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  1. Book ; Thesis: Funktionsergebnisse der Volumenreduktionschirurgie in der Thoraxklinik Heidelberg

    Maniatis, Nikolaos

    2000  

    Author's details vorgelegt von Nikolaos Maniatis
    Language German
    Size 66 Bl., Ill., graph. Darst.
    Edition [Mikrofiche-Ausg.]
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Mainz, Univ., Diss., 2000
    HBZ-ID HT013294230
    Database Catalogue ZB MED Medicine, Health

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  2. Article ; Online: Differential Expression of Aquaporins in Experimental Models of Acute Lung Injury.

    Vassiliou, Alice G / Manitsopoulos, Nikolaos / Kardara, Matina / Maniatis, Nikolaos A / Orfanos, Stylianos E / Kotanidou, Anastasia

    In vivo (Athens, Greece)

    2017  Volume 31, Issue 5, Page(s) 885–894

    Abstract: Aim: The mammalian lung expresses at least three aquaporin (AQP) water channels whose precise role in lung injury or inflammation is still controversial.: Materials and methods: Three murine models of lung inflammation and corresponding controls were ...

    Abstract Aim: The mammalian lung expresses at least three aquaporin (AQP) water channels whose precise role in lung injury or inflammation is still controversial.
    Materials and methods: Three murine models of lung inflammation and corresponding controls were used to evaluate the expression of Aqp1, Aqp4, Aqp5 and Aqp9: lipopolysaccharide (LPS)-induced lung injury; HCl-induced lung injury; and ventilation-induced lung injury (VILI).
    Results: All models yielded increased lung vascular permeability, and inflammatory cell infiltration in the broncho-alveolar lavage fluid; VILI additionally produced altered lung mechanics. Lung expression of Aqp4 decreased in the models that targeted primarily the alveolar epithelium, i.e. acid aspiration and mechanical ventilation, while Aqp5 expression decreased in the model that appeared to target both the capillary endothelium and alveolar epithelium, i.e. LPS.
    Conclusion: Participation of aquaporins in the acute inflammatory process depends on localization and the type of lung injury.
    MeSH term(s) Acute Lung Injury/etiology ; Acute Lung Injury/metabolism ; Acute Lung Injury/pathology ; Acute Lung Injury/physiopathology ; Animals ; Aquaporins/genetics ; Disease Models, Animal ; Gene Expression Regulation ; Lipopolysaccharides/adverse effects ; Male ; Mice ; Permeability ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Respiratory Function Tests
    Chemical Substances Aquaporins ; Lipopolysaccharides ; RNA, Messenger
    Language English
    Publishing date 2017-09-07
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 807031-3
    ISSN 1791-7549 ; 0258-851X
    ISSN (online) 1791-7549
    ISSN 0258-851X
    DOI 10.21873/invivo.11143
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  3. Article: The impact of wind and solar power generation on the level and volatility of wholesale electricity prices in Greece

    Maniatis, Georgios I. / Milonas, Nikolaos T.

    Energy policy. 2022 Nov., v. 170

    2022  

    Abstract: We investigate the impact of wind and solar power generation on the level and volatility of wholesale electricity prices in the Greek electricity market from August 2012 to December 2018. In the context of a GARCH-in-Mean model the empirical findings ... ...

    Abstract We investigate the impact of wind and solar power generation on the level and volatility of wholesale electricity prices in the Greek electricity market from August 2012 to December 2018. In the context of a GARCH-in-Mean model the empirical findings suggest the existence of the merit-order effect which is stronger in the case of wind power. Controlling for regulatory mechanisms that may affect price volatility, we find that while overall renewables have decreased price volatility, wind power tends to increase it and solar power tends to decrease it. Furthermore, during peak hours, wind and solar power generation tend to decrease price volatility, supporting the hypothesis that renewables’ output reduces the volatility of wholesale electricity prices when it is positively correlated with the electricity load. Finally, we find that the increase in the price-cap of the Greek wholesale electricity market was associated with a reduction in the volatility of wholesale electricity prices. This finding highlights the importance of the market structure and the degree of vertical integration of participants in liberalized electricity markets, which determines their behavior while also affecting market price volatility.
    Keywords electricity ; energy policy ; market prices ; markets ; models ; power generation ; solar energy ; vertical integration ; wind ; wind power ; Greece
    Language English
    Dates of publication 2022-11
    Publishing place Elsevier Ltd
    Document type Article
    ISSN 0301-4215
    DOI 10.1016/j.enpol.2022.113243
    Database NAL-Catalogue (AGRICOLA)

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  4. Article ; Online: Highly Selective Endothelin-1 Receptor A Inhibition Prevents Bleomycin-Induced Pulmonary Inflammation and Fibrosis in Mice.

    Manitsopoulos, Nikolaos / Nikitopoulou, Ioanna / Maniatis, Nikolaos A / Magkou, Christina / Kotanidou, Anastasia / Orfanos, Stylianos E

    Respiration; international review of thoracic diseases

    2017  Volume 95, Issue 2, Page(s) 122–136

    Abstract: Background: Pulmonary fibrosis is a chronic disease, which progressively leads to respiratory failure and ultimately death. Endothelin-1 (ET-1), a vasoconstrictor secreted by endothelial cells, promotes vasoconstriction by activation of its receptors A ... ...

    Abstract Background: Pulmonary fibrosis is a chronic disease, which progressively leads to respiratory failure and ultimately death. Endothelin-1 (ET-1), a vasoconstrictor secreted by endothelial cells, promotes vasoconstriction by activation of its receptors A and B.
    Objectives: We addressed the role of highly selective ET-1 receptor A (ETA) inhibition in the pathogenesis of experimental pulmonary fibrosis by bleomycin (BLM).
    Methods: BLM sulfate (2 U/mL) or saline was intratracheally administered to C57/Bl6 mice (4 groups; n = 5-11/group). Pretreatment with the highly selective ETA receptor inhibitor sitaxentan (15 mg/kg/day) was started 1 day prior to BLM injection and continued for the duration of the experiment. Lung mechanics were assessed prior to sacrifice at days 7, 14, and 21 after BLM, followed by procurement of bronchoalveolar lavage fluid (BALF), blood, and lung tissue samples.
    Results: Time-dependent effects of BLM exposure included decreased static compliance and increased lung elastance, airspace inflammation and microvascular permeability, histological acute lung injury and fibrosis, and lung collagen deposition. Pretreatment with highly selective ETA receptor inhibitor had no adverse effect on control mice but improved lung mechanics and lung injury score in addition to decreasing BALF pleocytosis, protein content, and collagen deposition in BLM-treated mice. Mortality from BLM reached 40% and occurred primarily during the inflammatory stage of the model but was abrogated by sitaxentan pretreatment.
    Conclusions: We conclude that in our BLM-induced pulmonary fibrosis model, prophylactic highly selective ETA inhibition improves survival, preserves lung function, attenuates lung injury, and reduces collagen deposition.
    MeSH term(s) Animals ; Bleomycin ; Collagen/metabolism ; Disease Models, Animal ; Drug Evaluation, Preclinical ; Endothelin Receptor Antagonists/therapeutic use ; Isoxazoles/therapeutic use ; Liver/drug effects ; Lung/drug effects ; Lung/metabolism ; Lung/pathology ; Male ; Mice, Inbred C57BL ; Pneumonia/chemically induced ; Pneumonia/complications ; Pneumonia/prevention & control ; Pulmonary Fibrosis/chemically induced ; Pulmonary Fibrosis/pathology ; Pulmonary Fibrosis/prevention & control ; Receptor, Endothelin A/metabolism ; Respiratory Function Tests ; Thiophenes/therapeutic use
    Chemical Substances Endothelin Receptor Antagonists ; Isoxazoles ; Receptor, Endothelin A ; Thiophenes ; Bleomycin (11056-06-7) ; Collagen (9007-34-5) ; sitaxsentan (J9QH779MEM)
    Language English
    Publishing date 2017-11-09
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 206674-9
    ISSN 1423-0356 ; 0025-7931
    ISSN (online) 1423-0356
    ISSN 0025-7931
    DOI 10.1159/000481201
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Integration in groups of donors may modify attitudes towards blood donation.

    Politou, Marianna / Gialeraki, Argyri / Valsami, Serena / Nearchakos, Nikolaos / Tsantes, Argyrios / Travlou, Anthi / Maniatis, Alice

    Blood transfusion = Trasfusione del sangue

    2015  Volume 13, Issue 2, Page(s) 336–337

    MeSH term(s) Attitude to Health ; Blood Donors ; Female ; Greece ; Humans ; Male ; Surveys and Questionnaires
    Language English
    Publishing date 2015-04
    Publishing country Italy
    Document type Letter
    ZDB-ID 2135732-8
    ISSN 1723-2007 ; 0041-1787
    ISSN 1723-2007 ; 0041-1787
    DOI 10.2450/2014.0153-14
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    Zs.A 798: Show issues Location:
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  6. Article: Highly Selective Endothelin-1 Receptor A Inhibition Prevents Bleomycin-Induced Pulmonary Inflammation and Fibrosis in Mice

    Manitsopoulos, Nikolaos / Nikitopoulou, Ioanna / Maniatis, Nikolaos A. / Magkou, Christina / Kotanidou, Anastasia / Orfanos, Stylianos E.

    Respiration

    2017  Volume 95, Issue 2, Page(s) 122–136

    Abstract: Background: Pulmonary fibrosis is a chronic disease, which progressively leads to respiratory failure and ultimately death. Endothelin-1 (ET-1), a vasoconstrictor secreted by endothelial cells, promotes vasoconstriction by activation of its receptors A ... ...

    Institution GP Livanos and M Simou Laboratories, 1st Department of Critical Care Medicine & Pulmonary Services, Evangelismos Hospital, University of Athens Medical School 1st Department of Critical Care Medicine & Pulmonary Services, Evangelismos Hospital, University of Athens Medical School 2nd Department of Critical Care, “Attikon” Hospital, University of Athens Medical School, and Department of Pathology, Evangelismos Hospital, Athens, Greece
    Abstract Background: Pulmonary fibrosis is a chronic disease, which progressively leads to respiratory failure and ultimately death. Endothelin-1 (ET-1), a vasoconstrictor secreted by endothelial cells, promotes vasoconstriction by activation of its receptors A and B. Objectives: We addressed the role of highly selective ET-1 receptor A (ETA) inhibition in the pathogenesis of experimental pulmonary fibrosis by bleomycin (BLM). Methods: BLM sulfate (2 U/mL) or saline was intratracheally administered to C57/Bl6 mice (4 groups; n = 5-11/group). Pretreatment with the highly selective ETA receptor inhibitor sitaxentan (15 mg/kg/day) was started 1 day prior to BLM injection and continued for the duration of the experiment. Lung mechanics were assessed prior to sacrifice at days 7, 14, and 21 after BLM, followed by procurement of bronchoalveolar lavage fluid (BALF), blood, and lung tissue samples. Results: Time-dependent effects of BLM exposure included decreased static compliance and increased lung elastance, airspace inflammation and microvascular permeability, histological acute lung injury and fibrosis, and lung collagen deposition. Pretreatment with highly selective ETA receptor inhibitor had no adverse effect on control mice but improved lung mechanics and lung injury score in addition to decreasing BALF pleocytosis, protein content, and collagen deposition in BLM-treated mice. Mortality from BLM reached 40% and occurred primarily during the inflammatory stage of the model but was abrogated by sitaxentan pretreatment. Conclusions: We conclude that in our BLM-induced pulmonary fibrosis model, prophylactic highly selective ETA inhibition improves survival, preserves lung function, attenuates lung injury, and reduces collagen deposition.
    Keywords Inflammation ; Fibrosis ; Bleomycin ; Endothelin-1 ; Sitaxentan ; Lung function
    Language English
    Publishing date 2017-11-09
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Basic Science Investigations
    ZDB-ID 206674-9
    ISSN 1423-0356 ; 0025-7931
    ISSN (online) 1423-0356
    ISSN 0025-7931
    DOI 10.1159/000481201
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  7. Article ; Online: Vascular endothelial-cadherin downregulation as a feature of endothelial transdifferentiation in monocrotaline-induced pulmonary hypertension.

    Nikitopoulou, Ioanna / Orfanos, Stylianos E / Kotanidou, Anastasia / Maltabe, Violetta / Manitsopoulos, Nikolaos / Karras, Panagiotis / Kouklis, Panos / Armaganidis, Apostolos / Maniatis, Nikolaos A

    American journal of physiology. Lung cellular and molecular physiology

    2016  Volume 311, Issue 2, Page(s) L352–63

    Abstract: Increased pulmonary vascular resistance in pulmonary hypertension (PH) is caused by vasoconstriction and obstruction of small pulmonary arteries by proliferating vascular cells. In analogy to cancer, subsets of proliferating cells may be derived from ... ...

    Abstract Increased pulmonary vascular resistance in pulmonary hypertension (PH) is caused by vasoconstriction and obstruction of small pulmonary arteries by proliferating vascular cells. In analogy to cancer, subsets of proliferating cells may be derived from endothelial cells transitioning into a mesenchymal phenotype. To understand phenotypic shifts transpiring within endothelial cells in PH, we injected rats with alkaloid monocrotaline to induce PH and measured lung tissue levels of endothelial-specific protein and critical differentiation marker vascular endothelial (VE)-cadherin. VE-cadherin expression by immonoblotting declined significantly 24 h and 15 days postinjection to rebound to baseline at 30 days. There was a concomitant increase in transcriptional repressors Snail and Slug, along with a reduction in VE-cadherin mRNA. Mesenchymal markers α-smooth muscle actin and vimentin were upregulated by immunohistochemistry and immunoblotting, and α-smooth muscle actin was colocalized with endothelial marker platelet endothelial cell adhesion molecule-1 by confocal microscopy. Apoptosis was limited in this model, especially in the 24-h time point. In addition, monocrotaline resulted in activation of protein kinase B/Akt, endothelial nitric oxide synthase (eNOS), nuclear factor (NF)-κB, and increased lung tissue nitrotyrosine staining. To understand the etiological relationship between nitrosative stress and VE-cadherin suppression, we incubated cultured rat lung endothelial cells with endothelin-1, a vasoconstrictor and pro-proliferative agent in pulmonary arterial hypertension. This resulted in activation of eNOS, NF-κB, and Akt, in addition to induction of Snail, downregulation of VE-cadherin, and synthesis of vimentin. These effects were blocked by eNOS inhibitor N(ω)-nitro-l-arginine methyl ester. We propose that transcriptional repression of VE-cadherin by nitrosative stress is involved in endothelial-mesenchymal transdifferentiation in experimental PH.
    MeSH term(s) Animals ; Antigens, CD/genetics ; Antigens, CD/metabolism ; Apoptosis ; Cadherins/genetics ; Cadherins/metabolism ; Cell Transdifferentiation ; Cells, Cultured ; Down-Regulation ; Endothelial Cells/physiology ; Endothelin-1/physiology ; Endothelium, Vascular/pathology ; Enzyme Activation ; Gene Silencing ; Hypertension, Pulmonary/chemically induced ; Hypertension, Pulmonary/metabolism ; Hypertension, Pulmonary/pathology ; Lung/pathology ; Monocrotaline ; Nitric Oxide Synthase Type III/metabolism ; Rats, Wistar ; Transcription, Genetic
    Chemical Substances Antigens, CD ; Cadherins ; Endothelin-1 ; cadherin 5 ; Monocrotaline (73077K8HYV) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Nos3 protein, rat (EC 1.14.13.39)
    Language English
    Publishing date 2016-05-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00156.2014
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  8. Article: The endothelium in acute lung injury/acute respiratory distress syndrome.

    Maniatis, Nikolaos A / Orfanos, Stylianos E

    Current opinion in critical care

    2008  Volume 14, Issue 1, Page(s) 22–30

    Abstract: Purpose of review: Since pulmonary edema from increased endothelial permeability is the hallmark of acute lung injury, a frequently encountered entity in critical care medicine, the study of endothelial responses in this setting is crucial to the ... ...

    Abstract Purpose of review: Since pulmonary edema from increased endothelial permeability is the hallmark of acute lung injury, a frequently encountered entity in critical care medicine, the study of endothelial responses in this setting is crucial to the development of effective endothelial-targeted treatments.
    Recent findings: From the enormous amount of research in the field of endothelial pathophysiology, we have focused on work delineating endothelial alterations elicited by noxious stimuli implicated in acute lung injury. The bulk of the material covered deals with molecular and cellular aspects of the pathogenesis, reflecting current trends in the published literature. We initially discuss pathways of endothelial dysfunction in acute lung injury and then cover the mechanisms of endothelial protection. Several experimental treatments in animal models are presented, which aid in the understanding of the disease pathogenesis and provide evidence for potentially useful therapies.
    Summary: Mechanistic studies have delivered several interventions, which are effective in preventing and treating experimental acute lung injury and have thus provided objectives for translational studies. Some of these modalities may evolve into clinically useful tools in the treatment of this devastating illness.
    MeSH term(s) Angiopoietins/metabolism ; Animals ; Cytoskeleton/metabolism ; Cytoskeleton/ultrastructure ; Endothelium, Vascular/pathology ; Endothelium, Vascular/physiopathology ; Humans ; Pulmonary Edema/pathology ; Pulmonary Edema/physiopathology ; Pulmonary Edema/prevention & control ; Reactive Nitrogen Species/metabolism ; Reactive Oxygen Species/metabolism ; Renin-Angiotensin System/physiology ; Respiratory Distress Syndrome, Adult/pathology ; Respiratory Distress Syndrome, Adult/physiopathology ; Respiratory Distress Syndrome, Adult/prevention & control ; Signal Transduction
    Chemical Substances Angiopoietins ; Reactive Nitrogen Species ; Reactive Oxygen Species
    Language English
    Publishing date 2008-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1235629-3
    ISSN 1531-7072 ; 1070-5295
    ISSN (online) 1531-7072
    ISSN 1070-5295
    DOI 10.1097/MCC.0b013e3282f269b9
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  9. Article: Caveolins and lung function.

    Maniatis, Nikolaos A / Chernaya, Olga / Shinin, Vasily / Minshall, Richard D

    Advances in experimental medicine and biology

    2012  Volume 729, Page(s) 157–179

    Abstract: The primary function of the mammalian lung is to facilitate diffusion of oxygen to venous blood and to ventilate carbon dioxide produced by catabolic reactions within cells. However, it is also responsible for a variety of other important functions, ... ...

    Abstract The primary function of the mammalian lung is to facilitate diffusion of oxygen to venous blood and to ventilate carbon dioxide produced by catabolic reactions within cells. However, it is also responsible for a variety of other important functions, including host defense and production of vasoactive agents to regulate not only systemic blood pressure, but also water, electrolyte and acid-base balance. Caveolin-1 is highly expressed in the majority of cell types in the lung, including epithelial, endothelial, smooth muscle, connective tissue cells, and alveolar macrophages. Deletion of caveolin-1 in these cells results in major functional aberrations, suggesting that caveolin-1 may be crucial to lung homeostasis and development. Furthermore, generation of mutant mice that under-express caveolin-1 results in severe functional distortion with phenotypes covering practically the entire spectrum of known lung diseases, including pulmonary hypertension, fibrosis, increased endothelial permeability, and immune defects. In this Chapter, we outline the current state of knowledge regarding caveolin-1-dependent regulation of pulmonary cell functions and discuss recent research findings on the role of caveolin-1 in various pulmonary disease states, including obstructive and fibrotic pulmonary vascular and inflammatory diseases.
    MeSH term(s) Animals ; Caveolins/metabolism ; Endothelium/cytology ; Endothelium/metabolism ; Endothelium/pathology ; Humans ; Lung/growth & development ; Lung/metabolism ; Lung/physiology ; Lung/physiopathology ; Lung Diseases/metabolism ; Lung Diseases/pathology ; Lung Diseases/physiopathology ; Pulmonary Alveoli/cytology ; Pulmonary Alveoli/pathology ; Pulmonary Alveoli/physiology ; Pulmonary Alveoli/physiopathology
    Chemical Substances Caveolins
    Language English
    Publishing date 2012-03-13
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-1-4614-1222-9_11
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Protective role of statins against ventilator-induced lung injury.

    Siempos, Ilias I / Kopterides, Petros / Maniatis, Nikolaos A / Armaganidis, Apostolos

    Critical care (London, England)

    2010  Volume 14, Issue 5, Page(s) 441

    MeSH term(s) Animals ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Ventilator-Induced Lung Injury/enzymology ; Ventilator-Induced Lung Injury/prevention & control
    Chemical Substances Hydroxymethylglutaryl-CoA Reductase Inhibitors
    Language English
    Publishing date 2010-09-16
    Publishing country England
    Document type Comment ; Letter
    ZDB-ID 2041406-7
    ISSN 1466-609X ; 1364-8535
    ISSN (online) 1466-609X
    ISSN 1364-8535
    DOI 10.1186/cc9245
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