Publications by authors named "Hanke Heun-Johnson"

Background: A long-term projection model based on nationally representative data and tracking disease progression across Alzheimer's disease continuum is important for economics evaluation of Alzheimer's disease and other dementias (ADOD) therapy.

Methods: The Health and Retirement Study (HRS) includes an adapted version of the Telephone Interview for Cognitive Status (TICS27) to evaluate respondents' cognitive function. We developed an ordered probit transition model to predict future TICS27 score.

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To improve access to and quality of affordable behavioral healthcare, there is a need for more research to identify which interventions can generate long-term, societal return-on-investment (ROI). Barriers to ROI studies in the behavioral health sector were explored by conducting semi-structured interviews with individuals from key stakeholder groups at state and national behavioral health-related organizations. Limited operating budgets, state-based payer systems, the lack of financial support, privacy laws, and other unique experiences of behavioral health providers and patients were identified as important factors that affect the collection and utilization of data.

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Background: Fully assessing the mortality burden of the COVID-19 pandemic requires measuring years of life lost (YLLs) and accounting for quality-of-life differences.

Objective: To measure YLLs and quality-adjusted life-years (QALYs) lost from the COVID-19 pandemic, by age, sex, race/ethnicity, and comorbidity.

Design: State-transition microsimulation model.

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Importance: Racial/ethnic disparities in health care use and clinical outcomes for behavioral health disorders, including psychosis, are well documented, but less is known about these disparities during the period leading up to first-episode psychosis (FEP).

Objective: To describe the racial/ethnic disparities in behavioral health care use and prescription drug use of children and young adults before the diagnosis of FEP.

Design, Setting, And Participants: An observational cohort study was conducted using medical and prescription drug claims from January 1, 2007, to September 30, 2015, obtained from Optum's deidentified Clinformatics Data Mart Database, a commercial claims database augmented with race/ethnicity and socioeconomic variables.

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Serious mental illness (SMI) is a disabling condition that develops early in life and imposes substantial economic burden. There is a growing belief that early intervention for SMI has lifelong benefits for patients. However, assessing the cost-effectiveness of early intervention efforts is hampered by a lack of evidence on the long-term benefits.

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Early adversity in childhood increases the risk of anxiety, mood, and post-traumatic stress disorders in adulthood, and specific gene-by-environment interactions may increase risk further. A common functional variant in the promoter region of the gene encoding the human MET receptor tyrosine kinase (rs1858830 ' allele) reduces expression of and is associated with altered cortical circuit function and structural connectivity. Mice with reduced expression exhibit changes in anxiety-like and conditioned fear behavior, precocious synaptic maturation in the hippocampus, and reduced neuronal arbor complexity and synaptogenesis.

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Animal models can help elucidate the mechanisms through which early-life stress (ELS) has pathophysiological effects on the developing brain. One model that has been developed for rodents consists of limiting the amount of bedding and nesting material during the first postnatal weeks of pup life. This ELS environment has been shown to induce "abusive" behaviors by rat dams towards pups, while mouse dams have been hypothesized to display "fragmented care".

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Duchenne muscular dystrophy (DMD) is a deadly and common childhood disease caused by mutations that disrupt dystrophin protein expression. Several miniaturized dystrophin/utrophin constructs are utilized for gene therapy, and while these constructs have shown promise in mouse models, the functional integrity of these proteins is not well described. Here, we compare the biophysical properties of full-length dystrophin and utrophin with therapeutically relevant miniaturized constructs using an insect cell expression system.

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Background: The loss of dystrophin compromises muscle cell membrane stability and causes Duchenne muscular dystrophy and/or various forms of cardiomyopathy. Increased expression of the dystrophin homolog utrophin by gene delivery or pharmacologic up-regulation has been demonstrated to restore membrane integrity and improve the phenotype in the dystrophin-deficient mdx mouse. However, the lack of a viable therapy in humans predicates the need to explore alternative methods to combat dystrophin deficiency.

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