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Lower concentrations in heparin lock are optimal for shortening APTT in haemodialysis patients; further studies are needed to elucidate the role of heparin concentration in the lock practice.
Lower concentrations in heparin lock are optimal for shortening APTT in haemodialysis patients; further studies are needed to elucidate the role of heparin concentration in the lock practice.To evaluate the effect of reduced calcium (Ca) and available P (aP) levels in starter diets on growth performance and tibia, sternum and serum characteristics, and to assay the association between Ca and P (aP) intakes and these variables, 600 one-day-old broiler chicks (Ross 308) were used in a 21-days trial. Broilers were randomly allotted to five treatments with five replicate pens. Chicks were fed on one of the five starter diets that were formulated with a 10% reduction in the Ca and aP contents, starting from the control diet and hence, named as C (0.96% Ca, 0.45% aP), L1 (0.85% Ca and 0.42% aP), L2 (0.77% Ca and 0.38% aP), L3 (0.68% Ca and 0.34% aP) and L4 (0.61% Ca and 0.31% aP). Declining dietary Ca and aP levels did not affect body weight and levels of Ca, P and alkaline phosphatase in serum, but reduced linearly feed intake, the feed conversion ratio and the bone weight and ash content. The Ca and aP intakes and CaaP ratio displayed a positive correlation with both tibia and sternum weights, and the mass of the bones were equally sensitive to dietary Ca and aP levels. In conclusion, the body weight of young broilers was irresponsive to changes in the skeleton when exposed to early dietary Ca and aP restrictions (up to 0.61% Ca and 0.31% aP) and the mechanostat had limits due to the association between Ca and aP intakes, and bone properties.Luteolin is a widely distributed flavone herbs and vegetables. It has anti-oxidant and anti-inflammatory activities and improves glucose metabolism by potentiating insulin sensitivity and improving β-cell function and mass. Alzheimer's disease (AD) is induced by the deposition of amyloid-beta (Aβ) in the hippocampus and the formation of neurotoxic Aβ plaques. The Aβ deposition is associated with increased formation of Aβ from amyloid precursor protein by up-regulation of β-secretase and β-site amyloid precursor protein-cleaving enzyme 1 (BACE1). Furthermore, Aβ accumulation is increased by brain insulin resistance. The impairment of insulin/IGF-1 signaling mainly in the hippocampus and brain insulin resistance is connected to signals originating in the liver and gut microbiota, known as the gut microbiota-liver-brain axis. This indicates that the changes in the production of short-chain fatty acids by the gut microbiota and pro-inflammatory cytokines can alter insulin resistance in the liver and brain. Luteolin is detected in the brain tissues after passing through the blood-brain barrier, where it can directly influence neuroinflammation and brain insulin resistance and modulate Aβ deposition. Luteolin (10-70 mg/kg bw for rodents) can modulate the systemic and brain insulin resistance, and it suppresses AD development directly, and it influences Aβ deposition by activation of the gut microbiota-liver-brain axis. In this review, we evaluate the potential of luteolin to mitigate two potential causes of AD, neuroinflammatory processes, and disruption of glucose metabolism in the brain. Metabolism inhibitor This review suggests that luteolin intake can enhance brain insulin resistance and neuroinflammation, directly and indirectly, to protect against the development of Alzheimer's-like disease, and the gut microbiota-liver-brain axis is mainly involved in the indirect pathway. However, most studies have been conducted in animal studies, and human clinical trials are needed.Evidence suggests that preventive dressings applied on sacral skin help to prevent pressure ulcers. However, possible performance differences of different dressing types are unclear. An exploratory randomized crossover trial with intra-individual comparisons was conducted to compare the effects of three different multi-layer foam dressings (Mepilex Border Sacrum, ALLEVYN Life Sacrum and Optifoam Gentle Sacrum) compared to no dressing on the sacral skin. Healthy female volunteers (n = 12, mean age 72 years) wore three different dressings on their sacral skin for 3.5 hours while lying supine on a standard hospital mattress. At regular intervals, subjects performed standardized movements to enhance shear loads. Skin surface temperature, stratum corneum hydration, erythema, skin roughness and the interleukin 1 alpha (IL-1α) concentration per total protein were measured at baseline and after the lying periods. After 3.5 hours, the median skin temperature increased in all four groups between 3.0°C and 3.8°C with only minor differences between the no dressing and the dressing groups. Median stratum corneum hydration increased during the lying period in all groups with highest increases in the Optifoam Gentle Sacrum (7.3 arbitrary units) and no dressing group (7.0 arbitrary units). There was a median decrease of the mean roughness (Rz) in the Optifoam Gentle Sacrum group of -6.3 μm but no relevant changes in the other groups. After loading, the erythema index was highest in the ALLEVYN Life Sacrum and no dressing groups. Highest releases of IL-1α were observed in the ALLEVYN Life Sacrum and Optifoam Gentle Sacrum groups, in the Mepilex Border Sacrum group changes were minor. Study results indicate, that the application of preventive dressings on sacral skin during loading do not cause additional occlusion compared to loading without dressings when lying supine. Different dressings cause different cutaneous responses during loading.
What is the central question of this study? The pathophysiology of acute mountain sickness (AMS), involving the respiratory, renal and cerebrovascular systems, remains poorly understood. How do the early adaptations in these systems during a simulated altitude of 5000m relate to AMS risk? What is the main finding and its importance? The rate of blood alkalosis and cerebral artery dilatation predict AMS severity during the first 10 h of exposure to a simulated altitude of 5000m. Slow metabolic compensation by the kidneys of respiratory alkalosis attributable to a brisk breathing response together with excessive brain blood vessel dilatation might be involved in early development of AMS.
The complex pathophysiology of acute mountain sickness (AMS) remains poorly understood and is likely to involve maladaptive responses of the respiratory, renal and cerebrovascular systems to hypoxia. Using stepwise linear regression, we tested the hypothesis that exacerbated respiratory alkalosis, as a result of a brisk ventilatory response, sluggish renal compensation in acute hypoxia and dysregulation of cerebral perfusion predict AMS severity.
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