Browsing by Subject "Aged, 80 and over"
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Item A Machine Learning Approach to Identify Predictors of Potentially Inappropriate Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Use in Older Adults with Osteoarthritis(MDPI, 2020-12-28) Patel, Jayeshkumar; Ladani, Amit; Sambamoorthi, Nethra; LeMasters, Traci; Dwibedi, Nilanjana; Sambamoorthi, UshaEvidence from some studies suggest that osteoarthritis (OA) patients are often prescribed non-steroidal anti-inflammatory drugs (NSAIDs) that are not in accordance with their cardiovascular (CV) or gastrointestinal (GI) risk profiles. However, no such study has been carried out in the United States. Therefore, we sought to examine the prevalence and predictors of potentially inappropriate NSAIDs use in older adults (age > 65) with OA using machine learning with real-world data from Optum De-identified Clinformatics((R)) Data Mart. We identified a retrospective cohort of eligible individuals using data from 2015 (baseline) and 2016 (follow-up). Potentially inappropriate NSAIDs use was identified using the type (COX-2 selective vs. non-selective) and length of NSAIDs use and an individual's CV and GI risk. Predictors of potentially inappropriate NSAIDs use were identified using eXtreme Gradient Boosting. Our study cohort comprised of 44,990 individuals (mean age 75.9 years). We found that 12.8% individuals had potentially inappropriate NSAIDs use, but the rate was disproportionately higher (44.5%) in individuals at low CV/high GI risk. Longer duration of NSAIDs use during baseline (AOR 1.02; 95% CI:1.02-1.02 for both non-selective and selective NSAIDs) was associated with a higher risk of potentially inappropriate NSAIDs use. Additionally, individuals with low CV/high GI (AOR 1.34; 95% CI:1.20-1.50) and high CV/low GI risk (AOR 1.61; 95% CI:1.34-1.93) were also more likely to have potentially inappropriate NSAIDs use. Heightened surveillance of older adults with OA requiring NSAIDs is warranted.Item Neuroprotective and neurotoxic outcomes of androgens and estrogens in an oxidative stress environment(BioMed Central Ltd., 2020-03-29) Duong, Phong; Tenkorang, Mavis A. A.; Trieu, Jenny; McCuiston, Clayton; Rybalchenko, Nataliya; Cunningham, Rebecca L.BACKGROUND: The role of sex hormones on cellular function is unclear. Studies show androgens and estrogens are protective in the CNS, whereas other studies found no effects or damaging effects. Furthermore, sex differences have been observed in multiple oxidative stress-associated CNS disorders, such as Alzheimer's disease, depression, and Parkinson's disease. The goal of this study is to examine the relationship between sex hormones (i.e., androgens and estrogens) and oxidative stress on cell viability. METHODS: N27 and PC12 neuronal and C6 glial phenotypic cell lines were used. N27 cells are female rat derived, whereas PC12 cells and C6 cells are male rat derived. These cells express estrogen receptors and the membrane-associated androgen receptor variant, AR45, but not the full-length androgen receptor. N27, PC12, and C6 cells were exposed to sex hormones either before or after an oxidative stressor to examine neuroprotective and neurotoxic properties, respectively. Estrogen receptor and androgen receptor inhibitors were used to determine the mechanisms mediating hormone-oxidative stress interactions on cell viability. Since the presence of AR45 in the human brain tissue was unknown, we examined the postmortem brain tissue from men and women for AR45 protein expression. RESULTS: Neither androgens nor estrogens were protective against subsequent oxidative stress insults in glial cells. However, these hormones exhibited neuroprotective properties in neuronal N27 and PC12 cells via the estrogen receptor. Interestingly, a window of opportunity exists for sex hormone neuroprotection, wherein temporary hormone deprivation blocked neuroprotection by sex hormones. However, if sex hormones are applied following an oxidative stressor, they exacerbated oxidative stress-induced cell loss in neuronal and glial cells. CONCLUSIONS: Sex hormone action on cell viability is dependent on the cellular environment. In healthy neuronal cells, sex hormones are protective against oxidative stress insults via the estrogen receptor, regardless of sex chromosome complement (XX, XY). However, in unhealthy (e.g., high oxidative stress) cells, sex hormones exacerbated oxidative stress-induced cell loss, regardless of cell type or sex chromosome complement. The non-genomic AR45 receptor, which is present in humans, mediated androgen's damaging effects, but it is unknown which receptor mediated estrogen's damaging effects. These differential effects of sex hormones that are dependent on the cellular environment, receptor profile, and cell type may mediate the observed sex differences in oxidative stress-associated CNS disorders.Item Shorter length of hospital stay for hip fracture in those with dementia and without a known diagnosis of osteoporosis in the USA(BioMed Central Ltd., 2020-12-03) Rasu, Rafia S.; Zalmai, Rana; Karpes Matusevich, Aliza R.; Hunt, Suzanne L.; Phadnis, Milind A.; Rianon, NahidBACKGROUND: About 50% of all hospitalized fragility fracture cases in older Americans are hip fractures. Approximately 3/4 of fracture-related costs in the USA are attributable to hip fractures, and these are mostly covered by Medicare. Hip fracture patients with dementia, including Alzheimer's disease, have worse health outcomes including longer hospital length of stay (LOS) and charges. LOS and hospital charges for dementia patients are usually higher than for those without dementia. Research describing LOS and acute care charges for hip fractures has mostly focused on these outcomes in trauma patients without a known pre-admission diagnosis of osteoporosis (OP). Lack of documented diagnosis put patients at risk of not having an appropriate treatment plan for OP. Whether having a diagnosis of OP would have an effect on hospital outcomes in dementia patients has not been explored. We aim to investigate whether having a diagnosis of OP, dementia, or both has an effect on LOS and hospital charges. In addition, we also report prevalence of common comorbidities in the study population and their effects on hospital outcomes. METHODS: We conducted a cross-sectional analysis of claims data (2012-2013) for 2175 Medicare beneficiaries (>/=65 years) in the USA. RESULTS: Compared to those without OP or dementia, patients with demenia only had a shorter LOS (by 5%; P = .04). Median LOS was 6 days (interquartile range [IQR]: 5-7), and the median hospital charges were $45,100 (IQR: 31,500 - 65,600). In general, White patients had a shorter LOS (by 7%), and those with CHF and ischemic heart disease (IHD) had longer LOS (by 7 and 4%, respectively). Hospital charges were 6% lower for women, and 16% lower for White patients. CONCLUSION: This is the first study evaluating LOS in dementia in the context of hip fracture which also disagrees with previous reporting about longer LOS in dementia patients. Patients with CHF and IHD remains at high risk for longer LOS regardless of their diagnosis of dementia or OP.Item Water T2 as an early, global and practical biomarker for metabolic syndrome: an observational cross-sectional study(BioMed Central Ltd., 2017-12-19) Robinson, Michelle D.; Mishra, Ina; Deodhar, Sneha; Patel, Vipulkumar; Gordon, Katrina V.; Vintimilla, Raul; Brown, Kim; Johnson, Leigh A.; O'Bryant, Sid E.; Cistola, David P.BACKGROUND: Metabolic syndrome (MetS) is a highly prevalent condition that identifies individuals at risk for type 2 diabetes mellitus and atherosclerotic cardiovascular disease. Prevention of these diseases relies on early detection and intervention in order to preserve pancreatic beta-cells and arterial wall integrity. Yet, the clinical criteria for MetS are insensitive to the early-stage insulin resistance, inflammation, cholesterol and clotting factor abnormalities that characterize the progression toward type 2 diabetes and atherosclerosis. Here we report the discovery and initial characterization of an atypical new biomarker that detects these early conditions with just one measurement. METHODS: Water T2, measured in a few minutes using benchtop nuclear magnetic resonance relaxometry, is exquisitely sensitive to metabolic shifts in the blood proteome. In an observational cross-sectional study of 72 non-diabetic human subjects, the association of plasma and serum water T2 values with over 130 blood biomarkers was analyzed using bivariate, multivariate and logistic regression. RESULTS: Plasma and serum water T2 exhibited strong bivariate correlations with markers of insulin, lipids, inflammation, coagulation and electrolyte balance. After correcting for confounders, low water T2 values were independently and additively associated with fasting hyperinsulinemia, dyslipidemia and subclinical inflammation. Plasma water T2 exhibited 100% sensitivity and 87% specificity for detecting early insulin resistance in normoglycemic subjects, as defined by the McAuley Index. Sixteen normoglycemic subjects with early metabolic abnormalities (22% of the study population) were identified by low water T2 values. Thirteen of the 16 did not meet the harmonized clinical criteria for metabolic syndrome and would have been missed by conventional screening for diabetes risk. Low water T2 values were associated with increases in the mean concentrations of 6 of the 16 most abundant acute phase proteins and lipoproteins in plasma. CONCLUSIONS: Water T2 detects a constellation of early abnormalities associated with metabolic syndrome, providing a global view of an individual's metabolic health. It circumvents the pitfalls associated with fasting glucose and hemoglobin A1c and the limitations of the current clinical criteria for metabolic syndrome. Water T2 shows promise as an early, global and practical screening tool for the identification of individuals at risk for diabetes and atherosclerosis.