTHrP in coronary endothelial cells that improves cell survival. In endothelial cells, the expression of PTHrP is regulated by alpha-adrenoceptor stimulation in a cell-cycle dependent and cell-type specific manner

Studio Recital: Jana Young\u27s Voice Studio

KSU School of Music presents Jana Young\u27s Voice Studio.https://digitalcommons.kennesaw.edu/musicprograms/1202/thumbnail.jp

Second Human Case of Cache Valley Virus Disease

We document the second known case of Cache Valley virus disease in a human. Cache Valley virus disease is rarely diagnosed in North America, in part because laboratories rarely test for it. Its true incidence, effect on public health, and full clinical spectrum remain to be determined

Timing of immune escape linked to success or failure of vaccination

Successful vaccination against HIV should limit viral replication sufficiently to prevent the emergence of viral immune escape mutations. Broadly directed immunity is likely to be required to limit opportunities for immune escape variants to flourish. We studied the emergence of an SIV Gag cytotoxic T cell immune escape variant in pigtail macaques expressing the Mane-A*10 MHC I allele using a quantitative RT-PCR to measure viral loads of escape and wild type variants. Animals receiving whole Gag expressing vaccines completely controlled an SIVmac251 challenge, had broader CTL responses and exhibited minimal CTL escape. In contrast, animals vaccinated with only a single CTL epitope and challenged with the same SIVmac251 stock had high levels of viral replication and rapid CTL escape. Unvaccinated na&iuml;ve animals exhibited a slower emergence of immune escape variants. Thus narrowly directed vaccination against a single epitope resulted in rapid immune escape and viral levels equivalent to that of na&iuml;ve unvaccinated animals. These results emphasize the importance of inducing broadly directed HIV-specific immunity that effectively quashes early viral replication and limits the generation of immune escape variants. This has important implications for the selection of HIV vaccines for expanded human trials.<br /

Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts