Search Results - "Ness, Emily C"
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1212-P: Cost-Related Medication Nonadherence in Alabama's Medicaid Population with Diabetes
Published in Diabetes (New York, N.Y.) (01-06-2022)“…Background: Cost-related medication nonadherence (CRMN) occurs when an individual takes less medication than what is prescribed due to difficulty affording…”
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Late mortality after bone marrow transplant for chronic myelogenous leukemia in the context of prior tyrosine kinase inhibitor exposure: A Blood or Marrow Transplant Survivor Study (BMTSS) report
Published in Cancer (15-11-2019)“…Background Late mortality was investigated in patients with chronic myelogenous leukemia (CML) who underwent blood or bone marrow transplant (BMT) with or…”
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Inter-α-inhibitor blocks epithelial sodium channel activation and decreases nasal potential differences in ΔF508 mice
Published in American journal of respiratory cell and molecular biology (01-05-2014)“…Increased activity of lung epithelial sodium channels (ENaCs) contributes to the pathophysiology of cystic fibrosis (CF) by increasing the rate of epithelial…”
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Journal Article -
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Long-Term Morbidity and Mortality Experienced By Chronic Myeloid Leukemia (CML) Patients after Allogeneic Hematopoietic Cell Transplantation (HCT) - a Report from BMTSS-2
Published in Blood (02-12-2016)“…▪ Background: Tyrosine kinase inhibitors have become the treatment of choice for CML. However, the high cost and need for life-long treatment contribute to…”
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Progressive Decline in Late Mortality after Hematopoietic Cell Transplantation (HCT) over 40 Years - a Report from BMTSS
Published in Blood (02-12-2016)“…Background: The high intensity of therapeutic exposures (for autologous and allogeneic HCT) and chronic GvHD and its management (in allogeneic HCT) increase…”
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Inter-[alpha]-Inhibitor Blocks Epithelial Sodium Channel Activation and Decreases Nasal Potential Differences in [Delta]F508 Mice
Published in American journal of respiratory cell and molecular biology (01-05-2014)“…Increased activity of lung epithelial sodium channels (ENaCs) contributes to the pathophysiology of cystic fibrosis (CF) by increasing the rate of epithelial…”
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Journal Article