Assessing the Dream-Lag Effect for REM and NREM Stage 2 Dreams

This study investigates evidence, from dream reports, for memory consolidation during sleep. It is well-known that events andmemories from waking life can be incorporated into dreams. These incorporations can be a literal replication of what occurredin waking life, or, more often, they can be partial or indirect. Two types of temporal relationship have been found tocharacterize the time of occurrence of a daytime event and the reappearance or incorporation of its features in a dream. Thesetemporal relationships are referred to as the day-residue or immediate incorporation effect, where there is the reappearance offeatures from events occurring on the immediately preceding day, and the dream-lag effect, where there is the reappearanceof features from events occurring 5–7 days prior to the dream. Previous work on the dream-lag effect has used spontaneoushome recalled dream reports, which can be from Rapid Eye Movement Sleep (REM) and from non-Rapid Eye Movement Sleep(NREM). This study addresses whether the dream-lag effect occurs only for REM sleep dreams, or for both REM and NREM stage2 (N2) dreams. 20 participants kept a daily diary for over a week before sleeping in the sleep laboratory for 2 nights. REM andN2 dreams collected in the laboratory were transcribed and each participant rated the level of correspondence between everydream report and every diary record. The dream-lag effect was found for REM but not N2 dreams. Further analysis indicatedthat this result was not due to N2 dream reports being shorter, in terms of number of words, than the REM dream reports.These results provide evidence for a 7-day sleep-dependent non-linear memory consolidation process that is specific to REMsleep, and accord with proposals for the importance of REM sleep to emotional memory consolidation

Mechanism of insulin resistance in a rat model of kidney disease and the risk of developing type 2 diabetes.

International audienceChronic kidney disease is associated with homeostatic imbalances such as insulin resistance. However, the underlying mechanisms leading to these imbalances and whether they promote the development of type 2 diabetes is unknown. The effect of chronic kidney disease on insulin resistance was studied on two different rat strains. First, in a 5/6th nephrectomised Sprague-Dawley rat model of chronic kidney disease, we observed a correlation between the severity of chronic kidney disease and hyperglycemia as evaluated by serum fructosamine levels (p<0.0001). Further, glucose tolerance tests indicated an increase of 25% in glycemia in chronic kidney disease rats (p<0.0001) as compared to controls whereas insulin levels remained unchanged. We also observed modulation of glucose transporters expression in several tissues such as the liver (decrease of ≈40%, p≤0.01) and muscles (decrease of ≈29%, p≤0.05). Despite a significant reduction of ≈37% in insulin-dependent glucose uptake in the muscles of chronic kidney disease rats (p<0.0001), the development of type 2 diabetes was never observed. Second, in a rat model of metabolic syndrome (Zucker Leprfa/fa), chronic kidney disease caused a 50% increased fasting hyperglycemia (p<0.0001) and an exacerbated glycemic response (p<0.0001) during glucose challenge. Similar modulations of glucose transporters expression and glucose uptake were observed in the two models. However, 30% (p<0.05) of chronic kidney disease Zucker rats developed characteristics of type 2 diabetes. Thus, our results suggest that downregulation of GLUT4 in skeletal muscle may be associated with insulin resistance in chronic kidney disease and could lead to type 2 diabetes in predisposed animals

Changes in Urinary and Serum Levels of Novel Biomarkers after Administration of Gadolinium-based Contrast Agents

Objective The aim of our study is to describe the changes in urinary and serum levels of novel biomarkers after gadolinium contrast administration in patients with normal renal function. Methods We measured four biomarkers in 28 volunteers: interleukin-18 (IL-18), N -acetyl-glucosaminidase (NAG), neutrophil gelatinase-associated lipocalin, and cystatin C. Urinary and serum samples were collected at 0, 3, and 24 hours following gadolinium administration. Results Baseline serum creatinine was 57.8 ± 34.5 μmol/L and remained stable. Urinary IL-18 levels increased significantly at three hours (10.7 vs. 7.3 ng/mg creatinine; P < 0.05). Similarly, urinary NAG levels increased significantly at three hours (3.9 vs. 2.2 IU/mg creatinine; P < 0.001). For both these markers, the difference was no longer significant at 24 hours. No statistically significant differences were observed for urinary and serum neutrophil gelatinase-associated lipocalin levels and for serum cystatin C levels. Conclusions Urinary IL-18 and NAG levels increased transiently after administration of gadolinium-based contrast agents in patients with normal renal function

Subchronic oral exposure of tungsten induces myofibroblast transformation and various markers of kidney fibrosis

Tungsten is a naturally occurring transition element used in a broad range of applications. As a result of its extensive use, we are increasingly exposed to tungsten from our environment, including potable water, since tungsten can become bioaccessible in ground sources. The kidneys are particularly susceptible to tungsten exposure as this is the main site for tungsten excretion. In this study, we investigated the prolonged effects of tungsten on the kidneys and how this may impact injury and function. When mice were exposed to tungsten in their drinking water for 1 mo, kidney function had not significantly changed. Following 3-mo exposure, mice were presented with deterioration in kidney function as determined by serum and urine creatinine levels. During 3 mo of tungsten exposure, murine kidneys demonstrated significant increases in the myofibroblast marker a-smooth muscle actin (aSMA) and extracellular matrix products: fibronectin, collagen, and matricellular proteins. In addition, Masson's trichrome and hematoxylin-eosin (H&E) staining revealed an increase in fibrotic tissue and vacuolization of tubular epithelial cells, respectively, from kidneys of tungsten-treated mice, indicative of renal injury. In vitro treatment of kidney fibroblasts with tungsten led to increased proliferation and upregulation of transforming growth factor b1 (TGFb1), which was consistent with the appearance of fibroblast-to-myofibroblast transition (FMT) markers. Our data suggest that continuous exposure to tungsten impairs kidney function that may lead to the development of chronic kidney disease (CKD)

Correspondence between REM dream reports and diary records as a function of time period.

<p>Mean correspondence scores (and Standard Deviations) between REM dream reports and diary records as a function of time period between diary day and dream. * p≤.05 (Wilcoxon test).</p

Correspondence between N2 dream reports and diary records as a function of time.

<p>Mean correspondence scores (and Standard Deviations) between N2 dream reports and diary records as a function of time between diary day and dream.</p

Example portion of a matrix used to record correspondence ratings (0–4) between dream reports and diary records.

<p>Example portion of a matrix used to record correspondence ratings (0–4) between dream reports and diary records.</p

Correspondence between N2 dream reports and diary records as a function of time period.

<p>Mean correspondence scores (and Standard Deviations) between N2 dream reports and diary records as a function of time period between diary day and dream. * p<.05 (Wilcoxon test).</p

Time of glycosuria apparition in Zucker Lepr^fa/fa rats.

<p>The graph shows the proportion of rats with glycosuria as confirmed by a positive Diastix^™ (Bayer) test on two consecutive days for 15 Zucker Lepr^fa/fa rats per group.</p

Glucose transporters mRNA expression in selected organs of CKD rats.

<p>mRNA encoding glucose transporters in CTL and CKD rats in the indicated tissues were measured by quantitative Real-Time PCR. mRNA levels are expressed in relative quantities and calculated using the ΔΔCT method [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0176650#pone.0176650.ref033" target="_blank">33</a>] with their respective housekeeping gene (Villin-1 for kidneys, β-actin for liver and GAPDH for muscles and adipose tissues). Data was normalized to the mean relative quantity of each gene in CTL rats. The graph shows the mean expression in CKD rats expressed as a percentage of controls ± S.D. of at least 10 rats in each group. *, p<0.05; **, p<0.01; ***, p<0.001; ****, p<0.0001 as compared to CTL rats. <b>(A)</b> Glucose transporters mRNA expression in the kidney and liver of SD rats. <b>(B)</b> GLUT1 and GLUT4 mRNA expression in skeletal muscle and white adipose tissue of SD rats. <b>(C)</b> GLUT1 and GLUT4 mRNA expression in skeletal muscle and white adipose tissue of Zucker Lepr^fa/fa rats. Measurements at Day 42.</p