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Article ; Online: T cell involvement in antiphospholipid syndrome.

Tektonidou, Maria G / Vlachogiannis, Nikolaos I / Sfikakis, Petros P

2024 Volume 263, Page(s) 110218

Abstract: Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by arterial and venous thrombosis, and obstetric complications in the presence of antiphospholipid antibodies (aPL), including lupus anticoagulant, anticardiolipin and anti- ... ...

Abstract	Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by arterial and venous thrombosis, and obstetric complications in the presence of antiphospholipid antibodies (aPL), including lupus anticoagulant, anticardiolipin and anti-β2-glycoprotein I antibodies. APS manifests as single, often as recurrent events, and rarely as a catastrophic condition. Most studies of APS pathogenesis to date have focused on the prothrombotic role of aPL, while innate immune responses such as monocyte, complement and neutrophil activation have been also recognized as part of the thrombo-inflammatory cascade in APS. While the presence of autoreactive T cells against β2-glycoprotein I has been long known, less data are available on their pathogenetic role in APS. In this review, we summarize current knowledge on the involvement of T cells in APS pathophysiology, alterations of T cell subsets in peripheral blood, and clinical associations. We also highlight potential therapeutic opportunities by targeting T helper-B cell interactions in these patients.
Language	English
Publishing date	2024-04-18
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2024.110218
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Article ; Online: Circulating Progenitor Cells Predict Clinical Outcomes in Patients With Coronary Artery Disease and Renal Insufficiency.

Vlachogiannis, Nikolaos I / Stellos, Konstantinos

JACC. Basic to translational science

2020 Volume 5, Issue 8, Page(s) 783–785

Language	English
Publishing date	2020-08-24
Publishing country	United States
Document type	Editorial ; Comment
ISSN	2452-302X
ISSN (online)	2452-302X
DOI	10.1016/j.jacbts.2020.07.002
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Article ; Online: Liver endothelial cells in NAFLD and transition to NASH and HCC.

Velliou, Rallia-Iliana / Legaki, Aigli-Ioanna / Nikolakopoulou, Polyxeni / Vlachogiannis, Nikolaos I / Chatzigeorgiou, Antonios

Cellular and molecular life sciences : CMLS

2023 Volume 80, Issue 11, Page(s) 314

Abstract: Non-alcoholic fatty liver disease (NAFLD) is considered as the hepatic manifestation of metabolic syndrome, which is characterised by obesity, insulin resistance, hypercholesterolemia and hypertension. NAFLD is the most frequent liver disease worldwide ... ...

Abstract	Non-alcoholic fatty liver disease (NAFLD) is considered as the hepatic manifestation of metabolic syndrome, which is characterised by obesity, insulin resistance, hypercholesterolemia and hypertension. NAFLD is the most frequent liver disease worldwide and more than 10% of NAFLD patients progress to the inflammatory and fibrotic stage of non-alcoholic steatohepatitis (NASH), which can lead to end-stage liver disease including hepatocellular carcinoma (HCC), the most frequent primary malignant liver tumor. Liver sinusoidal endothelial cells (LSEC) are strategically positioned at the interface between blood and hepatic parenchyma. LSECs are highly specialized cells, characterised by the presence of transcellular pores, called fenestrae, and exhibit anti-inflammatory and anti-fibrotic characteristics under physiological conditions. However, during NAFLD development they undergo capillarisation and acquire a phenotype similar to vascular endothelial cells, actively promoting all pathophysiological aspects of NAFLD, including steatosis, inflammation, and fibrosis. LSEC dysfunction is critical for the progression to NASH and HCC while restoring LSEC homeostasis appears to be a promising approach to prevent NAFLD progression and its complications and even reverse tissue damage. In this review we present current information on the role of LSEC throughout the progressive phases of NAFLD, summarising in vitro and in vivo experimental evidence and data from human studies.
MeSH term(s)	Humans ; Non-alcoholic Fatty Liver Disease/metabolism ; Carcinoma, Hepatocellular/genetics ; Endothelial Cells/metabolism ; Liver Neoplasms/metabolism ; Liver/metabolism ; Fibrosis
Language	English
Publishing date	2023-10-05
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-023-04966-7
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Article ; Online: PRIME Cells Predicting Rheumatoid Arthritis Flares.

Sfikakis, Petros P / Vlachogiannis, Nikolaos I / Sakkou, Maria

The New England journal of medicine

2020 Volume 383, Issue 16, Page(s) 1594–1595

MeSH term(s)	Arthritis, Rheumatoid ; Diagnostic Tests, Routine ; Humans ; RNA
Chemical Substances	RNA (63231-63-0)
Language	English
Publishing date	2020-10-09
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMc2027492
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Article ; Online: Geriatric Frailty Is Associated With Oxidative Stress, Accumulation, and Defective Repair of DNA Double-Strand Breaks Independently of Age and Comorbidities.

Kravvariti, Evrydiki / Ntouros, Panagiotis A / Vlachogiannis, Nikolaos I / Pappa, Maria / Souliotis, Vassilis L / Sfikakis, Petros P

The journals of gerontology. Series A, Biological sciences and medical sciences

2022 Volume 78, Issue 4, Page(s) 603–610

Abstract: Defects in the DNA damage response and repair (DDR/R) network accumulate during the aging process. Physical frailty, a state of reduced physiological function and decreased resilience to biological stressors, is also exacerbated by aging, but its link ... ...

Abstract	Defects in the DNA damage response and repair (DDR/R) network accumulate during the aging process. Physical frailty, a state of reduced physiological function and decreased resilience to biological stressors, is also exacerbated by aging, but its link with DDR/R aberrations beyond the effect of age and comorbidities is unclear. Fifty-three community-dwelling older adults, aged 65-102 years, who underwent frailty classification according to the Rockwood Clinical Frailty Scale (CFS), and 51 healthy adults younger than 45 years were examined in parallel. The following DDR/R parameters were determined in their peripheral blood mononuclear cells (PBMCs): (a) oxidative stress and abasic (apurinic/apyrimidinic; AP) sites, (b) endogenous DNA damage (alkaline comet assay olive tail moment [OTM] indicative of DNA single-strand breaks [SSBs] and double-strand breaks [DSBs] and γH2AX levels by immunofluorescence [DSBs only]), (c) capacity of the 2 main DNA repair mechanisms (DSB repair and nucleotide excision repair). Older individual-derived PBMCs displayed reduced-to-oxidized glutathione ratios indicative of increased levels of oxidative stress and increased AP sites, as well as increased accumulation of endogenous DNA damage (OTM and γH2AX) and defective DSB-repair capacity, compared with younger controls. These DDR/R aberrations were more pronounced in frail versus nonfrail older adults. Notably, oxidative stress, AP sites, DSBs, and DSB-repair capacity were associated with individual CFS levels after adjusting for chronological age, sex, Charlson Comorbidity Index, and polypharmacy. Geriatric frailty is independently associated with increased DNA damage formation and reduced DSB-R capacity, supporting further research into these measures as potential frailty biomarkers.
MeSH term(s)	Humans ; Aged ; DNA Breaks, Double-Stranded ; Leukocytes, Mononuclear ; Frailty/genetics ; DNA Repair/genetics ; Oxidative Stress/genetics ; DNA Damage ; DNA/genetics ; Comorbidity
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2022-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1223643-3
ISSN	1758-535X ; 1079-5006
ISSN (online)	1758-535X
ISSN	1079-5006
DOI	10.1093/gerona/glac214
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Article ; Online: Diurnal production of cortisol and prediction of treatment response in rheumatoid arthritis: a 6-month, real-life prospective cohort study.

Yavropoulou, Maria P / Filippa, Maria G / Vlachogiannis, Nikolaos I / Fragoulis, George E / Laskari, Katerina / Mantzou, Aimilia / Panopoulos, Stylianos / Fanouriakis, Antonis / Bournia, Vasiliki-Kalliopi / Evangelatos, Gerasimos / Papapanagiotou, Aggeliki / Tektonidou, Maria G / Chrousos, George P / Sfikakis, Petros P

RMD open

2024 Volume 10, Issue 1

Abstract: Objectives: A reduced adrenal reserve-associated cortisol production relative to the enhanced needs of chronic inflammation (: Methods: Diurnal cortisol production (measured at: 08-12:00/18:00-22:00) was assessed by electrochemiluminescence ... ...

Abstract	Objectives: A reduced adrenal reserve-associated cortisol production relative to the enhanced needs of chronic inflammation ( Methods: Diurnal cortisol production (measured at: 08-12:00/18:00-22:00) was assessed by electrochemiluminescence immunoassay in 28 consecutive patients with moderately/highly active RA, as well as 3 and 6 months after treatment initiation or/escalation. Twenty-eight COVID-19 patients and 28 age-matched healthy individuals (HC) served as controls. Results: Saliva diurnal cortisol production in patients with RA was similar to that of HC, despite 12-fold higher serum C reactive protein (CRP) levels, and lower than COVID-19 patients (area under the curve: RA: 87.0±37.6 vs COVID-19: 146.7±14.3, p<0.001), having similarly high CRP. Moreover, a disturbed circadian cortisol rhythm at baseline was evident in 15 of 28 of patients with RA vs 4 of 28 and 20 of 28 of HC and COVID-19 patients, respectively. Treatment-induced minimal disease activity (MDA) at 6 months was achieved by 16 of 28 patients. Despite comparable demographics and clinical characteristics at baseline, non-MDA patients had lower baseline morning cortisol and higher adrenocorticotropic hormone (ACTH) levels compared with patients on MDA (cortisol: 10.9±4.0 vs 18.4±8.2 nmol/L, respectively, p=0.005 and ACTH: 4.8±3.3 vs 2.4±0.4 pmol/L, respectively, p=0.047). Baseline morning cortisol <13.9 nmol/L predicted non-MDA at 6 months (75% sensitivity, 92% specificity, p=0.006). Prospective measurements revealed that individualised diurnal cortisol production remained largely unchanged from baseline to 3 and 6 months. Conclusions: An impaired adrenal reserve is present in patients with RA. Further studies to confirm that assessment of diurnal cortisol production may be useful in guiding treatment decisions and/or predicting treatment response in RA are warranted. Trial registration number: NCT05671627.
MeSH term(s)	Humans ; Hydrocortisone/metabolism ; Prospective Studies ; Arthritis, Rheumatoid/drug therapy ; Adrenocorticotropic Hormone/metabolism ; Adrenocorticotropic Hormone/pharmacology ; COVID-19
Chemical Substances	Hydrocortisone (WI4X0X7BPJ) ; Adrenocorticotropic Hormone (9002-60-2)
Language	English
Publishing date	2024-01-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2812592-7
ISSN	2056-5933 ; 2056-5933
ISSN (online)	2056-5933
ISSN	2056-5933
DOI	10.1136/rmdopen-2023-003575
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Article ; Online: The role of A-to-I RNA editing in infections by RNA viruses: Possible implications for SARS-CoV-2 infection.

Vlachogiannis, Nikolaos I / Verrou, Kleio-Maria / Stellos, Konstantinos / Sfikakis, Petros P / Paraskevis, Dimitrios

Clinical immunology (Orlando, Fla.)

2021 Volume 226, Page(s) 108699

Abstract: RNA editing is a fundamental biological process with 2 major forms, namely adenosine-to-inosine (A-to-I, recognized as A-to-G) and cytosine-to-uracil (C-to-U) deamination, mediated by ADAR and APOBEC enzyme families, respectively. A-to-I RNA editing has ... ...

Abstract	RNA editing is a fundamental biological process with 2 major forms, namely adenosine-to-inosine (A-to-I, recognized as A-to-G) and cytosine-to-uracil (C-to-U) deamination, mediated by ADAR and APOBEC enzyme families, respectively. A-to-I RNA editing has been shown to directly affect the genome/transcriptome of RNA viruses with significant repercussions for viral protein synthesis, proliferation and infectivity, while it also affects recognition of double-stranded RNAs by cytosolic receptors controlling the host innate immune response. Recent evidence suggests that RNA editing may be present in SARS-CoV-2 genome/transcriptome. The majority of mapped mutations in SARS-CoV-2 genome are A-to-G/U-to-C(opposite strand) and C-to-U/G-to-A(opposite strand) substitutions comprising potential ADAR-/APOBEC-mediated deamination events. A single nucleotide substitution can have dramatic effects on SARS-CoV-2 infectivity as shown by the D614G(A-to-G) substitution in the spike protein. Future studies utilizing serial sampling from patients with COVID-19 are warranted to delineate whether RNA editing affects viral replication and/or the host immune response to SARS-CoV-2.
MeSH term(s)	APOBEC Deaminases/genetics ; APOBEC Deaminases/metabolism ; Adenosine Deaminase/genetics ; Adenosine Deaminase/metabolism ; COVID-19/enzymology ; COVID-19/immunology ; COVID-19/virology ; Humans ; Immunity, Innate ; Mutation ; RNA Editing ; RNA Viruses/genetics ; RNA Viruses/pathogenicity ; RNA, Double-Stranded/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; SARS-CoV-2/genetics ; SARS-CoV-2/metabolism
Chemical Substances	RNA, Double-Stranded ; RNA-Binding Proteins ; ADAR protein, human (EC 3.5.4.37) ; Adenosine Deaminase (EC 3.5.4.4) ; APOBEC Deaminases (EC 3.5.4.5)
Language	English
Publishing date	2021-02-25
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2021.108699
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Article ; Online: Deregulated DNA damage response network in Behcet's disease.

Vlachogiannis, Nikolaos I / Ntouros, Panagiotis A / Pappa, Maria / Verrou, Kleio-Maria / Arida, Aikaterini / Souliotis, Vassilis L / Sfikakis, Petros P

Clinical immunology (Orlando, Fla.)

2022 Volume 246, Page(s) 109189

Abstract: Behcet's disease (BD) is a chronic, relapsing systemic vasculitis of unknown etiology. Since the DNA repair enzyme NEIL1 has been identified as one of the two genetic risk factors for BD by whole exome study, we examined the potential involvement of the ... ...

Abstract	Behcet's disease (BD) is a chronic, relapsing systemic vasculitis of unknown etiology. Since the DNA repair enzyme NEIL1 has been identified as one of the two genetic risk factors for BD by whole exome study, we examined the potential involvement of the DNA damage response (DDR) network in BD. Peripheral blood mononuclear cells from 26 patients and 26 age-/sex-matched healthy controls were studied. Endogenous DNA damage levels were increased in active BD patients compared to controls or patients in remission. In parallel, BD patients had defective nucleotide excision repair capacity. RNA-sequencing revealed reduced expression of NEIL1 that negatively correlated with DNA damage accumulation. On the other hand, expression of genes involved in senescence and senescence-associated secretory phenotype positively correlated with individual endogenous DNA damage levels. We conclude that deregulated DDR contributes to the proinflammatory environment in BD.
MeSH term(s)	Humans ; Behcet Syndrome/complications ; Leukocytes, Mononuclear ; Case-Control Studies ; DNA Glycosylases
Chemical Substances	NEIL1 protein, human (EC 3.2.2.-) ; DNA Glycosylases (EC 3.2.2.-)
Language	English
Publishing date	2022-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2022.109189
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Article: Microvasculopathy-Related Hemorrhagic Tissue Deposition of Iron May Contribute to Fibrosis in Systemic Sclerosis: Hypothesis-Generating Insights from the Literature and Preliminary Findings.

Sfikakis, Petros P / Vlachogiannis, Nikolaos I / Ntouros, Panagiotis A / Mavrogeni, Sophie / Maris, Thomas G / Karantanas, Apostolos H / Souliotis, Vassilis L

Life (Basel, Switzerland)

2022 Volume 12, Issue 3

Abstract: Microvascular wall abnormalities demonstrated by nailfold capillaroscopy in systemic sclerosis (SSc) may result in microhemorrhagic deposition of erythrocyte-derived iron. Such abnormalities precede fibrosis, which is orchestrated by myofibroblasts. Iron ...

Abstract	Microvascular wall abnormalities demonstrated by nailfold capillaroscopy in systemic sclerosis (SSc) may result in microhemorrhagic deposition of erythrocyte-derived iron. Such abnormalities precede fibrosis, which is orchestrated by myofibroblasts. Iron induces endothelial-to-mesenchymal transition in vitro, which is reversed by reactive oxygen species (ROS) scavengers. The conversion of quiescent fibroblasts into profibrotic myofibroblasts has also been associated with ROS-mediated activation of TGF-β1. Given that iron overload predisposes to ROS formation, we hypothesized that the uptake of erythrocyte-derived iron by resident cells promotes fibrosis. Firstly, we show that iron induces oxidative stress in skin-derived and synovial fibroblasts in vitro, as well as in blood mononuclear cells ex vivo. The biological relevance of increased oxidative stress was confirmed by showing the concomitant induction of DNA damage in these cell types. Similar results were obtained in vivo, following intravenous iron administration. Secondly, using magnetic resonance imaging we show an increased iron deposition in the fingers of a patient with early SSc and nailfold microhemorrhages. While a systematic magnetic resonance study to examine tissue iron levels in SSc, including internal organs, is underway, herein we propose that iron may be a pathogenetic link between microvasculopathy and fibrosis and an additional mechanism responsible for increased oxidative stress in SSc.
Language	English
Publishing date	2022-03-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662250-6
ISSN	2075-1729
ISSN	2075-1729
DOI	10.3390/life12030430
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Article ; Online: Targeting senescence and inflammation in chronic destructive TNF-driven joint pathology.

Vlachogiannis, Nikolaos I / Evangelou, Konstantinos / Ntari, Lydia / Nikolaou, Christoforos / Denis, Maria C / Karagianni, Niki / Veroutis, Dimitris / Gorgoulis, Vassilis / Kollias, George / Sfikakis, Petros P

Mechanisms of ageing and development

2023 Volume 214, Page(s) 111856

Abstract: We had shown that administration of the senolytic Dasatinib abolishes arthritis in the human TNF transgenic mouse model of chronic destructive arthritis when given in combination with a sub-therapeutic dose of the anti-TNF mAb Infliximab (1 mg/kg). ... ...

Abstract	We had shown that administration of the senolytic Dasatinib abolishes arthritis in the human TNF transgenic mouse model of chronic destructive arthritis when given in combination with a sub-therapeutic dose of the anti-TNF mAb Infliximab (1 mg/kg). Herein, we found that while the number of senescent chondrocytes (GL13
MeSH term(s)	Humans ; Mice ; Animals ; Cellular Senescence ; Dasatinib/pharmacology ; Infliximab/pharmacology ; Tumor Necrosis Factor Inhibitors/pharmacology ; Inflammation ; Mice, Transgenic ; Arthritis
Chemical Substances	Dasatinib (RBZ1571X5H) ; Infliximab (B72HH48FLU) ; Tumor Necrosis Factor Inhibitors
Language	English
Publishing date	2023-08-07
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	183915-9
ISSN	1872-6216 ; 0047-6374
ISSN (online)	1872-6216
ISSN	0047-6374
DOI	10.1016/j.mad.2023.111856
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