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10. Letter to the editor: Re: Pathogenic mechanisms of osteogenesis imperfecta, evidence for classification.

Author

Dalgleish, Raymond, Micha, Dimitra, Superti-Furga, Andrea, van Dijk, Fleur S., and Sillence, David O.

Subjects
*OSTEOGENESIS imperfecta, *CLASSIFICATION, *RARE diseases, *NOSOLOGY
Abstract

A paper published in Orphanet Journal of Rare Diseases proposes a new classification of osteogenesis imperfecta (OI) based upon underlying pathological mechanisms. The proposed numbering of OI types conflicts with the currently used numbering and is likely to lead to confusion. In addition, classification of OI according to underlying pathogenic mechanisms is not novel. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Elucidating the role of water in collagen self-assembly by isotopically modulating collagen hydration.

Author

Giubertoni, Giulia, Liru Feng, Klein, Kevin, Giannetti, Guido, Rutten, Luco, Yeji Choi, Anouk van der Net, Castro-Linares, Gerard, Caporaletti, Federico, Micha, Dimitra, Hunger, Johannes, Deblais, Antoine, Bonn, Daniel, Sommerdijk, Nico, Šarić, Anđela, Ilie, Ioana M., Koenderink, Gijsje H., and Woutersen, Sander

Subjects
COLLAGEN, CYTOSKELETAL proteins, RATE of nucleation, HYDRATION, STRUCTURAL dynamics
Abstract

Water is known to play an important role in collagen self-assembly, but it is still largely unclear how water--collagen interactions influence the assembly process and determine the fibril network properties. Here, we use the H2O/D2O isotope effect on the hydrogen-bond strength in water to investigate the role of hydration in collagen self-assembly. We dissolve collagen in H2O and D2O and compare the growth kinetics and the structure of the collagen assemblies formed in these water isotopomers. Surprisingly, collagen assembly occurs ten times faster in D2O than in H2O, and collagen in D2O self-assembles into much thinner fibrils, that form a more inhomogeneous and softer network, with a fourfold reduction in elastic modulus when compared to H2O. Combining spectroscopic measurements with atomistic simulations, we show that collagen in D2O is less hydrated than in H2O. This partial dehydration lowers the enthalpic penalty for water removal and reorganization at the collagen--water interface, increasing the self-assembly rate and the number of nucleation centers, leading to thinner fibrils and a softer network. Coarse-grained simulations show that the acceleration in the initial nucleation rate can be reproduced by the enhancement of electrostatic interactions. These results show that water acts as a mediator between collagen monomers, by modulating their interactions so as to optimize the assembly process and, thus, the final network properties. We believe that isotopically modulating the hydration of proteins can be a valuable method to investigate the role of water in protein structural dynamics and protein self-assembly. [ABSTRACT FROM AUTHOR]

Published
2024
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14. Elucidating the role of water in collagen self assembly by isotopically modulating collagen hydration

Author

Giubertoni, Giulia, primary, Feng, Liru, additional, Klein, Kevin, additional, Giannetti, Guido, additional, Choi, Yeji, additional, van der Net, Anouk, additional, Castro-Linares, Gerard, additional, Caporaletti, Federico, additional, Micha, Dimitra, additional, Hunger, Johannes, additional, Deblais, Antoine, additional, Bonn, Daniel, additional, Saric, Andel, additional, Ilie, Ioana M, additional, Koenderink, Gijsje H, additional, and Woutersen, Sander, additional

Published
2023
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16. IFT74 variants cause skeletal ciliopathy and motile cilia defects in mice and humans

Author

Bakey, Zeineb, primary, Cabrera, Oscar A., additional, Hoefele, Julia, additional, Antony, Dinu, additional, Wu, Kaman, additional, Stuck, Michael W., additional, Micha, Dimitra, additional, Eguether, Thibaut, additional, Smith, Abigail O., additional, van der Wel, Nicole N., additional, Wagner, Matias, additional, Strittmatter, Lara, additional, Beales, Philip L., additional, Jonassen, Julie A., additional, Thiffault, Isabelle, additional, Cadieux-Dion, Maxime, additional, Boyes, Laura, additional, Sharif, Saba, additional, Tüysüz, Beyhan, additional, Dunstheimer, Desiree, additional, Niessen, Hans W. M., additional, Devine, William, additional, Lo, Cecilia W., additional, Mitchison, Hannah M., additional, Schmidts, Miriam, additional, and Pazour, Gregory J., additional

Published
2023
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20. Pre-clinical evaluation of Bcl-2 inhibitor ABT-737 in small cell lung cancer

Author

Micha, Dimitra

Subjects
616.99424
Abstract

The evasion of apoptosis is a common feature of various malignancies and often depends on the overexpression of Bcl-2 family antiapoptotic proteins. Resistance to chemotherapy and radiotherapy is promoted because these tumour cells have a higher threshold for apoptosis-promoting signals than their normal cell counterparts. This has lead to the development of BH3 mimetic compounds that target the survival proteins of the Bcl-2 family.

Published
2009

23. Primary ciliary dyskinesia in Volendam

Author

Kos, Renate, Israëls, Joël, van Gogh, Christine D. L., Altenburg, Josje, Diepenhorst, Sandra, Paff, Tamara, Boon, Elles M. J., Micha, Dimitra, Pals, Gerard, Neerincx, Anne H., Maitland-van der Zee, Anke H., Haarman, Eric G., Pediatric surgery, Otolaryngology / Head & Neck Surgery, AII - Cancer immunology, CCA - Cancer Treatment and quality of life, CCA - Cancer biology and immunology, Pulmonary medicine, Clinical genetics, AMS - Rehabilitation & Development, AMS - Tissue Function & Regeneration, Amsterdam Reproduction & Development, Human genetics, ACS - Microcirculation, ACS - Atherosclerosis & ischemic syndromes, Amsterdam Reproduction & Development (AR&D), Pulmonology, General Paediatrics, Paediatric Pulmonology, and APH - Personalized Medicine

Subjects
phenotype, Mutation, Genetics, otorhinolaryngologic diseases, Humans, primary ciliary dyskinesia, CCDC114, lung function, Microtubule-Associated Proteins, Genetics (clinical), Ciliary Motility Disorders, Netherlands
Abstract

Primary ciliary dyskinesia (PCD) is a heterogeneous disease, with impaired mucociliary clearance causing respiratory tract infections. A founding CCDC114 mutation has led to a relatively homogeneous and large Dutch PCD population in Volendam. Our aim was to describe their phenotype. Therefore, all Volendam PCD patients seen at the Amsterdam UMC were included in this study. Data were collected on lung function, microbiology, radiology, and ear-nose-throat (ENT) symptoms. A mixed effects model estimated lung function decline in %point per year (95% confidence interval [CI]). Thirty-three (60%) out of approximately 56 Volendam PCD patients were treated at our center and included in this study. Only 30% of patients had situs inversus. FEV1 declined in children (-1.43%/year, CI: -1.80/-1.05), but not in adults (0.01%/year, CI: -0.36/0.38). Pseudomonas aeruginosa was cultured in 21% of children and 60% of adults, respectively. Patients who have been infected at some point with P. aeruginosa had a steeper decline in FEV1 as compared to patients that have never been infected. Neonatal symptoms (79%) and ENT problems (94%) were common; fertility issues however, were not (11%) common. Compared to other PCD cohorts, the Volendam/CCDC114 patients have a moderately severe phenotype with lung function decline predominantly occurring in childhood.

Published
2022

24. IFT74variants cause skeletal ciliopathy and motile cilia defects in mice and humans

Author

Bakey, Zeineb, primary, Cabrera, Oscar A., additional, Hoefele, Julia, additional, Antony, Dinu, additional, Wu, Kaman, additional, Stuck, Michael W., additional, Micha, Dimitra, additional, Eguether, Thibaut, additional, Smith, Abigail O., additional, van der Wel, Nicole N., additional, Wagner, Matias, additional, Strittmatter, Lara, additional, Beales, Philip L., additional, Jonassen, Julie A., additional, Thiffault, Isabelle, additional, Cadieux-Dion, Maxime, additional, Boyes, Laura, additional, Sharif, Saba, additional, Tüysüz, Beyhan, additional, Dunstheimer, Desiree, additional, Niessen, Hans W.M., additional, Devine, William, additional, Lo, Cecilia W, additional, Mitchison, Hannah M., additional, Schmidts, Miriam, additional, and Pazour, Gregory J., additional

Published
2023
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28. Novel Pathogenic Variants in Sparc as Cause of Osteogenesis Imperfecta: Two Case Reports

Author

Storoni, Silvia, primary, Celli, Luca, additional, Zhytnik, Lidiia, additional, Maasalu, Katre, additional, Märtson, Aare, additional, Kõks, Sulev, additional, Khmyzov, Sergey, additional, Pashenko, Andrei, additional, Maugeri, Alessandra, additional, Zambrano, Anna, additional, Celli, Mauro, additional, Eekhoff, Elisabeth M.W., additional, and Micha, Dimitra, additional

Published
2023
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30. Exploration of the skeletal phenotype of the Col1a1 +/Mov13 mouse model for haploinsufficient osteogenesis imperfecta type 1

Author

Claeys, Lauria, Zhytnik, Lidiia, Wisse, Lisanne E., van Essen, Huib W., Eekhoff, E. Marelise W., Pals, Gerard, Bravenboer, Nathalie, Micha, Dimitra, Human genetics, AMS - Musculoskeletal Health, AMS - Tissue Function & Regeneration, Clinical chemistry, Internal medicine, Amsterdam Gastroenterology Endocrinology Metabolism, AMS - Ageing & Vitality, ACS - Atherosclerosis & ischemic syndromes, ACS - Microcirculation, Laboratory Medicine, and Laboratory Specialized Diagnostics & Reseach

Subjects
Endocrinology, Diabetes and Metabolism
Abstract

IntroductionOsteogenesis Imperfecta is a rare genetic connective tissue disorder, characterized by skeletal dysplasia and fragile bones. Currently only two mouse models have been reported for haploinsufficient (HI) mild Osteogenesis Imperfecta (OI); the Col1a1+/Mov13 (Mov13) and the Col1a1+/-365 mouse model. The Mov13 mice were created by random insertion of the Mouse Moloney leukemia virus in the first intron of the Col1a1 gene, preventing the initiation of transcription. Since the development of the Mov13 mice almost four decades ago and its basic phenotypic characterization in the 90s, there have not been many further studies. We aimed to extensively characterize the Mov13 mouse model in order to critically evaluate its possible use for preclinical studies of HI OI.MethodsBone tissue from ten heterozygous Mov13 and ten wild-type littermates (WT) C57BL/6J mice (50% males per group) was analyzed at eight weeks of age with bone histomorphometry, micro computed tomography (microCT), 3-point bending, gene expression of different collagens, as well as serum markers of bone turnoverResultsThe Mov13 mouse presented a lower bone strength and impaired material properties based on our results of 3-point bending and microCT analysis respectively. In contrast, no significant differences were found for all histomorphometric parameters. In addition, no significant differences in Col1a1 bone expression were present, but there was a significant lower P1NP concentration, a bone formation marker, measured in serum. Furthermore, bone tissue of Mov13 mice presented significantly higher expression of collagens (Col1a2, Col5a1 and Col5a2), and bone metabolism markers (Bglap, Fgf23, Smad7, Edn1 and Eln) compared to WT. Finally, we measured a significantly lower Col1a1 expression in heart and skin tissue and also determined a higher expression of other collagens in the heart tissue.ConclusionAlthough we did not detect a significant reduction in Col1a1 expression in the bone tissue, a change in bone structure and reduction in bone strength was noted. Regrettably, the variability of the bone phenotype and the appearance of severe lymphoma in adult Mov13 mice, does not favor their use for the testing of new long-term drug studies. As such, a new HI OI type 1 mouse model is urgently needed.

Published
2023

32. The intricate mechanism of PLS3 in bone homeostasis and disease.

Author

Wenchao Zhong, Pathak, Janak L., Yueting Liang, Zhytnik, Lidiia, Pals, Gerard, Eekhoff, Elisabeth M. W., Bravenboer, Nathalie, and Micha, Dimitra

Subjects
BONE diseases, TISSUE metabolism, SYMPTOMS, HOMEOSTASIS, BONE cells, MECHANOTRANSDUCTION (Cytology)
Abstract

Since our discovery in 2013 that genetic defects in PLS3 lead to bone fragility, the mechanistic details of this process have remained obscure. It has been established that PLS3 variants cause syndromic and nonsyndromic osteoporosis as well as osteoarthritis. PLS3 codes for an actin-bundling protein with a broad pattern of expression. As such, it is puzzling how PLS3 specifically leads to bone-related disease presentation. Our review aims to summarize the current state of knowledge regarding the function of PLS3 in the predominant cell types in the bone tissue, the osteocytes, osteoblasts and osteoclasts. This is related to the role of PLS3 in regulating mechanotransduction, calcium regulation, vesicle trafficking, cell differentiation and mineralization as part of the complex bone pathology presented by PLS3 defects. Considering the consequences of PLS3 defects on multiple aspects of bone tissue metabolism, our review motivates the study of its mechanism in bone diseases which can potentially help in the design of suitable therapy. [ABSTRACT FROM AUTHOR]

Published
2023
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35. X-linked hypomyelination with spondylometaphyseal dysplasia (H-SMD) associated with mutations in AIFM1

Author

Miyake, Noriko, Wolf, Nicole I., Cayami, Ferdy K., Crawford, Joanna, Bley, Annette, Bulas, Dorothy, Conant, Alex, Bent, Stephen J., Gripp, Karen W., Hahn, Andreas, Humphray, Sean, Kimura-Ohba, Shihoko, Kingsbury, Zoya, Lajoie, Bryan R., Lal, Dennis, Micha, Dimitra, Pizzino, Amy, Sinke, Richard J., Sival, Deborah, Stolte-Dijkstra, Irene, Superti-Furga, Andrea, Ulrick, Nicole, Taft, Ryan J., Ogata, Tsutomu, Ozono, Keiichi, Matsumoto, Naomichi, Neubauer, Bernd A., Simons, Cas, and Vanderver, Adeline

Published
2017
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36. Gene Therapy for Fibrodysplasia Ossificans Progressiva: Feasibility and Obstacles

Author

Eekhoff, Elisabeth M.W., primary, de Ruiter, Ruben D., additional, Smilde, Bernard J., additional, Schoenmaker, Ton, additional, de Vries, Teun J., additional, Netelenbos, Coen, additional, Hsiao, Edward C., additional, Scott, Christiaan, additional, Haga, Nobuhiko, additional, Grunwald, Zvi, additional, De Cunto, Carmen L., additional, di Rocco, Maja, additional, Delai, Patricia L. R., additional, Diecidue, Robert J., additional, Madhuri, Vrisha, additional, Cho, Tae-Joon, additional, Morhart, Rolf, additional, Friedman, Clive S., additional, Zasloff, Michael, additional, Pals, Gerard, additional, Shim, Jae-Hyuck, additional, Gao, Guangping, additional, Kaplan, Frederick, additional, Pignolo, Robert J., additional, and Micha, Dimitra, additional

Published
2022
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38. Prevalence and Hospital Admissions in Patients With Osteogenesis Imperfecta in The Netherlands: A Nationwide Registry Study

Author

Storoni, Silvia, Treurniet, Sanne, Maugeri, Alessandra, Pals, Gerard, van den Aardweg, Joost G., van der Pas, Stéphanie L., Elting, Mariet W., Kloen, Peter, Micha, Dimitra, Eekhoff, Elisabeth Marelise W., Internal medicine, Amsterdam Movement Sciences, Human genetics, Pulmonary medicine, Epidemiology and Data Science, Amsterdam Reproduction & Development (AR&D), AMS - Rehabilitation & Development, AMS - Tissue Function & Regeneration, AMS - Musculoskeletal Health, Amsterdam Gastroenterology Endocrinology Metabolism, ACS - Microcirculation, ACS - Atherosclerosis & ischemic syndromes, Pulmonology, ACS - Pulmonary hypertension & thrombosis, Orthopedic Surgery and Sports Medicine, APH - Personalized Medicine, APH - Quality of Care, and ACS - Diabetes & metabolism

Subjects
Adult, Adolescent, Endocrinology, Diabetes and Metabolism, Infant, Newborn, Infant, morbidity, Osteogenesis Imperfecta, Hospitals, Hospitalization, hospital admission, Young Adult, CBS registry, pathogenic variant, Child, Preschool, Prevalence, Quality of Life, Humans, Registries, Child, Netherlands
Abstract

Osteogenesis Imperfecta (OI) is a complex disease caused by genetic alterations in production of collagen type I, and collagen-related proteins. Bone fragility is the most common patient issue, but extraskeletal complications also present an adverse factor in the quality of life and prognosis of patients with OI. However, still little is known about the morbidity and mortality of these patients. The objective of this paper is to determine and describe to what extent OI impacts patients’ life in terms of hospitalization and complications describing the incidence and prevalence of the Dutch cohort of OI patients and the characteristics of their hospital admissions. Information regarding OI patients and their hospital admission was extracted from the Statistics Netherlands Database and matched to the OI Genetics Database of Amsterdam UMC. Hospital admission data was available for 674 OI patients. This OI nationwide registry study shows that the life expectancy of OI patients is adversely affected by the disease. The median annual incidence risk of OI between 1992 and 2019 was 6.5 per 100,000 live births. Furthermore, patients with OI had a 2.9 times higher hospitalization rate compared to the general Dutch population. The highest hospitalization rate ratio of 8.4 was reported in the patient group between 0 and 19 years old. OI type and severity had impact on extraskeletal manifestations, which play a key role in the numerous hospital admissions. More awareness about the impact of OI on patients’ life is needed to improve and implement prevention and follow-up guidelines.

Published
2022

41. Exploration of the skeletal phenotype of the Col1a1+/Mov13 mouse model for haploinsufficient osteogenesis imperfecta type 1.

Author

Claeys, Lauria, Zhytnik, Lidiia, Wisse, Lisanne E., van Essen, Huib W., Eekhoff, E. Marelise W., Pals, Gerard, Bravenboer, Nathalie, and Micha, Dimitra

Subjects
OSTEOGENESIS imperfecta, X-ray computed microtomography, OSSEOINTEGRATION, LABORATORY mice, ANIMAL disease models, SKELETAL dysplasia, FIBRODYSPLASIA ossificans progressiva
Abstract

Introduction: Osteogenesis Imperfecta is a rare genetic connective tissue disorder, characterized by skeletal dysplasia and fragile bones. Currently only two mouse models have been reported for haploinsufficient (HI) mild Osteogenesis Imperfecta (OI); the Col1a1+/Mov13 (Mov13) and the Col1a1+/-365 mouse model. The Mov13 mice were created by random insertion of the Mouse Moloney leukemia virus in the first intron of the Col1a1 gene, preventing the initiation of transcription. Since the development of the Mov13 mice almost four decades ago and its basic phenotypic characterization in the 90s, there have not been many further studies. We aimed to extensively characterize the Mov13 mouse model in order to critically evaluate its possible use for preclinical studies of HI OI. Methods: Bone tissue from ten heterozygous Mov13 and ten wild-type littermates (WT) C57BL/6J mice (50% males per group) was analyzed at eight weeks of age with bone histomorphometry, micro computed tomography (microCT), 3-point bending, gene expression of different collagens, as well as serum markers of bone turnover Results: The Mov13 mouse presented a lower bone strength and impaired material properties based on our results of 3-point bending and microCT analysis respectively. In contrast, no significant differences were found for all histomorphometric parameters. In addition, no significant differences in Col1a1 bone expression were present, but there was a significant lower P1NP concentration, a bone formation marker, measured in serum. Furthermore, bone tissue of Mov13 mice presented significantly higher expression of collagens (Col1a2, Col5a1 and Col5a2), and bone metabolism markers (Bglap, Fgf23, Smad7, Edn1 and Eln) compared to WT. Finally, we measured a significantly lower Collai expression in heart and skin tissue and also determined a higher expression of other collagens in the heart tissue. Conclusion: Although we did not detect a significant reduction in Collai expression in the bone tissue, a change in bone structure and reduction in bone strength was noted. Regrettably, the variability of the bone phenotype and the appearance of severe lymphoma in adult Mov13 mice, does not favor their use for the testing of new long-term drug studies. As such, a new HI OI type 1 mouse model is urgently needed. [ABSTRACT FROM AUTHOR]

Published
2023
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43. Fibrodysplasia Ossificans Progressiva: What Have We Achieved and Where Are We Now? Follow-up to the 2015 Lorentz Workshop

Author

de Ruiter, Ruben D., primary, Smilde, Bernard J., additional, Pals, Gerard, additional, Bravenboer, Nathalie, additional, Knaus, Petra, additional, Schoenmaker, Ton, additional, Botman, Esmée, additional, Sánchez-Duffhues, Gonzalo, additional, Pacifici, Maurizio, additional, Pignolo, Robert J., additional, Shore, Eileen M., additional, van Egmond, Marjolein, additional, Van Oosterwyck, Hans, additional, Kaplan, Frederick S., additional, Hsiao, Edward C., additional, Yu, Paul B., additional, Bocciardi, Renata, additional, De Cunto, Carmen Laura, additional, Longo Ribeiro Delai, Patricia, additional, de Vries, Teun J., additional, Hilderbrandt, Susanne, additional, Jaspers, Richard T., additional, Keen, Richard, additional, Koolwijk, Peter, additional, Morhart, Rolf, additional, Netelenbos, Jan C., additional, Rustemeyer, Thomas, additional, Scott, Christiaan, additional, Stockklausner, Clemens, additional, ten Dijke, Peter, additional, Triffit, James, additional, Ventura, Francesc, additional, Ravazzolo, Roberto, additional, Micha, Dimitra, additional, and Eekhoff, Elisabeth M. W., additional

Published
2021
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45. SMAD2 Mutations Are Associated with Arterial Aneurysms and Dissections

Author

Micha, Dimitra, Guo, Dong-chuan, Hilhorst-Hofstee, Yvonne, van Kooten, Fop, Atmaja, Dian, Overwater, Eline, Cayami, Ferdy K., Regalado, Ellen S., van Uffelen, René, Venselaar, Hanka, Faradz, Sultana M.H., Vriend, Gerrit, Weiss, Marjan M., Sistermans, Erik A., Maugeri, Alessandra, Milewicz, Dianna M., Pals, Gerard, and van Dijk, Fleur S.

Published
2015
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46. Molecular phenotyping and functional assessment of smooth muscle-like cells with pathogenic variants in aneurysm genes ACTA2, MYH11, SMAD3 and FBN1

Author

Burger, Joyce, primary, Bogunovic, Natalija, additional, de Wagenaar, Nathalie P, additional, Liu, Hui, additional, van Vliet, Nicole, additional, IJpma, Arne, additional, Maugeri, Alessandra, additional, Micha, Dimitra, additional, Verhagen, Hence J M, additional, ten Hagen, Timo L M, additional, Majoor-Krakauer, Danielle, additional, van der Pluijm, Ingrid, additional, Essers, Jeroen, additional, and Yeung, Kak K, additional

Published
2021
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47. Inflammatory Gene Expression of Human Perivascular Adipose Tissue in Abdominal Aortic Aneurysms

Author

Meekel, Jorn P., primary, Dias-Neto, Marina, additional, Bogunovic, Natalija, additional, Conceição, Gloria, additional, Sousa-Mendes, Claudia, additional, Stoll, Gawin R., additional, Leite-Moreira, Adelino, additional, Huynh, Jennifer, additional, Micha, Dimitra, additional, Eringa, Etto C., additional, Balm, Ron, additional, Blankensteijn, Jan D., additional, and Yeung, Kak K., additional

Published
2021
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49. sj-pdf-1-jet-10.1177_15266028211009272 – Supplemental material for Patient-Specific 3-Dimensional Model of Smooth Muscle Cell and Extracellular Matrix Dysfunction for the Study of Aortic Aneurysms

Author

Bogunovic, Natalija, Meekel, Jorn P., Jisca Majolée, Hekhuis, Marije, Pyszkowski, Jakob, Jockenhövel, Stefan, Kruse, Magnus, Riesebos, Elise, Micha, Dimitra, Blankensteijn, Jan D., Hordijk, Peter L., Samaneh Ghazanfari, and Kak K. Yeung

Subjects
FOS: Clinical medicine, Cardiology, Medicine, 110323 Surgery
Abstract

Supplemental material, sj-pdf-1-jet-10.1177_15266028211009272 for Patient-Specific 3-Dimensional Model of Smooth Muscle Cell and Extracellular Matrix Dysfunction for the Study of Aortic Aneurysms by Natalija Bogunovic, Jorn P. Meekel, Jisca Majolée, Marije Hekhuis, Jakob Pyszkowski, Stefan Jockenhövel, Magnus Kruse, Elise Riesebos, Dimitra Micha, Jan D. Blankensteijn, Peter L. Hordijk, Samaneh Ghazanfari and Kak K. Yeung in Journal of Endovascular Therapy

Published
2021
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50. sj-pdf-2-jet-10.1177_15266028211009272 – Supplemental material for Patient-Specific 3-Dimensional Model of Smooth Muscle Cell and Extracellular Matrix Dysfunction for the Study of Aortic Aneurysms

Author

Bogunovic, Natalija, Meekel, Jorn P., Jisca Majolée, Hekhuis, Marije, Pyszkowski, Jakob, Jockenhövel, Stefan, Kruse, Magnus, Riesebos, Elise, Micha, Dimitra, Blankensteijn, Jan D., Hordijk, Peter L., Samaneh Ghazanfari, and Kak K. Yeung

Subjects
FOS: Clinical medicine, Cardiology, Medicine, 110323 Surgery
Abstract

Supplemental material, sj-pdf-2-jet-10.1177_15266028211009272 for Patient-Specific 3-Dimensional Model of Smooth Muscle Cell and Extracellular Matrix Dysfunction for the Study of Aortic Aneurysms by Natalija Bogunovic, Jorn P. Meekel, Jisca Majolée, Marije Hekhuis, Jakob Pyszkowski, Stefan Jockenhövel, Magnus Kruse, Elise Riesebos, Dimitra Micha, Jan D. Blankensteijn, Peter L. Hordijk, Samaneh Ghazanfari and Kak K. Yeung in Journal of Endovascular Therapy

Published
2021
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