The Vehicle, Spring 2010

Table of Contents ForgettingRashelle McNairpage 34 MuseMary Lieskepage 35 My CompulsionAshton Tembypage 38 MemoryKate Vandermeerpage 41 Killmercialize MeGreg Petersonpage 42 PenJake Smithpage 46 GrassKate Vandermeerpage 48 Character CreationMary Lieskepage 52 Ring Around TheKim Hunter-Perkinspage 54 The Great Cursive ScareJake Smithpage 55 OpiateDoug Urbanskipage 61 What Happens to Little Girls...Jennifer O\u27Neilpage 63 Poetry Sunny DaysRyan Poolpage 2 AtlantisDoug Urbanskipage 4 Garbage CityKate Vandermeerpage 6 Fat Girl ThongsKim Hunter-Perkinspage 7 MercilessRosalia Pecorapage 19 ChemistryMary Lieskepage 20 He-Who-Stopped-TalkingJustin Sudkamppage 22 In Which Iris Contemplates a Barren EarthSean Slatterypage 24 At the Bottom of the WorldNick Canadaypage 27 Dogma: Mush!Scott Maypage 28 ThiefMary Lieskepage 29 Prose Coming HomeDoug Urbanskipage 8 DodoDan Davispage 31 The Poet in the PedestrianScott Maypage 37 Toxic RainJacob Swansonpage 40 What\u27s Your Greatest Fear?Justine Fittonpage 43 Soul VoiceHolly Thomaspage 49 Conversations with a SniperKim Hunter-Perkinspage 56 LettersDaniel Paquinpage 65 Art San Marcos, MexicoKate Vandermeercover Contemplation of the World\u27s EndNicholas Giffordpage 18 Little Lady SitsSarah Hadwigerpage 26 MoodAlycia Rockeypage 30 Four Ducks in a RowMegan Mathypage 36 The Daily EasternBen Tillerypage 39 BirdsAlycia Rockeypage 45 March of the BugsMegan Mathypage 47 Mexico Work ExperienceKate Vandermeerpage 53 Feather and JewelsAlycia Rockeypage 60 The ForgottenMegan Mathypage 64 Special Features Fall 2009-Spring 2010 Vehicle Award Winnerspage 1 James K. Johnson Creative Writing Awardpage 74 Kim Hunter-PerkinsWinning Entries (Poetry)page 75 Clint WalkerWinning Entry (Fiction)page 86 Faculty Spotlight: Professor Jason Brownpage 99 About the Contributorspage 106 About the Editorspage 110https://thekeep.eiu.edu/vehicle/1093/thumbnail.jp

Genome-wide array-based copy number profiling in human placentas from unexplained stillbirths.

Accumulating evidence suggests that genomic structural variations, particularly copy number variations (CNV), are a common occurrence in humans that may bear phenotypic consequences for living individuals possessing the variant. While precise estimates vary, large-scale karyotypic abnormalities are present in 6-12\% of stillbirths (SB). However, due to inherent limitations of conventional cytogenetics, the contribution of genomic aberrations to stillbirth is likely underrepresented. High-resolution copy number variant analysis by genomic array-based profiling may overcome such limitations.Prospectively acquired SB cases > 22 weeks underwent classification of 'unexplained' stillbirth by Wigglesworth and Aberdeen criteria after extensive testing and rigorous multidisciplinary audit. Genome-wide analysis was conducted using high-resolution Illumina single nucleotide polymorphism (SNP) arrays (Human CNV370-Duo) on placental and fetal samples. Potential alternate detection methods were completed by one or more of three independent means (quantitative PCR, Illumina1M, or Agilent105K comparative genomic hybridization arrays).In our cohort of 54 stillbirths, 29 met strict unexplained criteria. Among these, we identified 24 putative novel CNVs. Subsequent interrogation detected 18 of 24 CNVs (75\%) in placental samples, 8 of which were also confirmed in available fetal samples; none were present in maternal blood.We describe the potential of whole-genome placental profiling to identify small genomic imbalances, which might contribute to a small proportion of well-characterized, unexplained stillbirths

The Vehicle, Spring 2010

Table of Contents ForgettingRashelle McNairpage 34 MuseMary Lieskepage 35 My CompulsionAshton Tembypage 38 MemoryKate Vandermeerpage 41 Killmercialize MeGreg Petersonpage 42 PenJake Smithpage 46 GrassKate Vandermeerpage 48 Character CreationMary Lieskepage 52 Ring Around TheKim Hunter-Perkinspage 54 The Great Cursive ScareJake Smithpage 55 OpiateDoug Urbanskipage 61 What Happens to Little Girls...Jennifer O\u27Neilpage 63 Poetry Sunny DaysRyan Poolpage 2 AtlantisDoug Urbanskipage 4 Garbage CityKate Vandermeerpage 6 Fat Girl ThongsKim Hunter-Perkinspage 7 MercilessRosalia Pecorapage 19 ChemistryMary Lieskepage 20 He-Who-Stopped-TalkingJustin Sudkamppage 22 In Which Iris Contemplates a Barren EarthSean Slatterypage 24 At the Bottom of the WorldNick Canadaypage 27 Dogma: Mush!Scott Maypage 28 ThiefMary Lieskepage 29 Prose Coming HomeDoug Urbanskipage 8 DodoDan Davispage 31 The Poet in the PedestrianScott Maypage 37 Toxic RainJacob Swansonpage 40 What\u27s Your Greatest Fear?Justine Fittonpage 43 Soul VoiceHolly Thomaspage 49 Conversations with a SniperKim Hunter-Perkinspage 56 LettersDaniel Paquinpage 65 Art San Marcos, MexicoKate Vandermeercover Contemplation of the World\u27s EndNicholas Giffordpage 18 Little Lady SitsSarah Hadwigerpage 26 MoodAlycia Rockeypage 30 Four Ducks in a RowMegan Mathypage 36 The Daily EasternBen Tillerypage 39 BirdsAlycia Rockeypage 45 March of the BugsMegan Mathypage 47 Mexico Work ExperienceKate Vandermeerpage 53 Feather and JewelsAlycia Rockeypage 60 The ForgottenMegan Mathypage 64 Special Features Fall 2009-Spring 2010 Vehicle Award Winnerspage 1 James K. Johnson Creative Writing Awardpage 74 Kim Hunter-PerkinsWinning Entries (Poetry)page 75 Clint WalkerWinning Entry (Fiction)page 86 Faculty Spotlight: Professor Jason Brownpage 99 About the Contributorspage 106 About the Editorspage 110https://thekeep.eiu.edu/vehicle/1093/thumbnail.jp

Liver gene regulatory networks: Contributing factors to nonalcoholic fatty liver disease

Metabolic diseases such as nonalcoholic fatty liver disease (NAFLD) result from complex interactions between intrinsic and extrinsic factors, including genetics and exposure to obesogenic environments. These risk factors converge in aberrant gene expression patterns in the liver, which are underlined by altered cis-regulatory networks. In homeostasis and in disease states, liver cis-regulatory networks are established by coordinated action of liver-enriched transcription factors (TFs), which define enhancer landscapes, activating broad gene programs with spatiotemporal resolution. Recent advances in DNA sequencing have dramatically expanded our ability to map active transcripts, enhancers and TF cistromes, and to define the 3D chromatin topology that contains these elements. Deployment of these technologies has allowed investigation of the molecular processes that regulate liver development and metabolic homeostasis. Moreover, genomic studies of NAFLD patients and NAFLD models have demonstrated that the liver undergoes pervasive regulatory rewiring in NAFLD, which is reflected by aberrant gene expression profiles. We have therefore achieved an unprecedented level of detail in the understanding of liver cis-regulatory networks, particularly in physiological conditions. Future studies should aim to map active regulatory elements with added levels of resolution, addressing how the chromatin landscapes of different cell lineages contribute to and are altered in NAFLD and NAFLD-associated metabolic states. Such efforts would provide additional clues into the molecular factors that trigger this disease. This article is categorized under: Biological Mechanisms > Metabolism Biological Mechanisms > Regulatory Biology Laboratory Methods and Technologies > Genetic/Genomic Methods

Modulation of neutrophil NETosis : interplay between infectious agents and underlying host physiology

The ability of neutrophils and other leucocyte members of the innate immune system to expel their DNA into the extracellular environment in a controlled manner in order to trap and kill pathogenic microorganisms lead to a paradigm shift in our understanding of host microbe interactions. Surprisingly, the neutrophil extracellular trap (NET) cast by neutrophils is very wide and extends to the entrapment of viruses as well as multicellular eukaryotic parasites. Not unexpectedly, it has emerged that pathogenic microorganisms can employ a wide array of strategies to avoid ensnarement, including expression of DNAse enzymes that destroy the lattice backbone of NETs. Alternatively, they may use molecular mimicry to avoid detection or trigger events leading to the expression of immune modulatory cytokines such as IL-10, which dampen the NETotic response of neutrophils. In addition, the host microenvironment may contribute to the innate immune response by the production of lectin-like molecules that bind to bacteria and promote their entrapment on NETs. An example of this is the production of surfactant protein D by the lung epithelium. In addition, pregnancy provides a different challenge, as the mother needs to mount an effective response against pathogens, without harming her unborn child. An examination of these decoy and host response mechanisms may open the path for new therapies to treat pathologies mediated by overt NETosis