Wearable Real-Time Skateboard Trick Visualization and Its Community Perception.

Motion visualization is an attractive way to provide support for a range of recreational and competitive sports. In skateboarding, sensor technology in particular can help visualization systems capture the motion of athletes to provide relevant information to athletes, judges, and spectators. This article describes the authors' proposed application of a 9D inertial-magnetic measurement unit (IMMU) based real-time trick classification and visualization system. It also reports on a survey they conducted with skateboarders that asked about the usefulness, acceptance, and future ideas of such a system.

Incidence and relevance of nonreentrant monomorphic ventricular tachycardia in patients with frequent implantable cardioverter defibrillator interventions.

BACKGROUND: Nonreentrant ventricular tachycardia (VT) originates in hearts without structural disease but occasionally can occur in patients with different cardiomyopathies equipped with an implantable cardioverter defibrillator (ICD). METHODS: In a series of 142 ICD recipients with structural heart disease undergoing ablation for recurrent or incessant monomorphic VT, nonreentrant VTs were identified. RESULTS: Nonreentrant VTs were the cause of appropriate ICD interventions in 12 patients (8.4%). The underlying heart disease was nonischemic cardiomyopathy in eight patients, prior myocardial infarction in two patients, and valvular cardiomyopathy in two patients with a mean left ventricular ejection fraction of 42 ± 7%. Unresponsiveness to antitachycardia pacing and repetitive spontaneous re-initiation of the VT after defibrillation was the cause of frequent ineffective ICD interventions including repetitive ICD shocks in these patients. Using ICD interrogation, one or more episodes of a severe electrical storm (≥3 serial efficacious ICD shocks within 15 min) were more frequently documented in patients with nonreentrant VTs (10/12) than in patients with scar-related reentrant VTs (36/115). The origin of the nonreentrant VT was the left ventricular outflow tract in seven patients, the right ventricular outflow tract in three patients, and the tricuspid and mitral annulus in each one patient. Catheter ablation including epicardial mapping in 2 patients eliminated the nonreentrant VT in 11 of 12 patients and prevented recurrent VT storm. CONCLUSIONS: Repetitive nonreentrant VTs may be ineffectively treated by ICD interventions and can be the cause of an electrical storm in different cardiomyopathies.

A Toxoplasma gondii pseudokinase inhibits host IRG resistance proteins.

The ability of mice to resist infection with the protozoan parasite, Toxoplasma gondii, depends in large part on the function of members of a complex family of atypical large GTPases, the interferon-gamma-inducible immunity-related GTPases (IRG proteins). Nevertheless, some strains of T. gondii are highly virulent for mice because, as recently shown, they secrete a polymorphic protein kinase, ROP18, from the rhoptries into the host cell cytosol at the moment of cell invasion. Depending on the allele, ROP18 can act as a virulence factor for T. gondii by phosphorylating and thereby inactivating mouse IRG proteins. In this article we show that IRG proteins interact not only with ROP18, but also strongly with the products of another polymorphic locus, ROP5, already implicated as a major virulence factor from genetic crosses, but whose function has previously been a complete mystery. ROP5 proteins are members of the same protein family as ROP18 kinases but are pseudokinases by sequence, structure, and function. We show by a combination of genetic and biochemical approaches that ROP5 proteins act as essential co-factors for ROP18 and present evidence that they work by enforcing an inactive GDP-dependent conformation on the IRG target protein. By doing so they prevent GTP-dependent activation and simultaneously expose the target threonines on the switch I loop for phosphorylation by ROP18, resulting in permanent inactivation of the protein. This represents a novel mechanism in which a pseudokinase facilitates the phosphorylation of a target by a partner kinase by preparing the substrate for phosphorylation, rather than by upregulation of the activity of the kinase itself.

[Intracoronary Stenting and Angiographic Results Strut Thickness Effect on Restenosis Outcome (ISAR-STEREO) Trial].

BACKGROUND: Increased thrombogenicity and smooth muscle cell proliferative response induced by the metal struts compromise the advantages of coronary stenting. The objective of this randomized, multicenter study was to ascertain whether a reduced strut thickness of a stent is associated with improved follow-up angiographic and clinical results. METHODS AND RESULTS: The study covered 651 patients with stenosis in the native coronary arteries > 2.8 mm in diameter. They were randomly assigned to receive 1 of 2 commercially available stents of comparable design but different thickness: 326 patients to the thin-strut stent (strut thickness of 50 microm) and 325 patients to the thicker-strut stent (strut thickness of 140 microm). The primary end point was the angiographic restenosis (> or = 50% diameter luminal stenosis at follow-up angiography). The secondary end points were the incidence of reinterventions due to restenosis-induced ischemia and the total rate of death and myocardial infarctions at 1 year (a combined end point). The incidence of angiographic restenosis was 15.0% in the thin-strut group and 25.8% in the thick-strut group (relative risk, 0.58; 95% CI, 0.39 to 0.87; p = 0.003). Clinical restenosis was also significantly reduced. Reinterventions were made in 8.6% of the thin-strut patients and in 13.8% of the thick-strut patients (relative risk, 0.62; 95% CI, 0.39 to 0.99; p = 0.03). No difference was observed in the combined 1-year rate of death and myocardial infarction. CONCLUSIONS: The use of a thin-strut device is associated with a significant reduction of angiographic and clinical restenosis after coronary artery stenting. These findings may have relevant implications for the currently most widely used percutaneous coronary intervention.

Two linked genes encoding a secreted effector and a membrane protein are essential for Ustilago maydis-induced tumour formation.

Ustilago maydis is a biotrophic fungal pathogen that colonizes living tissue of its host plant maize. Based on transcriptional upregulation during biotrophic development we identified the pit (proteins important for tumours) cluster, a novel gene cluster comprising four genes of which two are predicted to encode secreted effectors. Disruption of the gene cluster abolishes U. maydis-induced tumour formation and this phenotype can be caused by deleting either pit1 encoding a transmembrane protein or pit2 encoding a secreted protein. Pit1 localizes to the fungal plasma membrane at hyphal tips, endosomes and vacuoles while Pit2 is secreted to the biotrophic interface. Both Δpit1 and Δpit2 mutants are able to penetrate maize epidermis and grow intracellularly at sites of infection but fail to spread in the infected leaf. Microarray analysis shows an indistinguishable response of the plant to infection by Δpit1 and Δpit2 mutant strains. Transcriptional activation of maize defence genes in infections with Δpit1/2 mutant strains indicates that the mutants have a defect in suppressing plant immune responses. Our results suggest that the activity of Pit1 and Pit2 during tumour formation might be functionally linked and we discuss possibilities for a putative functional connection of the two proteins.

Reduction of right ventricular pacing with advanced atrioventricular search hysteresis: results of the PREVENT study.

BACKGROUND: Right ventricular pacing predisposes to the development of heart failure and atrial fibrillation. Automatic atrioventricular search hysteresis (AVSH) is a commonly used strategy to decrease the percentage of right ventricular pacing (%VP) in patients without permanent AV block, but the results have not been optimal. METHODS: The randomized, crossover PREVENT study evaluated whether an enhanced AVSH with two new features can reduce %VP compared with standard AVSH. The new features are the repetitive hysteresis [switch from extended to basic AV delay after a consistent loss of intrinsic AV conduction (IAVC) lasting for six consecutive atrial cycles] and the scan hysteresis (periodic IAVC search extension over six consecutive atrial cycles). Both standard AVSH and enhanced AVSH performed a periodic IAVC search every 180 cardiac cycles and operated with a basic AV-delay of 225 ms and a rate-independent maximum AV-delay of 300 ms for paced and sensed atrial events. RESULTS: Among 178 patients, 53.4% had no evidence of AV block at enrollment and 46.6% had history of intermittent AV block. The median %VP was decreased by enhanced AVSH compared to standard AVSH (4.0% vs 5.5%, P < 0.001), particularly in patients with a history of AV block (21.4% vs 25.5%, P < 0.001). The primary study hypothesis that 25% of all patients would experience > 20% relative %VP reduction was not met as 46 (25.8%) patients (95% confidence interval, 20.5-31.8%) presented such relative reduction. CONCLUSION: The enhanced AVSH algorithm reduces %VP compared with standard AVSH in patients with intermittent AV block.

Intracoronary stenting and angiographic results: strut thickness effect on restenosis outcome (ISAR-STEREO-2) trial.

OBJECTIVES: We tested the hypothesis that thinner-strut stents are associated with a reduced rate of restenosis when comparing two stents with different design. BACKGROUND: We have previously shown that, for two stents with similar design, the risk for restenosis is dependent on the strut thickness. It is unknown whether strut thickness preserves its relevance as a determinant of restenosis even in the presence of different stent designs. METHODS: A total of 611 patients with symptomatic coronary artery disease were randomly assigned to receive either the thin-strut ACS RX Multilink stent (Guidant, Advanced Cardiovascular Systems, Santa Clara, California) (strut thickness 50 microm, interconnected ring design; n = 309) or the thick-strut BX Velocity stent (Cordis Corp., Miami, Florida) (strut thickness 140 microm, closed cell design; n = 302). The primary end point was angiographic restenosis (> or =50% diameter stenosis at follow-up angiography). Secondary end points were the incidence of target-vessel revascularization (TVR) and the combined rate of death and myocardial infarction (MI) at one year. RESULTS: The incidence of angiographic restenosis was 17.9% in the thin-strut group and 31.4% in the thick-strut group, relative risk, 0.57 (95% confidence interval, 0.39 to 0.84), p < 0.001. A TVR due to restenosis was required in 12.3% of the thin-strut group and 21.9% of the thick-strut group, relative risk, 0.56 (95% confidence interval, 0.38 to 0.84), p = 0.002. No significant difference was observed in the combined incidence of death and MI at one year. CONCLUSIONS: When two stents with different design are compared, the stent with thinner struts elicits less angiographic and clinical restenosis than the thicker-strut stent.