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001-es BibID:BIBFORM076737
035-os BibID:(WOS)000440106900010 (Scopus)85048661448
Első szerző:Csípő Tamás
Cím:Short-term weight loss reverses obesity-induced microvascular endothelial dysfunction / Tamas Csipo, Gabor A. Fulop, Agnes Lipecz, Stefano Tarantini, Tamas Kiss, Priya Balasubramanian, Anna Csiszar, Zoltan Ungvari, Andriy Yabluchanskiy
Dátum:2018
ISSN:2509-2715 2509-2723
Megjegyzések:Obesity is one of the major risk factors for cardiovascular diseases and its prevalence is increasing in all age groups, with the biggest impact observed in middle-aged and older adults. A critical mechanism by which obesity promotes vascular pathologies in these patients involves impairment of endothelial function. While endothelial dysfunction in large vessels promotes atherogenesis, obesity-induced microvascular endothelial dysfunction impairs organ perfusion and thereby is causally related to the pathogenesis of ischemic heart disease, chronic kidney disease, intermittent claudication, exercise intolerance, and exacerbates cognitive decline in aging. Reduction of weight via calorie-based diet and exercise in animal models of obesity results in significant improvement of endothelial function both in large vessels and in the microcirculation, primarily due to attenuation of oxidative stress and inflammation. Clinical data on the protective effects of weight loss on endothelial function is limited to studies of flow-mediated dilation assessed in brachial arteries. Currently, there is no guideline on testing the effects of different weight management strategies on microvascular endothelial function in obese patients. Here, we provide proof-of-concept that weight loss-induced improvement of microvascular endothelial function can be reliably assessed in the setting of a geriatric outpatient clinic using a fast, reproducible, non-invasive method: laser speckle contrast imaging-based measurement of endothelium-dependent microvascular responses during post-occlusive reactive hyperemia tests. Our study also provides initial evidence that short-term weight loss induced by consumption of a low-carbohydrate low-calorie diet can reverse microvascular endothelial dysfunction associated with obesity.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Weight loss
Obesity
Endothelial function
Aging
Megjelenés:GeroScience. - 40 : 3 (2018), p. 337-346. -
További szerzők:Fülöp Gábor Áron (1988-) (általános orvos) Lipécz Ágnes Tarantini, Stefano Kiss Tamás Balasubramanian, Priya Csiszár Anna Ungvári Zoltán Yabluchanskiy, Andriy
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2.

001-es BibID:BIBFORM108985
035-os BibID:(scopus)85065594719 (wos)000467562000011
Első szerző:Fülöp Gábor Áron (általános orvos)
Cím:Role of age-related alterations of the cerebral venous circulation in the pathogenesis of vascular cognitive impairment / Fulop Gabor A., Tarantini Stefano, Yabluchanskiy Andriy, Molnar Andrea, Prodan Calin I., Kiss Tamas, Csipo Tamas, Lipecz Agnes, Balasubramanian Priya, Farkas Eszter, Toth Peter, Sorond Farzaneh, Csiszar Anna, Ungvari Zoltan
Dátum:2019
ISSN:0363-6135
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 316 : 5 (2019), p. H1124-H1140. -
További szerzők:Tarantini, Stefano Yabluchanskiy, Andriy Molnár Andrea (Budapest) Prodan, Calin I. Kiss Tamás Csípő Tamás (1990-) Lipécz Ágnes Balasubramanian, Priya Farkas Eszter Tóth Péter Sorond, Farzaneh A. Csiszár Anna Ungvári Zoltán
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM082128
035-os BibID:(WOS)000494370900001 (Scopus)85074926339
Első szerző:Fülöp Gábor Áron (általános orvos)
Cím:Cerebral venous congestion promotes blood-brain barrier disruption and neuroinflammation, impairing cognitive function in mice / Gabor A. Fulop, Chetan Ahire, Tamas Csipo, Stefano Tarantini, Tamas Kiss, Priya Balasubramanian, Andriy Yabluchanskiy, Eszter Farkas, Attila Toth, Ádám Nyúl-Tóth, Peter Toth, Anna Csiszar, Zoltan Ungvari
Dátum:2019
ISSN:2509-2715 2509-2723
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:GeroScience. - 41 : 5 (2019), p. 575-589. -
További szerzők:Ahire, Chetan Csípő Tamás (1990-) Tarantini, Stefano Kiss Tamás Balasubramanian, Priya Yabluchanskiy, Andriy Farkas Eszter Tóth Attila (1971-) (biológus) Nyúl-Tóth Ádám Tóth Péter Csiszár Anna Ungvári Zoltán
Pályázati támogatás:EFOP-3.6.1-16-2016-00008, 20765-3/2018/FEKUTSTRAT
EFOP
EFOP-3.6.2.-16-2017-00008
EFOP
GINOP-2.3.2-15-2016-00048
GINOP
GINOP-2.3.3-15-2016-00032
GINOP
NKFI-FK123798
NKFIH
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM082129
035-os BibID:(WOS)000493693900001 (Scopus)85074812973
Első szerző:Tarantini, Stefano
Cím:Treatment with the poly(ADP-ribose) polymerase inhibitor PJ-34 improves cerebromicrovascular endothelial function, neurovascular coupling responses and cognitive performance in aged mice, supporting the NAD+ depletion hypothesis of neurovascular aging / Tarantini Stefano, Yabluchanskiy Andriy, Csipo Tamas, Fulop Gabor, Kiss Tamas, Balasubramanian Priya, DelFavero Jordan, Ahire Chetan, Ungvari Anna, Nyúl-Tóth Ádám, Farkas Eszter, Benyo Zoltan, Tóth Attila, Csiszar Anna, Ungvari Zoltan
Dátum:2019
ISSN:2509-2715 2509-2723
Megjegyzések:Adjustment of cerebral blood flow (CBF) to neuronal activity via neurovascular coupling (NVC) plays an important role in the maintenance of healthy cognitive function. Strong evidence demonstrates that age-related cerebromicrovascular endothelial dysfunction and consequential impairment of NVC responses contribute importantly to cognitive decline. Recent studies demonstrate that NAD(+) availability decreases with age in the vasculature and that supplemental NAD(+) precursors can ameliorate cerebrovascular dysfunction, rescuing NVC responses and improving cognitive performance in aged mice. The mechanisms underlying the age-related decline in [NAD(+)] in cells of the neurovascular unit are likely multifaceted and may include increased utilization of NAD(+) by activated poly (ADP-ribose) polymerase (PARP-1). The present study was designed to test the hypothesis that inhibition of PARP-1 activity may confer protective effects on neurovascular function in aging, similar to the recently demonstrated protective effects of treatment with the NAD+ precursor nicotinamide mononucleotide (NMN). To test this hypothesis, 24-month-old C57BL/6 mice were treated with PJ-34, a potent PARP inhibitor, for 2 weeks. NVC was assessed by measuring CBF responses (laser speckle contrast imaging) in the somatosensory whisker barrel cortex evoked by contralateral whisker stimulation. We found that NVC responses were significantly impaired in aged mice. Treatment with PJ-34 improved NVC responses by increasing endothelial NO-mediated vasodilation, which was associated with significantly improved spatial working memory. PJ-34 treatment also improved endothelium-dependent acetylcholine-induced relaxation of aorta rings. Thus, PARP-1 activation, likely by decreasing NAD(+) availability, contributes to age-related endothelial dysfunction and neurovascular uncoupling, exacerbating cognitive decline. The cerebromicrovascular protective effects of pharmacological inhibition of PARP-1 highlight the preventive and therapeutic potential of treatments that restore NAD+ homeostasis as effective interventions in patients at risk for vascular cognitive impairment (VCI).
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Cellular energetics
Oxidative stress
ROS
Endothelial dysfunction
Functional hyperemia
Microcirculation
Senescence
Megjelenés:GeroScience. - 41 : 5 (2019), p. 533-542. -
További szerzők:Yabluchanskiy, Andriy Csípő Tamás (1990-) Fülöp Gábor Áron (1988-) (általános orvos) Kiss Tamás Balasubramanian, Priya DelFavero, Jordan Ahire, Chetan Ungvári Anna Nyúl-Tóth Ádám Farkas Eszter Benyó Zoltán Tóth Attila (1971-) (biológus) Csiszár Anna Ungvári Zoltán
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Intézményi repozitóriumban (DEA) tárolt változat
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