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Book: Advances in treatment of some common neurologic disorders; guest editor: William L. Griggs, III. Diagnosis, mechanisms, and treatment of hemolytic anemias; guest editors: Lawrence S. Lessin and Wendell F. Rosse

Griggs, William L / Lessin, Lawrence S / Rosse, Wendell F

(Modern treatment, ; v. 8, no. 2)

1971

Title variant	Diagnosis, mechanisms, and treatment of hemolytic anemias
Series title	Modern treatment, ; v. 8, no. 2
MeSH term(s)	Anemia, Hemolytic ; Nervous System Diseases/therapy
Language	English
Size	p. 217-458., illus.
Publisher	Medical Dept., Harper & Row
Publishing place	New York
Document type	Book
Database	Catalogue of the US National Library of Medicine (NLM)

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Article ; Online: Clinical benefit of eculizumab in patients with no transfusion history in the International Paroxysmal Nocturnal Haemoglobinuria Registry.

Almeida, Antonio M / Bedrosian, Camille / Cole, Alexander / Muus, Petra / Schrezenmeier, Hubert / Szer, Jeff / Rosse, Wendell F

Internal medicine journal

2017 Volume 47, Issue 9, Page(s) 1026–1034

Abstract: Background: Eculizumab reduces intravascular haemolysis and improves disease symptoms in patients with paroxysmal nocturnal haemoglobinuria (PNH).: Aims: To characterise, in a real-world setting, the effect of eculizumab in patients with haemolytic ... ...

Abstract	Background: Eculizumab reduces intravascular haemolysis and improves disease symptoms in patients with paroxysmal nocturnal haemoglobinuria (PNH). Aims: To characterise, in a real-world setting, the effect of eculizumab in patients with haemolytic PNH (lactase dehydrogenase (LDH) ≥ 1.5 upper limit of normal) and no history of red blood cell transfusion, including those with high disease activity (HDA). Methods: Three populations from the International PNH Registry were studied: (i) non-transfused, untreated; (ii) non-transfused, eculizumab-treated and (iii) transfused, eculizumab-treated (≥1 transfusions in 6 months prior to eculizumab initiation). Using multivariate linear regression, the primary outcome was mean absolute change from baseline to 6 months in LDH (U/L) in non-transfused patients who were treated with eculizumab versus those who remained untreated. Secondary outcomes were mean changes in functional assessment of chronic illness therapy (FACIT)-Fatigue and European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC-QLQ)-C30 Fatigue scores from baseline to last available assessment. Results: The study population included (i) 144 non-transfused, untreated patients; (ii) 45 non-transfused, eculizumab-treated patients and (iii) 105 transfused, eculizumab-treated patients. Of these, 136/144, 43/45 and 99/105 had HDA respectively. Compared with untreated patients, non-transfused, treated patients had greater absolute reduction in LDH (-1318.8 vs -39.4; P < 0.001) and greater percentage reduction in LDH (-69.9 vs -1.6%; P < 0.001). Clinically meaningful improvements in FACIT-Fatigue (73.7 vs 24.6%, respectively) and in EORTC-QLQ-C30 (84.2 vs 33.3%, respectively) were observed. Non-transfused, treated patients with HDA had significantly reduced LDH levels (P < 0.001) and clinically meaningful improvements in FACIT-Fatigue (P = 0.003) and EORTC-QLQ-C30 (P = 0.020) versus untreated patients. Conclusion: Significant LDH reduction and clinically meaningful improvement in fatigue were observed in patients with PNH and HDA treated with eculizumab versus untreated patients, irrespective of transfusion history.
Language	English
Publishing date	2017-09
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2045436-3
ISSN	1445-5994 ; 1444-0903
ISSN (online)	1445-5994
ISSN	1444-0903
DOI	10.1111/imj.13523
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Article: Clinical manifestations of paroxysmal nocturnal hemoglobinuria: present state and future problems.

Rosse, Wendell F / Nishimura, Junichi

International journal of hematology

2003 Volume 77, Issue 2, Page(s) 113–120

Abstract: The clinical pathology of paroxysmal nocturnal hemoglobinuria (PNH) involves 3 complications: hemolytic anemia, thrombosis, and hematopoietic deficiency. The first 2 are clearly the result of the cellular defect in PNH, the lack of proteins anchored to ... ...

Abstract	The clinical pathology of paroxysmal nocturnal hemoglobinuria (PNH) involves 3 complications: hemolytic anemia, thrombosis, and hematopoietic deficiency. The first 2 are clearly the result of the cellular defect in PNH, the lack of proteins anchored to the membrane by the glycosylphosphatidylinositol anchor. The hemolytic anemia results in syndromes primarily related to the fact that the hemolysis is extracellular. Thrombosis is most significant in veins within the abdomen, although a number of other thrombotic syndromes have been described. The hematopoietic deficiency may be the same as that in aplastic anemia, a closely related disorder, and may not be due to the primary biochemical defect. The relationship to aplastic anemia suggests a nomenclature that emphasizes the predominant clinical manifestations in a patient. This relationship does not explain cases that appear to be related to myelodysplastic syndromes or the transition of some cases of PNH to leukemia. Treatment, except for bone marrow transplantation, remains noncurative and in need of improvement.
MeSH term(s)	Anemia, Aplastic/etiology ; Anemia, Hemolytic/complications ; Anemia, Hemolytic/etiology ; Anemia, Hemolytic/therapy ; Bone Marrow Diseases/etiology ; Hematopoiesis/physiology ; Hemoglobinuria, Paroxysmal/classification ; Hemoglobinuria, Paroxysmal/complications ; Hemoglobinuria, Paroxysmal/therapy ; Humans ; Venous Thrombosis/drug therapy ; Venous Thrombosis/etiology ; Venous Thrombosis/pathology
Language	English
Publishing date	2003-11-03
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	1076875-0
ISSN	1865-3774 ; 0925-5710 ; 0917-1258
ISSN (online)	1865-3774
ISSN	0925-5710 ; 0917-1258
DOI	10.1007/bf02983209
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Article: Immune-mediated hemolytic anemia.

Rosse, Wendell F / Hillmen, Peter / Schreiber, Alan D

Hematology. American Society of Hematology. Education Program

2004 , Page(s) 48–62

Abstract: ... of these receptors is discussed. In Section III, Dr. Wendell Rosse discusses the forms of autoimmune hemolytic anemia ...

Abstract	Hemolytic anemia due to immune function is one of the major causes of acquired hemolytic anemia. In recent years, as more is known about the immune system, these entities have become better understood and their treatment improved. In this section, we will discuss three areas in which this progress has been apparent. In Section I, Dr. Peter Hillmen outlines the recent findings in the pathogenesis of paroxysmal nocturnal hemoglobinuria (PNH), relating the biochemical defect (the lack of glycosylphosphatidylinositol [GPI]-linked proteins on the cell surface) to the clinical manifestations, particularly hemolysis (and its effects) and thrombosis. He discusses the pathogenesis of the disorder in the face of marrow dysfunction insofar as it is known. His major emphasis is on innovative therapies that are designed to decrease the effectiveness of complement activation, since the lack of cellular modulation of this system is the primary cause of the pathology of the disease. He recounts his considerable experience with a humanized monoclonal antibody against C5, which has a remarkable effect in controlling the manifestations of the disease. Other means of controlling the action of complement include replacing the missing modulatory proteins on the cell surface; these studies are not as developed as the former agent. In Section II, Dr. Alan Schreiber describes the biochemistry, genetics, and function of the Fc gamma receptors and their role in the pathobiology of autoimmune hemolytic anemia and idiopathic thrombocytopenic purpura due to IgG antibodies. He outlines the complex varieties of these molecules, showing how they vary in genetic origin and in function. These variations can be related to three-dimensional topography, which is known in some detail. Liganding IgG results in the transduction of a signal through the tyrosine-based activation motif and Syk signaling. The role of these receptors in the pathogenesis of hematological diseases due to IgG antibodies is outlined and the potential of therapy of these diseases by regulation of these receptors is discussed. In Section III, Dr. Wendell Rosse discusses the forms of autoimmune hemolytic anemia characterized by antibodies that react preferentially in the cold-cold agglutinin disease and paroxysmal cold hemoglobinuria (PCH). The former is due to IgM antibodies with a common but particular structure that reacts primarily with carbohydrate or carbohydrate-containing antigens, an interaction that is diminished at body temperature. PCH is a less common but probably underdiagnosed illness due to an IgG antibody reacting with a carbohydrate antigen; improved techniques for the diagnosis of PCH are described. Therapy for the two disorders differs somewhat because of the differences in isotype of the antibody. Since the hemolysis in both is primarily due to complement activation, the potential role of its control, as by the monoclonal antibody described by Dr. Hillmen, is discussed.
MeSH term(s)	Anemia, Hemolytic, Autoimmune/diagnosis ; Anemia, Hemolytic, Autoimmune/immunology ; Anemia, Hemolytic, Autoimmune/therapy ; Antigen-Antibody Complex/immunology ; Autoantibodies/immunology ; Hemoglobinuria, Paroxysmal/diagnosis ; Hemoglobinuria, Paroxysmal/physiopathology ; Hemoglobinuria, Paroxysmal/therapy ; Humans ; Receptors, IgG/immunology
Chemical Substances	Antigen-Antibody Complex ; Autoantibodies ; Receptors, IgG
Language	English
Publishing date	2004
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1520-4391
ISSN	1520-4391
DOI	10.1182/asheducation-2004.1.48
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book: Clinical immunohematology

Rosse, Wendell F

basic concepts and clinical applications

1990

Author's details	Wendell F. Rosse
MeSH term(s)	Blood Cells/immunology ; Blood Group Antigens/immunology ; Blood Grouping and Crossmatching
Language	English
Size	ix, 677 p. :, ill.
Publisher	Blackwell Scientific Publications ; Chicago, Ill. : Distributors, USA and Canada, Year Book Medical Publishers
Publishing place	Boston
Document type	Book
Note	Includes index.
ISBN	9780865420380 ; 0865420386
Database	Catalogue of the US National Library of Medicine (NLM)

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Article ; Online: Pulmonary hypertension and nitric oxide depletion in sickle cell disease.

Bunn, H Franklin / Nathan, David G / Dover, George J / Hebbel, Robert P / Platt, Orah S / Rosse, Wendell F / Ware, Russell E

Blood

2010 Volume 116, Issue 5, Page(s) 687–692

Abstract: During the past decade a large body of experimental and clinical studies has focused on the hypothesis that nitric oxide (NO) depletion by plasma hemoglobin in the microcirculation plays a central role in the pathogenesis of many manifestations of sickle ...

Abstract	During the past decade a large body of experimental and clinical studies has focused on the hypothesis that nitric oxide (NO) depletion by plasma hemoglobin in the microcirculation plays a central role in the pathogenesis of many manifestations of sickle cell disease (SCD), particularly pulmonary hypertension. We have carefully examined those studies and believe that the conclusions drawn from them are not adequately supported by the data. We agree that NO depletion may well play a role in the pathophysiology of other hemolytic states such as paroxysmal nocturnal hemoglobinuria, in which plasma hemoglobin concentrations are often at least an order of magnitude greater than in SCD. Accordingly, we conclude that clinical trials in SCD designed to increase the bioavailability of NO or association studies in which SCD clinical manifestations are related to plasma hemoglobin via its surrogates should be viewed with caution.
MeSH term(s)	Adult ; Anemia, Sickle Cell/blood ; Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/drug therapy ; Anemia, Sickle Cell/physiopathology ; Animals ; Child ; Clinical Trials as Topic ; Disease Models, Animal ; Echocardiography, Doppler ; Endothelium, Vascular/physiopathology ; False Positive Reactions ; Female ; Hemoglobins/analysis ; Hemoglobins/chemistry ; Hemoglobinuria, Paroxysmal/complications ; Hemolysis ; Humans ; Hydroxyurea/pharmacology ; Hydroxyurea/therapeutic use ; Hypertension, Pulmonary/blood ; Hypertension, Pulmonary/diagnostic imaging ; Hypertension, Pulmonary/etiology ; Hypertension, Pulmonary/physiopathology ; L-Lactate Dehydrogenase/blood ; Leg Ulcer/etiology ; Leg Ulcer/physiopathology ; Male ; Microcirculation ; Models, Biological ; Multicenter Studies as Topic ; Nitric Oxide/administration & dosage ; Nitric Oxide/blood ; Nitric Oxide/deficiency ; Nitric Oxide/physiology ; Nitric Oxide/therapeutic use ; Priapism/etiology ; Priapism/physiopathology ; Thromboembolism/etiology ; Thromboembolism/physiopathology ; Tricuspid Valve Insufficiency/diagnostic imaging ; Tricuspid Valve Insufficiency/etiology ; Tricuspid Valve Insufficiency/physiopathology
Chemical Substances	Hemoglobins ; Nitric Oxide (31C4KY9ESH) ; L-Lactate Dehydrogenase (EC 1.1.1.27) ; Hydroxyurea (X6Q56QN5QC)
Language	English
Publishing date	2010-04-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2010-02-268193
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Article ; Online: New Views of Sickle Cell Disease Pathophysiology and Treatment.

Rosse, Wendell F. / Narla, Mohandas / Petz, Lawrence D. / Steinberg, Martin H.

Hematology. American Society of Hematology. Education Program

2000 , Page(s) 2–17

Abstract: ... Rosse examines the role of the increased whole blood viscosity. In Section III, Dr. Petz reviews common ...

Abstract	This review addresses several areas of concern in the care of patients with sickle cell disease. In Sections I and II, the fundamental pathogenetic mechanisms of sickle cell disease and their clinical consequences are discussed. Dr. Narla presents the evidence for abnormal cell adhesiveness by SS cells and Dr. Rosse examines the role of the increased whole blood viscosity. In Section III, Dr. Petz reviews common and uncommon alloimmune consequences of transfusion in sickle cell disease and discusses the diagnosis and management of sickle cell patients with hyperhemolysis after transfusion. In Section IV, Dr. Steinberg gives an update on the use of hydroxyurea in the treatment of sickle cell disease, including the SC and S-beta thalassemia variants.
Language	English
Publishing date	2000
Publishing country	United States
Document type	Journal Article
ZDB-ID	2084287-9
ISSN	1520-4383 ; 1520-4391
ISSN (online)	1520-4383
ISSN	1520-4391
DOI	10.1182/asheducation-2000.1.2
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Book: Transfusion support for patients with sickle cell disease

Rosse, Wendell F / Telen, Marilyn J / Ware, Russell E

1998

Author's details	Wendell F. Rosse, Marilyn J. Telen, Russell E. Ware
MeSH term(s)	Anemia, Sickle Cell/therapy ; Blood Transfusion
Language	English
Size	xii, 113 p. :, ill.
Publisher	AABB Press
Publishing place	Bethesda, Md
Document type	Book
ISBN	9781563951039 ; 1563951037
Database	Catalogue of the US National Library of Medicine (NLM)

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Article: Clinical course and flow cytometric analysis of paroxysmal nocturnal hemoglobinuria in the United States and Japan.

Nishimura, Jun-Ichi / Kanakura, Yuzuru / Ware, Russell E / Shichishima, Tsutomu / Nakakuma, Hideki / Ninomiya, Haruhiko / Decastro, Carlos M / Hall, Sharon / Kanamaru, Akihisa / Sullivan, Keith M / Mizoguchi, Hideaki / Omine, Mitsuhiro / Kinoshita, Taroh / Rosse, Wendell F

Medicine

2004 Volume 83, Issue 3, Page(s) 193–207

Abstract: To determine and directly compare the clinical course of white and Asian patients with paroxysmal nocturnal hemoglobinuria (PNH), data were collected for epidemiologic analysis on 176 patients from Duke University and 209 patients from Japan. White ... ...

Abstract	: To determine and directly compare the clinical course of white and Asian patients with paroxysmal nocturnal hemoglobinuria (PNH), data were collected for epidemiologic analysis on 176 patients from Duke University and 209 patients from Japan. White patients were younger with significantly more classical symptoms of PNH including thrombosis, hemoglobinuria, and infection, while Asian patients were older with more marrow aplasia. The mean fraction of CD59-negative polymorphonuclear cells (PMN) at initial analysis was higher among Duke patients than Japanese patients. In both cohorts, however, a larger PNH clone was associated with classical PNH symptoms, while a smaller PNH clone was associated with marrow aplasia. Thrombosis was significantly more prevalent in white patients than Asian patients, and was associated with a significantly higher proportion of CD59-negative PMN. For individual patients, CD59-negative populations varied considerably over time, but a decreasing PNH clone portended hematopoietic failure. Survival analysis revealed a similar death rate in each group, although causes of death were different and significantly more Duke patients died from thrombosis. Japanese patients had a longer mean survival time (32.1 yr vs. 19.4 yr), although Kaplan-Meier survival curves were not significantly different. Poor survival in both groups was associated with age over 50 years, severe leukopenia/neutropenia at diagnosis, and severe infection as a complication; additionally, thrombosis at diagnosis or follow-up for Duke patients and renal failure for Japanese patients were poor prognostic factors. These data identify important differences between white and Asian patients with PNH. Identification of prognostic factors will help the design of prospective clinical trials for PNH.
MeSH term(s)	Adolescent ; Adult ; Age of Onset ; Aged ; Aged, 80 and over ; CD55 Antigens/blood ; CD59 Antigens/blood ; Cause of Death ; Child ; Child, Preschool ; Female ; Flow Cytometry ; Hematologic Tests ; Hemoglobinuria, Paroxysmal/blood ; Hemoglobinuria, Paroxysmal/diagnosis ; Hemoglobinuria, Paroxysmal/mortality ; Humans ; Japan/epidemiology ; Male ; Middle Aged ; Risk Factors ; Survival Analysis ; Survival Rate ; United States/epidemiology
Chemical Substances	CD55 Antigens ; CD59 Antigens
Language	English
Publishing date	2004-04-17
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80184-7
ISSN	1536-5964 ; 0025-7974
ISSN (online)	1536-5964
ISSN	0025-7974
DOI	10.1097/01.md.0000126763.68170.46
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Article: The hematopoietic defect in PNH is not due to defective stroma, but is due to defective progenitor cells.

Nishimura, Jun-ichi / Ware, Russell E / Burnette, Angela / Pendleton, Andrew L / Kitano, Kiyoshi / Hirota, Toshiyuki / Machii, Takashi / Kitani, Teruo / Smith, Clay A / Rosse, Wendell F

Blood cells, molecules & diseases

2002 Volume 29, Issue 2, Page(s) 159–167

Abstract: Although paroxysmal nocturnal hemoglobinuria (PNH) is often associated with aplastic anemia (AA), the nature of the pathogenetic link between PNH and AA remains unclear. Moreover, the PIG-A mutation appears to be necessary but not sufficient for the ... ...

Abstract	Although paroxysmal nocturnal hemoglobinuria (PNH) is often associated with aplastic anemia (AA), the nature of the pathogenetic link between PNH and AA remains unclear. Moreover, the PIG-A mutation appears to be necessary but not sufficient for the development of PNH, suggesting other factors are involved. The ability of PNH marrow cells to form in vitro hematopoietic colonies and the ability of PNH marrow to generate stroma that could support hematopoiesis of normal or PNH marrow in cross culture were investigated. PNH marrow from both post-Ficoll and post-lineage depleted hematopoietic progenitor cells grew similarly significantly fewer colonies than normal marrow. Sorting of CD59(+) and CD59(-) CD34(+) CD38(-) cells from patients with PNH showed similarly impaired clonogenic efficiency, indicating that the hematopoietic defect in PNH does not directly relate to GPI-anchored protein expression. PNH marrow readily grew stroma similar to marrow from normal donors. Cross culture experiments revealed that PNH stroma appears to function normally in vitro; it can support growth of normal marrow cells as well as normal stroma does, but neither PNH nor normal stroma could support the growth of PNH marrow cells. The hematopoietic defect in PNH is not due to defective stroma, but is due to defective progenitor cell growth related to additional unknown factors.
MeSH term(s)	Adult ; Bone Marrow Cells/pathology ; Case-Control Studies ; Cell Division ; Coculture Techniques ; Colony-Forming Units Assay ; Dyspnea, Paroxysmal/etiology ; Dyspnea, Paroxysmal/pathology ; Female ; Glycosylphosphatidylinositols ; Hematopoiesis ; Hematopoietic Stem Cells/pathology ; Humans ; Male ; Stromal Cells/cytology
Chemical Substances	Glycosylphosphatidylinositols
Language	English
Publishing date	2002-12-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1237083-6
ISSN	1096-0961 ; 1079-9796
ISSN (online)	1096-0961
ISSN	1079-9796
DOI	10.1006/bcmd.2002.0552
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