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Article ; Online: Dr Goodpasture: "I was not aware of such a connection between lung and kidney disease".

Collins, Robert D

2010 Volume 14, Issue 3, Page(s) 194–198

Abstract: This article describes how Dr Ernest Goodpasture's 1919 study of influenza became the basis for his name being attached to pulmonary-renal syndromes by Stanton and Tange in 1958. Dr Goodpasture was an unwilling participant in this naming, and in ... ...

Abstract	This article describes how Dr Ernest Goodpasture's 1919 study of influenza became the basis for his name being attached to pulmonary-renal syndromes by Stanton and Tange in 1958. Dr Goodpasture was an unwilling participant in this naming, and in retrospect, the patient he described who served as the prototypic case probably had a vasculitic syndrome. Finally, Dr Goodpasture's major contributions to virology are summarized.
MeSH term(s)	Anti-Glomerular Basement Membrane Disease/history ; History, 20th Century ; Humans ; Influenza, Human/history ; Pathology/history ; Terminology as Topic ; Virology/history
Language	English
Publishing date	2010-06
Publishing country	United States
Document type	Biography ; Historical Article ; Journal Article ; Portraits
ZDB-ID	1440011-x
ISSN	1532-8198 ; 1092-9134
ISSN (online)	1532-8198
ISSN	1092-9134
DOI	10.1016/j.anndiagpath.2010.02.003
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Article: On being a pathologist.

Collins, Robert D

Human pathology

2006 Volume 37, Issue 12, Page(s) 1514–1518

MeSH term(s)	Education, Medical/history ; History, 20th Century ; History, 21st Century ; Pathology, Clinical/history ; Tennessee ; United States
Language	English
Publishing date	2006-12
Publishing country	United States
Document type	Autobiography ; Biography ; Historical Article ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207657-3
ISSN	1532-8392 ; 0046-8177
ISSN (online)	1532-8392
ISSN	0046-8177
DOI	10.1016/j.humpath.2006.08.021
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Article: Dr William DeMonbreun: description of his contributions to our understanding of histoplasmosis and analysis of the significance of his work.

Collins, Robert D

Human pathology

2005 Volume 36, Issue 5, Page(s) 453–464

Abstract: Histoplasmosis was proven to be a fungal infection 70 years ago by Dr William DeMonbreun, at the time an assistant professor in the Department of Pathology at Vanderbilt Medical School. The significance of his work is analyzed in relationship to the ... ...

Abstract	Histoplasmosis was proven to be a fungal infection 70 years ago by Dr William DeMonbreun, at the time an assistant professor in the Department of Pathology at Vanderbilt Medical School. The significance of his work is analyzed in relationship to the evolution of knowledge about this important fungal infection. His discovery was also central to establishing the legitimacy of the recently reorganized medical school. Vanderbilt Medical School in 1925 was an experiment in building an educational institution essentially from scratch-the outcome of the experiment could be judged in the near term only by research productivity and Dr DeMonbreun's work was one of the 5 major discoveries made at Vanderbilt in the first decade of its existence. Further, his work is the bedrock on which Christie and Peterson later showed that histoplasmosis was endemic in the Ohio River Valley. Their studies plus a host of case reports and reviews up to recent times have contributed significantly to the academic standing of Vanderbilt. Heretofore unpublished illustrations and details about the prototypic cases are included for historical purposes. New light is also shed on the chain of circumstances that led to Vanderbilt's role in the evolution of knowledge about histoplasmosis. Finally, information is provided about Dr DeMonbreun's career after his discovery.
MeSH term(s)	Animals ; Histoplasmosis/history ; Histoplasmosis/pathology ; Histoplasmosis/veterinary ; History, 20th Century ; Humans ; Pathology/history ; United States
Language	English
Publishing date	2005-05
Publishing country	United States
Document type	Biography ; Historical Article ; Journal Article ; Portraits ; Research Support, Non-U.S. Gov't
ZDB-ID	207657-3
ISSN	1532-8392 ; 0046-8177
ISSN (online)	1532-8392
ISSN	0046-8177
DOI	10.1016/j.humpath.2005.01.025
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Article: Theodore E. Woodward Award: The devastating backlash of a dread disease: poliomyelitis.

Billings, F Tremaine / Collins, Robert D

Transactions of the American Clinical and Climatological Association

2005 Volume 116, Page(s) 57–62; discussion 63

Abstract: The paper is in three parts. 1) A description of acute anterior poliomyelitis; 2) A summary of the condition of post-polio syndrome; 3) A description of two small epidemics of poliomyelitis juxtaposed and related to one another. ...

Abstract	The paper is in three parts. 1) A description of acute anterior poliomyelitis; 2) A summary of the condition of post-polio syndrome; 3) A description of two small epidemics of poliomyelitis juxtaposed and related to one another.
MeSH term(s)	Awards and Prizes ; Disease Outbreaks/history ; History, 20th Century ; Humans ; Poliomyelitis/epidemiology ; Poliomyelitis/history ; Poliomyelitis/pathology ; Postpoliomyelitis Syndrome/epidemiology ; Postpoliomyelitis Syndrome/history ; Postpoliomyelitis Syndrome/pathology ; Societies, Medical ; United States/epidemiology
Language	English
Publishing date	2005
Publishing country	United States
Document type	Historical Article ; Journal Article
ZDB-ID	603823-2
ISSN	0065-7778
ISSN	0065-7778
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Article ; Online: Lethality in a murine model of pulmonary anthrax is reduced by combining nuclear transport modifier with antimicrobial therapy.

Veach, Ruth Ann / Zienkiewicz, Jozef / Collins, Robert D / Hawiger, Jacek

PloS one

2012 Volume 7, Issue 1, Page(s) e30527

Abstract: Background: In the last ten years, bioterrorism has become a serious threat and challenge to public health worldwide. Pulmonary anthrax caused by airborne Bacillus anthracis spores is a life-threatening disease often refractory to antimicrobial therapy. ...

Abstract	Background: In the last ten years, bioterrorism has become a serious threat and challenge to public health worldwide. Pulmonary anthrax caused by airborne Bacillus anthracis spores is a life-threatening disease often refractory to antimicrobial therapy. Inhaled spores germinate into vegetative forms that elaborate an anti-phagocytic capsule along with potent exotoxins which disrupt the signaling pathways governing the innate and adaptive immune responses and cause endothelial cell dysfunction leading to vascular injury in the lung, hypoxia, hemorrhage, and death. Methods/principal findings: Using a murine model of pulmonary anthrax disease, we showed that a nuclear transport modifier restored markers of the innate immune response in spore-infected animals. An 8-day protocol of single-dose ciprofloxacin had no significant effect on mortality (4% survival) of A/J mice lethally infected with B. anthracis Sterne. Strikingly, mice were much more likely to survive infection (52% survival) when treated with ciprofloxacin and a cell-penetrating peptide modifier of host nuclear transport, termed cSN50. In B. anthracis-infected animals treated with antibiotic alone, we detected a muted innate immune response manifested by cytokines, tumor necrosis factor alpha (TNFα), interleukin (IL)-6, and chemokine monocyte chemoattractant protein-1 (MCP-1), while the hypoxia biomarker, erythropoietin (EPO), was greatly elevated. In contrast, cSN50-treated mice receiving ciprofloxacin demonstrated a restored innate immune responsiveness and reduced EPO level. Consistent with this improvement of innate immunity response and suppression of hypoxia biomarker, surviving mice in the combination treatment group displayed minimal histopathologic signs of vascular injury and a marked reduction of anthrax bacilli in the lungs. Conclusions: We demonstrate, for the first time, that regulating nuclear transport with a cell-penetrating modifier provides a cytoprotective effect, which enables the host's immune system to reduce its susceptibility to lethal B. anthracis infection. Thus, by combining a nuclear transport modifier with antimicrobial therapy we offer a novel adjunctive measure to control florid pulmonary anthrax disease.
MeSH term(s)	Active Transport, Cell Nucleus/drug effects ; Animals ; Anthrax/complications ; Anthrax/drug therapy ; Anthrax/mortality ; Anthrax/pathology ; Anti-Infective Agents/administration & dosage ; Anti-Infective Agents/pharmacology ; Cell-Penetrating Peptides/administration & dosage ; Cell-Penetrating Peptides/pharmacology ; Ciprofloxacin/administration & dosage ; Ciprofloxacin/pharmacology ; Cytokines/blood ; Cytokines/metabolism ; Disease Models, Animal ; Drug Combinations ; Female ; Lung Diseases/drug therapy ; Lung Diseases/etiology ; Lung Diseases/mortality ; Lung Diseases/pathology ; Membrane Proteins/administration & dosage ; Membrane Proteins/pharmacology ; Mice ; Peptides, Cyclic/administration & dosage ; Peptides, Cyclic/pharmacology ; Survival Analysis ; Treatment Outcome
Chemical Substances	Anti-Infective Agents ; Cell-Penetrating Peptides ; Cytokines ; Drug Combinations ; Membrane Proteins ; Peptides, Cyclic ; cSN50 peptide ; Ciprofloxacin (5E8K9I0O4U)
Language	English
Publishing date	2012-01-26
Publishing country	United States
Document type	Evaluation Study ; Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0030527
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Book: Pediatric hematopathology

Collins, Robert D / Swerdlow, Steven H

2001

Title variant	Hematopathology
Author's details	[edited by] Robert D. Collins, Steven H. Swerdlow
MeSH term(s)	Hematologic Diseases/pathology ; Child ; Hematologic Diseases/diagnosis ; Infant ; Lymphatic Diseases/diagnosis ; Lymphatic Diseases/pathology
Language	English
Size	xiv, 422 p. :, ill. (some col.) ;, 29 cm.
Publisher	Churchill Livingstone
Publishing place	New York
Document type	Book
ISBN	9780443075667 ; 0443075662
Database	Catalogue of the US National Library of Medicine (NLM)

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Book: Pediatric hematopathology

Collins, Robert D / Swerdlow, Steven H

2001

Author's details	[ed. by] Robert D. Collins; Steven H. Swerdlow
Language	English
Size	XIV, 422 S., Ill., 29 cm
Publisher	Churchill Livingstone
Publishing place	New York, NY u.a.
Document type	Book
Note	Literaturangaben
ISBN	0443075662 ; 9780443075667
Database	Former special subject collection: coastal and deep sea fishing

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Article ; Online: Nuclear transport modulation reduces hypercholesterolemia, atherosclerosis, and fatty liver.

Liu, Yan / Major, Amy S / Zienkiewicz, Jozef / Gabriel, Curtis L / Veach, Ruth Ann / Moore, Daniel J / Collins, Robert D / Hawiger, Jacek

Journal of the American Heart Association

2013 Volume 2, Issue 2, Page(s) e000093

Abstract: Background: Elevated cholesterol and triglycerides in blood lead to atherosclerosis and fatty liver, contributing to rising cardiovascular and hepatobiliary morbidity and mortality worldwide.: Methods and results: A cell-penetrating nuclear transport ...

Abstract	Background: Elevated cholesterol and triglycerides in blood lead to atherosclerosis and fatty liver, contributing to rising cardiovascular and hepatobiliary morbidity and mortality worldwide. Methods and results: A cell-penetrating nuclear transport modifier (NTM) reduced hyperlipidemia, atherosclerosis, and fatty liver in low-density lipoprotein receptor-deficient mice fed a Western diet. NTM treatment led to lower cholesterol and triglyceride levels in blood compared with control animals (36% and 53%, respectively; P<0.005) and liver (41% and 34%, respectively; P<0.05) after 8 weeks. Atherosclerosis was reduced by 63% (P<0.0005), and liver function improved compared with saline-treated controls. In addition, fasting blood glucose levels were reduced from 209 to 138 mg/dL (P<0.005), and body weight gain was ameliorated (P<0.005) in NTM-treated mice, although food intake remained the same as that in control animals. The NTM used in this study, cSN50.1 peptide, is known to modulate nuclear transport of stress-responsive transcription factors such as nuclear factor kappa B, the master regulator of inflammation. This NTM has now been demonstrated to also modulate nuclear transport of sterol regulatory element-binding protein (SREBP) transcription factors, the master regulators of cholesterol, triglyceride, and fatty acid synthesis. NTM-modulated translocation of SREBPs to the nucleus was associated with attenuated transactivation of their cognate genes that contribute to hyperlipidemia. Conclusions: Two-pronged control of inflammation and dyslipidemia by modulating nuclear transport of their critical regulators offers a new approach to comprehensive amelioration of hyperlipidemia, atherosclerosis, fatty liver, and their potential complications.
MeSH term(s)	Active Transport, Cell Nucleus/drug effects ; Animals ; Atherosclerosis/drug therapy ; Atherosclerosis/metabolism ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Cell-Penetrating Peptides/pharmacology ; Cell-Penetrating Peptides/therapeutic use ; Cholesterol/metabolism ; Dietary Fats/metabolism ; Disease Models, Animal ; Fatty Liver/drug therapy ; Fatty Liver/metabolism ; Female ; Hypercholesterolemia/drug therapy ; Hypercholesterolemia/metabolism ; Liver/drug effects ; Liver/metabolism ; Mice ; Mice, Transgenic ; NF-kappa B/drug effects ; NF-kappa B/metabolism ; Peptides/pharmacology ; Peptides/therapeutic use ; Sterol Regulatory Element Binding Proteins/drug effects ; Sterol Regulatory Element Binding Proteins/metabolism ; Transcription Factors/drug effects ; Transcription Factors/metabolism ; Triglycerides/metabolism
Chemical Substances	Cell-Penetrating Peptides ; Dietary Fats ; NF-kappa B ; Peptides ; SN50 peptide ; Sterol Regulatory Element Binding Proteins ; Transcription Factors ; Triglycerides ; cSN50.1 peptide ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2013-04-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.113.000093
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Article ; Online: Prostaglandin I2 Suppresses Proinflammatory Chemokine Expression, CD4 T Cell Activation, and STAT6-Independent Allergic Lung Inflammation.

Zhou, Weisong / Zhang, Jian / Goleniewska, Kasia / Dulek, Daniel E / Toki, Shinji / Newcomb, Dawn C / Cephus, Jacqueline Y / Collins, Robert D / Wu, Pingsheng / Boothby, Mark R / Peebles, R Stokes

Journal of immunology (Baltimore, Md. : 1950)

2016 Volume 197, Issue 5, Page(s) 1577–1586

Abstract: Allergic airway diseases are immune disorders associated with heightened type 2 immune responses and IL-5 and IL-13 production at the site of inflammation. We have previously reported that cyclooxygenase (COX) inhibition by indomethacin augmented ... ...

Abstract	Allergic airway diseases are immune disorders associated with heightened type 2 immune responses and IL-5 and IL-13 production at the site of inflammation. We have previously reported that cyclooxygenase (COX) inhibition by indomethacin augmented allergic airway inflammation in a STAT6-independent manner. However, the key COX product(s) responsible for restraining indomethacin-mediated STAT6-independent allergic inflammation is unknown. In this study, using the mouse model of OVA-induced allergic airway inflammation, we identified that PGI2 receptor (IP) signaling was critical for indomethacin-induced, STAT6-independent proallergic effects. We demonstrated that IP deficiency increased inflammatory cell infiltration, eosinophilia, and IL-5 and IL-13 expression in the lung in a STAT6-independent manner. The augmented STAT6-independent allergic inflammation correlated with enhanced primary immune responses to allergic sensitization and elevated production of multiple inflammatory chemokines (CCL11, CCL17, CCL22, and CXCL12) in the lung after allergen challenge. We also showed that the PGI2 analogue cicaprost inhibited CD4 T cell proliferation and IL-5 and IL-13 expression in vitro, and IP deficiency diminished the stimulatory effect of indomethacin on STAT6-independent IL-5 and IL-13 responses in vivo. The inhibitory effects of PGI2 and the IP signaling pathway on CD4 T cell activation, inflammatory chemokine production, and allergic sensitization and airway inflammation suggest that PGI2 and its analogue iloprost, both Food and Drug Administration-approved drugs, may be useful in treating allergic diseases and asthma. In addition, inhibiting PGI2 signaling by drugs that either block PGI2 production or restrain IP signaling may augment STAT6-independent pathways of allergic inflammation.
MeSH term(s)	Allergens/administration & dosage ; Allergens/immunology ; Animals ; Antihypertensive Agents/pharmacology ; Asthma/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/physiology ; Cell Proliferation ; Chemokines/biosynthesis ; Chemokines/immunology ; Epoprostenol/administration & dosage ; Epoprostenol/analogs & derivatives ; Epoprostenol/pharmacology ; Hypersensitivity ; Indomethacin ; Inflammation ; Interleukin-13/genetics ; Interleukin-13/immunology ; Interleukin-5/genetics ; Interleukin-5/immunology ; Lung/immunology ; Lung/physiopathology ; Lymphocyte Activation/drug effects ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Ovalbumin/immunology ; Receptors, Epoprostenol/deficiency ; Receptors, Epoprostenol/genetics ; Receptors, Epoprostenol/metabolism ; STAT6 Transcription Factor/deficiency ; STAT6 Transcription Factor/genetics ; STAT6 Transcription Factor/immunology ; STAT6 Transcription Factor/metabolism ; Signal Transduction ; Th2 Cells/immunology
Chemical Substances	Allergens ; Antihypertensive Agents ; Chemokines ; Interleukin-13 ; Interleukin-5 ; Receptors, Epoprostenol ; STAT6 Transcription Factor ; Stat6 protein, mouse ; Ovalbumin (9006-59-1) ; Epoprostenol (DCR9Z582X0) ; cicaprost (NE94J8CAMD) ; Indomethacin (XXE1CET956)
Language	English
Publishing date	2016-09-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1501063
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Article ; Online: In vivo islet protection by a nuclear import inhibitor in a mouse model of type 1 diabetes.

Moore, Daniel J / Zienkiewicz, Jozef / Kendall, Peggy L / Liu, Danya / Liu, Xueyan / Veach, Ruth Ann / Collins, Robert D / Hawiger, Jacek

PloS one

2010 Volume 5, Issue 10, Page(s) e13235

Abstract: Background: Insulin-dependent Type 1 diabetes (T1D) is a devastating autoimmune disease that destroys beta cells within the pancreatic islets and afflicts over 10 million people worldwide. These patients face life-long risks for blindness, ... ...

Abstract	Background: Insulin-dependent Type 1 diabetes (T1D) is a devastating autoimmune disease that destroys beta cells within the pancreatic islets and afflicts over 10 million people worldwide. These patients face life-long risks for blindness, cardiovascular and renal diseases, and complications of insulin treatment. New therapies that protect islets from autoimmune destruction and allow continuing insulin production are needed. Increasing evidence regarding the pathomechanism of T1D indicates that islets are destroyed by the relentless attack by autoreactive immune cells evolving from an aberrant action of the innate, in addition to adaptive, immune system that produces islet-toxic cytokines, chemokines, and other effectors of islet inflammation. We tested the hypothesis that targeting nuclear import of stress-responsive transcription factors evoked by agonist-stimulated innate and adaptive immunity receptors would protect islets from autoimmune destruction. Principal findings: Here we show that a first-in-class inhibitor of nuclear import, cSN50 peptide, affords in vivo islet protection following a 2-day course of intense treatment in NOD mice, which resulted in a diabetes-free state for one year without apparent toxicity. This nuclear import inhibitor precipitously reduces the accumulation of islet-destructive autoreactive lymphocytes while enhancing activation-induced cell death of T and B lymphocytes derived from autoimmune diabetes-prone, non-obese diabetic (NOD) mice that develop T1D. Moreover, in this widely used model of human T1D we noted attenuation of pro-inflammatory cytokine and chemokine production in immune cells. Conclusions: These results indicate that a novel form of immunotherapy that targets nuclear import can arrest inflammation-driven destruction of insulin-producing beta cells at the site of autoimmune attack within pancreatic islets during the progression of T1D.
MeSH term(s)	Animals ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/metabolism ; Disease Models, Animal ; Immunity, Innate ; Interleukin-11/metabolism ; Interleukin-5/metabolism ; Islets of Langerhans/drug effects ; Islets of Langerhans/immunology ; Islets of Langerhans/metabolism ; Mice ; Mice, Inbred NOD ; Signal Transduction
Chemical Substances	Interleukin-11 ; Interleukin-5
Language	English
Publishing date	2010-10-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0013235
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