bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Qualitative Evaluation of a Telemedicine‐Enhanced Emergency Care Program for Older Adults
Authors: Shah Manish N. , Morris Dylan , Jones Courtney M. C. , Gillespie Suzanne M. , Nelson Dallas L. , McConnochie Kenneth M. , Dozier Ann 
Published: March 2013

ObjectivesTo document the experiences of patients, their caregivers, healthcare personnel, and staff members with a program that provides telemedicine‐enhanced emergency care to older adults residing in senior living communities (SLCs) and to delineate perceived barriers and facilitators.DesignQualitative study.SettingA primary care geriatric medicine practice.ParticipantsStakeholders associated with telemedicine visits: patients, family caregivers, telemedicine dispatcher, certified telemedicine assistants, telemedicine providers, and SLC staff.MeasurementsBetween June and August 2011, telemedicine encounters were observed, and field notes were recorded. After each telemedicine visit, all participants were interviewed using a semistructured guide. Discrete statements from interviews and field notes were coded and arranged into themes. Concordance or discordance in field notes and stakeholder responses were grouped for analysis.ResultsAfter 10 telemedicine visits and 34 interviews from 21 unique participants, redundancy was achieved. Participants and their families overwhelmingly reported satisfaction with their care, remarking particularly on the convenience, speed, and completeness of the evaluation. Participants reported some unmet expectations regarding provider presence at home and visit length. Providers thought telemedicine made them more efficient overall and improved diagnostic certainty but considered in‐person visits to be superior. All stakeholders, including patients, noted inadequate telemedicine technician training, leading to low confidence levels and performance difficulties. Participants, providers, and telemedicine technicians cited problems with the reliability, weight, and size of the equipment as serious challenges, decreasing their satisfaction and increasing their frustration.ConclusionTelemedicine‐enhanced emergency care is an acceptable method of providing emergency care to older adults in SLCs. Stakeholders report a number of advantages. Training and technology barriers require particular attention.
Body Mass Index, Change in Body Mass Index, and Survival in Old and Very Old Persons
Authors: Dahl Anna K. , Fauth Elizabeth B. , Ernsth‐Bravell Marie , Hassing Linda B. , Ram Nilam , Gerstof Denis 
Published: March 2013

ObjectivesTo examine how body mass index (BMI) and change in BMI are associated with mortality in old (70–79) and very old (≥80) individuals.DesignPooled data from three multidisciplinary prospective population‐based studies: OCTO‐twin, Gender, and NONA.SettingSweden.ParticipantsEight hundred eighty‐two individuals aged 70 to 95.MeasurementsBMI was calculated from measured height and weight as kg/m2. Information about survival status and time of death was obtained from the Swedish Civil Registration System.ResultsMortality hazard was 20% lower for the overweight group than the normal–underweight group (relative risk (RR) = 0.80, P = .011), and the mortality hazard for the obese group did not differ significantly from that of the normal–underweight group (RR = 0.93, P = .603), independent of age, education, and multimorbidity. Furthermore, mortality hazard was 65% higher for the BMI loss group than for the BMI stable group (RR = 1.65, P < .001) and 53% higher for the BMI gain group than for the BMI stable group (RR = 1.53, P = .001). Age moderated the BMI change differences. That is, the higher mortality risks associated with BMI loss and gain were less severe in very old age.ConclusionOld persons who were overweight had a lower mortality risk than old persons who were of normal weight, even after controlling for weight change and multimorbidity. Persons who increased or decreased in BMI had a greater mortality risk than those who had a stable BMI, particularly those aged 70 to 79. This study lends further support to the belief that the World Health Organization guidelines for BMI are overly restrictive in old age.
A new scenario of the evolutionary derivation of the mammalian diaphragm from shoulder muscles
Authors: Hirasawa Tatsuya , Kuratani Shigeru 
Published: March 2013

AbstractThe evolutionary origin of the diaphragm remains unclear, due to the lack of a comparable structure in other extant taxa. However, recent researches into the developmental mechanism of this structure have yielded new insights into its origin. Here we summarize current understanding regarding the development of the diaphragm, and present a possible scenario for the evolutionary acquisition of this uniquely mammalian structure. Recent developmental analyses indicate that the diaphragm and forelimb muscles are derived from a shared cell population during embryonic development. Therefore, the embryonic positions of forelimb muscle progenitors, which correspond to the position of the brachial plexus, likely played an important role in the evolution of the diaphragm. We surveyed the literature to reexamine the position of the brachial plexus among living amniotes and confirmed that the cervico‐thoracic transition in ribs reflects the brachial plexus position. Using this osteological correlate, we concluded that the anterior borders of the brachial plexuses in the stem synapsids were positioned at the level of the fourth spinal nerve, suggesting that the forelimb buds were laid in close proximity of the infrahyoid muscles. The topology of the phrenic and suprascapular nerves of mammals is similar to that of subscapular and supracoracoid nerves, respectively, of the other amniotes, suggesting that the diaphragm evolved from a muscle positioned medial to the pectoral girdle (cf. subscapular muscle). We hypothesize that the diaphragm was acquired in two steps: first, forelimb muscle cells were incorporated into tissues to form a primitive diaphragm in the stem synapsid grade, and second, the diaphragm in cynodonts became entrapped in the region controlled by pulmonary development.
Ca2+/S100 proteins regulate HCV virus NS5A–FKBP8/FKBP38 interaction and HCV virus RNA replication
Authors: Tani Joji , Shimamoto Seiko , Mori Kyoko , Kato Nobuyuki , Moriishi Kohji , Matsuura Yoshiharu , Tokumitsu Hiroshi , Tsuchiya Mitsumasa , Fujimoto Tomohito , Kato Kiyohito , Miyoshi Hisaaki , Masaki Tsutomu , Kobayashi Ryoji 
Published: March 2013

AbstractBackground & AimFKBP8/FKBP38 is a unique FK506‐binding protein with a C‐terminal membrane anchor and localizes at the outer membranes of mitochondria and the endoplasmic reticulum. Similar to some immunophilins, such as FKBP51, FKBP52 and Cyclophilin 40, FKBP8/FKBP38 contain a putative Calmodulin‐binding domain and a tetratricopeptide‐repeat (TPR) domain for the binding of Hsp90. Both Hsp90 and the non‐structural protein 5A (NS5A) of the hepatitis C virus (HCV) interact specifically with FKBP8/FKBP38 through its TPR domain, and the ternary complex formation plays a critical role in HCV RNA replication. The goal of this study is to evaluate that the host factor inhibits the ternary complex formation and the replication of HCV in vitro and in vivo.MethodsS100 proteins, FKBP38, FKBP8, HCV NS5A, Hsp90, and calmodulin were expressed in E.coli and purified. In vitro binding studies were performed by GST pull‐down, S‐tag pull‐down and surface plasmon resonance analyses. The effect of S100 proteins on HCV replication was analysed by Western blotting using an HCV NS3 antibody following transfection of S100 proteins into the HCV replicon harbouring cell line (sO cells).ResultsIn vitro binding studies showed that S100A1, S100A2, S100A6, S100B and S100P directly interacted with FKBP8/FKBP38 in a Ca2+‐dependent manner and inhibited the FKBP8/FKBP38–Hsp90 and FKBP8/FKBP38–NS5A interactions. Furthermore, overexpression of S100A1, S100A2 and S100A6 in sO cells resulted in the efficient inhibition of HCV replication.ConclusionThe association of the S100 proteins with FKBP8/FKBP38 provides a novel Ca2+‐dependent regulatory role in HCV replication through the NS5A–host protein interaction.
IL‐6 cooperates with peroxisome proliferator‐activated receptor‐α‐ligands to induce liver fatty acid binding protein (LFABP) up‐regulation
Authors: Vida Margarita , Serrano Antonia , Romero‐Cuevas Miguel , Pavón Francisco J. , González‐Rodriguez Águeda , Gavito Ana L. , Cuesta Antonio L. , Valverde Ángela M. , Rodríguez de Fonseca Fernando , Baixeras Elena 
Published: March 2013

AbstractBackgroundLFABP plays a critical role in the uptake and intracellular transport of fatty acids (FA) and other peroxisome proliferator‐activated receptor alpha (PPARα) ligands. PPARα activation by PPARα ligands bound to LFABP results in gene expression of FA oxidation enzymes and de novo LFABP. The cytokine IL‐6 is involved in regulating liver lipid oxidation.AimsTo study the ability of IL‐6 to modulate the expression of the LFABP in hepatocytes. Methods: HepG2 and mouse primary hepatocytes were used to test LFABP mRNA and protein expression after IL‐6 and PPARα‐ligand treatments. Mice lacking IL‐6 and wild‐type C57Bl/6 were subjected to a fasting/re‐feeding cycle to monitor hepatic LFABP mRNA kinetics after food intake.ResultsIn hepatocyte cultures, IL‐6 treatment stimulated a LFABP mRNA sustained expression. Combined treatment of IL‐6 plus PPARα ligands further enhanced LFABP gene and protein expression. In contrast, pretreatment with the PPARα‐antagonist GW‐6471 prevented the up‐regulation of LFABP mRNA induced by IL‐6 in the late phase of LFABP kinetics. Furthermore, the up‐regulation of LFABP mRNA observed in the liver of wild‐type mice 8 h after re‐feeding was absent in mice lacking IL‐6.ConclusionsIL‐6 induces LFABP kinetics in hepatocytes and is partially dependent on PPARα. The maximum increase in LFABP expression occurs when the stimulation with IL‐6 and PPARα‐ligands takes place simultaneously. The in vivo results indicate a postprandial regulation of LFABP that correlates with the presence of IL‐6. These effects may have important implications in the postprandial increase in FA uptake and intracellular trafficking in the liver.
Thermal adaptation and acclimation of ectotherms from differing aquatic climates
Authors: Narum Shawn R. , Campbell Nathan R. , Meyer Kevin A. , Miller Michael R. , Hardy Ronald W. 
Published: March 2013

AbstractTo elucidate the mechanisms of thermal adaptation and acclimation in ectothermic aquatic organisms from differing climates, we used a common‐garden experiment for thermal stress to investigate the heat shock response of redband trout (Oncorhynchus mykiss gairdneri) from desert and montane populations. Evidence for adaptation was observed as expression of heat shock genes in fish from the desert population was more similar to control (unstressed) fish and significantly different (P ≤ 0.05) from those from the montane population, while F1 crosses were intermediate. High induction of heat shock proteins (Hsps) in the montane strain appeared to improve short‐term survival during first exposure to high water temperatures, but high physiological costs of Hsp production may have led to lower long‐term survival. In contrast, the desert strain had significantly lower heat shock response than the montane fish and F1 crosses, suggesting that these desert fish have evolved alternative mechanisms to deal with thermal stress that provide better balance of physiological costs. Genomewide tests of greater than 10 000 SNPs found multipleSNPs that were significantly associated with survival under thermal stress, including Hsp47 which consistently appeared as a strong candidate gene for adaption to desert climates. CandidateSNPs identified in this study are prime targets to screen more broadly across this species' range to predict the potential for adaptation under scenarios of climate change. These results demonstrate that aquatic species can evolve adaptive responses to thermal stress and provide insight for understanding how climate change may impact ectotherms.
Chaperone‐mediated autophagy components are upregulated in sporadic inclusion‐body myositis muscle fibres
Authors: Cacciottolo M. , Nogalska A. , D'Agostino C. , Engel W. K. , Askanas V. 
Published: March 2013

AimsSporadic inclusion‐body myositis (s‐IBM) is an age‐associated degenerative muscle disease. Characteristic features are muscle‐fibre vacuolization and intramuscle‐fibre accumulations of multiprotein aggregates, which may result from the demonstrated impairments of the 26S proteasome and autophagy. Chaperone‐mediated autophagy (CMA) is a selective form of lysosomal degradation targeting proteins carrying the KFERQ motif. Lysosome‐associated membrane protein type 2A (LAMP2A) and the heat‐shock cognate protein 70 (Hsc70) constitute specific CMA components. Neither CMA components nor CMA activity has been studied in normal or disease human muscle, to our knowledge.MethodsWe studied CMA components by immunocytochemistry, immunoblots, real‐time PCR and immunoprecipitation in: (a) 16 s‐IBM, nine aged‐matched normal and nine disease control muscle biopsies; and (b) cultured human muscle fibres (CHMFs) with experimentally inhibited activities of either the 26S proteasome or autophagy.ResultsCompared with age‐matched controls, in s‐IBM muscle, LAMP2A and Hsc70 were on a given transverse section accumulated as aggregates in approximately 5% of muscle fibres, where they (a) colocalized with each other and α‐synuclein (α‐syn), a CMA‐targeted protein; and (b) were bound to each other and to α‐syn by immunoprecipitation. By immunoblots, LAMP2A was increased sevenfold P < 0.001 and Hsc70 2.6‐fold P < 0.05. LAMP2A mRNA was increased 4.4‐fold P < 0.001 and Hsc70 mRNA 1.9‐fold P < 0.05. In CHMFs inhibition of either the 26S proteasome or autophagy induced CMA, evidenced by a significant increase of both LAMP2A and Hsc70.ConclusionsOur study demonstrates, for the first time, up‐regulation of CMA components in s‐IBM muscle, and it provides further evidence that altered protein degradation is likely an important pathogenic aspect in s‐IBM.
Fichte and the German Idiom: the Metaphysics of the Addresses to the German Nation
Authors: Keohane Oisín 
Published: March 2013

AbstractThis article argues against the dominant Anglophone and Francophone interpretation of Fichte, which reads him as advancing either a form of ethnic or cultural nationalism. It claims that what is missing from the current reception of Fichte is the essentially philosophical and cosmopolitan character of his nationalism – the fact that the Addresses to the German Nation uses non‐empirical and cosmopolitical concepts to develop and articulate its nationalistic viewpoint. It therefore claims that the notion of a national philosophical idiom that the Addresses present, far from being a screen for its nationalism, is its driving engine. It does this by considering the problems of translating the German locution ist unsers Geschlechts. Consequently, it is claimed that the cosmo‐nationalism of Fichte is not reducible to a set of claims regarding ethnicity or even the empirical world, even if a discourse on the organismic, on what counts as life, irreducibly haunts the Addresses.
A randomized maternal evaluation of epinephrine autoinjection devices
Authors: Brown Josephine , Tuthill David , Alfaham Mazin , Spear Elizabeth 
Published: March 2013

AbstractBackgroundIntramuscular epinephrine (adrenaline) is the first‐line therapy for anaphylaxis and prompt administration improves outcome. In 2011, two epinephrine autoinjectors existed in the United Kingdom, differing in their users' administration method: EpiPen® and Anapen®. We routinely train all families who receive these devices.AimTo evaluate:

Maternal competence in using epinephrine autoinjectors following our standard anaphylaxis training package.

Which device mothers found easier to use.

MethodsMothers with no previous epinephrine autoinjector experience were approached to participate. One clinician provided a standardized demonstration on using a randomly assigned autoinjector device. She immediately evaluated the mothers' performance using ten predetermined criteria. Four criteria were device specific and six were common criteria to both devices.ResultsOne hundred mothers participated: 50 EpiPen® and 50 Anapen®. A substantial proportion of mothers (15% overall) were not able to successfully ‘fire’ these training devices: Anapen® 4% and EpiPen® 26% (OR 8.43, p = 0.005). Only 22% of mothers overall were able to perform all ten procedures completely successfully: Anapen® 32% and EpiPen® 12%. Chi‐squared analysis showed a significantly higher proportion of mothers correctly performing all Anapen® specific procedures than EpiPen® (OR 14.24, p < 0.0001).ConclusionIt is concerning that 15% of mothers overall could not ‘fire’ these devices correctly despite a one‐to‐one demonstration, identifying a need for more user friendly devices and training. Mothers found the Anapen® device significantly easier to use, which may have implications for future prescribing. Evaluation of the next generation of autoinjectors and their training packages needs to be performed as important practical differences may be found.
Individual Responsibility for Climate Change
Authors: Banks Melany 
Published: March 2013

AbstractAs we become more aware of the potential causes and consequences of climate change we are left wondering: who is responsible? Climate change has the potential to harm large portions of the global population and, arguably, is already doing so. Further, climate change is argued to be human‐caused. If this is true, then it seems to be the case that we can analyze climate change in terms of responsibility. I argue that we can approach environmental harms, such as climate change, through a theory of collective responsibility. I propose an account of reductive collective responsibility that can apply to the unstructured collective causing climate change and determine what we are each individually morally responsible for. To avoid the critiques of reductive collective responsibility for large unstructured harms, I propose we separate the determination of membership and eligibility for responsibility from the attribution of responsibility. Through this method, I can speak to the individual responsibility of each member who contributes to climate change without holding them responsible for that which is outside their control.
The cis‐acting CTTC–P1BS module is indicative for gene function of LjVTI12, a Qb‐SNARE protein gene that is required for arbuscule formation in Lotus japonicus
Authors: Lota Frédéric , Wegmüller Sarah , Buer Benjamin , Sato Shusei , Bräutigam Andrea , Hanf Benjamin , Bucher Marcel 
Published: March 2013

SummaryThe majority of land plants live in symbiosis with arbuscular mycorrhizal fungi from the phylum Glomeromycota. This symbiosis improves acquisition of phosphorus (P) by the host plant in exchange for carbohydrates, especially under low‐P availability. The symbiosome, constituted by root cortex cells accommodating arbuscular mycorrhizal fungal hyphae, is the site at which bi‐directional exchange of nutrients and metabolites takes place. Uptake of orthophosphate (Pi) in the symbiosome is facilitated by mycorrhiza‐specific plant Pi transporters. Modifications of the potato Pi transporter 3 (StPT3) promoter were analysed in transgenic mycorrhizal roots, and it was found that the CTTC cis‐regulatory element is necessary and sufficient for a transcriptional response to fungal colonization under low‐Pi conditions. Phylogenetic footprinting also revealed binary combination of the CTTC element with the Pi starvation response‐associated PHR1‐binding site (P1BS) in the promoters of several mycorrhiza‐specific Pi transporter genes. Scanning of the Lotus japonicus genome for gene promoters containing both cis‐regulatory elements revealed a strong over‐representation of genes involved in transport processes. One of these, LjVTI12, encoding a member of the SNARE family of proteins involved in membrane transport, exhibited enhanced transcript levels in Lotus roots colonized with the arbuscular mycorrhizal fungus Glomus intraradices. Down‐regulation of LjVTI12 by RNA interference resulted in a mycorrhiza‐specific phenotype characterized by distorted arbuscule morphology. The results highlight cooperative cis‐regulation which integrates mycorrhiza and Pi starvation signaling with vesicle trafficking in symbiosome development.
Open stomata 1 (OST1) kinase controls R–type anion channel QUAC1 in Arabidopsis guard cells
Authors: Imes Dennis , Mumm Patrick , Böhm Jennifer , Al‐Rasheid Khaled A. S. , Marten Irene , Geiger Dietmar , Hedrich Rainer 
Published: March 2013

SummaryUnder drought stress, the stress hormone ABA addresses the SnR kinase OST1 via its cytosolic receptor and the protein phosphatase ABI1. Upon activation, OST1 phosphorylates the guard cell S–type anion channel SLAC1. Arabidopsis ABI1 and OST1 loss‐of‐function mutants are characterized by an extreme wilting 'open stomata′ phenotype. Given the fact that guard cells express both SLAC‐ and R–/QUAC‐type anion channels, we questioned whether OST1, besides SLAC1, also controls the QUAC1 channel. In other words, are ABI1/OST1 defects preventing both of the guard cell anion channel types from operating properly in terms of stomatal closure? The activation of the R–/QUAC‐type anion channel by ABA signaling kinase OST1 and phosphatase ABI1 was analyzed in two experimental systems: Arabidopsis guard cells and the plant cell‐free background of Xenopus oocytes. Patch‐clamp studies on guard cells show that ABA activates R–/QUAC‐type currents of wild‐type plants, but to a much lesser extent in those of abi1–1 and ost1–2 mutants. In the oocyte system the co‐expression of QUAC1 and OST1 resulted in a pronounced activation of the R–type anion channel. These studies indicate that OST1 is addressing both S–/SLAC‐ and R–/QUAC‐type guard cell anion channels, and explain why the ost1–2 mutant is much more sensitive to drought than single slac1 or quac1 mutants.
Arabidopsis transcription factor WRKY8 functions antagonistically with its interacting partner VQ9 to modulate salinity stress tolerance
Authors: Hu Yanru , Chen Ligang , Wang Houping , Zhang Liping , Wang Fang , Yu Diqiu 
Published: March 2013

SummaryThe WRKY transcription factors have been demonstrated to play crucial roles in regulating stress responses; however, the exact mechanisms underlying their involvement in stress responses are not fully understood. Arabidopsis WRKY8 was predominantly expressed in roots and was highly upregulated by salt treatment. Disruption of WRKY8 rendered plants hypersensitive to salt, showing delayed germination, inhibited post‐germination development and accelerated chlorosis. Further investigation revealed that WRKY8 interacted with VQ9, and their interaction decreased the DNA‐binding activity of WRKY8. The VQ9 protein was exclusively localized in the nucleus, and VQ9 expression was strongly responsive to NaCl treatment. Mutation of VQ9 enhanced tolerance to salt stress, indicating that VQ9 acts antagonistically with WRKY8 to mediate responses to salt stress. The antagonist functions of WRKY8 and VQ9 were consistent with an increased or reduced Na+/K+ concentration ratio, as well as contrasting expression patterns of downstream stress‐responsive genes in salt‐stressed wrky8 and vq9 mutants. Moreover, chromatin immunoprecipitation (ChIP) assays showed that WRKY8 directly bound the promoter of RD29A under salt conditions. These results provided strong evidence that the VQ9 protein acts as a repressor of the WRKY8 factor to maintain an appropriate balance of WRKY8‐mediated signaling pathways to establish salinity stress tolerance.