The Napping Company: bringing science to the workplace

Increasing emphasis is currently being given to the importance of bringing knowledge gained from science into places where people live and work, in order to increase the impact science has on the general public's quality of life. Scientific findings about the positive impact of napping on mood and performance are an example of research generated knowledge that needs to be brought to the workplace. A major goal of the Napping Company (www.napping.com) is to bring the science of napping to the workers and the workplace so that employees and employers can act on this knowledge and change worker napping behavior and employer napping policies. The present paper overviews the challenges inherent in making scientific knowledge useful to how we live our lives. The Napping Company is guided by five principles of knowledge transfer in the company's attempts to disseminate and increase utilization of napping research. Examples are given to illustrate how the Napping Company has used these principles to bridge the gap between napping science and nap behavior and policies in the workplace.     

Avoiding spectral leakage in objective detection of auditory steady-state evoked responses in the inferior colliculus of rat using coherence

Local field potentials (LFP) are bioelectric signals recorded from the brain that reflect neural activity in a high temporal resolution. Separating background activity from that evoked by specific somato-sensory input is a matter of great clinical relevance in neurology. The coherence function is a spectral coefficient that can be used as a detector of periodic responses in noisy environments. Auditory steady-state responses to amplitude-modulated tones generate periodic responses in neural networks that may be accessed by means of coherence between the stimulation signal and the LFP recorded from the auditory pathway. Such signal processing methodology was applied in this work to evaluate in vivo, anaesthetized Wistar rats, activation of neural networks due to single carrier sound stimulation frequencies, as well as to evaluate the effect of different modulating tones in the evoked responses. Our results show that an inappropriate choice of sound stimuli modulating frequencies can compromise coherence analysis, e.g. misleading conclusions due to mathematical artefact of signal processing. Two modulating frequency correction protocols were used: nearest integer and nearest prime number. The nearest prime number correction was successful in avoiding spectral leakage in the coherence analysis of steady-state auditory response, as predicted by Monte Carlo simulations.     

Proinflammatory cytokine-receptor interaction model improves the predictability of cerebral white matter injury in preterm infants

Proinflammatory cytokines have been variably linked to development of cerebral white matter injury (WMI) in preterm infants. Because soluble receptors tightly control cytokine bioactivity, we modeled cytokine-receptor interaction as a predictor of WMI. Plasma from 100 preterm infants was assayed for cytokines (tumor necrosis factor alpha, interleukin (IL-1beta, IL-6) and their soluble receptors (sTNF-RI), sTNF-RII, sIL-1RA, and sIL-6R). Cranial ultrasound (US) results were correlated with cytokine and receptor concentrations individually and with cytokine-receptor interaction models (PROC LOGISTIC; SAS Software). Receiver operating characteristic curves were constructed to determine the predictability of WMI. Fifty-two infants with normal US exams were compared with 21 infants with evidence of WMI. There was no association between individual cytokine or receptor concentrations and the development of WMI. However, modeling cytokines with their soluble receptors significantly improved the predictability of WMI. We concluded that consideration of cytokine-receptor interaction may be more important than individual cytokine concentrations alone in determining the role of inflammation in the pathogenesis of WMI in preterm infants.     

Classification and pathogenic models of unintentional postural cranial deformities in infants: plagiocephalies and brachycephalies

Unintentional postural deformities of the skull have increased in a pseudoepidemic manner in the last 15 years. Although dorsal decubitus and prenatal risk factors can play a role in the genesis of such deformities, we think that a crucial determinant is a postnatal defect of cervical mobility responsible for the infant's posture (ie, positional preference) when supine. Indeed, muscular factors, which limit the range of head and neck movements, have been underestimated in the genesis of skull deformities. Here, we have retrospectively analyzed data from 181 infants with unintentional skull deformities and propose a classification of these deformities into 3 types based on their pathogenic model and clinical appearance: fronto-occipital plagiocephalies due to severe muscle hypertonia in which the myogenic component is the first implicated, occipital plagiocephalies with muscle imbalance due to neurogenic muscle hypertonia, and posterior brachycephalies with neurogenic muscle hypertonia of the suboccipital muscles due to trauma to the occipitovertebral junction. Future studies on the size and density of specific muscles or group of muscles should help us to better understand their involvement in the pathogenesis of postural deformities. Our findings also highlight the importance of carefully assessing cervical mobility during the first week of life to detect possible limitations and to prescribe (if needed) an adapted rehabilitation. Rehabilitation should be associated with postural measures put in place when infants sleep supine to prevent the appearance of skull deformations.     

SOCS2 regulates T helper type 2 differentiation and the generation of type 2 allergic responses

The incidence of allergy and asthma in developed countries is on the increase and this trend looks likely to continue. CD4(+) T helper 2 (Th2) cells are major drivers of these diseases and their commitment is controlled by cytokines such as interleukin 4, which are in turn regulated by the suppressor of cytokine signaling (SOCS) proteins. We report that SOCS2(-/-) CD4(+) T cells show markedly enhanced Th2 differentiation. SOCS2(-/-) mice, as well as RAG-1(-/-) mice transferred with SOCS2(-/-) CD4(+) T cells, exhibit elevated type 2 responses after helminth antigen challenge. Moreover, in in vivo models of atopic dermatitis and allergen-induced airway inflammation, SOCS2(-/-) mice show significantly elevated IgE, eosinophilia, type 2 responses, and inflammatory pathology relative to wild-type mice. Finally, after T cell activation, markedly enhanced STAT6 and STAT5 phosphorylation is observed in SOCS2(-/-) T cells, whereas STAT3 phosphorylation is blunted. Thus, we provide the first evidence that SOCS2 plays an important role in regulating Th2 cell expansion and development of the type 2 allergic responses.