The Vehicle, Spring 1995

Table of Contents Poetry The SwimmersJennifer Moropage 2 Everlasting ArmsSue Songerpage 2 Talking to an AddictBridgett Jensenpage 3 SecretsTiffany Abbottpage 5 CryingMatthew Berrypage 6 winter fieldsKeith Spearpage 7 untitledKemp Nishan Munizpage 7 Rainy Night in ParisDiana Matijaspage 8 nap timeKelly A. Pricepage 10 Angel of the EarthHeather Anne Winterspage 10 Color DreamsMatthew J. Nelsonpage 12 Dandelion PaintSandy Beauchamppage 13 Merry Go Round MarathonElizabeth Bromleypage 14 The ArmadilloKeith Spearpage 15 The Shoe SagaJennifer Moropage 16 Coffee Cup Confessional BoothSue Songerpage 18 What Gravity, A Rock And A Rabbit Have To Do With My Love LifeMartin Paul Brittpage 19 Good Bye, Good KnightRich Birdpage 20 Photography Railroad Station IKelly A. Pricepage 22 1000 VinesKelly A. Pricepage 23 Self PortraitKelly A. Pricepage 24 Prose Queen of Dead AirBryan Levekpage 26 Closer to the noiseMichell Heidelpage 29 Somewhere in BetweenKimberly Hunterpage 32 Miss SteakBryan Levekpage 37 Chasing the ChasteTerry Bassettpage 43 Biographies Authors, editorspage 48https://thekeep.eiu.edu/vehicle/1065/thumbnail.jp

The Vehicle, Fall 1994

Table of Contents Poetry Noah\u27s WifeJennifer Moropage 8-9 The Intensity of a BreathHeather Anne Winterspage 10-11 When I Was RainNicole Moonpage 11 Wreckage at Low Tide, After a Storm On Cape FearMatt Parkspage 12-14 two belowKeith Spearpage 16 HeatScott Langrenpage 17 Plastic Shard WordsMatthew J. Nelsonpage 18 Mr. Snowplow ManMartin Paul Brittpage 19 Carpe DiemMichael Lairpage 19 untitledWalt Howardpage 20 The GameKellie J. Olsenpage 21 AT PEACEJennifer Surmanpage 22 SawdustSue Songerpage 23 Photography Unbound RealitiesKris Quiriconipage 26 untitled Mark Porter page 27 untitled Mark Porter page 28 untitled Mark Porter page 29 Prose I am Here...RememberingJ. Dylan McNeillpage 32-34 RecognitionSue Songerpage 35-36 SACCADICSteve Beinpage 37-40 The BurnBryan Levekpage 41-45 Biographiespage 46-48https://thekeep.eiu.edu/vehicle/1063/thumbnail.jp

The Vehicle, Fall 1994

Table of Contents Poetry Noah\u27s WifeJennifer Moropage 8-9 The Intensity of a BreathHeather Anne Winterspage 10-11 When I Was RainNicole Moonpage 11 Wreckage at Low Tide, After a Storm On Cape FearMatt Parkspage 12-14 two belowKeith Spearpage 16 HeatScott Langrenpage 17 Plastic Shard WordsMatthew J. Nelsonpage 18 Mr. Snowplow ManMartin Paul Brittpage 19 Carpe DiemMichael Lairpage 19 untitledWalt Howardpage 20 The GameKellie J. Olsenpage 21 AT PEACEJennifer Surmanpage 22 SawdustSue Songerpage 23 Photography Unbound RealitiesKris Quiriconipage 26 untitled Mark Porter page 27 untitled Mark Porter page 28 untitled Mark Porter page 29 Prose I am Here...RememberingJ. Dylan McNeillpage 32-34 RecognitionSue Songerpage 35-36 SACCADICSteve Beinpage 37-40 The BurnBryan Levekpage 41-45 Biographiespage 46-48https://thekeep.eiu.edu/vehicle/1063/thumbnail.jp

First Light LBT AO Images of HR 8799 bcde at 1.65 and 3.3 Microns: New Discrepancies between Young Planets and Old Brown Dwarfs

As the only directly imaged multiple planet system, HR 8799 provides a unique opportunity to study the physical properties of several planets in parallel. In this paper, we image all four of the HR 8799 planets at H-band and 3.3 microns with the new LBT adaptive optics system, PISCES, and LBTI/LMIRCam. Our images offer an unprecedented view of the system, allowing us to obtain H and 3.3$ micron photometry of the innermost planet (for the first time) and put strong upper-limits on the presence of a hypothetical fifth companion. We find that all four planets are unexpectedly bright at 3.3 microns compared to the equilibrium chemistry models used for field brown dwarfs, which predict that planets should be faint at 3.3 microns due to CH4 opacity. We attempt to model the planets with thick-cloudy, non-equilibrium chemistry atmospheres, but find that removing CH4 to fit the 3.3 micron photometry increases the predicted L' (3.8 microns) flux enough that it is inconsistent with observations. In an effort to fit the SED of the HR 8799 planets, we construct mixtures of cloudy atmospheres, which are intended to represent planets covered by clouds of varying opacity. In this scenario, regions with low opacity look hot and bright, while regions with high opacity look faint, similar to the patchy cloud structures on Jupiter and L/T transition brown-dwarfs. Our mixed cloud models reproduce all of the available data, but self-consistent models are still necessary to demonstrate their viability.Comment: Accepted to Ap

G9a regulates group 2 innate lymphoid cell development by repressing the group 3 innate lymphoid cell program.

Innate lymphoid cells (ILCs) are emerging as important regulators of homeostatic and disease-associated immune processes. Despite recent advances in defining the molecular pathways that control development and function of ILCs, the epigenetic mechanisms that regulate ILC biology are unknown. Here, we identify a role for the lysine methyltransferase G9a in regulating ILC2 development and function. Mice with a hematopoietic cell-specific deletion of G9a (Vav.G9a(-/-) mice) have a severe reduction in ILC2s in peripheral sites, associated with impaired development of immature ILC2s in the bone marrow. Accordingly, Vav.G9a(-/-) mice are resistant to the development of allergic lung inflammation. G9a-dependent dimethylation of histone 3 lysine 9 (H3K9me2) is a repressive histone mark that is associated with gene silencing. Genome-wide expression analysis demonstrated that the absence of G9a led to increased expression of ILC3-associated genes in developing ILC2 populations. Further, we found high levels of G9a-dependent H3K9me2 at ILC3-specific genetic loci, demonstrating that G9a-mediated repression of ILC3-associated genes is critical for the optimal development of ILC2s. Together, these results provide the first identification of an epigenetic regulatory mechanism in ILC development and function

The Scientific Investigation of Unidentified Aerial Phenomena (UAP) Using Multimodal Ground-based Observatories

Peer reviewedPublisher PD

Remodeling Lipid Metabolism and Improving Insulin Responsiveness in Human Primary Myotubes

OBJECTIVE: Disturbances in lipid metabolism are strongly associated with insulin resistance and type 2 diabetes (T2D). We hypothesized that activation of cAMP/PKA and calcium signaling pathways in cultured human myotubes would provide further insight into regulation of lipid storage, lipolysis, lipid oxidation and insulin responsiveness. METHODS: Human myoblasts were isolated from vastus lateralis, purified, cultured and differentiated into myotubes. All cells were incubated with palmitate during differentiation. Treatment cells were pulsed 1 hour each day with forskolin and ionomycin (PFI) during the final 3 days of differentiation to activate the cAMP/PKA and calcium signaling pathways. Control cells were not pulsed (control). Mitochondrial content, (14)C lipid oxidation and storage were measured, as well as lipolysis and insulin-stimulated glycogen storage. Myotubes were stained for lipids and gene expression measured. RESULTS: PFI increased oxidation of oleate and palmitate to CO(2) (p<0.001), isoproterenol-stimulated lipolysis (p = 0.01), triacylglycerol (TAG) storage (p<0.05) and mitochondrial DNA copy number (p = 0.01) and related enzyme activities. Candidate gene and microarray analysis revealed increased expression of genes involved in lipolysis, TAG synthesis and mitochondrial biogenesis. PFI increased the organization of lipid droplets along the myofibrillar apparatus. These changes in lipid metabolism were associated with an increase in insulin-mediated glycogen storage (p<0.001). CONCLUSIONS: Activation of cAMP/PKA and calcium signaling pathways in myotubes induces a remodeling of lipid droplets and functional changes in lipid metabolism. These results provide a novel pharmacological approach to promote lipid metabolism and improve insulin responsiveness in myotubes, which may be of therapeutic importance for obesity and type 2 diabetes

Glutamine versus Ammonia Utilization in the NAD Synthetase Family

NAD is a ubiquitous and essential metabolic redox cofactor which also functions as a substrate in certain regulatory pathways. The last step of NAD synthesis is the ATP-dependent amidation of deamido-NAD by NAD synthetase (NADS). Members of the NADS family are present in nearly all species across the three kingdoms of Life. In eukaryotic NADS, the core synthetase domain is fused with a nitrilase-like glutaminase domain supplying ammonia for the reaction. This two-domain NADS arrangement enabling the utilization of glutamine as nitrogen donor is also present in various bacterial lineages. However, many other bacterial members of NADS family do not contain a glutaminase domain, and they can utilize only ammonia (but not glutamine) in vitro. A single-domain NADS is also characteristic for nearly all Archaea, and its dependence on ammonia was demonstrated here for the representative enzyme from Methanocaldococcus jannaschi. However, a question about the actual in vivo nitrogen donor for single-domain members of the NADS family remained open: Is it glutamine hydrolyzed by a committed (but yet unknown) glutaminase subunit, as in most ATP-dependent amidotransferases, or free ammonia as in glutamine synthetase? Here we addressed this dilemma by combining evolutionary analysis of the NADS family with experimental characterization of two representative bacterial systems: a two-subunit NADS from Thermus thermophilus and a single-domain NADS from Salmonella typhimurium providing evidence that ammonia (and not glutamine) is the physiological substrate of a typical single-domain NADS. The latter represents the most likely ancestral form of NADS. The ability to utilize glutamine appears to have evolved via recruitment of a glutaminase subunit followed by domain fusion in an early branch of Bacteria. Further evolution of the NADS family included lineage-specific loss of one of the two alternative forms and horizontal gene transfer events. Lastly, we identified NADS structural elements associated with glutamine-utilizing capabilities