Trends From 2010 to 2019 in Opioid and Nonopioid Pain Management After Total Knee Arthroplasty.

INTRODUCTION: As the opioid epidemic enters its third decade, we reflect on how it has affected clinical practice within the orthopaedic community. Recent studies show prolonged opioid use after total knee arthroplasty (TKA) is associated with worse overall health outcomes. This study aims to elucidate trends in pain management after TKA over the past decade. METHODS: A retrospective analysis was performed using the PearlDiver database from 2010 to 2019. Patients who underwent primary TKA without a history of mental illness, complex pain syndromes, or opioids used 6 months before surgery were selected. Postoperative prescription filling rates of opioid and nonopioid at 30, 90 days, and 1 year from surgery were analyzed. Linear regression analysis and compound annual growth rates (CAGRs) were analyzed from 2010 to 2019, a P value <0.05 being considered significant. RESULTS: Between 2010 and 2019, 579,269 patients underwent primary TKA. At 30 days, filling of prescriptions for opioids (CAGR = 3.54%) and nonopioids (CAGR = 15.50%) markedly increased from 2010 to 2019. At 90 days, opioids decreased (CAGR = -4.42%). At 1 year, opioid (CAGR = -10.92%) and nonopioid (CAGR = -2.12%) prescriptions markedly decreased from 2010 to 2019. DISCUSSION: This study highlights patterns of decreased opioid prescription rates at 90 days and 1 year postoperatively from 2010 to 2019. Decreasing opioid rates may indicate effectiveness in targeted public health campaigns to curb opioid overuse.

Declining life expectancy in the Great Lakes region: contributors to Black and white longevity change across educational attainment.

BACKGROUND: The East North Central Census division (aka the Great Lakes region) experienced a decrease in life expectancy of 0.3 years from 2014 to 2016 - one of the largest declines across the nine Census divisions. Disadvantaged groups that typically have below-average life expectancy, including Black individuals and those without a college education, may have been disproportionately affected by this longevity shift. This investigation examines life expectancy changes among different sex, race, and education groups in the Great Lakes region, and how specific causes of death contributed to within-group longevity changes over time and across age. METHODS: We used 2008 to 2017 death counts from the National Center for Health Statistics and American Community Survey population estimates to measure within-group change in life expectancy at age 25 among non-Hispanic Black and white males and females by educational attainment. We decomposed life expectancy change over time for each subgroup by 24 causes of death and measured their contribution to longevity change across 13 age groups. RESULTS: Among persons with ≤ 12 years of education, white males and females experienced 1.3- and 1.7-year longevity declines respectively, compared to a 0.6-year decline among Black males and a 0.3-year decline among Black females. Life expectancy declined among all groups with 13-15 years of education, but especially Black females, who experienced a 2.2-year loss. With the exception of Black males, all groups with 16 + years of education experienced longevity gains. Homicide contributed 0.34 years to longevity decline among Black males with ≤ 12 years of education. Drug poisoning made large contributions to longevity losses among Black females with ≤ 12 years of education (0.31 years), white males and females with 13-15 years of education (0.35 and 0.21 years, respectively), and white males and females with ≤ 12 years of education (0.92 and 0.65 years, respectively). CONCLUSIONS: Public health efforts to reduce the risks of homicide among Black males without a college education and drug poisoning among all groups could improve life expectancy and reduce racial and educational longevity disparities in the Great Lakes region.

Using meditation in a control vs. acceptance context: A preliminary evaluation of relations with anxiety, depression, and indices of well-being.

BACKGROUND AND OBJECTIVES: Meditation practices have been marketed broadly to ameliorate human suffering. As such, individuals may seek out and use meditation to control or manage unpleasant thoughts and emotions. Emotion and thought control research suggest that meditation used in this way may potentiate unpleasant private experiences and contribute to negative outcomes. We aimed to evaluate the function or purpose guiding meditation and its relations with anxiety, depression, and other indices of well-being. DESIGN AND METHODS: In a cross-sectional design, undergraduate meditators (N = 98) reported intentions guiding their meditation practice (i.e., experiential/emotional control or acceptance/openness) and completed an assessment battery. RESULTS: Most participants (58.2%) indicated using meditation to manage, control, or avoid difficult experiences. Participants using meditation with control-based intentions reported greater worry, anxiety, depression, negative affect, and lower mindfulness relative to their acceptance-guided counterparts. After controlling for level of anxiety, viewing anxiety as a problem increased the likelihood of using meditation with control-based intentions. Similar relations were observed between viewing stress as a problem and the likelihood of using meditation for experiential control. CONCLUSIONS: Findings suggest that (a) how people meditate is significantly related to psychological distress and (b) highlight the importance of evaluating intentions guiding meditative practices, particularly in individuals struggling with unpleasant emotional or psychological experiences.

Habitual sleep, sleep duration differential, and weight change among adults: Findings from the Wisconsin Sleep Cohort Study.

OBJECTIVES: Assess longitudinal associations between diary-measured sleep duration and clinically assessed body mass index (BMI). DESIGN: Multilevel growth curve analyses examined how within-person changes and between-person differences in habitual sleep duration were associated with BMI trajectories. SETTING: Sleep diaries across 2-6 consecutive weekday and weekend nights at each data collection point, repeatedly collected at approximate 4-year intervals, for an average of 9.2 (standard deviation [SD] = 3.6) years between 1989 and 2011. PARTICIPANTS: About 784 participants (47% women) enrolled in the Wisconsin Sleep Cohort Study (mean [SD] age = 51.1 [8.0] years at baseline). MEASUREMENTS: The outcome variable was BMI (kg/m2). Key predictors were habitual sleep duration (defined as average weekday nighttime sleep duration) and sleep duration differential (defined as the difference between average weekday and average weekend nighttime sleep duration) at each data collection wave. RESULTS: Men with shorter habitual sleep duration on weekdays had higher BMI than men with longer habitual sleep duration on weekdays (ß = -0.90 kg/m2/hour, se = 0.34, p = .008). Participants with larger differentials between weekday and weekend sleep duration experienced more rapid BMI gain over time for both men (ß = 0.033 kg/m2/year per hour differential, se = 0.017, p = .044) and women (ß = 0.057 kg/m2/year per hour differential, se = 0.027, p = .036). CONCLUSION: This study suggests that habitual short sleep is associated with higher BMI levels in men and that a larger weekday-weekend sleep differential is associated with increasing BMI trajectories among both men and women in mid-to-late life.

Contributors to reduced life expectancy among Native Americans in the Four Corners States.

To assess trends in life expectancy and the contribution of specific causes of death to Native American-White longevity gaps in the Four Corners states, we used death records from the National Center for Health Statistics and population estimates from the U.S. Census Bureau from 1999-2017 to generate period life tables and decompose racial gaps in life expectancy. Native American-White life expectancy gaps narrowed between 2001 and 2012 but widened thereafter, reaching 4.92 years among males and 2.06 years among females in 2015. The life expectancy disadvantage among Native American males was primarily attributable to motor vehicle accidents (0.96 years), liver disease (1.22 years), and diabetes (0.78 years). These causes of deaths were also primary contributors to the gap among females, forming three successive waves of mortality that occurred in young adulthood, midlife, and late adulthood, respectively, among Native American males and females. Interventions to reduce motor vehicle accidents in early adulthood, alcohol-related mortality in midlife, and diabetes complications at older ages could reduce Native American-White longevity disparities in the Four Corners states.

Contributors to the black-white life expectancy gap in Washington D.C.

Although the black-white gap in life expectancy has been shrinking in the U.S., national improvement conceals ongoing disparities. Nowhere is this more evident than Washington D.C., where the black-white gap has persistently exceeded 10 years. Using 1999-2017 mortality data from the National Center for Health Statistics, we employed demographic techniques to pursue three aims: first, we created period life tables to examine longevity trends in Washington D.C.; second, we decomposed black-white life expectancy differences into 23 causes of death in three time periods (2000, 2008, 2016); third, we assessed age-specific contributions for each cause of death. Findings revealed that heart disease (4.14 years), homicide (2.43 years), and cancer (2.30 years) contributed most to the 17.23-year gap among males in 2016. Heart disease and cancer contributed most at ages 55-69; homicide contributed most at ages 20-29. Among females in 2016, heart disease (3.24 years), cancer (2.36 years), and unintentional injuries (0.85 years) contributed most to the 12.06-year gap. Heart disease and cancer contributed most at ages 55-69, and unintentional injuries at ages 50-59. Our investigation provides detailed evidence about contributors to the black-white longevity gap in Washington D.C., which can aid in the development of targeted public health interventions.

TRPV4 receptor as a functional sensory molecule in bladder urothelium: Stretch-independent, tissue-specific actions and pathological implications.

The newly recognized sensory role of bladder urothelium has generated intense interest in identifying its novel sensory molecules. Sensory receptor TRPV4 may serve such function. However, specific and physiologically relevant tissue actions of TRPV4, stretch-independent responses, and underlying mechanisms are unknown and its role in human conditions has not been examined. Here we showed TRPV4 expression in guinea-pig urothelium, suburothelium, and bladder smooth muscle, with urothelial predominance. Selective TRPV4 activation without stretch evoked significant ATP release-key urothelial sensory process, from live mucosa tissue, full-thickness bladder but not smooth muscle, and sustained muscle contractions. ATP release was mediated by Ca2+-dependent, pannexin/connexin-conductive pathway involving protein tyrosine kinase, but independent from vesicular transport and chloride channels. TRPV4 activation generated greater Ca2+ rise than purinergic activation in urothelial cells. There was intrinsic TRPV4 activity without exogeneous stimulus, causing ATP release. TRPV4 contributed to 50% stretch-induced ATP release. TRPV4 activation also triggered superoxide release. TRPV4 expression was increased with aging. Human bladder mucosa presented similarities to guinea pigs. Overactive bladders exhibited greater TRPV4-induced ATP release with age dependence. These data provide the first evidence in humans for the key functional role of TRPV4 in urothelium with specific mechanisms and identify TRPV4 up-regulation in aging and overactive bladders.

Contributors to Wisconsin's persistent black-white gap in life expectancy.

BACKGROUND: Although the black-white gap in life expectancy has narrowed in the U.S., there is considerable variability across states. In Wisconsin, the black-white gap exceeds 6 years, well above the national average. Reducing this disparity is an urgent public health priority, but there is limited understanding of what contributes to Wisconsin's racial gap in longevity. Our investigation identifies causes of death that contribute most to Wisconsin's black-white gap in life expectancy among males and females, and highlights specific ages where each cause of death contributes most to the gap. METHODS: Our study employs 1999-2016 restricted-use mortality data provided by the National Center for Health Statistics. After generating race- and sex-specific life tables for each 3-year period of observation (e.g., 1999-2001), we trace recent trends in the black-white life expectancy gap in Wisconsin. We subsequently conduct a series of analyses to decompose the black-white gap in three time periods into 13 separate causes and 19 different age groups. RESULTS: In 2014-16, Wisconsin's black-white gap in life expectancy was 7.34 years for males (67% larger than the national gap), and 5.61 years for females (115% larger than the national gap). Among males, homicide was the single largest contributor, accounting for 1.56 years of the total gap. Heart disease and cancer followed, contributing 1.43 and 1.42 years, respectively. Among females, heart disease and cancer were the two leading contributors to the gap, accounting for 1.12 and 1.00 years, respectively. Whereas homicide contributed most to the racial gap in male longevity during late adolescence and early adulthood, heart disease and cancer exerted most of their influence between ages 50-70 for both males and females. Other notable contributors were unintentional injuries (males), diabetes and cerebrovascular disease (females), and perinatal conditions (males and females). CONCLUSIONS: Our study identifies targets for future policy interventions that could substantially reduce Wisconsin's racial gap in life expectancy. Concerted efforts to eliminate racial disparities in perinatal mortality and homicide early in the life course, and chronic conditions such as cancer and heart disease in later life, promise to help Wisconsin achieve the public health objective of racial parity in longevity.

Purinergic and muscarinic modulation of ATP release from the urothelium and its paracrine actions.

The urothelium is a newly recognized sensory structure that detects bladder fullness. Pivotal to this sensory role is the release of ATP from the urothelium. However, the routes for urothelial ATP release, its modulation by receptor-mediated pathways, and the autocrine/paracrine role of ATP are poorly understood, especially in native tissue. We examined the action of key neurotransmitters: purinergic and muscarinic agonists on ATP release and its paracrine effect. Guinea pig and human urothelial mucosa were mounted in a perfusion trough; superfusate ATP was measured using a luciferin-luciferase assay, and tissue contractions were recorded with a tension transducer. Intracellular Ca²âº was measured in isolated urothelial cells with fura-2. The P2Y agonist UTP but not the P2X agonist α,ß-methylene-ATP generated ATP release. The muscarinic agonist carbachol and the M2-preferential agonist oxotremorine also generated ATP release, which was antagonized by the M2-specific agent methoctramine. Agonist-evoked ATP release was accompanied by mucosal contractions. Urothelial ATP release was differentially mediated by intracellular Ca²âº release, cAMP, exocytosis, or connexins. Urothelium-attached smooth muscle exhibited spontaneous contractions that were augmented by subthreshold concentrations of carbachol, which had little direct effect on smooth muscle. This activity was attenuated by desensitizing P2X receptors on smooth muscle. Urothelial ATP release was increased in aging bladders. Purinergic and muscarinic agents produced similar effects in human urothelial tissue. This is the first demonstration of specific modulation of urothelial ATP release in native tissue by purinergic and muscarinic neurotransmitters via distinct mechanisms. Released ATP produces paracrine effects on underlying tissues. This process is altered during aging and has relevance to human bladder pathologies.