Shift work and quality of sleep::Effect of working in designed dynamic light

PURPOSE: To examine the effect of designed dynamic light on staff’s quality of sleep with regard to sleep efficiency, level of melatonin in saliva, and subjective perceptions of quality of sleep. METHODS: An intervention group working in designed dynamic light was compared with a control group working in ordinary institutional light at two comparable intensive care units (ICUs). The study included examining (1) melatonin profiles obtained from saliva samples, (2) quality of sleep in terms of sleep efficiency, number of awakenings and subjective assessment of sleep through the use of sleep monitors and sleep diaries, and (3) subjective perceptions of well-being, health, and sleep quality using a questionnaire. Light conditions were measured at both locations. RESULTS: A total of 113 nurses (88 %) participated. There were no significant differences between the two groups regarding personal characteristics, and no significant differences in total sleep efficiency or melatonin level were found. The intervention group felt more rested (OR 2.03, p = 0.003) and assessed their condition on awakening as better than the control group (OR 2.35, p = 0.001). Intervention-ICU nurses received far more light both during day and evening shifts compared to the control-ICU. CONCLUSIONS: The study found no significant differences in monitored sleep efficiency and melatonin level. Nurses from the intervention-ICU subjectively assessed their sleep as more effective than participants from the control-ICU. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00420-015-1051-0) contains supplementary material, which is available to authorized users

Modelling the nucleon wave function from soft and hard processes

Current light-cone wave functions for the nucleon are unsatisfactory since they are in conflict with the data of the nucleon's Dirac form factor at large momentum transfer. Therefore, we attempt a determination of a new wave function respecting theoretical ideas on its parameterization and satisfying the following constraints: It should provide a soft Feynman contribution to the proton's form factor in agreement with data; it should be consistent with current parameterizations of the valence quark distribution functions and lastly it should provide an acceptable value for the \jp \to N \bar N decay width. The latter process is calculated within the modified perturbative approach to hard exclusive reactions. A simultaneous fit to the three sets of data leads to a wave function whose $x$-dependent part, the distribution amplitude, shows the same type of asymmetry as those distribution amplitudes constrained by QCD sum rules. The asymmetry is however much more moderate as in those amplitudes. Our distribution amplitude resembles the asymptotic one in shape but the position of the maximum is somewhat shifted.Comment: 32 pages RevTex + PS-file with 5 figures in uu-encoded, compressed fil

SNHG16 is regulated by the Wnt pathway in colorectal cancer and affects genes involved in lipid metabolism

It is well established that lncRNAs are aberrantly expressed in cancer where they have been shown to act as oncogenes or tumor suppressors. RNA profiling of 314 colorectal adenomas/adenocarcinomas and 292 adjacent normal colon mucosa samples using RNA‐sequencing demonstrated that the snoRNA host gene 16 (SNHG16) is significantly up‐regulated in adenomas and all stages of CRC. SNHG16 expression was positively correlated to the expression of Wnt‐regulated transcription factors, including ASCL2, ETS2, and c‐Myc. In vitro abrogation of Wnt signaling in CRC cells reduced the expression of SNHG16 indicating that SNHG16 is regulated by the Wnt pathway. Silencing of SNHG16 resulted in reduced viability, increased apoptotic cell death and impaired cell migration. The SNHG16 silencing particularly affected expression of genes involved in lipid metabolism. A connection between SNHG16 and genes involved in lipid metabolism was also observed in clinical tumors. Argonaute CrossLinking and ImmunoPrecipitation (AGO‐CLIP) demonstrated that SNHG16 heavily binds AGO and has 27 AGO/miRNA target sites along its length, indicating that SNHG16 may act as a competing endogenous RNA (ceRNA) “sponging” miRNAs off their cognate targets. Most interestingly, half of the miRNA families with high confidence targets on SNHG16 also target the 3′UTR of Stearoyl‐CoA Desaturase (SCD). SCD is involved in lipid metabolism and is down‐regulated upon SNHG16 silencing. In conclusion, up‐regulation of SNHG16 is a frequent event in CRC, likely caused by deregulated Wnt signaling. In vitro analyses demonstrate that SNHG16 may play an oncogenic role in CRC and that it affects genes involved in lipid metabolism, possible through ceRNA related mechanisms