TY - JOUR AU - Chen, Jia-Le AU - Liu, Lou AU - Peng, Xin-Rui AU - Wang, Yan AU - Xiang, Xiang AU - Chen, Yu AU - Xu, De-Xiang AU - Chen, Dao-Zhen TI - Role of the GalNAc-galectin pathway in the healing of premature rupture of membranes JF - MOLECULAR MEDICINE J2 - MOL MED VL - 30 PY - 2024 IS - 1 PG - 11 SN - 1076-1551 DO - 10.1186/s10020-024-00908-6 UR - https://m2.mtmt.hu/api/publication/35316198 ID - 35316198 N1 - Export Date: 27 February 2025; CODEN: MOMEE LA - English DB - MTMT ER - TY - JOUR AU - Miura, Y. AU - Fujii, S. AU - Ichinohe, T. TI - Cell-based and extracellular vesicle-based MSC therapies for acute radiation syndrome affecting organ systems JF - JOURNAL OF RADIATION RESEARCH J2 - J RADIAT RES VL - 65 PY - 2024 SP - i80 EP - i87 SN - 0449-3060 DO - 10.1093/jrr/rrae009 UR - https://m2.mtmt.hu/api/publication/35657394 ID - 35657394 N1 - Department of Hematology and Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima, 734-8553, Japan Department of Transfusion Medicine and Cell Therapy, Fujita Health University School of Medicine, 1-93 Dengakugakubo, Kutsukakecho, Toyoake, Aichi, 470-1192, Japan Export Date: 2 January 2025 Correspondence Address: Ichinohe, T.; Department of Hematology and Oncology, 1-2-3 Kasumi, Minami-ku, Japan; email: nohe@hiroshima-u.ac.jp LA - English DB - MTMT ER - TY - JOUR AU - Ruppert, Zsófia AU - Neuperger, Patricia AU - Rákóczi, Bettina AU - Gémes, Nikolett AU - Dukay, Brigitta AU - Hajdu, Petra AU - Péter, Mária AU - Balogh, Gábor AU - Tiszlavicz, László AU - Vigh, László AU - Török, Zsolt AU - Puskás, László AU - Szebeni, Gábor AU - Tóth, Erzsébet Melinda TI - Characterization of obesity-related diseases and inflammation using single cell immunophenotyping in two different diet-induced obesity models JF - INTERNATIONAL JOURNAL OF OBESITY J2 - INT J OBES (LOND) VL - 48 PY - 2024 IS - 11 SP - 1568 EP - 1576 PG - 9 SN - 0307-0565 DO - 10.1038/s41366-024-01584-6 UR - https://m2.mtmt.hu/api/publication/35133023 ID - 35133023 N1 - Laboratory of Molecular Stress Biology, Institute of Biochemistry, HUN-REN Biological Research Centre, Szeged, Hungary PhD School in Biology, University of Szeged, Szeged, Hungary Laboratory of Functional Genomics, Core Facility, HUN-REN Biological Research Centre, Szeged, Hungary Department of Pathology, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary Department of Internal Medicine, Hematology Centre, Faculty of Medicine, University of Szeged, Szeged, H6725, Hungary Export Date: 2 August 2024 CODEN: IJOBD Correspondence Address: Tóth, M.E.; Laboratory of Molecular Stress Biology, Hungary; email: toth.erzsebetmelinda@brc.hu Correspondence Address: Szebeni, G.J.; Laboratory of Functional Genomics, Hungary; email: szebeni.gabor@brc.hu A közlemény a Bolyai János Kutatási Ösztöndíj (BO/00582/22/8) segítségével jött létre. AB - Obesity is a growing problem worldwide and a major risk factor for many chronic diseases. The accumulation of adipose tissue leads to the release of significant amounts of pro-inflammatory cytokines and adipokines, resulting in a low-grade systemic inflammation. However, the mechanisms behind the development of obesity-related diseases are not fully understood. Therefore, our study aimed to investigate the pathological changes and inflammatory processes at systemic level and in individual organs in two different diet-induced mouse obesity models. LA - English DB - MTMT ER - TY - JOUR AU - Vukotić, M. AU - Kapor, S. AU - Simon, F. AU - Cokic, V. AU - Santibanez, J.F. TI - Mesenchymal stromal cells in myeloid malignancies: Immunotherapeutic opportunities JF - HELIYON J2 - HELIYON VL - 10 PY - 2024 IS - 3 SN - 2405-8440 DO - 10.1016/j.heliyon.2024.e25081 UR - https://m2.mtmt.hu/api/publication/34566506 ID - 34566506 N1 - Molecular Oncology Group, Institute for Medical Research, University of Belgrade, Belgrade, Serbia Department of Hematology, Clinical Hospital Center “Dr. Dragisa Misovic-Dedinje, ” University of Belgrade, Serbia Laboratory of Integrative Physiopathology, Faculty of Life Sciences, Universidad Andres Bello, Santiago, Chile Millennium Institute on Immunology and Immunotherapy, Santiago, Chile Millennium Nucleus of Ion Channel-Associated Diseases, Universidad de Chile, Santiago, Chile Centro Integrativo de Biología y Química Aplicada (CIBQA), Universidad Bernardo O'Higgins, Santiago, Chile Export Date: 8 February 2024 Correspondence Address: Santibanez, J.F.; Molecular oncology group, Dr. Subotica 4, POB 102, Serbia; email: jfsantibanez@imi.bg.ac.rs Correspondence Address: Kapor, S.; Department of Hematology, Serbia; email: suncicabjelica@gmail.com AB - Myeloid malignancies are clonal disorders of the progenitor cells or hematopoietic stem cells, including acute myeloid leukemia, myelodysplastic syndromes, myeloproliferative malignancies, and chronic myelomonocytic leukemia. Myeloid neoplastic cells affect the proliferation and differentiation of other hematopoietic lineages in the bone marrow and peripheral blood, leading to severe and life-threatening complications. Mesenchymal stromal cells (MSCs) residing in the bone marrow exert immunosuppressive functions by suppressing innate and adaptive immune systems, thus creating a supportive and tolerant microenvironment for myeloid malignancy progression. This review summarizes the significant features of MSCs in myeloid malignancies, including their role in regulating cell growth, cell death, and antineoplastic resistance, in addition to their immunosuppressive contributions. Understanding the implications of MSCs in myeloid malignancies could pave the path for potential use in immunotherapy. © 2024 The Authors LA - English DB - MTMT ER - TY - JOUR AU - Kiss, Tamás AU - Mir, Mohd Yaqub AU - Stefancsik, Gergely AU - Ganbat, Gantulga AU - Askarova, Aruzhan AU - Monostori, Éva AU - Dulka, Karolina AU - Szebeni, Gábor AU - Nyúl-Tóth, Ádám AU - Csiszar, Anna AU - Légrádi, Ádám TI - Galectin-1 as a marker for microglia activation in the aging brain JF - BRAIN RESEARCH J2 - BRAIN RES VL - 1818 PY - 2023 PG - 13 SN - 0006-8993 DO - 10.1016/j.brainres.2023.148517 UR - https://m2.mtmt.hu/api/publication/34093747 ID - 34093747 N1 - Funding Agency and Grant Number: American Heart Association [GINOP-2.3.2-15-2016-00034, 142877 FK22]; National Research, Development, and Innovation Office (NKFI) , Hungary [AHA834339]; Ministry for Innovation and Technology from the National Research, Development and Innovation Fund; American Heart Association; Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences; [EFOP-3.6.1-16-2016-00008]; [2020-1.1.6-JOVO-2021-00003]; [UNKP-22-5-SZTE-535]; [BO/00582/22/8] Funding text: This work was supported by a grant from EFOP-3.6.1-16-2016-00008 and GINOP-2.3.2-15-2016-00034 grants. ANyT was supported by American Heart Association (AHA834339) . (The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript) . This research was funded by the 2020-1.1.6-JOVO-2021-00003 and 142877 FK22, grant from the National Research, Development, and Innovation Office (NKFI) , Hungary. This work was supported by the UNKP-22-5-SZTE-535 New National Excellence Program (GJS) of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund. This work was supported by the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences BO/00582/22/8 (GJS) . AB - Microglia cells, the immune cells residing in the brain, express immune regulatory molecules that have a central role in the manifestation of age-related brain characteristics. Our hypothesis suggests that galectin-1, an anti-inflammatory member of the beta-galactoside-binding lectin family, regulates microglia and neuroinflammation in the aging brain. Through our in-silico analysis, we discovered a subcluster of microglia in the aged mouse brain that exhibited increased expression of galectin-1 mRNA. In our Western blotting experiments, we observed a decrease in galectin-1 protein content in our rat primary cortical cultures over time. Additionally, we found that the presence of lipopolysaccharide, an immune activator, significantly increased the expression of galectin-1 protein in microglial cells. Utilizing flow cytometry, we determined that a portion of the galectin-1 protein was localized on the surface of the microglial cells. As cultivation time increased, we observed a decrease in the expression of activation-coupled molecules in microglial cells, indicating cellular exhaustion. In our mixed rat primary cortical cell cultures, we noted a transition of amoeboid microglial cells labeled with OX42(CD11b/c) to a ramified, branched phenotype during extended cultivation, accompanied by a complete disappearance of galectin-1 expression. By analyzing the transcriptome of a distinct microglial subpopulation in an animal model of aging, we established a correlation between chronological aging and galectin-1 expression. Furthermore, our in vitro study demonstrated that galectin-1 expression is associated with the functional activation state of microglial cells exhibiting specific amoeboid morphological characteristics. Based on our findings, we identify galectin-1 as a marker for microglia activation in the context of aging. LA - English DB - MTMT ER - TY - JOUR AU - Fujii, Sumie AU - Miura, Yasuo TI - Immunomodulatory and Regenerative Effects of MSC-Derived Extracellular Vesicles to Treat Acute GVHD JF - STEM CELLS J2 - STEM CELLS VL - 40 PY - 2022 IS - 11 SP - 977 EP - 990 PG - 14 SN - 1066-5099 DO - 10.1093/stmcls/sxac057 UR - https://m2.mtmt.hu/api/publication/33081050 ID - 33081050 N1 - Funding Agency and Grant Number: Japan Society for the Promotion of Science KAKENHI [19K17856, 18K08323, 22K07485] Funding text: This work was supported in part by Grants-in-Aid from Japan Society for the Promotion of Science KAKENHI (grant number 19K17856 for S.F., and 18K08323 and 22K07485 for Y.M.). AB - The development of human mesenchymal stromal/stem cell (MSC)-based therapy has focused on exploring biological nanoparticles secreted from MSCs. There is emerging evidence that the immunomodulatory and regenerative effects of MSCs can be recapitulated by extracellular vesicles released from MSCs (MSC-EVs). Off-the-shelf allogeneic human MSC products are clinically available to treat acute graft-versus-host disease (GVHD), but real-world data have revealed the limitations of these products as well as their feasibility, safety, and efficacy. MSC-EVs may have advantages over parental MSCs as drugs because of their distinguished biodistribution and importantly dose-dependent therapeutic effects. Recent research has shed light on the role of microRNAs in the mode-of-action of MSC-EVs. A group of specific microRNAs alone or in combination with membrane proteins, membrane lipids, and soluble factors present in MSC-EVs play key roles in the regulation of GVHD. In this concise review, we review the regulation of T-cell-mediated adaptive immunity and antigen-presenting cell-mediated innate immunity by MSC-EVs and the direct regenerative effects on damaged cells in association with the immunopathology of GVHD. LA - English DB - MTMT ER - TY - JOUR AU - Hermenean, Anca AU - Oatis, Daniela AU - Herman, Hildegard AU - Ciceu, Alina AU - D'Amico, Giovanbattista AU - Trotta, Maria Consiglia TI - Galectin 1-A Key Player between Tissue Repair and Fibrosis JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 10 PG - 12 SN - 1661-6596 DO - 10.3390/ijms23105548 UR - https://m2.mtmt.hu/api/publication/32888529 ID - 32888529 N1 - Funding Agency and Grant Number: Romanian Ministry of Research, Innovation and Digitization, CNCS/CCCDI-UEFISCDI within PNCDI III [PN-III-P4-ID-PCE-2020-1772] Funding text: This research was funded by a grant of the Romanian Ministry of Research, Innovation and Digitization, CNCS/CCCDI-UEFISCDI, project number PN-III-P4-ID-PCE-2020-1772, within PNCDI III. AB - Galectins are ten family members of carbohydrate-binding proteins with a high affinity for beta galactose-containing oligosaccharides. Galectin-1 (Gal-1) is the first protein discovered in the family, expressed in many sites under normal and pathological conditions. In the first part of the review article, we described recent advances in the Gal-1 modulatory role on wound healing, by focusing on the different phases triggered by Gal-1, such as inflammation, proliferation, tissue repair and re-epithelialization. On the contrary, Gal-1 persistent over-expression enhances angiogenesis and extracellular matrix (ECM) production via PI3K/Akt pathway activation and leads to keloid tissue. Therefore, the targeted Gal-1 modulation should be considered a method of choice to treat wound healing and avoid keloid formation. In the second part of the review article, we discuss studies clarifying the role of Gal-1 in the pathogenesis of proliferative diabetic retinopathy, liver, renal, pancreatic and pulmonary fibrosis. This evidence suggests that Gal-1 may become a biomarker for the diagnosis and prognosis of tissue fibrosis and a promising molecular target for the development of new and original therapeutic tools to treat fibrosis in different chronic diseases. LA - English DB - MTMT ER - TY - JOUR AU - Li, Jingman AU - Pan, Yuchen AU - Yang, Jingjing AU - Wang, Jiali AU - Jiang, Qi AU - Dou, Huan AU - Hou, Yayi TI - Tumor necrosis factor-alpha-primed mesenchymal stem cell-derived exosomes promote M2 macrophage polarization via Galectin-1 and modify intrauterine adhesion on a novel murine model JF - FRONTIERS IN IMMUNOLOGY J2 - FRONT IMMUNOL VL - 13 PY - 2022 PG - 15 SN - 1664-3224 DO - 10.3389/fimmu.2022.945234 UR - https://m2.mtmt.hu/api/publication/33586986 ID - 33586986 AB - BackgroundIntrauterine adhesion (IUA) is a condition caused due to damage or infection of the endometrium. It is characterized by continuous inflammation and following fibrosis and dysfunction. However, the current animal IUA models have several disadvantages, including complex operation, high mortality, and many extra distractions owing to opening of the abdominal cavity to expose the uterus. Mesenchymal stem cells (MSCs), which have been used in treatment of IUA, are heterogeneous and immunosuppressive. However, their therapeutic effect is not as good as expected. MethodsHere, we successfully built a new murine IUA model, called electric tool-scratching IUA model, and applied it in our experiments to investigate the efficacy of tumor necrosis factor-alpha (TNF-alpha) primed MSCs (T-MSCs). In the new model, we used a self-made electric tool that can cause mechanical damage to the endometrium without opening the abdominal cavity. ELISA and histological staining analysis were performed to evaluate pathological features of IUA. qRT-PCR, flow cytometry and immunofluoresence staining were performed to detect the phenotypes of macrophages. TMT proteomics quantification and western blotting assay were performed to analyze the differentially expressed proteins of MSC exosomes. ResultsBased on the new IUA model, we found TNF-alpha pretreatment could enhance the ability of MSCs to relieve inflammation and reduce endometrium fibrosis. Mechanistically, T-MSC promoted macrophage polarization to M2 phenotype through exosomes. Subsequently, we found the expression of Galectin-1 was increased in T-MSC exosomes. Finally, we analyzed the gene expression pattern of Galectin-1 treated macrophages and found Galectin-1 promoted macrophage polarization to M2 phenotype mainly through the Jak-STAT signaling pathway. ConclusionsOur studies proposed an innovative mouse model and a better MSC treatment strategy for IUA. LA - English DB - MTMT ER - TY - JOUR AU - Oatis, Daniela AU - Simon-Repolski, Erika AU - Balta, Cornel AU - Mihu, Alin AU - Pieretti, Gorizio AU - Alfano, Roberto AU - Peluso, Luisa AU - Trotta, Maria Consiglia AU - D'Amico, Michele AU - Hermenean, Anca TI - Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1,-3,-8,-9 JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 15 PG - 13 SN - 1661-6596 DO - 10.3390/ijms23158210 UR - https://m2.mtmt.hu/api/publication/33066488 ID - 33066488 AB - Pulmonary fibrosis is a consequence of the pathological accumulation of extracellular matrix (ECM), which finally leads to lung scarring. Although the pulmonary fibrogenesis is almost known, the last two years of the COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its post effects added new particularities which need to be explored. Many questions remain about how pulmonary fibrotic changes occur within the lungs of COVID-19 patients, and whether the changes will persist long term or are capable of resolving. This review brings together existing knowledge on both COVID-19 and pulmonary fibrosis, starting with the main key players in promoting pulmonary fibrosis, such as alveolar and endothelial cells, fibroblasts, lipofibroblasts, and macrophages. Further, we provide an overview of the main molecular mechanisms driving the fibrotic process in connection with Galactin-1, -3, -8, and -9, together with the currently approved and newly proposed clinical therapeutic solutions given for the treatment of fibrosis, based on their inhibition. The work underlines the particular pathways and processes that may be implicated in pulmonary fibrosis pathogenesis post-SARS-CoV-2 viral infection. The recent data suggest that galectin-1, -3, -8, and -9 could become valuable biomarkers for the diagnosis and prognosis of lung fibrosis post-COVID-19 and promising molecular targets for the development of new and original therapeutic tools to treat the disease. LA - English DB - MTMT ER - TY - JOUR AU - Ge, X. AU - Shi, K. AU - Hou, J. AU - Fu, Y. AU - Xiao, H. AU - Chi, F. AU - Xu, J. AU - Cai, F. AU - Bai, C. TI - Galectin-1 secreted by bone marrow-derived mesenchymal stem cells mediates anti-inflammatory responses in acute airway disease JF - EXPERIMENTAL CELL RESEARCH J2 - EXP CELL RES VL - 407 PY - 2021 IS - 1 SN - 0014-4827 DO - 10.1016/j.yexcr.2021.112788 UR - https://m2.mtmt.hu/api/publication/32182436 ID - 32182436 N1 - Department of Respiratory Medicine, Seventh People's Hospital of Shanghai University of TCM, Shanghai, 200137, China Department of Respiratory Medicine, Shanghai Hospital of Traditional Chinese Medicine, Shanghai, 200071, China Department of Respiratory and Critical Care Medicine, General Hospital of Ningxia Medical University, Ningxia, 750004, China Department of Respiratory and Critical Care Medicine, Changhai Hospital, Naval Medical University (Second Military Medical University), Shanghai, 200433, China Export Date: 7 September 2021 CODEN: ECREA Correspondence Address: Ge, X.; Department of Respiratory Medicine, China; email: 15000760961@126.com Correspondence Address: Bai, C.; Department of Respiratory and Critical Care Medicine, China; email: bc7878@sohu.com Funding details: PKJ2019-Y13 Funding details: BDX2019-01 Funding details: Natural Science Foundation of Shanghai, 20ZR1442600 Funding details: National Natural Science Foundation of China, NNSFC, 81300018, 81570020, 81873405 Funding text 1: This study was supported by funding from the National Natural Science Foundation of China ( 81300018 , 81570020 , 81873405 ); Fund of Pudong New Area Science and Technology Commission ( PKJ2019-Y13 ); Natural Science Foundation of Shanghai ( 20ZR1442600 ); Fund for the Seventh People's Hospital ( BDX2019-01 ). AB - The hallmarks of allergic airway disease (AAD) include infiltration of inflammatory cells into the bronchoalveolar space. Bone marrow derived mesenchymal stem cells (BMSCs) show anti-inflammatory properties in AAD. In addition, galectin-1 (Gal-1) is a lectin significantly upregulated upon inflammation and is also known to mediate potential anti-inflammatory responses. We hypothesized that BMSCs regulated inflammatory responses by secretion of Gal-1 during AAD pathogenesis. BMSCs were isolated from murine femurs and tibiae and adoptively transferred into an ovalbumin-induced AAD mouse model. Knockdown of Gal-1 in BMSCs was performed using shRNA. Flow cytometry, ELISAs, and immunohistology were performed to analyze inflammatory responses in mice, and a Transwell system was used to establish an in vitro co-culture system of lung epithelial cells (MLE-12) and BMSCs. Administration of BMSCs significantly upregulated Gal-1 expression upon inflammation and decreased infiltration of inflammatory cells and secretion of proinflammatory cytokines in vivo. In addition, we showed that this function was mediated by reduced activation of the MAPK p38 signaling pathway. Similar observations were found using an in vitro lipopolysaccharide-induced model when MLE-12 cells were co-cultured with BMSCs. Gal-1 secretion by BMSCs alleviated inflammatory responses observed in AAD and hence provides a promising therapeutic alternative to AAD patients insensitive to conventional drug treatments. © 2021 Elsevier Inc. LA - English DB - MTMT ER - TY - JOUR AU - Kapor, Suncica AU - Santibanez, Juan F. TI - Myeloid-Derived Suppressor Cells and Mesenchymal Stem/Stromal Cells in Myeloid Malignancies JF - JOURNAL OF CLINICAL MEDICINE J2 - J CLIN MED VL - 10 PY - 2021 IS - 13 PG - 26 SN - 2077-0383 DO - 10.3390/jcm10132788 UR - https://m2.mtmt.hu/api/publication/32106566 ID - 32106566 AB - Myeloid malignancies arise from an altered hematopoietic stem cell and mainly comprise acute myeloid leukemia, myelodysplastic syndromes, myeloproliferative malignancies, and chronic myelomonocytic leukemia. Myeloid neoplastic leukemic cells may influence the growth and differentiation of other hematopoietic cell lineages in peripheral blood and bone marrow. Myeloid-derived suppressor cells (MDSCs) and mesenchymal stromal cells (MSCs) display immunoregulatory properties by controlling the innate and adaptive immune systems that may induce a tolerant and supportive microenvironment for neoplasm development. This review analyzes the main features of MDSCs and MSCs in myeloid malignancies. The number of MDSCs is elevated in myeloid malignancies exhibiting high immunosuppressive capacities, whereas MSCs, in addition to their immunosuppression contribution, regulate myeloid leukemia cell proliferation, apoptosis, and chemotherapy resistance. Moreover, MSCs may promote MDSC expansion, which may mutually contribute to the creation of an immuno-tolerant neoplasm microenvironment. Understanding the implication of MDSCs and MSCs in myeloid malignancies may favor their potential use in immunotherapeutic strategies. LA - English DB - MTMT ER - TY - JOUR AU - Golubinskaya, P. A. AU - Sarycheva, M. V AU - Dolzhikov, A. A. AU - Bondarev, V. P. AU - Stefanova, M. S. AU - Soldatov, V. O. AU - Nadezhdin, S. V AU - Korokin, M. V AU - Pokrovsky, M. V AU - Burda, Yu E. TI - APPLICATION OF MULTIPOTENT MESENCHYMAL STEM CELL SECRETOME IN THE TREATMENT OF ADJUVANT ARTHRITIS AND CONTACT-ALLERGIC DERMATITIS IN ANIMAL MODELS JF - PHARMACY & PHARMACOLOGY-FARMATSIYA I FARMAKOLOGIYA J2 - PHARM PHARMACOL-RUSS VL - 8 PY - 2020 IS - 6 SP - 416 EP - 425 PG - 10 SN - 2307-9266 DO - 10.19163/2307-9266-2020-8-6-416-425 UR - https://m2.mtmt.hu/api/publication/32073571 ID - 32073571 N1 - Belgorod State National Research University, 85 Pobeda St., Belgorod, 308015, Russian Federation Regional Pathoanatomical Bureau of the Health Committee of the Kursk Region, 45a St. Sumskaya, Kursk, 305007, Russian Federation City Hospital No. 246, Gubkin St., Belgorod, 308036, Russian Federation Export Date: 22 June 2021 Correspondence Address: Golubinskaya, P.A.; Belgorod State National Research University, 85 Pobeda St., Russian Federation; email: polinapigeon@gmail.com Chemicals/CAS: 1 fluoro 2,4 dinitrobenzene, 25376-51-6, 70-34-8; dexamethasone, 50-02-2; fluocinolone, 807-38-5; Freund adjuvant, 9007-81-2 AB - The therapeutic effect of multipotent mesenchymal stem cells has been proven on various disease models. One of the mechanisms is the paracrine effect of the cells on the surrounding tissues. The aim. To investigate the secretome effectiveness of the multipotent mesenchymal stem cells in the treatment of adjuvant arthritis and contact-allergic dermatitis in Wistar rats. Materials and methods. Adjuvant arthritis was simulated in 26 female rats by the administration of Freund's complete adjuvant and then treated with the administration of 100 mu l of multipotent mesenchymal stem cell secretome or saline. Contact-allergic dermatitis was modeled on 30 female rats by applying 200 mu l of an oil solution of dinitrofluorobenzene to the skin on days 1, 5 and 6. Then the rats were treated with fluocinolone ointment (a positive control), baby cream (a negative control), baby cream with a secretome of native multipotent mesenchymal stem cells or from the cells processed with dexamethasone. Results. Judging by the indicators of the longitudinal and transverse dimensions of the paws in rats and a histological examination, the secretome did not have any anti-inflammatory effect on adjuvant arthritis. A cream with a secretome from multipotent mesenchymal stem cells processed with dexamethasone, was the most effective on the model of contact-allergic dermatitis: the clinical improvement occurred on the 2nd day. The secretome from native multipotent mesenchymal stem cells and fluocinolone had a therapeutic effect on the 3rd day of application, the negative control - on the 4th day. The lymphocytic infiltration coefficient was significantly lower (p<0.05) in all the cases compared to the negative control (2.8 +/- 0.1). However, the lowest infiltration was observed when the cream with secretome from native (1.75 +/- 0.1) and dexamethasone-stimulated (1.76 +/- 0.1) multipotent mesenchymal stem cells was being used. Conclusion. The cream with the secretome of multipotent mesenchymal stem cells suppresses lymphocytic infiltration more strongly than the highly active topical glucocorticosteroid - fluocinolone - on the model of contact-allergic dermatitis, which is a classic local delayed-type hypersensitivity reaction. However, a further study of the therapeutic effect of the secretome on models of systemic inflammatory diseases is required after its preliminary purification from large-molecular proteins. LA - Russian DB - MTMT ER - TY - JOUR AU - Juárez-Navarro, K.J. AU - Padilla-Camberos, E. AU - Díaz, N.F. AU - Miranda-Altamirano, A. AU - Díaz-Martínez, N.E. TI - Human Mesenchymal Stem Cells: The Present Alternative for High-Incidence Diseases, even SARS-Cov-2 JF - STEM CELLS INTERNATIONAL J2 - STEM CELLS INT VL - 2020 PY - 2020 SN - 1687-966X DO - 10.1155/2020/8892189 UR - https://m2.mtmt.hu/api/publication/31824428 ID - 31824428 N1 - Biotecnologia Medica y Farmaceut. Ctro. de Invest. y Asistencia en Tecn. y Diseno Del Estado de Jalisco, Guadalajara, Mexico Departamento de Fisiología y Desarrollo Celular, Instituto Nacional de Perinatología Isidro Espinosa de Los Reyes, Mexico City, Mexico Departamento de Atención A Niños Con Quemaduras, Hospital Civil de Guadalajara, Mexico Export Date: 22 January 2021 Correspondence Address: Díaz-Martínez, N.E.; Biotecnologia Medica y Farmaceut. Ctro. de Invest. y Asistencia en Tecn. y Diseno Del Estado de JaliscoMexico; email: ediaz@ciatej.mx Biotecnologia Medica y Farmaceut. Ctro. de Invest. y Asistencia en Tecn. y Diseno Del Estado de Jalisco, Guadalajara, Mexico Departamento de Fisiología y Desarrollo Celular, Instituto Nacional de Perinatología Isidro Espinosa de Los Reyes, Mexico City, Mexico Departamento de Atención A Niños Con Quemaduras, Hospital Civil de Guadalajara, Mexico Cited By :1 Export Date: 22 June 2021 Correspondence Address: Díaz-Martínez, N.E.; Biotecnologia Medica y Farmaceut. Ctro. de Invest. y Asistencia en Tecn. y Diseno Del Estado de JaliscoMexico; email: ediaz@ciatej.mx Chemicals/CAS: galectin 1, 258495-34-0; interleukin 8, 114308-91-7; prostaglandin E2, 363-24-6; protein tyrosine phosphatase; receptor type tyrosine protein phosphatase C; scatter factor, 67256-21-7, 72980-71-3; vasculotropin, 127464-60-2 AB - Mesenchymal stem cells (MSCs), defined as plastic adherent cells with multipotent differentiation capacity in vitro, are an emerging and valuable tool to treat a plethora of diseases due to their therapeutic mechanisms such as their paracrine activity, mitochondrial and organelle transfer, and transfer of therapeutic molecules via exosomes. Nowadays, there are more than a thousand registered clinical trials related to MSC application around the world, highlighting MSC role on difficult-to-treat high-incidence diseases such as the current COVID-19, HIV infections, and autoimmune and metabolic diseases. Here, we summarize a general overview of MSCs and their therapeutic mechanisms; also, we discuss some of the novel clinical trial protocols and their results as well as a comparison between the number of registries, countries, and search portals. © 2020 Karen J. Juárez-Navarro et al. LA - English DB - MTMT ER - TY - JOUR AU - Liu, Siyu AU - Liu, Fei AU - Zhou, You AU - Jin, Baeku AU - Sun, Qiang AU - Guo, Shu TI - Immunosuppressive Property of MSCs Mediated by Cell Surface Receptors JF - FRONTIERS IN IMMUNOLOGY J2 - FRONT IMMUNOL VL - 11 PY - 2020 SN - 1664-3224 DO - 10.3389/fimmu.2020.01076 UR - https://m2.mtmt.hu/api/publication/31432181 ID - 31432181 N1 - Department of Plastic Surgery, The First Hospital of China Medical University, Shenyang, China Department of Breast Surgery, Shengjing Hospital of China Medical University, Shenyang, China Export Date: 6 October 2020 Correspondence Address: Guo, S.; Department of Plastic Surgery, The First Hospital of China Medical UniversityChina; email: sguo@cmu.edu.cn Department of Plastic Surgery, The First Hospital of China Medical University, Shenyang, China Department of Breast Surgery, Shengjing Hospital of China Medical University, Shenyang, China Cited By :2 Export Date: 10 February 2021 Correspondence Address: Guo, S.; Department of Plastic Surgery, China; email: sguo@cmu.edu.cn Department of Plastic Surgery, The First Hospital of China Medical University, Shenyang, China Department of Breast Surgery, Shengjing Hospital of China Medical University, Shenyang, China Cited By :5 Export Date: 22 June 2021 Correspondence Address: Guo, S.; Department of Plastic Surgery, China; email: sguo@cmu.edu.cn Chemicals/CAS: chemokine receptor CXCR4, 188900-71-2; galectin 1, 258495-34-0; galectin 3, 208128-56-7; intercellular adhesion molecule 1, 126547-89-5; B7-H1 Antigen; Cell Adhesion Molecules; Galectins; Receptors, Cell Surface; Receptors, Chemokine; Receptors, Immunologic LA - English DB - MTMT ER - TY - JOUR AU - Luis, J. AU - Eastlake, K. AU - Khaw, P.T. AU - Limb, G.A. TI - Galectins and their involvement in ocular disease and development JF - EXPERIMENTAL EYE RESEARCH J2 - EXP EYE RES VL - 197 PY - 2020 SN - 0014-4835 DO - 10.1016/j.exer.2020.108120 UR - https://m2.mtmt.hu/api/publication/31405452 ID - 31405452 N1 - Export Date: 18 August 2020 CODEN: EXERA Correspondence Address: Luis, J.; National Institute for Health Research (NIHR), Biomedical Research Centre at Moorfields Eye Hospital, NHS Foundation Trust, UCL Institute of OphthalmologyUnited Kingdom; email: Joshua.Luis@ucl.ac.uk Funding details: National Institute for Health Research Biomedical Research Centre at Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology Funding details: Fight for Sight UK Funding text 1: This work was supported by Fight for Sight , Moorfields Eye Charity, and the NIHR Biomedical Research Centre at Moorfields Eye Hospital and UCL Institute of Ophthalmology, London, UK. Export Date: 22 June 2021 CODEN: EXERA Correspondence Address: Luis, J.; National Institute for Health Research (NIHR), United Kingdom; email: Joshua.Luis@ucl.ac.uk Chemicals/CAS: Galectins LA - English DB - MTMT ER - TY - JOUR AU - Sepehr, Koushan Sineh AU - Razavi, Alireza AU - Hassan, Zuhair Mohammad AU - Fazel, Abdolreza AU - Abdollahpour-Alitappeh, Meghdad AU - Mossahebi-Mohammadi, Majid AU - Yekaninejad, Mir Saeed AU - Farhadihosseinabadi, Behrouz AU - Hashemi, Seyed Mahmoud TI - Comparative immunomodulatory properties of mesenchymal stem cells derived from human breast tumor and normal breast adipose tissue JF - CANCER IMMUNOLOGY IMMUNOTHERAPY J2 - CANCER IMMUNOL IMMUN VL - 69 PY - 2020 IS - 9 SP - 1841 EP - 1854 PG - 14 SN - 1432-0851 DO - 10.1007/s00262-020-02567-y UR - https://m2.mtmt.hu/api/publication/31316898 ID - 31316898 N1 - Funding Agency and Grant Number: Tehran University of Medical Sciences and Health ServicesTehran University of Medical Sciences [30069] Funding text: The authors would like to thank those normal individuals and breast cancer patients for their kind participation in this project. This work was supported by a grant from Tehran University of Medical Sciences and Health Services (Grant Number: 30069). Laboratory Sciences Research Center, Golestan University of Medical Sciences, Gorgan, Iran Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran Cancer Research Center, Golestan University of Medical Sciences, Gorgan, Iran Cellular and Molecular Biology Research Center, Larestan University of Medical Sciences, Larestan, Iran Sarem Cell Research Center(SCRC), Sarem Women’s Hospital, Tehran, Iran Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran Neuroscience Research Center (NRC), Iran University of Medical Sciences, Tehran, Iran Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran Urogenital Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran Department of Tissue Engineering and Applied Cell Sciences, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran Export Date: 22 January 2021 CODEN: CIIMD Correspondence Address: Razavi, A.; Department of Immunology, Iran; email: razavial@tums.ac.ir Correspondence Address: Hashemi, S.M.; Department of Immunology, Iran; email: smmhashemi@sbmu.ac.ir Chemicals/CAS: galectin 1, 258495-34-0; gamma interferon, 82115-62-6; gelatinase A, 146480-35-5; gelatinase B, 146480-36-6; indoleamine 2,3 dioxygenase; interleukin 14, 150740-44-6; prostaglandin E2, 363-24-6; vasculotropin, 127464-60-2; vasculotropin A, 489395-96-2; Cytokines; Dinoprostone; Vascular Endothelial Growth Factor A Funding details: Tehran University of Medical Sciences and Health Services, TUMS, 30069 Funding text 1: The authors would like to thank those normal individuals and breast cancer patients for their kind participation in this project. This work was supported by a grant from Tehran University of Medical Sciences and Health Services (Grant Number: 30069). Laboratory Sciences Research Center, Golestan University of Medical Sciences, Gorgan, Iran Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran Cancer Research Center, Golestan University of Medical Sciences, Gorgan, Iran Cellular and Molecular Biology Research Center, Larestan University of Medical Sciences, Larestan, Iran Sarem Cell Research Center(SCRC), Sarem Women’s Hospital, Tehran, Iran Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran Neuroscience Research Center (NRC), Iran University of Medical Sciences, Tehran, Iran Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran Urogenital Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran Department of Tissue Engineering and Applied Cell Sciences, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran Export Date: 22 June 2021 CODEN: CIIMD Correspondence Address: Razavi, A.; Department of Immunology, Iran; email: razavial@tums.ac.ir Correspondence Address: Hashemi, S.M.; Department of Immunology, Iran; email: smmhashemi@sbmu.ac.ir Chemicals/CAS: galectin 1, 258495-34-0; gamma interferon, 82115-62-6; gelatinase A, 146480-35-5; gelatinase B, 146480-36-6; indoleamine 2,3 dioxygenase; interleukin 14, 150740-44-6; prostaglandin E2, 363-24-6; vasculotropin, 127464-60-2; vasculotropin A, 489395-96-2; Cytokines; Dinoprostone; Vascular Endothelial Growth Factor A LA - English DB - MTMT ER - TY - JOUR AU - Hornung, Ákos AU - Monostori, Éva AU - Kovács, László TI - Systemic lupus erythematosus in the light of the regulatory effects of galectin-1 on T-cell function JF - LUPUS J2 - LUPUS VL - 26 PY - 2017 IS - 4 SP - 339 EP - 347 PG - 9 SN - 0961-2033 DO - 10.1177/0961203316686846 UR - https://m2.mtmt.hu/api/publication/3190069 ID - 3190069 N1 - Institute of Genetics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary Department of Rheumatology and Immunology, University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Health Centre, Ká lvária sgt. 57, Szeged, 6725, Hungary Cited By :1 Export Date: 18 September 2019 CODEN: LUPUE Correspondence Address: Kovács, L.; Department of Rheumatology and Immunology, University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Health Centre, Ká lvária sgt. 57, Hungary; email: kovacs.laszlo@med.u-szeged.hu Chemicals/CAS: galectin 1, 258495-34-0; ganglioside GM1, 37758-47-7; phosphatidylinositol 3 kinase, 115926-52-8; phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase, 210488-47-4; protein kinase Lck, 114051-78-4; protein kinase Syk, 138674-26-7; protein kinase ZAP 70, 148047-34-1; Galectin 1; LGALS1 protein, human Institute of Genetics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary Department of Rheumatology and Immunology, University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Health Centre, Ká lvária sgt. 57, Szeged, 6725, Hungary Cited By :1 Export Date: 29 November 2019 CODEN: LUPUE Correspondence Address: Kovács, L.; Department of Rheumatology and Immunology, University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Health Centre, Ká lvária sgt. 57, Hungary; email: kovacs.laszlo@med.u-szeged.hu Chemicals/CAS: galectin 1, 258495-34-0; ganglioside GM1, 37758-47-7; phosphatidylinositol 3 kinase, 115926-52-8; phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase, 210488-47-4; protein kinase Lck, 114051-78-4; protein kinase Syk, 138674-26-7; protein kinase ZAP 70, 148047-34-1; Galectin 1; LGALS1 protein, human Institute of Genetics, Biological Research Centre, Hungarian Academy of Sciences, Szeged, Hungary Department of Rheumatology and Immunology, University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Health Centre, Ká lvária sgt. 57, Szeged, 6725, Hungary Cited By :1 Export Date: 2 December 2019 CODEN: LUPUE Correspondence Address: Kovács, L.; Department of Rheumatology and Immunology, University of Szeged, Faculty of Medicine, Albert Szent-Györgyi Health Centre, Ká lvária sgt. 57, Hungary; email: kovacs.laszlo@med.u-szeged.hu Chemicals/CAS: galectin 1, 258495-34-0; ganglioside GM1, 37758-47-7; phosphatidylinositol 3 kinase, 115926-52-8; phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase, 210488-47-4; protein kinase Lck, 114051-78-4; protein kinase Syk, 138674-26-7; protein kinase ZAP 70, 148047-34-1; Galectin 1; LGALS1 protein, human AB - Galectin-1 is an endogenous immunoregulatory lectin-type protein. Its most important effects are the inhibition of the differentiation and cytokine production of Th1 and Th17 cells, and the induction of apoptosis of activated T-cells. Galectin-1 has been identified as a key molecule in antitumor immune surveillance, and data are accumulating about the pathogenic role of its deficiency, and the beneficial effects of its administration in various autoimmune disease models. Initial animal and human studies strongly suggest deficiencies in both galectin-1 production and responsiveness in systemic lupus erythematosus (SLE) T-cells. Since lupus features widespread abnormalities in T-cell activation, differentiation and viability, in this review the authors wished to highlight potential points in T-cell signalling processes that may be influenced by galectin-1. These points include GM-1 ganglioside-mediated lipid raft aggregation, early activation signalling steps involving p56Lck, the exchange of the CD3 zeta-ZAP-70 to the FcRgamma-Syk pathway, defective mitogen-activated protein kinase pathway activation, impaired regulatory T-cell function, the failure to suppress the activity of interleukin 17 (IL-17) producing T-cells, and decreased suppression of the PI3K-mTOR pathway by phosphatase and tensin homolog (PTEN). These findings place galectin-1 into the group of potential pathogenic molecules in SLE. LA - English DB - MTMT ER - TY - JOUR AU - Reesink, Heidi L AU - Sutton, Ryan M AU - Shurer, Carolyn R AU - Peterson, Ryan P AU - Tan, Julie S AU - Su, Jin AU - Paszek, Matthew J AU - Nixon, Alan J TI - Galectin-1 and galectin-3 expression in equine mesenchymal stromal cells (MSCs), synovial fibroblasts and chondrocytes, and the effect of inflammation on MSC motility JF - STEM CELL RESEARCH & THERAPY J2 - STEM CELL RES THER VL - 8 PY - 2017 PG - 12 SN - 1757-6512 DO - 10.1186/s13287-017-0691-2 UR - https://m2.mtmt.hu/api/publication/27049125 ID - 27049125 N1 - Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, United States Robert Frederick Smith School of Chemical and Biomolecular Engineering, Cornell University, Ithaca, NY 14853, United States Cited By :15 Export Date: 22 June 2021 Correspondence Address: Reesink, H.L.; Department of Clinical Sciences, United States; email: hlr42@cornell.edu Chemicals/CAS: galectin 1, 258495-34-0; galectin 3, 208128-56-7; lactose, 10039-26-6, 16984-38-6, 63-42-3, 64044-51-5; Galectin 1; Galectin 3; Interleukin-1beta; Lactose; Lipopolysaccharides; Tumor Necrosis Factor-alpha LA - English DB - MTMT ER - TY - JOUR AU - Matula, Zsolt AU - Németh, Andrea AU - Lőrincz, Péter AU - Szepesi, Áron AU - Brózik, Anna AU - Buzás, Edit Irén AU - Lőw, Péter AU - Német, Katalin AU - Uher, Ferenc AU - Suhajdáné Urbán, Veronika TI - The role of extracellular vesicle and tunneling nanotube-mediated intercellular cross-talk between mesenchymal stem cells and human peripheral T cells. JF - STEM CELLS AND DEVELOPMENT J2 - STEM CELLS DEV VL - 25 PY - 2016 IS - 23 SP - 1818 EP - 1832 PG - 15 SN - 1547-3287 DO - 10.1089/scd.2016.0086 UR - https://m2.mtmt.hu/api/publication/3110431 ID - 3110431 N1 - Institute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, 1117, Hungary Department of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary Department of Anatomy, Cell and Developmental Biology, Eötvos Loránd University, Budapest, Hungary Creative Cell Ltd., Budapest, Hungary Stem Cell Biology, National Blood Service, Budapest, Hungary Department of Morphology and Physiology, Faculty of Health Sciences, Semmelweis University, Budapest, Hungary Cited By :18 Export Date: 5 August 2019 CODEN: SCDTA Correspondence Address: Matula, Z.; Institute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of SciencesHungary; email: matula.zsolt@ttk.mta.hu Institute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, 1117, Hungary Department of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary Department of Anatomy, Cell and Developmental Biology, Eötvos Loránd University, Budapest, Hungary Creative Cell Ltd., Budapest, Hungary Stem Cell Biology, National Blood Service, Budapest, Hungary Department of Morphology and Physiology, Faculty of Health Sciences, Semmelweis University, Budapest, Hungary Cited By :18 Export Date: 7 August 2019 CODEN: SCDTA Correspondence Address: Matula, Z.; Institute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of SciencesHungary; email: matula.zsolt@ttk.mta.hu Institute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, 1117, Hungary Department of Genetics, Cell- and Immunobiology, Semmelweis University, Budapest, Hungary Department of Anatomy, Cell and Developmental Biology, Eötvos Loránd University, Budapest, Hungary Creative Cell Ltd., Budapest, Hungary Stem Cell Biology, National Blood Service, Budapest, Hungary Department of Morphology and Physiology, Faculty of Health Sciences, Semmelweis University, Budapest, Hungary Cited By :25 Export Date: 1 June 2020 CODEN: SCDTA Correspondence Address: Matula, Z.; Institute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of SciencesHungary; email: matula.zsolt@ttk.mta.hu Chemicals/CAS: gamma interferon, 82115-62-6 AB - The role of extracellular vesicles in mediating the immunosuppressory properties of mesenchymal stem cells has recently attracted remarkable scientific interest. The aim of this work was to analyze the transport mechanisms of membrane and cytoplasmic components between T lymphocytes and adipose tissue-derived mesenchymal stem cells, by focusing on the role of distinct populations of extracellular vesicles, direct cell-cell contacts and the soluble mediators per se in modulating T lymphocyte function. We found that neither murine thymocytes and human primary T cells, nor Jurkat lymphoblastoid cells incorporated appreciable amounts of MSC-derived microvesicles or exosomes. Moreover, these particles had no effect on the proliferation and IFN-gamma production of in vitro stimulated primary T cells. In contrast, AD-MSCs incorporated large amounts of membrane components from T cells as an intensive uptake of exosomes and microvesicles could be observed. Interestingly, we found a bi-directional exchange of cytoplasmic components between human AD-MSCs and primary T lymphocytes, mediated by tunneling nanotubes derived exclusively from the T cells. In contrast, tunneling nanotubes couldn't be observed between AD-MSCs and the Jurkat cells. Our results reveal a novel and efficient way of intercellular communication between MSCs and T cells, and may help a better understanding of the immunomodulatory function of MSCs. LA - English DB - MTMT ER - TY - JOUR AU - Nishizawa, Kazuhisa AU - Seki, Reiko TI - Mechanisms of immunosuppression by mesenchymal stromal cells: a review with a focus on molecules JF - Biomedical Research and Clinical Practice J2 - Biomed Res Clin Prac VL - 1 PY - 2016 IS - 3 SP - 82 EP - 96 PG - 15 SN - 2397-9631 DO - 10.15761/BRCP.1000116 UR - https://m2.mtmt.hu/api/publication/31390785 ID - 31390785 LA - English DB - MTMT ER -