Online physical exercise intervention in older adults during lockdown: Can we improve the recipe?

BACKGROUND: Recorded and live online physical exercise (PE) interventions are known to provide health benefits. However, the effects of prioritizing the number of live or recorded sessions remain unclear. AIMS: To explore which recorded-live sessions ratio leads to the best implementation and benefits in older adults. METHODS: Forty-six community-dwelling adults (> 60y.o.) were randomized into two groups completing a 12-week online PE intervention. Each group had a different ratio of live-recorded online sessions as follows: Live-Recorded-Live sessions (LRL; n = 22) vs. Recorded-Live-Recorded sessions (RLR; n = 24). RESULTS: Drop-out rates did not reach significance (LRL:14% vs. RLR: 29%, p = 0.20), and adherence was similar (> 85%) between groups. Both groups reported similar levels of satisfaction (> 70%), enjoyment (> 75%), and perceived exertion (> 60%). Both groups increased physical health and functional capacities, with greater improvements in muscle power (LRL: LRL: + 35 ± 16.1% vs. RLR: + 7 ± 13.9%; p = 0.010) and endurance (LRL: + 34.7 ± 15.4 vs. RLR: + 27.0 ± 26.5, p < 0.001) in the LRL group. DISCUSSION: Both online PE intervention modalities were adapted to the participants' capacities and led to a high level of enjoyment and retention. The greater physical improvements observed in the LRL group are likely due to the higher presence of the instructor compared to the RLR group. Indeed, participants received likely more feedback to appropriately adjust postures and movements, increasing the quality of the exercises. CONCLUSION: When creating online PE interventions containing both recorded and live sessions, priority should be given to maximizing the number of live sessions and not the number of recorded sessions.

[Sleep disorders in patients with a neurocognitive disorder]. / Les troubles du sommeil chez les patients atteints d'un trouble neurocognitif.

INTRODUCTION: Sleep disorders are prevalent in patients with a neurocognitive disorder, and diagnosis and treatment in these patients remain challenging in clinical practice. METHODS: This narrative review offers a systematic approach to diagnose and treat sleep disorders in neurocognitive disorders. RESULTS: Alzheimer's disease is often associated with circadian rhythm disorders, chronic insomnia, and sleep apnea-hypopnea syndrome. Alpha-synucleinopathies (e.g., Parkinson's disease and Lewy body dementia) are often associated with a rapid eye movement sleep behavior disorder, restless legs syndrome, chronic insomnia, and sleep apnea-hypopnea syndrome. A focused history allows to diagnose most sleep disorders. Clinicians should ensure to gather the following information in all patients with a neurocognitive disorder: (1) the presence of difficulties falling asleep or staying asleep, (2) the impact of sleep disturbances on daily functioning (fatigue, sleepiness and other daytime consequences), and (3) abnormal movements in sleep. Sleep diaries and questionnaires can assist clinicians in screening for specific sleep disorders. Polysomnography is recommended if a rapid eye movement sleep behavior disorder or a sleep apnea-hypopnea syndrome are suspected. Sleep complaints should prompt clinicians to ensure that comorbidities interfering with sleep are properly managed. The main treatment for moderate to severe obstructive sleep apnea-hypopnea syndrome remains continuous positive airway pressure, as its efficacy has been demonstrated in patients with neurocognitive disorders. Medications should also be reviewed, and time of administration should be optimized (diuretics and stimulating medications in the morning, sedating medications in the evening). Importantly, cholinesterase inhibitors (especially donepezil) may trigger insomnia. Switching to morning dosing or to an alternative drug may help. Cognitive-behavioral therapy for insomnia is indicated to treat chronic insomnia in neurocognitive disorders. False beliefs regarding sleep should be addressed with the patient and their caregiver. The sleep environment should be optimized (decrease light exposure at night, minimize noise, avoid taking vital signs, etc.). Sleep restriction can be considered as patients with a neurocognitive disorder often spend too much time in bed. The need for naps should be assessed case by case as naps may contribute to insomnia in some patients but allow others to complete their diurnal activities. Trazodone (50mg) may also be used under certain circumstances in chronic insomnia. Recent evidence does not support a role for exogenous melatonin in patients with a neucognitive disorder and insomnia. Patients in long-term care facilities are often deprived of an adequate diurnal exposure to light. Increasing daytime exposure to light may improve sleep and mood. Patients with circadian rhythm disorders can also benefit from light therapy (morning bright light therapy in case of phase delay and evening bright light therapy in case of phase advance). Rapid eye movement sleep behavior disorder can lead to violent behaviors, and the sleeping environment should be secured (e.g., mattress on the floor, remove surrounding objects). Medication exacerbating this disorder should be stopped if possible. High dose melatonin (6 to 18mg) or low dose clonazepam (0.125-0.25mg) at bedtime may be used to reduce symptoms. Melatonin is preferred in first-line as it is generally well tolerated with few side effects. Patients with restless legs syndrome should be investigated for iron deficiency. Medication decreasing dopaminergic activity should be reduced or stopped if possible. Behavioral strategies such as exercise and leg massages may be beneficial. Low-dose dopamine agonists (such as pramipexole 0.125mg two hours before bedtime) can be used to treat the condition, but a prolonged treatment may paradoxically worsen the symptoms. Alpha-2-delta calcium channel ligands can also be used while monitoring for the risk of falls. CONCLUSION: Multiple and sustained nonpharmacological approaches are recommended for the treatment of sleep disturbances in patients with neurocognitive disorder. Pharmacological indications remain limited, and further randomized clinical trials integrating a multimodal approach are warranted to evaluate the treatment of sleep disorders in specific neurocognitive disorders.

Fasting enhances TRAIL-mediated liver natural killer cell activity via HSP70 upregulation.

Acute starvation, which is frequently observed in clinical practice, sometimes augments the cytolytic activity of natural killer cells against neoplastic cells. In this study, we investigated the molecular mechanisms underlying the enhancement of natural killer cell function by fasting in mice. The total number of liver resident natural killer cells in a unit weight of liver tissue obtained from C57BL/6J mice did not change after a 3-day fast, while the proportions of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)+ and CD69+ natural killer cells were significantly elevated (n = 7, p <0.01), as determined by flow cytometric analysis. Furthermore, we found that TRAIL- natural killer cells that were adoptively transferred into Rag-2-/- γ chain-/- mice could convert into TRAIL+ natural killer cells in fasted mice at a higher proportion than in fed mice. Liver natural killer cells also showed high TRAIL-mediated antitumor function in response to 3-day fasting. Since these fasted mice highly expressed heat shock protein 70 (n = 7, p <0.05) in liver tissues, as determined by western blot, the role of this protein in natural killer cell activation was investigated. Treatment of liver lymphocytes with 50 µg/mL of recombinant heat shock protein 70 led to the upregulation of both TRAIL and CD69 in liver natural killer cells (n = 6, p <0.05). In addition, HSP70 neutralization by intraperitoneally injecting an anti- heat shock protein 70 monoclonal antibody into mice prior to fasting led to the downregulation of TRAIL expression (n = 6, p <0.05). These findings indicate that acute fasting enhances TRAIL-mediated liver natural killer cell activity against neoplastic cells through upregulation of heat shock protein 70.

Neuroimaging findings in primary insomnia.

State-of-the-art neuroimaging techniques have accelerated progress in the study and understanding of sleep in humans. Neuroimaging studies in primary insomnia remain relatively few, considering the important prevalence of this disorder in the general population. This review examines the contribution of functional and structural neuroimaging to our current understanding of primary insomnia. Functional studies during sleep provided support for the hyperarousal theory of insomnia. Functional neuroimaging also revealed abnormalities in cognitive and emotional processing in primary insomnia. Results from structural studies suggest neuroanatomical alterations in primary insomnia, mostly in the hippocampus, anterior cingulate cortex and orbitofrontal cortex. However, these results are not well replicated across studies. A few magnetic resonance spectroscopy studies revealed abnormalities in neurotransmitter concentrations and bioenergetics in primary insomnia. The inconsistencies among neuroimaging findings on insomnia are likely due to clinical heterogeneity, differences in imaging and overall diversity of techniques and designs employed. Larger samples, replication, as well as innovative methodologies are necessary for the progression of this perplexing, yet promising area of research.

Sleep and dreaming are for important matters.

Recent studies in sleep and dreaming have described an activation of emotional and reward systems, as well as the processing of internal information during these states. Specifically, increased activity in the amygdala and across mesolimbic dopaminergic regions during REM sleep is likely to promote the consolidation of memory traces with high emotional/motivational value. Moreover, coordinated hippocampal-striatal replay during NREM sleep may contribute to the selective strengthening of memories for important events. In this review, we suggest that, via the activation of emotional/motivational circuits, sleep and dreaming may offer a neurobehavioral substrate for the offline reprocessing of emotions, associative learning, and exploratory behaviors, resulting in improved memory organization, waking emotion regulation, social skills, and creativity. Dysregulation of such motivational/emotional processes due to sleep disturbances (e.g., insomnia, sleep deprivation) would predispose to reward-related disorders, such as mood disorders, increased risk-taking and compulsive behaviors, and may have major health implications, especially in vulnerable populations.

Equilibrium and kinetics of biosorption of cadmium(II) and copper(II) ions by wheat straw.

Biosorption equilibrium and kinetics of Cd(2+) and Cu(2+) ions on wheat straw, Triticum aestivum, in an aqueous system were investigated. Among the models tested, namely the Langmuir, Freundlich, Temkin, and Dubinin-Radushkevich isotherms, the biosorption equilibrium for both Cd(2+) and Cu(2+) was best described by the Langmuir model. The Langmuir biosorption capacity for Cd(2+) was about 27% higher than that for Cu(2+). It was also found that biosorption of Cd(2+) and Cu(2+) by wheat straw followed second-order kinetics. The equilibrium amount of metal ions adsorbed onto the wheat straw increased with increasing of pH from 4.0 to 7.0, and the effect was more pronounced for Cd(2+) than for Cu(2+). The equilibrium adsorbed amount also increased with the initial concentration of the metal ions, as expected. On the other hand, an increase of temperature from 25 to 30 degrees C only enhanced the biosorption of Cd(2+) and Cu(2+) slightly. The apparent temperature independence and the strong pH dependence of the amount of metal ions adsorbed along with moderate mean free energies of biosorption (between 8.0 and 12.9 kJ mol(-1)) altogether indicate that biosorption of Cd(2+) and Cu(2+) by wheat straw might follow a chemisorption mechanism.

Intrinsic brain activity in altered states of consciousness: how conscious is the default mode of brain function?

Spontaneous brain activity has recently received increasing interest in the neuroimaging community. However, the value of resting-state studies to a better understanding of brain-behavior relationships has been challenged. That altered states of consciousness are a privileged way to study the relationships between spontaneous brain activity and behavior is proposed, and common resting-state brain activity features observed in various states of altered consciousness are reviewed. Early positron emission tomography studies showed that states of extremely low or high brain activity are often associated with unconsciousness. However, this relationship is not absolute, and the precise link between global brain metabolism and awareness remains yet difficult to assert. In contrast, voxel-based analyses identified a systematic impairment of associative frontoparieto-cingulate areas in altered states of consciousness, such as sleep, anesthesia, coma, vegetative state, epileptic loss of consciousness, and somnambulism. In parallel, recent functional magnetic resonance imaging studies have identified structured patterns of slow neuronal oscillations in the resting human brain. Similar coherent blood oxygen level-dependent (BOLD) systemwide patterns can also be found, in particular in the default-mode network, in several states of unconsciousness, such as coma, anesthesia, and slow-wave sleep. The latter results suggest that slow coherent spontaneous BOLD fluctuations cannot be exclusively a reflection of conscious mental activity, but may reflect default brain connectivity shaping brain areas of most likely interactions in a way that transcends levels of consciousness, and whose functional significance remains largely in the dark.

Hemodynamic cerebral correlates of sleep spindles during human non-rapid eye movement sleep.

In humans, some evidence suggests that there are two different types of spindles during sleep, which differ by their scalp topography and possibly some aspects of their regulation. To test for the existence of two different spindle types, we characterized the activity associated with slow (11-13 Hz) and fast (13-15 Hz) spindles, identified as discrete events during non-rapid eye movement sleep, in non-sleep-deprived human volunteers, using simultaneous electroencephalography and functional MRI. An activation pattern common to both spindle types involved the thalami, paralimbic areas (anterior cingulate and insular cortices), and superior temporal gyri. No thalamic difference was detected in the direct comparison between slow and fast spindles although some thalamic areas were preferentially activated in relation to either spindle type. Beyond the common activation pattern, the increases in cortical activity differed significantly between the two spindle types. Slow spindles were associated with increased activity in the superior frontal gyrus. In contrast, fast spindles recruited a set of cortical regions involved in sensorimotor processing, as well as the mesial frontal cortex and hippocampus. The recruitment of partially segregated cortical networks for slow and fast spindles further supports the existence of two spindle types during human non-rapid eye movement sleep, with potentially different functional significance.

A role for sleep in brain plasticity.

The idea that sleep might be involved in brain plasticity has been investigated for many years through a large number of animal and human studies, but evidence remains fragmentary. Large amounts of sleep in early life suggest that sleep may play a role in brain maturation. In particular, the influence of sleep in developing the visual system has been highlighted. The current data suggest that both Rapid Eye Movement (REM) and non-REM sleep states would be important for brain development. Such findings stress the need for optimal paediatric sleep management. In the adult brain, the role of sleep in learning and memory is emphasized by studies at behavioural, systems, cellular and molecular levels. First, sleep amounts are reported to increase following a learning task and sleep deprivation impairs task acquisition and consolidation. At the systems level, neurophysiological studies suggest possible mechanisms for the consolidation of memory traces. These imply both thalamocortical and hippocampo-neocortical networks. Similarly, neuroimaging techniques demonstrated the experience-dependent changes in cerebral activity during sleep. Finally, recent works show the modulation during sleep of cerebral protein synthesis and expression of genes involved in neuronal plasticity.

Regional organisation of brain activity during paradoxical sleep (PS).

Human brain function is regionally organised during paradoxical sleep (PS) in a very different way than during wakefulness or slow wave sleep. The important activity in the pons and in the limbic/paralimbic areas constitutes the key feature of the functional neuroanatomy of PS, together with a relative quiescence of prefrontal and parietal associative cortices. Two questions are still outstanding. What neurocognitive and neurophysiological mechanisms may explain this original organization of brain function during PS? How the pattern of regional brain function may relate to dream content? Although some clues are already available, the experimental answer to both questions is still pending.

Memory processing during human sleep as assessed by functional neuroimaging.

Sleep is believed to participate in memory consolidation, possibly through off-line processing of recent memory traces. In this paper, we summarize functional neuroimaging data testing this hypothesis. First, sleep deprivation disrupts the processing of recent memory traces and hampers the changes in functional segregation and connectivity which underpin the gain in performance usually observed in subjects allowed to sleep on the first post-training night. Second, experience-dependent changes in regional brain activity occur during post-training sleep. These changes are shown to be related to the processing of high-level material and to be modulated by the amount of learning achieved during the training session. These changes do not involve isolated brain areas but entire macroscopic cerebral networks. These data suggest a role for sleep in the processing of recent memory traces.

The Laboratory Information System (LIS): I-Application to the clinical chemistry laboratory.

The Laboratory Information System (LIS) was designed as a "turn-key" system. The main functions are operated interactively on a mini-computer which gives the laboratory complete control over daily processing. Collection of results from automated analyzers is accomplished via a micro-computer/micro-processor network. Links are provided with a central main frame computer for immediate patient identification and historical data processing. LIS is designed to manage all the operations involved in laboratory activities. The system has 14 major functions: registration of test requests, production of specimen collection sheets and identification labels, confirmation of specimen collection, production of aliquot labels, workload inquiry, production of worksheets, manual entry of test results, automated entry of test results, results inquiry, preliminary report, final report, daily activities reports, statistical reports, billing. System security is provided along three directions: data entry validation, system access control, and memory protection. The main advantages of LIS are: reduced clerical work, better evaluation of workload, faster communication, improvement of information given to the clinician: adapted reference values, interpretation, comments, improved retrieval operations, faster billing.

[Growth hormone specific binding sites : characteristics of lactogenic receptors induced by estrogens (author's transl)]. / Récepteurs de l'hormone de croissance. Caractéristiques des récepteurs lactogéniques induits par les oestrogènes.

In vitro binding of growth hormone was characterized in rat liver. Microsomal preparations were found more active than membranes purified with an aqueous two-phase polymer system. Binding conducted at 4 degrees C was found optimal after 72 hours of incubation in 5 mM Tris-Maleate buffer pH 6.4 with 25 mM CaCl2. Injecting estrone (25 microgram/100 g B.W.) for one week induced the formation of lactogenic receptors, and increased the specific binding of hGH from 2.8 +/- 1.9 to 22.3 +/- 7.1%. Prolactin and hGH, but not rGH or other pituitary hormones, could displace radioactive hGH. With incubations conducted at 37 degrees C, equilibrium was reached more rapidly but at the cost of a more extensive degradation. The presence of membrane receptors in the medium partly protected the hormone against aggregation and degradation. Scatchard plots were obtained from experiments conducted under optimal conditions and analyzed on computer using a program based on an iterative method. Data indicated that lactogenic receptors possessed a single specific binding site for hGH with a constant (Ka) of 2.18 +/- 0.22 x 10(9) M-1 and a binding capacity of 304 +/- 91 fm/mg proteins.