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001-es BibID:BIBFORM092976
Első szerző:Gebri Enikő Zsuzsa (fogszakorvos)
Cím:Salivary Osteopontin as a Potential Biomarker for Oral Mucositis / Enikő Gebri, Attila Kiss, Ferenc Tóth, Tibor Hortobágyi
Dátum:2021
Megjegyzések:Abstract: Osteopontin (OPN), a multifunctional phosphoglycoprotein also presents in saliva, plays a crucial role in tumour progression, inflammation and mucosal protection. Mucosal barrier injury due to high-dose conditioning regimen administered during autologous and allogeneic peripheral stem cell transplantation (APSCT) has neither efficient therapy nor established biomarkers. Our aim was to assess the biomarker role of OPN during APSCT, with primary focus on oral mucositis (OM). Serum and salivary OPN levels were determined by ELISA in 10 patients during APSCT at four stages of transplantation (day ??3/??7, 0, +7, +14), and in 23 respective healthy controls. Results: There was a negative correlation between both salivary and serum OPN levels and grade of OM severity during APSCT (r = ??0.791, p = 0.019; r = ??0.973, p = 0.001). Salivary OPN increased at days +7 (p = 0.011) and +14 (p = 0.034) compared to controls. Among patients, it was higher at day +14 compared to the time of admission (day ??3/??7) (p = 0.039) and transplantation (day 0) (p = 0.011). Serum OPN remained elevated at all four stages of transplantation compared to controls (p = 0.013, p = 0.02, p = 0.011, p = 0.028). During APSCT elevated salivary OPN is a potential non-invasive biomarker of oral mucositis whereas the importance of high serum OPN warrants further studies.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Metabolites. - 11 : 4 (2021), p. 1-16. -
További szerzők:Kiss Attila (1942-) (belgyógyász, haematológus) Tóth Ferenc (fogorvos) Hortobágyi Tibor (1965-) (patológus)
Internet cím:DOI
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001-es BibID:BIBFORM108726
035-os BibID:(cikkazonosító)270 (Scopus)85148902237 (WoS)000940561800001
Első szerző:Lőrincz Hajnalka (biológus)
Cím:Crucial Regulatory Role of Organokines in Relation to Metabolic Changes in Non-Diabetic Obesity / Lőrincz Hajnalka, Somodi Sándor, Ratku Balázs, Harangi Mariann, Paragh György
Dátum:2023
ISSN:2218-1989
Megjegyzések:Obesity is characterized by an excessive accumulation of fat leading to a plethora of medical complications, including coronary artery disease, hypertension, type 2 diabetes mellitus or impaired glucose tolerance and dyslipidemia. Formerly, several physiological roles of organokines, including adipokines, hepatokines, myokines and gut hormones have been described in obesity, especially in the regulation of glucose and lipid metabolism, insulin sensitivity, oxidative stress, and low-grade inflammation. The canonical effect of these biologically active peptides and proteins may serve as an intermediate regulatory level that connects the central nervous system and the endocrine, autocrine, and paracrine actions of organs responsible for metabolic and inflammatory processes. Better understanding of the function of this delicately tuned network may provide an explanation for the wide range of obesity phenotypes with remarkable inter-individual differences regarding comorbidities and therapeutic responses. The aim of this review is to demonstrate the role of organokines in the lipid and glucose metabolism focusing on the obese non-diabetic subgroup. We also discuss the latest findings about sarcopenic obesity, which has recently become one of the most relevant metabolic disturbances in the aging population.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
metabolically healthy obesity
non-diabetic obesity
adipokine
hepatokine
myokine
sarcopenic obesity
prediabetes
insulin resistance
cardiovascular risk
Megjelenés:Metabolites. - 13 : 2 (2023), p. 1-27. -
További szerzők:Somodi Sándor (1977-) (belgyógyász) Ratku Balázs (1985-) (mentőtiszt) Harangi Mariann (1974-) (belgyógyász, endokrinológus) Paragh György (1953-) (belgyógyász)
Pályázati támogatás:OTKA K142273
Egyéb
OTKA PD124126
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Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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