Publications by authors named "O Rawashdeh"

Melatonin supplementation strengthens non-restorative sleep rhythms and its temporal alignment in both humans and night-active rodents. Of note, although the sleep cycle is reversed in day-active and night-active (nocturnal) mammals, both, produce melatonin at night under the control of the circadian clock. The effects of exogenous melatonin on sleep and sleepiness are relatively clear, but its endogenous role in sleep, particularly, in timing sleep onset (SO), remains poorly understood.

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Article Synopsis
  • The suprachiasmatic nucleus (SCN) in the hypothalamus is the central control hub for circadian rhythms in mammals, producing various neurotransmitters.
  • Researchers confirmed the presence of β-adrenergic receptors in the SCN and examined their effects on energy signaling through cAMP-regulated elements.
  • The study's findings suggest that stress-related increases in adrenaline can impact circadian functions and may help explain side effects of β-blockers used for hypertension.
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  • Thyroid hormones (THs) play a crucial role in regulating energy metabolism, particularly in the liver, where they influence lipid and cholesterol levels as well as overall energy availability.
  • A study using a mouse model of hypothyroidism found that low TH levels reduced activity, food intake, and body temperature primarily during the active phase, with minimal effects on liver gene expression compared to high TH levels.
  • Circadian analysis revealed changes in gene expression patterns related to cholesterol metabolism in low-TH mice, identifying 516 genes as potential markers for assessing liver TH state throughout the day.
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Poor sleep is thought to enhance pain via increasing peripheral and/or central sensitization. Aerobic exercise, conversely, relives pain via reducing sensitization, among other mechanisms. This raises two clinical questions: (1) does poor sleep contribute to the transition from acute-to-persistent pain, and (2) can exercise protect against this transition? This study tested these questions and explored underlying mechanisms in a controlled injury model.

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Graft-versus-host disease (GVHD) is a serious complication of otherwise curative allogeneic haematopoietic stem cell transplants. Chronic GVHD induces pathological changes in peripheral organs as well as the brain and is a frequent cause of late morbidity and death after bone-marrow transplantation. In the periphery, bone-marrow-derived macrophages are key drivers of pathology, but recent evidence suggests that these cells also infiltrate into cGVHD-affected brains.

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