bluuebunny/crossref_metadata_2025_split huggingface dataset:
Development of an improved urea-selective catalytic reduction—diesel particulate filter system for heavy-duty commercial vehicles
Authors: Hirata K , Masaki N , Yano M , Akagawa H , Takada K , Kusaka J , Mori T 
Published: July 2009

Many heavy-duty commercial vehicles are now equipped with urea-selective catalytic reduction (SCR) systems, which can reduce NO x emissions sufficiently to meet the requirements of legislation such as Japan's New Long-term Diesel Emissions Regulations. However, in order to meet even stricter exhaust emissions regulations (and fuel consumption standards) due to be imposed in many parts of the world in the near future, urea-SCR systems with greater catalytic efficiency combined with diesel particulate filters (DPFs) will be needed. Therefore, in the study presented here the scope for enhancing the efficiency of a urea-SCR system was explored by optimizing the urea dosing system and injection strategies, and the gas flow in the exhaust pipe. However, since improving the catalysis parameters could have the greatest overall effect on conversion efficiency, work focused on modifying the catalyst materials to increase their adsorption capacity for the NH3 reducing agent, and thus increase the collision frequency between NO x and NH3 absorbed on the surface of the catalyst. In addition, the oxidation parameters of the oxidation catalyst were optimized, which enhanced the NO x conversion efficiency of the system, not only in a steady cycle but also in a transient cycle. Following these adjustments, a DPF-plus-SCR system with the new catalytic material delivered 90 per cent conversions of NO x and particulate matter to N2 and CO2 respectively, in the JE05 test cycle. In addition, a new concept, a miniaturized ‘urea-SCR with DPF function system’ was proposed and tested, which delivered 90 per cent NO x conversion rates and 90 per cent reductions in particulate matter emissions in the JE05 test cycle.
Fatigue to Fracture: An Informative, Fast, and Reliable Approach for Assessing Medical Implant Durability
Authors: Gong X.-Y. , Chwirut D. J. , Mitchell M. R. , Choules B. D. 
Published: July 2009

Abstract
This paper compares the differences between the “test to success” and “test to fracture” paradigms for medical implant durability assessment. It recognizes that test to success can be one of the tests within test to fracture, in addition to a series of shorter cycle, higher force/deformation tests. In addition, by “testing to fracture,” one can validate the fatigue analysis capability, learn the consequences of in vitro fractures, and provide information that can either be used for product improvement or for clinicians to make life-saving decisions.
A New Technology of Recycling 100 % Reclaimed Asphalt Pavements
Authors: Do Huh Jung , Park Joo Young 
Published: July 2009

Abstract
Recycling of 100 % reclaimed asphalt pavement (RAP) without adding any virgin materials is a challenging task. Most of the present RAP-recycling technology is limited to use the 20 %–30 % RAP as a maximum content for wearing courses of asphalt pavements. The main goal of the existing recycling technology is focused to restore original properties of the straight asphalt pavement mixtures by using rejuvenators. Here, a new technology is introduced to use 100 % RAP-recycling by adding a specially developed polymer-modifier. The hot mix asphalt design is used to figure out the content of the modifier. Quality of the new recycled mixtures is excellent such that their properties are superior over the virgin straight asphalt mixtures. Excellent quality, maximum use of RAP, simple process, and competitive price will make this technology very attractive.
Study on Low-Temperature Cracking Performance of Asphalt Mortar Modified by an Aluminate Coupling Agent
Authors: Liu Shu-tang , Hou Feng , Cao Wei-dong , Liu Ying 
Published: July 2009

Abstract
The low-temperature performance properties of asphalt mortar modified by an aluminate coupling agent (ACA) were investigated and are reported in this paper. An orthogonal experiment design method was used, and the creep stiffness and m-value were adopted as the indicators to investigate the modifier effects of the filler-asphalt ratio, ACA, and stearic acid on the low-temperature performance of asphalt mortar. The influence of other factors on the high-temperature, anti-rutting performance and intermediate-temperature fatigue performance of asphalt mortar was also evaluated. Analysis indicated that ACA could improve significantly the low-temperature performance and intermediate-temperature fatigue performance of asphalt mortar but reduced the high-temperature performance. Asphalt mortar modified by a moderate filler-asphalt ratio, a significant amount of ACA, and stearic acid showed better low-temperature performance properties.
Prediction of In-Service Fatigue Life of Flexible Pavements Based on Accelerated Pavement Testing
Authors: Guo Runhua , Prozzi Jorge A. 
Published: July 2009

Abstract
Full-scale accelerated pavement testing (APT) is a supplement to typical laboratory procedures. As such, it leads to significant advances in practice and economic savings for the evaluation of new pavement configurations, stress level related factors, new materials, and design improvements. This type of testing closely simulates field conditions; however, it does not capture actual pavement performance because of the limited ability to address long-term phenomena. Therefore, to fully utilize the benefits of APT, there is a need for a methodology to predict the long-term performance of in-service pavement structures based on the generated test results in order to account for such differences. The bias correction factor (BCF) or bias correction functions should account for the quantifiable differences between the fatigue life of the pavement site under APT and the in-service conditions. The BCF represents an improvement of the currently used “shift factors” since they are more general and are based on laboratory testing or computer simulations. By applying the proposed methodology, APT performance results from a structure similar to an in-service structure can be used to perform four-point bending beam tests and structural analysis to obtain an accurate estimate of the necessary BCF to estimate in-service performance.
Buchbesprechungen
Authors: Voß Christian 
Published: July 2009

Zusammenfassung

Fremdes Europa? Selbstbilder und Europa-Vorstellungen in Bulgarien (18501945). Hrsg. von Petǎr PETROV, Katerina GEHL und Klaus ROTH. Berlin: LIT Verlag 2007, 366 S. ( Kulturgeschichtliche Perspektiven, 6) ISBN 978-3-8258-0793-1
curledEncodes the Drosophila Homolog of the Vertebrate Circadian Deadenylase Nocturnin
Authors: Grönke Sebastian , Bickmeyer Iris , Wunderlich Roman , Jäckle Herbert , Kühnlein Ronald P 
Published: July 2009

AbstractDrosophila melanogaster curled, one of the first fly mutants described by T. H. Morgan &gt;90 years ago, is the founding member of a series of curled wing phenotype mutants widely used as markers in fruit fly genetics. The expressivity of the wing phenotype is environmentally modulated, suggesting that the mutation affects the metabolic status of cells rather than a developmental control gene. However, the molecular identity of any of the curled wing marker mutant genes is still unknown. In a screen for starvation-responsive genes, we previously identified the single fly homolog of the vertebrate nocturnin genes, which encode cytoplasmic deadenylases that act in the post-transcriptional control of genes by poly(A) tail removal of target mRNAs prior to their degradation. Here we show that curled encodes Drosophila Nocturnin and that the gene is required at pupal stage for proper wing morphogenesis after eclosion of the fly. Despite the complex ontogenetic expression pattern of the gene, curled is not expressed in the developing wing, and wing-specific curled knockdown mediated by RNAi does not result in the curled wing phenotype, indicating a tissue-nonautonomous, systemic mode of curled gene function. Our study not only presents an entry point into the functional analysis of invertebrate nocturnins but also paves the way for the identification of the still elusive Nocturnin target mRNAs by genetic suppressor screens on the curled wing phenotype.
Quantitative Analysis of CPR Quality During In-Hospital Resuscitation of Older Children and Adolescents
Authors: Sutton Robert M. , Niles Dana , Nysaether Jon , Abella Benjamin S. , Arbogast Kristy B. , Nishisaki Akira , Maltese Matthew R. , Donoghue Aaron , Bishnoi Ram , Helfaer Mark A. , Myklebust Helge , Nadkarni Vinay 
Published: July 2009

OBJECTIVE: Few data exist on pediatric cardiopulmonary resuscitation (CPR) quality. This study is the first to evaluate actual in-hospital pediatric CPR. We hypothesized that with bedside CPR training and corrective feedback, CPR quality can approach American Heart Association (AHA) targets.
PATIENTS AND METHODS: Using CPR recording/feedback defibrillators, quality of CPR was assessed for patients ≥8 years of age who suffered a cardiac arrest in the PICU or emergency department (ED). Before and during the study, a bedside CPR training program was initiated.
RESULTS: Between October 2006 and February 2008, twenty events in 18 patients met inclusion criteria and resulted in 36749 evaluable chest compressions (CCs) during 392.3 minutes of arrest. CCs were shallow (&lt;38 mm or &lt;1.5 in) in 27.2% (9998 of 36749), with excessive residual leaning force (≥2500 g) in 23.4% (8611 of 36749). Segmental analysis of the first 5 minutes of the events demonstrated that shallow CCs and excessive residual leaning force were less prevalent during the first 5 minutes. AHA targets were not achieved for CC rate in 62 (43.1%) of 144 segments, CC depth in 52 (36.1%) of 144 segments, and residual leaning force in 53 (36.8%) of 144 segments.
CONCLUSIONS: This prospective, observational study demonstrates feasibility of monitoring in-hospital pediatric CPR. Even with bedside CPR retraining and corrective audiovisual feedback, CPR quality frequently did not meet AHA targets. Importantly, no flow fraction target of 10% was achieved. Future studies should investigate novel educational methods and targeted feedback technologies.
13C-Sucrose Breath Test: Novel Use of a Noninvasive Biomarker of Environmental Gut Health
Authors: Ritchie Brett K. , Brewster David R. , Davidson Geoffrey P. , Tran Cuong D. , McNeil Yvette , Hawkes Joanna S. , Butler Ross N. 
Published: July 2009

OBJECTIVE: Environmental enteropathy syndrome may compromise growth and predispose to infectious diseases in children in the developing world, including Australian Aboriginal children from remote communities of the Northern Territory. In this study, we described the use of a biomarker 13C-sucrose breath test (SBT) to measure enterocyte sucrase activity as a marker of small intestinal villus integrity and function.
METHODS: This was a hospital-based prospective case-control study of Aboriginal and non-Aboriginal children with and without acute diarrheal disease. Using the SBT, we compared 36 Aboriginal case subjects admitted to a hospital (18 diarrheal and 18 nondiarrheal disease), with 7 healthy non-Aboriginal control subjects. Intestinal permeability using the lactulose/rhamnose (L/R) ratio on a timed 90-minute blood test was performed simultaneously with the SBT. The SBT results are expressed as a cumulative percentage of the dose recovered at 90 minutes.
RESULTS: Aboriginal children with acute diarrheal disease have a significantly decreased absorptive capacity, as determined by the SBT, with a mean of 1.9% compared with either Aboriginal children without diarrhea (4.1%) or non-Aboriginal (6.1%) control subjects. The mean L/R ratio in the diarrhea group was 31.8 compared with 11.4 in Aboriginal children without diarrhea. There was a significant inverse correlation between the SBT and the L/R ratio.
CONCLUSIONS: The SBT was able to discriminate among Aboriginal children with diarrhea, asymptomatic Aboriginal children with an underlying environmental enteropathy, and healthy non-Aboriginal controls. This test provides a noninvasive, easy-to-use, integrated marker of the absorptive capacity and integrity of the small intestine and could be a valuable tool in evaluating the efficacy of interventions aimed at improving gut health.
The Role of Src in Solid Tumors
Authors: Wheeler Deric L. , Iida Mari , Dunn Emily F. 
Published: July 2009

Abstract
The proto-oncogene c-Src (Src) encodes a nonreceptor tyrosine kinase whose expression and activity are correlated with advanced malignancy and poor prognosis in a variety of human cancers. Nine additional enzymes with homology to Src have been identified and collectively are referred to as Src family kinases (SFKs). Together, SFKs represent the largest family of nonreceptor tyrosine kinases and interact directly with receptor tyrosine kinases, G-protein-coupled receptors, steroid receptors, signal transducers and activators of transcription, and molecules involved in cell adhesion and migration. These interactions lead to a diverse array of biological functions including proliferation, cell growth, differentiation, cell shape, motility, migration, angiogenesis, and survival. Studies investigating mutational activation of Src in human cancers suggest that this may be a rare event and that wild-type Src is weakly oncogenic. Thus, the role of Src in the development and progression of human cancer remains unclear. Recently, it was suggested that increased SFK protein levels and, more importantly, SFK tyrosine kinase activity are linked to cancer progression and metastatic disease by facilitating the action of other signaling proteins. This accumulating body of evidence indicates that SFKs may represent a promising therapeutic target for the treatment of solid tumors. This review discusses the role of SFKs in solid tumors and the recent therapeutic advances aimed at targeting this family of tyrosine kinases in cancer.
Dispersal pathways, seed rains, and the dynamics of larval behavior
Authors: Zimmer Richard K. , Fingerut Jonathan T. , Zimmer Cheryl Ann 
Published: July 2009

Dispersing propagules (larvae, seeds, and spores) establish and maintain populations, which serve as templates for subsequent species interactions. Connectivity among demes derives, in large part, from connectivity between consecutive steps, release, transport, and settlement, in dispersal pathways. Concurrent measurements of individuals in each step are a necessary precursor to identifying governing mechanisms. Here we directly and definitively resolved the roles of physics and behavior in mediating dispersal pathways of an estuarine parasite between its intermediate hosts. Planktonic cercariae of Himasthla rhigedana, a parasitic flatworm, are functionally similar to lecithotrophic larvae of many free‐living marine invertebrates. The combination of parasite life cycle characteristics and the relatively simple tidal flows in their habitat renders this system an effective model for dispersal studies.Simultaneous field measurements of larval release, transport, settlement, and the flow regime, together with mechanistic experiments, led to empirical understanding of host colonization. All dispersal steps were highly and significantly correlated over time and in space. This tight coupling resulted, unequivocally, from a suite of larval behaviors. Cercariae emerged from first intermediate host snails only during daytime flood tides, enhancing larval retention in the marsh. Daylight triggered downward swimming, and within seconds, cercariae overpowered turbulent mixing, landing in benthic habitat of second intermediate host snails and crabs. Larvae settled (encysted) on external regions of snails/crabs that, presumably, were most vulnerable to ingestion by definitive host shorebirds. In total, cercarial behaviors greatly foreshortened dispersal distances, magnified local parasite prevalence, and increased the likelihood of large‐scale transmission by definitive hosts. Cracking open the black box of dispersal thus revealed mechanisms, connectivity, and ecological consequences of the larval stage.
Mitochondrial Networking Protects β-Cells From Nutrient-Induced Apoptosis
Authors: Molina Anthony J.A. , Wikstrom Jakob D. , Stiles Linsey , Las Guy , Mohamed Hibo , Elorza Alvaro , Walzer Gil , Twig Gilad , Katz Steve , Corkey Barbara E. , Shirihai Orian S. 
Published: July 2009

OBJECTIVE
Previous studies have reported that β-cell mitochondria exist as discrete organelles that exhibit heterogeneous bioenergetic capacity. To date, networking activity, and its role in mediating β-cell mitochondrial morphology and function, remains unclear. In this article, we investigate β-cell mitochondrial fusion and fission in detail and report alterations in response to various combinations of nutrients.

RESEARCH DESIGN AND METHODS
Using matrix-targeted photoactivatable green fluorescent protein, mitochondria were tagged and tracked in β-cells within intact islets, as isolated cells and as cell lines, revealing frequent fusion and fission events. Manipulations of key mitochondrial dynamics proteins OPA1, DRP1, and Fis1 were tested for their role in β-cell mitochondrial morphology. The combined effects of free fatty acid and glucose on β-cell survival, function, and mitochondrial morphology were explored with relation to alterations in fusion and fission capacity.

RESULTS
β-Cell mitochondria are constantly involved in fusion and fission activity that underlies the overall morphology of the organelle. We find that networking activity among mitochondria is capable of distributing a localized green fluorescent protein signal throughout an isolated β-cell, a β-cell within an islet, and an INS1 cell. Under noxious conditions, we find that β-cell mitochondria become fragmented and lose their ability to undergo fusion. Interestingly, manipulations that shift the dynamic balance to favor fusion are able to prevent mitochondrial fragmentation, maintain mitochondrial dynamics, and prevent apoptosis.

CONCLUSIONS
These data suggest that alterations in mitochondrial fusion and fission play a critical role in nutrient-induced β-cell apoptosis and may be involved in the pathophysiology of type 2 diabetes.
Increased MAPK Activation and Impaired Insulin Signaling in Subcutaneous Microvascular Endothelial Cells in Type 2 Diabetes: The Role of Endothelin-1
Authors: Gogg Silvia , Smith Ulf , Jansson Per-Anders 
Published: July 2009

OBJECTIVE
To establish a method for isolation and culture of subcutaneous microvascular endothelial cells (MVEC) from small human tissue biopsies to compare gene and protein expression of insulin signaling molecules in MVEC from insulin-resistant and healthy control subjects.

RESEARCH DESIGN AND METHODS
Stromavascular cells from subcutaneous needle biopsies of type 2 diabetic and control subjects were expanded in culture and the endothelial cells selected with magnetic immune separation. Western blots and RT-PCR were used for protein and gene expression assays.

RESULTS
At least 99% of the expanded primary MVEC could be characterized as endothelial cells. The expression of insulin receptors was low, but insulin increased tyrosine phosphorylation of both the insulin receptor and insulin receptor substrate (IRS)-1 and activated protein kinase B (PKB). The IRS-1 protein expression was reduced and the serine phosphorylation of PKB in response to insulin attenuated whereas basal and insulin-stimulated phosphorylation of extracellular signal–related kinase (ERK)1/2 was increased in type 2 diabetes MVEC. Endothelin (ET)-1 mRNA levels were significantly higher in type 2 diabetes cells. The addition of ET-1 increased the phosphorylation of mitogen-activated protein kinase (MAPK), an effect antagonized by the MEK-1 inhibitor PD98059. Furthermore, the endothelin ETA and ETB receptor antagonists BQ123 and BQ788 decreased basal MAPK activity in type 2 diabetes MVEC and prevented the ET-1–induced activation.

CONCLUSIONS
We developed a system for isolation and culture of human MVEC from small needle biopsies. Our observations support the concept of “selective” insulin resistance, involving IRS-1 and the PI3kinase pathway, as an underlying factor for a dysregulated microvascular endothelium in type 2 diabetes. Our data also support a role of ET-1 for the increased MAPK activity seen in nonstimulated type 2 diabetes MVEC.
Gene Profiling of Human Adipose Tissue During Evoked Inflammation In Vivo
Authors: Shah Rachana , Lu Yun , Hinkle Christine C. , McGillicuddy Fiona C. , Kim Roy , Hannenhalli Sridhar , Cappola Thomas P. , Heffron Sean , Wang XingMei , Mehta Nehal N. , Putt Mary , Reilly Muredach P. 
Published: July 2009

OBJECTIVE
Adipose inflammation plays a central role in obesity-related metabolic and cardiovascular complications. However, few human adipose-secreted proteins are known to mediate these processes. We hypothesized that microarray mRNA profiling of human adipose during evoked inflammation could identify novel adipocytokines.

RESEARCH DESIGN AND METHODS
Healthy human volunteers (n = 14) were treated with intravenous endotoxin (3 ng/kg lipopolysaccharide [LPS]) and underwent subcutaneous adipose biopsies before and after LPS. On Affymetrix U133Plus 2.0 arrays, adipose mRNAs modulated &gt;1.5-fold (with P &lt; 0.00001) were selected. SignalP 3.0 and SecretomeP 2.0 identified genes predicted to encode secreted proteins. Of these, 86 candidates were chosen for validation in adipose from an independent human endotoxemia protocol (N = 7, with 0.6 ng/kg LPS) and for exploration of cellular origin in primary human adipocytes and macrophages in vitro.

RESULTS
Microarray identified 776 adipose genes modulated by LPS; 298 were predicted to be secreted. Of detectable prioritized genes, 82 of 85 (96% [95% CI 90–99]) were upregulated (fold changes &gt;1.0) during the lower-dose (LPS 0.6 ng/kg) validation study and 51 of 85 (59% [49–70]) were induced greater than 1.5-fold. Treatment of primary adipocytes with LPS and macrophage polarization to M1 proinflammatory phenotype increased expression by 1.5-fold for 58 and 73% of detectable genes, respectively.

CONCLUSIONS
We demonstrate that evoked inflammation of human adipose in vivo modulated expression of multiple genes likely secreted by adipocytes and monocytes. These included established adipocytokines and chemokines implicated in recruitment and activation of lymphocytes, adhesion molecules, antioxidants, and several novel genes with unknown function. Such candidates may represent biomarkers and therapeutic targets for obesity-related complications.