Kooperativer Bibliotheksverbund

In: Diabetologia, Springer Science and Business Media LLC, Vol. 42, No. S1 ( 1999-8), p. A1-A330

Type of Medium: Online Resource

ISSN: 0012-186X , 1432-0428

URL: Article

DOI: 10.1007/BF03375458

Language: English

Publisher: Springer Science and Business Media LLC

Publication Date: 1999

detail.hit.zdb_id: 1458993-X

In: Annals of the Rheumatic Diseases, BMJ, Vol. 81, No. Suppl 1 ( 2022-06), p. 256-257

Abstract: Drug survival is an important proxy measure for effectiveness of treatments for inflammatory diseases such as rheumatoid arthritis (RA), axial spondyloarthritis (AxSpA), psoriatic arthritis (PsA), and psoriasis [1-4]. Objectives The objective of this study was to examine the real-life drug survival of biologics and novel small-molecule therapies across various disease entities such as RA, AxSpA, PsA, and psoriasis. Methods We performed a nationwide cohort study using the prospective nationwide registries DANBIO and DERMBIO, comprising all patients treated with biologics or novel small-molecule therapies for RA, AxSpA, PsA, and psoriasis between January 2015 through May 2021 (DANBIO) and November 2009 to November 2019 (DERMBIO). Drug survival was visualized using Kaplan-Meier curves, and Cox proportional hazards models were used to calculate adjusted Hazard Ratios (HRs) with 95% confidence intervals (CIs) for risk of discontinuing therapy. Results The study comprised a total of 12,089 patients (17,903 treatment series), including 5,104 RA patients (7,867 series), 2,157 AxSpA patients (3,016 series3), 2,551 PsA patients (3,313 series), and 2,577 psoriasis patients (3,707 series). In confounder-adjusted models drug survival in RA was highest for rituximab followed by baricitinib, etanercept and tocilizumab respectively. For AxSpA drug survival was high for golimumab compared to all other drugs, followed by secukinumab and etanercept and lowest for infliximab. For PsA tofacitinib and infliximab had the lowest drug survival compared to all other drugs. All other drugs performed almost equally well with a tendency of a generally higher drug survival for golimumab, followed by secukinumab and ixekizumab. For psoriasis drug survival was generally highest for guselkumab. Figure 1. Conclusion Differing treatment responses to drugs with various types of action across RA, AxSpA, PsA and psoriasis emphasize that although these diseases have many overlaps in their pathogenesis, there is a need for an individualized treatment approach that considers the underlying disease, patient profile, and treatment history. References [1]Egeberg A, Ottosen MB, Gniadecki R, et al. Safety, efficacy and drug survival of biologics and biosimilars for moderate-to-severe plaque psoriasis. Br J Dermatol 2018; 178(2): 509-19. [2]Gron KL, Glintborg B, Norgaard M, et al. Comparative Effectiveness of Certolizumab Pegol, Abatacept, and Biosimilar Infliximab in Patients With Rheumatoid Arthritis Treated in Routine Care: Observational Data From the Danish DANBIO Registry Emulating a Randomized Trial. Arthritis Rheumatol 2019; 71(12): 1997-2004. [3]Lindstrom U, Glintborg B, Di Giuseppe D, et al. Comparison of treatment retention and response to secukinumab versus tumour necrosis factor inhibitors in psoriatic arthritis. Rheumatology 2020. [4]Glintborg B, Lindstrom U, Di Giuseppe D, et al. One-year treatment outcomes of secukinumab versus tumor necrosis factor inhibitors in Spondyloarthritis. Arthritis Care Res (Hoboken) 2020. Acknowledgements We acknowledge the substantial contribution of the academic hospitals and private clinics and their physicians that report data to DANBIO and DERMBIO. Disclosure of Interests Alexander Egeberg Speakers bureau: AbbVie, Almirall, Leo Pharma, Zuellig Pharma Ltd., Galápagos NV, Sun Pharmaceuticals, Samsung Bioepis Co., Ltd., Pfizer, Eli Lilly and Company, Novartis, Galderma, Dermavant, UCB, Mylan, Bristol-Myers Squibb, and Janssen Pharmaceuticals, Paid instructor for: AbbVie, Almirall, Leo Pharma, Zuellig Pharma Ltd., Galápagos NV, Sun Pharmaceuticals, Samsung Bioepis Co., Ltd., Pfizer, Eli Lilly and Company, Novartis, Galderma, Dermavant, UCB, Mylan, Bristol-Myers Squibb, and Janssen Pharmaceuticals, Consultant of: AbbVie, Almirall, Leo Pharma, Zuellig Pharma Ltd., Galápagos NV, Sun Pharmaceuticals, Samsung Bioepis Co., Ltd., Pfizer, Eli Lilly and Company, Novartis, Galderma, Dermavant, UCB, Mylan, Bristol-Myers Squibb, and Janssen Pharmaceuticals, Grant/research support from: Pfizer, Eli Lilly, Novartis, Bristol-Myers Squibb, AbbVie, Janssen Pharmaceuticals, Nana Lippert Rosenoe: None declared, David Aagaard: None declared, Erik Lørup: None declared, Lea Nymand: None declared, Lars Erik Kristensen Speakers bureau: Dr. LE Kristensen has received fees for speaking and consultancy from Pfizer, AbbVie, Amgen, Forward pharma, UCB, Gilead, Biogen, BMS, MSD, Novartis, Eli Lilly, and Janssen pharmaceuticals, Paid instructor for: Dr. LE Kristensen has received fees for speaking and consultancy from Pfizer, AbbVie, Amgen, Forward pharma, UCB, Gilead, Biogen, BMS, MSD, Novartis, Eli Lilly, and Janssen pharmaceuticals, Consultant of: Dr. LE Kristensen has received fees for speaking and consultancy from Pfizer, AbbVie, Amgen, Forward pharma, UCB, Gilead, Biogen, BMS, MSD, Novartis, Eli Lilly, and Janssen pharmaceuticals, Grant/research support from: Dr. LE Kristensen has received fees for speaking and consultancy from Pfizer, AbbVie, Amgen, Forward pharma, UCB, Gilead, Biogen, BMS, MSD, Novartis, Eli Lilly, and Janssen pharmaceuticals, Jacob Thyssen Speakers bureau: Dr. Thyssen has attended advisory boards for Almirall, Eli Lilly & Co, Pfizer, LEO Pharma, Asana, Regeneron, AbbVie, Union Therapeutics, and Sanofi-Genzyme and received speaker honorarium from LEO Pharma, Regeneron, Almirall, Abbvie, Eli Lilly & Co, and Sanofi-Genzyme, and been an investigator for AbbVie, Pfizer, Eli Lilly & Co, LEO Pharma and Sanofi-Genzyme., Paid instructor for: Dr. Thyssen has attended advisory boards for Almirall, Eli Lilly & Co, Pfizer, LEO Pharma, Asana, Regeneron, AbbVie, Union Therapeutics, and Sanofi-Genzyme and received speaker honorarium from LEO Pharma, Regeneron, Almirall, Abbvie, Eli Lilly & Co, and Sanofi-Genzyme, and been an investigator for AbbVie, Pfizer, Eli Lilly & Co, LEO Pharma and Sanofi-Genzyme., Consultant of: Dr. Thyssen has attended advisory boards for Almirall, Eli Lilly & Co, Pfizer, LEO Pharma, Asana, Regeneron, AbbVie, Union Therapeutics, and Sanofi-Genzyme and received speaker honorarium from LEO Pharma, Regeneron, Almirall, Abbvie, Eli Lilly & Co, and Sanofi-Genzyme, and been an investigator for AbbVie, Pfizer, Eli Lilly & Co, LEO Pharma and Sanofi-Genzyme., Grant/research support from: Dr. Thyssen has attended advisory boards for Almirall, Eli Lilly & Co, Pfizer, LEO Pharma, Asana, Regeneron, AbbVie, Union Therapeutics, and Sanofi-Genzyme and received speaker honorarium from LEO Pharma, Regeneron, Almirall, Abbvie, Eli Lilly & Co, and Sanofi-Genzyme, and been an investigator for AbbVie, Pfizer, Eli Lilly & Co, LEO Pharma and Sanofi-Genzyme., Simon F. Thomsen Speakers bureau: Dr. Thomsen has been a speaker or has served on advisory boards for Sanofi-Genzyme, AbbVie, LEO Pharma, Pfizer, Eli Lilly and Company, Novartis, UCB Pharma, Almirall, and Janssen Pharmaceuticals; has received research support from Sanofi-Genzyme, AbbVie, LEO Pharma, Novartis, UCB Pharma, and Janssen Pharmaceuticals; and has been an investigator for Sanofi-Genzyme, Regeneron, AbbVie, LEO Pharma, Novartis and Pfizer., Paid instructor for: Dr. Thomsen has been a speaker or has served on advisory boards for Sanofi-Genzyme, AbbVie, LEO Pharma, Pfizer, Eli Lilly and Company, Novartis, UCB Pharma, Almirall, and Janssen Pharmaceuticals; has received research support from Sanofi-Genzyme, AbbVie, LEO Pharma, Novartis, UCB Pharma, and Janssen Pharmaceuticals; and has been an investigator for Sanofi-Genzyme, Regeneron, AbbVie, LEO Pharma, Novartis and Pfizer., Consultant of: Dr. Thomsen has been a speaker or has served on advisory boards for Sanofi-Genzyme, AbbVie, LEO Pharma, Pfizer, Eli Lilly and Company, Novartis, UCB Pharma, Almirall, and Janssen Pharmaceuticals; has received research support from Sanofi-Genzyme, AbbVie, LEO Pharma, Novartis, UCB Pharma, and Janssen Pharmaceuticals; and has been an investigator for Sanofi-Genzyme, Regeneron, AbbVie, LEO Pharma, Novartis and Pfizer., Grant/research support from: Dr. Thomsen has been a speaker or has served on advisory boards for Sanofi-Genzyme, AbbVie, LEO Pharma, Pfizer, Eli Lilly and Company, Novartis, UCB Pharma, Almirall, and Janssen Pharmaceuticals; has received research support from Sanofi-Genzyme, AbbVie, LEO Pharma, Novartis, UCB Pharma, and Janssen Pharmaceuticals; and has been an investigator for Sanofi-Genzyme, Regeneron, AbbVie, LEO Pharma, Novartis and Pfizer., René Lindholm Cordtz: None declared, Nikolai Loft Speakers bureau: speaker for Eli Lilly and Janssen Cilag., Lone Skov Speakers bureau: Dr. Skov has been a paid speaker for AbbVie, Eli Lilly, Novartis, and LEO Pharma, and has been a consultant or has served on Advisory Boards with AbbVie, Janssen Cilag, Novartis, Eli Lilly, LEO Pharma, UCB, Almirall, and Sanofi. She has served as an investigator for AbbVie, Sanofi, Janssen Cilag, Boehringer Ingelheim, AstraZenica, Eli Lilly, Novartis, Regeneron, and LEO Pharma, and has received research and educational grants from Novartis, Sanofi, Janssen Cilag, and LEO Pharma., Paid instructor for: Dr. Skov has been a paid speaker for AbbVie, Eli Lilly, Novartis, and LEO Pharma, and has been a consultant or has served on Advisory Boards with AbbVie, Janssen Cilag, Novartis, Eli Lilly, LEO Pharma, UCB, Almirall, and Sanofi. She has served as an investigator for AbbVie, Sanofi, Janssen Cilag, Boehringer Ingelheim, AstraZenica, Eli Lilly, Novartis, Regeneron, and LEO Pharma, and has received research and educational grants from Novartis, Sanofi, Janssen Cilag, and LEO Pharma., Consultant of: Dr. Skov has been a paid speaker for AbbVie, Eli Lilly, Novartis, and LEO Pharma, and has been a consultant or has served on Advisory Boards with AbbVie, Janssen Cilag, Novartis, Eli Lilly, LEO Pharma, UCB, Almirall, and Sanofi. She has served as an investigator for AbbVie, Sanofi, Janssen Cilag, Boehringer Ingelheim, AstraZenica, Eli Lilly, Novartis, Regeneron, and LEO Pharma, and has received research and educational grants from Novartis, Sanofi, Janssen Cilag, and LEO Pharma., Grant/research support from: Dr. Skov has been a paid speaker for AbbVie, Eli Lilly, Novartis, and LEO Pharma, and has been a consultant or has served on Advisory Boards with AbbVie, Janssen Cilag, Novartis, Eli Lilly, LEO Pharma, UCB, Almirall, and Sanofi. She has served as an investigator for AbbVie, Sanofi, Janssen Cilag, Boehringer Ingelheim, AstraZenica, Eli Lilly, Novartis, Regeneron, and LEO Pharma, and has received research and educational grants from Novartis, Sanofi, Janssen Cilag, and LEO Pharma., Lars Erik Bryld: None declared, Mads Rasmussen Speakers bureau: Dr. Rasmussen has been a paid speaker for AbbVie, Almirall, and LEO Pharma. Consulting, or serving on expert/advisory boards with AbbVie, Almirall, Janssen Cilag, and Eli Lilly. He served as investigator for Janssen Cilag, UCB, and Novartis., Paid instructor for: Dr. Rasmussen has been a paid speaker for AbbVie, Almirall, and LEO Pharma. Consulting, or serving on expert/advisory boards with AbbVie, Almirall, Janssen Cilag, and Eli Lilly. He served as investigator for Janssen Cilag, UCB, and Novartis., Consultant of: Dr. Rasmussen has been a paid speaker for AbbVie, Almirall, and LEO Pharma. Consulting, or serving on expert/advisory boards with AbbVie, Almirall, Janssen Cilag, and Eli Lilly. He served as investigator for Janssen Cilag, UCB, and Novartis., Grant/research support from: Dr. Rasmussen has been a paid speaker for AbbVie, Almirall, and LEO Pharma. Consulting, or serving on expert/advisory boards with AbbVie, Almirall, Janssen Cilag, and Eli Lilly. He served as investigator for Janssen Cilag, UCB, and Novartis., Pil Højgaard: None declared, Salome Kristensen: None declared, Lene Dreyer Speakers bureau: Dr. Dreyer has received research grant/research support from BMS, and speakers bureau from Eli Lilly and Galderma., Paid instructor for: Dr. Dreyer has received research grant/research support from BMS, and speakers bureau from Eli Lilly and Galderma., Consultant of: Dr. Dreyer has received research grant/research support from BMS, and speakers bureau from Eli Lilly and Galderma., Grant/research support from: Dr. Dreyer has received research grant/research support from BMS, and speakers bureau from Eli Lilly and Galderma.

Type of Medium: Online Resource

ISSN: 0003-4967 , 1468-2060

URL: Article

DOI: 10.1136/annrheumdis-2022-eular.1054

Language: English

Publisher: BMJ

Publication Date: 2022

detail.hit.zdb_id: 1481557-6

In: Diabetologia, Springer Science and Business Media LLC, Vol. 47, No. S1 ( 2004-8), p. A1-A464

Type of Medium: Online Resource

ISSN: 0012-186X , 1432-0428

URL: Article

DOI: 10.1007/BF03375463

Language: English

Publisher: Springer Science and Business Media LLC

Publication Date: 2004

detail.hit.zdb_id: 1458993-X

In: Annals of the Rheumatic Diseases, BMJ, Vol. 81, No. Suppl 1 ( 2022-06), p. 392.1-392

Abstract: Immune-mediated inflammatory arthritis (IMIA) is a group of diseases characterized by chronic synovitis including rheumatoid arthritis (RA), psoriatic arthritis (PsA), and spondyloarthritis (SpA). Some disease modifying antirheumatic drugs (DMARDs) have demonstrated efficacy in several of these diseases (e.g. TNFα inhibitors) while others have not (e.g. IL-17A inhibitors in RA). Furthermore, within each disease there are patient subgroups experiencing different responses to the same drug, which underlines the need for further elucidation of pathogenic processes to guide personalized in IMIAs. Objectives Here we investigated if clinical features and synovial transcriptional signature could predict in vitro efficacy of specific DMARDs across different IMIAs. Methods Synovial fluid mononuclear cells (SFMCs) from patients with SpA (n=13), RA (n=16), PsA (n=13), juvenile idiopathic arthritis (JIA) (n=7) or undifferentiated arthritis (n=5) were included. SFMCs from each patient were cultured for 48 hours (drugs listed in Table 1). Culture medium and DMSO were used as negative controls. In vitro drug response was assessed by measuring monocyte chemoattractant protein 1 (MCP-1) by ELISA. SFMC baseline gene expression of 270 genes related to inflammation was measured using the NanoString nCounter Human Inflammation V2 Panel. Drug responses (ΔMCP-1) were compared with clinical diagnosis, serostatus in RA patients, HLA-B27 status in SpA patients, DAS28-CRP score, years since diagnosis, failed modes of action and transcriptional signatures. Table 1. Drug Target Adalimumab TNFα Etanercept TNFα Tocilizumab IL-6 Anakinra IL-1β Ustekinumab IL-12/23 Secukinumab IL-17A Tofacitinib JAK1/3 Baricitinib JAK2/3 Results DMARDs with a similar molecular target had comparable effects on ΔMCP-1. The TNFα inhibitors adalimumab and etanercept (r=0.86) had similar drug responses, and so had the JAK inhibitors tofacitinib and baricitinib (r=0,71). In contrast, drugs with different modes of action had diverse responses (Figure 1). High HLA-DRA gene expression associated with high responses to TNFα inhibitors (both p 〈 0.05). JAK inhibitors reduced MCP-1 secretion significantly more in SFMCs from seropositive than seronegative RA patients (p 〈 0.05). Drug response was greater in SFMCs from patients with low DAS28-CRP scores (DAS28-CRP 〈 2.5) compared with patients with a high DAS28-CRP score (DAS28-CRP 〉 5.2) for TNFα inhibitors, tocilizumab and JAK inhibitors (all p 〈 0.05). Patients clustered with either an overall high or an overall low response to almost all DMARDs, or with a significant response to only one or a few of the DMARDs. Transcriptional signature of patient SFMCs primarily responding to TNFα inhibitors was different compared with the signature of patient SFMCs primarily responding to JAK inhibitors. Diagnosis, HLA-B27 status, failed modes of action and years since diagnosis did not affect ΔMCP-1 in this in vitro setup. Figure 1. Association between DMARD molecular target and in vitro response as measured by change in MCP-1 secretion . Conclusion Similarities and differences in mode of action for 8 different DMARDs were captured in drug response as measured by MCP-1 change in SFMC cultures from 54 patients with inflammatory arthritis. We were able to identify interesting differences in gene expression when comparing cells responding to TNF inhibitors to cells responding to JAK inhibitors. Drug responses were only to a minor extent associated with clinical features. Acknowledgements Sincere thanks to Stinne Greisen, Malene Hvid, Maithri Aspari and Amalie Broksø for continuous guidance during the laboratory work. Disclosure of Interests Mads Brüner Kristensen: None declared, Ulvi Ahmadov: None declared, Morten Aagaard Nielsen: None declared, Lasse Sommer Kristensen: None declared, Tue Wenzel Kragstrup Shareholder of: Co-founder and clinical developer in iBio tech ApS., Speakers bureau: Speaking fees from Pfizer, Bristol-Myers Squibb, Eli Lilly, Novartis, UCB, and Abbvie., Consultant of: Consultancy fees from Bristol-Myers Squibb and Gilead., Grant/research support from:. Research grants from Gilead.

Type of Medium: Online Resource

ISSN: 0003-4967 , 1468-2060

URL: Article

DOI: 10.1136/annrheumdis-2022-eular.2512

Language: English

Publisher: BMJ

Publication Date: 2022

detail.hit.zdb_id: 1481557-6

In: Blood, American Society of Hematology, Vol. 102, No. 10 ( 2003-11-15), p. 3615-3620

Abstract: It is currently debated whether the mechanism of action of therapeutic doses of recombinant factor VIIa (rFVIIa, Novo-Seven) relies on the tissue factor (TF)-independent activity of the enzyme. The present study was conducted to investigate the in vivo hemostatic effects of rFVIIa and 3 analogs thereof with superior intrinsic activity (FVIIaIIa, K337A-FVIIaIia, and M298Q-FVIIa) in mice with antibody-induced hemophilia A. A highly significant dose response was observed for the bleeding time and blood loss for each of the rFVIIa variants. The bleeding time and blood loss were normalized after administration of 10 mg/kg rFVIIa, 3 mg/kg K337A-FVIIaIia, and 3 mg/kg M298Q-FVIIa, indicating a potency of these FVIIa analogs 3-4 times above that of rFVIIa in FVIII-depleted mice. The different in vivo potencies of the various forms of FVIIa could not be explained by the pharmacokinetics. Histopathological evaluation of kidneys revealed no signs of treatment-related pathological changes even after treatment with the superactive variants. The fact that FVIIa analogs with enhanced intrinsic activity are more efficacious in the murine hemophilia A model strongly suggests that the TF-independent procoagulant activity of FVIIa contributes to its clinical hemostatic effect. (Blood. 2003; 102:3615-3620)

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood-2003-05-1369

Language: English

Publisher: American Society of Hematology

Publication Date: 2003

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: British Journal of Haematology, Wiley, Vol. 199, No. 4 ( 2022-11), p. 539-548

Abstract: Overweight patients with cancer are frequently reduced in chemotherapy dose due to toxicity concerns, although previous studies have indicated that dose reduction (DR) of overweight patients results in comparable toxicity but may compromise overall survival (OS). Current evidence regarding DR in patients with acute myeloid leukaemia (AML) is limited. To investigate the association between DR and outcome among overweight patients with AML we analysed a Danish nationwide cohort of overweight adult AML patients treated with remission induction chemotherapy. Among 536 patients identified, 10.1% were categorized as DR defined as 95% or less of full body surface area (BSA)‐based dose. Risk factors for DR were high body mass index (BMI) and BSA, therapy‐related AML and favourable cytogenetics. No significant differences were observed for rates of complete remission (CR), 30‐ and 90‐day mortality between DR and non‐DR patients. Furthermore, DR did not affect median relapse‐free survival (RFS) [DR, 14.5 (95% confidence interval, 9.0–41.7) months; non‐DR, 15.0 (12.3–19.3)] with an adjusted difference in five‐year restricted mean survival time (Δ5y‐RMST) of 0.2 (−8.4 to 8.8) months nor median OS (DR, 17.0 [11.9 to 45.5] months; non‐DR, 17.5 [14.8 to 20.5] ) with an adjusted Δ5y‐RMST of 0.8 (−5.7 to 7.3) months. In conclusion, we found no statistically significant association between DR and outcomes among overweight patients with AML. However, we acknowledge the limited sample size and encourage further studies in this important subject.

Type of Medium: Online Resource

ISSN: 0007-1048 , 1365-2141

URL: Issue

URL: Article

DOI: 10.1111/bjh.v199.4

DOI: 10.1111/bjh.18448

Language: English

Publisher: Wiley

Publication Date: 2022

detail.hit.zdb_id: 1475751-5

In: Acta Anaesthesiologica Scandinavica, Wiley, Vol. 67, No. 5 ( 2023-05), p. 649-654

Abstract: The duration of apnoeic oxygenation with high‐flow nasal oxygen is limited by hypercapnia and acidosis and monitoring of arterial carbon dioxide level is therefore essential. We have performed a study in patients undergoing prolonged apnoeic oxygenation where we monitored the progressive hypercapnia with transcutaneous carbon dioxide. In this paper, we compared the transcutaneous carbon dioxide level with arterial carbon dioxide tension. Methods This is a secondary publication based on data from a study exploring the limits of apnoeic oxygenation. We compared transcutaneous carbon dioxide monitoring with arterial carbon dioxide tension using Bland–Altman analyses in anaesthetised and paralysed patients undergoing prolonged apnoeic oxygenation until a predefined limit of pH 7.15 or PCO 2 of 12 kPa was reached. Results We included 35 patients with a median apnoea duration of 25 min. Mean pH was 7.14 and mean arterial carbon dioxide tension was 11.2 kPa at the termination of apnoeic oxygenation. Transcutaneous carbon dioxide monitoring initially slightly underestimated the arterial tension but at carbon dioxide levels above 10 kPa it overestimated the value. Bias ranged from −0.55 to 0.81 kPa with limits of agreement between −1.25 and 2.11 kPa. Conclusion Transcutaneous carbon dioxide monitoring provided a clinically acceptable substitute for arterial blood gases but as hypercapnia developed to considerable levels, we observed overestimation at high carbon dioxide tensions in patients undergoing apnoeic oxygenation with high‐flow nasal oxygen.

Type of Medium: Online Resource

ISSN: 0001-5172 , 1399-6576

URL: Issue

URL: Article

DOI: 10.1111/aas.v67.5

DOI: 10.1111/aas.14216

Language: English

Publisher: Wiley

Publication Date: 2023

detail.hit.zdb_id: 2004319-3

In: European Journal of Vascular and Endovascular Surgery, Elsevier BV, Vol. 15, No. 6 ( 1998-06), p. 515-520

Type of Medium: Online Resource

ISSN: 1078-5884

URL: Article

DOI: 10.1016/S1078-5884(98)80112-3

Language: English

Publisher: Elsevier BV

Publication Date: 1998

detail.hit.zdb_id: 2005354-X

In: The Lancet, Elsevier BV, Vol. 394, No. 10204 ( 2019-09), p. 1169-1180

Type of Medium: Online Resource

ISSN: 0140-6736

URL: Article

DOI: 10.1016/S0140-6736(19)31887-2

Language: English

Publisher: Elsevier BV

Publication Date: 2019

detail.hit.zdb_id: 2067452-1

detail.hit.zdb_id: 3306-6

detail.hit.zdb_id: 1476593-7

SSG: 5,21

In: Acta Neuropathologica, Springer Science and Business Media LLC, Vol. 54, No. 1 ( 1981-3), p. 31-41

Type of Medium: Online Resource

ISSN: 0001-6322 , 1432-0533

URL: Article

DOI: 10.1007/BF00691330

Language: English

Publisher: Springer Science and Business Media LLC

Publication Date: 1981

detail.hit.zdb_id: 1458410-4