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  1. Article ; Online: Inflammation control and improvement of cognitive function in COVID-19 infections: is there a role for kynurenine 3-monooxygenase inhibition?

    Collier, Mary Ew / Zhang, Shaowei / Scrutton, Nigel S / Giorgini, Flaviano

    Drug discovery today

    2021  Volume 26, Issue 6, Page(s) 1473–1481

    Abstract: The novel respiratory virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), emerged during late 2019 and spread rapidly across the world. It is now recognised that the nervous system can be ... ...

    Abstract The novel respiratory virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), emerged during late 2019 and spread rapidly across the world. It is now recognised that the nervous system can be affected in COVID-19, with several studies reporting long-term cognitive problems in patients. The metabolic pathway of tryptophan degradation, known as the kynurenine pathway (KP), is significantly activated in patients with COVID-19. KP metabolites have roles in regulating both inflammatory/immune responses and neurological functions. In this review, we speculate on the effects of KP activation in patients with COVID-19, and how modulation of this pathway might impact inflammation and reduce neurological symptoms.
    MeSH term(s) Animals ; COVID-19/immunology ; COVID-19/psychology ; Cognition/drug effects ; Cognition/physiology ; Humans ; Inflammation/metabolism ; Kynurenine/metabolism ; Kynurenine 3-Monooxygenase/antagonists & inhibitors ; Neuroprotective Agents/pharmacology ; Signal Transduction ; Sulfonamides/pharmacology ; Thiazoles/pharmacology ; Tryptophan/metabolism
    Chemical Substances Neuroprotective Agents ; Ro 61-8048 ; Sulfonamides ; Thiazoles ; Kynurenine (343-65-7) ; Tryptophan (8DUH1N11BX) ; Kynurenine 3-Monooxygenase (EC 1.14.13.9)
    Language English
    Publishing date 2021-02-18
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1324988-5
    ISSN 1878-5832 ; 1359-6446
    ISSN (online) 1878-5832
    ISSN 1359-6446
    DOI 10.1016/j.drudis.2021.02.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4725: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article: Analysis of the potential of cancer cell lines to release tissue factor-containing microvesicles: correlation with tissue factor and PAR2 expression.

    Ettelaie, Camille / Collier, Mary Ew / Featherby, Sophie / Benelhaj, Naima E / Greenman, John / Maraveyas, Anthony

    Thrombosis journal

    2016  Volume 14, Page(s) 2

    Abstract: Background: Despite the association of cancer-derived circulating tissue factor (TF)-containing microvesicles and hypercoagulable state, correlations with the incidence of thrombosis remain unclear.: Methods: In this study the upregulation of TF ... ...

    Abstract Background: Despite the association of cancer-derived circulating tissue factor (TF)-containing microvesicles and hypercoagulable state, correlations with the incidence of thrombosis remain unclear.
    Methods: In this study the upregulation of TF release upon activation of various cancer cell lines, and the correlation with TF and PAR2 expression and/or activity was examined. Microvesicle release was induced by PAR2 activation in seventeen cell lines and released microvesicle density, microvesicle-associated TF activity, and phoshpatidylserine-mediated activity were measured. The time-course for TF release was monitored over 90 min in each cell line. In addition, TF mRNA expression, cellular TF protein and cell-surface TF activities were quantified. Moreover, the relative expression of PAR2 mRNA and cellular protein were analysed. Any correlations between the above parameters were examined by determining the Pearson's correlation coefficients.
    Results: TF release as microvesicles peaked between 30-60 min post-activation in the majority of cell lines tested. The magnitude of the maximal TF release positively correlated with TF mRNA (c = 0.717; p < 0.001) and PAR2 mRNA (c = 0.770; p < 0.001) expressions while the percentage increase correlated with PAR2 mRNA (c = 0.601; p = 0.011) and protein (c = 0.714; p < 0.001). There was only a weak correlation between resting TF release, and microvesicle release. However, TF release in resting cells did not significantly correlate with any of the parameters examined. Furthermore, TF mRNA expression correlated with PAR2 mRNA expression (c = 0.745; p < 0.001).
    Discussion and conclusions: In conclusion, our data suggest that TF and PAR2 mRNA, and PAR2 protein are better indicators of the ability of cancer cells to release TF and may constitute more accurate predictors of risk of thrombosis.
    Language English
    Publishing date 2016-01-19
    Publishing country England
    Document type Journal Article
    ISSN 1477-9560
    ISSN 1477-9560
    DOI 10.1186/s12959-016-0075-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Advantages of brain penetrating inhibitors of kynurenine-3-monooxygenase for treatment of neurodegenerative diseases

    Zhang, Shaowei / Collier, Mary E.W / Heyes, Derren J / Giorgini, Flaviano / Scrutton, Nigel S

    Archives of biochemistry and biophysics. 2021 Jan. 15, v. 697

    2021  

    Abstract: Kynurenine-3-monooxygenase (KMO) is an important therapeutic target for several brain disorders that has been extensively studied in recent years. Potent inhibitors towards KMO have been developed and tested within different disease models, showing great ...

    Abstract Kynurenine-3-monooxygenase (KMO) is an important therapeutic target for several brain disorders that has been extensively studied in recent years. Potent inhibitors towards KMO have been developed and tested within different disease models, showing great therapeutic potential, especially in models of neurodegenerative disease. The inhibition of KMO reduces the production of downstream toxic kynurenine pathway metabolites and shifts the flux to the formation of the neuroprotectant kynurenic acid. However, the efficacy of KMO inhibitors in neurodegenerative disease has been limited by their poor brain permeability. Combined with virtual screening and prodrug strategies, a novel brain penetrating KMO inhibitor has been developed which dramatically decreases neurotoxic metabolites. This review highlights the importance of KMO as a drug target in neurological disease and the benefits of brain permeable inhibitors in modulating kynurenine pathway metabolites in the central nervous system.
    Keywords biophysics ; brain ; drugs ; kynurenine pathway ; metabolites ; neurodegenerative diseases ; neurotoxicity ; permeability ; therapeutics
    Language English
    Dates of publication 2021-0115
    Publishing place Elsevier Inc.
    Document type Article
    Note NAL-AP-2-clean
    ZDB-ID 523-x
    ISSN 1096-0384 ; 0003-9861
    ISSN (online) 1096-0384
    ISSN 0003-9861
    DOI 10.1016/j.abb.2020.108702
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

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    Archiv: Show issues

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  4. Article ; Online: An Open-label Phase I Study of GDC-0927 in Postmenopausal Women with Locally Advanced or Metastatic Estrogen Receptor-Positive Breast Cancer.

    Chandarlapaty, Sarat / Dickler, Maura N / Perez Fidalgo, Jose Alejandro / Villanueva-Vázquez, Rafael / Giltnane, Jennifer / Gates, Mary / Chang, Ching-Wei / Cheeti, Sravanthi / Fredrickson, Jill / Wang, Xiaojing / Collier, Ann / Moore, Heather M / Metcalfe, Ciara / Lauchle, Jennifer / Humke, Eric W / Bardia, Aditya

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2023  Volume 29, Issue 15, Page(s) 2781–2790

    Abstract: Purpose: GDC-0927 is a novel, potent, nonsteroidal, orally bioavailable, selective estrogen receptor (ER) degrader that induces tumor regression in ER+ breast cancer xenograft models.: Patients and methods: This phase I dose-escalation multicenter ... ...

    Abstract Purpose: GDC-0927 is a novel, potent, nonsteroidal, orally bioavailable, selective estrogen receptor (ER) degrader that induces tumor regression in ER+ breast cancer xenograft models.
    Patients and methods: This phase I dose-escalation multicenter study enrolled postmenopausal women with ER+/HER2- metastatic breast cancer to determine the safety, pharmacokinetics, and recommended phase II dose of GDC-0927. Pharmacodynamics was assessed with [18F]-fluoroestradiol (FES) PET scans.
    Results: Forty-two patients received GDC-0927 once daily. The MTD was not reached. The most common adverse events (AE) regardless of causality were nausea, constipation, diarrhea, arthralgia, fatigue, hot flush, back pain, and vomiting. There were no deaths, grade 4/5 AEs, or treatment-related serious AEs. Two patients experienced grade 2 AEs of special interest of deep vein thrombosis and jugular vein thrombosis, both considered unrelated to GDC-0927. Following dosing, approximately 1.6-fold accumulation was observed, consistent with the observed half-life and dosing frequency. There were no complete or partial responses. Pharmacodynamics was supported by >90% reduction in FES uptake and an approximately 40% reduction in ER expression, suggesting ER degradation is not the mechanistic driver of ER antagonism. Twelve patients (29%) achieved clinical benefit; 17 patients (41%) showed a confirmed best overall response of stable disease. Baseline levels of ER and progesterone receptor protein and mutant ESR1 circulating tumor DNA did not correlate with clinical benefit.
    Conclusions: GDC-0927 appeared to be well tolerated with pharmacokinetics supporting once-daily dosing. There was evidence of target engagement and preliminary evidence of antitumor activity in heavily pretreated patients with advanced/metastatic ER+/HER2- breast cancer with and without ESR1 mutations.
    MeSH term(s) Humans ; Female ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Receptors, Estrogen/genetics ; Postmenopause ; Estrogen Receptor Antagonists ; Positron-Emission Tomography
    Chemical Substances Receptors, Estrogen ; Estrogen Receptor Antagonists
    Language English
    Publishing date 2023-06-01
    Publishing country United States
    Document type Multicenter Study ; Clinical Trial, Phase I ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-23-0011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4223: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
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  5. Article: Accumulation of tissue factor in endothelial cells induces cell apoptosis, mediated through p38 and p53 activation

    ElKeeb, Azza M / Collier, Mary E.W. / Maraveyas, Anthony / Ettelaie, Camille

    Thrombosis and Haemostasis

    2015  Volume 113, Issue 02, Page(s) 364–378

    Abstract: We previously reported that high levels of tissue factor (TF) can induce cellular apoptosis in endothelial cells. In this study, TF-mediated mechanisms of induction of apoptosis were explored. Endothelial cells were transfected to express wild-type TF. ... ...

    Abstract We previously reported that high levels of tissue factor (TF) can induce cellular apoptosis in endothelial cells. In this study, TF-mediated mechanisms of induction of apoptosis were explored. Endothelial cells were transfected to express wild-type TF. Additionally, cells were transfected to express Asp253-substituted, or Ala253-substitued TF to enhance or prevent TF release, respectively. Alternatively, cells were pre-incubated with TF-rich and TF-poor microvesicles. Cell proliferation, apoptosis and the expression of cyclin D1, p53, bax and p21 were measured following activation of cells with PAR2-agonist peptide. Greatest levels of cell proliferation and cyclin D1 expression were observed in cells expressing wild-type or Asp253-substituted TF. In contrast, increased cellular apoptosis was observed in cells expressing Ala253-substituted TF, or cells pre-incubated with TF-rich microvesicles. The level of p53 protein, p53-phosphorylation at ser33, p53 nuclear localisation and transcriptional activity, but not p53 mRNA, were increased in cells expressing wild-type and Ala253-substituted TF, or in cells pre-incubated with TF-rich microvesicles. However, the expression of bax and p21 mRNA, and Bax protein were only increased in cells pre-incubated with TF-rich microvesicle and in cells expressing Ala253-substituted TF. Inhibition of the transcriptional activity of p53 using pifithrin-α suppressed the expression of Bax. Finally, siRNA- mediated suppression of p38α, or inhibition using SB202190 significantly reduced the p53 protein levels, p53 nuclear localisation and transcriptional activity, suppressed Bax expression and prevented cellular apoptosis. In conclusion, accumulation of TF within endothelial cells, or sequestered from the surrounding can induce cellular apoptosis through mechanisms mediated by p38, and involves the stabilisation of p53.
    Keywords Tissue factor ; serine-phosphorylation ; p38-MAP kinase ; p53 activation ; apoptosis
    Language English
    Publishing date 2015-01-01
    Publisher Schattauer GmbH
    Publishing place Stuttgart ; New York
    Document type Article
    ZDB-ID 518294-3
    ISSN 2567-689X ; 0340-6245
    ISSN (online) 2567-689X
    ISSN 0340-6245
    DOI 10.1160/TH14-09-0795
    Database Thieme publisher's database

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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.192: Show issues Location:
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    Zs.MO 433: Show issues

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  6. Article ; Online: Erratum to: Methods for evaluating medical tests and biomarkers.

    Gopalakrishna, Gowri / Langendam, Miranda / Scholten, Rob / Bossuyt, Patrick / Leeflang, Mariska / Noel-Storr, Anna / Thomas, James / Marshall, Iain / Wallace, Byron / Whiting, Penny / Davenport, Clare / GopalaKrishna, Gowri / de Salis, Isabel / Mallett, Sue / Wolff, Robert / Riley, Richard / Westwood, Marie / Kleinen, Jos / Collins, Gary /
    Reitsma, Hans / Moons, Karel / Zapf, Antonia / Hoyer, Annika / Kramer, Katharina / Kuss, Oliver / Ensor, J / Deeks, J J / Martin, E C / Riley, R D / Rücker, Gerta / Steinhauser, Susanne / Schumacher, Martin / Ensor, Joie / Snell, Kym / Willis, Brian / Debray, Thomas / Deeks, Jon / di Ruffano, Lavinia Ferrante / Taylor-Phillips, Sian / Hyde, Chris / Taylor, Stuart A / Batnagar, Gauraang / Di Ruffano, Lavinia Ferrante / Seedat, Farah / Clarke, Aileen / Byron, Sarah / Nixon, Frances / Albrow, Rebecca / Walker, Thomas / Deakin, Carla / Zhelev, Zhivko / Hunt, Harriet / Yang, Yaling / Abel, Lucy / Buchanan, James / Fanshawe, Thomas / Shinkins, Bethany / Wynants, Laure / Verbakel, Jan / Van Huffel, Sabine / Timmerman, Dirk / Van Calster, Ben / Zwinderman, Aeliko / Oke, Jason / O'Sullivan, Jack / Perera, Rafael / Nicholson, Brian / Bromley, Hannah L / Roberts, Tracy E / Francis, Adele / Petrie, Denniis / Mann, G Bruce / Malottki, Kinga / Smith, Holly / Billingham, Lucinda / Sitch, Alice / Gerke, Oke / Holm-Vilstrup, Mie / Segtnan, Eivind Antonsen / Halekoh, Ulrich / Høilund-Carlsen, Poul Flemming / Francq, Bernard G / Dinnes, Jac / Parkes, Julie / Gregory, Walter / Hewison, Jenny / Altman, Doug / Rosenberg, William / Selby, Peter / Asselineau, Julien / Perez, Paul / Paye, Aïssatou / Bessede, Emilie / Proust-Lima, Cécile / Naaktgeboren, Christiana / de Groot, Joris / Rutjes, Anne / Reitsma, Johannes / Ogundimu, Emmanuel / Cook, Jonathan / Le Manach, Yannick / Vergouwe, Yvonne / Pajouheshnia, Romin / Groenwold, Rolf / Moons, Karen / Peelen, Linda / Nieboer, Daan / De Cock, Bavo / Pencina, Micael J / Steyerberg, Ewout W / Cooper, Jennifer / Parsons, Nick / Stinton, Chris / Smith, Steve / Dickens, Andy / Jordan, Rachel / Enocson, Alexandra / Fitzmaurice, David / Adab, Peymane / Boachie, Charles / Vidmar, Gaj / Freeman, Karoline / Connock, Martin / Court, Rachel / Moons, Carl / Harris, Jessica / Mumford, Andrew / Plummer, Zoe / Lee, Kurtis / Reeves, Barnaby / Rogers, Chris / Verheyden, Veerle / Angelini, Gianni D / Murphy, Gavin J / Huddy, Jeremy / Ni, Melody / Good, Katherine / Cooke, Graham / Hanna, George / Ma, Jie / Moons, K G M Carl / de Groot, Joris A H / Altman, Doug G / Reitsma, Johannes B / Collins, Gary S / Moons, Karel G M / Altman, Douglas G / Kamarudin, Adina Najwa / Kolamunnage-Dona, Ruwanthi / Cox, Trevor / Borsci, Simone / Pérez, Teresa / Pardo, M Carmen / Candela-Toha, Angel / Muriel, Alfonso / Zamora, Javier / Sanghera, Sabina / Mohiuddin, Syed / Martin, Richard / Donovan, Jenny / Coast, Joanna / Seo, Mikyung Kelly / Cairns, John / Mitchell, Elizabeth / Smith, Alison / Wright, Judy / Hall, Peter / Messenger, Michael / Calder, Nicola / Wickramasekera, Nyantara / Vinall-Collier, Karen / Lewington, Andrew / Damen, Johanna / Cairns, David / Hutchinson, Michelle / Sturgeon, Cathie / Mitchel, Liz / Kift, Rebecca / Christakoudi, Sofia / Rungall, Manohursingh / Mobillo, Paula / Montero, Rosa / Tsui, Tjir-Li / Kon, Sui Phin / Tucker, Beatriz / Sacks, Steven / Farmer, Chris / Strom, Terry / Chowdhury, Paramit / Rebollo-Mesa, Irene / Hernandez-Fuentes, Maria / Damen, Johanna A A G / Debray, Thomas P A / Heus, Pauline / Hooft, Lotty / Scholten, Rob J P M / Schuit, Ewoud / Tzoulaki, Ioanna / Lassale, Camille M / Siontis, George C M / Chiocchia, Virginia / Roberts, Corran / Schlüssel, Michael Maia / Gerry, Stephen / Black, James A / van der Schouw, Yvonne T / Peelen, Linda M / Spence, Graeme / McCartney, David / van den Bruel, Ann / Lasserson, Daniel / Hayward, Gail / Vach, Werner / de Jong, Antoinette / Burggraaff, Coreline / Hoekstra, Otto / Zijlstra, Josée / de Vet, Henrica / Graziadio, Sara / Allen, Joy / Johnston, Louise / O'Leary, Rachel / Power, Michael / Johnson, Louise / Waters, Ray / Simpson, John / Fanshawe, Thomas R / Phillips, Peter / Plumb, Andrew / Helbren, Emma / Halligan, Steve / Gale, Alastair / Sekula, Peggy / Sauerbrei, Willi / Forman, Julia R / Dutton, Susan J / Takwoingi, Yemisi / Hensor, Elizabeth M / Nichols, Thomas E / Kempf, Emmanuelle / Porcher, Raphael / de Beyer, Jennifer / Altman, Douglas / Hopewell, Sally / Dennis, John / Shields, Beverley / Jones, Angus / Henley, William / Pearson, Ewan / Hattersley, Andrew / Scheibler, Fueloep / Rummer, Anne / Sturtz, Sibylle / Großelfinger, Robert / Banister, Katie / Ramsay, Craig / Azuara-Blanco, Augusto / Burr, Jennifer / Kumarasamy, Manjula / Bourne, Rupert / Uchegbu, Ijeoma / Murphy, Jennifer / Carter, Alex / Murphy, Jen / Marti, Joachim / Eatock, Julie / Robotham, Julie / Dudareva, Maria / Gilchrist, Mark / Holmes, Alison / Monaghan, Phillip / Lord, Sarah / StJohn, Andrew / Sandberg, Sverre / Cobbaert, Christa / Lennartz, Lieselotte / Verhagen-Kamerbeek, Wilma / Ebert, Christoph / Horvath, Andrea / Jenniskens, Kevin / Peters, Jaime / Grigore, Bogdan / Ukoumunne, Obi / Levis, Brooke / Benedetti, Andrea / Levis, Alexander W / Ioannidis, John P A / Shrier, Ian / Cuijpers, Pim / Gilbody, Simon / Kloda, Lorie A / McMillan, Dean / Patten, Scott B / Steele, Russell J / Ziegelstein, Roy C / Bombardier, Charles H / Osório, Flavia de Lima / Fann, Jesse R / Gjerdingen, Dwenda / Lamers, Femke / Lotrakul, Manote / Loureiro, Sonia R / Löwe, Bernd / Shaaban, Juwita / Stafford, Lesley / van Weert, Henk C P M / Whooley, Mary A / Williams, Linda S / Wittkampf, Karin A / Yeung, Albert S / Thombs, Brett D / Cooper, Chris / Nieto, Tom / Smith, Claire / Tucker, Olga / Dretzke, Janine / Beggs, Andrew / Rai, Nirmala / Bayliss, Sue / Stevens, Simon / Mallet, Sue / Sundar, Sudha / Hall, Emma / Porta, Nuria / Estelles, David Lorente / de Bono, Johann

    Diagnostic and prognostic research

    2017  Volume 1, Page(s) 11

    Abstract: This corrects the article DOI: 10.1186/s41512-016-0001-y.]. ...

    Abstract [This corrects the article DOI: 10.1186/s41512-016-0001-y.].
    Language English
    Publishing date 2017-03-30
    Publishing country England
    Document type Published Erratum
    ISSN 2397-7523
    ISSN (online) 2397-7523
    DOI 10.1186/s41512-017-0011-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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