807 research outputs found

    From Daimones to Demons: Exorcisms and Cultural Constructions of the Demonic in Late Antique Egypt

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    Christian conceptions of demonic forces and possession in Late Antique Egypt were heavily shaped by pre-existing Greek, Egyptian, and Jewish traditions. The syncretic nature of Christianization facilitated an integration of local traditions with new beliefs. A process of demonization occurred as pre-existing views of daimones from the Underworld were transformed from morally ambiguous beings into inherently evil figures. Demons and exorcism rituals served important anthropological functions as they revealed the underlying social conflicts that arose as Christianity spread and changed earlier traditions. This study focuses on magical texts, amulets, and early Christian literature to analyze the effects of Christianization on Egyptian cultural practices and beliefs regarding demons and possession. Demonic entities came to symbolize the cultural “Other,” while exorcisms acted as a ritual performance of these deep-seated tensions and became a form of ritual power over the “Other.

    Summary Report on Information Technology Integration Activities For project to Enhance NASA Tools for Coastal Managers in the Gulf of Mexico and Support Technology Transfer to Mexico

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    Deliverable to NASA Stennis Space Center summarizing summarizes accomplishments made by Battelle and its subcontractors to integrate NASA's COAST visualization tool with the Noesis search tool developed under the Gulf of Mexico Regional Collaborative project

    Enteric glia mediate neuron death in colitis through purinergic pathways that require connexin-43 and nitric oxide

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    The concept of enteric glia as regulators of intestinal homeostasis is slowly gaining acceptance as a central concept in neurogastroenterology. Yet how glia contribute to intestinal disease is still poorly understood. Purines generated during inflammation drive enteric neuron death by activating neuronal P2X7 purine receptors (P2X7R), triggering ATP release via neuronal pannexin-1 channels that subsequently recruits intracellular calcium ([Ca(2+)]i) responses in the surrounding enteric glia. We tested the hypothesis that the activation of enteric glia contributes to neuron death during inflammation.We studied neuroinflammation in vivo using the 2,4-dinitrobenzenesulfonic acid model of colitis and in situ using whole-mount preparations of human and mouse intestine. Transgenic mice with a targeted deletion of glial connexin-43 (Cx43) [GFAP∷Cre (ERT2+/-)/Cx43(f/f) ] were used to specifically disrupt glial signaling pathways. Mice deficient in inducible nitric oxide (NO) synthase (iNOS (-/-)) were used to study NO production. Protein expression and oxidative stress were measured using immunohistochemistry and in situ Ca(2+) and NO imaging were used to monitor glial [Ca(2+)]i and [NO]i.Purinergic activation of enteric glia drove [Ca(2+)]i responses and enteric neuron death through a Cx43-dependent mechanism. Neurotoxic Cx43 activity, driven by NO production from glial iNOS, was required for neuron death. Glial Cx43 opening liberated ATP and Cx43-dependent ATP release was potentiated by NO.Our results show that the activation of glial cells in the context of neuroinflammation kills enteric neurons. Mediators of inflammation that include ATP and NO activate neurotoxic pathways that converge on glial Cx43 hemichannels. The glial response to inflammatory mediators might contribute to the development of motility disorders

    Designing Digital COVID-19 Screening: Insights and Deliberations

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    Due to the global COVID-19 pandemic, public health control and screening measures have been introduced at healthcare facilities, including those housing our most vulnerable populations. These warning measures situated at hospital entrances are presently labour-intensive, requiring additional staff to conduct manual temperature checks and risk-assessment questionnaires of every individual entering the premises. To make this process more efficient, we present eGate, a digital COVID-19 health-screening smart Internet of Things system deployed at multiple entry points around a children's hospital. This paper reports on design insights based on the experiences of concierge screening staff stationed alongside the eGate system. Our work contributes towards social-technical deliberations on how to improve design and deploy of digital health-screening systems in hospitals. It specifically outlines a series of design recommendations for future health screening interventions, key considerations relevant to digital screening control systems and their implementation, and the plausible effects on the staff who work alongside them

    Selvkost i Bodø kommune

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    Studentarbeid i økonomi og ledelse (bachelorgrad) - Høgskolen i Bodø, 2009Selvkostkalkulasjon er en av de tradisjonelle kalkulasjonsmetodene med størst oppmerksomhet rettet mot de indirekte kostnadene (Sending og Tangenes, 2007). De fleste kommuner i Norge anvender selvkost for å beregne gebyrgrunnlaget på ulike tjenester, som vann, avløp, renovasjon og lignende. Derfor vil dette berøre de aller fleste av innbyggerne i Norge. I oppsettet av denne type kalkulasjon vil det ofte oppstå problemer og utfordringer, da spesielt med hensyn på de indirekte kostnadene. Vi har derfor valgt å se på følgende problemstilling: Hvilke utfordringer er forbundet med selvkostkalkulering tilknyttet kommunal tjenesteproduksjon? Denne problemstillingen er forsøkt besvart gjennom relevant teori innenfor Selvkost, ABC, Norm- praksis-bruk, Systemteori og en Sensitivitetsnalyse. Videre knyttes dette opp mot diverse intervjuer og samtaler med ansatte i Bodø kommune som er vårt case-objekt. I empirien presenteres de funnene som vi har gjort gjennom intervju og samtaler. Noe av det vi fant var ulik oppfatning av regnskapspraksis og ulike meninger om hvor stor detaljeringsgraden skal være. Vi tror at ved å ha en jevnlig oppdatering av de ulike systemene, vil det være mulig å finne de mest korrekte kostnadene. Gjennom drøfting og analysering har vi prøvd å finne ulike årsaker til de problemer som har oppstått. I løpet av denne skriveprosessen har vi funnet ut at mange av de utfordringer som kan oppstå i kalkuleringen er mangel på dokumentasjon, ulik oppfatning av regnskapsbruk, manglende oppdatering av regnskapstall, samt ulik praksis mellom avdelinger

    Predictive Validity of the MAYSI-2 and PAI-A for Suicide-Related Behavior and Nonsuicidal Self-Injury Among Adjudicated Adolescent Offenders on Probation

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    This prospective study evaluated the ability of the MAYSI-2 and PAI-A to predict suicide-related behavior (SRB) and non-suicidal self-injury (NSSI) among adjudicated adolescent offenders on probation. Predictive validity of the MAYSI-2 for SRB and NSSI has generally been postdictively examined among detained adolescents. In addition, no published studies have examined the predictive validity of the PAI-A for SRB and NSSI among adolescent offenders. Neither the MAYSI-2 nor PAI-A added incremental predictive validity above lifetime SRB or NSSI. However, several MAYSI-2 and PAI-A subscales were predictive of SRB or NSSI. With some exceptions, most recommended instrument cut-off scores differentiated between low-risk and high-risk youth. These findings suggest that the MAYSI-2 and PAI-A hold promise for evaluating SRB and NSSI among justice-involved youth. In addition, these findings contribute to more informed decisions regarding the use of these tools and can be used to inform SRB and NSSI prevention efforts

    High-fat diet impairs duodenal barrier function and elicits glia-dependent changes along the gut-brain axis that are required for anxiogenic and depressive-like behaviors

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    Background: Mood and metabolic disorders are interrelated and may share common pathological processes. Autonomic neurons link the brain with the gastrointestinal tract and constitute a likely pathway for peripheral metabolic challenges to affect behaviors controlled by the brain. The activities of neurons along these pathways are regulated by glia, which exhibit phenotypic shifts in response to changes in their microenvironment. How glial changes might contribute to the behavioral effects of consuming a high-fat diet (HFD) is uncertain. Here, we tested the hypothesis that anxiogenic and depressive-like behaviors driven by consuming a HFD involve compromised duodenal barrier integrity and subsequent phenotypic changes to glia and neurons along the gut-brain axis. Methods: C57Bl/6 male mice were exposed to a standard diet or HFD for 20 weeks. Bodyweight was monitored weekly and correlated with mucosa histological damage and duodenal expression of tight junction proteins ZO-1 and occludin at 0, 6, and 20 weeks. The expression of GFAP, TLR-4, BDNF, and DCX were investigated in duodenal myenteric plexus, nodose ganglia, and dentate gyrus of the hippocampus at the same time points. Dendritic spine number was measured in cultured neurons isolated from duodenal myenteric plexuses and hippocampi at weeks 0, 6, and 20. Depressive and anxiety behaviors were also assessed by tail suspension, forced swimming, and open field tests. Results: HFD mice exhibited duodenal mucosa damage with marked infiltration of immune cells and decreased expression of ZO-1 and occludin that coincided with increasing body weight. Glial expression of GFAP and TLR4 increased in parallel in the duodenal myenteric plexuses, nodose ganglia, and hippocampus in a time-dependent manner. Glial changes were associated with a progressive decrease in BDNF, and DCX expression, fewer neuronal dendritic spines, and anxiogenic/depressive symptoms in HFD-treated mice. Fluorocitrate (FC), a glial metabolic poison, abolished these effects both in the enteric and central nervous systems and prevented behavioral alterations at week 20. Conclusions: HFD impairs duodenal barrier integrity and produces behavioral changes consistent with depressive and anxiety phenotypes. HFD-driven changes in both peripheral and central nervous systems are glial-dependent, suggesting a potential glial role in the alteration of the gut-brain signaling that occurs during metabolic disorders and psychiatric co-morbidity
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