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Article ; Online: Optimization of Xenografting Methods for Generating Human Skeletal Muscle in Mice.

O'Neill, Andrea / Martinez, Anna Llach / Mueller, Amber L / Huang, Weiliang / Accorsi, Anthony / Kane, Maureen A / Eyerman, David / Bloch, Robert J

Cell transplantation

2024 Volume 33, Page(s) 9636897241242624

Abstract: Xenografts of human skeletal muscle generated in mice can be used to study muscle pathology and to test drugs designed to treat myopathies and muscular dystrophies for their efficacy and specificity in human tissue. We previously developed methods to ... ...

Abstract	Xenografts of human skeletal muscle generated in mice can be used to study muscle pathology and to test drugs designed to treat myopathies and muscular dystrophies for their efficacy and specificity in human tissue. We previously developed methods to generate mature human skeletal muscles in immunocompromised mice starting with human myogenic precursor cells (hMPCs) from healthy individuals and individuals with facioscapulohumeral muscular dystrophy (FSHD). Here, we examine a series of alternative treatments at each stage in order to optimize engraftment. We show that (i) X-irradiation at 25Gy is optimal in preventing regeneration of murine muscle while supporting robust engraftment and the formation of human fibers without significant murine contamination; (ii) hMPC lines differ in their capacity to engraft; (iii) some hMPC lines yield grafts that respond better to intermittent neuromuscular electrical stimulation (iNMES) than others; (iv) some lines engraft better in male than in female mice; (v) coinjection of hMPCs with laminin, gelatin, Matrigel, or Growdex does not improve engraftment; (vi) BaCl
MeSH term(s)	Adult ; Humans ; Male ; Mice ; Female ; Animals ; Heterografts ; Transplantation, Heterologous ; Cardiotoxins ; Muscle, Skeletal/pathology ; Muscular Dystrophy, Facioscapulohumeral/pathology
Chemical Substances	Cardiotoxins
Language	English
Publishing date	2024-04-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	1135816-6
ISSN	1555-3892 ; 0963-6897
ISSN (online)	1555-3892
ISSN	0963-6897
DOI	10.1177/09636897241242624
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Article ; Online: Regulatory T cells shield muscle mitochondria from interferon-γ-mediated damage to promote the beneficial effects of exercise.

Langston, P Kent / Sun, Yizhi / Ryback, Birgitta A / Mueller, Amber L / Spiegelman, Bruce M / Benoist, Christophe / Mathis, Diane

Science immunology

2023 Volume 8, Issue 89, Page(s) eadi5377

Abstract: Exercise enhances physical performance and reduces the risk of many disorders such as cardiovascular disease, type 2 diabetes, dementia, and cancer. Exercise characteristically incites an inflammatory response, notably in skeletal muscles. Although some ... ...

Abstract	Exercise enhances physical performance and reduces the risk of many disorders such as cardiovascular disease, type 2 diabetes, dementia, and cancer. Exercise characteristically incites an inflammatory response, notably in skeletal muscles. Although some effector mechanisms have been identified, regulatory elements activated in response to exercise remain obscure. Here, we have addressed the roles of Foxp3
MeSH term(s)	Mice ; Animals ; T-Lymphocytes, Regulatory ; Interferon-gamma ; Diabetes Mellitus, Type 2/metabolism ; Transcription Factors/metabolism ; Mitochondria, Muscle
Chemical Substances	Interferon-gamma (82115-62-6) ; Transcription Factors
Language	English
Publishing date	2023-11-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2470-9468
ISSN (online)	2470-9468
DOI	10.1126/sciimmunol.adi5377
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Article ; Online: Skeletal muscle cell transplantation: models and methods.

Mueller, Amber L / Bloch, Robert J

Journal of muscle research and cell motility

2019 Volume 41, Issue 4, Page(s) 297–311

Abstract: Xenografts of skeletal muscle are used to study muscle repair and regeneration, mechanisms of muscular dystrophies, and potential cell therapies for musculoskeletal disorders. Typically, xenografting involves using an immunodeficient host that is pre- ... ...

Abstract	Xenografts of skeletal muscle are used to study muscle repair and regeneration, mechanisms of muscular dystrophies, and potential cell therapies for musculoskeletal disorders. Typically, xenografting involves using an immunodeficient host that is pre-injured to create a niche for human cell engraftment. Cell type and method of delivery to muscle depend on the specific application, but can include myoblasts, satellite cells, induced pluripotent stem cells, mesangioblasts, immortalized muscle precursor cells, and other multipotent cell lines delivered locally or systemically. Some studies follow cell engraftment with interventions to enhance cell proliferation, migration, and differentiation into mature muscle fibers. Recently, several advances in xenografting human-derived muscle cells have been applied to study and treat Duchenne muscular dystrophy and Facioscapulohumeral muscular dystrophy. Here, we review the vast array of techniques available to aid researchers in designing future experiments aimed at creating robust muscle xenografts in rodent hosts.
MeSH term(s)	Animals ; Cell Transplantation/methods ; Humans ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Muscle, Skeletal/metabolism
Language	English
Publishing date	2019-08-07
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	283053-x
ISSN	1573-2657 ; 0142-4319
ISSN (online)	1573-2657
ISSN	0142-4319
DOI	10.1007/s10974-019-09550-w
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Article ; Online: "Rogue" neutrophil-subset [DEspR+CD11b+/CD66b+] immunotype is an actionable therapeutic target for neutrophilic inflammation-mediated tissue injury -

Carstensen, Saskia / Müller, Meike / Tan, Glaiza L A / Pasion, Khristine Amber / Hohlfeld, Jens M / Herrera, Victoria L M / Ruiz-Opazo, Nelson

Frontiers in immunology

2022 Volume 13, Page(s) 1008390

Abstract: Background and objective: The correlation (Rs > 0.7) of neutrophils expressing the dual endothelin1/signal peptide receptor (DEspR+CD11b+/CD66b+) with severity of hypoxemia (SF-ratio) and multi-organ failure (SOFA-score) in patients with acute ... ...

Abstract	Background and objective: The correlation (Rs > 0.7) of neutrophils expressing the dual endothelin1/signal peptide receptor (DEspR+CD11b+/CD66b+) with severity of hypoxemia (SF-ratio) and multi-organ failure (SOFA-score) in patients with acute respiratory distress syndrome (ARDS) suggest the hypothesis that the DEspR+ neutrophil-subset is an actionable therapeutic target in ARDS. To test this hypothesis, we conducted Methods: We performed tests in lipopolysaccharide (LPS)-induced acute neutrophilic inflammation in three species - human, rhesus macaque, rat - with increasing dose-dependent severity. We measured DEspR+CD66b+ neutrophils in bronchoalveolar lavage fluid (BALF) in healthy volunteers (HVs) 24-hours after segmental LPS-challenge by ChipCytometry, and DEspR+CD11b+ neutrophils in whole blood and BALF in an LPS-induced transient acute lung injury (ALI) model in macaques. We determined anti-DEspR antibody efficacy Results: ChipCytometry detected increased BALF total neutrophil and DEspR+CD66b+ neutrophil counts after segmental LPS-challenge compared to baseline ( Conclusion: Detection of increased DEspR+ neutrophil-subset in human BALF after segmental LPS-challenge supports the correlation of circulating DEspR+ neutrophil counts with severity measure (SOFA-score) in ARDS. Efficacy and safety of targeted inhibition of DEspR+CD11b+ neutrophil-subset in LPS-induced transient-ALI and high-mortality encephalopathy models identify a potential therapeutic target for neutrophil-mediated secondary tissue injury.
MeSH term(s)	Humans ; Rats ; Animals ; Lipopolysaccharides/adverse effects ; Neutrophils ; Macaca mulatta ; Acute Lung Injury/metabolism ; Inflammation/metabolism ; Respiratory Distress Syndrome/drug therapy ; Hypoxia/metabolism ; Brain Diseases/metabolism
Chemical Substances	Lipopolysaccharides
Language	English
Publishing date	2022-10-04
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.1008390
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Article ; Online: Why does COVID-19 disproportionately affect older people?

Mueller, Amber L / McNamara, Maeve S / Sinclair, David A

Aging

2020 Volume 12, Issue 10, Page(s) 9959–9981

Abstract: The severity and outcome of coronavirus disease 2019 (COVID-19) largely depends on a patient's age. Adults over 65 years of age represent 80% of hospitalizations and have a 23-fold greater risk of death than those under 65. In the clinic, COVID-19 ... ...

Abstract	The severity and outcome of coronavirus disease 2019 (COVID-19) largely depends on a patient's age. Adults over 65 years of age represent 80% of hospitalizations and have a 23-fold greater risk of death than those under 65. In the clinic, COVID-19 patients most commonly present with fever, cough and dyspnea, and from there the disease can progress to acute respiratory distress syndrome, lung consolidation, cytokine release syndrome, endotheliitis, coagulopathy, multiple organ failure and death. Comorbidities such as cardiovascular disease, diabetes and obesity increase the chances of fatal disease, but they alone do not explain why age is an independent risk factor. Here, we present the molecular differences between young, middle-aged and older people that may explain why COVID-19 is a mild illness in some but life-threatening in others. We also discuss several biological age clocks that could be used in conjunction with genetic tests to identify both the mechanisms of the disease and individuals most at risk. Finally, based on these mechanisms, we discuss treatments that could increase the survival of older people, not simply by inhibiting the virus, but by restoring patients' ability to clear the infection and effectively regulate immune responses.
MeSH term(s)	Aged ; Aging/physiology ; Betacoronavirus/isolation & purification ; Betacoronavirus/physiology ; COVID-19 ; Comorbidity ; Coronavirus Infections/epidemiology ; Coronavirus Infections/immunology ; Coronavirus Infections/therapy ; Cytokine Release Syndrome/etiology ; Cytokine Release Syndrome/immunology ; Epigenesis, Genetic/physiology ; Humans ; Immunity/physiology ; Pandemics ; Patient Care Management/methods ; Pneumonia, Viral/epidemiology ; Pneumonia, Viral/immunology ; Pneumonia, Viral/therapy ; Respiratory Distress Syndrome/etiology ; Respiratory Distress Syndrome/immunology ; Risk Assessment ; Risk Factors ; SARS-CoV-2 ; Severity of Illness Index
Keywords	covid19
Language	English
Publishing date	2020-05-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.103344
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Article ; Online: TIME-seq reduces time and cost of DNA methylation measurement for epigenetic clock construction.

Griffin, Patrick T / Kane, Alice E / Trapp, Alexandre / Li, Jien / Arnold, Matthew / Poganik, Jesse R / Conway, Ryan J / McNamara, Maeve S / Meer, Margarita V / Hoffman, Noah / Amorim, João A / Tian, Xiao / MacArthur, Michael R / Mitchell, Sarah J / Mueller, Amber L / Carmody, Colleen / Vera, Daniel L / Kerepesi, Csaba / Ying, Kejun /

Noren Hooten, Nicole / Mitchell, James R / Evans, Michele K / Gladyshev, Vadim N / Sinclair, David A

Nature aging

2024 Volume 4, Issue 2, Page(s) 261–274

Abstract: Epigenetic 'clocks' based on DNA methylation have emerged as the most robust and widely used aging biomarkers, but conventional methods for applying them are expensive and laborious. Here we develop tagmentation-based indexing for methylation sequencing ( ...

Abstract	Epigenetic 'clocks' based on DNA methylation have emerged as the most robust and widely used aging biomarkers, but conventional methods for applying them are expensive and laborious. Here we develop tagmentation-based indexing for methylation sequencing (TIME-seq), a highly multiplexed and scalable method for low-cost epigenetic clocks. Using TIME-seq, we applied multi-tissue and tissue-specific epigenetic clocks in over 1,800 mouse DNA samples from eight tissue and cell types. We show that TIME-seq clocks are accurate and robust, enriched for polycomb repressive complex 2-regulated loci, and benchmark favorably against conventional methods despite being up to 100-fold less expensive. Using dietary treatments and gene therapy, we find that TIME-seq clocks reflect diverse interventions in multiple tissues. Finally, we develop an economical human blood clock (R > 0.96, median error = 3.39 years) in 1,056 demographically representative individuals. These methods will enable more efficient epigenetic clock measurement in larger-scale human and animal studies.
MeSH term(s)	Pregnancy ; Female ; Humans ; Mice ; Animals ; DNA Methylation/genetics ; Epigenesis, Genetic ; Aging/genetics ; Epigenomics/methods ; Labor, Obstetric
Language	English
Publishing date	2024-01-10
Publishing country	United States
Document type	Journal Article
ISSN	2662-8465
ISSN (online)	2662-8465
DOI	10.1038/s43587-023-00555-2
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Article: Why does COVID-19 disproportionately affect older people?

Mueller, Amber L / McNamara, Maeve S / Sinclair, David A

Aging (Albany NY)

Abstract	The severity and outcome of coronavirus disease 2019 (COVID-19) largely depends on a patient's age. Adults over 65 years of age represent 80% of hospitalizations and have a 23-fold greater risk of death than those under 65. In the clinic, COVID-19 patients most commonly present with fever, cough and dyspnea, and from there the disease can progress to acute respiratory distress syndrome, lung consolidation, cytokine release syndrome, endotheliitis, coagulopathy, multiple organ failure and death. Comorbidities such as cardiovascular disease, diabetes and obesity increase the chances of fatal disease, but they alone do not explain why age is an independent risk factor. Here, we present the molecular differences between young, middle-aged and older people that may explain why COVID-19 is a mild illness in some but life-threatening in others. We also discuss several biological age clocks that could be used in conjunction with genetic tests to identify both the mechanisms of the disease and individuals most at risk. Finally, based on these mechanisms, we discuss treatments that could increase the survival of older people, not simply by inhibiting the virus, but by restoring patients' ability to clear the infection and effectively regulate immune responses.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #32470948
Database	COVID19

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Article ; Online: Diltiazem improves contractile properties of skeletal muscle in dysferlin-deficient BLAJ mice, but does not reduce contraction-induced muscle damage.

Begam, Morium / Collier, Alyssa F / Mueller, Amber L / Roche, Renuka / Galen, Sujay S / Roche, Joseph A

Physiological reports

2018 Volume 6, Issue 11, Page(s) e13727

Abstract: ... B6.A- ... ...

Abstract	B6.A-Dysf
MeSH term(s)	Animals ; Calcium Channel Blockers/administration & dosage ; Diltiazem/administration & dosage ; Disease Models, Animal ; Dysferlin/genetics ; Male ; Mice, Knockout ; Muscle Contraction/drug effects ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/pathology ; Muscle, Skeletal/physiopathology ; Muscular Dystrophies, Limb-Girdle/genetics ; Muscular Dystrophies, Limb-Girdle/physiopathology ; Muscular Dystrophies, Limb-Girdle/prevention & control
Chemical Substances	Calcium Channel Blockers ; Dysf protein, mouse ; Dysferlin ; Diltiazem (EE92BBP03H)
Language	English
Publishing date	2018-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.13727
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Article ; Online: "Rogue" neutrophil-subset [DEspR+CD11b+/CD66b+] immunotype is an actionable therapeutic target for neutrophilic inflammation-mediated tissue injury - studies in human, macaque and rat LPS-inflammation models

Carstensen, Saskia / Müller, Meike / Tan, Glaiza L.A. / Pasion, Khristine Amber / Hohlfeld, Jens / Herrera, Victoria L.M. / Ruiz-Opazo, Nelson

2022

Abstract	Background and objective: The correlation (Rs > 0.7) of neutrophils expressing the dual endothelin1/signal peptide receptor (DEspR+CD11b+/CD66b+) with severity of hypoxemia (SF-ratio) and multi-organ failure (SOFA-score) in patients with acute respiratory distress syndrome (ARDS) suggest the hypothesis that the DEspR+ neutrophil-subset is an actionable therapeutic target in ARDS. To test this hypothesis, we conducted in vivo studies to validate DEspR+ neutrophil-subset as therapeutic target and test efficacy of DEspR-inhibition in acute neutrophilic hyperinflammation models. Methods: We performed tests in lipopolysaccharide (LPS)-induced acute neutrophilic inflammation in three species – human, rhesus macaque, rat - with increasing dose-dependent severity. We measured DEspR+CD66b+ neutrophils in bronchoalveolar lavage fluid (BALF) in healthy volunteers (HVs) 24-hours after segmental LPS-challenge by ChipCytometry, and DEspR+CD11b+ neutrophils in whole blood and BALF in an LPS-induced transient acute lung injury (ALI) model in macaques. We determined anti-DEspR antibody efficacy in vivo in LPS-ALI macaque model and in high-mortality LPS-induced encephalopathy in hypertensive rats. Results: ChipCytometry detected increased BALF total neutrophil and DEspR+CD66b+ neutrophil counts after segmental LPS-challenge compared to baseline (P =0.034), as well as increased peripheral neutrophil counts and neutrophil-lymphocyte ratio (NLR) compared to pre-LPS level (P <0.05). In the LPS-ALI macaque model, flow cytometry detected increased DEspR+ and DEspR[-] neutrophils in BALF, which was associated with moderate-severe hypoxemia. After determining pharmacokinetics of single-dose anti-DEspR[hu6g8] antibody, one-time pre-LPS anti-DEspR treatment reduced hypoxemia (P =0.03) and neutrophil influx into BALF (P =0.0001) in LPS-ALI vs vehicle mock-treated LPS-ALI macaques. Ex vivo live cell imaging of macaque neutrophils detected greater “intrinsic adhesion to hard-surface” in DEspR+ vs DEspR[-] neutrophils (P <0.001). ...
Subject code	630
Language	English
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Combined PD-L1/TGFβ blockade allows expansion and differentiation of stem cell-like CD8 T cells in immune excluded tumors.

Castiglioni, Alessandra / Yang, Yagai / Williams, Katherine / Gogineni, Alvin / Lane, Ryan S / Wang, Amber W / Shyer, Justin A / Zhang, Zhe / Mittman, Stephanie / Gutierrez, Alan / Astarita, Jillian L / Thai, Minh / Hung, Jeffrey / Yang, Yeqing Angela / Pourmohamad, Tony / Himmels, Patricia / De Simone, Marco / Elstrott, Justin / Capietto, Aude-Hélène /

Cubas, Rafael / Modrusan, Zora / Sandoval, Wendy / Ziai, James / Gould, Stephen E / Fu, Wenxian / Wang, Yulei / Koerber, James T / Sanjabi, Shomyseh / Mellman, Ira / Turley, Shannon J / Müller, Sören

Nature communications

2023 Volume 14, Issue 1, Page(s) 4703

Abstract: TGFβ signaling is associated with non-response to immune checkpoint blockade in patients with advanced cancers, particularly in the immune-excluded phenotype. While previous work demonstrates that converting tumors from excluded to inflamed phenotypes ... ...

Abstract	TGFβ signaling is associated with non-response to immune checkpoint blockade in patients with advanced cancers, particularly in the immune-excluded phenotype. While previous work demonstrates that converting tumors from excluded to inflamed phenotypes requires attenuation of PD-L1 and TGFβ signaling, the underlying cellular mechanisms remain unclear. Here, we show that TGFβ and PD-L1 restrain intratumoral stem cell-like CD8 T cell (T
MeSH term(s)	Female ; Animals ; Mice ; Cell Differentiation ; CD8-Positive T-Lymphocytes/immunology ; Stem Cells ; B7-H1 Antigen/antagonists & inhibitors ; Transforming Growth Factor beta/antagonists & inhibitors ; Interferon-gamma/immunology ; T-Cell Exhaustion ; Immune Checkpoint Inhibitors/pharmacology ; Mice, Inbred BALB C ; Cell Line, Tumor ; Breast Neoplasms/drug therapy ; Breast Neoplasms/immunology ; RNA-Seq
Chemical Substances	B7-H1 Antigen ; Transforming Growth Factor beta ; Interferon-gamma (82115-62-6) ; Immune Checkpoint Inhibitors
Language	English
Publishing date	2023-08-05
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-40398-4
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