Publications by authors named "Nicole Reed"

Background: While the advantages of using the internet and social media for research recruitment are well documented, the evolving online environment also enhances motivations for misrepresentation to receive incentives or to "troll" research studies. Such fraudulent assaults can compromise data integrity, with substantial losses in project time; money; and especially for vulnerable populations, research trust. With the rapid advent of new technology and ever-evolving social media platforms, it has become easier for misrepresentation to occur within online data collection.

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Native WYSE CHOICES adapted an Alcohol Exposed Pregnancy (AEP) prevention curriculum for mobile health delivery for young urban American Indian and Alaska Native (AIAN) women. This qualitative study explored the relevance of culture in adapting a health intervention with a national sample of urban AIAN youth. In total, the team conducted 29 interviews across three iterative rounds.

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Background: Fetal Alcohol Spectrum Disorders (FASD) result in lifelong disability and are a leading cause of preventable birth defects in the US, including for American Indian and Alaska Natives (AIANs). Prevention of alcohol exposed pregnancies (AEPs), which can cause FASD, is typically aimed at adult women who are risky drinkers and have unprotected sex. Among AIANs, AEP prevention research has been primarily conducted in reservation communities, even though over 70% of AIANs live in urban areas.

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Health advocates are increasingly using social media and mobile technology to reach American Indian and Alaska Native (AI/AN) youth to address important health topics and enhance protective factors. Public health experts did not know to what extent AI/AN youth used these tools to access health resources during the pandemic. The Native Youth Health Tech Survey was administered online from October to November 2020 with 349 AI/AN youth 15 to 24 years old.

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Background: Community-based participatory research is a particularly powerful approach to research with American Indian and Alaska Native (AIAN) communities who have been subject to a history of mistreatment and unethical research. In person meetings, discussion, and engagement with tribal members and the community have become an essential component of community-based participatory research in AIAN communities. With the advent of the coronavirus disease 2019 pandemic, AIAN communities have moved to close or sharply curtail in-person activities, precluding in-person research methods.

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Sporadic inclusion body myositis (IBM) is the most common acquired muscle disease in adults over age 50, yet it remains unclear whether the disease is primarily driven by T cell–mediated autoimmunity. IBM muscle biopsies display nuclear clearance and cytoplasmic aggregation of TDP-43 in muscle cells, a pathologic finding observed initially in neurodegenerative diseases, where nuclear loss of TDP-43 in neurons causes aberrant RNA splicing. Here, we show that loss of TDP-43–mediated splicing repression, as determined by inclusion of cryptic exons, occurs in skeletal muscle of subjects with IBM.

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The M7.5 Palu-Donggala earthquake occurred on 28 September 2018 and caused significant damage in Palu City and the surrounding Central Sulawesi region of Indonesia. The earthquake initiated a series of catastrophic landslides (classified as ) [1,2], collapsed buildings, and generated tsunami waves that impacted Palu Bay's coast.

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Cisplatin is a commonly used chemotherapy agent with significant dose-limiting neurotoxicity resulting in peripheral neuropathy. Although it is postulated that formation of DNA-platinum adducts is responsible for both its cytotoxicity in cancer cells and side effects in neurons, downstream mechanisms that lead to distal axonal degeneration are unknown. Here we show that activation of calpains is required for both neurotoxicity and formation of DNA-platinum adduct formation in neurons but not in cancer cells.

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Distal axon degeneration seen in many peripheral neuropathies is likely to share common molecular mechanisms with Wallerian degeneration. Although several studies in mouse models of peripheral neuropathy showed prevention of axon degeneration in the slow Wallerian degeneration (Wlds) mouse, the role of a recently identified player in Wallerian degeneration, Sarm1, has not been explored extensively. In this study, we show that mice lacking the Sarm1 gene are resistant to distal axonal degeneration in a model of chemotherapy induced peripheral neuropathy caused by paclitaxel and a model of high fat diet induced putative metabolic neuropathy.

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Ethoxyquin was recently identified as a neuroprotective compound against toxic neuropathies and efficacy was demonstrated against paclitaxel-induced neurotoxicity in vivo. In this study we examined the efficacy of ethoxyquin in preventing neurotoxicity of cisplatin in rodent models of chemotherapy-induced peripheral neuropathy and explored its mechanism of action. Ethoxyquin prevented neurotoxicity of cisplatin in vitro in a sensory neuronal cell line and primary rat dorsal root ganglion neurons.

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Previous studies demonstrated that Schwann cells (SCs) express distinct motor and sensory phenotypes, which impact the ability of these pathways to selectively support regenerating neurons. In the present study, unbiased microarray analysis was used to examine differential gene expression in denervated motor and sensory pathways in rats. Several genes that were significantly upregulated in either denervated sensory or motor pathways were identified and two secreted factors were selected for further analysis: osteopontin (OPN) and clusterin (CLU) which were upregulated in denervated motor and sensory pathways, respectively.

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Objective: Peripheral neurotoxicity is a major dose-limiting side effect of many chemotherapeutic drugs. Currently there are no effective disease-modifying therapies for chemotherapy-induced peripheral neuropathies, but these side effects of chemotherapy are potentially ideal targets for development of neuroprotective therapies, because candidate drugs can be co- or preadministered before the injury to peripheral axons takes place.

Methods: We used a phenotypic drug screening approach to identify ethoxyquin as a potential neuroprotective drug and carried out additional biochemical experiments to identify its mechanism of action.

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Nitric oxide (NO) is a signaling molecule that can trigger adaptive (physiological) or maladaptive (pathological) responses to stress stimuli in a context-dependent manner. We have previously reported that NO may signal axonal injury to neighboring glial cells. In this study, we show that mice deficient in neuronal nitric oxide synthase (nNOS-/-) are more vulnerable than WT mice to toxin-induced peripheral neuropathy.

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The tryptophans of integral membrane proteins have been suggested to play specific roles as "interfacial anchors", based on their preference for a location near the lipid head groups. Still, the underlying mechanism behind this behavior remains unclear. NMR experiments can provide an important tool to study this interaction in an actual bilayer environment.

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Clinically relevant peripheral neuropathies (such as diabetic and human immunodeficiency virus sensory neuropathies) are characterized by distal axonal degeneration, rather than neuronal death. Here, we describe a novel, endogenous pathway that prevents axonal degeneration. We show that in response to axonal injury, periaxonal Schwann cells release erythropoietin (EPO), which via EPO receptor binding on neurons, prevents axonal degeneration.

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