Aroused and Impulsive Effects of Colour Stimuli on Lateral and Logical Abilities.

The purpose of this study was to explore the influence of environmental colour on people's lateral and logical abilities. This was done by evaluating study participants' response time and error rate when completing six types of psychometric tests that were performed in various hue backgrounds on a computer. To maximise the colour stimulation provided by the monitor, the experiment was carried out in a dark laboratory. Analysis of participants' response time and error rate showed that different colours could significantly influence arousal and impulsiveness, which suggests that colour has indirect impacts on cognitive abilities. Further analysis revealed that different colours had various effects depending on the type of psychometric test given. These findings suggest that future research on environmental design should consider how to effectively use colour to impact people's performance and behaviour.

A Comparative Study of Colour Effects on Cognitive Performance in Real-World and VR Environments.

This research explores the influence of colour on cognitive performance and intellectual abilities (i.e., logical and lateral thinking abilities and people's attention to detail) in a conventional laboratory setting and an approximately identical virtual reality (VR) environment. Comparative experiments using psychological methods were carried out in both settings to explore the impact of immersive colour experience. This work builds on earlier studies that suggest that the VR environment enhances user experiences, with results evidencing that a considered approach to colour design can trigger a positive impact on user engagement. The experiments further evaluated the positive effects of immersive colour stimuli in VR by evaluating participants' logical and lateral thinking abilities, as well as their attention to detail. Their response time and error rate when completing each psychometric test were recorded with different hue backgrounds in both environments. The data collected from participants reveal the differential impacts of colour between the reality setting using standard colour imaging displays and in an approximately identical VR environment. Analysis of the psychometric tests shows the differential influence of colours on logical and lateral thinking abilities and people's attention to detail between the physical environment and the VR environment. Our findings add to the data demonstrating that a well-designed immersive colour experience in VR can trigger positive user engagement and, as explored in this study, improve cognitive performance. This again positions immersive colour experience as an important design tool to be fully considered in the creation of effective VR research and applications.

In vivo tissue response to ultrasound assisted application of biodegradable pins into cortical and cancellous bone structures: a histological and densitometric analysis in rabbits.

In orthopaedic traumatology biodegradable pins are increasingly used for fixation of small bone fragments. In the present study, the ultrasound-assisted anchoring technique (SonicFusion technique), a osteosynthesis method being recently introduced in cranial applications, in which ultrasonic energy is used to insert and anchor polymer pins in bone, was compared with the conventional pin application procedure. The aim of the present study was to assess the short and long term thermal impact of two different ultrasonic energy levels on different bone structures in the distal medial femur of rabbits. The treatment groups consisted of customized polylactide pins applied at a low and a high energy level, the Reference Control and a Negative Control. The thermal effect on bone tissues was evaluated by means of qualitative and semi-quantitative histology and micro-computerized tomography. Five days following surgery, all implant sites showed no tissue damage but normal signs of early ongoing tissue repair. Enhancing the energy level by about 30% had no significant impact on the tissue response. At 4 weeks after surgery test sites covered by ultrasound-aided implantation showed a significantly enhanced bone/implant contact as compared to pins applied by conventional application. In conclusion, the ultrasound assisted anchoring technique not only did not impair bone regeneration, but even improved implant integration.

Candida endocarditis associated with cardiac rhythm management devices: review with current treatment guidelines.

Coincident with an increased use of cardiac rhythm management devices (CRMD) has been an increase in the number of pacemaker and cardioverter-defibrillator infections. CRMD endocarditis accounts for about 10% of all device-related infections, and cardiac infection caused by Candida sp. is a rare event. To date, only sporadic reports of this unusual and life-threatening event have been reported. By describing a case of CRMD-related Candida endocarditis and conducting a literature review, we provide a detailed characterisation of this unusual clinical entity with an emphasis on diagnosis, management and treatment. A case of CRMD-related Candida endocarditis is presented and a computer search for confirmed cases of CRMD-Candida endocarditis was conducted. Current recommendations for management and treatment were documented. From 1969 to 2009, 15 patients with CRMD-Candida endocarditis (12 pacemaker and three implanted cardioverter-defibrillator) were documented. All were males, non-albicans Candida sp. were frequently recovered, a major fungal embolus occurred in 27% of patients and two of 10 patients who received defined antifungal therapy and device explantation expired. CRMD Candida endocarditis is a rare and serious clinical event; isolates can include Candida albicans and other Candida sp., and treatment involves both targeted antifungal therapy and device removal.

Spontaneous coronary artery dissection in a woman on fenfluramine.

Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome, cardiogenic shock, and sudden cardiac death in women of reproductive age who have no traditional risk factors for coronary artery disease. The etiology, prognosis, and treatment of SCAD remain poorly defined. Coronary angiography is the gold standard for diagnosis. Management includes medical therapy and revascularization procedures using percutaneous intervention and coronary artery bypass grafting. Possible mechanisms of SCAD include rupture of atherosclerotic plaque or vasa vasorum, hemorrhage between the outer media and external lamina with intramedial hematoma expansion, and compression of the vessel lumen. We report a case of SCAD in a 39-year-old woman presenting with ST-elevation myocardial infarction midway through her menstrual cycle. Her medications included fenfluramine for obesity and hydrochlorothiazide, amlodipine, and atenolol for hypertension.

Fibroblast growth factor 2: from laboratory evidence to clinical application.

Fibroblast growth factor 2 (FGF2) is expressed ubiquitously in mesodermal and neuroectodermal cells. Human FGF2 occurs in isoforms translated from a common mRNA by alternative use of AUG (low-molecular weight isoforms) and CUG (high-molecular weight isoforms) start codons. Whereas the high-molecular weight isoforms function in an intracrine manner, the low-molecular weight isoform functions as autocrine, paracrine, and intracrine ligands. FGF2's signals are mediated by a family of high- and low-affinity receptors. The nuclear localization of FGF2 appears to be essential for its mitogenic effects with different isoforms localizing in different nuclear substructures. By regulating the transcription or activity of multiple other genes, FGF2 plays an important role in proliferation, differentiation, and survival of cells of almost all organ systems. Its potent angiogenic effects observed in tissue culture models and healthy animals have prompted clinical trials testing effects of FGF2 protein or genetic material on ischemic tissues. Unfortunately, FGF2-mediated therapeutic angiogenesis has yielded inconclusive results. One possible reason is that single-gene therapy is not sufficient to support the numerous effectors required to generate mature vessels assembled by multiple cells, including pericytes, smooth muscle cells, and endothelial cell subtypes. Another possible reason is that potentially negative effects of dyslipidemia, a common finding in patients with macro- and microvascular disease, on gene therapy have not been taken into account. We have demonstrated that electronegative low-density lipoprotein (LDL) from hypercholesterolemic human plasma downregulates FGF2 by both transcriptional and posttranscriptional mechanisms. In our models, FGF2 downregulation results in angiostasis and endothelial cell apoptosis. Deprivation of endogenous FGF2 may lead to dysregulation of the activities of other survival and angiogenesis-related genes. Delineation of the molecular mechanisms modulating the expression and actions of FGF2 may provide the basis for novel therapeutic interventions.

Ablation for atrial fibrillation: are cures really achieved?

During the past 10 years numerous studies on the treatment of paroxysmal atrial fibrillation (AF) by right and left atrial ablation procedures have been published. The results of studies based on follow-up periods of a few months have been repeatedly interpreted as providing evidence for curative therapy. However, insufficient focus on the variability of the natural history of paroxysmal AF, the inadequate detection of silent arrhythmic events, the eclectic post-interventional use of antiarrhythmic drugs, and the lack of appropriate control groups make the reports unconvincing. Randomized controlled trials are needed to confirm postulated long-term cure rates for AF.

Class I or class III agents for atrial fibrillation: are asking the right question?

Atrial fibrilliation (AF) is often combined with advanced age and structural heart disease, conditions known to invite serious proarrhythmic complications of antiarrhythmic drug therapy. Recent controlled trials comparing two AF treatment strategies-rhythm control requiring atrial defibrilliation and antiarrhythmic drugs to prevent AF and ventiricular rate control obviating sinus rhythm maintenance with such drugs-showed equal or superior results with rate control. AF is associated with derepressions of "fetospecific" expression patterns that may profoundly alter the responsiveness of atrial muscle to antiarrhythmic drugs. Therefore, effects of drugs predicted according to pharmacological classifications evaluating drug actions in intact myocardium only should be interpreted cautiously. The classification proposed by Vaughan Williams fails to distinguish between acute and chronic drug efficacy and toxicity as recommended in classical pharmacology. There is, however, overwhelming evidence that acute and chronic drug effects often differ fundamentally. For instance, amiodarone acts acutely as a sodium channel blocker, whereas chronic effects may be mediated by a downregulation of thyroid hormone receptors. Meaningful direct effects of amiodarone on atrial potassium channels is questionable, since the main candidate target-current (IKr) may not be expressed in human atrial muscle. Multiple biophysical factors contribute to the lack of ion channel-selective actions of antiarrhythmic agents. Nonselectivity becomes particularly important in the context of mechanisms of action of Vaughan Williams Class I and III agents on human atrial muscle. Preclinical studies indicate that Class I agents such as flecainide and propafenone may act in AF predominantly as Class III agents. Meta-analyses of antiarrhythmic agents for the prevention of AF have failed to reveal superior drugs or drug classes. Superiority of amiodarone over other agents may depend on arbitrary amiodarone-favoring loading protocols producing significant differential effects exclusively during the acute phase of treatment. In conclusion, the classification of current antiarrhythmic agents into Class I and III may not be a useful simplification when applied to the pharmacotherapy of AF.

Structural pathways and prevention of heart failure and sudden death.

We review the macroscopic and microscopic anatomy of myocardial disease associated with heart failure (HF) and sudden cardiac death (SCD) and focus on the prevention of SCD in light of its structural pathways. Compared to patients without SCD, patients with SCD exhibit 5- to 6-fold increases in the risks of ventricular arrhythmias and SCD. Epidemiologically, left ventricular hypertrophy by ECG or echocardiography acts as a potent dose-dependent SCD predictor. Dyslipidemia, a coronary disease risk factor, independently predicts echocardiographic hypertrophy. In adult SCD autopsy studies, increases in heart weight and severe coronary disease are constant findings, whereas rates of acute coronary thrombi vary remarkably. The microscopic myocardial anatomy of SCD is incompletely defined but may include prevalent changes of advanced myocardial disease, including cardiomyocyte hypertrophy, cardiomyocyte apoptosis, fibroblast hyperplasia, diffuse and focal matrix protein accumulation, and recruitment of inflammatory cells. Hypertrophied cardiomyocytes express "fetospecific" genetic programs that can account for acquired long QT physiology with risk for polymorphic ventricular arrhythmias. Structural heart disease associated with HF and high SCD risk is causally related to an up-regulation of the adrenergic renin-angiotensin-aldosterone pathway. In outcome trials, suppression of this pathway with combinations of beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin-II receptor blockers, and mineralocorticoid receptor blockers have achieved substantial total mortality and SCD reductions. Contrarily, trials with ion channel-active agents that are not known to reduce structural heart disease have failed to reduce these risks. Device therapy effectively prevents SCD, but whether biventricular pacing-induced remodeling decreases left ventricular mass remains uncertain.

Low-density lipoprotein in hypercholesterolemic human plasma induces vascular endothelial cell apoptosis by inhibiting fibroblast growth factor 2 transcription.

BACKGROUND: Apoptosis of vascular endothelial cells (ECs) can be induced in vitro by experimentally modified LDL. Description of proapoptotic circulating lipoproteins may significantly enhance understanding of atherothrombosis pathophysiology. METHODS AND RESULTS: Fast protein liquid chromatography of LDL samples from 7 asymptomatic, hypercholesterolemic patients yielded subfractions L1-L5 in increasing electronegativity. L4 and L5 were not detectable or collectible in normolipidemic samples. In bovine aortic EC cultures, L5 induced marked apoptosis and L4 had a mild effect, whereas hypercholesterolemic or normolipidemic L1-L3 had negligible effects. Compared with copper-oxidized LDL, L5 was only mildly oxidized, although its propensity to form conjugated dienes in response to copper exceeded that of other subfractions. L5-induced apoptosis was associated with suppressed fibroblast growth factor 2 (FGF-2) transcription, as assessed by nuclear run-on analysis. Degrading platelet-activating factor (PAF)-like lipids in L5 by a recombinant PAF acetylhydrolase prevented both FGF-2 downregulation and apoptosis. Furthermore, the ability of L5 lipid extract to induce calcium influx into neutrophils was lost after pretreatment of the extract with PAF acetylhydrolase. FGF-2 supplementation, PAF receptor (PAFR) blockade with WEB-2086, and inactivation of PAFR-coupled Gi protein with pertussis toxin all effectively attenuated L5-induced apoptosis. CONCLUSIONS: Our findings indicate that a highly electronegative, mildly oxidized LDL subfraction present in human hypercholesterolemic but not normolipidemic plasma can induce apoptosis in cultured ECs. The evidence that a freshly isolated LDL species modulates transcription of FGF-2 may provide a physiological insight into the mechanism of vascular EC apoptosis in hypercholesterolemia.