| 1. |
- Arfvidsson, John, et al.
(author)
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Monocyte subsets in myocardial infarction: A review
- 2017
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In: International Journal of Cardiology. - : ELSEVIER IRELAND LTD. - 0167-5273 .- 1874-1754. ; 231, s. 47-53
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Research review (peer-reviewed)abstract
- Background: Monocytes form an important part of the human innate immune system by taking part in inflammatory reactions. With time, monocytes have gained interest in the role they may play during the event of myocardial infarction (MI). The current paradigm suggests that monocytes consist of three subdivisions which differ in phenotypic and dynamic patterns after an MI. In the inflammation that ensues, the different subsets have been shown to have an impact on reparative processes and patient recovery. Methods results: We searched Medline and Embase until April 5, 2016, for observational studies or clinical trials regarding monocyte functions and dynamics in MI. Apart from studies in humans, extensive work has been done in mice in an effort to understand the complex nature of monocyte dynamics. Animal models might add useful information on mapping these processes. Conclusion: The question still remains whether animal data can, to a certain degree, be extrapolated to monocyte functions during human MI. This review aims to summarize current available evidence on both mice and men with particular focus on the understanding of monocyte subsets dynamics and effects in human MI. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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| 2. |
- Humar, Miha, et al.
(author)
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Introduction of the COST FP 1303 Cooperative Performance Test
- 2015
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In: Proceedings of the 46th IRG Annual Meeting.
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Conference paper (peer-reviewed)abstract
- COST Action FP 1303 “Performance of bio-based building materials” successfully started in October 2013 and an ambitious program was set up for the four year programme. COST Actions provide an excellent opportunity for collaborative research, e.g. in the frame of Round Robin tests.The idea of this respective test was to distribute a fairly simple test set up to as many places in Europe as possible in order to collect performance data reflecting the range of climatic exposure conditions. Furthermore we wanted to consider performance in its manifold meaning, i.e. optical, aesthetical, moisture and functional performance and durability. In contrast to traditional Round Robin tests aiming on comparative evaluation and validation of results from different test laboratories, this initiative aims on collecting performance data under climatically different exposure conditions. Therefore it was required to provide weather data from the respective test sites to allow establishing relationships between climate conditions and the following measured, which shall be evaluated regularly: decay, discolouration, development of mould and other staining fungi, corrosion, formation of cracks and moisture performance (if data logging device is included). Further details about the test and the first outcomes are presented in this paper.
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| 3. |
- Stojkovic, Stefan, et al.
(author)
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IL-33 stimulates the release of procoagulant microvesicles from human monocytes and differentially increases tissue factor in human monocyte subsets
- 2017
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In: Thrombosis and Haemostasis. - : SCHATTAUER GMBH-VERLAG MEDIZIN NATURWISSENSCHAFTEN. - 0340-6245 .- 2567-689X. ; 117:7, s. 1379-1390
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Journal article (peer-reviewed)abstract
- Monocytes and monocyte-derived microvesicles (MVs) are the main source of circulating tissue factor (TF). Increased monocyte TF expression and increased circulating levels of procoagulant MVs contribute to the formation of a prothrombotic state in patients with cardiovascular disease. Interleukin (IL)-33 is a pro-inflammatory cytokine involved in atherosclerosis and other inflammatory diseases, but its role in regulating thrombosis is still unclear. The aim of the present study was to investigate the effects of IL-33 on the procoagulant properties of human monocytes and monocyte-derived MVs. IL-33 induced a time- and concentration-dependent increase of monocyte TF mRNA and protein levels via binding to the ST2-receptor and activation of the NF-kappa B-pathway. The IL-33 treated monocytes also released CD14+TF+ MVs and IL-33 was found to increase the TF activity of both the isolated monocytes and monocyte-derived MVs. The monocytes were classified into subsets according to their CD14 and CD16 expression. Intermediate monocytes (IM) showed the highest ST2 receptor expression, followed by non-classical monocytes (NCM), and classical monocytes (CM). IL-33 induced a significant increase of TF only in the IM (p<0.01), with a tendency in NCM (p=0.06), but no increase was observed in CM. Finally, plasma levels of IL-33 were positively correlated with CD14+TF+ MVs in patients undergoing carotid endarterectomy (r=0.480; p=0.032; n=20). We hereby provide novel evidence that the proinflammatory cytokine IL-33 induces differential TF expression and activity in monocyte subsets, as well as the release of procoagulant MVs. In this manner, IL-33 may contribute to the formation of a prothrombotic state characteristic for cardiovascular disease.
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| 4. |
- Ugovšek, Aleš, et al.
(author)
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Short-term performance of wooden windows and facade elements made of thermally modified and non-modified Norway spruce in different natural environments
- 2018
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In: Wood Material Science & Engineering. - : Taylor & Francis. - 1748-0272 .- 1748-0280. ; 14:1, s. 42-47
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Journal article (peer-reviewed)abstract
- Thermally modified wood is becoming an increasingly popular material for different applications in buildings. Laboratory tests indicated a positive effect of thermal modification on durability, dimensional stability and thermal conductivity of wood. Therefore, windows and facade elements made of thermally modified Norway spruce and non-modified Norway spruce were tested in the field and installed in different test objects which were exposed at five locations in Europe (Slovenia, Germany, Sweden, and Spain). Results from monitoring showed that elements and windows made of thermally modified spruce (TMS) had considerably lower wood moisture content compared to the ones made of non-modified spruce and that wax further positively influenced moisture performance. Colour changes of TMS were more intensive compared to non-modified spruce but were successfully retarded by adding pigments to the wax. Mould and stain growth was largely dependent on the location, amount of precipitation and relative humidity.
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| 5. |
- Witman, Nevin, 1982-, et al.
(author)
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miR-128 regulates non-myocyte hyperplasia, deposition of extracellular matrix and Islet1 expression during newt cardiac regeneration
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Other publication (other academic/artistic)abstract
- Cardiovascular disease is a global scourge to society, with novel therapeutic approaches required in order to alleviate the suffering caused by sustained cardiac damage. MicroRNAs (miRNAs) are being touted as one such approach in the fight against heart disease, acting as possible post-transcriptional molecular triggers responsible for invoking cardiac regeneration. To further ones understanding of miRNAs and cardiac regeneration, it is prudent to learn from organisms that can intrinsically regenerate their hearts following injury. Using the red-spotted newt, an adult chordate capable of cardiac regeneration, we decided to delve deeper into the role miRNAs play during this process. RNA isolated from regenerating newt heart samples, was used in a microarray screen, to identify significantly expressed candidate miRNAs during newt cardiac regeneration. We performed quantitative qPCR analysis on several conserved miRNAs and found one in particular, miR-128, to be significantly elevated when cardiac hyperplasia is at its peak following injury. In-situ hybridisation techniques revealed a localised expression pattern for miR-128 in the cardiomyocytes and non-cardiomyocytes in close proximity to the regeneration zone and in vivo knockdown studies revealed a regulatory role for miR-128 in proliferating non-cardiomyocyte populations and extracellular matrix deposition. Finally, 3’UTR reporter assays revealed Islet1 as a biological target for miR-128, which was confirmed further through in vivo Islet1 transcriptional and translational expression analysis in regenerating newt hearts. From these studies we conclude that miR-128 regulates both cardiac hyperplasia and Islet1 expression during newt heart regeneration and that this information could be translated into future mammalian cardiac studies.
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| 6. |
- Witman, Nevin, et al.
(author)
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miR-128 regulates non-myocyte hyperplasia, deposition of extracellular matrix and Islet1 expression during newt cardiac regeneration
- 2013
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In: Developmental Biology. - : Elsevier. - 0012-1606 .- 1095-564X. ; 383:2, s. 253-263
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Journal article (peer-reviewed)abstract
- Cardiovascular disease is a global scourge to society, with novel therapeutic approaches required in order to alleviate the suffering caused by sustained cardiac damage. MicroRNAs (miRNAs) are being touted as one such approach in the fight against heart disease, acting as possible post-transcriptional molecular triggers responsible for invoking cardiac regeneration. To further ones understanding of miRNAs and cardiac regeneration, it is prudent to learn from organisms that can intrinsically regenerate their hearts following injury. Using the red-spotted newt, an adult chordate capable of cardiac regeneration, we decided to delve deeper into the role miRNAs play during this process. RNA isolated from regenerating newt heart samples, was used in a microarray screen, to identify significantly expressed candidate miRNAs during newt cardiac regeneration. We performed quantitative qPCR analysis on several conserved miRNAs and found one in particular, miR-128, to be significantly elevated when cardiac hyperplasia is at its peak following injury. In-situ hybridisation techniques revealed a localised expression pattern for miR-128 in the cardiomyocytes and non-cardiomyocytes in close proximity to the regeneration zone and in vivo knockdown studies revealed a regulatory role for miR-128 in proliferating non-cardiomyocyte populations and extracellular matrix deposition. Finally, 3'UTR reporter assays revealed Islet1 as a biological target for miR-128, which was confirmed further through in vivo Islet1 transcriptional and translational expression analysis in regenerating newt hearts. From these studies we conclude that miR-128 regulates both cardiac hyperplasia and Islet1 expression during newt heart regeneration and that this information could be translated into future mammalian cardiac studies.
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