A "virtually minimal" visuo-haptic training of attention in severe traumatic brain injury.

Background: Although common during the early stages of recovery from severe traumatic brain injury (TBI), attention deficits have been scarcely investigated. Encouraging evidence suggests beneficial effects of attention training in more chronic and higher functioning patients. Interactive technology may provide new opportunities for rehabilitation in inpatients who are earlier in their recovery.

Treatment challenges with profound behaviour disturbance after traumatic brain injury: a case report.

Background: Severe behavioural disturbances exhibited during the earliest stages of recovery from severe traumatic brain injury often limit the ability to provide standard care. Studies that focus on treatment options for inpatients with such behaviours are scarce. There is limited guidance on how to approach therapy that will maximize the patient's tolerance and participation and how to measure meaningful progress.

Tolerance of a virtual reality intervention for attention remediation in persons with severe TBI.

Objective: To evaluate the feasibility of applying virtual reality and robotics technology to improve attention in patients with severe traumatic brain injury (TBI) in the early stages of recovery.

Methods: A sample of TBI patients (n=18, aged 19-73) who were receiving acute inpatient rehabilitation completed three-dimensional cancellation exercises over two consecutive days in an interactive virtual environment that minimized distractions and that integrated both visual and haptic (tactile) stimuli. Observations of behaviour during the intervention and of the instructions needed to encourage compliance were recorded.

p66SHC promotes apoptosis and antagonizes mitogenic signaling in T cells.

Of the three Shc isoforms, p66Shc is responsible for fine-tuning p52/p46Shc signaling to Ras and has been implicated in apoptotic responses to oxidative stress. Here we show that human peripheral blood lymphocytes and mouse thymocytes and splenic T cells acquire the capacity to express p66Shc in response to apoptogenic stimulation. Using a panel of T-cell transfectants and p66Shc(-/-) T cells, we show that p66Shc expression results in increased susceptibility to apoptogenic stimuli, which depends on Ser36 phosphorylation and correlates with an altered balance in apoptosis-regulating gene expression.

Extensive temporally regulated reorganization of the lipid raft proteome following T-cell antigen receptor triggering.

Signalling by immunoreceptors is orchestrated at specific plasma membrane microdomains, referred to as lipid rafts. Here we present a proteomics approach to the temporal analysis of protein association with lipid rafts following T-cell antigen receptor (TCR) triggering. We show that TCR engagement promotes the temporally regulated recruitment of proteins participating in the TCR signalling cascade to lipid rafts.

The p66Shc longevity gene is silenced through epigenetic modifications of an alternative promoter.

The mammal Shc locus encodes three overlapping isoforms (46, 52, and 66 kDa) that differ in the length of their N-terminal regions. p46/p52Shc and p66Shc have been implicated, respectively, in the cytoplasmic propagation of growth and apoptogenic signals. Levels of p66Shc expression correlate with life span duration in mice.

F-actin dynamics control segregation of the TCR signaling cascade to clustered lipid rafts.

Following ligand binding the TCR segregates to plasma membrane microdomains, termed lipid rafts, characterized by a highly ordered lipid structure favoring partitioning of glycosyl phosphatidyl inositol-linked costimulatory receptors and acylated signaling molecules. Here we show that the inducible association of the TCR and key signaling proteins with lipid rafts is dependent on the actin cytoskeleton through a mechanism involving raft coalescence. Although lipid rafts are required for full activation of the TCR-dependent tyrosine phosphorylation cascade and sustained signaling, triggering of TCR-proximal events, including Fyn activation and a first wave of Vav phosphorylation, is independent of lipid rafts, while a second wave of raft-dependent Vav phosphorylation occurs after raft coalescence, as also supported by the finding that Vav is phosphorylated in response to lipid raft clustering by GM1 aggregation.