208 research outputs found

    Looking for Group: Sociality, Embodiment, and Institutions in World of Warcraft

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    This ethnography examines the varying degrees of conflict between multiple stakeholders involved in the massively multiplayer online role-playing game World of Warcraft (WoW). The game’s designers, like many software developers in the contemporary world, tend to be guided by an ideology influenced by classical liberalism, but also inspired by a utopian view of technology in general. That ideological position has directly affected many aspects of the game, from the largely unregulated in-game economy, to the strong emphasis on individual mastery of the game’s systems to progress through the complete content of the game world. World of Warcraft advertises itself not just on its narrative and combat mechanics; it also entices players to participate because of its very nature as a multiplayer game. The structure of WoW encourages players to join together in tight-knit communities (“guilds”) not just to overcome powerful opponents, but to socialize as well. In this way the game exists for many players as a significant social outlet in their everyday lives. However, players, guilds, and designers exist in a state of tension due to the ideological and architected constraints of the game. Due to the classical liberal bent of WoW promoting individual achievement through the game’s many obstacles, players oftentimes find themselves having to break away from close friends they game with in order to follow the primary goals of the narrative. This leads to an environment where players are constantly weighing the social bonds they establish and/or maintain through play against the concerns of software programmers intent on directing them to endgame content above all else

    Mechanosensing of shear by Pseudomonas aeruginosa leads to increased levels of the cyclic-di-GMP signal initiating biofilm development

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    Biofilms are communities of sessile microbes that are phenotypically distinct from their genetically identical, free-swimming counterparts. Biofilms initiate when bacteria attach to a solid surface. Attachment triggers intracellular signaling to change gene expression from the planktonic to the biofilm phenotype. For Pseudomonas aeruginosa, it has long been known that intracellular levels of the signal cyclic-di-GMP increase upon surface adhesion and that this is required to begin biofilm development. However, what cue is sensed to notify bacteria that they are attached to the surface has not been known. Here, we show that mechanical shear acts as a cue for surface adhesion and activates cyclic-di-GMP signaling. The magnitude of the shear force, and thereby the corresponding activation of cyclic-di-GMP signaling, can be adjusted both by varying the strength of the adhesion that binds bacteria to the surface and by varying the rate of fluid flow over surface-bound bacteria. We show that the envelope protein PilY1 and functional type IV pili are required mechanosensory elements. An analytic model that accounts for the feedback between mechanosensors, cyclic-di-GMP signaling, and production of adhesive polysaccharides describes our data well

    College Students, Technology, and Time

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    Our research explores CUNY students’ lived experiences using digital technology in and out of class, on and off campus. Beyond checking grades or emailing a professor, students use digital technology to create space and time for their schoolwork. However, technology can also impede students’ opportunities for making space and time. Understanding how students use digital technology is crucial for colleges and universities to better support students in their academic work

    Liquid Sucrose Consumption Promotes Obesity and Impairs Glucose Tolerance Without Altering Circulating Insulin Levels

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    © 2018 The Obesity Society Objective: Multiple factors contribute to the rising rates of obesity and to difficulties in weight reduction that exist in the worldwide population. Caloric intake via sugar-sweetened beverages may be influential. This study tested the hypothesis that liquid sucrose intake promotes obesity by increasing serum insulin levels and tissue lipid accumulation. Methods: C57BL/6J mice were given 30% sucrose in liquid form. Changes in weight gain, body composition, energy expenditure (EE), and tissue lipid content were measured. Results: Mice drinking sucrose gained more total body mass (TBM), had greater fat mass, and displayed impaired glucose tolerance relative to control mice. These metabolic changes occurred without alterations in circulating insulin levels and despite increases in whole body EE. Lipid accrued in liver, but not skeletal muscle, of sucrose-consuming mice. Oxygen consumption (VO2) correlated with fat-free mass and moderately with TBM, but not with fat mass. ANCOVA for treatment effects on EE, with TBM, VO2, lean body mass, and fat-free mass taken as potential covariates for EE, revealed VO2 as the most significant correlation. Conclusions: Weight gain induced by intake of liquid sucrose in mice is associated with lipid accrual in liver, but not skeletal muscle, and occurs without an increase in circulating insulin

    Targeted disruption of cubilin reveals essential developmental roles in the structure and function of endoderm and in somite formation

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    BACKGROUND: Cubilin is a peripheral membrane protein that interacts with the integral membrane proteins megalin and amnionless to mediate ligand endocytosis by absorptive epithelia such as the extraembryonic visceral endoderm (VE). RESULTS: Here we report the effects of the genetic deletion of cubilin on mouse embryonic development. Cubilin gene deletion is homozygous embryonic lethal with death occurring between 7.5–13.5 days post coitum (dpc). Cubilin-deficient embryos display developmental retardation and do not advance morphologically beyond the gross appearance of wild-type 8–8.5 dpc embryos. While mesodermal structures such as the allantois and the heart are formed in cubilin mutants, other mesoderm-derived tissues are anomalous or absent. Yolk sac blood islands are formed in cubilin mutants but are unusually large, and the yolk sac blood vessels fail to undergo remodeling. Furthermore, somite formation does not occur in cubilin mutants. Morphological abnormalities of endoderm occur in cubilin mutants and include a stratified epithelium in place of the normally simple columnar VE epithelium and a stratified cuboidal epithelium in place of the normally simple squamous epithelium of the definitive endoderm. Cubilin-deficient VE is also functionally defective, unable to mediate uptake of maternally derived high-density lipoprotein (HDL). CONCLUSION: In summary, cubilin is required for embryonic development and is essential for the formation of somites, definitive endoderm and VE and for the absorptive function of VE including the process of maternal-embryo transport of HDL

    Census politics in deeply divided societies

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    Population censuses in societies that are deeply divided along ethnic, religious or linguistic lines can be sensitive affairs – particularly where political settlements seek to maintain peace through the proportional sharing of power between groups. This brief sets out some key findings from a research project investigating the relationship between census politics and the design of political institutions in Bosnia and Herzegovina, Kenya, Lebanon and Northern Ireland

    Fibulin-1 is required for morphogenesis of neural crest-derived structures

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    AbstractHere we report that mouse embryos homozygous for a gene trap insertion in the fibulin-1 (Fbln1) gene are deficient in Fbln1 and exhibit cardiac ventricular wall thinning and ventricular septal defects with double outlet right ventricle or overriding aorta. Fbln1 nulls also display anomalies of aortic arch arteries, hypoplasia of the thymus and thyroid, underdeveloped skull bones, malformations of cranial nerves and hemorrhagic blood vessels in the head and neck. The spectrum of malformations is consistent with Fbln1 influencing neural crest cell (NCC)-dependent development of these tissues. This is supported by evidence that Fbln1 expression is associated with streams of cranial NCCs migrating adjacent to rhombomeres 2–7 and that Fbln1-deficient embryos display patterning anomalies of NCCs forming cranial nerves IX and X, which derive from rhombomeres 6 and 7. Additionally, Fbln1-deficient embryos show increased apoptosis in areas populated by NCCs derived from rhombomeres 4, 6 and 7. Based on these findings, it is concluded that Fbln1 is required for the directed migration and survival of cranial NCCs contributing to the development of pharyngeal glands, craniofacial skeleton, cranial nerves, aortic arch arteries, cardiac outflow tract and cephalic blood vessels

    Heme oxygenase-1 deficiency alters erythroblastic Island formation, steady-state erythropoiesis and red blood cell lifespan in mice

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    Heme oxygenase-1 is critical for iron recycling during red blood cell turnover, whereas its impact on steady-state erythropoiesis and red blood cell lifespan is not known. We show here that in 8- to 14-week old mice, heme oxygenase- 1 deficiency adversely affects steady-state erythropoiesis in the bone marrow. This is manifested by a decrease in Ter-119+-erythroid cells, abnormal adhesion molecule expression on macrophages and erythroid cells, and a greatly diminished ability to form erythroblastic islands. Compared with wild-type animals, red blood cell size and hemoglobin content are decreased, while the number of circulating red blood cells is increased in heme oxygenase-1 deficient mice, overall leading to microcytic anemia. Heme oxygenase-1 deficiency increases oxidative stress in circulating red blood cells and greatly decreases the frequency of macrophages expressing the phosphatidylserine receptor Tim4 in bone marrow, spleen and liver. Heme oxygenase-1 deficiency increases spleen weight and Ter119+-erythroid cells in the spleen, although α4β1-integrin expression by these cells and splenic macrophages positive for vascular cell adhesion molecule 1 are both decreased. Red blood cell lifespan is prolonged in heme oxygenase-1 deficient mice compared with wild-type mice. Our findings suggest that while macrophages and relevant receptors required for red blood cell formation and removal are substantially depleted in heme oxygenase- 1 deficient mice, the extent of anemia in these mice may be ameliorated by the prolonged lifespan of their oxidatively stressed erythrocytes

    Ocean and coastal acidification off New England and Nova Scotia

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    Author Posting. © The Oceanography Society, 2015. This article is posted here by permission of The Oceanography Society for personal use, not for redistribution. The definitive version was published in Oceanography 28, no. 2 (2015): 182-197, doi:10.5670/oceanog.2015.41.New England coastal and adjacent Nova Scotia shelf waters have a reduced buffering capacity because of significant freshwater input, making the region’s waters potentially more vulnerable to coastal acidification. Nutrient loading and heavy precipitation events further acidify the region’s poorly buffered coastal waters. Despite the apparent vulnerability of these waters, and fisheries’ and mariculture’s significant dependence on calcifying species, the community lacks the ability to confidently predict how the region’s ecosystems will respond to continued ocean and coastal acidification. Here, we discuss ocean and coastal acidification processes specific to New England coastal and Nova Scotia shelf waters and review current understanding of the biological consequences most relevant to the region. We also identify key research and monitoring needs to be addressed and highlight existing capacities that should be leveraged to advance a regional understanding of ocean and coastal acidification.This project was supported in part by an appointment to the Internship/Research Participation Program at the Office of Water, US Environmental Protection Agency (EPA), administered by the Oak Ridge Institute for Science and Education through an interagency agreement between the US Department of Energy and the EPA. JS acknowledges support from NASA grant from NNX14AL84G NASA-CCS
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