Traceability for Model Driven, Software Product Line Engineering

Traceability is an important challenge for software organizations. This is true for traditional software development and even more so in new approaches that introduce more variety of artefacts such as Model Driven development or Software Product Lines. In this paper we look at some aspect of the interaction of Traceability, Model Driven development and Software Product Line

A study on the protective effects of calcium channel blockers against anoxic brain damage

Introduction It is now widely accepted that a rapid neuronal influx of Ca2+ following cerebral ischaemia! hypoxia is intimately connected with the cascade of events- including activation of enzymes which give rise to the production of reactive oxygen species and nitric oxide, thereby leading to free-radical induced damage -which reseult in neuronal injury and death. It is also known that a burst of free radical generation I occurs during re-oxygenation of the tissues following a period,ofischaernialhypoxia as also a prolonged purturbation of the membrane functions continues after the perfusion/oxygenation has been restored, which leads to continued accumulnnon of calcium intracellularly ; resulting ultimately in delayed damage and death of the neurone. Estimation of lipid peroxidation products proviqes a reliable estimate of free radical induced damage to tissues, and has been widely used for this purpose

Cracking Behavior of Coating during Hot Tensile Tests of AlSi-Coated Press Hardening Steel

For industrial hot stamping applications, press hardening steel is usually coated with Al-10wt.%Si, in order to prevent substrate decarburization and oxidation at elevated temperatures. However, during hot stamping, the AlSi coating layer fractures, causing severe tool wear, substrate oxidation and increased friction coefficient between the tool and stamped part. The initiation of coating fracture can largely be attributed to the formation of several intermetallic compounds (i.e., FeAl & Fe2Al5) via Fe-diffusion, which also results in void formation throughout the coating layer. These intermetallics are formed mainly during the heating stage, with decreasing Fe-content from the coating-substrate interface. Due to distinctive thermo-mechanical properties of intermetallics compared to the steel substrate, the interaction between different intermetallics, including voids, causes high strain localization around the voids, leading to coating fracture. The goal of this study is to detect the initiation of cracks in a ~45 mu-m coating layer during uniaxial tensile deformation of a 1.5 mm AlSi-coated press hardening steel. For this purpose, isothermal tensile tests were performed at elevated temperatures. The coating cracks were detected by means of acoustic emission (AE) sensors during deformation. The distribution of coating cracks at hot stamping condition was examined via optical measurements. The tensile strain was measured from a strain grid on the sample gauge. The experiment involves heating the coated steel in a furnace to 920 ̊C for 6 minutes, followed by uniaxial tensile deformation (at 600 ̊C and 800 ̊C), and finally quenching at ambient air. The first AE signal from the sample was observed during the tensile deformation at 600 ̊C, indicating that tensile strain initiates fracture in the coating layer. At cooling stage, the temperature change with time triggered more AE signals, which may correspond to substrate phase transformation and additional fractures in the coated steel; the latter is owing to thermal expansion mismatch between the intermetallics in the coating layer, and steel substrate. Interestingly, no AE signals were observed during the heating stage; i.e., no coating cracks occur prior to deformation and quenching

Uterine arteriovenous malformation: a rare cause of abnormal uterine bleeding

Uterine arteriovenous malformation (AVM) is a rare gynecological entity that usually presents with vaginal bleeding of variable spectrum. High level of suspicion aided by color Doppler ultrasound is needed to confirm the diagnosis. This case report describes a 52-year-old woman G7P6A1 who presented with irregular pervaginal bleeding for 5 years. Her symptom was recurrent, on and off and refractory to hormone therapy. She was diagnosed with uterine AVM on pelvic color Doppler ultrasound that revealed a dilated and hypervascular cystic mass of 6.2×4.1 cm located at right uterine wall where blood flow was bidirectional. As a definitive treatment, open abdominal hysterectomy was performed successfully. This report reminds gynecologists to consider uterine AVM as a rare differential diagnosis of abnormal uterine bleeding (AUB)

Clinical outcome and virological characteristics of hepatitis B-related acute liver failure in the United States

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72563/1/j.1365-2893.2005.00581.x.pd

IQGAP1 promotes chronic pain by regulating the trafficking and sensitization of TRPA1 channels

TRPA1 channels have been implicated in mechanical and cold hypersensitivity in chronic pain. But how TRPA1 mediates this process is unclear. Here we show that IQ-motif containing GTPase activating protein 1 (IQGAP1) is responsible using a combination of biochemical, molecular, Ca2+ imaging and behavioural approaches. TRPA1 and IQGAP1 bind to each other and are highly colocalised in sensory DRG neurons in mice. The expression of IQGAP1 but not TRPA1 is increased in chronic inflammatory and neuropathic pain. However, TRPA1 undergoes increased trafficking to the membrane of DRG neurons catalysed by the small GTPase Cdc42 associated with IQGAP1, leading to functional sensitization of the channel. Activation of PKA is also sufficient to evoke TRPA1 trafficking and sensitization. All these responses are, however, completely prevented in the absence of IQGAP1. Concordantly, deletion of IQGAP1 markedly reduces mechanical and cold hypersensitivity in chronic inflammatory and neuropathic pain in mice. IQGAP1 thus promotes chronic pain by coupling the trafficking and signalling machineries to TRPA1 channels

IQGAP1 promotes chronic pain by regulating the trafficking and sensitization of TRPA1 channels

TRPA1 channels have been implicated in mechanical and cold hypersensitivity in chronic pain. But how TRPA1 mediates this process is unclear. Here we show that IQ-motif containing GTPase activating protein 1 (IQGAP1) is responsible using a combination of biochemical, molecular, Ca2+ imaging and behavioural approaches. TRPA1 and IQGAP1 bind to each other and are highly colocalised in sensory DRG neurons in mice. The expression of IQGAP1 but not TRPA1 is increased in chronic inflammatory and neuropathic pain. However, TRPA1 undergoes increased trafficking to the membrane of DRG neurons catalysed by the small GTPase Cdc42 associated with IQGAP1, leading to functional sensitization of the channel. Activation of PKA is also sufficient to evoke TRPA1 trafficking and sensitization. All these responses are, however, completely prevented in the absence of IQGAP1. Concordantly, deletion of IQGAP1 markedly reduces mechanical and cold hypersensitivity in chronic inflammatory and neuropathic pain in mice. IQGAP1 thus promotes chronic pain by coupling the trafficking and signalling machineries to TRPA1 channels

Hypoxia induces dilated cardiomyopathy in the chick embryo: mechanism, intervention, and long-term consequences

Background: Intrauterine growth restriction is associated with an increased future risk for developing cardiovascular diseases. Hypoxia in utero is a common clinical cause of fetal growth restriction. We have previously shown that chronic hypoxia alters cardiovascular development in chick embryos. The aim of this study was to further characterize cardiac disease in hypoxic chick embryos. Methods: Chick embryos were exposed to hypoxia and cardiac structure was examined by histological methods one day prior to hatching (E20) and at adulthood. Cardiac function was assessed in vivo by echocardiography and ex vivo by contractility measurements in isolated heart muscle bundles and isolated cardiomyocytes. Chick embryos were exposed to vascular endothelial growth factor (VEGF) and its scavenger soluble VEGF receptor-1 (sFlt-1) to investigate the potential role of this hypoxia-regulated cytokine. Principal Findings: Growth restricted hypoxic chick embryos showed cardiomyopathy as evidenced by left ventricular (LV) dilatation, reduced ventricular wall mass and increased apoptosis. Hypoxic hearts displayed pump dysfunction with decreased LV ejection fractions, accompanied by signs of diastolic dysfunction. Cardiomyopathy caused by hypoxia persisted into adulthood. Hypoxic embryonic hearts showed increases in VEGF expression. Systemic administration of rhVEGF165 to normoxic chick embryos resulted in LV dilatation and a dose-dependent loss of LV wall mass. Lowering VEGF levels in hypoxic embryonic chick hearts by systemic administration of sFlt-1 yielded an almost complete normalization of the phenotype. Conclusions/Significance: Our data show that hypoxia causes a decreased cardiac performance and cardiomyopathy in chick embryos, involving a significant VEGF-mediated component. This cardiomyopathy persists into adulthood

Five decades of the International Endodontic Journal: bibliometric overview 1967–2020

Aim The International Endodontic Journal (IEJ) has served as a platform for research and clinical practice in Endodontics since 1967. This study provides a bibliographic analysis and overview of the publications that have appeared in the IEJ from 1967 to 2020. Methodology A literature search was performed in Elsevier's Scopus database to locate all the publications of the International Endodontic Journal. Various bibliometric software packages including the open-source visualization software Gephi and Biblioshiny (version 2.0) were employed for data visualization and analysis. Results A total of 3739 records with citation and bibliographic details were selected and retrieved to allow a bibliometric analysis to be performed. The bibliometric analysis indicates that the IEJ has grown both in terms of productivity and influence. Over time, the journal has been associated with an increase in the number of manuscripts published and the citations they have attracted, but with minor downward fluctuations in citations in the last few years. Bibliographic coupling of the IEJ articles revealed that the major research themes published in the journal include ‘endodontics’, ‘root canal treatment’, ‘calcium hydroxide’, ‘apical periodontitis’, ‘mineral trioxide aggregate’, ‘microbiology’, ‘cyclic fatigue’, ‘cone-beam computed tomography’ and ‘micro-computed tomography’. Authors affiliated to institutions in the UK were the major contributors to the journal and were linked with other countries such as Brazil, USA and Malaysia. The largest number of publications were from the University of São Paulo, Brazil. Conclusion The IEJ is one of the leading journals in Endodontology and has been providing a platform for innovative research and clinical reports for more than 50 years. Publications have been associated with a wide range of authors, institutions and countries around the world

Hypoxia induces dilated cardiomyopathy in the chick embryo: mechanism; intervention; and long-term consequences.

Background Intrauterine growth restriction is associated with an increased future risk for developing cardiovascular diseases. Hypoxia in utero is a common clinical cause of fetal growth restriction. We have previously shown that chronic hypoxia alters cardiovascular development in chick embryos. The aim of this study was to further characterize cardiac disease in hypoxic chick embryos. Methods Chick embryos were exposed to hypoxia and cardiac structure was examined by histological methods one day prior to hatching (E20) and at adulthood. Cardiac function was assessed in vivo by echocardiography and ex vivo by contractility measurements in isolated heart muscle bundles and isolated cardiomyocytes. Chick embryos were exposed to vascular endothelial growth factor (VEGF) and its scavenger soluble VEGF receptor-1 (sFlt-1) to investigate the potential role of this hypoxia-regulated cytokine. Principal Findings Growth restricted hypoxic chick embryos showed cardiomyopathy as evidenced by left ventricular (LV) dilatation, reduced ventricular wall mass and increased apoptosis. Hypoxic hearts displayed pump dysfunction with decreased LV ejection fractions, accompanied by signs of diastolic dysfunction. Cardiomyopathy caused by hypoxia persisted into adulthood. Hypoxic embryonic hearts showed increases in VEGF expression. Systemic administration of rhVEGF165 to normoxic chick embryos resulted in LV dilatation and a dose-dependent loss of LV wall mass. Lowering VEGF levels in hypoxic embryonic chick hearts by systemic administration of sFlt-1 yielded an almost complete normalization of the phenotype. Conclusions/Significance Our data show that hypoxia causes a decreased cardiac performance and cardiomyopathy in chick embryos, involving a significant VEGF-mediated component. This cardiomyopathy persists into adulthood