@book{MTMT:34446677,
	title = {2023. évi Orvos- és Egészségtudományi TDK Konferencia},
	url = {https://m2.mtmt.hu/api/publication/34446677},
	isbn = {9789633069592},
	editor = {Tolnai, József and Peták, Ferenc and Fodor, Gergely and Rakonczay, Zoltán},
	publisher = {Universití of Szeged},
	unique-id = {34446677},
	year = {2023},
	orcid-numbers = {Tolnai, József/0000-0002-7648-764X; Peták, Ferenc/0000-0001-6249-9327; Fodor, Gergely/0000-0002-4736-4966; Rakonczay, Zoltán/0000-0002-1499-3416}
}

@article{MTMT:34183455,
	title = {The anti-inflammatory effect of dimethyl trisulfide in experimental acute pancreatitis},
	url = {https://m2.mtmt.hu/api/publication/34183455},
	author = {Orján, Erik Márk and Kormányos, Eszter Sára and Fűr, Gabriella and Dombi, Ágnes and Bálint, Emese Réka and Balla, Zsolt and Balog, Beáta Adél and Dágó, Ágnes and Totonji, Ahmad and Bátai, István Zoárd and Jurányi, Eszter Petra and Ditrói, Tamás and Al-omari, Ammar and Pozsgai, Gábor and Kormos, Viktória and Nagy, Péter and Pintér, Erika and Rakonczay, Zoltán and Kiss, Lóránd},
	doi = {10.1038/s41598-023-43692-9},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {13},
	unique-id = {34183455},
	issn = {2045-2322},
	abstract = {Various organosulfur compounds, such as dimethyl trisulfide (DMTS), display anti-inflammatory properties. We aimed to examine the effects of DMTS on acute pancreatitis (AP) and its mechanism of action in both in vivo and in vitro studies. AP was induced in FVB/n mice or Wistar rats by caerulein, ethanol-palmitoleic acid, or L-ornithine-HCl. DMTS treatments were administered subcutaneously. AP severity was assessed by pancreatic histological scoring, pancreatic water content, and myeloperoxidase activity measurements. The behaviour of animals was followed. Pancreatic heat shock protein 72 (HSP72) expression, sulfide, and protein persulfidation were measured. In vitro acinar viability, intracellular Ca 2+ concentration, and reactive oxygen species production were determined. DMTS dose-dependently decreased the severity of AP. It declined the pancreatic infiltration of leukocytes and cellular damage in mice. DMTS upregulated the HSP72 expression during AP and elevated serum sulfide and low molecular weight persulfide levels. DMTS exhibited cytoprotection against hydrogen peroxide and AP-inducing agents. It has antioxidant properties and modulates physiological but not pathophysiological Ca 2+ signalling. Generally, DMTS ameliorated AP severity and protected pancreatic acinar cells. Our findings indicate that DMTS is a sulfur donor with anti-inflammatory and antioxidant effects, and organosulfur compounds require further investigation into this potentially lethal disease.},
	year = {2023},
	eissn = {2045-2322},
	orcid-numbers = {Orján, Erik Márk/0000-0003-4176-0834; Balog, Beáta Adél/0009-0008-3568-4090; Jurányi, Eszter Petra/0000-0002-0563-4876; Nagy, Péter/0000-0003-3393-235X; Pintér, Erika/0000-0001-9898-632X; Rakonczay, Zoltán/0000-0002-1499-3416}
}

@article{MTMT:33636629,
	title = {Suprapapillary Biliary Stents Have Longer Patency Times than Transpapillary Stents-A Systematic Review and Meta-Analysis.},
	url = {https://m2.mtmt.hu/api/publication/33636629},
	author = {Kovács, Norbert and Pécsi, Dániel and Sipos, Zoltán and Borbásné Farkas, Kornélia and Földi, Mária and Hegyi, Péter and Bajor, Judit and Erőss, Bálint Mihály and Márta, Katalin and Mikó, Alexandra and Rakonczay, Zoltán and Sarlós, Patrícia and Ábrahám, Szabolcs and Vincze, Áron},
	doi = {10.3390/jcm12030898},
	journal-iso = {J CLIN MED},
	journal = {JOURNAL OF CLINICAL MEDICINE},
	volume = {12},
	unique-id = {33636629},
	abstract = {Endoscopic biliary stent placement is a minimally invasive intervention for patients with biliary strictures. Stent patency and function time are crucial factors. Suprapapillary versus transpapillary stent positioning may contribute to stent function time, so a meta-analysis was performed in this comparison.A comprehensive literature search was conducted in the CENTRAL, Embase, and MEDLINE databases to find data on suprapapillary stent placement compared to the transpapillary method via endoscopic retrograde cholangiopancreatography in cases of biliary stenosis of any etiology and any stent type until December 2020. We carried out a meta-analysis focusing on the following outcomes: stent patency, stent migration, rate of cholangitis and pancreatitis, and other reported complications.Three prospective and ten retrospective studies involving 1028 patients were included. Suprapapillary stent placement appeared to be superior to transpapillary stent positioning in patency (weighted mean difference = 50.23 days, 95% CI: 8.56, 91.98; p = 0.0.018). In a subgroup analysis of malignant indications, suprapapillary positioning showed a lower rate of cholangitis (OR: 0.34, 95% CI: 0.13, 0.93; p = 0.036). Another subgroup analysis investigating metal stents in a suprapapillary position resulted in a lower rate of pancreatitis (OR: 0.16, 95% CI: 0.03, 0.95; p = 0.043) compared to transpapillary stent placement. There was no difference in stent migration rates between the two groups (OR: 0.67, 95% CI: 0.17, 2.72; p = 0.577).Based on our results, suprapapillary biliary stenting has longer stent patency. Moreover, the stent migration rate did not differ between the suprapapillary and transpapillary groups.},
	keywords = {endoscopy; Stent; ERCP; intraductal; inside; [Meta-analysis]},
	year = {2023},
	eissn = {2077-0383},
	orcid-numbers = {Pécsi, Dániel/0000-0003-0499-6004; Sipos, Zoltán/0000-0001-7845-8116; Borbásné Farkas, Kornélia/0000-0002-5349-6527; Hegyi, Péter/0000-0003-0399-7259; Erőss, Bálint Mihály/0000-0003-3658-8427; Márta, Katalin/0000-0002-2213-4865; Rakonczay, Zoltán/0000-0002-1499-3416; Sarlós, Patrícia/0000-0002-5086-9455; Ábrahám, Szabolcs/0000-0002-2191-1714; Vincze, Áron/0000-0003-2217-7686}
}

@article{MTMT:33620612,
	title = {Mechanisms linking hypertriglyceridemia to acute pancreatitis},
	url = {https://m2.mtmt.hu/api/publication/33620612},
	author = {Kiss, Lóránd and Fűr, Gabriella and Sailaja, Pisipati and Prasad, Rajalingamgari and Nils, Ewald and Vijay, Singh and Rakonczay, Zoltán},
	doi = {10.1111/apha.13916},
	journal-iso = {ACTA PHYSIOL},
	journal = {ACTA PHYSIOLOGICA},
	volume = {237},
	unique-id = {33620612},
	issn = {1748-1708},
	abstract = {Hypertriglyceridemia (HTG) is a metabolic disorder, defined when serum or plasma triglyceride concentration (seTG) is >1.7 mM. HTG can be categorized as mild to very severe groups based on the seTG value. The risk of acute pancreatitis (AP), a serious disease with high mortality and without specific therapy, increases with the degree of HTG. Furthermore, even mild or moderate HTG aggravates AP initiated by other important etiological factors, including alcohol or bile stone. This review briefly summarizes the pathophysiology of HTG, the epidemiology of HTG-induced AP and the clinically observed effects of HTG on the outcomes of AP. Our main focus is to discuss the pathophysiological mechanisms linking HTG to AP. HTG is accompanied by an increased serum fatty acid (FA) concentration, and experimental results have demonstrated that these FAs have the most prominent role in causing the consequences of HTG during AP. FAs inhibit mitochondrial complexes in pancreatic acinar cells, induce pathological elevation of intracellular Ca2+ concentration, cytokine release and tissue injury, and reduce the function of pancreatic ducts. Furthermore, high FA concentrations can induce respiratory, kidney, and cardiovascular failure in AP. All these effects may contribute to the observed increased AP severity and frequent organ failure in patients. Importantly, experimental results suggest that the reduction of FA production by lipase inhibitors can open up new therapeutic options of AP. Overall, investigating the pathophysiology of HTG-induced AP or AP in the presence of HTG and determining possible treatments are needed.},
	keywords = {FATTY-ACIDS; PROTEIN-KINASE-C; fatty acid; mitochondrial dysfunction; Acute pancreatitis; ENDOPLASMIC-RETICULUM STRESS; LIPOPROTEIN-LIPASE; RETROSPECTIVE ANALYSIS; INFLAMMATORY CYTOKINE; ELEVATED SERUM TRIGLYCERIDES; ACID ETHYL-ESTERS},
	year = {2023},
	eissn = {1748-1716},
	orcid-numbers = {Rakonczay, Zoltán/0000-0002-1499-3416}
}

@CONFERENCE{MTMT:34657419,
	title = {Defective CFTR expression promotes epithelial cell damage in alcoholic pancreatitis and hepatitis by the impaired regulation of PMCA activity},
	url = {https://m2.mtmt.hu/api/publication/34657419},
	author = {Madácsy, Tamara and Varga, Árpád and Csákány-Papp, Noémi and Tél, Bálint and Pallagi, Petra and Szabó, Viktória and Kiss, Aletta Kata and Fanczal, Júlia and Rakonczay, Zoltán and Tiszlavicz, László and Rázga, Zsolt and Hohweiler, Meike and Kleger, Alexander and Gray, Mike and Hegyi, Péter and Maléth, József},
	booktitle = {European Cystic Fibrosis Society 17th ECFS Basic Science Conference},
	unique-id = {34657419},
	year = {2022},
	pages = {135},
	orcid-numbers = {Madácsy, Tamara/0000-0001-5598-9723; Varga, Árpád/0000-0002-2379-139X; Csákány-Papp, Noémi/0000-0002-3614-2698; Tél, Bálint/0000-0003-2066-6494; Pallagi, Petra/0000-0001-8906-0840; Szabó, Viktória/0000-0001-6547-9102; Kiss, Aletta Kata/0000-0001-6404-1555; Fanczal, Júlia/0000-0001-7356-3857; Rakonczay, Zoltán/0000-0002-1499-3416; Tiszlavicz, László/0000-0003-1134-6587; Rázga, Zsolt/0000-0003-4717-8482; Hegyi, Péter/0000-0003-0399-7259; Maléth, József/0000-0001-5768-3090}
}

@book{MTMT:33399502,
	title = {Szegedi Tudományegyetem - Szent-Györgyi Albert Orvostudományi Kar, Fogorvostudományi Kar, Gyógyszerésztudományi Kar és Egészségtudományi és Szociális Képzési Kar 2022. évi Tudományos Diákköri Konferenciája},
	url = {https://m2.mtmt.hu/api/publication/33399502},
	isbn = {9789633068908},
	editor = {Tolnai, József and Peták, Ferenc and Rakonczay, Zoltán},
	publisher = {SZTE},
	unique-id = {33399502},
	year = {2022},
	orcid-numbers = {Tolnai, József/0000-0002-7648-764X; Peták, Ferenc/0000-0001-6249-9327; Rakonczay, Zoltán/0000-0002-1499-3416}
}

@article{MTMT:32800045,
	title = {Impaired regulation of PMCA activity by defective CFTR expression promotes epithelial cell damage in alcoholic pancreatitis and hepatitis.},
	url = {https://m2.mtmt.hu/api/publication/32800045},
	author = {Madácsy, Tamara and Varga, Árpád and Csákány-Papp, Noémi and Tél, Bálint and Pallagi, Petra and Szabó, Viktória and Kiss, Aletta Kata and Fanczal, Júlia and Rakonczay, Zoltán and Tiszlavicz, László and Rázga, Zsolt and Hohwieler, Meike and Kleger, Alexander and Gray, Mike and Hegyi, Péter and Maléth, József},
	doi = {10.1007/s00018-022-04287-1},
	journal-iso = {CELL MOL LIFE SCI},
	journal = {CELLULAR AND MOLECULAR LIFE SCIENCES},
	volume = {79},
	unique-id = {32800045},
	issn = {1420-682X},
	abstract = {Alcoholic pancreatitis and hepatitis are frequent, potentially lethal diseases with limited treatment options. Our previous study reported that the expression of CFTR Cl- channel is impaired by ethanol in pancreatic ductal cells leading to more severe alcohol-induced pancreatitis. In addition to determining epithelial ion secretion, CFTR has multiple interactions with other proteins, which may influence intracellular Ca2+ signaling. Thus, we aimed to investigate the impact of ethanol-mediated CFTR damage on intracellular Ca2+ homeostasis in pancreatic ductal epithelial cells and cholangiocytes. Human and mouse pancreas and liver samples and organoids were used to study ion secretion, intracellular signaling, protein expression and interaction. The effect of PMCA4 inhibition was analyzed in a mouse model of alcohol-induced pancreatitis. The decreased CFTR expression impaired PMCA function and resulted in sustained intracellular Ca2+ elevation in ethanol-treated and mouse and human pancreatic organoids. Liver samples derived from alcoholic hepatitis patients and ethanol-treated mouse liver organoids showed decreased CFTR expression and function, and impaired PMCA4 activity. PMCA4 co-localizes and physically interacts with CFTR on the apical membrane of polarized epithelial cells, where CFTR-dependent calmodulin recruitment determines PMCA4 activity. The sustained intracellular Ca2+ elevation in the absence of CFTR inhibited mitochondrial function and was accompanied with increased apoptosis in pancreatic epithelial cells and PMCA4 inhibition increased the severity of alcohol-induced AP in mice. Our results suggest that improving Ca2+ extrusion in epithelial cells may be a potential novel therapeutic approach to protect the exocrine pancreatic function in alcoholic pancreatitis and prevent the development of cholestasis in alcoholic hepatitis.},
	keywords = {CFTR; Ca2+ signaling; Alcoholic pancreatitis; Alcoholic Hepatitis; Epithelial ion secretion},
	year = {2022},
	eissn = {1420-9071},
	orcid-numbers = {Madácsy, Tamara/0000-0001-5598-9723; Varga, Árpád/0000-0002-2379-139X; Csákány-Papp, Noémi/0000-0002-3614-2698; Tél, Bálint/0000-0003-2066-6494; Pallagi, Petra/0000-0001-8906-0840; Szabó, Viktória/0000-0001-6547-9102; Kiss, Aletta Kata/0000-0001-6404-1555; Fanczal, Júlia/0000-0001-7356-3857; Rakonczay, Zoltán/0000-0002-1499-3416; Tiszlavicz, László/0000-0003-1134-6587; Rázga, Zsolt/0000-0003-4717-8482; Hegyi, Péter/0000-0003-0399-7259; Maléth, József/0000-0001-5768-3090}
}

@article{MTMT:32692193,
	title = {Noninvasive ventilation improves the outcome in patients with pneumonia-associated respiratory failure: Systematic review and meta-analysis},
	url = {https://m2.mtmt.hu/api/publication/32692193},
	author = {Ruzsics, István and Mátrai, Péter and Hegyi, Péter and Németh, Dávid and Tenk, Judit and Csenkey, Alexandra and Erőss, Bálint Mihály and Varga, Gábor and Balaskó, Márta and Pétervári, Erika and Veres, Gábor and Sepp, Róbert and Rakonczay, Zoltán and Vincze, Áron and Garami, András and Rumbus, Zoltán},
	doi = {10.1016/j.jiph.2022.02.004},
	journal-iso = {J INFECT PUBLIC HEALTH},
	journal = {JOURNAL OF INFECTION AND PUBLIC HEALTH},
	volume = {15},
	unique-id = {32692193},
	issn = {1876-0341},
	abstract = {Background
		Noninvasive ventilation (NIV) is beneficial in exacerbations of chronic obstructive pulmonary disease (COPD), but its effectiveness in pneumonia-associated respiratory failure is still controversial. In the current meta-analysis, we aimed to investigate whether the use of NIV before intubation in pneumonia improves the mortality and intubation rates of respiratory failure as compared to no use of NIV in adults.
		
		Methods
		We searched three databases from inception to December 2019. We included studies, in which pneumonia patients were randomized initially into either NIV-treated or non-NIV-treated groups. Five full-text publications, including 121 patients, reported eligible data for statistical analysis.
		
		Results
		With NIV the overall hospital mortality rate seemed lower in patients with pneumonia-associated respiratory failure, but this was not significant [odds ratio (OR) = 0.39; 95% confidence interval (CI): 0.13–1.14; P = 0.085]. In the intensive care unit, the mortality was significantly lower when NIV was applied compared to no NIV treatment (OR = 0.22; 95% CI: 0.07–0.75; P = 0.015). NIV also decreased mortality compared to no NIV in patient groups, which did not exclude patients with COPD (OR = 0.25; 95% CI: 0.08–0.74; P = 0.013). The need for intubation was significantly reduced in NIV-treated patients (OR = 0.22; 95% CI: 0.09–0.53; P = 0.001), which effect was more prominent in pneumonia patient groups not excluding patients with pre-existing COPD (OR = 0.13; 95% CI: 0.03–0.46; P = 0.002).
		
		Conclusion
		NIV markedly decreases the death rate in the intensive care unit and reduces the need for intubation in patients with pneumonia-associated respiratory failure. The beneficial effects of NIV seem more pronounced in populations that include patients with COPD. Our findings suggest that NIV should be considered in the therapeutic guidelines of pneumonia, given that future clinical trials confirm the results of our meta-analysis.
		
		Availability of data and materials
		All data and materials generated during the current study are available from the corresponding author on reasonable request.},
	keywords = {MORTALITY; Meta-analysis; pneumonia; Noninvasive ventilation; INVASIVE VENTILATION; [Meta-analysis]},
	year = {2022},
	eissn = {1876-035X},
	pages = {349-359},
	orcid-numbers = {Ruzsics, István/0000-0002-6381-8884; Hegyi, Péter/0000-0003-0399-7259; Erőss, Bálint Mihály/0000-0003-3658-8427; Varga, Gábor/0000-0002-5506-8198; Pétervári, Erika/0000-0002-3673-8491; Veres, Gábor/0000-0002-0911-1941; Sepp, Róbert/0000-0003-4964-1661; Rakonczay, Zoltán/0000-0002-1499-3416; Vincze, Áron/0000-0003-2217-7686; Garami, András/0000-0003-2493-0571}
}

@article{MTMT:32667372,
	title = {Blood–brain barrier dysfunction in l-ornithine induced acute pancreatitis in rats and the direct effect of l-ornithine on cultured brain endothelial cells},
	url = {https://m2.mtmt.hu/api/publication/32667372},
	author = {Walter, Fruzsina and Harazin, András and Tóth, Andrea and Veszelka, Szilvia and Santa Maria, Anaraquel and Barna, Lilla and Kincses, András and Biczo, G and Balla, Zsolt and Kui, Balázs and Maléth, József and Cervenak, László and Tubak, Vilmos and Kittel, Ágnes and Rakonczay, Zoltán and Deli, Mária Anna},
	doi = {10.1186/s12987-022-00308-0},
	journal-iso = {FLUIDS BARRIERS CNS},
	journal = {FLUIDS AND BARRIERS OF THE CNS},
	volume = {19},
	unique-id = {32667372},
	issn = {2045-8118},
	year = {2022},
	eissn = {2045-8118},
	orcid-numbers = {Walter, Fruzsina/0000-0001-8145-2823; Harazin, András/0000-0002-0904-5606; Santa Maria, Anaraquel/0000-0003-3505-5477; Maléth, József/0000-0001-5768-3090; Cervenak, László/0000-0003-0166-8697; Tubak, Vilmos/0000-0002-6141-3920; Rakonczay, Zoltán/0000-0002-1499-3416; Deli, Mária Anna/0000-0001-6084-6524}
}

@article{MTMT:32624010,
	title = {Fentanyl but Not Morphine or Buprenorphine Improves the Severity of Necrotizing Acute Pancreatitis in Rats},
	url = {https://m2.mtmt.hu/api/publication/32624010},
	author = {Bálint, Emese Réka and Fűr, Gabriella and Kui, Balázs and Balla, Zsolt and Kormányos, Eszter Sára and Orján, Erik Márk and Tóth, Brigitta and Horváth, Gyöngyi and Szűcs, Edina and Benyhe, Sándor and Ducza, Eszter and Pallagi, Petra and Maléth, József and Venglovecz, Viktória and Hegyi, Péter and Kiss, Lóránd and Rakonczay, Zoltán},
	doi = {10.3390/ijms23031192},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {32624010},
	issn = {1661-6596},
	abstract = {Opioids are widely used for the pain management of acute pancreatitis (AP), but their impact on disease progression is unclear. Therefore, our aim was to study the effects of clinically relevant opioids on the severity of experimental AP. Various doses of fentanyl, morphine, or buprenorphine were administered as pre- and/or post-treatments in rats. Necrotizing AP was induced by the intraperitoneal injection of L-ornithine-HCl or intra-ductal injection of Na-taurocholate, while intraperitoneal caerulein administration caused edematous AP. Disease severity was determined by laboratory and histological measurements. Mu opioid receptor (MOR) expression and function was assessed in control and AP animals. MOR was expressed in both the pancreas and brain. The pancreatic expression and function of MOR were reduced in AP. Fentanyl post-treatment reduced necrotizing AP severity, whereas pre-treatment exacerbated it. Fentanyl did not affect the outcome of edematous AP. Morphine decreased vacuolization in edematous AP, while buprenorphine pre-treatment increased pancreatic edema during AP. The overall effects of morphine on disease severity were negligible. In conclusion, the type, dosing, administration route, and timing of opioid treatment can influence the effects of opioids on AP severity. Fentanyl post-treatment proved to be beneficial in AP. Clinical studies are needed to determine which opioids are best in AP.},
	keywords = {MORPHINE; ANALGESIA; fentanyl; Acute pancreatitis; Opioids; buprenorphine},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Kormányos, Eszter Sára/0000-0002-6201-1341; Orján, Erik Márk/0000-0003-4176-0834; Horváth, Gyöngyi/0000-0002-6025-4577; Pallagi, Petra/0000-0001-8906-0840; Maléth, József/0000-0001-5768-3090; Venglovecz, Viktória/0000-0002-2316-7247; Hegyi, Péter/0000-0003-0399-7259; Rakonczay, Zoltán/0000-0002-1499-3416}
}