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Authors: Yonca B. Kabak, Mahmut Sozmen, Alparslan K. Devrim, Mert Sudagidan, Funda Yildirim, Tolga Guvenc, Murat Yarim, Yavuz M. Gulbahar, Ishtiaq Ahmed, Efe Karaca and Sinem Inal

). Immunohistochemistry (IHC) Sections (5 μm) from the tissue samples were subjected to immunohistochemistry (IHC) using the streptavidin-biotin peroxidase complex technique for the detection of bFGF, VEGF-C, TGFβ1, PDGF-A, PDGF-C and PDGFR-α. Comparison of the VEGF and

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Authors: Gabriella Pár, Áron Vincze, Timea Berki, Attila Miseta, László Kereskai, László Pajor, Angela Oszter, Ferenc Jakab, Zoltán Szereday, Ágnes Nagy, Béla Hunyady and Alajos Pár

Abstract

Background: Although liver biopsy (LB) is the gold standard for the morphological diagnosis of diseases of the liver, recent noninvasive tests may also help in the evaluation of liver fibrosis. We have studied blood fibrosis markers and liver stiffness (LS) measurement to assess fibrosis in different forms of chronic hepatitis C virus (HCV) infection. Patients and methods: Out of 119 HCV-infected patients, 75 had biopsy-proven chronic hepatitis C, 24 had HCV cirrhosis, 20 individuals were symptom-free HCV carriers with persistently normal alanine aminotransferase (PNA), and 30 healthy blood donors served as controls. Wai's aspartate-aminotransferase (AST) to platelet ratio index (APRI) was calculated from serum AST and blood platelet number. Serum HCV-RNA (hepatitis C virus ribonucleic acid), procollagen-III-peptide (P-III-P) and hyaluronic acid (HA), plasma transforming growth factor β-1 (TGFβ-1), Knodell's histological activity index (HAI), and METAVIR fibrosis score were determined, and for LS measurement transient elastography (TE) (FibroScan) was applied. Results: In chronic hepatitis C patients, all fibrosis markers were significantly elevated compared to normal controls. HA, APRI, and LS values were highest in HCV cirrhosis and nonresponders to PEG-IFN + ribavirin (P/R) therapy. High P-III-P values occurred only in advanced fibrosis. Serum HA correlated with the fibrosis stage. Plasma TGFβ-1 was significantly higher in patients with chronic hepatitis C than in symptom-free HCV carriers, and it correlated with HAI. After 3–6 months of P/R therapy, both HA and TGFβ-1 levels significantly decreased even in virological nonresponders. APRI was 0.21 ± 0.05 in normal controls, 0.20 ± 0.08 in symptom-free HCV carriers, 0.70 ± 0.40 in patients with chronic hepatitis C, and 3.21 ± 2.3 in HCV cirrhosis cases. LS values were 5.10 ± 1.19 kPa in controls, 5.38 ± 1.37 kPa in HCV carriers with PNA, 9.67 ± 4.11 kPa in chronic hepatitis C patients, 6.56 ± 2.61 kPa in patients with sustained virological response, 18.55 ± 11.65 kPa in nonresponders to P/R, and 37.40 ± 16.85 kPa in HCV cirrhosis cases. On the basis of a novel sequential algorithm that comprises APRI and LS for assessment of fibrosis, 47% of our HCV patients did not need biopsy for diagnosing significant (F ≥ 2) fibrosis. Conclusion: Both blood fibrosis markers and LS, particularly in combination, represent an advance in the noninvasive assessment of fibrosis in HCV infection. P/R treatment may inhibit fibrosis progression even independently of virological response.

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Authors: Balázs Liktor, Andor Hirschberg and Tamás Karosi

Absztrakt:

Az otosclerosis egy jelenleg is ismeretlen etiológiájú megbetegedés, mely kizárólagosan az emberi temporalis csont oticus kapszulájában mutatható ki. Az elmúlt évtizedekben számtalan etiopatogenetikai faktor lehetséges szerepe merült fel, azonban a legtöbb kísérletet klinikai tünetek alapján diagnosztizált otosclerosisos beteganyagon végezték, amelynek nagyjából egyharmada nem is otosclerosisos eredetű stapesfixáció. Kísérletsorozatainkban szövettani vizsgálat alapján diagnosztizáltuk és stadizáltuk az otosclerosisos betegcsoportot, és ezúton vizsgáltuk a lehetséges patogenetikai tényezőket. Kísérletes munkánknak köszönhetően mára egyértelmű etiológiai tényezőként tartják számon a kanyaróvírus-fertőzést és a transzformáló növekedési faktor-béta-1 (TGFβ1)-gén rs1800472-SNP-jét, melyeknek ez idáig még nincs terápiás konzekvenciájuk. Továbbá a jelen tanulmányban végigkövetjük az irodalomban fellelhető genetikai és környezeti tényezőket, melyek alapvető szerepet játszhatnak az otosclerosis patogenezisében. Orv Hetil. 2018; 159(30): 1215–1220.

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-inflammatory macrophages induce Foxp 3 + GITR + CD 25 regulatory T cells, which suppress via membrane-bound TGFβ-1. J. Immunol., 2008, 181 (3), 2220–2226. Lakatos, P.: Osteoimmunology: How does inflammation affect bone metabolism

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): The pro-inflammatory role of TGFβ1: a paradox ? Int. J. Biol. Sci. 8 , 228 – 235 . Hermans , D. , Van Steendam , K. , Verbrugghe , E. , Verlinden , M. , Martel , A

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Authors: B. Sági, A. Peti, O. Lakatos, T. Gyimesi, E. Sulyok, I. Wittmann and Botond Csiky

/l) Fetuin A (g/l) α-Klotho (pg/mL) TNF-α (pg/mL) TGFβ-1 (ng/mL) hsCRP (mg/l) Patients 11.4 ± 7.5 0.43 ± 0.11 299.3 ± 124.7 20.2 ± 15.9 2.85 ± 1.35 11.8 ± 10.4 Controls 52.2 ± 13.1 0.55 ± 0.09 602 ± 100 5.2 ± 1.3 0.69 ± 0.42 4.51 ± 5.31 P 0.001 0.05 0.01 0

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adaptive myocardial hypertension and could lead to the preservation of the right ventricle function in early stage of PAH. VEGFR: vascular endothelial growth factor receptor; TGFβ1R: transforming growth factor-β1 receptor; FGFR: fibroblast growth factor

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