TY - BOOK ED - Tolnai, József ED - Peták, Ferenc ED - Fodor, Gergely ED - Rakonczay, Zoltán TI - 2023. évi Orvos- és Egészségtudományi TDK Konferencia PB - Szegedi Tudományegyetem CY - Szeged PY - 2023 SP - 301 SN - 9789633069592 UR - https://m2.mtmt.hu/api/publication/34446677 ID - 34446677 LA - English DB - MTMT ER - TY - JOUR AU - Orján, Erik Márk AU - Kormányos, Eszter Sára AU - Fűr, Gabriella AU - Dombi, Ágnes AU - Bálint, Emese Réka AU - Balla, Zsolt AU - Balog, Beáta Adél AU - Dágó, Ágnes AU - Totonji, Ahmad AU - Bátai, István Zoárd AU - Jurányi, Eszter Petra AU - Ditrói, Tamás AU - Al-omari, Ammar AU - Pozsgai, Gábor AU - Kormos, Viktória AU - Nagy, Péter AU - Pintér, Erika AU - Rakonczay, Zoltán AU - Kiss, Lóránd TI - The anti-inflammatory effect of dimethyl trisulfide in experimental acute pancreatitis JF - SCIENTIFIC REPORTS J2 - SCI REP VL - 13 PY - 2023 IS - 1 PG - 19 SN - 2045-2322 DO - 10.1038/s41598-023-43692-9 UR - https://m2.mtmt.hu/api/publication/34183455 ID - 34183455 N1 - * Megosztott szerzőség AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Kovács, Norbert AU - Pécsi, Dániel AU - Sipos, Zoltán AU - Borbásné Farkas, Kornélia AU - Földi, Mária AU - Hegyi, Péter AU - Bajor, Judit AU - Erőss, Bálint Mihály AU - Márta, Katalin AU - Mikó, Alexandra AU - Rakonczay, Zoltán AU - Sarlós, Patrícia AU - Ábrahám, Szabolcs AU - Vincze, Áron TI - Suprapapillary Biliary Stents Have Longer Patency Times than Transpapillary Stents-A Systematic Review and Meta-Analysis. JF - JOURNAL OF CLINICAL MEDICINE J2 - J CLIN MED VL - 12 PY - 2023 IS - 3 PG - 16 SN - 2077-0383 DO - 10.3390/jcm12030898 UR - https://m2.mtmt.hu/api/publication/33636629 ID - 33636629 N1 - * Megosztott szerzőség AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Kiss, Lóránd AU - Fűr, Gabriella AU - Sailaja, Pisipati AU - Prasad, Rajalingamgari AU - Nils, Ewald AU - Vijay, Singh AU - Rakonczay, Zoltán TI - Mechanisms linking hypertriglyceridemia to acute pancreatitis JF - ACTA PHYSIOLOGICA J2 - ACTA PHYSIOL VL - 237 PY - 2023 IS - 3 PG - 21 SN - 1748-1708 DO - 10.1111/apha.13916 UR - https://m2.mtmt.hu/api/publication/33620612 ID - 33620612 N1 - Funding Agency and Grant Number: DOD [PR 191945]; Emberi Eroforrasok Miniszteriuma [EFOP- 3.6.2- 16- 2017- c]; Innovacios es Technologiai Miniszterium [UNKP- 21- 5- SZTE- 577]; Magyar Tudomanyos Akademia [BO/00866/20/5]; European Regional Development Fund [GINOP- 2.3.2- 15- 2016- 00048]; National Institute of Diabetes and Digestive and Kidney Diseases [R01DK092460, R01DK119646]; Nemzeti Kutatasi Fejlesztesi es Innovacios Hivatal [K135874, PD129114]; University of Szeged Open Access Fund [6038] Funding text: DOD, Grant/Award Number: PR 191945; Emberi Eroforrasok Miniszteriuma, Grant/Award Number: EFOP- 3.6.2- 16- 2017- 00006; Innovacios es Technologiai Miniszterium, Grant/Award Number: UNKP- 21- 5- SZTE- 577; Magyar Tudomanyos Akademia, Grant/Award Number: BO/00866/20/5; European Regional Development Fund, Grant/Award Number: GINOP- 2.3.2- 15- 2016- 00048; National Institute of Diabetes and Digestive and Kidney Diseases, Grant/Award Number: R01DK092460 and R01DK119646; Nemzeti Kutatasi Fejlesztesi es Innovacios Hivatal, Grant/Award Number: K135874 and PD129114; University of Szeged Open Access Fund, Grant/Award Number: 6038 AB - 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. LA - English DB - MTMT ER - TY - CONF AU - Madácsy, Tamara AU - Varga, Árpád AU - Csákány-Papp, Noémi AU - Tél, Bálint AU - Pallagi, Petra AU - Szabó, Viktória AU - Kiss, Aletta Kata AU - Fanczal, Júlia AU - Rakonczay, Zoltán AU - Tiszlavicz, László AU - Rázga, Zsolt AU - Hohweiler, Meike AU - Kleger, Alexander AU - Gray, Mike AU - Hegyi, Péter AU - Maléth, József TI - Defective CFTR expression promotes epithelial cell damage in alcoholic pancreatitis and hepatitis by the impaired regulation of PMCA activity T2 - European Cystic Fibrosis Society 17th ECFS Basic Science Conference C1 - Albufeira PY - 2022 SP - 135 UR - https://m2.mtmt.hu/api/publication/34657419 ID - 34657419 LA - English DB - MTMT ER - TY - BOOK ED - Tolnai, József ED - Peták, Ferenc ED - Rakonczay, Zoltán TI - Szegedi Tudományegyetem - Szent-Györgyi Albert Orvostudományi Kar, Fogorvostudományi Kar, Gyógyszerésztudományi Kar és Egészségtudományi és Szociális Képzési Kar 2022. évi Tudományos Diákköri Konferenciája PB - Szegedi Tudományegyetem (SZTE) CY - Szeged PY - 2022 SP - 255 SN - 9789633068908 UR - https://m2.mtmt.hu/api/publication/33399502 ID - 33399502 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Madácsy, Tamara AU - Varga, Árpád AU - Csákány-Papp, Noémi AU - Tél, Bálint AU - Pallagi, Petra AU - Szabó, Viktória AU - Kiss, Aletta Kata AU - Fanczal, Júlia AU - Rakonczay, Zoltán AU - Tiszlavicz, László AU - Rázga, Zsolt AU - Hohwieler, Meike AU - Kleger, Alexander AU - Gray, Mike AU - Hegyi, Péter AU - Maléth, József TI - Impaired regulation of PMCA activity by defective CFTR expression promotes epithelial cell damage in alcoholic pancreatitis and hepatitis. JF - CELLULAR AND MOLECULAR LIFE SCIENCES J2 - CELL MOL LIFE SCI VL - 79 PY - 2022 IS - 5 PG - 18 SN - 1420-682X DO - 10.1007/s00018-022-04287-1 UR - https://m2.mtmt.hu/api/publication/32800045 ID - 32800045 N1 - Department of Medicine, University of Szeged, Szeged, 6720, Hungary HAS-USZ Momentum Epithelial Cell Signaling and Secretion Research Group, University of Szeged, Szeged, 6720, Hungary First Department of Pediatrics, Semmelweis University, Budapest, Hungary Department of Pathophysiology, University of Szeged, Szeged, 6720, Hungary Department of Pathology, University of Szeged, Szeged, Hungary Department of Internal Medicine I, Ulm University Hospital, Ulm, Germany Biosciences Institute, Newcastle University, Newcastle upon Tyne, United Kingdom Institute for Translational Medicine, University of Pécs, Pécs, Hungary Centre for Translational Medicine and Division for Pancreatic Disorders, Semmelweis University, Budapest, Hungary HCEMM-USZ Molecular Gastroenterology Research Group, University of Szeged, Szeged, 6720, Hungary Cited By :4 Export Date: 26 January 2024 CODEN: CMLSF Correspondence Address: Maléth, J.; Department of Medicine, Hungary; email: jozsefmaleth1@gmail.com AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Ruzsics, István AU - Mátrai, Péter AU - Hegyi, Péter AU - Németh, Dávid AU - Tenk, Judit AU - Csenkey, Alexandra AU - Erőss, Bálint Mihály AU - Varga, Gábor AU - Balaskó, Márta AU - Pétervári, Erika AU - Veres, Gábor AU - Sepp, Róbert AU - Rakonczay, Zoltán AU - Vincze, Áron AU - Garami, András AU - Rumbus, Zoltán TI - Noninvasive ventilation improves the outcome in patients with pneumonia-associated respiratory failure: Systematic review and meta-analysis JF - JOURNAL OF INFECTION AND PUBLIC HEALTH J2 - J INFECT PUBLIC HEALTH VL - 15 PY - 2022 IS - 3 SP - 349 EP - 359 PG - 11 SN - 1876-0341 DO - 10.1016/j.jiph.2022.02.004 UR - https://m2.mtmt.hu/api/publication/32692193 ID - 32692193 AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Walter, Fruzsina AU - Harazin, András AU - Tóth, Andrea AU - Veszelka, Szilvia AU - Santa Maria, Anaraquel AU - Barna, Lilla AU - Kincses, András AU - Biczo, G AU - Balla, Zsolt AU - Kui, Balázs AU - Maléth, József AU - Cervenak, László AU - Tubak, Vilmos AU - Kittel, Ágnes AU - Rakonczay, Zoltán AU - Deli, Mária Anna TI - Blood–brain barrier dysfunction in l-ornithine induced acute pancreatitis in rats and the direct effect of l-ornithine on cultured brain endothelial cells JF - FLUIDS AND BARRIERS OF THE CNS J2 - FLUIDS BARRIERS CNS VL - 19 PY - 2022 IS - 1 PG - 20 SN - 2045-8118 DO - 10.1186/s12987-022-00308-0 UR - https://m2.mtmt.hu/api/publication/32667372 ID - 32667372 N1 - Institute of Biophysics, Biological Research Centre, Temesvári krt. 62, Szeged, 6726, Hungary Department of Medicine, University of Szeged, Kálvária sgt 57, Szeged, 6725, Hungary Department of Pathophysiology, University of Szeged, Semmelweis u. 1, Szeged, 6701, Hungary HAS-USZ Momentum Epithelial Cell Signaling and Secretion Research Group, University of Szeged, Dóm sqr. 10, Szeged, 6720, Hungary HCEMM-SZTE Molecular Gastroenterology Research Group, University of Szeged, Dóm sqr. 10, Szeged, 6720, Hungary Department of Internal Medicine and Hematology, Research Laboratory, Semmelweis University, Üllői út 26, Budapest, 1085, Hungary Creative Laboratory Ltd, Temesvári krt. 62, Szeged, 6726, Hungary Institute of Experimental Medicine, Eötvös Loránd Research Network, Szigony u. 43, Budapest, 1083, Hungary Wyss Institute for Biologically Inspired Engineering at Harvard University, 3 Blackfan Circle, Boston, MA 02115, United States Department of Biomedicine, Faculty of Health, Aarhus University, Høegh-Guldbergs Gade 10, Aarhus C, 8000, Denmark Institute of Applied Sciences, Department of Environmental Biology and Education, Juhász Gyula Faculty of Education, University of Szeged, Boldogasszony sgt. 6, Szeged, 6725, Hungary Cited By :1 Export Date: 23 November 2022 Correspondence Address: Deli, M.A.; Institute of Biophysics, Temesvári krt. 62, Hungary; email: deli.maria@brc.hu LA - English DB - MTMT ER - TY - JOUR AU - Bálint, Emese Réka AU - Fűr, Gabriella AU - Kui, Balázs AU - Balla, Zsolt AU - Kormányos, Eszter Sára AU - Orján, Erik Márk AU - Tóth, Brigitta AU - Horváth, Gyöngyi AU - Szűcs, Edina AU - Benyhe, Sándor AU - Ducza, Eszter AU - Pallagi, Petra AU - Maléth, József AU - Venglovecz, Viktória AU - Hegyi, Péter AU - Kiss, Lóránd AU - Rakonczay, Zoltán TI - Fentanyl but Not Morphine or Buprenorphine Improves the Severity of Necrotizing Acute Pancreatitis in Rats JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 3 PG - 23 SN - 1661-6596 DO - 10.3390/ijms23031192 UR - https://m2.mtmt.hu/api/publication/32624010 ID - 32624010 N1 - Department of Pathophysiology, University of Szeged, Szeged, 6725, Hungary Department of Medicine, University of Szeged, Szeged, 6725, Hungary Department of Physiology, University of Szeged, Szeged, 6725, Hungary Institute of Biochemistry, Biological Research Center, Szeged, 6726, Hungary Department of Pharmacodynamics and Biopharmacy, Faculty of Pharmacy, University of Szeged, Szeged, 6725, Hungary Department of Pharmacology and Pharmacotherapy, University of Szeged, Szeged, 6725, Hungary Institute for Translational Medicine, Medical School, University of Pecs, Pecs, 7624, Hungary Cited By :4 Export Date: 16 October 2023 Correspondence Address: Kiss, L.; Department of Pathophysiology, Hungary; email: lorand.kiss.work@gmail.com Correspondence Address: Rakonczay, Z.; Department of Pathophysiology, Hungary; email: rakonczay.zoltan@med.u-szeged.hu Chemicals/CAS: amylase, 9000-90-2, 9000-92-4, 9001-19-8; buprenorphine, 52485-79-7, 53152-21-9; ceruletide, 17650-98-5; enkephalin[2 dextro alanine 4 methylphenylalanine 5 glycine], 78123-71-4; fentanyl, 437-38-7, 1443-54-5; gentamicin, 1392-48-9, 1403-66-3, 1405-41-0; ketamine, 1867-66-9, 6740-88-1, 81771-21-3; morphine, 52-26-6, 57-27-2; myeloperoxidase; naloxone, 357-08-4, 465-65-6; ornithine, 70-26-8, 7006-33-9; taurocholic acid, 145-42-6, 59005-70-8, 81-24-3; xylazine, 23076-35-9, 7361-61-7; Analgesics, Opioid; Buprenorphine; Fentanyl; Morphine; Receptors, Opioid, mu Tradenames: PE-10, Becton Dickinson, United States; PE-10, Clay Adams, United States Manufacturers: CP Pharmaceuticals, Germany; Sigma Aldrich, HungaryBecton Dickinson, United States; Clay Adams, United States Funding text 1: Funding: This work was supported by EFOP-3.6.2–16–2017–00006, GINOP-2.3.2-15-2016-00048, Bólyai János Research Grant (BO/00866/20/5), ÚNKP Grant (ÚNKP-20-5-SZTE-163), NKFIH PD129114 and NKFIH K119938. The funders did not influence the interpretation of results in any way. AB - 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. LA - English DB - MTMT ER -