Acedia in the Local Church: Cultivating the Virtue of Charity as a Remedy for the Vice of Acedia

The vice of acedia is one of the greatest challenges the church is currently facing. Acedia lies at the root of indifference, apathy, idleness, and a lack of engagement in the life of a community of faith. Paradoxically, acedia also manifests as dutiful, distracted service that seeks to maintain status quo or personal preferences. Adding to the complexity further, acedia will also produce an overwhelming desire to leave one’s faith community for any other place that promises to meet one’s needs or provide a more hospitable environment for one’s growth. The first step that must be undertaken against this forgotten vice is to describe acedia, name the primary ways it is attacking the local church, and identify the way scripture portrays its effects. This initial exploration is essential to the church’s recovery because of the anonymity acedia currently enjoys. In order to begin to recover from the symptoms of acedia, the church must first be able to accurately name and diagnose acedia. Prescribing a remedy for the vice of acedia will begin with a description of the teleological, teachable, and habitual nature of virtue. From this basic foundation a framework for combatting the vice of acedia and cultivating the virtue of charity will be constructed. The principle components of this framework include a narrative approach to forming telos and identity, a working understanding of habit and habit formation, and a practical introduction to the practices and habits that can rescue from acedia and cultivate friendship with God. Ultimately it is the implementation of a series of practices and habits that will enable the church to equip her members to live in the union and friendship with God and one another we have been designed for, that has been frustrated and destroyed by the vicious effects of acedia

A Theology of Weakness: Word Studies from the Greek Text of II Corinithians 12:9 in Context With Exegesis of Seven Select Passages of Scripture

Excerpt: In his commentary on the second letter of Paul to the Corinthians , R. C. H. Lenski proposes that the verb teleo in II Corinthians 12 :9 is mistranslated . Whereas most translations say, My grace is sufficient for you, for my strength is made perfect in weakness , Lenski believes that the last phrase should read, for the power is brought to its finish in weakness. It seems that he stands unsupported in this conviction, for my research uncovered no other commentator who suggested such an interpretation

Advancing the Knowledge of Organic Farming Data in New Mexico: Health and Injury Surveillance Systems

While the concept and practice of organic farming has been around since the mid-1800s, there is little data currently being collected on injury, illness, or fatality within the organic farming population, leaving the health risks unknown. This paper intends to look at the surveillance systems currently in place to collect injury and illness data as it relates to organic farmers, and in particular, the New Mexico organic farmer. Evaluations of the current surveillance systems were conducted, and organic farmer demographics were analyzed using rate ratio comparisons of United States(U.S.), Texas, and New Mexico. The results show that the current surveillance systems do not generally include organic farming in their results, and what is collected is limited to demographic and economic counts. The analysis of the demographic data show that New Mexico organic farmers have a roughly similar demographic make-up as that of both U.S. and Texas organic farmers, but are younger and have been farming their current organic farms less time than New Mexico farmers on the whole. New Mexico farmers also has a significantly larger Hispanic population than is seen in either the U.S. or Texas. Understanding the demographic makeup of New Mexico organic farmers is important in the future to identify injury and illness risk factors within the population. However, without further data collection in the areas of injury and illness among organic farmers, there will be no way to measure the true health risks of this profession, or evaluate any potential interventions

Chronic cocaine exposure in Drosophila: Life, cell death and oogenesis

AbstractDevelopmental signaling cascades that can be perturbed by cocaine and other drugs of abuse have been difficult to study in humans and vertebrate models. Although numerous direct neural targets of cocaine have been elucidated at the molecular level, little is known about the specific cellular events that are impacted indirectly as a result of the drug's perturbation of neural circuits. We have developed oogenesis in Drosophila melanogaster as a model in which to identify downstream biochemical and/or cellular processes that are disrupted by chronic cocaine exposure. In this model, cocaine feeding resulted not only in expected reductions in viability, but also in unanticipated developmental defects during oogenesis, including aberrant follicle morphogenesis and vitellogenic follicle degeneration. To identify mechanisms through which cocaine exerted its deleterious effects on oogenesis, we examined candidate components of neural and hormonal signaling pathways. Cocaine-induced disruptions in follicle formation were enhanced by juvenile hormone exposure and phenocopied by serotonin feeding, while cocaine-activated follicle apoptosis was enhanced by concomitant dopamine feeding. HPLC analysis of dopamine and serotonin in the ovary suggests that these neurotransmitters could variably mediate cocaine's effects on oogenesis indirectly in the brain and/or directly in the ovary itself. We confirmed the involvement of hormone signaling by measuring ecdysteroids, which increase following cocaine exposure, and by demonstrating suppression of cocaine-induced follicle loss by hormone receptor mutants. Cocaine-induced ovarian follicle apoptosis and adult lethality appear to be caused by modulation of dopamine levels, while morphological defects during follicle formation likely result from perturbing serotonin signaling during cocaine exposure. Our work suggests not only a new role for juvenile hormone and/or serotonin in Drosophila ovarian follicle formation, but also a cocaine-sensitive role for dopamine in modulating hormone levels in the female fly

Trick or re-treat : towards a new treasure-seeking ethic in Canada's north

This project explores the notion that the summer camping community in Dawson City, Yukon, epitomizes the possibility that the retreat and the quest, often considered distinct forms of travel and discovery, are closely related in the contemporary Canadian context. The journey North to Dawson City--a town and region famous for the Klondike Gold Rush and treasure-seeking--is akin to a rite of passage and to the questing patterns that are evident in many myths of heroism. Every hero reckons with a threat and saves the day. While boreal "wilderness" has traditionally been depicted as potentially dangerous and challenging terrain, the location of the threat has shifted significantly over the past three or four decades in North America. Pollution and the rat race are the new raging river and pack of wolves. Framed in this way, the hero's quest for adventure and treasure shares a seat with the weakling's retreat. I believe that what has been referred to as "the Myth of the North" is intact to this day. The symbolic structure of the North is communicated by oral tradition and in text through story, song, slang, and fashion. A limen is a margin and a threshold and discussions of the Canadian North are at home in the field of religious studies when we conceptualize the North as liminal space and place. The North is physically liminal as the end of the road, politically liminal as a colonial state and conceptually liminal as a frontier. The following writing has been largely inspired by the conversations and scenery that I experienced upon my three-time journey to Dawson City. The ideas presented in this paper have developed from a combination of text-based and primary research, largely informed by the theories of anthropologist Victor Turner and by my friends, colleagues, and acquaintances in Dawson

Manipulation of P-TEFb control machinery by HIV: recruitment of P-TEFb from the large form by Tat and binding of HEXIM1 to TAR

Basal transcription of the HIV LTR is highly repressed and requires Tat to recruit the positive transcription elongation factor, P-TEFb, which functions to promote the transition of RNA polymerase II from abortive to productive elongation. P-TEFb is found in two forms in cells, a free, active form and a large, inactive complex that also contains 7SK RNA and HEXIM1 or HEXIM2. Here we show that HIV infection of cells led to the release of P-TEFb from the large form. Consistent with Tat being the cause of this effect, transfection of a FLAG-tagged Tat in 293T cells caused a dramatic shift of P-TEFb out of the large form to a smaller form containing Tat. In vitro, Tat competed with HEXIM1 for binding to 7SK, blocked the formation of the P-TEFb–HEXIM1–7SK complex, and caused the release P-TEFb from a pre-formed P-TEFb–HEXIM1–7SK complex. These findings indicate that Tat can acquire P-TEFb from the large form. In addition, we found that HEXIM1 binds tightly to the HIV 5′ UTR containing TAR and recruits and inhibits P-TEFb activity. This suggests that in the absence of Tat, HEXIM1 may bind to TAR and repress transcription elongation of the HIV LTR

The Drosophila 7SK snRNP and the essential role of dHEXIM in development

Regulation of the positive transcription elongation factor, P-TEFb, plays a major role in controlling mammalian transcription and this is accomplished in part by controlled release of P-TEFb from the 7SK snRNP that sequesters the kinase in an inactive state. We demonstrate here that a similar P-TEFb control system exists in Drosophila. We show that an RNA previously suggested to be a 7SK homolog is, in fact, associated with P-TEFb, through the action of a homolog of the human HEXIM1/2 proteins (dHEXIM). In addition, a Drosophila La related protein (now called dLARP7) is shown to be the functional homolog of human LARP7. The Drosophila 7SK snRNP (d7SK snRNP) responded to treatment of cells with P-TEFb inhibitors and to nuclease treatment of cell lysates by releasing P-TEFb. Supporting a critical role for the d7SK snRNP in Drosophila development, dLARP7 and dHEXIM were found to be ubiquitously expressed throughout embryos and tissues at all stages. Importantly, knockdown of dHEXIM was embryonic lethal, and reduction of dHEXIM in specific tissues led to serious developmental defects. Our results suggest that regulation of P-TEFb by the d7SK snRNP is essential for the growth and differentiation of tissues required during Drosophila development

UNBOUND

Featured here, are the extraordinary works of our graduating Fashion Design class. This accomplishment is truly a celebration of the tree years of passion, hard work, and dedication of our students. It\u27s our hope that the fashion industry will partake in the creative endeavors of the emerging designers from the Fashion Design program at Fanshawe College in London, Ontario.https://first.fanshawec.ca/famd_design_fashiondesign_unbound/1002/thumbnail.jp

Small Molecules Targeted to a Non-Catalytic “RVxF” Binding Site of Protein Phosphatase-1 Inhibit HIV-1

HIV-1 Tat protein recruits host cell factors including CDK9/cyclin T1 to HIV-1 TAR RNA and thereby induces HIV-1 transcription. An interaction with host Ser/Thr protein phosphatase-1 (PP1) is critical for this function of Tat. PP1 binds to a Tat sequence, Q35VCF38, which resembles the PP1-binding “RVxF” motif present on PP1-binding regulatory subunits. We showed that expression of PP1 binding peptide, a central domain of Nuclear Inhibitor of PP1, disrupted the interaction of HIV-1 Tat with PP1 and inhibited HIV-1 transcription and replication. Here, we report small molecule compounds that target the “RVxF”-binding cavity of PP1 to disrupt the interaction of PP1 with Tat and inhibit HIV-1 replication. Using the crystal structure of PP1, we virtually screened 300,000 compounds and identified 262 small molecules that were predicted to bind the “RVxF”-accommodating cavity of PP1. These compounds were then assayed for inhibition of HIV-1 transcription in CEM T cells. One of the compounds, 1H4, inhibited HIV-1 transcription and replication at non-cytotoxic concentrations. 1H4 prevented PP1-mediated dephosphorylation of a substrate peptide containing an RVxF sequence in vitro. 1H4 also disrupted the association of PP1 with Tat in cultured cells without having an effect on the interaction of PP1 with the cellular regulators, NIPP1 and PNUTS, or on the cellular proteome. Finally, 1H4 prevented the translocation of PP1 to the nucleus. Taken together, our study shows that HIV- inhibition can be achieved through using small molecules to target a non-catalytic site of PP1. This proof-of-principle study can serve as a starting point for the development of novel antiviral drugs that target the interface of HIV-1 viral proteins with their host partners