bluuebunny/crossref_metadata_2025_split huggingface dataset:
Imaging Selection in Ischemic Stroke: Feasibility of Automated CT-Perfusion Analysis
Authors: Campbell Bruce C.V. , Yassi Nawaf , Ma Henry , Sharma Gagan , Salinas Simon , Churilov Leonid , Meretoja Atte , Parsons Mark W. , Desmond Patricia M. , Lansberg Maarten G. , Donnan Geoffrey A. , Davis Stephen M. 
Published: October 2014

Background Advanced imaging may refine patient selection for ischemic stroke treatment but delays to acquire and process the imaging have limited implementation. Aims We examined the feasibility of imaging selection in clinical practice using fully automated software in the EXTEND trial program. Methods CTP and perfusion-diffusion MRI data were processed using fully-automated software to generate a yes/no ‘mismatch’ classification that determined eligibility for trial therapies. The technical failure/mismatch classification error rate and time to image and treat with CT vs. MR-based selection were examined. Results In a consecutive series of 776 patients from five sites over six-months the technical failure rate of CTP acquisition/processing (uninterpretable maps) was 3·4% (26/776, 95%CI 2·2–4·9%). Mismatch classification was overruled by expert review in an additional 9·0% (70/776, 95%CI 7·1–11·3%) due to artifactual ‘perfusion lesion’. In 154 consecutive patients at one site, median additional time to acquire CTP after noncontrast CT was 6·5 min. Subsequent RAPID processing time varied from 3–10 min across 20 trial centers (median 5 min 20 s). In the EXTEND trial, door-to-needle times in patients randomized on the basis of CTP ( n = 47) were median 78 min shorter than MRI-selected ( n = 16) patients ( P < 0·001). Conclusions Automated CTP-based mismatch selection is rapid, robust in clinical practice, and associated with faster treatment decisions than MRI. This technological advance has the potential to improve the standardization and reproducibility of interpretation of advanced imaging and extend use to practice settings beyond highly specialized academic centers.
Validation of the Korean language version of the incontinence‐quality of life scale
Authors: Kang Youngmi 
Published: October 2014

ABSTRACTThe purpose of this study is to determine the reliability and validity of the translated Korean version of the incontinence‐quality of life (I‐QOL) in a sample of community‐dwelling Korean American women with urinary incontinence in the USA. A survey design was used and a convenience sampling method of 176 Korean American women who reported having urinary incontinence symptoms was used. Translation–back translation procedures were used to translate the English version of the I‐QOL into Korean version. Reliability of the Korean I‐QOL questionnaire was demonstrated by Cronbach's α coefficients. Pearson's correlations of an item with its own scale and other scales were calculated to evaluate item‐convergent and item‐discriminant validity. Confirmatory factor analysis was performed to examine the underlying factor structure of the Korean version of the I‐QOL. Cronbach's α coefficient for all three subscales was greater than 0·70. The results of item‐convergent validity indicated that each item was strongly correlated with the originally belonged subscale. Item‐discriminant validity was evidenced by all lower correlations of an item to the other subscales than that of own subscale. Three factors were extracted from I‐QOL, accounting for 67·37% of the variance. The findings supported the reliability and validity of Korean version of I‐QOL questionnaire. It would be considered as a valuable instrument to assess the different aspects of health‐related quality of life in incontinence patients and recommended for use in clinical research.
A decade of progress in adipose tissue macrophage biology
Authors: Hill Andrea A. , Reid Bolus W. , Hasty Alyssa H. 
Published: October 2014

SummaryOne decade has passed since seminal publications described macrophage infiltration into adipose tissue (AT) as a key contributor to inflammation and obesity‐related insulin resistance. Currently, a PubMed search for ‘adipose tissue inflammation’ reveals over 3500 entries since these original reports. We now know that resident macrophages in lean AT are alternatively activated, M2‐like, and play a role in AT homeostasis. In contrast, the macrophages in obese AT are dramatically increased in number and are predominantly classically activated, M1‐like, and promote inflammation and insulin resistance. Mediators of AT macrophage (ATM) phenotype include adipokines and fatty acids secreted from adipocytes as well as cytokines secreted from other immune cells in AT. There are several mechanisms that could explain the large increase in ATMs in obesity. These include recruitment‐dependent mechanisms such as adipocyte death, chemokine release, and lipolysis of fatty acids. Newer evidence also points to recruitment‐independent mechanisms such as impaired apoptosis, increased proliferation, and decreased egress. Although less is known about the homeostatic function of M2‐like resident ATMs, recent evidence suggests roles in AT expansion, thermoregulation, antigen presentation, and iron homeostasis. The field of immunometabolism has come a long way in the past decade, and many exciting new discoveries are bound to be made in the coming years that will expand our understanding of how AT stands at the junction of immune and metabolic co‐regulation.
Macrophage proliferation, provenance, and plasticity in macroparasite infection
Authors: Rückerl Dominik , Allen Judith E. 
Published: October 2014

SummaryMacrophages have long been center stage in the host response to microbial infection, but only in the past 10–15 years has there been a growing appreciation for their role in helminth infection and the associated type 2 response. Through the actions of the IL‐4 receptor α (IL‐4Rα), type 2 cytokines result in the accumulation of macrophages with a distinctive activation phenotype. Although our knowledge of IL‐4Rα‐induced genes is growing rapidly, the specific functions of these macrophages have yet to be established in most disease settings. Understanding the interplay between IL‐4Rα‐activated macrophages and the other cellular players is confounded by the enormous transcriptional heterogeneity within the macrophage population and by their highly plastic nature. Another level of complexity is added by the new knowledge that tissue macrophages can be derived either from a resident prenatal population or from blood monocyte recruitment and that IL‐4 can increase macrophage numbers through proliferative expansion. Here, we review current knowledge on the contribution of macrophages to helminth killing and wound repair, with specific attention paid to distinct cellular origins and plasticity potential.
Macrophage heterogeneity in tissues: phenotypic diversity and functions
Authors: Gordon Siamon , Plüddemann Annette , Martinez Estrada Fernando 
Published: October 2014

SummaryDuring development and throughout adult life, macrophages derived from hematopoietic progenitors are seeded throughout the body, initially in the absence of inflammatory and infectious stimuli as tissue‐resident cells, with enhanced recruitment, activation, and local proliferation following injury and pathologic insults. We have learned a great deal about macrophage properties ex vivo and in cell culture, but their phenotypic heterogeneity within different tissue microenvironments remains poorly characterized, although it contributes significantly to maintaining local and systemic homeostasis, pathogenesis, and possible treatment. In this review, we summarize the nature, functions, and interactions of tissue macrophage populations within their microenvironment and suggest questions for further investigation.
Tissue macrophage identity and self‐renewal
Authors: Gentek Rebecca , Molawi Kaaweh , Sieweke Michael H. 
Published: October 2014

SummaryMacrophages are cellular components of the innate immune system that reside in virtually all tissues and contribute to immunity, repair, and homeostasis. The traditional view that all tissue‐resident macrophages derive from the bone marrow through circulating monocyte intermediates has dramatically shifted recently with the observation that macrophages from embryonic progenitors can persist into adulthood and self‐maintain by local proliferation. In several tissues, however, monocytes also contribute to the resident macrophage population, on which the local environment can impose tissue‐specific macrophage functions. These observations have raised important questions: What determines resident macrophage identity and function, ontogeny or environment? How is macrophage proliferation regulated? In this review, we summarize the current knowledge about the identity, proliferation, and turnover of tissue‐resident macrophages and how they differ from freshly recruited short‐lived monocyte‐derived cells. We examine whether macrophage proliferation can be qualified as self‐renewal of mature differentiated cells and whether the concepts and molecular pathways are comparable to self‐renewal mechanisms in stem cells. Finally, we discuss how improved understanding of macrophage identity and self‐renewal could be exploited for therapeutic intervention of macrophage‐mediated pathologies by selectively targeting freshly recruited or resident macrophages.
Platelet thromboembolism
Authors: KESSLER C. M. , HANSON S. R. 
Published: October 2014

Abstract. Platelet‐dependent thrombosis and subsequent embolization are major causes of cerebral ischaemia. Beside aspirin which irreversibly blocks platelet cyclo‐oxygenase, several other substances interfere in different platelet metabolic pathways and block platelet adhesion and aggregation. We found in an experimental model using non‐human primates that a specific peptide inhibitor blocking GP IIb/IIIa platelet receptor which binds fibrinogen completely, prevents the retention of embolized platelet aggregates in the cerebral circulation. As thrombin may play a key role for platelet activation in vivo leech‐derived hirudin, a direct thrombin inhibitor as well as activated protein C which limits thrombin production and also prevents platelet dependent thrombus formation very effective.We demonstrated in the same non‐human primate model of platelet embolization that the amount of retention of platelet emboli in the vascular bed depends on the nature of the vasculature. For example, platelet emboli were cleared very quickly from brain microcirculation, whereas platelet embolization into the lower limb via the femoral artery caused a significantly longer retention of the embolized material. Such specific mechanisms may be caused by different levels of local vasodilators as PGI2 or EDRF.
Model‐Based Nitrogen and Phosphorus (Nutrient) Criteria for Large Temperate Rivers: 2. Criteria Derivation
Authors: Suplee Michael W. , Flynn Kyle F. , Chapra Steven C. 
Published: October 2014

AbstractNitrogen and phosphorus criteria were developed for 233 km of the Yellowstone River, one of the first cases where a mechanistic model has been used to derive large river numeric nutrient criteria. A water quality model and a companion model which simulates lateral algal biomass across transects were used to simulate effects of increasing nutrients on five variables (dissolved oxygen, total organic carbon, total dissolved gas,pH, and benthic algal biomass in depths ≤1 m). Incremental increases in nutrients were evaluated relative to their impact on predefined thresholds for each variable; the first variable to exceed a threshold set the nutrient criteria. Simulations were made at a low flow, the 14Q5 (lowest average 14 consecutive day flow, July‐September, recurring one in five years), which was derived using benthic algae growth curves and EPA guidance on excursion frequency. An extant climate dataset with an annual recurrence was used, and tributary water quality and flows were coincident with the river's 10 lowest flow years. The river had different sensitivities to nutrients longitudinally,pHbeing the most sensitive variable in the upstream reach and algal biomass in the lower. Model‐based criteria for the Yellowstone River are as follows: between the Bighorn and Powder river confluences, 55 μg TP/l and 655 μg TN/l; from the Powder River confluence to Montana state line, 95 μg TP/l and 815 μg TN/l. Pros and cons of using steady‐state models to derive river nutrient criteria are discussed.
Rapid onset of syndrome of inappropriate antidiuretic hormone secretion induced by duloxetine in an elderly type 2 diabetic patient with painful diabetic neuropathy
Authors: Kamei Shinji , Kaneto Hideaki , Tanabe Akihito , Irie Shintaro , Hirata Yurie , Shimoda Masashi , Kohara Kenji , Mune Tomoatsu , Kaku Kohei 
Published: October 2014

AbstractDiabetic neuropathy is the most common diabetic complication. Duloxetine, a serotonin noradrenaline reuptake inhibitor (SNRI), is widely used for the treatment of diabetic painful neuropathy (DPN) because of the efficacy and safety profile. Syndrome of inappropriate antidiuretic hormone secretion, which is strongly associated duloxetine, is a rare but occasionally life‐threatening adverse effect. Here, we report a case of syndrome of inappropriate antidiuretic hormone secretion that rapidly developed after starting duloxetine in an elderly Japanese female type 2 diabetes mellitus patient. Furthermore, we discuss the possible relationship between the onset of syndrome of inappropriate antidiuretic hormone secretion and the gene polymorphism of cytochrome P450 isoform 1A2 and 2D6, both of which are responsible for duloxetine metabolism.
More explicit communication after classroom‐based crew resource management training: results of a pragmatic trial
Authors: Verbeek‐van Noord Inge , de Bruijne Martine C. , Twisk Jos W. R. , van Dyck Cathy , Wagner Cordula 
Published: October 2014

AbstractRationale, aims and objectivesAviation‐based crew resource management trainings to optimize non‐technical skills among professionals are often suggested for health care as a way to increase patient safety. Our aim was to evaluate the effect of a 2‐day classroom‐based crew resource management (CRM) training at emergency departments (EDs) on explicit professional oral communication (EPOC; non‐technical skills).MethodA pragmatic controlled before‐after trial was conducted. Four EDs of general teaching hospitals were recruited (two intervention and two control departments). ED nurses and ED doctors were observed on their non‐technical skills by means of a validated observation tool (EPOC). Our main outcome measure was the amount of EPOC observed per interaction in 30 minutes direct observations. Three outcome measures from EPOC were analysed: human interaction, anticipation on environment and an overall EPOC score. Linear and logistic mixed model analyses were performed. Models were corrected for the outcome measurement at baseline, days between training and observation, patient safety culture and error management culture at baseline.ResultsA statistically significant increase after the training was found on human interaction (β = 0.27, 95% CI 0.08–0.49) and the overall EPOC score (β = 0.25, 95% CI 0.06–0.43), but not for anticipation on environment (OR = 1.19, 95% CI .45–3.15). This means that approximately 25% more explicit communication was shown after CRM training.ConclusionsWe found an increase in the use of CRM skills after classroom‐based crew resource management training. This study adds to the body of evidence that CRM trainings have the potential to increase patient safety by reducing communication flaws, which play an important role in health care‐related adverse events.
Effect of medication adherence on blood pressure control and risk factors for antihypertensive medication adherence
Authors: Yue Zhao , Bin Wang , Weilin Qi , Aifang Yang 
Published: October 2014

AbstractRationale, aims and objectivesWe aim to investigate a range of risk factors associated with medication adherence among Chinese hypertensive patients. We also aim to investigate the association between medication adherence and blood pressure control.MethodsA cross‐sectional study was conducted among Chinese hypertensive patients in a comprehensive teaching hospital in Shanghai, China, using a validated scale, a self‐designed questionnaire and patients' medical records.ResultsOf the 232 eligible participants, 61 (26.3%), 51 (22.0%) and 120 (51.7%) showed low, medium and high adherence, respectively. Adjusted for socio‐demographic, clinical and patient‐related factors, antihypertensive medication adherence was significantly associated with better systolic blood pressure control (P = 0.001), whereas the association with diastolic blood pressure control was relatively weak (P = 0.334). In the multivariate analysis, patients with longer duration of drug use [P = 0.012, odds ratio (OR) = 0.46, 95% confidence interval (CI) 0.25–0.84], combination of antiplatelet agents (0.002, 0.38, 0.20–0.71), less concerns of medical cost (0.001, 0.18, 0.02–0.51), more availability of professional guidance (0.002, 0.34, 0.17–0.66) and more availability of family support (0.036, 0.51, 0.27–0.96) were more likely to adhere to their drug regimens.ConclusionsThe rate of suboptimal medication adherence among Chinese hypertensive patients is quite high. Interventions could focus upon the risk factors to improve antihypertensive medication adherence in clinical practice.
P301L tau expression affects glutamate release and clearance in the hippocampal trisynaptic pathway
Authors: Hunsberger Holly C. , Rudy Carolyn C. , Batten Seth R. , Gerhardt Greg A. , Reed Miranda N. 
Published: October 2014

AbstractIndividuals at risk of developing Alzheimer's disease (AD) often exhibit hippocampal hyperexcitability. A growing body of evidence suggests that perturbations in the glutamatergic tripartite synapse may underlie this hyperexcitability. Here, we used a tau mouse model of AD (rTg(TauP301L)4510) to examine the effects of tau pathology on hippocampal glutamate regulation. We found a 40% increase in hippocampal vesicular glutamate transporter, which packages glutamate into vesicles, and has previously been shown to influence glutamate release, and a 40% decrease in hippocampal glutamate transporter 1, the major glutamate transporter responsible for removing glutamate from the extracellular space. To determine whether these alterations affected glutamate regulation in vivo, we measured tonic glutamate levels, potassium‐evoked glutamate release, and glutamate uptake/clearance in the dentate gyrus, cornu ammonis 3(CA3), and cornu ammonis 1(CA1) regions of the hippocampus. P301L tau expression resulted in a 4‐ and 7‐fold increase in potassium‐evoked glutamate release in the dentate gyrus and CA3, respectively, and significantly decreased glutamate clearance in all three regions. Both release and clearance correlated with memory performance in the hippocampal‐dependent Barnes maze task. Alterations in mice expressing P301L were observed at a time when tau pathology was subtle and before readily detectable neuron loss. These data suggest novel mechanisms by which tau may mediate hyperexcitability.
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Pre‐synaptic vesicular glutamate transporters (vGLUTs) package glutamate into vesicles before exocytosis into the synaptic cleft. Once in the extracellular space, glutamate acts on glutamate receptors. Glutamate is removed from the extracellular space by excitatory amino acid transporters, including GLT‐1, predominantly localized to glia. P301L tau expression increases vGLUT expression and glutamate release, while also decreasing GLT‐1 expression and glutamate clearance.
Zinc transporter‐1: a novel NMDA receptor‐binding protein at the postsynaptic density
Authors: Mellone Manuela , Pelucchi Silvia , Alberti Lorenzo , Genazzani Armando A. , Di Luca Monica , Gardoni Fabrizio 
Published: October 2014

AbstractZinc (Zn2+) is believed to play a relevant role in the physiology and pathophysiology of the brain. Hence, Zn2+ homeostasis is critical and involves different classes of molecules, including Zn2+ transporters. The ubiquitous Zn2+ transporter‐1 (ZNT‐1) is a transmembrane protein that pumps cytosolic Zn2+ to the extracellular space, but its function in the central nervous system is not fully understood. Here, we show that ZNT‐1 interacts with GluN2A‐containing NMDA receptors, suggesting a role for this transporter at the excitatory glutamatergic synapse. First, we found that ZNT‐1 is highly expressed at the hippocampal postsynaptic density (PSD) where NMDA receptors are enriched. Two‐hybrid screening, coimmunoprecipitation experiments and clustering assay in COS‐7 cells demonstrated that ZNT‐1 specifically binds the GluN2A subunit of the NMDA receptor. GluN2A deletion mutants and pull‐down assays indicated GluN2A(1390–1464) domain as necessary for the binding to ZNT‐1. Most importantly, ZNT‐1/GluN2A complex was proved to be dynamic, since it was regulated by induction of synaptic plasticity. Finally, modulation of ZNT‐1 expression in hippocampal neurons determined a significant change in dendritic spine morphology, PSD‐95 clusters and GluN2A surface levels, supporting the involvement of ZNT‐1 in the dynamics of excitatory PSD.
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Zn2+ transporter‐1 (ZNT‐1) pumps cytosolic Zn2+ to the extracellular space, but its function in the central nervous system is not fully understood. We show that ZNT‐1 interacts with GluN2A‐containing NMDA receptors at the glutamatergic synapse. Most importantly, ZNT‐1/GluN2A complex is regulated by induction of synaptic plasticity. Modulation of ZNT‐1 expression in hippocampal neurons determined a shrinkage of dendritic spines and a reduction of GluN2A surface levels supporting the involvement of ZNT‐1 in the dynamics of the excitatory synapse.
Localization of heat shock protein HSPA6 (HSP70B') to sites of transcription in cultured differentiated human neuronal cells following thermal stress
Authors: Khalouei Sam , Chow Ari M. , Brown Ian R. 
Published: October 2014

AbstractHeat shock proteins (Hsps) are a set of highly conserved proteins that are involved in cellular repair and protective mechanisms. In order to identify potential stress‐sensitive sites in differentiated SH‐SY5Y human neuronal cells, localization of two inducible members of the HSPA (HSP70) family was investigated, namely HSPA6 (HSP70B') and HSPA1A (HSP70‐1). Following heat shock, yellow fluorescent protein (YFP)‐tagged HSPA6 and HSPA1A proteins localized to nuclear speckles that are enriched in RNA splicing factors (identified by SC35 and SON marker proteins) and then to the granular component of the nucleolus (identified by nucleophosmin). Subsequently, YFP‐HSPA6 protein, but not YFP‐HSPA1A, localized to the periphery of nuclear speckles that are sites of RNA transcription. The HSPA6 gene is present in the human genome but not in genomes of rat and mouse. Hence, current animal models of neurodegenerative diseases are lacking a potentially protective member of the HSPA family.
imagePotential stress‐sensitive sites were identified in differentiated human SH‐SY5Y cells by the localization of HSPA6 (HSP70B') and HSPA1A (HSP70‐1) to nuclear components following heat shock. HSPA6 and HSPA1A rapidly moved to nuclear speckles, enriched in RNA splicing factors, then to the granular layer of the nucleolus. Subsequently, HSPA6 exhibited a novel localization not observed for the more widely studied HSPA1A, namely association with the periphery of nuclear speckles that are sites of transcription. HS = heat shock; HSPA6 = HSP70B' protein; HSPA1A = HSP70‐1 protein.