Guidance on personal dosimetry for occupational exposure in interventional radiology

During examinations that involve significant levels of exposure, radiology staff wear protective aprons and move towards various exposure orientations. The resulting body exposure is extremely non-uniform. Under such conditions the partially unshielded organs in the trunk together with tissues and organs in the head and neck region determine the effective dose equivalent. In principle, the same will be true for the newly introduced primary quantity effective dose. New calculations are required for quantitative assessments, because the selection of relevant organs and their weighting factors were changed. In this paper we describe our calculations and present and discuss conversion factors for the assessment of effective dose in typical exposure situations for radiology staff in interventional radiology.</p

In vivo imaging of the central and peripheral effects of sleep deprivation and suprachiasmatic nuclei lesion on PERIOD-2 protein in mice.

STUDY OBJECTIVES: That sleep deprivation increases the brain expression of various clock genes has been well documented. Based on these and other findings we hypothesized that clock genes not only underlie circadian rhythm generation but are also implicated in sleep homeostasis. However, long time lags have been reported between the changes in the clock gene messenger RNA levels and their encoded proteins. It is therefore crucial to establish whether also protein levels increase within the time frame known to activate a homeostatic sleep response. We report on the central and peripheral effects of sleep deprivation on PERIOD-2 (PER2) protein both in intact and suprachiasmatic nuclei-lesioned mice. DESIGN: In vivo and in situ PER2 imaging during baseline, sleep deprivation, and recovery. SETTINGS: Mouse sleep-recording facility. PARTICIPANTS: Per2::Luciferase knock-in mice. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Six-hour sleep deprivation increased PER2 not only in the brain but also in liver and kidney. Remarkably, the effects in the liver outlasted those observed in the brain. Within the brain the increase in PER2 concerned the cerebral cortex mainly, while leaving suprachiasmatic nuclei (SCN) levels unaffected. Against expectation, sleep deprivation did not increase PER2 in the brain of arrhythmic SCN-lesioned mice because of higher PER2 levels in baseline. In contrast, liver PER2 levels did increase in these mice similar to the sham and partially lesioned controls. CONCLUSIONS: Our results stress the importance of considering both sleep-wake dependent and circadian processes when quantifying clock-gene levels. Because sleep deprivation alters PERIOD-2 in the brain as well as in the periphery, it is tempting to speculate that clock genes constitute a common pathway mediating the shared and well-known adverse effects of both chronic sleep loss and disrupted circadian rhythmicity on metabolic health

Depriving Mice of Sleep also Deprives of Food.

Both sleep-wake behavior and circadian rhythms are tightly coupled to energy metabolism and food intake. Altered feeding times in mice are known to entrain clock gene rhythms in the brain and liver, and sleep-deprived humans tend to eat more and gain weight. Previous observations in mice showing that sleep deprivation (SD) changes clock gene expression might thus relate to altered food intake, and not to the loss of sleep per se. Whether SD affects food intake in the mouse and how this might affect clock gene expression is, however, unknown. We therefore quantified (i) the cortical expression of the clock genes Per1, Per2, Dbp, and Cry1 in mice that had access to food or not during a 6 h SD, and (ii) food intake during baseline, SD, and recovery sleep. We found that food deprivation did not modify the SD-incurred clock gene changes in the cortex. Moreover, we discovered that although food intake during SD did not differ from the baseline, mice lost weight and increased food intake during subsequent recovery. We conclude that SD is associated with food deprivation and that the resulting energy deficit might contribute to the effects of SD that are commonly interpreted as a response to sleep loss