Publications by authors named "Sherry Dadgar"

The long-term mortality of patients with kidney failure remains unacceptably high. There are a multitude of reasons for the unfavorable status quo of dialysis care, such as the inadequate and suboptimal pattern of uremic toxin removal resulting in a metabolic and hemodynamic "roller coaster" induced by thrice-weekly in-center hemodialysis. Innovation in dialysis delivery systems is needed to build an adaptive and self-improving process to change the status quo of dialysis care with the aim of transforming it from being reactive to being proactive.

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Desirable outcomes including rejection- and infection-free kidney transplantation are not guaranteed despite current strategies for immunosuppression and using prophylactic antimicrobial medications. Graft survival depends on factors beyond human leukocyte antigen matching such as the level of immunosuppression, infections, and management of other comorbidities. Risk stratification of transplant patients based on predisposing genetic modifiers and applying precision pharmacotherapy may help improving the transplant outcomes.

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What is the central question of this study? What is the functional relevance of OPN isoform expression in muscle pathology? What is the main finding and its importance? The full-length human OPN-a isoform is the most pro-inflammatory isoform in the muscle microenvironment, acting on macrophages and myoblasts in an RGD-integrin-dependent manner. OPN-a upregulates expression of tenascin-C (TNC), a known Toll-like receptor 4 (TLR4) agonist. Blocking TLR4 signalling inhibits the pro-inflammatory effects of OPN-a, suggesting that a potential mechanism of OPN action is by promoting TNC-TLR4 signalling.

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Article Synopsis
  • The study investigates why muscle regeneration fails in dystrophic muscle by using data from human dystrophy and mouse models.
  • It reveals that transforming growth factor β networks, which are linked to fibrosis and poor regeneration, are activated during normal muscle repair but at different times.
  • By creating an experimental model that mimics differing regeneration rates, the researchers found that specific treatments improved muscle recovery, suggesting the model could help understand tissue failure in other chronic conditions.
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Article Synopsis
  • The absence of dystrophin in Duchenne muscular dystrophy (DMD) makes muscles vulnerable to injury, leading to cell membrane damage and ongoing inflammation, while current glucocorticoid treatments pose significant side effects and unclear benefits.
  • Researchers discovered a new oral drug, VBP15, that provides muscle protection and promotes repair through anti-inflammatory and membrane-stabilizing actions, without triggering hormonal or immune suppression.
  • In DMD model mice, VBP15 demonstrated improved muscle strength and pathology, suggesting it could be a promising option for clinical use in DMD and other chronic inflammatory conditions.
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Background: Mitochondrial activity inhibits proliferation and is required for differentiation of myoblasts. Myoblast proliferation is also inhibited by the ~20% oxygen level used in standard tissue culture. We hypothesize that mitochondrial activity would be greater at hyperoxia (20% O(2)) relative to more physiological oxygen (5% O(2)).

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Uncharacterized open reading frames (ORFs) in human genomic sequence often show a high degree of evolutionary conservation, yet have little or no tissue EST or protein data suggestive of protein product function. The encoded proteins may have highly restricted expression in specialized cells, subcellular specializations, and/or narrow windows during development. One such highly specialized and minute subcellular compartment is the neuromuscular junction (NMJ), where motorneurons contact muscle fibers.

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Background: To date, there are no criteria for diagnosing autosomal dominant polycystic kidney disease (ADPKD) in at-risk children 15 years or younger.

Study Design: Longitudinal (retrospective cohort study).

Setting & Participants: 420 children (mean age, 8.

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Chromatin remodeling is an essential event for HIV-1 transcription. Over the last two decades this field of research has come to the forefront, as silencing of the HIV-1 provirus through chromatin modifications has been linked to latency. Here, we focus on chromatin remodeling, especially in relation to the transactivator Tat, and review the most important and newly emerging studies that investigate remodeling mechanisms.

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