Polar Hydration is a company whose mission is to combat the risk of dehydration in cold climates and inspire the adventurer with all of us. Through ASU’s Founders Lab and a partnership with NASA, we set out to take NASA patented technology and develop a business plan through gauging public interest via surveys and interviews, and implementing a marketing strategy based on those results. Our product consists of a freeze-resistant hydration pack which uses insulation and electronics to actively heat its water contents and prevent freezing. With outdoor activities, the colder the weather the higher the risk of dehydration. This is due to the intake of colder dryer air as well as it being harder to recognize that you are losing liquids through sweat as it is in warmer climates. In winter sports such as skiing and snowboarding as well as colder conditions for hiking and hunting, this can become a huge problem as water is not readily available. That’s why, at Polar Hydration, we took NASA patented technology to design our freeze-resistant hydration pack. It’s designed like most other hydration packs, consisting of a backpack with a plastic bladder holding water and straw to drink from, but with additional layers of insulation and electronics to prevent water from freezing. With this, we will combat dehydration and inspire the adventurer within all of us.

This story ---Under Still Faces--- is a horror fiction story. It is influenced primarily by classic, gothic literature with themes from the horror and true crime genres. The story includes critical/theoretical concepts, literary devices, and techniques from gothic literature primarily including Freud’s Uncanny, uneven framing, and an unreliable narrator. It employs themes from Edgar Allan Poe’s novels as well as his thesis regarding plot in The Philosophy of Composition. Particular descriptive themes in conjunction with the use of gothic elements surprise the reader about the story’s true ending similar to Poe’s The Oval Portrait. Included is an analysis of the literary decisions made in the piece to evoke specific reactions and feelings from the reader.

Sphingosine-1-phosphate receptors (S1PRs) and their signaling pathways play an important role in mediating vascular health and function. Upon ligand mediated activation, S1PRs 1-5 couple with diverse heterotrimeric G-protein subunits (Gαi, Gαq/11, Gα12/13), initiating multimodal downstream signaling pathways which result in various physiological outcomes in the vasculature, including cell proliferation and migration, barrier integrity preservation or loss, contraction, and inflammation. Specifically, S1PR2 activation has been linked to endothelial activation, barrier integrity loss, and inflammation, whereas S1PR1 activation contributes to barrier integrity preservation, vasodilation, and anti-inflammatory properties. Although the role of S1PRs during pathophysiological conditions such as acute ischemic stroke is under current investigation, the complete S1PR expression profile in the cerebrovasculature following acute ischemic injury has not yet been investigated. Therefore, the present study was aimed to characterize the expression profiles of S1PRs 1-5 in human brain microvascular endothelial cells (HBMECs) and human brain vascular smooth muscle cells (HBVSMCs) following 3h hypoxia plus glucose deprivation (HGD; in vitro ischemic injury) exposure. At the mRNA level, we observed expression of S1PRs 1-5 in HBVSMCs and S1PRs 1-4 in HBMECs. Under basal conditions, we employed real-time RT-PCR and observed that mRNA levels of S1PR1 were highest in expression followed by S1PR3 then S1PR2 in HBMECs. On the other hand, S1PR3 mRNA was the highest followed by S1PR2 then S1PR1 in HBVSMCs. In HBMECs, HGD exposure increased S1PR1 mRNA and protein levels, but decreased S1PR1 mRNA in HBVSMCs. Similarly, HGD induced increased S1PR3 mRNA in HBMECs and decreased S1PR3 mRNA in HBVSMCs. For S1PR2, HGD did not alter mRNA or protein expression in HBMECs but increased mRNA levels in HBVSMCs. These data suggest that acute exposure to HGD appears to differentially regulate expression of S1PRs in HBMECs and HBVSMCs. The differential expression in S1PRs both basally and following HGD exposure may suggest distinct signaling mechanisms at play within the two cerebrovascular cell types, implicating these receptors as potential therapeutic targets following ischemic injury.