The influence of lexical selection disruptions on articulation

Interactive models of language production predict that it should be possible to observe long-distance interactions; effects that arise at one level of processing influence multiple subsequent stages of representation and processing. We examine the hypothesis that disruptions arising in nonform-based levels of planning—specifically, lexical selection—should modulate articulatory processing. A novel automatic phonetic analysis method was used to examine productions in a paradigm yielding both general disruptions to formulation processes and, more specifically, overt errors during lexical selection. This analysis method allowed us to examine articulatory disruptions at multiple levels of analysis, from whole words to individual segments. Baseline performance by young adults was contrasted with young speakers’ performance under time pressure (which previous work has argued increases interaction between planning and articulation) and performance by older adults (who may have difficulties inhibiting nontarget representations, leading to heightened interactive effects). The results revealed the presence of interactive effects. Our new analysis techniques revealed these effects were strongest in initial portions of responses, suggesting that speech is initiated as soon as the first segment has been planned. Interactive effects did not increase under response pressure, suggesting interaction between planning and articulation is relatively fixed. Unexpectedly, lexical selection disruptions appeared to yield some degree of facilitation in articulatory processing (possibly reflecting semantic facilitation of target retrieval) and older adults showed weaker, not stronger interactive effects (possibly reflecting weakened connections between lexical and form-level representations)

Scanning spreading resistance microscopy of two-dimensional diffusion of boron implanted in free-standing silicon nanostructures

B implants of 1keV, 1×10¹⁵at.cm⁻² into 125-nm-wide, free-standing Si nanostructures have been characterized using scanning spreading resistancemicroscopy following a 0s, 1050°Canneal in N₂. A curved diffusion front has been observed. B in the center of the ridge diffuses further than at the sides. A similar effect has been observed in SUPREM-IV simulations. It is attributed to a reduction in transient enhanced diffusion close to the vertical surfaces due to recombination of ion-implantation-induced excess Si self-interstitials

Design and Evaluation of a Magnetic Rotablation Catheter for Arterial Stenosis

Arterial stenosis is a high-risk disease accompanied by large amounts of calcified deposits and plaques that develop inside the vasculature. These deposits should be reduced to improve blood flow. However, current methods used to reduce stenosis require externally-controlled actuation systems resulting in limited workspace or patient risks. This results in an unexplored preference regarding the revascularization strategy for symptomatic artery stenosis. In this paper, we propose a novel internally-actuated solution: a magnetic spring-loaded rotablation catheter. The catheter is developed to achieve stenosis-debulking capabilities by actuating drill bits using two internal electromagnetic coils and a magnetic reciprocating spring-loaded shaft. The state-space model of the catheter is validated by comparing the simulation results of the magnetic fields of the internal coils with the experimental results of a fabricated prototype. Contact forces of the catheter tip are measured experimentally, resulting in a maximum axial force of 2.63 N and a torque of 5.69 mN-m. Finally, we present interventions in which the catheter is inserted to a vascular target site and demonstrate plaque-specific treatment using different detachable actuator bits. Calcified deposits are debulked and visualized via ultrasound imaging. The catheter can reduce a stenosis cross-sectional area by up to 35%, indicating the potential for the treatment of calcified lesions, which could prevent restenosis

Requirement of JNK1 for endothelial cell injury in atherogenesis

AbstractObjectiveThe c-Jun N-terminal kinase (JNK) family regulates fundamental physiological processes including apoptosis and metabolism. Although JNK2 is known to promote foam cell formation during atherosclerosis, the potential role of JNK1 is uncertain. We examined the potential influence of JNK1 and its negative regulator, MAP kinase phosphatase-1 (MKP-1), on endothelial cell (EC) injury and early lesion formation using hypercholesterolemic LDLR−/− mice.Methods and resultsTo assess the function of JNK1 in early atherogenesis, we measured EC apoptosis and lesion formation in LDLR−/− or LDLR−/−/JNK1−/− mice exposed to a high fat diet for 6 weeks. En face staining using antibodies that recognise active, cleaved caspase-3 (apoptosis) or using Sudan IV (lipid deposition) revealed that genetic deletion of JNK1 reduced EC apoptosis and lesion formation in hypercholesterolemic mice. By contrast, although EC apoptosis was enhanced in LDLR−/−/MKP-1−/− mice compared to LDLR−/− mice, lesion formation was unaltered.ConclusionWe conclude that JNK1 is required for EC apoptosis and lipid deposition during early atherogenesis. Thus pharmacological inhibitors of JNK may reduce atherosclerosis by preventing EC injury as well as by influencing foam cell formation

Proarrhythmic proclivity of left-stellate ganglion stimulation in a canine model of drug-induced long-QT syndrome type 1

Background Left-stellate ganglion stimulation (LSGS) can modify regional dispersion of ventricular refractoriness, promote triggered activity, and reduce the threshold for ventricular fibrillation (VF). Sympathetic hyperactivity precipitates torsades de pointes (TdP) and VF in susceptible patients with long-QT syndrome type 1 (LQT1). We investigated the electromechanical effects of LSGS in a canine model of drug-induced LQT1, gaining novel arrhythmogenic insights. Methods In nine mongrel dogs, the left and right stellate ganglia were exposed for electrical stimulation. ECG, left- and right-ventricular endocardial monophasic action potentials (MAPs) and pressures (LVP, RVP) were recorded. The electromechanical window (EMW; Q to LVP at 90% relaxation minus QT interval) was calculated. LQT1 was mimicked by infusion of the KCNQ1/IKs blocker HMR1556. Results At baseline, LSGS and right-stellate ganglion stimulation (RSGS) caused similar heart-rate acceleration and QT shortening. Positive inotropic and lusitropic effects were more pronounced under LSGS than RSGS. IKs blockade prolonged QTc, triggered MAP-early afterdepolarizations (EADs) and rendered the EMW negative, but no ventricular tachyarrhythmias occurred. Superimposed LSGS exaggerated EMW negativity and evoked TdP in 5/9 dogs within 30 s. Preceding extrasystoles originated mostly from the outflow-tracts region. TdP deteriorated into therapy-refractory VF in 4/5 animals. RSGS did not provoke TdP/VF. Conclusions In this model of drug-induced LQT1, LSGS readily induced TdP and VF during repolarization prolongation and MAP-EAD generation, but only if EMW turned from positive to very negative. We postulate that altered mechano-electric coupling can exaggerate regional dispersion of refractoriness and facilitates ventricular ectopy

MEN-2 Syndrome: The Value of Screening and Central Registration; A Study of Six Kindreds in The Netherlands

Since 1975, six families with the MEN-2A syndrome including 66 patients have been identified in The Netherlands. All these patients underwent thyroidectomy for C-cell hyperplasia and/or medullary thyroid carcinoma (MTC); eight were symptomatic (Group A), 51 were relatives of patients found to be affected (Group B), and seven had had a negative screening test that became positive (Group C). To assess the effect of screening, we compared these groups with respect to the occurrence of metastatic MTC at thyroidectomy and the results of the postoperative calcitonin (CT) tests. We found that 87% of Group A, 37% of Group B; and none of Group C had metastatic disease at surgery. The cure rates in these three groups with MEN-2A, as determined by stimulated CT measurement, was 0%, 51%, and 100%, respectively. From these results it may be concluded that screening can lead to the detection of MTC at an earlier stage which in turn could permit curative treatment and improvement of both prognosis and life expectancy. The need for supervision of affected families by central registration to guarantee the continuity of screening is stressed