Using relaxation techniques to improve sleep during naps.

Insufficient sleep is a common occurrence in occupational settings (e.g. doctors, drivers, soldiers). The resulting sleep debt can lead to daytime sleepiness, fatigue, mood disorder, and cognitive deficits as well as altered vascular, immune and inflammatory responses. Short daytime naps have been shown to be effective at counteracting negative outcomes related to sleep debt with positive effects on daytime sleepiness and performance after a normal or restricted night of sleep in laboratory settings. However, the environmental settings in the workplace and the emotional state of workers are generally not conducive to beneficial effects. Here, we tested whether relaxation techniques (RT) involving hypnosis might increase total sleep time (TST) and/or deepen sleep. In this study, eleven volunteers (aged 37-52) took six early-afternoon naps (30 min) in their occupational workplace, under two different conditions: control 'Naps' or 'Naps + RT' with a within-subjects design. Our results demonstrate that adding RT to naps changes sleep architecture, with a significant increase in the TST, mostly due to N2 sleep stage (and N3, to a lesser extent). Therefore, the deepening of short naps with RT involving hypnosis might be a successful non-pharmacological way to extend sleep duration and to deepen sleep in occupational settings.

The role of athletes' pain-related anxiety in pain-related attentional processes.

Numerous researchers have highlighted the social determinants of athletes' attitude toward pain, yet little is known about the role of cognitive processes and emotions that are related to pain in sport endeavors. There is evidence, in a dot probe paradigm, that individuals with chronic pain selectively orient their attention toward pain-related stimuli, but no studies have differentiated between the two attentional processes of hypervigilance that are evident in athletes: facilitated detection of threat and difficulty in disengaging attention from threatening stimuli. In the present study using a dot probe paradigm, we examined whether professional rugby players (N=58) with high pain-related anxiety (HPA) would show an attentional bias for pain-related threat, and whether this hypervigilance would reflect difficulty disengaging from threat or facilitated detection of threat. Rugby players with HPA oriented their attention toward pain-related threat with a concomitant difficulty disengaging from threat. Difficulty disengaging from painful stimuli may increase anxiety, and thus be maladaptive in sport. This is the first study to identify pain-related anxiety as a vulnerability marker in athletes' attentional biases.

SAR103168: a tyrosine kinase inhibitor with therapeutic potential in myeloid leukemias.

SAR103168, a tyrosine kinase inhibitor of the pyrido [2,3-d] pyridimidine subclass, inhibited the kinase activities of the entire Src kinase family, Abl kinase, angiogenic receptor kinases (vascular endothelial growth factor receptor [VEGFR] 1 and 2), Tie2, platelet derived growth factor (PDGF), fibroblast growth factor receptor (FGFR) 1 and 3, and epidermal growth factor receptor (EGFR). SAR103168 was a potent Src inhibitor, with 50% inhibitory concentration (IC50) = 0.65 ± 0.02 nM (at 100 µM ATP), targeting the auto-phosphorylation of the kinase domain (Src(260-535)) and activity of the phosphorylated kinase. Phosphorylation of Src, Lyn and Src downstream signaling pathways (PYK2, P-130CAS, FAK, JNK and MAPK) were inhibited in a dose-dependent manner. SAR103168 inhibited the phosphorylation of STAT5 in KG1 cells and fresh cells from patients with acute myeloid leukemia (AML). SAR103168 inhibited proliferation and induced apoptosis in acute and chronic myeloid leukemic cells at nanomolar IC50. SAR103168 induced anti-proliferation of leukemic progenitors (CFU-L) from 29 patients with AML, and > 85% of AML patient samples were sensitive to SAR103168. These antagonist activities of SAR103168 were independent of FLT3 expression. SAR103168 treatment was effective in 50% of high-risk patient samples carrying chromosome 7 abnormalities or complex rearrangement. SAR103168 administration (intravenous or oral) impaired tumor growth and induced tumor regression in animals bearing human AML leukemic cells, correlating with potent inhibition of Src downstream signaling pathways in AML tumors. SAR103168 showed potent anti-tumor activity in SCID (severe combined immunodeficiency) mice bearing AML (KG1, EOL-1, Kasumi-1, CTV1) and chronic myeloid leukemia (CML) (K562) tumors. The combination of cytarabine and SAR103168 showed synergistic activity in AML and CML tumor models. These results highlight the therapeutic potential of SAR103168 in myeloid leukemias and support the rationale for clinical investigations.