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1.

001-es BibID:BIBFORM125809
Első szerző:Ádám Dorottya (molekuláris biológus)
Cím:The TRPM5 antagonist triphenylphosphine oxide increases sebaceous lipogenesis and modulates immune phenotype of human sebocytes in a TRPM5-independent manner / Ádám D., Arany J., Tóth K. F., Petö O., Nyitrai T., Tóth B. I., Póliska S., Zouboulis C. C., Oláh A.
Dátum:2024
Megjegyzések:It has recently been shown that transient receptor potential melastatin 5 (TRPM5) ion channels contributed to the maintenance of the anagen phase of the hair cycle. Because adjacent sebaceous glands also exhibited TRPM5 immunopositivity, topically applied TRPM5 modulators administered with the intention to influence hair growth may also affect sebaceous glands (SGs). Hence, we aimed to assess expression of TRPM5 as well as effects of 2 agonists and 1 antagonist (triphenylphosphine oxide [TPPO]) of TRPM5 on human SZ95 sebocytes. First, using complementary methods (RNA-Seq, RT-qPCR, western blot, siRNA-mediated gene silencing, fluorescent Na+- and Ca2+-measurements), we found that TRPM5 is not expressed in human sebocytes in a functionally active form.While non- cytotoxic (MTT-assay) concentrations of the activators were ineffective, TPPO promoted sebaceous lipogenesis (Nile Red). This effect was TRPM5-independent and was found to be mediated in an Akt- and epidermal growth factor receptor (EGFR)-dependent manner, most likely via the Akt-induced up-regulation of diacylglycerol O-acyltransferase-2. Moreover, TPPO up-regulated interleukin (IL)-6 in an EGFR- and p38a MAPKdependent manner (RT-qPCR), while it decreased release of IL-8 (ELISA), and it down-regulated additional pro-inflammatory cytokines (chemokine (C-X-C motif) ligand [CXCL]-1, CXCL2, CXCL6, colony-stimulating factor 2, IL-32). Collectively, specific TRPM5 modulators are unlikely to exert direct SG-related side effects, while safe TPPO analogues may induce beneficial moderate lipogenic and anti-inflammatory effects in dry skin dermatoses.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
sebocyte
acne
TRPM5
TPPO
Megjelenés:The Journal of Investigative Dermatology. - 144 : 12_Suppl (2024), p. S313. -
További szerzők:Arany József (1990-) (klinikai laboratóriumi kutató, vegyész) Tóth Kinga Fanni (1992-) (molekuláris biológus, élettanász) Pető Orsolya Nyitrai Tamara (1999-) (molekuláris biológus) Tóth István Balázs (1978-) (élettanász) Póliska Szilárd (1978-) (biológus) Zouboulis, Christos C. (1960-) (bőrgyógyász) Oláh Attila (1984-) (élettanász)
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Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM116424
Első szerző:Ádám Dorottya (molekuláris biológus)
Cím:The TRPM5 antagonist TPPO increases sebaceous lipogenesis and exerts pro-inflammatory effects via activation of Akt and p38 MAPK cascades / Ádám D., Arany J., Pető O., Tóth B. I., Zouboulis C. C., Oláh A.
Dátum:2023
ISSN:0022-202X 1523-1747
Megjegyzések:We have previously shown that transient receptor potential vanilloid (TRPV)-1, -3, and -4 ion channels are negative regulators of sebaceous lipogenesis. Moreover, the transient receptor potential melastatin 5 (TRPM5) was recently demonstrated to be expressed in human hair follicles, where its homeostatic activity appeared to promote the anagen phase (PMID: 33773986). Because the immunofluorescent images published in said article indicated that sebaceous glands also exhibited TRPM5 positivity, TRPM5 modulators administered with the intention of influencing hair growth may also have an unintended impact on sebaceous gland functions. Thus, we aimed to investigate the effects of TRPM5 modulators on human SZ95 sebocytes. SZ95 sebocytes were treated with TRPM5 modulators (activators: 2,5-dimethylpyrazine [DMP], 2-heptanone [HEP]; antagonist: triphenylphosphine oxide [TPPO]), and viability (MTT-assay), lipid synthesis (Nile Red labeling), gene expression (Q-PCR, western blot), mediator release (ELISA), as well as time-dependent activation of relevant second messenger pathways (phosphokinase array) were monitored. Expression of TRPM5 was knocked down by siRNA-transfection. Expression of TRPM5 was found to be around detection limit at the mRNA level, and western blotting did not produce bands at the predicted molecular weights either. Because siRNA-mediated silencing of TRPM5 failed to alter the intensity of the apparently nonspecific bands, we concluded that TRPM5 is most likely not expressed in human sebocytes. Furthermore, we found that the activators did not influence viability and lipid synthesis. Interestingly TPPO promoted sebaceous lipogenesis, and increased interleukin (IL)-6 expression and release. Phosphokinase array revealed the time-dependent activation of several kinase cascades in response to TPPO-treatment. Using pharmacological inhibitors, we could demonstrate that lipogenic effect of TPPO was mediated via the activation of the Akt1/2/3 and p38 MAPK. We concluded that the use of TPPO is likely to influence sebaceous gland biology via activating certain cellular off-targets.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
TRPM5
sebocyte
TPPO
acne
dry skin
Megjelenés:Journal Of Investigative Dermatology. - 143 : 11 (2023), p. S354. -
További szerzők:Arany József (1990-) (klinikai laboratóriumi kutató, vegyész) Pető Orsolya Tóth István Balázs (1978-) (élettanász) Zouboulis, Christos C. (1960-) (bőrgyógyász) Oláh Attila (1984-) (élettanász)
Pályázati támogatás:EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
EFOP-3.6.1-16-2016-00022
EFOP
134235
OTKA
ÚNKP-23-5-DE-477
Egyéb
János Bolyai Research Scholarship
MTA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

3.

001-es BibID:BIBFORM116425
Első szerző:Arany József (klinikai laboratóriumi kutató, vegyész)
Cím:Adenosine receptors are novel regulators of human sebocyte biology / Arany J., Ádám D., Cseszlai M., Nyitrai T., Zouboulis C. C., Oláh A.
Dátum:2023
ISSN:0022-202X 1523-1747
Megjegyzések:We have previously shown that (-)-cannabidiol, a non-psychotropic phytocannabinoid, exerted complex anti-acne effects, some of which were found to be mediated by the A2A adenosine receptor. Thus, in the current study, we aimed to investigate the expression and functional role of adenosine receptors on human SZ95 sebocytes. First, besides confirming the expression of A2A receptor, we showed that A1 and A2B adenosine receptors were also expressed in human sebocytes (Q-PCR, western blot), whereas expression of A3 was found to be around detection limit (Q-PCR). Next, by using non-cytotoxic concentrations (MTT-assay) of selective modulators of A2A and A2B receptors, we found that administration of the A2B agonist BAY 60-6583 led to a small, but significant increase in the basal, homeostatic sebaceous lipogenesis, while the A2B antagonist alloxazine reduced the lipid synthesis (24- and 48-hour treatments; Nile Red). Interestingly, administration of ZM 241385 (an A2A antagonist that can also block A2B receptor at higher concentrations) resulted in a concentration-dependent decrease of the lipid synthesis in course of 24-hr treatments, but did not influence lipogenesis in case of longer (48-hr) experiments (Nile Red). Importantly, the A2A agonist CGS 21680 slightly, but significantly decreased basal sebaceous lipogenesis (24- and 48-hr treatments; Nile Red), and could also suppress the lipogenic effect of the "acne-mimicking" inflammatory lipid mediator arachidonic acid (48-hr treatments; Nile Red). Last, but not least, our preliminary data suggest that activation of A2A, but, intriguingly, not of A2B, receptor is efficient in suppressing the Toll-like receptor 4 activator lipopolysaccharide-induced pro-inflammatory response as well (Q-PCR). Taken together, our data indicate that several adenosine receptors are expressed on human sebocytes. These receptors differentially influence sebocyte biology, and activation of A2A receptor appears to exert promising anti-acne effects in our in vitro model systems.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
sebocyte
acne
adenosine receptor
sebaceous lipogenesis
Megjelenés:Journal Of Investigative Dermatology. - 143 : Suppl_11 (2023), p. S355. -
További szerzők:Ádám Dorottya (1991-) (molekuláris biológus) Cseszlai M. Nyitrai Tamara (1999-) (molekuláris biológus) Zouboulis, Christos C. (1960-) (bőrgyógyász) Oláh Attila (1984-) (élettanász)
Pályázati támogatás:EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
EFOP-3.6.1-16-2016-00022
EFOP
János Bolyai Research Scholarship
MTA
134235
OTKA
ÚNKP-23-5-DE-477
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM125810
Első szerző:Dull Katalin (molekuláris biológus, genetikus)
Cím:Sebum lipids selectively modulate gene expression in keratinocytes / Dull K., Ádám D., Póliska S., Aboud H., Szegedi A., Oláh A., Töröcsik D.
Dátum:2024
ISSN:0022-202X 1523-1747
Megjegyzések:Changes in sebum quantity and composition have been reported in several skin diseases, suggesting a (patho) physiological role, but their effect on different cell types is not well characterized. Based on our previous findings that sebum lipids can penetrate the epidermis, this study aimed to investigate their effects on keratinocytes using pro-inflammatory (stearic acid and palmitic acid), anti- inflammatory lipids (linoleic acid and oleic acid) and squalene. In our experimental settings, HaCaT keratinocytes in subconfluent cultures with high proliferation rates (representing basal epidermal keratinocytes) and those in advanced differentiation in postconfluent cultures maintained under high Ca2+ concentrations (representing suprabasal epidermal layers) were treated with different sebum-composing lipids. The cell differentiation state was validated by measuring the expression of markers by RT-qPCR, and whole transcriptome analysis was performed using STRING platform. We found that keratinocytes exhibited differentiation-dependent unique gene expression patterns in response to the lipids. While squalene had the most significant effect on proliferating keratinocytes, palmitic and oleic acid treatments had a greater effect on differentiated cells. All lipids influenced cell proliferation and pathways related to cell cycle regulation. All treatments affected immune system-related pathways: in both differentiated and proliferating keratinocytes squalene, palmitic acid, and stearic acid treatments affected IL-17 signaling, cytokine signaling, interferon a/b, and TLR signaling. In this regard, the effect of stearic acid was the least pronounced. In conclusion, our results suggest that keratinocytes are able to selectively recognize and respond to the different lipids that make up sebum. Further characterization of the pathways involved may bring us closer to understanding the relevance of changes in sebum composition in different conditions such as acne and may provide the basis for improving sebum modulation therapies.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
sebocyte
acne
keratinocyte
Megjelenés:Journal Of Investigative Dermatology. - 144 : 12 (2024), p. S264. -
További szerzők:Ádám Dorottya (1991-) (molekuláris biológus) Póliska Szilárd (1978-) (biológus) Aboud, H. Szegedi Andrea (1964-) (bőrgyógyász) Oláh Attila (1984-) (élettanász) Töröcsik Dániel (1979-) (bőrgyógyász)
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM083558
035-os BibID:(WOS)000574374700009 (Scopus)85083011579
Első szerző:Markovics Arnold (molekuláris biológus)
Cím:GPR119 is a potent regulator of human sebocyte biology / Arnold Markovics, Ágnes Angyal, Kinga Fanni Tóth, Dorottya Ádám, Zsófia Pénzes, József Magi, Ágnes Pór, Ilona Kovács, Dániel Törőcsik, Christos C. Zouboulis, Tamás Bíró, Attila Oláh
Dátum:2020
ISSN:0022-202X 1523-1747
Megjegyzések:We have previously shown that endocannabinoids promote sebaceous lipogenesis, and sebocytes are involved in the metabolism of the "endocannabinoid-like" substance oleoylethanolamide (OEA). OEA is an endogenous activator of GPR119, a recently de-orphanized receptor, which is currently being investigated as a promising anti-diabetic drug target. Thus, in the current study, we investigated the effects of OEA as well as the expression and role of GPR119 in human sebocytes. We found that OEA promoted differentiation of human SZ95 sebocytes (elevated lipogenesis, enhanced granulation, and the induction of early apoptotic events), and it switched the cells to a pro-inflammatory phenotype (increased expression and release of several pro-inflammatory cytokines). Moreover, we could also demonstrate that GPR119 was expressed in human sebocytes, and its siRNA-mediated gene silencing suppressed OEA-induced sebaceous lipogenesis, which was mediated via JNK, ERK1/2, Akt/PKB, and CREB activation. Finally, our pilot data demonstrated that GPR119 was down-regulated in sebaceous glands of acne patients, arguing that GPR119 signaling may indeed be disturbed in acne. Collectively, our findings introduce the OEA?GPR119 signaling as a new positive regulator of sebocyte differentiation, and highlight the possibility that dysregulation of this pathway may contribute to the development of seborrhea and acne.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
GPR119
acne
sebocyte
oleoylethanolamide
seborrhea
inflammation
Megjelenés:Journal of Investigative Dermatology. - 140 : 10 (2020), p. 1909-1918. -
További szerzők:Angyal Ágnes (1987-) (molekuláris biológus) Tóth Kinga Fanni (1992-) (molekuláris biológus, élettanász) Ádám Dorottya (1991-) (molekuláris biológus) Pénzes Zsófia (1992-) (klinikai laboratóriumi kutató) Magi József Pór Ágnes Kovács Ilona (1965-) (patológus) Töröcsik Dániel (1979-) (bőrgyógyász) Zouboulis, Christos C. (1960-) (bőrgyógyász) Bíró Tamás (1968-) (élettanász) Oláh Attila (1984-) (élettanász)
Pályázati támogatás:120552
OTKA
121360
OTKA
125055
OTKA
Bolyai János Kutatási Ösztöndíj
MTA
GINOP-2.3.2-15-2016-00050
GINOP
Galderma Acne and Rosacea Basic Research Award
Egyéb
ÚNKP-19-4-DE-287
Egyéb
ÚNKP-19-4-DE-15
Egyéb
ÚNKP-19-3-I-DE-141
Egyéb
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

6.

001-es BibID:BIBFORM116427
Első szerző:Tóth Kinga Fanni (molekuláris biológus, élettanász)
Cím:Fluoxetine exerts anti-inflammatory effects on human epidermal keratinocytes, and suppresses their endothelin release / Tóth K. F., Ádám D., Arany J., Ramirez Y. A., Bíró T., Drake J. I., O'Mahony A., Szöllősi A. G., Kilic A., Soeberdt M., Abels C., Oláh A.
Dátum:2023
ISSN:0022-202X 1523-1747
Megjegyzések:Pathological activity Toll-like receptor (TLR)-3 plays an important role in the pathogenesis of pruritic dermatoses and in the development of itch. Fluoxetine is a safe antidepressant with remarkable anti-inflammatory actions in various systems, including the skin. Thus, we aimed to investigate the effects of fluoxetine in a TLR3-activator induced inflammatory model by using immortalized (HaCaT) as well as primary human epidermal keratinocytes. When applied at a non-cytotoxic concentration (MTT-assay, CyQUANT-assay), fluoxetine significantly suppressed polyinosinic-polycytidylic acid (p(I:C))-induced expression and release of several proinflammatory cytokines, and it decreased the release of the itch mediator endothelins (Q-PCR, cytokine array, ELISA). Fluoxetine did not interfere with the p(I:C)-induced activation of the p38 MAPK cascade, and did not inhibit phosphorylation (and hence inactivation) of IkBa, an important inhibitor of the NF-kB pathway (western blot). Moreover, co-administration of fluoxetine failed to significantly suppress p(I:C)-induced elevation ofmitochondrial ROS production (MitoSOX Red). Instead, the anti-inflammatory effects of fluoxetine were most likely mediated via the inhibition of the phosphoinositide 3-kinase (PI3K)-pathway (unbiased activity profiling). Importantly, the PI3K-inhibitor GDC0941 fully mimicked the effects of fluoxetine. Although fluoxetine was found to be able to occupy the binding site of GDC0941 (in silico molecular docking), and to exert direct inhibitory effect on PI3K, it exhibited much lower potency and efficacy as compared to GDC0941 (cell-free PI3K activity assay). Collectively, our findings demonstrate that fluoxetine exerts potent anti-inflammatory effects, and suppresses the release of the endogenous itch mediator endothelins in human keratinocytes, most likely via indirect inhibition of PI3K. Thus, clinical studies are encouraged to explore whether the currently reported beneficial effects translate in vivo following its topical administration in inflammatory and pruritic dermatoses. Supported by: NRDIO (125055, 134235, 134993, GINOP-2.3.2-15-2016-00015, GINOP-2.3.3-15-2016-00020, EFOP-3.6.3-VEKOP-16-2017-00009); János Bolyai Research Scholarship; ÚNKP-23-5-DE-477; "Deutscher Akademischer Austauschdienst" (DAAD); Dr. AugustWolff GmbH & Co. KG Arzneimittel.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
fluoxetine
itch
inflammation
skin
keratinocyte
endothelin
Toll-like receptor 3
Megjelenés:Journal Of Investigative Dermatology. - 143 : 11 (2023), p. S361. -
További szerzők:Ádám Dorottya (1991-) (molekuláris biológus) Arany József (1990-) (klinikai laboratóriumi kutató, vegyész) Ramirez, Yesid A. Bíró Tamás (1968-) (élettanász) (absztraktok) Drake, Jennifer I. O'Mahony, Alison Szöllősi Attila Gábor (1982-) (élettanász) Kilic, Ana Soeberdt, Michael Abels, Christoph Oláh Attila (1984-) (élettanász)
Pályázati támogatás:125055
OTKA
134235
OTKA
134993
OTKA
GINOP-2.3.2-15-2016-00015
GINOP
GINOP-2.3.3-15-2016-00020
GINOP
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
János Bolyai Research Scholarship
MTA
ÚNKP-23-5-DE-477
Egyéb
Deutscher Akademischer Austauschdienst
Egyéb
Dr. AugustWolff GmbH & Co. KG Arzneimittel
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

7.

001-es BibID:BIBFORM115844
Első szerző:Tóth Kinga Fanni (molekuláris biológus, élettanász)
Cím:Fluoxetine exerts anti-inflammatory effects on human epidermal keratinocytes, and suppresses endothelin release via inhibiting PI3K / Tóth K., Ádám D., Arany J., Ramirez Y. A., Bíró T., Drake J. I., O'Mahony A., Szöllösi A. G., Kilic A., Soeberdt M., Abels C., Oláh A.
Dátum:2023
ISSN:0022-202X 1523-1747
Megjegyzések:Fluoxetine (FX) is a safe antidepressant belonging to the group of selective serotonin reuptake inhibitors. It exhibits remarkable anti-inflammatory activity in various systems; thus, we aimed to investigate its biological effects on immortalized (HaCaT) and primary human epidermal keratinocytes. We found that, when applied at its highest non-cytotoxic concentration (14 mM), FX significantly suppressed the Toll-like receptor 3 activator polyinosinicpolycytidylic acid (p(I:C))-induced expression (Q-PCR: interleukin [IL]-1a, IL-1b, and IL-8) and release (cytokine array and ELISA: IL-8) of several pro-inflammatory cytokines, and it decreased the release of the itch mediator endothelins as well. Surprisingly, unbiased activity profiling revealed that the effects of FX (4.7 and 14 mM) did not resemble the effects of different doses of serotonin, but were rather similar to the effects of the phosphoinositide 3-kinase (PI3K) inhibitor GDC0941 (370 nM). In addition, GDC0941 mimicked the effects of FX in our experimental models, and in silico docking analysis revealed that FX may be able to occupy the same binding site on PI3K isoenzymes as GDC0941. Finally, we found that FX was indeed able to directly suppress activity of PI3K (cell-free PI3K activity assay). Collectively, our findings demonstrate that FX (14 mM) exerts potent anti-inflammatory effects, and suppresses the release of the endogenous itch mediator endothelins in human keratinocytes, most likely via the inhibition of PI3K. Thus, our data highlight the possibility of dermatological repositioning of FX to treat various inflammatory and pruritic dermatoses.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
fluoxetine
keratinocyte
itch
inflammation
Megjelenés:Journal Of Investigative Dermatology. - 143 : 5 (2023), p. S126. -
További szerzők:Ádám Dorottya (1991-) (molekuláris biológus) Arany József (1990-) (klinikai laboratóriumi kutató, vegyész) Ramirez, Yesid A. Bíró Tamás (1968-) (élettanász) (absztraktok) Drake, Jennifer I. O'Mahony, Alison Szöllősi Attila Gábor (1982-) (élettanász) Kilic, Ana Soeberdt, Michael Abels, Christoph Oláh Attila (1984-) (élettanász)
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

8.

001-es BibID:BIBFORM082876
035-os BibID:(WOS)000485661500602
Első szerző:Tóth Kinga Fanni (molekuláris biológus, élettanász)
Cím:The putative tribbles homolog 3 (TRIB3) activator honokiol suppresses lipogenesis, and exerts anti-proliferative as well as anti-inflammatory effects on human sebocytes / Tóth K., Ádám D., Arany J., Faragó P., Arbiser J. L., Zouboulis C. C., Bíró T., Oláh A.
Dátum:2019
Megjegyzések:We have previously shown that cannabidiol (CBD) exerts complex anti-acne effects in vitro, and in vivo efficiency of topically administered CBD in moderate to severe acne is currently being assessed in a phase II clinical trial (ID at clinicaltrials.gov: NCT03573518). We have also demonstrated that anti-acne effects of CBD were at least in part mediated by the activation/upregulation of tribbles homolog 3 (TRIB3). Thus, here, we aimed to assess the effects of the plantderived TRIB3-activator honokiol (HNK) on human SZ95 sebocytes. We showed that, up to 20 uM, HNK did not impair viability (24/48 hrs; MTT-assay), but concentration-dependently decreased sebaceous lipogenesis (SLG) (24/48 hrs; Nile Red). To explore its putative anti-acne potential, we further assessed the effects of HNK on arachidonic acid (AA)-induced enhanced, acne-mimicking SLG. Importantly, non-cytotoxic HNK concentrations suppressed the lipogenic action of AA (24/48 hrs; Nile Red), and exerted significant anti-proliferative actions (72 hrs; CyQUANT-assay). Moreover, HNK was able to suppress the lipopolysaccharide-induced proinflammatory response of human sebocytes, as monitored by the expression (interleukin [IL]-1a, IL-1b, IL-6, IL-8, and tumor necrosis factor-a) and release (IL-8) of pro-inflammatory cytokines (3 hrs; Q-PCR and ELISA). Collectively, our data demonstrate that HNK exhibits complex anti-acne effects in vitro. These findings may therefore encourage the systematic exploration of topically applied HNK in the clinical management of acne.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
acne
honokiol
sebaceous lipid synthesis
inflammation
TRIB3
sebocyte
Megjelenés:Journal of Investigative Dermatology. - 139 : 9S (2019), p. S319. -
További szerzők:Ádám Dorottya (1991-) (molekuláris biológus) Arany József (1990-) (klinikai laboratóriumi kutató, vegyész) Faragó Péter Arbiser, J. L. Zouboulis, Christos C. (1960-) (bőrgyógyász) Bíró Tamás (1968-) (élettanász) (absztraktok) Oláh Attila (1984-) (élettanász)
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Intézményi repozitóriumban (DEA) tárolt változat
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