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Intramuscular Anabolic Signaling and Endocrine Response Following Different Resistance Exercise Protocols In Trained MenGonzalez, Adam 01 January 2015 (has links)
The mammalian/mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway appears to be the primary regulator of protein synthesis and growth. While resistance exercise paradigms are often divided into hypertrophy (HYP) and strength (STR) protocols, it is unknown whether these protocols differentially stimulate mTORC1 signaling. The purpose of this study was to examine mTORC1 signaling in conjunction with circulating hormone concentrations following a typical lower-body HYP and STR resistance exercise protocol. Ten resistance-trained men (24.7±3.4y; 90.1±11.3kg; 176.0±4.9cm) performed each resistance exercise protocol in a random, counterbalanced order. Blood samples were obtained at baseline (BL), immediately (IP), 30 minutes (30P), 1 hour (1H), 2 hours (2H), and 5 hours (5H) post-exercise. Fine needle muscle biopsies were completed at BL, 1H, and 5H. Electromyography of the vastus lateralis was also recorded during each protocol. HYP and STR produced a similar magnitude of muscle activation across sets. Myoglobin and lactate dehydrogenase concentrations were significantly greater following STR compared to HYP (p=0.01-0.02), whereas the lactate response was significantly higher following HYP compared to STR (p=0.003). The GH, cortisol, and insulin responses were significantly greater following HYP compared to STR (p=0.0001-0.04). No significant differences between protocols were observed for the IGF-1 or testosterone response. Intramuscular anabolic signaling analysis revealed a significantly greater (p=0.03) phosphorylation of IGF-1 receptor at 1H following HYP compared to STR. Phosphorylation status of all other signaling proteins including mTOR (mammalian target of rapamycin), p70S6k (ribosomal S6 kinase 1), and RPS6 (ribosomal protein S6) were not significantly different between trials. Despite significant differences in markers of muscle damage and the endocrine response following STR and HYP, both protocols appeared to elicit similar mTORC1 activation in resistance-trained men.
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The role of NCOA4-mediated ferritinophagy in iron overloadDorman, Matthew J. 31 January 2023 (has links)
Iron homeostasis is a vital process that balances access to free iron to fuel physiological processes with iron storage to reduce the deleterious aspects of excess free iron. Dysfunctional iron homeostasis can lead to iron overload, in which excess free iron can promote cellular injury, ferroptosis, and eventual organ damage as a result. The cellular consequences of long-term iron overload including the cellular pathways that lead to pathological changes or those that may provide protection against damage are incompletely defined. Here, we use dietary and genetically engineered mouse models of iron overload combined with mass spectrometry-based quantitative proteomics to determine the iron overload liver proteome. We identify and quantify over 8,000 proteins representing the most in-depth iron overload proteome evaluation to date. Using bioinformatics, we identify conserved upregulated pathways including ‘response to oxidative stress’ and downregulated pathways including ‘steroid homeostasis.’ Furthermore, we identify an unexpected role for NCOA4, an autophagy adaptor that targets ferritin for autophagic degradation during iron deprivation, during iron overload. This work highlights the importance of further investigation into NCOA4 and its role in diseases of iron overload. / 2025-01-30T00:00:00Z
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Promotion of Neuronal Regeneration: Upregulation of Intrinsic Neuronal Growth Capacity versus Microtubule StabilizationLe, Cathy 01 January 2020 (has links)
Central Nervous System (CNS) injury may lead to irreversible damage to cognitive and motor abilities when injured. This is due to the inability of axons to regenerate. This thesis focuses on two methods of promoting axonal regeneration: microtubule stabilization and upregulation of the intrinsic growth capacity of the neuron via the mechanistic target of rapamycin (mTOR) pathway. Both have shown promising results in potentially being a therapeutic treatment for CNS trauma. This research seeks to (1) test a combinatorial method of axonal regeneration utilizing both methods simultaneously and (2) compare microtubule stabilization and upregulation of the mTOR pathway as neuronal regeneration methods. Aim 1 serves to test the combinatorial treatment of Taxol, a microtubule stabilizer, and cRheb transfection, which upregulates the mTOR pathway, on neuronal cell cultures. Cells were cultured in either a growth-promoting substrate or a mix of growth-promoting and growth-inhibitory substrates. The results of this study revealed combinatorial treatment of 2DIV Taxol application with cRheb transfection as a promising treatment that yielded significantly greater axonal outgrowth than either treatment alone. Aim 2 serves to compare the two established methods of axonal regeneration in the scientific community. Based off of a meta-analysis, results of this aim indicate upregulation of mTOR is more effective at promoting axonal regeneration than microtubule stabilization.
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THE ANALYSIS AND UTILIZATION OF GLOBAL GENE EXPRESSION DATA FOR THE STUDY AND TREATMENT OF BREAST CANCERMosley, Jonathan D. 13 July 2007 (has links)
No description available.
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mTOR Regulation of Hippocampal Granule Cell Pathology in Temporal Lobe EpilepsyHester, Michael S. January 2014 (has links)
No description available.
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Role of autophagy in normal and malignant hematopoiesisChen, Xiaoyi 16 June 2017 (has links)
No description available.
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OSTEOACTIVIN PLAYS A NOVEL ROLE IN AUTOPHAGY-MEDIATED BONE HOMEOSTASISJaber, Fatima A. 17 April 2018 (has links)
No description available.
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Development and Maturation of Endocrine Cells of the Gastrointestinal SystemSinagoga, Katie Lynn January 2017 (has links)
No description available.
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Identification of Targeted Therapeutics for Malignant Peripheral Nerve Sheath TumorsJohansson, L. Gunnar 26 September 2008 (has links)
No description available.
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Inhibition of mTOR for the treatment and prevention of lung cancerMemmott, Regan 05 August 2010 (has links)
No description available.
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