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Full-Text Articles in Engineering
Friend Or Foe? The Role Of Transforming Growth Factor-Β (Tgfβ) Signaling In Calcineurin Inhibitor-Induced Renal Damage, Adaku Ume
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With its incorporation into clinical practice in the early 1980s, the class of pharmacological agents known as calcineurin inhibitors (CNIs) quickly became the cornerstone of immunosuppressive therapy post-organ transplantation. However, its use is limited by irreversible kidney damage in the form of renal fibrosis. The molecular mechanism by which CNIs induce renal fibrosis remains to be better understood, and to date, there are no specific therapeutic strategies to mitigate this damage. This dilemma presents a critical need to explain mechanisms by which CNIs cause renal damage. Kidneys of patients on chronic CNI therapy show increased expression of the proinflammatory cytokine …
Identifying A Novel Ferrocene Derivative As A K-Ras Inhibitor, Kristen Marie Rehl
Identifying A Novel Ferrocene Derivative As A K-Ras Inhibitor, Kristen Marie Rehl
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Ras proteins are small GTPases that regulate cell proliferation, differentiation and survival at the plasma membrane (PM). There are three Ras isoforms ubiquitously expressed in mammalian cells: H-, N- and K-Ras. Constitutively active Ras mutations are found in ~19% of all human cancers, with ~75% of those being in K-Ras. There are K-Ras inhibitors in clinic but they only target the oncogenic K-RasG12C mutant, which only makes up a small sub-set of K-Ras-driven cancers. Thus, there still exists a need for a pan anti-K-Ras drug. Ferrocene derivatives are a class of compounds that have been shown to inhibit the growth …
Contributors To Pathologic Depolarization In Myotonia Congenita, Jessica Hope Myers
Contributors To Pathologic Depolarization In Myotonia Congenita, Jessica Hope Myers
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Myotonia congenita is an inherited skeletal muscle disorder caused by loss-of-function mutation in the CLCN1 gene. This gene encodes the ClC-1 chloride channel, which is almost exclusively expressed in skeletal muscle where it acts to stabilize the resting membrane potential. Loss of this chloride channel leads to skeletal muscle hyperexcitability, resulting in involuntary muscle action potentials (myotonic discharges) seen clinically as muscle stiffness (myotonia). Stiffness affects the limb and facial muscles, though specific muscle involvement can vary between patients. Interestingly, respiratory distress is not part of this disease despite muscles of respiration such as the diaphragm muscle also carrying this …
Monitoring Blood Flow In Animal Models Using A Camera-Based Technique, Dharminder Singh Langri
Monitoring Blood Flow In Animal Models Using A Camera-Based Technique, Dharminder Singh Langri
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Blood flow dynamics plays a critical role in maintaining tissue health, as it delivers nutrients and oxygen while removing waste products. It is especially important when there is a disruption in cerebral autoregulation due to trauma, which can induce ischemia or hyperemia and can lead to secondary brain injury. Thus, there is a need for noninvasive techniques that can allow continuous monitoring of blood flow during intervention. Optical techniques have become increasingly practical for measuring blood flow due to their non-invasive, continuous, and relatively lower-cost nature. This research focused on developing a low-cost, scalable optical technique for measuring blood flow …
Friend Or Foe? The Role Of Transforming Growth Factor-Β (Tgfβ) Signaling In Calcineurin Inhibitor-Induced Renal Damage, Adaku Uwe
Browse all Theses and Dissertations
With its incorporation into clinical practice in the early 1980s, the class of pharmacological agents known as calcineurin inhibitors (CNIs) quickly became the cornerstone of immunosuppressive therapy post-organ transplantation. However, its use is limited by irreversible kidney damage in the form of renal fibrosis. The molecular mechanism by which CNIs induce renal fibrosis remains to be better understood, and to date, there are no specific therapeutic strategies to mitigate this damage. This dilemma presents a critical need to explain mechanisms by which CNIs cause renal damage. Kidneys of patients on chronic CNI therapy show increased expression of the proinflammatory cytokine …