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Artikel ; Online: Measuring Diaphragm Thickness and Function Using Point-of-Care Ultrasound.

Bellissimo, Catherine A / Morris, Idunn S / Wong, Jenna / Goligher, Ewan C

Journal of visualized experiments : JoVE

2023 , Heft 201

Abstract: The diaphragm is the main component of the respiratory muscle pump. Diaphragm dysfunction can cause dyspnea and exercise intolerance, and predisposes affected individuals to respiratory failure. In mechanically ventilated patients, the diaphragm is ... ...

Abstract	The diaphragm is the main component of the respiratory muscle pump. Diaphragm dysfunction can cause dyspnea and exercise intolerance, and predisposes affected individuals to respiratory failure. In mechanically ventilated patients, the diaphragm is susceptible to atrophy and dysfunction through disuse and other mechanisms. This contributes to failure to wean and poor long-term clinical outcomes. Point-of-care ultrasound provides a valid and reproducible method for evaluating diaphragm thickness and contractile activity (thickening fraction during inspiration) that can be readily employed by clinicians and researchers alike. This article presents best practices for measuring diaphragm thickness and quantifying diaphragm thickening during tidal breathing or maximal inspiration. Once mastered, this technique can be used to diagnose and prognosticate diaphragm dysfunction, and guide and monitor response to treatment over time in both healthy individuals and acute or chronically ill patients.
Mesh-Begriff(e)	Humans ; Diaphragm/diagnostic imaging ; Point-of-Care Systems ; Thorax ; Respiratory Muscles ; Point-of-Care Testing
Sprache	Englisch
Erscheinungsdatum	2023-11-03
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/65431
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Mitochondrial stress responses in Duchenne muscular dystrophy: metabolic dysfunction or adaptive reprogramming?

Bellissimo, Catherine A / Garibotti, Madison C / Perry, Christopher G R

American journal of physiology. Cell physiology

2022 Band 323, Heft 3, Seite(n) C718–C730

Abstract: Mitochondrial stress may be a secondary contributor to muscle weakness in inherited muscular dystrophies. Duchenne muscular dystrophy has received the majority of attention, whereby most discoveries suggest mitochondrial ATP synthesis may be reduced. ... ...

Abstract	Mitochondrial stress may be a secondary contributor to muscle weakness in inherited muscular dystrophies. Duchenne muscular dystrophy has received the majority of attention, whereby most discoveries suggest mitochondrial ATP synthesis may be reduced. However, not all studies support this finding. Furthermore, some studies have reported increased mitochondrial reactive oxygen species and propensity for permeability transition pore formation as an inducer of apoptosis, although divergent findings have also been described. A closer examination of the literature suggests the degree and direction of mitochondrial stress responses may depend on the progression of the disease, the muscle type examined, the mouse model used with regard to preclinical research, the precise metabolic pathways in consideration, and in some cases, the in vitro technique used to assess a given mitochondrial bioenergetic function. One intent of this review is to provide careful considerations for future experimental designs to resolve the heterogeneous nature of mitochondrial stress during the progression of Duchenne muscular dystrophy. Such considerations have implications for other muscular dystrophies as well which are addressed briefly herein. A renewed perspective of the term "mitochondrial dysfunction" is presented whereby stress responses might be re-explored in future investigations as direct contributors to myopathy versus an adaptive "reprogramming" intended to maintain homeostasis in the face of disease stressors themselves. In so doing, the prospective development of mitochondrial enhancement therapies can be driven by advances in perspectives as much as experimental approaches when resolving the precise relationships between mitochondrial remodeling and muscle weakness in Duchenne and, indeed, other muscular dystrophies.
Mesh-Begriff(e)	Animals ; Mice ; Mitochondria/metabolism ; Muscle Weakness/metabolism ; Muscle, Skeletal/metabolism ; Muscular Dystrophy, Duchenne/genetics ; Muscular Dystrophy, Duchenne/metabolism ; Prospective Studies
Sprache	Englisch
Erscheinungsdatum	2022-07-11
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00249.2022
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Sex differences in the regulation of hepatic mitochondrial turnover following physical activity: do males need more quality control than females?

Bellissimo, Catherine A / Perry, Christopher G R

The Journal of physiology

2018 Band 596, Heft 24, Seite(n) 6125–6126

Mesh-Begriff(e)	Exercise ; Female ; Liver ; Male ; Mitophagy ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Quality Control ; Sex Characteristics
Chemische Substanzen	Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
Sprache	Englisch
Erscheinungsdatum	2018-10-28
Erscheinungsland	England
Dokumenttyp	Journal Article ; Comment
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP276896
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Mitochondrial bioenergetic dysfunction in the D2.mdx model of Duchenne muscular dystrophy is associated with microtubule disorganization in skeletal muscle.

Ramos, Sofhia V / Hughes, Meghan C / Delfinis, Luca J / Bellissimo, Catherine A / Perry, Christopher G R

PloS one

2020 Band 15, Heft 10, Seite(n) e0237138

Abstract: In Duchenne muscular dystrophy, a lack of dystrophin leads to extensive muscle weakness and atrophy that is linked to cellular metabolic dysfunction and oxidative stress. This dystrophinopathy results in a loss of tethering between microtubules and the ... ...

Abstract	In Duchenne muscular dystrophy, a lack of dystrophin leads to extensive muscle weakness and atrophy that is linked to cellular metabolic dysfunction and oxidative stress. This dystrophinopathy results in a loss of tethering between microtubules and the sarcolemma. Microtubules are also believed to regulate mitochondrial bioenergetics potentially by binding the outer mitochondrial membrane voltage dependent anion channel (VDAC) and influencing permeability to ADP/ATP cycling. The objective of this investigation was to determine if a lack of dystrophin causes microtubule disorganization concurrent with mitochondrial dysfunction in skeletal muscle, and whether this relationship is linked to altered binding of tubulin to VDAC. In extensor digitorum longus (EDL) muscle from 4-week old D2.mdx mice, microtubule disorganization was observed when probing for α-tubulin. This cytoskeletal disorder was associated with a reduced ability of ADP to stimulate respiration and attenuate H2O2 emission relative to wildtype controls. However, this was not associated with altered α-tubulin-VDAC2 interactions. These findings reveal that microtubule disorganization in dystrophin-deficient EDL is associated with impaired ADP control of mitochondrial bioenergetics, and suggests that mechanisms alternative to α-tubulin's regulation of VDAC2 should be examined to understand how cytoskeletal disruption in the absence of dystrophin may cause metabolic dysfunctions in skeletal muscle.
Mesh-Begriff(e)	Animals ; Dystrophin/metabolism ; Energy Metabolism ; Mice ; Mice, Inbred mdx ; Microtubules/metabolism ; Microtubules/pathology ; Mitochondria/metabolism ; Mitochondria/pathology ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscular Dystrophy, Duchenne/metabolism ; Tubulin/metabolism ; Voltage-Dependent Anion Channels/metabolism
Chemische Substanzen	Dystrophin ; Tubulin ; Voltage-Dependent Anion Channels
Sprache	Englisch
Erscheinungsdatum	2020-10-01
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0237138
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Proof of Concept for Continuous On-Demand Phrenic Nerve Stimulation to Prevent Diaphragm Disuse during Mechanical Ventilation (STIMULUS): A Phase 1 Clinical Trial.

Morris, Idunn S / Bassi, Thiago / Bellissimo, Catherine A / de Perrot, Marc / Donahoe, Laura / Brochard, Laurent / Mehta, Nawzer / Thakkar, Viral / Ferguson, Niall D / Goligher, Ewan C

American journal of respiratory and critical care medicine

2023 Band 208, Heft 9, Seite(n) 992–995

Mesh-Begriff(e)	Humans ; Diaphragm/innervation ; Electric Stimulation Therapy ; Electrodes, Implanted ; Phrenic Nerve ; Respiration, Artificial/adverse effects ; Thorax ; Proof of Concept Study
Sprache	Englisch
Erscheinungsdatum	2023-08-29
Erscheinungsland	United States
Dokumenttyp	Clinical Trial, Phase I ; Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202305-0791LE
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Memory impairment in the D2.mdx mouse model of Duchenne muscular dystrophy is prevented by the adiponectin receptor agonist ALY688.

Bellissimo, Catherine A / Castellani, Laura N / Finch, Michael S / Murugathasan, Mayoorey / Gandhi, Shivam / Sweeney, Gary / Abdul-Sater, Ali A / MacPherson, Rebecca E K / Perry, Christopher G R

Experimental physiology

2023 Band 108, Heft 9, Seite(n) 1108–1117

Abstract: New findings: What is the central question of this study? Can adiponectin receptor agonism improve recognition memory in a mouse model of Duchenne muscular dystrophy? What is the main finding and its importance? Short-term treatment with the new ... ...

Abstract	New findings: What is the central question of this study? Can adiponectin receptor agonism improve recognition memory in a mouse model of Duchenne muscular dystrophy? What is the main finding and its importance? Short-term treatment with the new adiponectin receptor agonist ALY688 improves recognition memory in D2.mdx mice. This finding suggests that further investigation into adiponectin receptor agonism is warranted, given that there remains an unmet need for clinical approaches to treat this cognitive dysfunction in people with Duchenne muscular dystrophy. Abstract: Memory impairments have been well documented in people with Duchenne muscular dystrophy (DMD). However, the underlying mechanisms are poorly understood, and there is an unmet need to develop new therapies to treat this condition. Using a novel object recognition test, we show that recognition memory impairments in D2.mdx mice are completely prevented by daily treatment with the new adiponectin receptor agonist ALY688 from day 7 to 28 of age. In comparison to age-matched wild-type mice, untreated D2.mdx mice demonstrated lower hippocampal mitochondrial respiration (carbohydrate substrate), greater serum interleukin-6 cytokine content and greater hippocampal total tau and Raptor protein contents. Each of these measures was partly or fully preserved after treatment with ALY688. Collectively, these results indicate that adiponectin receptor agonism improves recognition memory in young D2.mdx mice.
Mesh-Begriff(e)	Animals ; Mice ; Muscular Dystrophy, Duchenne/drug therapy ; Muscular Dystrophy, Duchenne/metabolism ; Mice, Inbred mdx ; Receptors, Adiponectin/metabolism ; Receptors, Adiponectin/therapeutic use ; Adiponectin/metabolism ; Respiration ; Disease Models, Animal ; Memory Disorders/drug therapy ; Memory Disorders/metabolism ; Muscle, Skeletal/metabolism
Chemische Substanzen	Receptors, Adiponectin ; Adiponectin
Sprache	Englisch
Erscheinungsdatum	2023-07-06
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1016295-1
ISSN	1469-445X ; 0958-0670
ISSN (online)	1469-445X
ISSN	0958-0670
DOI	10.1113/EP091274
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: The slow-release adiponectin analog ALY688-SR modifies early-stage disease development in the D2.

Bellissimo, Catherine A / Gandhi, Shivam / Castellani, Laura N / Murugathasan, Mayoorey / Delfinis, Luca J / Thuhan, Arshdeep / Garibotti, Madison C / Seo, Yeji / Rebalka, Irena A / Hsu, Henry H / Sweeney, Gary / Hawke, Thomas J / Abdul-Sater, Ali A / Perry, Christopher G R

American journal of physiology. Cell physiology

2023 Band 326, Heft 4, Seite(n) C1011–C1026

Abstract: Fibrosis is associated with respiratory and limb muscle atrophy in Duchenne muscular dystrophy (DMD). Current standard of care partially delays the progression of this myopathy but there remains an unmet need to develop additional therapies. Adiponectin ... ...

Abstract	Fibrosis is associated with respiratory and limb muscle atrophy in Duchenne muscular dystrophy (DMD). Current standard of care partially delays the progression of this myopathy but there remains an unmet need to develop additional therapies. Adiponectin receptor agonism has emerged as a possible therapeutic target to lower inflammation and improve metabolism in
Mesh-Begriff(e)	Animals ; Mice ; Mice, Inbred mdx ; Muscular Dystrophy, Duchenne/drug therapy ; Muscular Dystrophy, Duchenne/genetics ; Muscular Dystrophy, Duchenne/pathology ; Adiponectin/genetics ; Disease Models, Animal ; Interleukin-6/metabolism ; Mice, Inbred C57BL ; Hydrogen Peroxide/metabolism ; Receptors, Adiponectin/genetics ; Receptors, Adiponectin/metabolism ; Mice, Inbred DBA ; Muscle, Skeletal/metabolism ; Diaphragm/metabolism ; Fibrosis ; Inflammation/metabolism ; Disease Progression ; Atrophy/metabolism ; Atrophy/pathology
Chemische Substanzen	Adiponectin ; Interleukin-6 ; Hydrogen Peroxide (BBX060AN9V) ; Receptors, Adiponectin
Sprache	Englisch
Erscheinungsdatum	2023-12-25
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00638.2023
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Mitochondrial creatine sensitivity is lost in the D2.

Bellissimo, Catherine A / Delfinis, Luca J / Hughes, Meghan C / Turnbull, Patrick C / Gandhi, Shivam / DiBenedetto, Sara N / Rahman, Fasih A / Tadi, Peyman / Amaral, Christina A / Dehghani, Ali / Cobley, James N / Quadrilatero, Joe / Schlattner, Uwe / Perry, Christopher G R

American journal of physiology. Cell physiology

2023 Band 324, Heft 5, Seite(n) C1141–C1157

Abstract: Duchenne muscular dystrophy (DMD) is associated with distinct mitochondrial stress responses. Here, we aimed to determine whether the prospective mitochondrial-enhancing compound Olesoxime, prevents early-stage mitochondrial stress in limb and ... ...

Abstract	Duchenne muscular dystrophy (DMD) is associated with distinct mitochondrial stress responses. Here, we aimed to determine whether the prospective mitochondrial-enhancing compound Olesoxime, prevents early-stage mitochondrial stress in limb and respiratory muscle from D2.
Mesh-Begriff(e)	Animals ; Mice ; Muscular Dystrophy, Duchenne/metabolism ; Mice, Inbred mdx ; Creatine/metabolism ; Mice, Inbred C57BL ; Prospective Studies ; Diaphragm/metabolism ; Muscle, Skeletal ; Disease Models, Animal
Chemische Substanzen	Creatine (MU72812GK0) ; olesoxime (A6778U5IFY)
Sprache	Englisch
Erscheinungsdatum	2023-01-23
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00377.2022
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Muscle weakness precedes atrophy during cancer cachexia and is linked to muscle-specific mitochondrial stress.

Delfinis, Luca J / Bellissimo, Catherine A / Gandhi, Shivam / DiBenedetto, Sara N / Garibotti, Madison C / Thuhan, Arshdeep K / Tsitkanou, Stavroula / Rosa-Caldwell, Megan E / Rahman, Fasih A / Cheng, Arthur J / Wiggs, Michael P / Schlattner, Uwe / Quadrilatero, Joe / Greene, Nicholas P / Perry, Christopher Gr

JCI insight

2022 Band 7, Heft 24

Abstract: Muscle weakness and wasting are defining features of cancer-induced cachexia. Mitochondrial stress occurs before atrophy in certain muscles, but the possibility of heterogeneous responses between muscles and across time remains unclear. Using mice ... ...

Abstract	Muscle weakness and wasting are defining features of cancer-induced cachexia. Mitochondrial stress occurs before atrophy in certain muscles, but the possibility of heterogeneous responses between muscles and across time remains unclear. Using mice inoculated with Colon-26 cancer, we demonstrate that specific force production was reduced in quadriceps and diaphragm at 2 weeks in the absence of atrophy. At this time, pyruvate-supported mitochondrial respiration was lower in quadriceps while mitochondrial H2O2 emission was elevated in diaphragm. By 4 weeks, atrophy occurred in both muscles, but specific force production increased to control levels in quadriceps such that reductions in absolute force were due entirely to atrophy. Specific force production remained reduced in diaphragm. Mitochondrial respiration increased and H2O2 emission was unchanged in both muscles versus control while mitochondrial creatine sensitivity was reduced in quadriceps. These findings indicate muscle weakness precedes atrophy and is linked to heterogeneous mitochondrial alterations that could involve adaptive responses to metabolic stress. Eventual muscle-specific restorations in specific force and bioenergetics highlight how the effects of cancer on one muscle do not predict the response in another muscle. Exploring heterogeneous responses of muscle to cancer may reveal new mechanisms underlying distinct sensitivities, or resistance, to cancer cachexia.
Mesh-Begriff(e)	Mice ; Animals ; Cachexia/etiology ; Cachexia/metabolism ; Muscle, Skeletal/metabolism ; Hydrogen Peroxide/metabolism ; Muscle Weakness/metabolism ; Atrophy/metabolism ; Atrophy/pathology ; Colonic Neoplasms/metabolism
Chemische Substanzen	Hydrogen Peroxide (BBX060AN9V)
Sprache	Englisch
Erscheinungsdatum	2022-12-22
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.155147
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Sexual dimorphism in human skeletal muscle mitochondrial bioenergetics in response to type 1 diabetes.

Monaco, Cynthia M F / Bellissimo, Catherine A / Hughes, Meghan C / Ramos, Sofhia V / Laham, Robert / Perry, Christopher G R / Hawke, Thomas J

American journal of physiology. Endocrinology and metabolism

2019 Band 318, Heft 1, Seite(n) E44–E51

Abstract: Sexual dimorphism in mitochondrial respiratory function has been reported in young women and men without diabetes, which may have important implications for exercise. The purpose of this study was to determine if sexual dimorphism exists in skeletal ... ...

Abstract	Sexual dimorphism in mitochondrial respiratory function has been reported in young women and men without diabetes, which may have important implications for exercise. The purpose of this study was to determine if sexual dimorphism exists in skeletal muscle mitochondrial bioenergetics in people with type 1 diabetes (T1D). A resting muscle microbiopsy was obtained from women and men with T1D (
Mesh-Begriff(e)	Adult ; Calcium/metabolism ; Case-Control Studies ; Diabetes Mellitus, Type 1/metabolism ; Electron Transport Complex I/metabolism ; Electron Transport Complex II/metabolism ; Energy Metabolism ; Female ; Humans ; Hydrogen Peroxide/metabolism ; Male ; Mitochondria/metabolism ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/metabolism ; Sex Characteristics ; Sex Factors ; Young Adult
Chemische Substanzen	Hydrogen Peroxide (BBX060AN9V) ; Electron Transport Complex II (EC 1.3.5.1) ; Electron Transport Complex I (EC 7.1.1.2) ; Calcium (SY7Q814VUP)
Sprache	Englisch
Erscheinungsdatum	2019-12-03
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00411.2019
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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