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  1. Article ; Online: Hydrogen sulfide supplementation as a potential treatment for primary mitochondrial diseases.

    Slade, Luke / Deane, Colleen S / Szewczyk, Nathaniel J / Etheridge, Timothy / Whiteman, Matthew

    Pharmacological research

    2024  Volume 203, Page(s) 107180

    Abstract: Primary mitochondrial diseases (PMD) are amongst the most common inborn errors of metabolism causing fatal outcomes within the first decade of life. With marked heterogeneity in both inheritance patterns and physiological manifestations, these conditions ...

    Abstract Primary mitochondrial diseases (PMD) are amongst the most common inborn errors of metabolism causing fatal outcomes within the first decade of life. With marked heterogeneity in both inheritance patterns and physiological manifestations, these conditions present distinct challenges for targeted drug therapy, where effective therapeutic countermeasures remain elusive within the clinic. Hydrogen sulfide (H
    MeSH term(s) Hydrogen Sulfide/metabolism ; Hydrogen Sulfide/therapeutic use ; Humans ; Animals ; Mitochondrial Diseases/drug therapy ; Mitochondrial Diseases/metabolism ; Mitochondria/metabolism ; Mitochondria/drug effects ; Dietary Supplements ; Signal Transduction/drug effects
    Chemical Substances Hydrogen Sulfide (YY9FVM7NSN)
    Language English
    Publishing date 2024-04-09
    Publishing country Netherlands
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1003347-6
    ISSN 1096-1186 ; 0031-6989 ; 1043-6618
    ISSN (online) 1096-1186
    ISSN 0031-6989 ; 1043-6618
    DOI 10.1016/j.phrs.2024.107180
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 721: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Caenorhabditis elegans

    Ellwood, Rebecca A / Piasecki, Mathew / Szewczyk, Nathaniel J

    International journal of molecular sciences

    2021  Volume 22, Issue 9

    Abstract: The nematode ... ...

    Abstract The nematode worm
    MeSH term(s) Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/physiology ; Disease Models, Animal ; Epistasis, Genetic ; Humans ; Muscular Dystrophy, Duchenne/genetics ; Muscular Dystrophy, Duchenne/pathology ; Mutation/genetics ; Phenotype
    Language English
    Publishing date 2021-05-05
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22094891
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  3. Article ; Online: Caenorhabditis elegans

    Scott, Amanda / Willis, Craig R G / Muratani, Masafumi / Higashitani, Atsushi / Etheridge, Timothy / Szewczyk, Nathaniel J / Deane, Colleen S

    iScience

    2023  Volume 26, Issue 7, Page(s) 107189

    Abstract: The application of omics to ... ...

    Abstract The application of omics to study
    Language English
    Publishing date 2023-06-20
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2023.107189
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  4. Article ; Online: Adaptability to eccentric exercise training is diminished with age in female mice.

    Baumann, Cory W / Deane, Colleen S / Etheridge, Timothy / Szewczyk, Nathaniel J / Willis, Craig R G / Lowe, Dawn A

    Journal of applied physiology (Bethesda, Md. : 1985)

    2023  Volume 135, Issue 5, Page(s) 1135–1145

    Abstract: The ability of skeletal muscle to adapt to eccentric contractions has been suggested to be blunted in older muscle. If eccentric exercise is to be a safe and efficient training mode for older adults, preclinical studies need to establish if older muscle ... ...

    Abstract The ability of skeletal muscle to adapt to eccentric contractions has been suggested to be blunted in older muscle. If eccentric exercise is to be a safe and efficient training mode for older adults, preclinical studies need to establish if older muscle can effectively adapt and if not, determine the molecular signatures that are causing this impairment. The purpose of this study was to quantify the extent age impacts functional adaptations of muscle and identify genetic signatures associated with adaptation (or lack thereof). The anterior crural muscles of young (4 mo) and older (28 mo) female mice performed repeated bouts of eccentric contractions in vivo (50 contractions/wk for 5 wk) and isometric torque was measured across the initial and final bouts. Transcriptomics was completed by RNA-sequencing 1 wk following the fifth bout to identify common and differentially regulated genes. When torques post eccentric contractions were compared after the first and fifth bouts, young muscle exhibited a robust ability to adapt, increasing isometric torque 20%-36%, whereas isometric torque of older muscle decreased up to 18% (
    MeSH term(s) Female ; Animals ; Mice ; Muscle, Skeletal/physiology ; Torque
    Language English
    Publishing date 2023-10-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 219139-8
    ISSN 1522-1601 ; 0021-8987 ; 0161-7567 ; 8750-7587
    ISSN (online) 1522-1601
    ISSN 0021-8987 ; 0161-7567 ; 8750-7587
    DOI 10.1152/japplphysiol.00428.2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.249: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Increased mitochondrial Ca

    Higashitani, Atsushi / Teranishi, Mika / Nakagawa, Yui / Itoh, Yukou / Sudevan, Surabhi / Szewczyk, Nathaniel J / Kubota, Yukihiko / Abe, Takaaki / Kobayashi, Takeshi

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2023  Volume 37, Issue 4, Page(s) e22851

    Abstract: Sarcopenia is a geriatric syndrome characterized by an age-related decline in skeletal muscle mass and strength. Here, we show that suppression of mitochondrial calcium uniporter (MCU)-mediated ... ...

    Abstract Sarcopenia is a geriatric syndrome characterized by an age-related decline in skeletal muscle mass and strength. Here, we show that suppression of mitochondrial calcium uniporter (MCU)-mediated Ca
    MeSH term(s) Animals ; Caenorhabditis elegans ; Mitochondria/pathology ; Muscle, Skeletal/metabolism ; Sarcopenia/pathology ; Muscular Dystrophies/metabolism ; Calcium/metabolism
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2023-03-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.202201489RR
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2266: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 296: Show issues

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  6. Article: Links Between Testosterone, Oestrogen, and the Growth Hormone/Insulin-Like Growth Factor Axis and Resistance Exercise Muscle Adaptations.

    Gharahdaghi, Nima / Phillips, Bethan E / Szewczyk, Nathaniel J / Smith, Ken / Wilkinson, Daniel J / Atherton, Philip J

    Frontiers in physiology

    2021  Volume 11, Page(s) 621226

    Abstract: Maintenance of skeletal muscle mass throughout the life course is key for the regulation of health, with physical activity a critical component of this, in part, due to its influence upon key hormones such as testosterone, estrogen, growth hormone (GH), ... ...

    Abstract Maintenance of skeletal muscle mass throughout the life course is key for the regulation of health, with physical activity a critical component of this, in part, due to its influence upon key hormones such as testosterone, estrogen, growth hormone (GH), and insulin-like growth factor (IGF). Despite the importance of these hormones for the regulation of skeletal muscle mass in response to different types of exercise, their interaction with the processes controlling muscle mass remain unclear. This review presents evidence on the importance of these hormones in the regulation of skeletal muscle mass and their responses, and involvement in muscle adaptation to resistance exercise. Highlighting the key role testosterone plays as a primary anabolic hormone in muscle adaptation following exercise training, through its interaction with anabolic signaling pathways and other hormones via the androgen receptor (AR), this review also describes the potential importance of fluctuations in other hormones such as GH and IGF-1 in concert with dietary amino acid availability; and the role of estrogen, under the influence of the menstrual cycle and menopause, being especially important in adaptive exercise responses in women. Finally, the downstream mechanisms by which these hormones impact regulation of muscle protein turnover (synthesis and breakdown), and thus muscle mass are discussed. Advances in our understanding of hormones that impact protein turnover throughout life offers great relevance, not just for athletes, but also for the general and clinical populations alike.
    Language English
    Publishing date 2021-01-15
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2020.621226
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  7. Article ; Online: Sulfur amino acid supplementation displays therapeutic potential in a C. elegans model of Duchenne muscular dystrophy.

    Ellwood, Rebecca A / Slade, Luke / Lewis, Jonathan / Torregrossa, Roberta / Sudevan, Surabhi / Piasecki, Mathew / Whiteman, Matthew / Etheridge, Timothy / Szewczyk, Nathaniel J

    Communications biology

    2022  Volume 5, Issue 1, Page(s) 1255

    Abstract: Mutations in the dystrophin gene cause Duchenne muscular dystrophy (DMD), a common muscle disease that manifests with muscle weakness, wasting, and degeneration. An emerging theme in DMD pathophysiology is an intramuscular deficit in the gasotransmitter ... ...

    Abstract Mutations in the dystrophin gene cause Duchenne muscular dystrophy (DMD), a common muscle disease that manifests with muscle weakness, wasting, and degeneration. An emerging theme in DMD pathophysiology is an intramuscular deficit in the gasotransmitter hydrogen sulfide (H
    MeSH term(s) Animals ; Muscular Dystrophy, Duchenne/drug therapy ; Muscular Dystrophy, Duchenne/genetics ; Caenorhabditis elegans/genetics ; Sulfur ; Cysteine ; Dietary Supplements
    Chemical Substances Sulfur (70FD1KFU70) ; Cysteine (K848JZ4886)
    Language English
    Publishing date 2022-11-16
    Publishing country England
    Document type Journal Article
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-022-04212-z
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  8. Article: Editorial: Integrative Physiology of Common Chronic Musculoskeletal Disorders.

    Clark, Brian C / Grooms, Dustin R / Etheridge, Timothy / Wilkinson, Daniel J / Zhu, Shouan / Arnold, W David / Szewczyk, Nathaniel J

    Frontiers in physiology

    2022  Volume 13, Page(s) 971103

    Language English
    Publishing date 2022-07-11
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2022.971103
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  9. Article ; Online: Comparative Analysis of Muscle Atrophy During Spaceflight, Nutritional Deficiency and Disuse in the Nematode

    Kim, Ban-Seok / Alcantara, Alfredo V / Moon, Je-Hyun / Higashitani, Atsushi / Higashitani, Nahoko / Etheridge, Timothy / Szewczyk, Nathaniel J / Deane, Colleen S / Gaffney, Christopher J / Higashibata, Akira / Hashizume, Toko / Yoon, Kyoung-Hye / Lee, Jin I

    International journal of molecular sciences

    2023  Volume 24, Issue 16

    Abstract: While spaceflight is becoming more common than before, the hazards spaceflight and space microgravity pose to the human body remain relatively unexplored. Astronauts experience muscle atrophy after spaceflight, but the exact reasons for this and ... ...

    Abstract While spaceflight is becoming more common than before, the hazards spaceflight and space microgravity pose to the human body remain relatively unexplored. Astronauts experience muscle atrophy after spaceflight, but the exact reasons for this and solutions are unknown. Here, we take advantage of the nematode
    MeSH term(s) Humans ; Animals ; Caenorhabditis elegans/genetics ; Malnutrition ; Space Flight ; Starvation ; Muscular Atrophy/etiology
    Language English
    Publishing date 2023-08-10
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms241612640
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  10. Article ; Online: Bisphosphonates attenuate age-related muscle decline in Caenorhabditis elegans.

    Slade, Luke / Bollen, Shelby E / Bass, Joseph J / Phillips, Bethan E / Smith, Kenneth / Wilkinson, Daniel J / Szewczyk, Nathaniel J / Atherton, Philip J / Etheridge, Timothy

    Journal of cachexia, sarcopenia and muscle

    2023  Volume 14, Issue 6, Page(s) 2613–2622

    Abstract: Background: Age-related muscle decline (sarcopenia) associates with numerous health risk factors and poor quality of life. Drugs that counter sarcopenia without harmful side effects are lacking, and repurposing existing pharmaceuticals could expedite ... ...

    Abstract Background: Age-related muscle decline (sarcopenia) associates with numerous health risk factors and poor quality of life. Drugs that counter sarcopenia without harmful side effects are lacking, and repurposing existing pharmaceuticals could expedite realistic clinical options. Recent studies suggest bisphosphonates promote muscle health; however, the efficacy of bisphosphonates as an anti-sarcopenic therapy is currently unclear.
    Methods: Using Caenorhabditis elegans as a sarcopenia model, we treated animals with 100 nM, 1, 10, 100 and 500 μM zoledronic acid (ZA) and assessed lifespan and healthspan (movement rates) using a microfluidic chip device. The effects of ZA on sarcopenia were examined using GFP-tagged myofibres or mitochondria at days 0, 4 and 6 post-adulthood. Mechanisms of ZA-mediated healthspan extension were determined using combined ZA and targeted RNAi gene knockdown across the life-course.
    Results: We found 100 nM and 1 μM ZA increased lifespan (P < 0.001) and healthspan [954 ± 53 (100 nM) and 963 ± 48 (1 μM) vs. 834 ± 59% (untreated) population activity AUC, P < 0.05]. 10 μM ZA shortened lifespan (P < 0.0001) but not healthspan (758.9 ± 37 vs. 834 ± 59, P > 0.05), whereas 100 and 500 μM ZA were larval lethal. ZA (1 μM) significantly improved myofibrillar structure on days 4 and 6 post-adulthood (83 and 71% well-organized myofibres, respectively, vs. 56 and 34% controls, P < 0.0001) and increased well-networked mitochondria at day 6 (47 vs. 16% in controls, P < 0.01). Genes required for ZA-mediated healthspan extension included fdps-1/FDPS-1 (278 ± 9 vs. 894 ± 17% population activity AUC in knockdown + 1 μM ZA vs. untreated controls, respectively, P < 0.0001), daf-16/FOXO (680 ± 16 vs. 894 ± 17%, P < 0.01) and agxt-2/BAIBA (531 ± 23 vs. 552 ± 8%, P > 0.05). Life/healthspan was extended through knockdown of igdb-1/FNDC5 (635 ± 10 vs. 523 ± 10% population activity AUC in gene knockdown vs. untreated controls, P < 0.01) and sir-2.3/SIRT-4 (586 ± 10 vs. 523 ± 10%, P < 0.05), with no synergistic improvements in ZA co-treatment vs. knockdown alone [651 ± 12 vs. 635 ± 10% (igdb-1/FNDC5) and 583 ± 9 vs. 586 ± 10% (sir-2.3/SIRT-4), both P > 0.05]. Conversely, let-756/FGF21 and sir-2.2/SIRT-4 were dispensable for ZA-induced healthspan [630 ± 6 vs. 523 ± 10% population activity AUC in knockdown + 1 μM ZA vs. untreated controls, P < 0.01 (let-756/FGF21) and 568 ± 9 vs. 523 ± 10%, P < 0.05 (sir-2.2/SIRT-4)].
    Conclusions: Despite lacking an endoskeleton, ZA delays Caenorhabditis elegans sarcopenia, which translates to improved neuromuscular function across the life course. Bisphosphonates might, therefore, be an immediately exploitable anti-sarcopenia therapy.
    MeSH term(s) Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans Proteins/genetics ; Diphosphonates/pharmacology ; Diphosphonates/therapeutic use ; Sarcopenia ; Quality of Life ; Muscles
    Chemical Substances Caenorhabditis elegans Proteins ; Diphosphonates
    Language English
    Publishing date 2023-09-18
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 2586864-0
    ISSN 2190-6009 ; 2190-5991
    ISSN (online) 2190-6009
    ISSN 2190-5991
    DOI 10.1002/jcsm.13335
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