Browsing by Author "Myburgh, K. H."

Now showing 1 - 5 of 5
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    Cellular regenerative therapy for acquired noncongenital musculoskeletal disorders
    (South African Medical Association, 2019-08-10) Niesler, C. U.; van de Vyver, M.; Myburgh, K. H.
    ENGLISH ABSTRACT: Stem cells have an inherent capacity to facilitate regeneration; this has led to unprecedented growth in their experimental use in various clinical settings, particularly in patients with diseases with few alternative treatment options. However, their approved clinical use has to date been restricted largely to haematological diseases and epidermal transplantation to treat severe burns. After thorough searching of two databases, this review illuminates the role of stem cell therapy for treatment of musculoskeletal diseases. Research suggests that successful application of stem cells as regenerative mediators is in all likelihood dependent on the ability of endogenous tissue-resident reparative mediators to respond to paracrine signals provided by the applied stem cells. Therefore, an understanding of how the pathological environment influences this process is crucial for the ultimate success of stem cell therapies. The current review presents both the progress and limitations of stem cells as regenerative mediators in the context of musculoskeletal disorders.
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    Endocrine and immune effects of dexamethasone in unilateral total knee replacement
    (SAGE Publications, 2006) Smith, Carine; Erasmus, P. J.; Myburgh, K. H.
    The effect of acute pre-surgery dexamethasone treatment on the inflammatory immune and endocrine responses to orthopaedic surgery was investigated. Whole blood samples were obtained before and 5 days after surgery for immune analysis, and serum was obtained before and 6 h, 3 days and 5 days after surgery for endocrine assessment. Dexamethasone did not affect the post-surgery granulocyte response, but inhibited the increase in monocyte count (an average increase of 38.5% was seen in the control group). Peak C-reactive protein concentration (3 days after surgery) was 51.4% lower in the dexamethasone group than in the control group. Dexamethasone had a major effect on cortisol concentrations and the cortisol:testosterone and cortisol: dehydroepiandrosterone ratios, but no effect on anabolic hormone concentrations. In conclusion, acute pre-surgery dexamethasone reatment may have beneficial effects in the post-surgery period, by limiting the extent of systemic inflammation and the cortisol response.
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    Illuminating the interrelated immune and endocrine adaptations after multiple exposures to short immobilization stress by in vivo blocking of IL-6
    (American Physiological Society, 2006-12) Smith, C.; Wilson, N. W.; Louw, Ann; Myburgh, K. H.
    ACUTE PSYCHOLOGICAL STRESS is known to activate the hypothalamic- pituitary-adrenal (HPA) axis, resulting in transiently increased release of inflammatory cytokines (28) and glucocorticoids (45). In contrast, multiple exposures to stress lead to adaptive responses in target tissues such as liver, skeletal muscle, and immune cells. These responses may be influenced by the severity of the stressor and the duration of the stress exposure. The endocrine and cytokine responses are known to be interrelated but are complex and still incompletely understood.
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    Redox status and muscle pathology in rheumatoid arthritis : insights from various rat hindlimb muscles
    (Hindawi, 2019-03-26) Oyenihi, A. B.; Ollewagen, T.; Myburgh, K. H.; Powrie, Y. S. L.; Smith, C.; Peluso, Ilaria
    Due to atrophy, muscle weakness is a common occurrence in rheumatoid arthritis (RA). The majority of human studies are conducted on the vastus lateralis muscle—a muscle with mixed fiber type—but little comparative data between multiple muscles in either rodent or human models are available. The current study therefore assessed both muscle ultrastructure and selected redox indicators across various muscles in a model of collagen-induced rheumatoid arthritis in female Sprague-Dawley rats. Only three muscles, the gastrocnemius, extensor digitorum longus (EDL), and soleus, had lower muscle mass (38%, 27%, and 25% loss of muscle mass, respectively; all at least P < 0. 01), while the vastus lateralis muscle mass was increased by 35% (P < 0. 01) in RA animals when compared to non-RA controls. However, all four muscles exhibited signs of deterioration indicative of rheumatoid cachexia. Cross-sectional area was similarly reduced in gastrocnemius, EDL, and soleus (60%, 58%, and 64%, respectively; all P < 0. 001), but vastus lateralis (22% smaller, P < 0. 05) was less affected, while collagen deposition was significantly increased in muscles. This pathology was associated with significant increases in tissue levels of reactive oxygen species (ROS) in all muscles except the vastus lateralis, while only the gastrocnemius had significantly increased levels of lipid peroxidation (TBARS) and antioxidant activity (FRAP). Current data illustrates the differential responses of different skeletal muscles of the hindlimb to a chronic inflammatory challenge both in terms of redox changes and resistance to cachexia.
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    Rheumatoid cachexia : the underappreciated role of myoblast, macrophage and fibroblast interplay in the skeletal muscle niche
    (BioMed Central, 2021-03-03) Ollewagen, T.; Myburgh, K. H.; van de Vyver, M.; Smith, C.
    ENGLISH ABSTRACT: Although rheumatoid arthritis affects 1% of the global population, the role of rheumatoid cachexia, which occurs in up to a third of patients, is relatively neglected as research focus, despite its significant contribution to decreased quality of life in patients. A better understanding of the cellular and molecular processes involved in rheumatoid cachexia, as well as its potential treatment, is dependent on elucidation of the intricate interactions of the cells involved, such as myoblasts, fibroblasts and macrophages. Persistent RA-associated inflammation results in a relative depletion of the capacity for regeneration and repair in the satellite cell niche. The repair that does proceed is suboptimal due to dysregulated communication from the other cellular role players in this multi-cellular environment. This includes the incomplete switch in macrophage phenotype resulting in a lingering pro-inflammatory state within the tissues, as well as fibroblast-associated dysregulation of the dynamic control of the extracellular matrix. Additional to this endogenous dysregulation, some treatment strategies for RA may exacerbate muscle wasting and no multi-cell investigation has been done in this context. This review summarizes the most recent literature characterising clinical RA cachexia and links these features to the roles of and complex communication between multiple cellular contributors in the muscle niche, highlighting the importance of a targeted approach to therapeutic intervention.