4%) were detected by PHES; only six cases (8.7%) were diagnosed by both methods. Half of the cases (50%) had diabetes, and 61% were on hemodialysis. Cognitive function scores did not differ significantly between those receiving dialysis, hemodialysis, or no renal replacement therapy.
 
  It is essential to identify cerebral dysfunction when uremic encephalopathy is in early subclinical stages to reduce preventable events as traffic and work accidents.
 It is essential to identify cerebral dysfunction when uremic encephalopathy is in early subclinical stages to reduce preventable events as traffic and work accidents.This study evaluated changes in fatty acids from sera, red blood cells, and colonic biopsies from a phase Ib clinical trial of personalized ω-3 fatty acid dosing in 47 healthy volunteers. The trial aimed to reduce colonic prostaglandin E2 (PGE2), a pro-inflammatory product of arachidonic acid (AA) oxidation. The personalized doses ranged 2-10 grams/day (54% eicosapentaenoic acid, EPA, 24% other ω-3 fatty acids). In colon, increases in ω-3 highly unsaturated fatty acids (HUFA) and EPAAA ratios each were correlated with decreases in PGE2. Changes in either colonic EPAAA ratios or ω-3 HUFA were significantly correlated with changes in the same fatty acid measures in red blood cells or serum. The only blood-based measure significantly correlated with changes in colonic PGE2 was change in red blood cell ω-3 HUFA (ρ = -0.39), and the increase in red blood cell ω-3 HUFA was significantly greater in participants who had at least a median reduction in colonic PGE2 vs. those who did not. In summary, fatty acid changes in blood did reflect fatty acid changes in the colon, but additional factors will be needed for optimizing dosing models that seek to predict the anti-inflammatory effects of ω-3 fatty acids on the colon.Aldosterone exerts an enormous function on proximal tubular cells (PTC) senescence, which is a common pathomechanism contributing to renal dysfunction. Numerous studies have shown that oxidative stress is deeply involved in the pathophysiologic processes of chronic kidney diseases. The study aims to investigate whether autophagy could regulate the process of senescence through oxidative stress in PTC both in vivo and ex vivo. Our results suggested that aldosterone treatment increased the senescence and oxidative stress as evidenced by increased percent of SA-β-Gal positive cells, reactive oxygen species level, expression of NADPH oxidase 4 (NOX4) rather than NOX2, and the up-regulation of p21 in cultured PTC. Furthermore, the alternation of the expression of p62 and LC3-II/LC3-I demonstrated that aldosterone treatment remarkably influenced autophagic flux. NOX4 siRNA treatment or autophagy induction with rapamycin reduced the oxidative stress and senescence in aldosterone-induced PTC. On the contrary, inhibition of autophagy with chloroquine worsened these changes. Similar results were further confirmed in vivo. Our results suggested that autophagy may become a realistic therapeutic strategy against aldosterone-induced PTC injury via improving oxidative stress.Sleep impairment is highly prevalent in night shift workers, but evidence on the association of former night shift work (NSW) and its metrics (duration and frequency) in relation to sleep complaints is lacking. We evaluated the association of former and current NSW with chronic insomnia or circadian rhythm sleep disorder in a sample of the general worker (GW) population and in hospital workers (HW) in Austria. Information on sleep, NSW history, sociodemographic, and lifestyle factors was collected through an online cross-sectional survey in a representative sample of GW (N= 1,004) and a sample of HW (N= 799) between 2017 and 2019. Multi-variable adjusted logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for various measures of sleep (including chronic insomnia, daytime sleepiness, sleep duration, napping habits) and doctor-diagnosed chronic insomnia across NSW exposure (never night shift work; ever; ever/former; ever/current) and related metrics (cumulative duration, average frequency), compared to never NSW. Effect modification by chronotype and daytime napping was investigated. Former NSW was associated with higher odds of chronic insomnia in both samples (GW OR = 2.28, 95% CI = 1.07-4.83; HW OR = 1.17, 95% CI = 0.60-2.27). Chronic insomnia odds tended to increase among current night shift workers (HW OR = 1.50, 95% CI = 0.79-2.83), compared to day workers. Higher NSW frequency (shifts/month) was associated with higher chronic insomnia odds in former night shift workers in both samples (GW ORper shift/month = 1.06, 95% CI = 1.00-1.12; HW ORper shift/month = 1.12, 95% CI = 1.00-1.25). Former NSW was also associated with increased daytime sleepiness among GW (OR = 2.26, 95% CI 1.28-3.99). Associations were more pronounced among early chronotypes and participants who reported no daytime naps. Our results suggest that NSW is associated with chronic insomnia even in the years after cessation of involvement in working it.Mitochondria are the main cellular energy powerhouses and supply most of the energy in the form of ATP to fuel essential neuronal functions through oxidative phosphorylation (OXPHOS). In Alzheimer disease (AD), metabolic and mitochondrial disruptions are an early feature preceding any histopathological and clinical manifestations. Mitochondrial malfunction is also linked to synaptic defects in early AD. Mitophagy serves as a key cellular quality control mechanism involving sequestration of damaged mitochondria within autophagosomes and their subsequent degradation in lysosomes.  https://www.selleckchem.com/products/go-6983.html  However, it remains largely unknown whether mitophagy is involved in the regulation of energy metabolism in neurons, and if so, whether metabolic deficiency in AD is attributed to mitophagy dysfunction. Here we reveal that mitophagy is broadly activated in metabolically enhanced neurons upon OXPHOS stimulation, which sustains high energetic activity by increasing mitochondrial turnover and hence facilitating mitochondrial maintenance. Unexpectedly, in AD-related mutant HsAPP Tg mouse brains, early stimulation of OXPHOS activity fails to correct energy deficits but exacerbates synapse loss as a consequence of mitophagy failure.