Use of salivary cortisol and cortisone in the high and low dose synacthen test

CONTEXT: Salivary cortisone reflects serum cortisol levels, is more sensitive than salivary cortisol at lower values of serum cortisol and is non-invasive. OBJECTIVE: To investigate the relationship between serum cortisol and salivary cortisol and cortisone following low and high-dose synacthen. DESIGN AND SETTING: Prospective pharmacodynamic studies in clinical research facilities. PARTICIPANTS AND INTERVENTION: 35 dexamethasone-suppressed, healthy adult males underwent an intravenous synacthen test: N=23 low-dose (1mcg), N=12 high-dose (250mcg). Paired serum and salivary samples were taken at 15 sampling points over 120 minutes. MAIN OUTCOME MEASURE: Serum cortisol and salivary cortisol and cortisone were analyzed for correlations and by a mixed effects model. RESULTS: At baseline the correlation between serum cortisol and salivary cortisol was weak with many samples undetectable (r=0.45, NS), but there was a strong correlation with salivary cortisone (r=0.94, p<0.001). Up to 50 minutes following synacthen the correlation coefficient between serum cortisol and salivary cortisol and cortisone was <0.8, but both had a stronger correlation at 60 minutes (salivary cortisol r=0.89, p<0.001, salivary cortisone r=0.85, p<0.001). The relationship was examined excluding samples in the dynamic phase (baseline to 60 minutes). Salivary cortisol and cortisone showed a close relationship to serum cortisol. Salivary cortisone showing the stronger correlation: Salivary cortisol r=0.82, p<0.001, salivary cortisone r=0.96, p<0.001. CONCLUSION: Following synacthen, both salivary cortisol and cortisone reflect serum cortisol levels but there is a lag in their rise up to 60mins. The results support further research for possible future use of a 60min salivary cortisone measurement during the synacthen test

Behandlungsempfehlungen Insomnie der Gruppe «Schlaf & Psychiatrie» der SGSSC

Die Insomnie ist eine häufige Störung der Schlaf-Wach-Regulation und tritt oft komorbid auf. Die nachfolgenden Behandlungsempfehlungen stellen evidenzbasierte Diagnostik- und Therapiestrategien vor und umfassen sowohl psychotherapeutische wie auch pharmakotherapeutische Interventionen. Diese Empfehlungen der Schweizerischen Gesellschaft für Schlafforschung, Schlafmedizin und Chronobiologie (SGSSC) für die Behandlung der Insomnie wurden auf Grundlage der Leitlinien der «European Sleep Research Society» (ESRS) von 2023 [1] sowie der S3-Leitlinie/Nationalen Versorgungsleitlinie «Nicht erholsamer Schlaf/Schlafstörungen» der Deutschen Gesellschaft für Schlafforschung und Schlafmedizin (DGSM) von 2017 [2] erstellt. Sie geben nicht unbedingt die Ansicht der SMF-Redaktion wieder. Der Inhalt untersteht der redaktionellen Verantwortung der unterzeichnenden Fachgesellschaft bzw. Arbeitsgruppe

The neural correlates of dreaming.

Consciousness never fades during waking. However, when awakened from sleep, we sometimes recall dreams and sometimes recall no experiences. Traditionally, dreaming has been identified with rapid eye-movement (REM) sleep, characterized by wake-like, globally 'activated', high-frequency electroencephalographic activity. However, dreaming also occurs in non-REM (NREM) sleep, characterized by prominent low-frequency activity. This challenges our understanding of the neural correlates of conscious experiences in sleep. Using high-density electroencephalography, we contrasted the presence and absence of dreaming in NREM and REM sleep. In both NREM and REM sleep, reports of dream experience were associated with local decreases in low-frequency activity in posterior cortical regions. High-frequency activity in these regions correlated with specific dream contents. Monitoring this posterior 'hot zone' in real time predicted whether an individual reported dreaming or the absence of dream experiences during NREM sleep, suggesting that it may constitute a core correlate of conscious experiences in sleep

The interrelated effect of sleep and learning in dogs (Canis familiaris); an EEG and behavioural study

The active role of sleep in memory consolidation is still debated, and due to a large between-species variation, the investigation of a wide range of different animal species (besides humans and laboratory rodents) is necessary. The present study applied a fully non-invasive methodology to study sleep and memory in domestic dogs, a species proven to be a good model of human awake behaviours. Polysomnography recordings performed following a command learning task provide evidence that learning has an effect on dogs’ sleep EEG spectrum. Furthermore, spectral features of the EEG were related to post-sleep performance improvement. Testing an additional group of dogs in the command learning task revealed that sleep or awake activity during the retention interval has both short- and long-term effects. This is the first evidence to show that dogs’ human-analogue social learning skills might be related to sleep-dependent memory consolidation

Having a creative day:understanding entrepreneurs’ daily idea generation through a recovery lens

Prior research has shown that trait creativity is important for becoming an entrepreneur and successful in business. We explore a new perspective by investigating how recovery from work stress influences entrepreneurs’ daily idea generation, a key aspect of creativity. Physio-logical and mental recovery enables the cognitive processes of creative problem-solving. Moreover, differences in mental recovery processes help to explain age-related changes in en-trepreneurs’ creativity. Multilevel analyses based on 415 daily data from 62 entrepreneurs support our predictions. Our study introduces a new “state” perspective to understanding en-trepreneurs’ creativity, and highlights the critical role of recovery processes for idea genera-tion

Bioreactor technologies to support liver function in vitro

Liver is a central nexus integrating metabolic and immunologic homeostasis in the human body, and the direct or indirect target of most molecular therapeutics. A wide spectrum of therapeutic and technological needs drives efforts to capture liver physiology and pathophysiology in vitro, ranging from prediction of metabolism and toxicity of small molecule drugs, to understanding off-target effects of proteins, nucleic acid therapies, and targeted therapeutics, to serving as disease models for drug development. Here we provide perspective on the evolving landscape of bioreactor-based models to meet old and new challenges in drug discovery and development, emphasizing design challenges in maintaining long-term liver-specific function and how emerging technologies in biomaterials and microdevices are providing new experimental models.National Institutes of Health (U.S.) (R01 EB010246)National Institutes of Health (U.S.) (P50-GM068762-08)National Institutes of Health (U.S.) (R01-ES015241)National Institutes of Health (U.S.) (P30-ES002109)5UH2TR000496-02National Science Foundation (U.S.). Emergent Behaviors of Integrated Cellular Systems (CBET-0939511)United States. Defense Advanced Research Projects Agency. Microphysiological Systems Program (W911NF-12-2-0039

Modulation of 11β-hydroxysteroid dehydrogenase as a strategy to reduce vascular inflammation

Atherosclerosis is a chronic inflammatory disease in which initial vascular damage leads to extensive macrophage and lymphocyte infiltration. Although acutely glucocorticoids suppress inflammation, chronic glucocorticoid excess worsens atherosclerosis, possibly by exacerbating systemic cardiovascular risk factors. However, glucocorticoid action within the lesion may reduce neointimal proliferation and inflammation. Glucocorticoid levels within cells do not necessarily reflect circulating levels due to pre-receptor metabolism by 11β-hydroxysteroid dehydrogenases (11β-HSDs). 11β-HSD2 converts active glucocorticoids into inert 11-keto forms. 11β-HSD1 catalyses the reverse reaction, regenerating active glucocorticoids. 11β-HSD2-deficiency/ inhibition causes hypertension, whereas deficiency/ inhibition of 11β-HSD1 generates a cardioprotective lipid profile and improves glycemic control. Importantly, 11β-HSD1-deficiency/ inhibition is atheroprotective, whereas 11β-HSD2-deficiency accelerates atherosclerosis. These effects are largely independent of systemic risk factors, reflecting modulation of glucocorticoid action and inflammation within the vasculature. Here, we consider whether evidence linking the 11β-HSDs to vascular inflammation suggests these isozymes are potential therapeutic targets in vascular injury and atherosclerosis