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Fahed Hakim

Researcher at Technion – Israel Institute of Technology

Publications -  62
Citations -  2113

Fahed Hakim is an academic researcher from Technion – Israel Institute of Technology. The author has contributed to research in topics: Spirometry & Sleep apnea. The author has an hindex of 20, co-authored 55 publications receiving 1554 citations. Previous affiliations of Fahed Hakim include Nazareth Hospital EMMS & University of Chicago.

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Fragmented Sleep Accelerates Tumor Growth and Progression through Recruitment of Tumor-Associated Macrophages and TLR4 Signaling

TL;DR: It was found that sleep fragmentation enhanced tumor size and weight compared with control mice, and the more aggressive features produced by sleep fragmentation persisted, but were abolished completely in TLR4(-/-) mice.
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Intermittent hypoxia-induced changes in tumor-associated macrophages and tumor malignancy in a mouse model of sleep apnea.

TL;DR: The notion that IH-induced alterations in TAMs participate in the adverse cancer outcomes reported in OSA is supported, as well as the possibility that these alterations are limited to tumor-associated macrophages.
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Activation of the reward system boosts innate and adaptive immunity

TL;DR: It is shown that activation of the ventral tegmental area (VTA), a key component of the reward system, strengthens immunological host defense and establishes a causal relationship between the activity of the VTA and the immune response to bacterial infection.
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Sleep fragmentation induces cognitive deficits via nicotinamide adenine dinucleotide phosphate oxidase-dependent pathways in mouse.

TL;DR: An important role for NADPH oxidase is substantiated in hippocampal memory impairments induced by SF, which is expected to minimize hippocampal impairments from both intermittent hypoxia and SF associated with the disease.
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Disrupted sleep without sleep curtailment induces sleepiness and cognitive dysfunction via the tumor necrosis factor-α pathway.

TL;DR: It is shown that recurrent arousals during sleep, as happens during sleep apnea, induce excessive sleepiness via activation of inflammatory mechanisms, and more specifically TNF-α-dependent pathways, despite preserved sleep duration.