3,170 research outputs found
A Protocol for Assessing and Developing Spiritual Formation among Council for Christian Colleges and Universities Schools in North America
The purpose of this dissertation is to develop a protocol for assessing and developing spiritual formation among schools affiliated with the Council for Christian Colleges and Universities in North America.
Problem: A paradigm that is deeply rooted in scripture, practical theology, and an understanding of spiritual formation is needed to assess programs for spiritual formation of traditional college students.
1. What is the need within its context? Articulates why a need exists among schools of Council for Christian Colleges and Universities? I will describe the historical context and provide original research from forty-two CCCV schools.
2: What is the approach to the problem? Practical theology is asserted as the proper approach and is helpfully nuanced by the work of practitioners, Don Browning, Thomas Groome, and Howard Snyder whose work suggests comprehensive paradigms for understanding spiritual formation.
3: What is spiritual formation? Since spiritual formation among evangelical colleges is the desired outcome for a program review, Dallas Willard, Richard Foster and Eugene Peterson and others provide an evangelical understanding of spiritual development, what it is and how it happens.
4: What is spiritual formation among university students? Developmental theories of James Fowler and the teachings of Sharon Parks and Steve Garber provide a structure for understanding the faith development of traditional college students. I will articulate sixteen premises and their implications for effective campus ministry.
5: What methodologies are appropriate for a campus ministry program review? The nature of a valid assessment of spiritual formation is articulated. Elements of a campus ministry program review are outlined. In order to develop an effective paradigm, a review of program assessment tools from congregational reviews, as well as campus ministry practices among CCCV campus pastors are reviewed. This chapter defines appropriate steps and gives an overview of the actual audit.
6: What is a protocol for a campus program audit? I will offer a detailed step-by-step strategy for an effective program review, including actual questions and sample data-gathering instruments
The Fixed Weighting Nature of a Cross-Evaluation Model
Cross-evaluation has been touted as a powerful extension of Data Envelopment Analysis that provides, not only a unique ordering among the Decision Making Units (DMUs), but also eliminates unrealistic weighting schemes without requiring the elicitation of weight restrictions from application area experts. The goal of this paper is to prove, in the single-input, multiple-output case, cross-evaluation implicitly uses a single fixed set of weights. We demonstrate how this unseen fixed set of weights may still be unrealistic
Regulation of Neurod1 Contributes to the Lineage Potential of Neurogenin3+ Endocrine Precursor Cells in the Pancreas
During pancreatic development, transcription factor cascades gradually commit precursor populations to the different endocrine cell fate pathways. Although mutational analyses have defined the functions of many individual pancreatic transcription factors, the integrative transcription factor networks required to regulate lineage specification, as well as their sites of action, are poorly understood. In this study, we investigated where and how the transcription factors Nkx2.2 and Neurod1 genetically interact to differentially regulate endocrine cell specification. In an Nkx2.2 null background, we conditionally deleted Neurod1 in the Pdx1+ pancreatic progenitor cells, the Neurog3+ endocrine progenitor cells, or the glucagon+ alpha cells. These studies determined that, in the absence of Nkx2.2 activity, removal of Neurod1 from the Pdx1+ or Neurog3+ progenitor populations is sufficient to reestablish the specification of the PP and epsilon cell lineages. Alternatively, in the absence of Nkx2.2, removal of Neurod1 from the Pdx1+ pancreatic progenitor population, but not the Neurog3+ endocrine progenitor cells, restores alpha cell specification. Subsequent in vitro reporter assays demonstrated that Nkx2.2 represses Neurod1 in alpha cells. Based on these findings, we conclude that, although Nkx2.2 and Neurod1 are both necessary to promote beta cell differentiation, Nkx2.2 must repress Neurod1 in a Pdx1+ pancreatic progenitor population to appropriately commit a subset of Neurog3+ endocrine progenitor cells to the alpha cell lineage. These results are consistent with the proposed idea that Neurog3+ endocrine progenitor cells represent a heterogeneous population of unipotent cells, each restricted to a particular endocrine lineage
Evaluation of evidence that the organophosphorus insecticide chlorpyrifos is a potential persistent organic pollutant (POP) or persistent, bioaccumulative, and toxic (PBT)
Identification of known and novel pancreas genes expressed downstream of Nkx2.2 during development
<p>Abstract</p> <p>Background</p> <p>The homeodomain containing transcription factor Nkx2.2 is essential for the differentiation of pancreatic endocrine cells. Deletion of Nkx2.2 in mice leads to misspecification of islet cell types; insulin-expressing β cells and glucagon-expressing α cells are replaced by ghrelin-expressing cells. Additional studies have suggested that Nkx2.2 functions both as a transcriptional repressor and activator to regulate islet cell formation and function. To identify genes that are potentially regulated by Nkx2.2 during the major wave of endocrine and exocrine cell differentiation, we assessed gene expression changes that occur in the absence of Nkx2.2 at the onset of the secondary transition in the developing pancreas.</p> <p>Results</p> <p>Microarray analysis identified 80 genes that were differentially expressed in e12.5 and/or e13.5 Nkx2.2<sup>-/- </sup>embryos. Some of these genes encode transcription factors that have been previously identified in the pancreas, clarifying the position of Nkx2.2 within the islet transcriptional regulatory pathway. We also identified signaling factors and transmembrane proteins that function downstream of Nkx2.2, including several that have not previously been described in the pancreas. Interestingly, a number of known exocrine genes are also misexpressed in the Nkx2.2<sup>-/- </sup>pancreas.</p> <p>Conclusions</p> <p>Expression profiling of Nkx2.2<sup>-/- </sup>mice during embryogenesis has allowed us to identify known and novel pancreatic genes that function downstream of Nkx2.2 to regulate pancreas development. Several of the newly identified signaling factors and transmembrane proteins may function to influence islet cell fate decisions. These studies have also revealed a novel function for Nkx2.2 in maintaining appropriate exocrine gene expression. Most importantly, Nkx2.2 appears to function within a complex regulatory loop with Ngn3 at a key endocrine differentiation step.</p
Dual Requirement for Yeast hnRNP Nab2p in mRNA poly(A) Tail Length Control and Nuclear Export
Recent studies of mRNA export factors have provided additional evidence for a mechanistic link between mRNA 3′‐end formation and nuclear export. Here, we identify Nab2p as a nuclear poly(A)‐binding protein required for both poly(A) tail length control and nuclear export of mRNA. Loss of NAB2 expression leads to hyperadenylation and nuclear accumulation of poly(A)+ RNA but, in contrast to mRNA export mutants, these defects can be uncoupled in a nab2 mutant strain. Previous studies have implicated the cytoplasmic poly(A) tail‐binding protein Pab1p in poly(A) tail length control during polyadenylation. Although cells are viable in the absence of NAB2 expression when PAB1 is overexpressed, Pab1p fails to resolve the nab2Δ hyperadenylation defect even when Pab1p is tagged with a nuclear localization sequence and targeted to the nucleus. These results indicate that Nab2p is essential for poly(A) tail length control in vivo, and we demonstrate that Nab2p activates polyadenylation, while inhibiting hyperadenylation, in the absence of Pab1p in vitro. We propose that Nab2p provides an important link between the termination of mRNA polyadenylation and nuclear export
AST-120 (spherical carbon adsorbent) lowers ammonia levels and attenuates brain edema in bile duct-ligated rats
The pathogenesis of hepatic encephalopathy is multifactorial, involving gut-derived toxins such as ammonia, which has been demonstrated to induce oxidative stress. Therefore, a primary hepatic encephalopathy treatment target is reducing ammonia production in the gastrointestinal tract. AST-120, an oral adsorbent of engineered activated carbon microspheres with surface areas exceeding 1600 m(2) /g, acts as a sink for neurotoxins and hepatotoxins present in the gut. We evaluated the capacity of AST-120 to adsorb ammonia in vitro and to lower blood ammonia, oxidative stress and brain edema in cirrhotic rats. Cirrhosis was induced in rats by bile duct ligation for 6 weeks. AST-120 was administered by gavage preventively for 6 weeks (0.1, 1, and 4 g/kg/day). In addition, AST-120 was evaluated as a short-term treatment for 2 weeks and 3 days (1 g/kg/day) and as a sink to adsorb intravenously infused ammonium acetate. In vitro, AST-120 efficiently adsorbed ammonia. Ammonia levels significantly decreased in a dose-dependent manner for all AST-120-treated bile duct-ligated rats (nontreated: 177.3 ± 30.8 μM; AST-120, 0.1 g/kg/day: 121.9 ± 13.8 μM; AST-120, 1 g/kg/day: 80.9 ± 30.0 μM; AST-120, 4 g/kg/day: 48.8 ± 19.6 μM) and significantly correlated with doses of AST-120 (r = -0.6603). Brain water content and locomotor activity normalized after AST-120 treatments, whereas arterial reactive oxygen species levels remained unchanged. Furthermore, AST-120 significantly attenuated a rise in arterial ammonia after ammonium acetate administration (intravenously). Conclusion:AST-120 treatment decreased arterial ammonia levels, normalized brain water content and locomotor activity but did not demonstrate an effect on systemic oxidative stress. Also, AST-120 acts as an ammonia sink, efficiently removing blood-derived ammonia. Additional studies are warranted to evaluate the effects of AST-120 on hepatic encephalopathy in patients with advanced liver disease. (HEPATOLOGY 2011;)
Evolution of a Reconfigurable Processing Platform for a Next Generation Space Software Defined Radio
The National Aeronautics and Space Administration (NASA)Harris Ka-Band Software Defined Radio (SDR) is the first, fully reprogrammable space-qualified SDR operating in the Ka-Band frequency range. Providing exceptionally higher data communication rates than previously possible, this SDR offers in-orbit reconfiguration, multi-waveform operation, and fast deployment due to its highly modular hardware and software architecture. Currently in operation on the International Space Station (ISS), this new paradigm of reconfigurable technology is enabling experimenters to investigate navigation and networking in the space environment.The modular SDR and the NASA developed Space Telecommunications Radio System (STRS) architecture standard are the basis for Harris reusable, digital signal processing space platform trademarked as AppSTAR. As a result, two new space radio products are a synthetic aperture radar payload and an Automatic Detection Surveillance Broadcast (ADS-B) receiver. In addition, Harris is currently developing many new products similar to the Ka-Band software defined radio for other applications. For NASAs next generation flight Ka-Band radio development, leveraging these advancements could lead to a more robust and more capable software defined radio.The space environment has special considerations different from terrestrial applications that must be considered for any system operated in space. Each space mission has unique requirements that can make these systems unique. These unique requirements can make products that are expensive and limited in reuse. Space systems put a premium on size, weight and power. A key trade is the amount of reconfigurability in a space system. The more reconfigurable the hardware platform, the easier it is to adapt to the platform to the next mission, and this reduces the amount of non-recurring engineering costs. However, the more reconfigurable platforms often use more spacecraft resources. Software has similar considerations to hardware. Having an architecture standard promotes reuse of software and firmware. Space platforms have limited processor capability, which makes the trade on the amount of amount of flexibility paramount
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