bluuebunny/crossref_metadata_2025_split huggingface dataset:
Beyond Deep Incarnation: Rethinking Christology in Radical Lutheran Terms
Authors: Peterson Daniel J. 
Published: September 2014

AbstractThis article takes the demise of Christendom and what Diana Butler Bass calls the end of religion as its point of departure for a “radical” rethinking of God in fully kenotic terms. It rejects any vestige of otherworldly transcendence as a temptation to escapism, inviting us instead to seek God's complete presence among us here in the world. Going beyond Niels Gregersen's understanding of the deep incarnation of the Logos and starting instead with a complete commitment to the infra‐Lutheranum, the author presents a radical Lutheran theology that embraces a total kenosis of God whose liberating and life‐giving reappearance we must find implicit among us in unexpected places, not least of which might include the embers of a dying church or the crumbling of our religious institutions.
Hospice Care and a Theology for Patients at the End of Life
Authors: Tracy Tara Flanagan 
Published: September 2014

AbstractIn Richard Kearney's text Anatheism, he claims that one can respond to the call of the stranger in two ways, with hospitality or with hostility. However, because the stranger possibly bears the presence of the divine, he urges one to risk responding to the stranger's call with hospitality rather than hostility, opening oneself up to encountering the sacred in the form of the stranger. In the present analysis, I claim that hospitality toward the stranger is modeled in the hospice philosophy of care for dying patients. I note the distinctions between the biomedical model of health care and the biopsychosoical model of care, and draw on Kearney's framework and Dorothee Soelle's text Suffering to suggest that, with regard to how to interpret pain, the act of hosting can be an option more viable than that of demonstrating hospitality.
Brain glucose sensing, glucokinase and neural control of metabolism and islet function
Authors: Ogunnowo‐Bada E. O. , Heeley N. , Brochard L. , Evans M. L. 
Published: September 2014

It is increasingly apparent that the brain plays a central role in metabolic homeostasis, including the maintenance of blood glucose. This is achieved by various efferent pathways from the brain to periphery, which help control hepatic glucose flux and perhaps insulin‐stimulated insulin secretion. Also, critically important for the brain given its dependence on a constant supply of glucose as a fuel – emergency counter‐regulatory responses are triggered by the brain if blood glucose starts to fall. To exert these control functions, the brain needs to detect rapidly and accurately changes in blood glucose. In this review, we summarize some of the mechanisms postulated to play a role in this and examine the potential role of the low‐affinity hexokinase, glucokinase, in the brain as a key part of some of this sensing. We also discuss how these processes may become altered in diabetes and related metabolic diseases.
Signal transducer and activator of transcription 3 and the phosphatidylinositol 3‐kinase regulatory subunits p55α and p50α regulate autophagy in vivo
Authors: Pensa Sara , Lloyd‐Lewis Bethan , Sargeant Timothy J. , Resemann Henrike K. , Kahn C. Ronald , Watson Christine J. 
Published: September 2014

Mammary gland involution involves a process that includes one of the most dramatic examples of cell death in an adult mammalian organism. We have previously shown that signal transducer and activator of transcription 3 (Stat3) regulates a lysosomal pathway of cell death in the first 48 h of involution and induces lysosome leakiness in mammary epithelial cells. Interestingly, Stat3 is associated also with the striking induction of autophagy that occurs concomitantly with cell death, presumably as a transient survival mechanism. The phosphatidylinositol 3‐kinase regulatory subunits p55α and p50α are dramatically and specifically upregulated at the transcriptional level by Stat3 at the onset of involution. We show here that ablation of either Stat3 or p55α/p50α in vivo affects autophagy during involution. We used two different cell culture models (normal mammary epithelial cells and mouse embryonic fibroblasts) to further investigate the role of p55α/p50α in autophagy regulation. Our results demonstrate a direct role for p55α/p50α as inhibitors of autophagy mediated by p85α. Thus, Stat3 and its downstream targets p55α/p50α are key regulators of the balance between autophagy and cell death in vivo.
Control of periphyton standing crop in an Atlantic Forest stream: the relative roles of nutrients, grazers and predators
Authors: Lourenço‐Amorim Christine , Neres‐Lima Vinicius , Moulton Timothy Peter , Sasada‐Sato Cristiano Yuji , Oliveira‐Cunha Priscila , Zandonà Eugenia 
Published: September 2014

Summary

Periphytic algae are an important source of energy fuelling stream food webs. Periphytic algal biomass can be controlled by bottom‐up and top‐down forces, but there are few studies that have investigated these effects simultaneously, especially in tropical streams, where periphyton can be a very important carbon source. Here, we investigated the bottom‐up effects of nutrients and the top‐down effects of grazers and predators in a coastal tropical stream in Brazil.

We employed nutrient‐diffusing substrata to test for nutrient limitation, placed inside electric exclosures of different intensities, which prevented consumers from entering the electrified area. We used four types of substrata: one enriched with nitrogen alone (N), one with phosphorus alone (P), one with nitrogen + phosphorus (NP) and one control with no nutrients added (C). The electric exclosure had three treatments: high electricity that excluded both predators (Macrobrachium olfersi shrimps) and grazers (Baetidae mayflies), low electricity that excluded only shrimps, and a control treatment with no electricity where both shrimps and mayflies were allowed to enter.

The limiting nutrient in the stream was nitrogen. Our results showed a greater magnitude of bottom‐up effects, with periphytic algae responding more strongly to nutrient addition than to grazers or predators. Top‐down control was not as strong, but periphytic algae responded negatively to grazers, especially in the absence of predators. This suggests that shrimps, either directly or indirectly, inhibit mayfly grazing activity. The response of periphytic algae to nutrients was stronger in the absence of grazers. Thus, top‐down effects, both directly and indirectly through a trophic cascade, can dampen the response to nitrogen addition, diminishing the degree of resource limitation.
Ten years of vegetation assembly after a North American mega fire
Authors: Abella Scott R. , Fornwalt Paula J. 
Published: September 2014

AbstractAltered fuels and climate change are transforming fire regimes in many of Earth's biomes. Postfire reassembly of vegetation – paramount to C storage and biodiversity conservation – frequently remains unpredictable and complicated by rapid global change. Using a unique data set of pre and long‐term postfire data, combined with long‐term data from nearby unburned areas, we examined 10 years of understory vegetation assembly after the 2002 Hayman Fire. This fire was the largest wildfire in recorded history in Colorado,USA. Resistance (initial postfire deviance from prefire condition) and resilience (return to prefire condition) declined with increasing fire severity. However, via both resistance and resilience, ‘legacy’ species of the prefire community constituted >75% of total plant cover within 3 years even in severely burned areas. Perseverance of legacy species, coupled with new colonizers, created a persistent increase in community species richness and cover over prefire levels. This was driven by a first‐year increase (maintained over time) in forbs with short life spans; a 2–3‐year delayed surge in long‐lived forbs; and a consistent increase in graminoids through the 10th postfire year. Burning increased exotic plant invasion relative to prefire and unburned areas, but burned communities always were >89% native. This study informs debate in the literature regarding whether these increasingly large fires are ‘ecological catastrophes.’ Landscape‐scale severe burning was catastrophic from a tree overstory perspective, but from an understory perspective, burning promoted rich and productive native understories, despite the entire 10‐year postfire period receiving below‐average precipitation.
Severe cardiomyopathy revealing antineutrophil cytoplasmic antibodies‐negative eosinophilic granulomatosis with polyangiitis
Authors: Bouiller K. , Samson M. , Eicher J.‐C. , Audia S. , Berthier S. , Leguy V. , Humbert O. , Martin L. , Lorgis L. , Cottin Y. , Bonnotte B. , Lorcerie B. 
Published: September 2014

AbstractEosinophilic granulomatosis with polyangiitis (EGPA) is a rare form of systemic vasculitis in which cardiac involvement is frequent and severe, and accounts for half of EGPA‐related deaths. ANCA‐positive EGPA differs from ANCA‐negative EGPA in that the former is significantly associated with renal involvement, peripheral neuropathy and biopsy proven vasculitis, whereas the latter is associated with cardiac involvement. Herein, we report a case of EGPA with myocarditis in a woman, who was successfully treated with steroids and cyclophosphamide. This report highlights the importance of diagnosing cardiac involvement in EGPA early, especially in ANCA‐negative patients.
Rapid rule out of myocardial infarction with the use of copeptin as a biomarker for cardiac injury
Authors: Jayasinghe R. , Narasimhan S. , Tran T. H. , Paskaranandavadivel A. 
Published: September 2014

AbstractCopeptin is a non‐specific marker of an endogenous stress response. A dual biomarker marker approach involving the simultaneous use of troponin and copeptin assays may assist early exclusion of acute coronary syndrome in Australian emergency departments. The utility and limitations of this approach are discussed.
Prospective Surgical Site Infection Surveillance in Dogs
Authors: Turk Ryen , Singh Ameet , Weese J. Scott 
Published: September 2014

ObjectiveTo 1) describe the incidence of surgical site infections (SSI) in dogs undergoing surgery at the Ontario Veterinary College Health Sciences Centre; 2) describe and compare procedure‐specific SSI rates; and 3) identify factors associated with development of SSI.Study DesignProspective, cohort studyAnimalsDogs (n = 846) undergoing surgery during 45 weeks (September 2010–July 2011).MethodsFollow‐up telephone conversation with dog owners was performed 30 days postoperatively, with additional 1‐year follow‐up performed for cases with surgical implants. A standardized questionnaire was administered to detect and characterize SSI.ResultsSSI were identified in 26 (3.0%) dogs; 11 (42%) were classified as superficial SSI, whereas 13 were deep, and 2 were organ/space. Of the confirmed SSI, only 17 (65%) were documented in the medical records. Hypotension (P = .011), class of surgery (P = .029), and use of an implant (P = .001) increased the risk of SSI. Microbial cultures were submitted for 19 cases (73%) and of those, 74% were staphylococci.ConclusionsSSI can result in devastating consequences in dogs and understanding risk factors is critical to target prevention practices. Whereas some risk factors such as hypotension are modifiable, others such as class of surgery are not. When possible, active surveillance should be used as part of a hospital infection control program.
Perioperative Administration of Antimicrobials During Tibial Plateau Leveling Osteotomy
Authors: Nazarali Alim , Singh Ameet , Weese J. Scott 
Published: September 2014

ObjectiveTo evaluate perioperative antimicrobial administration during tibial plateau leveling osteotomy (TPLO) in dogs at the Ontario Veterinary College Health Sciences Centre.Study DesignRetrospective case series.AnimalsDogs (n = 184) that had TPLO (n = 226).MethodsMedical records were reviewed and data collected included timing and dosage of pre, intra, and postoperative antimicrobial administration, method of stifle inspection, duration of surgery, duration of anesthesia, development of surgical site infection (SSI), microbiological investigation, implant removal, and possible comorbidities. Univariable analysis was conducted, followed by stepwise forward logistic regression to determine factors associated with SSI.ResultsOf the 225 cases administered perioperative antimicrobials, 96 (42.5%) received appropriate perioperative antimicrobial prophylaxis based on target times for preoperative and intraoperative dosing. Postoperative antimicrobials were administered to 54 (23.9%) of cases. Surgical site infection was documented in 30 (13.3%) cases.Staphylococcus pseudintermediuswas isolated from 15/17 (88.2%) SSI from which a bacterium was isolated, with 6/15 (40%) being methicillin‐resistantStaphylococcus pseudintermedius(MRSP). Postoperative administration of antimicrobials was protective for SSI (OR 0.1367;P = .0001; 95% CI = 0.021, 0.50). Duration of anesthesia time was associated with the likelihood of development of SSI (OR = 1.0094;P = .001; 95% CI = 1.00, 1.02).ConclusionCurrent practices for administration of antimicrobial prophylaxis during TPLO can be improved. There was no association between timing of antibiotic administration that was inconsistent with the target and development of SSI. Further study into risk factors of TPLO SSI is required.
Effect of Angiotensin Converting Enzyme Inhibitors on Soluble Tumor‐Necrosis‐Factor‐Related Apoptosis‐Inducing Ligand Levels – Association With Neointimal Hyperplasia in Drug Eluting Stents
Authors: GIANNOPOULOS GEORGIOS , PANAGOPOULOU VASILIKI , DEFTEREOS SPYRIDON , ANGELIDIS CHRISTOS , DAVLOUROS PERIKLIS , SYNETOS ANDREAS , TOUTOUZAS KONSTANTINOS , ALEXOPOULOS DIMITRIOS , CLEMAN MICHAEL W. , TOUSOULIS DIMITRIOS 
Published: September 2014

ObjectiveTo test the hypothesis that angiotensin converting enzyme inhibitors (ACEi) affect soluble tumor‐necrosis‐factor‐related apoptosis‐inducing ligand (sTRAIL) and this interaction is associated with less in‐drug‐eluting‐stent (DES) neointimal hyperplasia following percutaneous coronary intervention (PCI).MethodsFrom our database of patients with elective PCI and baseline intravascular ultrasound (IVUS) evaluation of the implanted DES, we randomly selected 60 patients who were prescribed an ACEi and 60 matched controls, who did not receive an ACEi following PCI. All patients underwent coronary angiography and IVUS. sTRAIL was measured in samples from the stented coronary artery and a peripheral vein.ResultssTRAIL concentration was higher in the ACEi group, both in coronary and peripheral samples: 104 [78–139] pg/ml versus 63 [45–100] pg/ml (P < 0.001) and 99 [73–135] pg/ml versus 69 [49–103] pg/ml (P = 0.002), respectively. There was an inverse association (standardized beta −0.760; P < 0.001) between sTRAIL and lumen area loss in both treatment groups. In the multivariable analysis, log(sTRAIL) was an independent negative predictor of lumen area loss (standardized beta −0.660, adjusted 95% confidence interval −0.722 to −0.466).ConclusionsTreatment with ACEi was associated with higher sTRAIL levels and lower lumen area loss in the IVUS evaluation of implanted DES. sTRAIL levels were negatively associated with in‐stent neointima hyperplasia in these postPCI patients.
Brain‐derived neurotrophic factor prevents the endothelial barrier dysfunction induced by interleukin‐1β and tumor necrosis factor‐α
Authors: Matsuda S. , Fujita T. , Kajiya M. , Kashiwai K. , Takeda K. , Shiba H. , Kurihara H. 
Published: September 2014

Background and ObjectiveBrain‐derived neurotrophic factor (BDNF) promotes the regeneration of periodontal tissue. Although a local inflammatory step is required to initiate the subsequent process of tissue regeneration, excessive inflammation may inhibit or delay tissue regeneration. Therefore, the regulation of inflammation is essential for periodontal tissue regeneration. In the present study, we examined the influence of BDNF on the human microvascular endothelial cell (HMVEC) barrier dysfunction induced by interleukin (IL)‐1β or tumor necrosis factor (TNF)‐α to determine the effects of BDNF on the regulation of local inflammation in periodontal tissue regeneration.Material and MethodsEndothelial permeability was analyzed using a Dextran transport assay with transwell plates. The expression of vascular endothelial (VE)‐cadherin was assessed by immunoblotting and immunofluorescence microscopy.ResultsBDNF (25 ng/mL) inhibited increase induced in endothelial permeability by IL‐1β and TNF‐α. IL‐1β and TNF‐α decreased VE‐cadherin protein levels, while BDNF recovered the reduction in HMVECs. BDNF protected the increase induced in endothelial permeability by IL‐1β and TNF‐α through TrkB. The single addition of BDNF into the culture increased the expression of VE‐cadherin in HMVECs.ConclusionBDNF played an important role in inhibiting endothelial barrier dysfunction, which suggests that it may assist in enhancing periodontal tissue regeneration.
Identification of transactivation‐responsive DNA‐binding protein 43 (TARDBP43; TDP‐43) as a novel factor for TNF‐α expression upon lipopolysaccharide stimulation in human monocytes
Authors: Murata H. , Hattori T. , Maeda H. , Takashiba S. , Takigawa M. , Kido J. , Nagata T. 
Published: September 2014

Background and ObjectiveTumor necrosis factor alpha (TNF‐α) is a major cytokine implicated in various inflammatory diseases. The nature of the nuclear factors associated with human TNF‐α gene regulation is not well elucidated. We previously identified a novel region located from −550 to −487 in human TNF‐α promoter that did not contain the reported binding sites for nuclear factor kappa B (NF‐κB) but showed lipopolysaccharide (LPS)‐induced transcriptional activity. The purpose of this study is to identify novel factors that bind to the promoter region and regulate TNF‐α expression.Material and MethodsTo identify DNA‐binding proteins that bound to the target region of TNF‐α promoter, a cDNA library from LPS‐stimulated human monocytic cell line THP‐1 was screened using a yeast one‐hybrid system. Cellular localizations of the DNA‐binding protein in the cells were examined by subcellular immunocytochemistry. Nuclear amounts of the protein in LPS‐stimulated THP‐1 cells were identified by western blot analysis. Expression of mRNA of the protein in the cells was quantified by real‐time polymerase chain reaction. Electrophoretic mobility shift assays were performed to confirm the DNA‐binding profile. Overexpression of the protein and knockdown of the gene were also performed to investigate the role for TNF‐α expression.ResultsSeveral candidates were identified from the cDNA library and transactivation‐responsive DNA‐binding protein 43 (TARDBP43; TDP‐43) was focused on. Western blot analysis revealed that nuclear TDP‐43 protein was increased in the LPS‐stimulated THP‐1 cells. Expression of TDP‐43 mRNA was already enhanced before TNF‐α induction by LPS. Electrophoretic mobility shift assay analysis showed that nuclear extracts obtained by overexpressing FLAG‐tagged TDP‐43 bound to the −550 to −487 TNF‐α promoter fragments. Overexpression of TDP‐43 in THP‐1 cells resulted in an increase of TNF‐α expression. Knockdown of TDP‐43 in THP‐1 cells downregulated TNF‐α expression.ConclusionWe identified TDP‐43 as one of the novel TNF‐α factors and found that it bound to the LPS‐responsive element in the TNF‐α promoter to increase TNF‐α expression.
Calving location selection patterns of saiga antelope in Mongolia
Authors: Buuveibaatar B. , Fuller T. K. , Young J. K. , Berger J. 
Published: September 2014

AbstractHabitat selection for calving by ungulates is an important behavioral trait because it affects neonate survival. Generally, ungulate calving site selection varies by vulnerability to predators, local topography, habitat quality and level of human disturbance. The Mongolian saiga (Saiga tatarica mongolica) is endemic to Mongolia where a threatened population of ∼7000 exists in the northern Gobi Desert. We analyzed factors that could affect selection of saiga calving locations in the Sharga Nature Reserve, western Mongolia, using data obtained from ground surveys over 4 years between 2008 and 2012. Multiple factors explain calving location selection by saiga antelopes, based on the results of a generalized linear mixed model within a use availability framework. Individual saiga females preferred calving locations that were away from settlements and closer to water sources and avoided steeper slopes in comparison with random locations. These results demonstrate that the choice of calving locations for saiga antelope is driven by both internal and external factors. Understanding which factors influence calving location selection for saiga provides insights to protect important habitats.
Circulating mannan‐binding lectin, M‐, L‐, H‐ficolin and collectin‐liver‐1 levels in patients with acute liver failure
Authors: Laursen Tea L. , Sandahl Thomas D. , Støy Sidsel , Schiødt Frank V. , Lee William M. , Vilstrup Hendrik , Thiel Steffen , Grønbæk Henning ,   US Acute Liver Failure Study Group
Published: September 2014

AbstractBackground & AimsThe complement system is activated in liver diseases including acute liver failure (ALF); however, the role of the lectin pathway of complement has scarcely been investigated in ALF. The pathway is initiated by soluble pattern recognition molecules: mannan‐binding lectin (MBL), M‐, L‐, and H‐ficolin and collectin‐liver‐1 (CL‐L1), which are predominantly synthesized in the liver. We aimed to study lectin levels in ALF patients and associations with clinical outcome.MethodsSerum samples from 75 patients enrolled by the US ALF Study Group were collected on days 1 and 3. We included 75 healthy blood donors and 20 cirrhosis patients as controls. Analyses were performed using sandwich‐type immunoassays (ELISA, TRIFMA).ResultsAt day 1, the MBL level in ALF patients was 40% lower compared with healthy controls {[median (interquartile range) 0.72 μg/ml(0.91) vs. 1.15 (1.92)(P = 0.02]}, and increased significantly by day 3 [0.83 μg/ml(0.94)(P = 0.01)]. The M‐ficolin level was 60% lower [0.54 μg/ml(0.50) vs. 1.48(1.01)(P < 0.0001)]. The CL‐L1 level at day 1 was slightly higher compared with healthy controls [3.20 μg/ml(2.37) vs. 2.64(0.72)(P = 0.11)]; this was significant at day 3 [3.35(1.84)(P = 0.006)]. H‐ and L‐ficolin levels were similar to healthy controls. Spontaneous ALF survivors had higher levels of MBL at day 1 [0.96 μg/ml(1.15) vs. 0.60(0.60)(P = 0.02)] and lower levels of L‐ficolin by day 3 compared with patients who died or were transplanted [1.61 μg/ml(1.19) vs. 2.17(2.19)(P = 0.02)].ConclusionWe observed significant dynamics in lectin levels in ALF patients, which may suggest they play a role in ALF pathogenesis. High MBL and low L‐ficolin levels are associated with survival.