@{MTMT:34817497,
	title = {Kalcium-anyagcsere zavarai, osteoporosis},
	url = {https://m2.mtmt.hu/api/publication/34817497},
	author = {Horváth, Csaba and Takács, István},
	booktitle = {Belgyógyászat 1 tantárgyi jegyzet},
	unique-id = {34817497},
	year = {2024},
	pages = {170-185},
	orcid-numbers = {Horváth, Csaba/0000-0002-0490-7932; Takács, István/0000-0002-7810-4833}
}

@{MTMT:34804137,
	title = {A mellékpajzsmirigy betegségei},
	url = {https://m2.mtmt.hu/api/publication/34804137},
	author = {Takács, István},
	booktitle = {Belgyógyászat 1 tantárgyi jegyzet},
	unique-id = {34804137},
	year = {2024},
	pages = {70-72},
	orcid-numbers = {Takács, István/0000-0002-7810-4833}
}

@{MTMT:34804134,
	title = {Pajzsmirigyhormon-adaptációs szindróma (nonthyroidal illness – PASz)},
	url = {https://m2.mtmt.hu/api/publication/34804134},
	author = {Takács, István},
	booktitle = {Belgyógyászat 1 tantárgyi jegyzet},
	unique-id = {34804134},
	year = {2024},
	pages = {68-69},
	orcid-numbers = {Takács, István/0000-0002-7810-4833}
}

@{MTMT:34803088,
	title = {Hyperthyreosis},
	url = {https://m2.mtmt.hu/api/publication/34803088},
	author = {Bakos, Bence and Takács, István},
	booktitle = {Belgyógyászat 1 tantárgyi jegyzet},
	unique-id = {34803088},
	year = {2024},
	pages = {46-49},
	orcid-numbers = {Bakos, Bence/0000-0003-2073-6536; Takács, István/0000-0002-7810-4833}
}

@book{MTMT:34802851,
	title = {Belgyógyászat 1 tantárgyi jegyzet},
	url = {https://m2.mtmt.hu/api/publication/34802851},
	isbn = {9789633316122},
	editor = {Takács, István},
	publisher = {Semmelweis Kiadó és Multimédia Stúdió},
	unique-id = {34802851},
	year = {2024},
	orcid-numbers = {Takács, István/0000-0002-7810-4833}
}

@article{MTMT:34795043,
	title = {Analysis of SIRT1 Gene SNPs and Clinical Characteristics in Medication-Related Osteonecrosis of the Jaw},
	url = {https://m2.mtmt.hu/api/publication/34795043},
	author = {Bojtor, Bence and Vaszilkó, Mihály Tamás and Ármós, Richárd Levente and Tóbiás, Bálint and Podani, János and Szentpéteri, Szófia Katalin and Balla, Bernadett and Lengyel, Balazs and Pikó, Henriett and Illés, Anett and Kiss, András and Putz, Zsuzsanna and Takács, István and Kósa, János and Lakatos, Péter},
	doi = {10.3390/ijms25073646},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34795043},
	issn = {1661-6596},
	abstract = {Certain genetic factors, including single-nucleotide polymorphisms (SNPs) in the SIRT1 gene, have been linked to medication-related osteonecrosis of the jaw (MRONJ). This study examined four SNPs in the SIRT1 gene and implemented multivariate statistical analysis to analyze genetic and clinical factors in MRONJ patients. Genomic DNA was isolated from peripheral blood samples of 63 patients of European origin treated for MRONJ, and four SNP genotypes in the gene encoding the SIRT-1 protein were determined by Sanger sequencing. The allele frequencies measured in the MRONJ population were compared with allele frequencies measured in the European population in the National Center for Biotechnology Information Allele Frequency Aggregator (NCBI ALFA) database. Genetic and clinical factors were examined with multivariate statistical analysis. A C:A allele distribution ratio of 77.8:22.2 was measured in the rs932658 SNP. In the ALFA project, a C:A allele distribution ratio of 59.9:40.1 was detected in the European population, which was found to be a significant difference (p = 4.5 × 10−5). Multivariate statistical analysis revealed a positive correlation (0.275) between the genotype of SNP rs932658 and the number of stages improved during appropriate MRONJ therapy. It is concluded that allele A in SNP rs932658 in the SIRT1 gene acts as a protective factor in MRONJ.},
	year = {2024},
	eissn = {1422-0067},
	orcid-numbers = {Vaszilkó, Mihály Tamás/0000-0002-2570-0009; Tóbiás, Bálint/0000-0003-4343-1866; Podani, János/0000-0002-1452-1486; Szentpéteri, Szófia Katalin/0000-0003-0073-4154; Balla, Bernadett/0000-0003-2465-1804; Pikó, Henriett/0000-0002-3579-5451; Illés, Anett/0000-0001-5351-9015; Putz, Zsuzsanna/0000-0002-0674-337X; Takács, István/0000-0002-7810-4833; Lakatos, Péter/0000-0002-7652-3671}
}

@article{MTMT:34780698,
	title = {Az első hazai tapasztalatok összegzése kromoszomális microarray-analízis és teljesexom-szekvenálás módszerekkel a magzati diagnosztikában},
	url = {https://m2.mtmt.hu/api/publication/34780698},
	author = {Pikó, Henriett and Illés, Anett and Nagy, Sándor and Beke, Artúr and Árvai, Kristóf and Elekes, Tibor and Ferdinandyné Horváth, Emese and Ferenczy, Miklós and Mosonyi, Péter and Lukács, Valéria and Klujber, Valéria and Török, Olga and Kiss, Zsuzsanna and P Tardy, Erika and Tidrenczel, Zsolt and Tóbiás, Bálint and Balla, Bernadett and Lakatos, Péter and Kósa, János and Takács, István},
	doi = {10.1556/650.2024.33028},
	journal-iso = {ORV HETIL},
	journal = {ORVOSI HETILAP},
	volume = {165},
	unique-id = {34780698},
	issn = {0030-6002},
	abstract = {Bevezetés: Az elmúlt évtized egyik jelentős technológiai újdonsága az ún. ’high-throughput’ molekuláris genetikai vizsgálati módszerek – mint a kromoszomális microarray-analízis (chromosomal microarray analysis, CMA) és a teljesexom-szekvenálás (whole-exome sequencing, WES) – elterjedése a praenatalis diagnosztikában. Célkitűzés: Az elmúlt 5 évben munkacsoportunk több mint 252 praenatalis vizsgálatot végzett hazai laboratóriumi háttérrel, amelyek indikációját különböző súlyosságú strukturális magzati ultrahangeltérések képezték. A klasszikus citogenetikai vizsgálatok eredményétől függően végeztük el a nagy felbontású CMA- és WES-analíziseket a praenatalis diagnosztika érdekében. Módszer: A CMA-vizsgálatokat a „GeneChip System 3000 Instrument” platformmal végeztük az SNP-alapú komparatív hibridizálás módszerével. Az általunk elvégzett újgenerációs szekvenálás során a teljes humán exom szekvenciájának meghatározása IonTorrent és Illumina platformokkal történt. Eredmények: Összesen 252 magzati CMA-vizsgálatot végeztünk, és 42%-ban mutattunk ki valamilyen hiányt vagy többletet, ebből 22%-ban igazoltunk kóros eltérést. 42 esetben végeztünk WES-t, amelyből 9 esetben (21,4%) azonosítottunk kóros eltérést az öröklésmenetet támogató, a magzati fenotípussal feltételezhetően összefüggésben lévő, a ClinVar adatbázis vagy az ACMG-klasszifikáció alapján. Megbeszélés: Tekintettel arra, hogy a magzati fenotípus értékelése közvetett, a praenatalis CMA- és WES-elemzésnek elsősorban a magzati ultrahangvizsgálat során azonosítható strukturális anomáliákkal összefüggő génekre, kromoszomális régiókra kell korlátozódnia. A szülők vizsgálata mind a CMA-, mind a WES-analízisek során kiemelt jelentőséggel bír, főleg azokban az esetekben, amelyeknél a kapott eltérés nem hozható egyértelmű összefüggésbe az ultrahangeltérésekkel. Következtetés: Fontos meghatározni azokat a paramétereket, amelyek alapján a magzati mintában talált kópiaszám-eltéréseket és WES-vizsgálattal igazolt variánsokat a leletben közöljük (figyelembe véve a nemzetközi ajánlásokat). Ezek alapján a praenatalis klinikai genetikai tanácsadáskor sokkal használhatóbb információk adhatók. Orv Hetil. 2024; 165(14): 523–530.},
	year = {2024},
	eissn = {1788-6120},
	pages = {523-530},
	orcid-numbers = {Pikó, Henriett/0000-0002-3579-5451; Illés, Anett/0000-0001-5351-9015; Beke, Artúr/0000-0002-6826-7751; Árvai, Kristóf/0000-0001-8774-937X; Tidrenczel, Zsolt/0000-0001-7223-1551; Tóbiás, Bálint/0000-0003-4343-1866; Balla, Bernadett/0000-0003-2465-1804; Lakatos, Péter/0000-0002-7652-3671; Takács, István/0000-0002-7810-4833}
}

@article{MTMT:34729561,
	title = {An Open-Label Phase 2 Study of Eneboparatide, a Novel PTH Receptor 1 Agonist, in Hypoparathyroidism},
	url = {https://m2.mtmt.hu/api/publication/34729561},
	author = {Takács, István and Mezősi, Emese and Soto, Alfonso and Kamenický, Peter and Figueres, Lucile and Galvez Moreno, Maria Angeles and Lemoine, Sandrine and Borson-Chazot, Francoise and Capel, Ismael and Ouldrouis, Taha and Lucas, Nadège and Allas, Soraya and Sumeray, Mark and Ovize, Michel and Mannstadt, Michael},
	doi = {10.1210/clinem/dgae121},
	journal-iso = {J CLIN ENDOCR METAB},
	journal = {JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM},
	unique-id = {34729561},
	issn = {0021-972X},
	abstract = {Hypoparathyroidism is a rare disorder characterized by a deficiency in parathyroid hormone (PTH) resulting in hypocalcemia, hyperphosphatemia, and hypercalciuria. Eneboparatide is an investigational peptide agonist of the PTH1 receptor for the treatment of chronic hypoparathyroidism (HP).To evaluate the efficacy, safety, and tolerability of eneboparatide in HP patients.Open-label, phase 2 study.Twenty-eight patients (21 women, 7 men), mean age (range): 58 years (28-72), with HP were enrolled into 2 consecutive cohorts (C1, n = 12, and C2, n = 16).Following an optimization period, daily subcutaneous injections of eneboparatide were administered for 3 months at 20 µg/day (C1) or 10 µg/day (C2) starting dose. Conventional therapy was progressively removed and eneboparatide could be titrated up to 60 µg (C1) or 80 µg (C2).Proportion of patients achieving independence from conventional therapy, albumin-adjusted serum calcium (ADsCa), 24-h urine calcium (uCa), serum bone turnover markers (s-CTX and P1NP), bone mineral density (BMD), and adverse events (AEs).After 3 months,  ≥ 88% patients achieved independence from conventional therapy while mean ADsCa was maintained within target range (7.8-9 mg/dL). Eneboparatide induced a rapid and sustained reduction of mean 24-hour uCa, even among patients with hypercalciuria. Bone turnover markers slightly increased and BMD remained unchanged, consistent with progressive resumption of physiologic bone turnover. Eneboparatide was well tolerated with no serious AEs.Eneboparatide allowed independence from conventional therapy and maintenance of serum calcium within a target range, while normalizing uCa excretion and producing a balanced resumption of bone turnover.},
	keywords = {calcium; REPLACEMENT THERAPY; Parathyroid Hormone; hypoparathyroidism; bone biomarkers; eneboparatide},
	year = {2024},
	eissn = {1945-7197},
	orcid-numbers = {Takács, István/0000-0002-7810-4833; Mezősi, Emese/0000-0001-9367-3877}
}

@article{MTMT:34452050,
	title = {Efficacy and safety of aldosterone synthase inhibition with and without empagliflozin for chronic kidney disease. a randomised, controlled, phase 2 trial},
	url = {https://m2.mtmt.hu/api/publication/34452050},
	author = {Tuttle, Katherine R and Hauske, Sibylle J and Canziani, Maria Eugenia and Caramori, Maria Luiza and Cherney, David and Cronin, Lisa and Heerspink, Hiddo J L and Hugo, Christian and Nangaku, Masaomi and Rotter, Ricardo Correa and Silva, Arnold and Shah, Shimoli V and Sun, Zhichao and Urbach, Dorothea and de Zeeuw, Dick and Rossing, Peter},
	doi = {10.1016/S0140-6736(23)02408-X},
	journal-iso = {LANCET},
	journal = {LANCET},
	volume = {403},
	unique-id = {34452050},
	issn = {0140-6736},
	abstract = {Excess aldosterone accelerates chronic kidney disease progression. This phase 2 clinical trial assessed BI 690517, an aldosterone synthase inhibitor, for efficacy, safety, and dose selection.This was a multinational, randomised, controlled, phase 2 trial. People aged 18 years or older with an estimated glomerular filtration rate (eGFR) of 30 to less than 90 mL/min/1·73 m2, a urine albumin to creatinine ratio (UACR) of 200 to less than 5000 mg/g, and serum potassium of 4·8 mmol/L or less, taking an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, were enrolled. Participants were randomly assigned (1:1) to 8 weeks of empagliflozin or placebo run-in, followed by a second randomisation (1:1:1:1) to 14 weeks of treatment with once per day BI 690517 at doses of 3 mg, 10 mg, or 20 mg, or placebo. Study participants, research coordinators, investigators, and the data coordinating centre were masked to treatment assignment. The primary endpoint was the change in UACR measured in first morning void urine from baseline (second randomisation) to the end of treatment. This study is registered with ClinicalTrials.gov (NCT05182840) and is completed.Between Feb 18 and Dec 30, 2022, of the 714 run-in participants, 586 were randomly assigned to receive BI 690517 or placebo. At baseline, 33% (n=196) were women, 67% (n=390) were men, 42% (n=244) had a racial identity other than White, and mean participant age was 63·8 years (SD 11·3). Mean baseline eGFR was 51·9 mL/min/1·73 m2 (17·7) and median UACR was 426 mg/g (IQR 205 to 889). Percentage change in first morning void UACR from baseline to the end of treatment at week 14 was -3% (95% CI -19 to 17) with placebo, -22% (-36 to -7) with BI 690517 3 mg, -39% (-50 to -26) with BI 690517 10 mg, and -37% (-49 to -22) with BI 690517 20 mg monotherapy. BI 690517 produced similar UACR reductions when added to empagliflozin. Investigator-reported hyperkalaemia occurred in 10% (14/146) of those in the BI 690517 3 mg group, 15% (22/144) in the BI 690517 10 mg group, and 18% (26/146) in the BI 690517 20 mg group, and in 6% (nine of 147) of those receiving placebo, with or without empagliflozin. Most participants with hyperkalaemia did not require intervention (86% [72/84]). Adrenal insufficiency was an adverse event of special interest reported in seven of 436 study participants (2%) receiving BI 690517 and one of 147 participants (1%) receiving matched placebo. No treatment-related deaths occurred during the study.BI 690517 dose-dependently reduced albuminuria with concurrent renin-angiotensin system inhibition and empagliflozin, suggesting an additive efficacy for chronic kidney disease treatment without unexpected safety signals.Boehringer Ingelheim.},
	year = {2024},
	eissn = {1474-547X},
	pages = {379-390},
	orcid-numbers = {Takács, István/0000-0002-7810-4833; Pethő, Ákos/0000-0001-9776-9841; Szili, Balázs/0000-0002-2816-9487}
}

@article{MTMT:34425939,
	title = {The Semmelweis Study: a longitudinal occupational cohort study within the framework of the Semmelweis Caring University Model Program for supporting healthy aging},
	url = {https://m2.mtmt.hu/api/publication/34425939},
	author = {Ungvári, Zoltán István and Tabák, Ádám and Ádány, Róza and Purebl, György and Kaposvári, Csilla and Fazekas-Pongor, Vince and Csípő, Tamás and Szarvas, Zsófia and Horváth, Krisztián and Mukli, Péter and Balog, Piroska and Bódizs, Róbert and Ujma, Przemyslaw Péter and Stauder, Adrienne and Belsky, Daniel W. and Kovács, Illés and Yabluchanskiy, Andriy and Maier, Andrea B. and Moizs, Mariann and Östlin, Piroska and Yon, Yongjie and Varga, Péter and Vokó, Zoltán and Papp, Magor Csongor and Takács, István and Vásárhelyi, Barna and Torzsa, Péter and Ferdinandy, Péter and Csiszar, Anna and Benyó, Zoltán and Szabó, Attila and Bednárikné Dörnyei, Gabriella and Kivimäki, Mika and Kellermayer, Miklós and Merkely, Béla Péter},
	doi = {10.1007/s11357-023-01018-7},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34425939},
	issn = {2509-2715},
	abstract = {The Semmelweis Study is a prospective occupational cohort study that seeks to enroll all employees of Semmelweis University (Budapest, Hungary) aged 25 years and older, with a population of 8866 people, 70.5% of whom are women. The study builds on the successful experiences of the Whitehall II study and aims to investigate the complex relationships between lifestyle, environmental, and occupational risk factors, and the development and progression of chronic age-associated diseases. An important goal of the Semmelweis Study is to identify groups of people who are aging unsuccessfully and therefore have an increased risk of developing age-associated diseases. To achieve this, the study takes a multidisciplinary approach, collecting economic, social, psychological, cognitive, health, and biological data. The Semmelweis Study comprises a baseline data collection with open healthcare data linkage, followed by repeated data collection waves every 5 years. Data are collected through computer-assisted self-completed questionnaires, followed by a physical health examination, physiological measurements, and the assessment of biomarkers. This article provides a comprehensive overview of the Semmelweis Study, including its origin, context, objectives, design, relevance, and expected contributions.},
	year = {2024},
	eissn = {2509-2723},
	pages = {191-218},
	orcid-numbers = {Ungvári, Zoltán István/0000-0002-6035-6039; Tabák, Ádám/0000-0002-6234-3936; Purebl, György/0000-0002-9750-2001; Fazekas-Pongor, Vince/0000-0002-6405-4003; Szarvas, Zsófia/0000-0002-0022-5053; Mukli, Péter/0000-0003-4355-8103; Balog, Piroska/0000-0001-5025-8649; Bódizs, Róbert/0000-0001-5341-060X; Ujma, Przemyslaw Péter/0000-0002-7981-3009; Stauder, Adrienne/0000-0002-0358-3657; Kovács, Illés/0000-0001-5763-0482; Vokó, Zoltán/0000-0002-1004-1848; Takács, István/0000-0002-7810-4833; Vásárhelyi, Barna/0000-0003-0055-7346; Torzsa, Péter/0000-0002-8148-4961; Ferdinandy, Péter/0000-0002-6424-6806; Benyó, Zoltán/0000-0001-6015-0359; Szabó, Attila/0000-0001-7321-9861; Bednárikné Dörnyei, Gabriella/0000-0001-7007-6252; Kellermayer, Miklós/0000-0002-5553-6553; Merkely, Béla Péter/0000-0001-6514-0723}
}