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001-es BibID:	BIBFORM077996
035-os BibID:	(PMID)30952206 (cikkazonosító)67
Első szerző:	Móré Elek Csaba (pszichiáter szakorvos)
Cím:	Altered irisin/BDNF axis parallels excessive daytime sleepiness in obstructive sleep apnea patients / Csaba E. More, Csaba Papp, Szilvia Harsanyi, Rudolf Gesztelyi, Angela Mikaczo, Gabor Tajti, Laszlo Kardos, Ildiko Seres, Hajnalka Lorincz, Krisztina Csapo, Judit Zsuga
Dátum:	2019
ISSN:	1465-9921
Megjegyzések:	Study objectives: Obstructive sleep apnea hypopnea syndrome (OSAHS) is a sleep-related breathing disorder, characterized by excessive daytime sleepiness (EDS), paralleled by intermittent collapse of the upper airway. EDS may be the symptom of OSAHS per se but may also be due to the alteration of central circadian regulation. Irisin is a putative myokine and has been shown to induce BDNF expression in several sites of the brain. BDNF is a key factor regulating photic entrainment and consequent circadian alignment and adaptation to the environment. Therefore, we hypothesized that EDS accompanying OSAHS is reflected by alteration of irisin/BDNF axis. Methods: Case history, routine laboratory parameters, serum irisin and BDNF levels, polysomnographic measures and Epworth Sleepiness Scale questionnaire (ESS) were performed in a cohort of OSAHS patients (n=69). Simple and then multiple linear regression was used to evaluate data. Results: We found that EDS reflected by the ESS is associated with higher serum irisin and BDNF levels; ?: 1.53; CI: 0.35, 6.15; p=0.012 and ?: 0.014; CI: 0.0.005, 0.023; p=0.02, respectively. Furthermore, influence of irisin and BDNF was significant even if the model accounted for their interaction (p=0.006 for the terms serum irisin, serum BDNF and their interaction). Furthermore, a concentration-dependent effect of both serum irisin and BDNF was evidenced with respect to their influence on the ESS. Conclusions: These results suggest that the irisin-BDNF axis influences subjective daytime sleepiness in OSAS patients reflected by the ESS. These results further imply the possible disruption of the circadian regulation in OSAHS. Future interventional studies are needed to confirm this observation.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban irisin BDNF sleep apnea circadian rhythm
Megjelenés:	Respiratory Research. - 20 : 1 (2019), p. 1-15. -
További szerzők:	Papp Csaba (1966-) (aneszteziológus és intenzív terápiás szakorvos) Kolozsváriné Harsányi Szilvia (1983-) (okleveles egészségpolitikai szakértő) Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Mikáczó Angéla (1980-) (tüdőgyógyász) Tajti Gábor (1988-) (gyógyszerész, biofizikus, sejtbiológus) Kardos László (1970-) (megelőző orvostan és népegészségtan szakorvos) Seres Ildikó (1954-) (biokémikus) Lőrincz Hajnalka (1986-) (biológus) Csapó Krisztina (1979-) (neurológus) Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager)
Pályázati támogatás:	EFOP-3.6.2-16-2017-00009 EFOP Establishing Thematic Scientific and Cooperation Network for Clinical Research GINOP-2.3.2-15-2016-00005 GINOP 2017-1.2.1-NKP-2017-00002 Egyéb
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM075286
035-os BibID:	(cikkazonosító)818
Első szerző:	Zsuga Judit (neurológus, pszichoterapeuta, egészségügyi szakmanager)
Cím:	Blind spot for sedentarism : redefining the diseasome of physical inactivity in view of circadian system and the irisin/BDNF axis / Judit Zsuga, Csaba E. More, Tamas Erdei, Csaba Papp, Szilvia Harsanyi, Rudolf Gesztelyi
Dátum:	2018
ISSN:	1664-2295
Megjegyzések:	Introduction: The term "diseasome of physical inactivity" was coined by Pedersen to explain clustering of chronic diseases linked to physical inactivity. Accordingly, physical inactivity per se contributes to the accumulation of visceral fat, which, generates chronic low-grade systemic inflammation, contributes to emergence of chronic, non-communicable diseases. Diversity of these disorders posits the possible involvement of a supraphysiological system. Methods: Hypothesis driven literature search and deductive reasoning was used to review relevant literature and formulate a novel theory. Results: We have identified the circadian system, omnipresent in virtually every cell, as a possible vehicle for brain muscle crosstalk, explaining some aspects of the diseasome of physical inactivity This system is hierarchically organized, with the suprachiasmatic nucleus (SCN) being the master clock that entrains to the dark/light cycle and synchronizes subsidiary molecular clocks in the periphery. Insufficient photic entrainment also causes chronic disease evolution. The recently identified irisin, was shown to induce brain-derived neurotrophic factor (BDNF) production in several brain areas. BDNF assumes significant role in gating light's influence in the retinohypothalamic synapse, by having a permissive effect on glutamate signal transduction underlying photic entrainment. Conclusions: Here we provide theoretical evidence to support the hypothesis that irisin may facilitate photic entrainment of the SCN, via BDNF. By this irisin opens up possible pathways for peripheral non-photic entrainment signals to exert influence on the master clock that is otherwise resistant to these. Furthermore, we suggest that intertwining processes of circadian, redox, inflammatory and myokine systems lay underneath the diseasome of physical inactivity.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban cirkadián ritmus circadian rhythm irisin BDNF
Megjelenés:	Frontiers in Neurology. - 9 (2018), p. 1-13. -
További szerzők:	Móré Elek Csaba (1966-) (pszichiáter szakorvos) Erdei Tamás Dániel (1992-) (kísérletes farmakológus) Papp Csaba (1966-) (aneszteziológus és intenzív terápiás szakorvos) Kolozsváriné Harsányi Szilvia (1983-) (okleveles egészségpolitikai szakértő) Gesztelyi Rudolf (1969-) (kísérletes farmakológus)
Pályázati támogatás:	EFOP-3.6.2-16-2017-00009 EFOP Establishing Thematic Scientific and Cooperation Network for Clinical Research GINOP-2.3.2-15-2016-00005 GINOP 2017-1.2.1-NKP-2017-00002 egyéb
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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