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Article ; Online: Melanocortin therapies to resolve fibroblast-mediated diseases.

Khodeneva, Natalya / Sugimoto, Michelle A / Davan-Wetton, Camilla S A / Montero-Melendez, Trinidad

2023 Volume 13, Page(s) 1084394

Abstract: Stromal cells have emerged as central drivers in multiple and diverse diseases, and consequently, as potential new cellular targets for the development of novel therapeutic strategies. In this review we revise the main roles of fibroblasts, not only as ... ...

Abstract	Stromal cells have emerged as central drivers in multiple and diverse diseases, and consequently, as potential new cellular targets for the development of novel therapeutic strategies. In this review we revise the main roles of fibroblasts, not only as structural cells but also as players and regulators of immune responses. Important aspects like fibroblast heterogeneity, functional specialization and cellular plasticity are also discussed as well as the implications that these aspects may have in disease and in the design of novel therapeutics. An extensive revision of the actions of fibroblasts on different conditions uncovers the existence of numerous diseases in which this cell type plays a pathogenic role, either due to an exacerbation of their 'structural' side, or a dysregulation of their 'immune side'. In both cases, opportunities for the development of innovative therapeutic approaches exist. In this regard, here we revise the existing evidence pointing at the melanocortin pathway as a potential new strategy for the treatment and management of diseases mediated by aberrantly activated fibroblasts, including scleroderma or rheumatoid arthritis. This evidence derives from studies involving models of
MeSH term(s)	Humans ; Melanocortins/metabolism ; Melanocortins/therapeutic use ; Fibroblasts/metabolism ; Myofibroblasts/metabolism ; Collagen/metabolism ; Arthritis, Rheumatoid/metabolism
Chemical Substances	Melanocortins ; Collagen (9007-34-5)
Language	English
Publishing date	2023-01-30
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.1084394
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Oncogenic Kras

bioRxiv : the preprint server for biology

2023

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is associated with mutations in Kras, a known oncogenic driver of PDAC; and ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is associated with mutations in Kras, a known oncogenic driver of PDAC; and the
Language	English
Publishing date	2023-02-18
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.02.15.528757
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Article ; Online: KRAS

Mahadevan, Krishnan K / McAndrews, Kathleen M / LeBleu, Valerie S / Yang, Sujuan / Lyu, Hengyu / Li, Bingrui / Sockwell, Amari M / Kirtley, Michelle L / Morse, Sami J / Moreno Diaz, Barbara A / Kim, Michael P / Feng, Ningping / Lopez, Anastasia M / Guerrero, Paola A / Paradiso, Francesca / Sugimoto, Hikaru / Arian, Kent A / Ying, Haoqiang / Barekatain, Yasaman /

Sthanam, Lakshmi Kavitha / Kelly, Patience J / Maitra, Anirban / Heffernan, Timothy P / Kalluri, Raghu

Cancer cell

2023 Volume 41, Issue 9, Page(s) 1606–1620.e8

Abstract: ... The ... ...

Abstract	The KRAS
MeSH term(s)	Humans ; CD8-Positive T-Lymphocytes ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Proto-Oncogene Proteins p21(ras)/antagonists & inhibitors ; Proto-Oncogene Proteins p21(ras)/genetics ; Tumor Microenvironment
Chemical Substances	KRAS protein, human ; KRASG12D inhibitor MRTX1133 ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2023-08-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2078448-X
ISSN	1878-3686 ; 1535-6108
ISSN (online)	1878-3686
ISSN	1535-6108
DOI	10.1016/j.ccell.2023.07.002
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Zs.MG 104: Show issues

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Article ; Online: Fibrinolysis in COVID-19: Impact on Clot Lysis and Modulation of Inflammation.

Sugimoto, Michelle A / Perucci, Luiza O / Tavares, Luciana P / Teixeira, Mauro M / Sousa, Lirlândia P

Current drug targets

2022 Volume 23, Issue 17, Page(s) 1578–1592

Abstract: COVID-19 is a multisystem disease caused by SARS-CoV-2 and is associated with an imbalance between the coagulation and fibrinolytic systems. Overall, hypercoagulation, hypofibrinolysis and fibrin-clot resistance to fibrinolysis predispose patients to ... ...

Abstract	COVID-19 is a multisystem disease caused by SARS-CoV-2 and is associated with an imbalance between the coagulation and fibrinolytic systems. Overall, hypercoagulation, hypofibrinolysis and fibrin-clot resistance to fibrinolysis predispose patients to thrombotic and thromboembolic events. In the lungs, the virus triggers alveolar and interstitial fibrin deposition, endothelial dysfunction, and pulmonary intravascular coagulation, all events intrinsically associated with the activation of inflammation and organ injury. Adding to the pathogenesis of COVID-19, there is a positive feedback loop by which local fibrin deposition in the lungs can fuel inflammation and consequently dysregulates coagulation, a process known as immunothrombosis. Therefore, fibrinolysis plays a central role in maintaining hemostasis and tissue homeostasis during COVID-19 by cleaning fibrin clots and controlling feed-forward products of coagulation. In addition, components of the fibrinolytic system have important immunomodulatory roles, as evidenced by studies showing the contribution of Plasminogen/Plasmin (Plg/Pla) to the resolution of inflammation. Herein, we review clinical evidence for the dysregulation of the fibrinolytic system and discuss its contribution to thrombosis risk and exacerbated inflammation in severe COVID-19. We also discuss the current concept of an interplay between fibrinolysis and inflammation resolution, mirroring the well-known crosstalk between inflammation and coagulation. Finally, we consider the central role of the Plg/Pla system in resolving thromboinflammation, drawing attention to the overlooked consequences of COVID-19-associated fibrinolytic abnormalities to local and systemic inflammation.
MeSH term(s)	Humans ; Inflammation/drug therapy ; COVID-19/complications ; SARS-CoV-2 ; Thrombosis/etiology
Language	English
Publishing date	2022-10-12
Publishing country	United Arab Emirates
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2064859-5
ISSN	1873-5592 ; 1389-4501
ISSN (online)	1873-5592
ISSN	1389-4501
DOI	10.2174/1389450123666221011102250
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Article ; Online: Engineered exosomes targeting MYC reverse the proneural-mesenchymal transition and extend survival of glioblastoma.

Haltom, Amanda R / Hassen, Wafa E / Hensel, Janine / Kim, Jiha / Sugimoto, Hikaru / Li, Bingrui / McAndrews, Kathleen M / Conner, Meagan R / Kirtley, Michelle L / Luo, Xin / Xie, Bingqing / Volpert, Olga V / Olalekan, Susan / Maltsev, Natalia / Basu, Anindita / LeBleu, Valerie S / Kalluri, Raghu

Extracellular vesicle

2022 Volume 1

Abstract: Dysregulated Myc signaling is a key oncogenic pathway in glioblastoma multiforme (GBM). Yet, effective therapeutic targeting of Myc continues to be challenging. Here, we demonstrate that exosomes generated from human bone marrow mesenchymal stem cells ( ... ...

Abstract	Dysregulated Myc signaling is a key oncogenic pathway in glioblastoma multiforme (GBM). Yet, effective therapeutic targeting of Myc continues to be challenging. Here, we demonstrate that exosomes generated from human bone marrow mesenchymal stem cells (MSCs) engineered to encapsulate siRNAs targeting Myc (iExo-Myc) localize to orthotopic GBM tumors in mice. Treatment of late stage GBM tumors with iExo-Myc inhibits proliferation and angiogenesis, suppresses tumor growth, and extends survival. Transcriptional profiling of tumors reveals that the mesenchymal transition and estrogen receptor signaling pathways are impacted by Myc inhibition. Single nuclei RNA sequencing (snRNA-seq) shows that iExo-Myc treatment induces transcriptional repression of multiple growth factor and interleukin signaling pathways, triggering a mesenchymal to proneural transition and shifting the cellular landscape of the tumor. These data confirm that Myc is an effective anti-glioma target and that iExo-Myc offers a feasible, readily translational strategy to inhibit challenging oncogene targets for the treatment of brain tumors.
Language	English
Publishing date	2022-10-27
Publishing country	United States
Document type	Journal Article
ISSN	2773-0417
ISSN (online)	2773-0417
DOI	10.1016/j.vesic.2022.100014
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Article ; Online: RvE1 Attenuates Polymicrobial Sepsis-Induced Cardiac Dysfunction and Enhances Bacterial Clearance.

Chen, Jianmin / Purvis, Gareth S D / Collotta, Debora / Al Zoubi, Sura / Sugimoto, Michelle A / Cacace, Antonino / Martin, Lukas / Colas, Roman A / Collino, Massimo / Dalli, Jesmond / Thiemermann, Christoph

Frontiers in immunology

2020 Volume 11, Page(s) 2080

Abstract: The development of cardiac dysfunction caused by microbial infection predicts high mortality in sepsis patients. Specialized pro-resolving mediators (SPMs) mediate resolution of inflammation in many inflammatory diseases, and are differentially expressed ...

Abstract	The development of cardiac dysfunction caused by microbial infection predicts high mortality in sepsis patients. Specialized pro-resolving mediators (SPMs) mediate resolution of inflammation in many inflammatory diseases, and are differentially expressed in plasma of sepsis patients. Here, we investigated whether the levels of SPMs are altered in the murine septic heart following polymicrobial sepsis-induced cardiac dysfunction. Ten weeks-old male C57BL/6 mice were subjected to polymicrobial sepsis induced by cecal ligation and puncture (CLP), which is a clinically relevant sepsis model receiving analgesics, antibiotics, and fluid resuscitation. CLP caused a significant systolic dysfunction assessed by echocardiography. The hearts were subjected to LC-MS/MS based lipid mediator profiling. Many SPMs were significantly reduced in septic hearts, among which RvE1 had a ~93-fold reduction. Treatment of CLP mice with synthetic RvE1 (1 μg/mouse
MeSH term(s)	Animals ; Bacterial Load/drug effects ; Biomarkers ; Disease Models, Animal ; Echocardiography ; Eicosapentaenoic Acid/analogs & derivatives ; Eicosapentaenoic Acid/pharmacology ; Flow Cytometry ; Gene Expression Regulation/drug effects ; Heart Diseases/diagnosis ; Heart Diseases/drug therapy ; Heart Diseases/etiology ; Heart Diseases/metabolism ; Heart Function Tests ; Immunity/drug effects ; Inflammation Mediators/metabolism ; Lipid Metabolism/drug effects ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Models, Biological ; Phagocytosis/drug effects ; Phagocytosis/immunology ; Prognosis ; Sepsis/complications ; Sepsis/immunology ; Sepsis/microbiology ; Signal Transduction/drug effects
Chemical Substances	Biomarkers ; Inflammation Mediators ; Eicosapentaenoic Acid (AAN7QOV9EA) ; 5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid (GND3JH08JA)
Language	English
Publishing date	2020-09-02
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.02080
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Article ; Online: Mediators of the Resolution of the Inflammatory Response.

Sugimoto, Michelle A / Vago, Juliana P / Perretti, Mauro / Teixeira, Mauro M

Trends in immunology

2019 Volume 40, Issue 3, Page(s) 212–227

Abstract: The termination of inflammation is governed by endogenous molecules collectively referred to as 'mediators of resolution' of inflammation. There is now strong evidence to suggest that failed resolution may underpin autoimmune and inflammatory diseases ... ...

Abstract	The termination of inflammation is governed by endogenous molecules collectively referred to as 'mediators of resolution' of inflammation. There is now strong evidence to suggest that failed resolution may underpin autoimmune and inflammatory diseases and could thus be targeted to decrease inflammation. There are many molecules that have been described as mediators of resolution, and new players are still being continuously discovered. To support the emerging field of 'resolution pharmacology', here we discuss the scientific strategies required to qualify a molecule as a resolution mediator. Systematic definition of the players of resolution, their receptors, and downstream mechanisms remains a necessary knowledge to move the field forward and suggest new targets for the development of novel therapies to treat inflammatory diseases.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/metabolism ; Autoimmune Diseases/immunology ; Cytokines/metabolism ; Homeostasis ; Humans ; Inflammation/immunology ; Inflammation Mediators/metabolism ; Mice ; Phagocytosis
Chemical Substances	Anti-Inflammatory Agents ; Cytokines ; Inflammation Mediators
Language	English
Publishing date	2019-02-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2019.01.007
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Article ; Online: Formyl Peptide Receptor Type 2 Deficiency in Myeloid Cells Amplifies Sepsis-Induced Cardiac Dysfunction.

Chen, Jianmin / Austin-Williams, Shani / O'Riordan, Caroline Elizabeth / Claria-Ribas, Pol / Sugimoto, Michelle A / Norling, Lucy V / Thiemermann, Christoph / Perretti, Mauro

Journal of innate immunity

2023 Volume 15, Issue 1, Page(s) 548–561

Abstract: Using a global formyl peptide receptor (Fpr) 2 knockout mouse colony, we have reported the modulatory properties of this pro-resolving receptor in polymicrobial sepsis. Herein, we have used a humanized FPR2 (hFPR2) mouse colony, bearing an intact or a ... ...

Abstract	Using a global formyl peptide receptor (Fpr) 2 knockout mouse colony, we have reported the modulatory properties of this pro-resolving receptor in polymicrobial sepsis. Herein, we have used a humanized FPR2 (hFPR2) mouse colony, bearing an intact or a selective receptor deficiency in myeloid cells to dwell on the cellular mechanisms. hFPR2 mice and myeloid cell-specific hFPR2 KO (KO) mice were subjected to cecal ligation and puncture (CLP)-induced polymicrobial sepsis. Compared with hFPR2 mice, CLP caused exacerbated cardiac dysfunction (assessed by echocardiography), worsened clinical outcome, and impaired bacterial clearance in KO mice. This pathological scenario was paralleled by increased recruitment of pro-inflammatory monocytes and reduced M2-like macrophages within the KO hearts. In peritoneal exudates of KO mice, we quantified increased neutrophil and MHC II+ macrophage numbers but decreased monocyte/macrophage and MHC II- macrophage recruitment. hFPR2 upregulation was absent in myeloid cells, and local production of lipoxin A4 was reduced in septic KO mice. Administration of the FPR2 agonist annexin A1 (AnxA1) improved cardiac function in hFPR2 septic mice but had limited beneficial effects in KO mice, in which the FPR2 ligand failed to polarize macrophages toward an MHC II- phenotype. In conclusion, FPR2 deficiency in myeloid cells exacerbates cardiac dysfunction and worsens clinical outcome in polymicrobial sepsis. The improvement of cardiac function and the host immune response by AnxA1 is more effective in hFPR2-competent septic mice.
MeSH term(s)	Animals ; Mice ; Heart Diseases/etiology ; Heart Diseases/genetics ; Heart Diseases/metabolism ; Leukocytes ; Macrophages ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, Formyl Peptide/agonists ; Receptors, Formyl Peptide/genetics ; Receptors, Formyl Peptide/metabolism ; Sepsis/complications
Chemical Substances	Receptors, Formyl Peptide ; formyl peptide receptor 2, mouse
Language	English
Publishing date	2023-04-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2454158-8
ISSN	1662-8128 ; 1662-811X
ISSN (online)	1662-8128
ISSN	1662-811X
DOI	10.1159/000530284
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Article ; Online: Targeting the Annexin A1-FPR2/ALX pathway for host-directed therapy in dengue disease.

Costa, Vivian Vasconcelos / Sugimoto, Michelle A / Hubner, Josy / Bonilha, Caio S / Queiroz-Junior, Celso Martins / Gonçalves-Pereira, Marcela Helena / Chen, Jianmin / Gobbetti, Thomas / Libanio Rodrigues, Gisele Olinto / Bambirra, Jordana L / Passos, Ingredy B / Machado Lopes, Carla Elizabeth / Moreira, Thaiane P / Bonjour, Kennedy / Melo, Rossana C N / Oliveira, Milton A P / Andrade, Marcus Vinicius M / Sousa, Lirlândia Pires / Souza, Danielle Gloria /

Santiago, Helton da Costa / Perretti, Mauro / Teixeira, Mauro Martins

eLife

2022 Volume 11

Abstract: Host immune responses contribute to dengue's pathogenesis and severity, yet the possibility that failure in endogenous inflammation resolution pathways could characterise the disease has not been contemplated. The pro-resolving protein Annexin A1 (AnxA1) ...

Abstract	Host immune responses contribute to dengue's pathogenesis and severity, yet the possibility that failure in endogenous inflammation resolution pathways could characterise the disease has not been contemplated. The pro-resolving protein Annexin A1 (AnxA1) is known to counterbalance overexuberant inflammation and mast cell (MC) activation. We hypothesised that inadequate AnxA1 engagement underlies the cytokine storm and vascular pathologies associated with dengue disease. Levels of AnxA1 were examined in the plasma of dengue patients and infected mice. Immunocompetent, interferon (alpha and beta) receptor one knockout (KO), AnxA1 KO, and formyl peptide receptor 2 (FPR2) KO mice were infected with
MeSH term(s)	Animals ; Annexin A1/metabolism ; Dengue/drug therapy ; Humans ; Inflammation/pathology ; Mice ; Peptides/metabolism ; Receptors, Formyl Peptide/metabolism ; Receptors, Lipoxin/metabolism
Chemical Substances	Annexin A1 ; FPR2 protein, human ; Peptides ; Receptors, Formyl Peptide ; Receptors, Lipoxin
Language	English
Publishing date	2022-03-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.73853
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Article ; Online: Angiotensin-(1-7)/MasR axis promotes migration of monocytes/macrophages with a regulatory phenotype to perform phagocytosis and efferocytosis

Isabella Zaidan / Luciana P. Tavares / Michelle A. Sugimoto / Kátia M. Lima / Graziele L. Negreiros-Lima / Lívia C.R. Teixeira / Thais C. Miranda / Bruno V.S. Valiate / Allysson Cramer / Juliana Priscila Vago / Gabriel H. Campolina-Silva / Jéssica A.M. Souza / Laís C. Grossi / Vanessa Pinho / Maria Jose Campagnole-Santos / Robson A.S. Santos / Mauro M. Teixeira / Izabela Galvão / Lirlândia P. Sousa

JCI Insight, Vol 7, Iss

2022 Volume 1

Abstract: Nonphlogistic migration of macrophages contributes to the clearance of pathogens and apoptotic cells, a critical step for the resolution of inflammation and return to homeostasis. Angiotensin-(1-7) [Ang-(1-7)] is a heptapeptide of the renin-angiotensin ... ...

Abstract	Nonphlogistic migration of macrophages contributes to the clearance of pathogens and apoptotic cells, a critical step for the resolution of inflammation and return to homeostasis. Angiotensin-(1-7) [Ang-(1-7)] is a heptapeptide of the renin-angiotensin system that acts through Mas receptor (MasR). Ang-(1-7) has recently emerged as a novel proresolving mediator, yet Ang-(1-7) resolution mechanisms are not fully determined. Herein, Ang-(1-7) stimulated migration of human and murine monocytes/macrophages in a MasR-, CCR2-, and MEK/ERK1/2–dependent manner. Pleural injection of Ang-(1-7) promoted nonphlogistic mononuclear cell influx alongside increased levels of CCL2, IL-10, and macrophage polarization toward a regulatory phenotype. Ang-(1-7) induction of CCL2 and mononuclear cell migration was also dependent on MasR and MEK/ERK. Of note, MasR was upregulated during the resolution phase of inflammation, and its pharmacological inhibition or genetic deficiency impaired mononuclear cell recruitment during self-resolving models of LPS pleurisy and E. coli peritonitis. Inhibition/absence of MasR was associated with reduced CCL2 levels, impaired phagocytosis of bacteria, efferocytosis, and delayed resolution of inflammation. In summary, we have uncovered a potentially novel proresolving feature of Ang-(1-7), namely the recruitment of mononuclear cells favoring efferocytosis, phagocytosis, and resolution of inflammation. Mechanistically, cell migration was dependent on MasR, CCR2, and the MEK/ERK pathway.
Keywords	Infectious disease ; Inflammation ; Medicine ; R
Subject code	610
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	American Society for Clinical investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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