@article{MTMT:34813506, title = {Antitrombin-III-deficites gravidák - kezelési lehetőségek}, url = {https://m2.mtmt.hu/api/publication/34813506}, author = {Bíró, Krisztina and Ujhelyi, Zoltán and Schlammadinger, Ágota and Rázsó, Katalin and Buchholcz, Gyula and Boda, Zoltán}, journal-iso = {GYÓGYSZERÉSZET}, journal = {GYÓGYSZERÉSZET}, volume = {68}, unique-id = {34813506}, issn = {0017-6036}, year = {2024}, pages = {62-66}, orcid-numbers = {Bíró, Krisztina/0000-0002-2070-0608} } @CONFERENCE{MTMT:34756237, title = {4CPS-036 Evaluation of the diagnosis and antibiotic prescription pattern in patients hospitalised with urinary tract infections (UTIs)}, url = {https://m2.mtmt.hu/api/publication/34756237}, author = {Fésüs, Adina and Matuz, M and Hambalek, H and Ruzsa, R and Tánczos, B and Bácskay, I and Illés, Á and Benkő, R}, booktitle = {Section 4: Clinical pharmacy services}, doi = {10.1136/ejhpharm-2024-eahp.140}, unique-id = {34756237}, year = {2024}, pages = {A68.2-A68}, orcid-numbers = {Fésüs, Adina/0000-0002-6351-7715} } @CONFERENCE{MTMT:34756232, title = {4CPS-035 Impact of antibiotic stewardship programme (ASP) on antibiotic use and clinical outcomes in patients hospitalised with community-acquired pneumonia (CAP): retrospective observational before-after study}, url = {https://m2.mtmt.hu/api/publication/34756232}, author = {Fésüs, Adina and Baluku, P and Sipos, É and Somodi, S and Vaskó, A and Lekli, I and Berczi-Kun, E and Bácskay, I}, booktitle = {Section 4: Clinical pharmacy services}, doi = {10.1136/ejhpharm-2024-eahp.139}, unique-id = {34756232}, year = {2024}, pages = {A68.1-A68}, orcid-numbers = {Fésüs, Adina/0000-0002-6351-7715} } @article{MTMT:34722559, title = {Direct modulation of TRPM8 ion channels by rapamycin and analog macrolide immunosuppressants}, url = {https://m2.mtmt.hu/api/publication/34722559}, author = {Tóth, Balázs István and Bahar, Bazeli and Annelies, Janssens and Lisztes, Erika and Racskó, Márk and Kelemen, Balázs and Herczeg, Mihály and Nagy, Tamás Milán and E Kövér, Katalin and Argha, Mitra and Attila, Borics and Bíró, Tamás and Thomas, Voets}, journal-iso = {ELIFE}, journal = {ELIFE}, unique-id = {34722559}, issn = {2050-084X}, year = {2024}, eissn = {2050-084X}, orcid-numbers = {Herczeg, Mihály/0000-0002-7938-9789} } @article{MTMT:34618976, title = {High glucose promotes osteogenic differentiation of human lens epithelial cells through hypoxia-inducible factor (HIF) activation}, url = {https://m2.mtmt.hu/api/publication/34618976}, author = {Ababneh, Haneen and Balogh, Enikő and Csiki, Dávid Máté and Lente, Gréta and Fenyvesi, Ferenc and Tóth, Andrea and Jeney, Viktória}, doi = {10.1002/jcp.31211}, journal-iso = {J CELL PHYSIOL}, journal = {JOURNAL OF CELLULAR PHYSIOLOGY}, unique-id = {34618976}, issn = {0021-9541}, abstract = {Cataract, a leading cause of blindness, is characterised by lens opacification. Type 2 diabetes is associated with a two- to fivefold higher prevalence of cataracts. The risk of cataract formation increases with the duration of diabetes and the severity of hyperglycaemia. Hydroxyapatite deposition is present in cataractous lenses that could be the consequence of osteogenic differentiation and calcification of lens epithelial cells (LECs). We hypothesised that hyperglycaemia might promote the osteogenic differentiation of human LECs (HuLECs). Osteogenic medium (OM) containing excess phosphate and calcium with normal (1 g/L) or high (4.5 g/L) glucose was used to induce HuLEC calcification. High glucose accelerated and intensified OM-induced calcification of HuLECs, which was accompanied by hyperglycaemia-induced upregulation of the osteogenic markers Runx2, Sox9, alkaline phosphatase and osteocalcin, as well as nuclear translocation of Runx2. High glucose-induced calcification was abolished in Runx2-deficient HuLECs. Additionally, high glucose stabilised the regulatory alpha subunits of hypoxia-inducible factor 1 (HIF-1), triggered nuclear translocation of HIF-1 alpha and increased the expression of HIF-1 target genes. Gene silencing of HIF-1 alpha or HIF-2 alpha attenuated hyperglycaemia-induced calcification of HuLECs, while hypoxia mimetics (desferrioxamine, CoCl2) enhanced calcification of HuLECs under normal glucose conditions. Overall, this study suggests that high glucose promotes HuLEC calcification via Runx2 and the activation of the HIF-1 signalling pathway. These findings may provide new insights into the pathogenesis of diabetic cataracts, shedding light on potential factors for intervention to treat this sight-threatening condition.}, keywords = {cataract; hyperglycaemia; Osteogenic differentiation; hypoxia-inducible factor (HIF); Lens epithelial cell; lens calcification}, year = {2024}, eissn = {1097-4652} } @article{MTMT:34572686, title = {Effects of H2S-donor ascorbic acid derivative and ischemia/reperfusion-induced injury in isolated rat hearts}, url = {https://m2.mtmt.hu/api/publication/34572686}, author = {Tánczos, Bence and Vass, Virág and Szabó, Erzsébet and Lovas, Miklós and Kattoub, Rasha Ghanem and Bakai-Bereczki, Ilona and Borbás, Anikó and Herczegh, Pál and Tósaki, Árpád}, doi = {10.1016/j.ejps.2024.106721}, journal-iso = {EUR J PHARM SCI}, journal = {EUROPEAN JOURNAL OF PHARMACEUTICAL SCIENCES}, volume = {195}, unique-id = {34572686}, issn = {0928-0987}, year = {2024}, eissn = {1879-0720}, pages = {106721}, orcid-numbers = {Bakai-Bereczki, Ilona/0000-0003-4601-7257; Borbás, Anikó/0000-0001-8462-4547} } @article{MTMT:34564621, title = {Serum afamin and its implications in adult growth hormone deficiency: a prospective GH-withdrawal study}, url = {https://m2.mtmt.hu/api/publication/34564621}, author = {Ratku, Balázs and Lőrincz, Hajnalka and Bak-Csiha, Sára and Sebestyén, Veronika and Berta, Eszter and Bodor, Miklós and Nagy, Endre and Szabó, Zoltán and Harangi, Mariann and Somodi, Sándor}, doi = {10.3389/fendo.2024.1348046}, journal-iso = {FRONT ENDOCRINOL}, journal = {FRONTIERS IN ENDOCRINOLOGY}, volume = {15}, unique-id = {34564621}, issn = {1664-2392}, year = {2024}, eissn = {1664-2392}, orcid-numbers = {Somodi, Sándor/0000-0002-3615-2300} } @article{MTMT:34546012, title = {Changes in the Composition of Unstimulated and Stimulated Saliva Due to Chewing Sour Cherry Gum and a Toothbrush Change}, url = {https://m2.mtmt.hu/api/publication/34546012}, author = {Skopkó, Boglárka Emese and Homoki, Judit Rita and Fazekas, Mónika Éva and Paholcsek, Melinda and Fauszt, Péter and Dávid, Péter and Stündl, László and Molnár, Piroska Bíróné and Forgács, Ildikó Noémi and Váradi, Judit and Bágyi, Kinga, Ágnes and Gálné Remenyik, Judit}, doi = {10.3390/cells13030251}, journal-iso = {CELLS-BASEL}, journal = {CELLS}, volume = {13}, unique-id = {34546012}, abstract = {Background: Our previous studies demonstrated that sour cherry anthocyanins (AC) reduce the salivary count of Streptococcus mutans and inhibit salivary amylase activity within 30 minutes after chewing AC gum. AC gum and changing toothbrushes after scaling reduced the Gram-negative species in the unstimulated salivary microbiota. The present study examined the effect of AC gums on salivary factors, including changes in microbiome. Methods: The study was conducted over three weeks with two groups; young adults (18–30) and adults (30–45). Ten participants changed their toothbrushes, while the other 10 participants did not change after the control period. After scaling, all participants received three doses of AC gum daily. The salivary mRNA and protein levels of cytokines, mucins, melatonin, and the microbiota of unstimulated and stimulated saliva were determined by polymerase chain reaction, enzyme-linked immunosorbent assay, and 16S rRNA gene sequencing. Results: Significantly higher levels of tumor necrosis factor α (TNFα), interleukin-1β (IL-1β), mucin5B (MUC5B), mucin7 (MUC7), and melatonin were detected in stimulated saliva. Correlation analysis of these factors with the microbiota showed positive correlations with the genera Lachnospiraceae, Eikenella, Saccharibacteria_(TM7), Streptococcus, Prevotella, and Haemophilus. Conclusions: AC chewing gum has a beneficial effect on the composition of the oral microbiome, and toothbrush replacement leads to changes in the levels of salivary pro-inflammatory cytokines.}, year = {2024}, eissn = {2073-4409}, orcid-numbers = {Dávid, Péter/0000-0002-6451-1200} } @article{MTMT:34534306, title = {DNA methylome, R-loop and clinical exome profiling of patients with sporadic amyotrophic lateral sclerosis}, url = {https://m2.mtmt.hu/api/publication/34534306}, author = {Feró, Orsolya and Varga, Dóra and Nagy, Éva and Karányi, Zsolt and Sipos, Éva and Engelhardt, József and Török, Nóra and Balogh, István and Vető, Borbála and Likó, István and Fóthi, Ábel and Szabó, Zoltán and Halmos, Gábor and Vécsei, László and Arányi, Tamás and Székvölgyi, Lóránt}, doi = {10.1038/s41597-024-02985-y}, journal-iso = {SCI DATA}, journal = {SCIENTIFIC DATA}, volume = {11}, unique-id = {34534306}, abstract = {Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the death of motor neurons, the aetiology of which is essentially unknown. Here, we present an integrative epigenomic study in blood samples from seven clinically characterised sporadic ALS patients to elucidate molecular factors associated with the disease. We used clinical exome sequencing (CES) to study DNA variants, DNA-RNA hybrid immunoprecipitation sequencing (DRIP-seq) to assess R-loop distribution, and reduced representation bisulfite sequencing (RRBS) to examine DNA methylation changes. The above datasets were combined to create a comprehensive repository of genetic and epigenetic changes associated with the ALS cases studied. This repository is well-suited to unveil new correlations within individual patients and across the entire patient cohort. The molecular attributes described here are expected to guide further mechanistic studies on ALS, shedding light on the underlying genetic causes and facilitating the development of new epigenetic therapies to combat this life-threatening disease.}, year = {2024}, eissn = {2052-4463}, orcid-numbers = {Fóthi, Ábel/0000-0001-7398-9700; Vécsei, László/0000-0001-8037-3672} } @article{MTMT:34502650, title = {Block Synthesis and Step-Growth Polymerization of C-6-Sulfonatomethyl-Containing Sulfated Malto-Oligosaccharides and Their Biological Profiling}, url = {https://m2.mtmt.hu/api/publication/34502650}, author = {Herczeg, Mihály and Demeter, Fruzsina and Nagy, Tibor and Rusznyák, Ágnes and Hodek, Jan and Sipos, Éva and Lekli, István and Fenyvesi, Ferenc and Weber, Jan and Kéki, Sándor and Borbás, Anikó}, doi = {10.3390/ijms25010677}, journal-iso = {INT J MOL SCI}, journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES}, volume = {25}, unique-id = {34502650}, issn = {1661-6596}, abstract = {Highly sulfated malto-oligomers, similar to heparin and heparan-sulfate, have good antiviral, antimetastatic, anti-inflammatory and cell growth inhibitory effects. Due to their broad biological activities and simple structure, sulfated malto-oligomer derivatives have a great therapeutic potential, therefore, the development of efficient synthesis methods for their production is of utmost importance. In this work, preparation of α-(1→4)-linked oligoglucosides containing a sulfonatomethyl moiety at position C-6 of each glucose unit was studied by different approaches. Malto-oligomeric sulfonic acid derivatives up to dodecasaccharides were prepared by polymerization using different protecting groups, and the composition of the product mixtures was analyzed by MALDI-MS methods and size-exclusion chromatography. Synthesis of lower oligomers was also accomplished by stepwise and block synthetic methods, and then the oligosaccharide products were persulfated. The antiviral, anti-inflammatory and cell growth inhibitory activity of the fully sulfated malto-oligosaccharide sulfonic acids were determined by in vitro tests. Four tested di- and trisaccharide sulfonic acids effectively inhibited the activation of the TNF-α-mediated inflammatory pathway without showing cytotoxicity.}, year = {2024}, eissn = {1422-0067}, orcid-numbers = {Herczeg, Mihály/0000-0002-7938-9789; Nagy, Tibor/0000-0001-8568-914X; Sipos, Éva/0009-0001-9561-2450; Borbás, Anikó/0000-0001-8462-4547} }