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3 results on '"Louisa Smitherman"'

1. The feasibility of health professional student delivered social visits for stroke survivors with loneliness

Author

Jason Burnett, Jordan Broussard, Bronson Ciavarra, Louisa Smitherman, Mary Li, Emma Thames, Sharon Zachariah, Grace Kim, Rachel Pijnnaken, Hannah Zeller, John Halphen, Sean I. Savitz, Namkee Choi, and Jennifer E. S. Beauchamp

Subjects
stroke, loneliness, social isolation (SI), student-led, social connectedness, Medicine
Abstract

ObjectivesTo examine the feasibility of a social phone call program to address social isolation and loneliness in stroke survivors.Materials and methodsWe paired 14 lonely community-living stroke survivors with 14 health professional students for 6-weekly unstructured social phone calls. Feasibility data and measures of social isolation, loneliness and other psychosocial metrics were collected pre- and post-intervention. Students journaled following each unstructured call to capture the informal conversation and their sentiments.ResultsSixty-two percent of the targeted sample was interested. Fourteen eligible and interested participants were enrolled. The 13 (93%) participants completing all calls and surveys were an average of 57 years old, 85% female, and 77% non-Hispanic white. At baseline, participants were highly lonely and moderately depressed. Participants disclosed physical and emotional challenges, previous valued employment, and enjoyment from the calls. Students reported enjoying the connections, learning about the struggles of aging-in-place after stroke, and valuing compassionate care for the stroke population.ConclusionsKnowledge gaps remain regarding effective social support interventions to provide continuity of care directed at managing social disconnection after stroke. A health professional student-delivered social phone call intervention with stroke survivors appears to be a feasible, in part, and encouraging approach for addressing social isolation and loneliness. Future trials require re-evaluation of eligibility criteria and strategies to boost enrollment before efficacy testing is conducted in a larger trial.

Published
2024
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2. The TP53-Induced Glycolysis and Apoptosis Regulator mediates cooperation between HTLV-1 p30II and the retroviral oncoproteins Tax and HBZ and is highly expressed in an in vivo xenograft model of HTLV-1-induced lymphoma

Author

Rachel Bergeson, Carolyn K. Harrod, Jordan Pope, Tetiana Hutchison, Lee Ratner, Louisa Smitherman, Courtney Yates, Lacin Yapindi, Wesleigh Gwinn, Kendra Peck, Megan Romeo, Robert Harrod, and Aditi Malu

Subjects
0301 basic medicine, Oncogene, Apoptosis Regulator, Angiogenesis, Biology, medicine.disease, medicine.disease_cause, Virus, Lymphoma, 03 medical and health sciences, Leukemia, 030104 developmental biology, hemic and lymphatic diseases, Virology, medicine, Cancer research, Carcinogenesis, Cytotoxicity
Abstract

The human T-cell leukemia virus type-1 (HTLV-1) is an oncoretrovirus that infects and transforms CD4+ T-cells and causes adult T-cell leukemia/lymphoma (ATLL) -an aggressive lymphoproliferative disease that is highly refractive to most anticancer therapies. The HTLV-1 proviral genome encodes several regulatory products within a conserved 3' nucleotide sequence, known as pX; however, it remains unclear how these factors might cooperate or dynamically interact in virus-infected cells. Here we demonstrate that the HTLV-1 latency-maintenance factor p30II induces the TP53-induced glycolysis and apoptosis regulator (TIGAR) and counters the oxidative stress, mitochondrial damage, and cytotoxicity caused by the viral oncoproteins Tax and HBZ. The p30II protein cooperates with Tax and HBZ and enhances their oncogenic potential in colony transformation/foci-formation assays. Further, we have shown that TIGAR is highly expressed in HTLV-1-induced tumors associated with oncogene dysregulation and increased angiogenesis in an in vivo xenograft model of HTLV-1-induced T-cell lymphoma. These findings provide the first evidence that p30II likely collaborates as an ancillary factor for the major oncoproteins Tax and HBZ during retroviral carcinogenesis.

Published
2018

3. The TP53-Induced Glycolysis and Apoptosis Regulator mediates cooperation between HTLV-1 p30

Author

Tetiana, Hutchison, Aditi, Malu, Laçin, Yapindi, Rachel, Bergeson, Kendra, Peck, Megan, Romeo, Carolyn, Harrod, Jordan, Pope, Louisa, Smitherman, Wesleigh, Gwinn, Lee, Ratner, Courtney, Yates, and Robert, Harrod

Subjects
CD4-Positive T-Lymphocytes, Gene Expression Regulation, Viral, Human T-lymphotropic virus 1, Lymphoma, Neovascularization, Pathologic, Carcinogenesis, viruses, Genes, pX, Intracellular Signaling Peptides and Proteins, Mitophagy, Retroviridae Proteins, Gene Products, tax, Phosphoric Monoester Hydrolases, Article, Mice, Oxidative Stress, Basic-Leucine Zipper Transcription Factors, hemic and lymphatic diseases, Animals, Heterografts, Humans, Apoptosis Regulatory Proteins, Reactive Oxygen Species
Abstract

The human T-cell leukemia virus type-1 (HTLV-1) is an oncoretrovirus that infects and transforms CD4+ T-cells and causes adult T-cell leukemia/lymphoma (ATLL) –an aggressive lymphoproliferative disease that is highly refractive to most anticancer therapies. The HTLV-1 proviral genome encodes several regulatory products within a conserved 3′ nucleotide sequence, known as pX; however, it remains unclear how these factors might cooperate or dynamically interact in virus-infected cells. Here we demonstrate that the HTLV-1 latency-maintenance factor p30(II) induces the TP53-induced glycolysis and apoptosis regulator (TIGAR) and counters the oxidative stress, mitochondrial damage, and cytotoxicity caused by the viral oncoproteins Tax and HBZ. The p30(II) protein cooperates with Tax and HBZ and enhances their oncogenic potential in colony transformation/foci-formation assays. Further, we have shown that TIGAR is highly expressed in HTLV-1-induced tumors associated with oncogene dysregulation and increased angiogenesis in an in vivo xenograft model of HTLV-1-induced T-cell lymphoma. These findings provide the first evidence that p30(II) likely collaborates as an ancillary factor for the major oncoproteins Tax and HBZ during retroviral carcinogenesis.

Published
2018

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