Effects of Surveillance on Intrinsic Motivation

Previous research indicates that explicit surveillance should induce subjects to attribute their performance at a task to the surveillance; hence, such subjects should persist to a lesser extent than subjects not exposed to such surveillance. Two forms of explicit surveillance were utilized: human and camera, as well as the appropriate opposites (human non- and camera non-surveillance). Subjects were directed to perform a model construction task, then were unobtrusively observed during a post-task “waiting period.” No difference in persistence was found for type of surveillance utilized. However, as predicted, subjects exposed to surveillance persisted less with the task materials than subjects not exposed

STAT3 activation in large granular lymphocyte leukemia is associated with cytokine signaling and DNA hypermethylation

Large granular lymphocyte leukemia (LGLL) is characterized by somatic gain-of-function STAT3 mutations. However, the functional effects of STAT3 mutations on primary LGLL cells have not been studied in detail. In this study, we show that CD8+ T cells isolated from STAT3 mutated LGLL patients have high protein levels of epigenetic regulators, such as DNMT1, and are characterized by global hypermethylation. Correspondingly, treatment of healthy CD8+ T cells with IL-6, IL-15, and/or MCP-1 cytokines resulted in STAT3 activation, increased DNMT1, EZH2, c-MYC, l-MYC, MAX, and NF kappa B levels, increased DNA methylation, and increased oxidative stress. Similar results were discovered in KAI3 NK cells overexpressing gain-of-function STAT3(Y640F) and STAT3(G618R) mutants compared to KAI3 NK cells overexpressing STAT3(WT). Our results also confirm that STAT3 forms a direct complex with DNMT1, EZH2, and HDAC1. In STAT3 mutated LGLL cells, DNA methyltransferase (DNMT) inhibitor azacitidine abrogated the activation of STAT3 via restored SHP1 expression. In conclusion, STAT3 mutations cause DNA hypermethylation resulting in sensitivity to DNMT inhibitors, which could be considered as a novel treatment option for LGLL patients with resistance to standard treatments.Peer reviewe

Sensorimotor Function in Progressive Multiple Sclerosis

Background: A sensitive test reflecting subtle sensorimotor changes throughout disease progression independent of mobility impairment is currently lacking in progressive multiple sclerosis. Objectives: We examined non-ambulatory measures of upper and lower extremity sensorimotor function that may reveal differences between relapsing–remitting and progressive forms of multiple sclerosis. Methods: Cutaneous sensitivity, proprioception, central motor function and mobility were assessed in 32 relapsing–remitting and 31 progressive multiple sclerosis patients and 30 non-multiple sclerosis controls. Results: Cutaneous sensation differed between relapsing–remitting and progressive multiple sclerosis at the foot and to a lesser extent the hand. Proprioception function in the upper but not the lower extremity differed between relapsing–remitting and progressive multiple sclerosis, but was different for both upper and lower extremities between multiple sclerosis patients and non-multiple sclerosis controls. Foot-tap but not hand-tap speed was slower in progressive compared to relapsing–remitting multiple sclerosis, suggestive of greater central motor function impairment in the lower extremity in progressive multiple sclerosis. In addition, the non-ambulatory sensorimotor measures were more sensitive in detecting differences between relapsing–remitting and progressive multiple sclerosis than mobility assessed with the 25-foot walk test. Conclusion: This study provides novel information about changes in sensorimotor function in progressive compared with relapsing–remitting forms of multiple sclerosis, and in particular the importance of assessing both upper and lower extremity function. Importantly, our findings showed loss of proprioceptive function in multiple sclerosis but also in progressive compared to relapsing–remitting multiple sclerosis

Socialt kapital och politiskt deltagande : En studie av sju afrikanska stater

Avsikten med avhandlingen har varit att undersöka om socialt kapital har en positiv effekt på politiskt deltagande i Afrika. Totalt studerades sju afrikanska demokratier, nämligen Kap Verde, Ghana, Benin, Namibia, Botswana, Mauritius och Sydafrika. Datamaterialet hämtades från Afrobarometer. För denna avhandling användes surveydata från omgång fem som utkom mellan åren 2011–2013. Analysen gjordes i olika faser. Först presenterades deskriptiv statistik för socialt kapital och politiskt deltagande. Sedan testades sambanden mellan socialt kapital och politiskt deltagande med hjälp av bivariata analyser. Analysen fullbordades i form av en multivariat logistisk regressionsanalys. Tidigare studier på området har påvisat att socialt kapital har en gynnande effekt på politiskt deltagande. Därmed var syftet att pröva om detta även gäller för Afrika där sambandet mellan socialt kapital och politiskt deltagande inte studerats i samma utsträckning som på övriga håll i världen. I avhandlingen operationaliserades socialt kapital med hjälp av två indikatorer, nämligen förtroende och föreningsaktivitet. Föreningsaktiviteten mättes genom engagemang i frivilliga- och religiösa organisationer. Politiskt deltagande undersöktes med hjälp av fem indikatorer. Dessa utgjordes av att rösta i val, att arbeta för ett parti eller en kandidat, att delta i kampanjorienterat arbete, att kontakta politiker och slutligen att delta i demonstrationer eller protestmarscher. Av resultaten framgick att föreningsaktivitet utövade en positiv effekt på samtliga former av politiskt deltagande. Studien intygar att det politiska deltagandet var högre bland individer som uppvisade högre föreningsengagemang. Förtroende präglades av ett annorlunda mönster. Förtroende saknade statistisk effekt i fyra av fem fall. Endast i förhållande till demonstrationer och protestmarscher identifierades ett positivt samband. Till följd därav fastställs att den positiva effekten av socialt kapital på politiskt deltagandet även gällde i de sju afrikanska staterna med särskild betoning på föreningsaktivitet. Detta medan förtroende saknade genomgående positiv effekt på politiskt deltagande

History of forest insect investigations in British Columbia III. The Vernon Laboratory and federal entomology in British Columbia

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Phosphoinositide Lipids in Ocular Tissues

Inositol phospholipids play an important role in cell physiology. The inositol head groups are reversibly phosphorylated to produce seven distinct phosphorylated inositides, commonly referred to as phosphoinositides (PIs). These seven PIs are dynamically interconverted from one PI to another by the action of PI kinases and PI phosphatases. The PI signals regulate a wide variety of cellular functions, including organelle distinction, vesicular transport, cytoskeletal organization, nuclear events, regulation of ion channels, cell signaling, and host–pathogen interactions. Most of the studies of PIs in ocular tissues are based on the PI enzymes and PI phosphatases. In this study, we examined the PI levels in the cornea, retinal pigment epithelium (RPE), and retina using PI-binding protein as probes. We have examined the lipids PI(3)P, PI(4)P, PI(3,4)P2, PI(4,5)P2, and PI(3,4,5)P3, and each is present in the cornea, RPE, and retina. Alterations in the levels of these PIs in mouse models of retinal disease and corneal infections have been reported, and the results of our study will help in the management of anomalous phosphoinositide metabolism in ocular tissues

Insulin receptor signaling regulates actin cytoskeletal organization in developing photoreceptors

The insulin receptor (ir) and ir signaling proteins are widely distributed throughout the cns. ir signaling provides a trophic signal for transformed retinal neurons in culture and we recently reported that deletion of ir in rod photoreceptors by cre/lox system resulted in stress‐induced photoreceptor degeneration. these studies suggest a neuroprotective role of ir in rod photoreceptor cell function. however, there are no studies available on the role of insulin‐induced ir signaling in the development of normal photoreceptors. to examine the role of insulin‐induced ir signaling, we analyzed cultured neuronal cells isolated from newborn rodent retinas. in insulin‐lacking cultures, photoreceptors from wild‐type rat retinas exhibited an abnormal morphology with a wide axon cone and disorganization of the actin and tubulin cytoskeleton. photoreceptors from ir knockout mouse retinas also exhibited a similar abnormal morphology. a novel finding in this study was that addition of docosahexaenoic acid, a photoreceptor trophic factor, restored normal axonal outgrowth in insulin‐lacking cultures. these data suggest that ir signaling pathways regulate actin and tubulin cytoskeletal organization in photoreceptors; they also imply that insulin and docosahexaenoic acid activate at least partially overlapping signaling pathways that are essential for the development of normal photoreceptors.Fil: Rajala, Raju V. S.. University of Oklahoma Health Sciences Center; Estados UnidosFil: Rajala, Ammaji. University of Oklahoma Health Sciences Center; Estados UnidosFil: Brush, Richard S.. University of Oklahoma Health Sciences Center; Estados UnidosFil: Rotstein, Nora Patricia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: Politi, Luis Enrique. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentin