Hospitality in the House of God: Deconstructing Habit and Building Missio Dei

This research project addresses neighborliness, change, and hospitality in the life of a mainline church of 1,200 members. It is a congregation that has traditional worship and programming with progressive values. The congregants are not comfortable with change and are coming to terms with the missing Millennial generation. Mixed method Action Research using missional practices of hospitality and neighbor interviews offered new faith formation and relationship growth with neighbors. There were also educational opportunities on change, the missional church movement, and neighborliness. The work relies on the theology of Serene Jones, Kosuke Koyama, and Miroslav Volf

Leptin fails to blunt the lipopolysaccharide-induced activation of the hypothalamic-pituitary-adrenal axis in rats

Copyright @ 2013 The authors. This work is licensed under a Creative Commons Attribution 3.0 Unported License.Obesity is a risk factor for sepsis morbidity and mortality, whereas the hypothalamic-pituitary-adrenal (HPA) axis plays a protective role in the body's defence against sepsis. Sepsis induces a profound systemic immune response and cytokines serve as excellent markers for sepsis as they act as mediators of the immune response. Evidence suggests that the adipokine leptin may play a pathogenic role in sepsis. Mouse endotoxaemic models present with elevated leptin levels and exogenously added leptin increased mortality whereas human septic patients have elevated circulating levels of the soluble leptin receptor (Ob-Re). Evidence suggests that leptin can inhibit the regulation of the HPA axis. Thus, leptin may suppress the HPA axis, impairing its protective role in sepsis.We hypothesised that leptin would attenuate the HPA axis response to sepsis.We investigated the direct effects of an i.p. injection of 2 mg/kg leptin on the HPA axis response to intraperitoneally injected 25 μg/kg lipopolysaccharide (LPS) in the male Wistar rat. We found that LPS potently activated the HPA axis, as shown by significantly increased plasma stress hormones, ACTH and corticosterone, and increased plasma interleukin 1β (IL1β) levels, 2 h after administration. Pre-treatment with leptin, 2 h before LPS administration, did not influence the HPA axis response to LPS. In turn, LPS did not affect plasma leptin levels. Our findings suggest that leptin does not influence HPA function or IL1b secretion in a rat model of LPS-induced sepsis, and thus that leptin is unlikely to be involved in the acute-phase endocrine response to bacterial infection in rats.The section is funded by grants from the MRC, BBSRC, NIHR and an Integrative Mammalian Biology (IMB) Capacity Building Award, and by a FP7-HEALTH-2009-241592 EuroCHIP grant and is supported by the NIHR Imperial Biomedical Research Centre Funding Scheme. This work is supported by a BBSRC Doctoral Training-Strategic Skills Award grant (BB/F017340/1)

The Spatial Distribution of Dust and Stellar Emission of the Magellanic Clouds

We study the emission by dust and stars in the Large and Small Magellanic Clouds, a pair of low-metallicity nearby galaxies, as traced by their spatially resolved spectral energy distributions (SEDs). This project combines Herschel Space Observatory PACS and SPIRE far-infrared photometry with other data at infrared and optical wavelengths. We build maps of dust and stellar luminosity and mass of both Magellanic Clouds, and analyze the spatial distribution of dust/stellar luminosity and mass ratios. These ratios vary considerably throughout the galaxies, generally between the range $0.01\leq L_{\rm dust}/L_\ast\leq 0.6$ and $10^{-4}\leq M_{\rm dust}/M_\ast\leq 4\times10^{-3}$. We observe that the dust/stellar ratios depend on the interstellar medium (ISM) environment, such as the distance from currently or previously star-forming regions, and on the intensity of the interstellar radiation field (ISRF). In addition, we construct star formation rate (SFR) maps, and find that the SFR is correlated with the dust/stellar luminosity and dust temperature in both galaxies, demonstrating the relation between star formation, dust emission and heating, though these correlations exhibit substantial scatter.Comment: 15 pages, 18 figures; ApJ, in press; version published in the journal will have higher-resolution figure

HECTD2 Is Associated with Susceptibility to Mouse and Human Prion Disease

Prion diseases are fatal transmissible neurodegenerative disorders, which include Scrapie, Bovine Spongiform Encephalopathy (BSE), Creutzfeldt-Jakob Disease (CJD), and kuru. They are characterised by a prolonged clinically silent incubation period, variation in which is determined by many factors, including genetic background. We have used a heterogeneous stock of mice to identify Hectd2, an E3 ubiquitin ligase, as a quantitative trait gene for prion disease incubation time in mice. Further, we report an association between HECTD2 haplotypes and susceptibility to the acquired human prion diseases, vCJD and kuru. We report a genotype-associated differential expression of Hectd2 mRNA in mouse brains and human lymphocytes and a significant up-regulation of transcript in mice at the terminal stage of prion disease. Although the substrate of HECTD2 is unknown, these data highlight the importance of proteosome-directed protein degradation in neurodegeneration. This is the first demonstration of a mouse quantitative trait gene that also influences susceptibility to human prion diseases. Characterisation of such genes is key to understanding human risk and the molecular basis of incubation periods

A Copine family member, Cpne8, is a candidate quantitative trait gene for prion disease incubation time in mouse

Prion disease incubation time in mice is determined by many factors including genetic background. The prion gene itself plays a major role in incubation time; however, other genes are also known to be important. Whilst quantitative trait loci (QTL) studies have identified multiple loci across the genome, these regions are often large, and with the exception of Hectd2 on Mmu19, no quantitative trait genes or nucleotides for prion disease incubation time have been demonstrated. In this study, we use the Northport heterogeneous stock of mice to reduce the size of a previously identified QTL on Mmu15 from approximately 25 to 1.2 cM. We further characterised the genes in this region and identify Cpne8, a member of the copine family, as the most promising candidate gene. We also show that Cpne8 mRNA is upregulated at the terminal stage of disease, supporting a role in prion disease. Applying these techniques to other loci will facilitate the identification of key pathways in prion disease pathogenesis

Electrophysiological resting state brain network and episodic memory in healthy aging adults

Recent studies have emphasized the changes in large-scale brain networks related to healthy aging, with the ultimate purpose to aid in differentiating normal neurocognitive aging from neurodegenerative disorders that also arise with age. Emerging evidence from functional Magnetic Resonance Imaging (fMRI) indicates that connectivity patterns within specific brain networks, especially the Default Mode Network (DMN), distinguish those with Alzheimer's disease from healthy individuals. In addition, disruptive alterations in the large-scale brain systems that support high-level cognition are shown to accompany cognitive decline at the behavioral level, which is commonly observed in the aging populations, even in the absence of disease. Although fMRI is useful for assessing functional changes in brain networks, its high costs and limited accessibility discourage studies that need large populations. In this study, we investigated the aging-effect on large-scale networks of the human brain using high-density electroencephalography and electrophysiological source imaging, which is a less costly and more accessible alternative to fMRI. In particular, our study examined a group of healthy subjects in the age range from middle- to older-aged adults, which is an under-studied range in the literature. Employing a high-resolution computation model, our results revealed age associations in the connectivity pattern of DMN in a consistent manner with previous fMRI findings. Particularly, in combination with a standard battery of cognitive tests, our data showed that in the posterior cingulate / precuneus area of DMN higher brain connectivity was associated with lower performance on an episodic memory task. The findings demonstrate the feasibility of using electrophysiological imaging to characterize large-scale brain networks and suggest that changes in network connectivity are associated with normal aging.This study was supported by National Science Foundation RII Track-2 FEC 1539068, Oklahoma Center for the Advancement of Science & Technology HR16–057, and Institute for Biomedical Engineering, Science, and Technology at University of Oklahoma. Financial support was provided by the University of Oklahoma Libraries’ Open Access Fund.Ye

Shadoo (Sprn) and prion disease incubation time in mice

Prion diseases are transmissible neurodegenerative disorders of mammalian species and include scrapie, bovine spongiform encephalopathy (BSE), and variant Creutzfeldt-Jakob disease (vCJD). The prion protein (PrP) plays a key role in the disease, with coding polymorphism in both human and mouse influencing disease susceptibility and incubation time, respectively. Other genes are also thought to be important and a plausible candidate is Sprn, which encodes the PrP-like protein Shadoo (Sho). Sho is expressed in the adult central nervous system and exhibits neuroprotective activity reminiscent of PrP in an in vitro assay. To investigate the role of Sprn in prion disease incubation time we sequenced the open reading frame (ORF) in a diverse panel of mice and saw little variation except in strains derived from wild-trapped mice. Sequencing the untranslated regions revealed polymorphisms that allowed us to carry out an association study of incubation period in the Northport heterogeneous stock of mice inoculated with Chandler/RML prions. We also examined the expression level of Sprn mRNA in the brains of normal and prion-infected mice and saw no correlation with either genotype or incubation time. We therefore conclude that Sprn does not play a major role in prion disease incubation time in these strains of mice

The Role of Heterotrophic Bacteria and Archaea in the Transformation of Lignin in the Open Ocean

The pelagic ocean receives terrigenous inputs of a range of organic compounds; however, the role that this terrigenous material plays in the ocean carbon cycle and biological pump is not entirely understood, and questions remain as to how oceanic cycles of terrigenous and autochthonous carbon interact. A significant portion of organic carbon that cannot be utilized by marine microbes in the epipelagic ocean escapes microbial remineralization to be sequestered in the deep ocean as refractory dissolved organic matter (DOM). Lignin, a “model” terrigenous compound, is thought to be refractory in the open ocean unless chemically altered. However, in this study, incubation experiments performed using lignin-amended oligotrophic seawater from the Sargasso Sea exhibited bacteria and archaea growth that doubled compared to unamended control treatments. The increase in bacteria and archaea cell abundance in lignin-amended treatments coincided with a 21–25% decrease in absorbance (250–400 nm) of chromophoric dissolved organic matter (CDOM), suggesting that certain microbes may be capable of altering fractions of this ostensibly recalcitrant organic matter. Furthermore, the microbial response to the lignin-amended treatments appears to be taxon-specific. Two phyla of Archaea, Euryarchaeota and Thaumarchaeota, exhibited an increase in abundance of 7-fold and 28-fold (from 2.42 × 106 cells L–1 to 1.72 × 107 cells L–1, and from 1.60 × 106 cells L–1 to 4.54 × 107 cells L–1, respectively), over 4 days of incubation in lignin-amended treatments. Additionally, an increase of 11-fold and 13-fold (from 2.93 × 106 cells L–1 to 3.30 × 107 cells L–1, and from 3.26 × 106 cells L–1 to 4.28 × 107 cells L–1, respectively), was observed in the abundance of these phyla in treatments containing lignin with added nitrogen and phosphorus, thus raising questions regarding primary and/or secondary responses to lignin degradation. Our findings indicate that marine bacteria and archaea play a role in the transformation of the optical properties of lignin in the open ocean and that they may serve as a potential sink for a portion of the lignin macromolecule

Overfishing Drives Over One-Third of All Sharks and Rays Toward a Global Extinction Crisis

The scale and drivers of marine biodiversity loss are being revealed by the International Union for Conservation of Nature (IUCN) Red List assessment process. We present the first global reassessment of 1,199 species in Class Chondrichthyes-sharks, rays, and chimeras. The first global assessment (in 2014) concluded that one-quarter (24%) of species were threatened. Now, 391 (32.6%) species are threatened with extinction. When this percentage of threat is applied to Data Deficient species, more than one-third (37.5%) of chondrichthyans are estimated to be threatened, with much of this change resulting from new information. Three species are Critically Endangered (Possibly Extinct), representing possibly the first global marine fish extinctions due to overfishing. Consequently, the chondrichthyan extinction rate is potentially 25 extinctions per million species years, comparable to that of terrestrial vertebrates. Overfishing is the universal threat affecting all 391 threatened species and is the sole threat for 67.3% of species and interacts with three other threats for the remaining third: loss and degradation of habitat (31.2% of threatened species), climate change (10.2%), and pollution (6.9%). Species are disproportionately threatened in tropical and subtropical coastal waters. Science-based limits on fishing, effective marine protected areas, and approaches that reduce or eliminate fishing mortality are urgently needed to minimize mortality of threatened species and ensure sustainable catch and trade of others. Immediate action is essential to prevent further extinctions and protect the potential for food security and ecosystem functions provided by this iconic lineage of predators

Fibrinogen beta variants confer protection against coronary artery disease in a Greek case-control study

<p>Abstract</p> <p>Background</p> <p>Although plasma fibrinogen levels are related to cardiovascular risk, data regarding the role of fibrinogen genetic variation in myocardial infarction (MI) or coronary artery disease (CAD) etiology remain inconsistent. The purpose of the present study was to investigate the effect of <it>fibrinogen A (FGA)</it>, <it>fibrinogen B (FGB) </it>and <it>fibrinogen G (FGG) </it>gene SNPs and haplotypes on susceptibility to CAD in a homogeneous Greek population.</p> <p>Methods</p> <p>We genotyped for rs2070022, rs2070016, rs2070006 in <it>FGA </it>gene, the rs7673587, rs1800789, rs1800790, rs1800788, rs1800787, rs4681 and rs4220 in <it>FGB </it>gene and for the rs1118823, rs1800792 and rs2066865 SNPs in <it>FGG </it>gene applying an arrayed primer extension-based genotyping method (APEX-2) in a sample of CAD patients (n = 305) and controls (n = 305). Logistic regression analysis was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs), before and after adjustment for potential confounders.</p> <p>Results</p> <p>None of the <it>FGA </it>and <it>FGG </it>SNPs and <it>FGA, FGB, FGG </it>and <it>FGA-FGG </it>haplotypes was associated with disease occurrence after adjustment. Nevertheless, rs1800787 and rs1800789 SNPs in <it>FGB </it>gene seem to decrease the risk of CAD, even after adjustment for potential confounders (OR = 0.42, 95%CI: 0.19-0.90, p = 0.026 and OR = 0.44, 95%CI:0.21-0.94, p = 0.039, respectively).</p> <p>Conclusions</p> <p><it>FGA </it>and <it>FGG </it>SNPs as well as <it>FGA, FGB, FGG </it>and <it>FGA-FGG </it>haplotypes do not seem to be important contributors to CAD occurrence in our sample. On the contrary, <it>FGB </it>rs1800787 and rs1800789 SNPs seem to confer protection to disease onset lowering the risk by about 50% in homozygotes for the minor alleles.</p