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1.
Cureus ; 16(1): e51616, 2024 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-38313965

RESUMO

Pectoralis major (PM) tendon ruptures are rare. Typically, they are caused by eccentric contractions from weight lifting. Due to the rarity of pectoralis major tendon ruptures, clinicians might misdiagnose this condition. We report a 16-year-old male with a right pectoralis major tendon rupture and an avulsion fracture after falling on a grass field playing soccer. He was initially misdiagnosed with biceps tendonitis, which highlights the importance of including pectoralis major tendon ruptures in one's differential diagnoses.

2.
Antioxidants (Basel) ; 12(5)2023 May 19.
Artigo em Inglês | MEDLINE | ID: mdl-37237990

RESUMO

Non-rapid eye movement sleep (NREMS) is accompanied by a decrease in cerebral metabolism, which reduces the consumption of glucose as a fuel source and decreases the overall accumulation of oxidative stress in neural and peripheral tissues. Enabling this metabolic shift towards a reductive redox environment may be a central function of sleep. Therefore, biochemical manipulations that potentiate cellular antioxidant pathways may facilitate this function of sleep. N-acetylcysteine increases cellular antioxidant capacity by serving as a precursor to glutathione. In mice, we observed that intraperitoneal administration of N-acetylcysteine at a time of day when sleep drive is naturally high accelerated the onset of sleep and reduced NREMS delta power. Additionally, N-acetylcysteine administration suppressed slow and beta electroencephalographic (EEG) activities during quiet wake, further demonstrating the fatigue-inducing properties of antioxidants and the impact of redox balance on cortical circuit properties related to sleep drive. These results implicate redox reactions in the homeostatic dynamics of cortical network events across sleep/wake cycles, illustrating the value of timing antioxidant administration relative to sleep/wake cycles. A systematic review of the relevant literature, summarized herein, indicates that this "chronotherapeutic hypothesis" is unaddressed within the clinical literature on antioxidant therapy for brain disorders such as schizophrenia. We, therefore, advocate for studies that systematically address the relationship between the time of day at which an antioxidant therapy is administered relative to sleep/wake cycles and the therapeutic benefit of that antioxidant treatment in brain disorders.

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