Outcomes of three different ways to train medical students as ultrasound tutors.

Background: In order to provide faculty-wide undergraduate ultrasound training in times of scarce resources, many medical faculties employ trained peer-student tutors to oversee the hands-on training. However, data to guide the training of ultrasound peer-student tutors are scarce. We conducted a prospective quasi-randomized study to assess the gain in theoretical knowledge and practical scanning skills of peer-student tutors who were trained with a course only, an internship only, or the combination of a course and an internship.

Online EEG-Based Workload Adaptation of an Arithmetic Learning Environment.

In this paper, we demonstrate a closed-loop EEG-based learning environment, that adapts instructional learning material online, to improve learning success in students during arithmetic learning. The amount of cognitive workload during learning is crucial for successful learning and should be held in the optimal range for each learner. Based on EEG data from 10 subjects, we created a prediction model that estimates the learner's workload to obtain an unobtrusive workload measure.

Asynchronous P300 classification in a reactive brain-computer interface during an outlier detection task.

Objective: In this study, the feasibility of detecting a P300 via an asynchronous classification mode in a reactive EEG-based brain-computer interface (BCI) was evaluated. The P300 is one of the most popular BCI control signals and therefore used in many applications, mostly for active communication purposes (e.g.

Cognitive state monitoring and the design of adaptive instruction in digital environments: lessons learned from cognitive workload assessment using a passive brain-computer interface approach.

According to Cognitive Load Theory (CLT), one of the crucial factors for successful learning is the type and amount of working-memory load (WML) learners experience while studying instructional materials. Optimal learning conditions are characterized by providing challenges for learners without inducing cognitive over- or underload. Thus, presenting instruction in a way that WML is constantly held within an optimal range with regard to learners' working-memory capacity might be a good method to provide these optimal conditions.

TRAF5 deficiency accelerates atherogenesis in mice by increasing inflammatory cell recruitment and foam cell formation.

Rationale: Tumor necrosis factor receptor-associated factors (TRAFs) are cytoplasmic adaptor proteins for the TNF/interleukin-1/Toll-like receptor superfamily. Ligands of this family comprise multiple important cytokines such as TNFα, CD40L, and interleukin-1β that promote chronic inflammatory diseases such as atherosclerosis. We recently reported overexpression of TRAF5 in murine and human atheromata and that TRAF5 promotes inflammatory functions of cultured endothelial cells and macrophages.

Tumor necrosis factor receptor associated factor 6 is not required for atherogenesis in mice and does not associate with atherosclerosis in humans.

Background: Tumor necrosis factor receptor-associated factors (TRAFs) are important signaling molecules for a variety of pro-atherogenic cytokines including CD40L, TNF alpha, and IL1beta. Several lines of evidence identified TRAF6 as a pro-inflammatory signaling molecule in vitro and we previously demonstrated overexpression of TRAF6 in human and Murine atherosclerotic plaques. This study investigated the role of TRAF6-deficiency in mice developing atherosclerosis, a chronic inflammatory disease.

Tumor necrosis factor receptor-associated factor 1 (TRAF1) deficiency attenuates atherosclerosis in mice by impairing monocyte recruitment to the vessel wall.

Background: Members of the tumor necrosis factor superfamily, such as tumor necrosis factor-alpha, potently promote atherogenesis in mice and humans. Tumor necrosis factor receptor-associated factors (TRAFs) are cytoplasmic adaptor proteins for this group of cytokines.

Methods And Results: This study tested the hypothesis that TRAF1 modulates atherogenesis in vivo.

CD40L induces inflammation and adipogenesis in adipose cells--a potential link between metabolic and cardiovascular disease.

CD40L figures prominently in atherogenesis. Recent data demonstrate elevated levels of sCD40L in the serum of patients with the metabolic syndrome (MS). This study investigated the role of CD40L in pro-inflammatory gene expression and cellular differentiation in adipose tissue to obtain insight into mechanisms linking the MS with atherosclerosis.