Financial Health of People Living With Dementia and Their Informal Care Partners: Protocol for a Mixed Methods Study.

BACKGROUND: There is a growing body of academic literature focusing on the significant financial burdens placed on people living with cancer, but little evidence exists on the impact of rising costs of care in other vulnerable populations. This financial strain, also known as financial toxicity, can impact behavioral, psychosocial, and material domains of life for people diagnosed with chronic conditions and their care partners. New evidence suggests that populations experiencing health disparities, including those with dementia, face limited access to health care, employment discrimination, income inequality, higher burdens of disease, and exacerbating financial toxicity. OBJECTIVE: The three study aims are to (1) adapt a survey to capture financial toxicity in people living with dementia and their care partners; (2) characterize the degree and magnitude of different components of financial toxicity in this population; and (3) empower the voice of this population through imagery and critical reflection on their perceptions and experiences relating to financial toxicity. METHODS: This study uses a mixed methods approach to comprehensively characterize financial toxicity among people living with dementia and their care partners. To address aim 1, we will adapt elements from previously validated and reliable instruments, including the Comprehensive Score for Financial Toxicity and Patient-Reported Outcomes Measurement Information System, to develop a financial toxicity survey specific to dyads of people living with dementia and their care partners. A total of 100 dyads will complete the survey, and data will be analyzed using descriptive statistics and regression models to address aim 2. Aim 3 will be addressed using the process of "photovoice," which is a qualitative, participatory research method that combines photography, verbal narratives, and critical reflection by groups of individuals to capture aspects of their environment and experiences with a certain topic. Quantitative results and qualitative findings will be integrated using a validated, joint display table mixed methods approach called the pillar integration process. RESULTS: This study is ongoing, with quantitative findings and qualitative results anticipated by December 2023. Integrated findings will enhance the understanding of financial toxicity in individuals living with dementia and their care partners by providing a comprehensive baseline assessment. CONCLUSIONS: As one of the first studies on financial toxicity related to dementia care, findings from our mixed methods approach will support the development of new strategies for improving the costs of care. While this work focuses on those living with dementia, this protocol could be replicated for people living with other diseases and serve as a blueprint for future research efforts in this space. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): DERR1-10.2196/47255.

Dysregulation of miR-155 Expression in Professional Mixed Martial Arts (MMA) Fighters.

Psychological and physical stress can induce dysregulation of gene expression via changes in DNA methylation and microRNA (miRNA) expression. Such epigenetic modifications are yet to be investigated in professional Mixed Martial Arts (MMA) fighters subject to highly stressful training involving repetitive head impacts. This study examined differences in DNA methylation and miRNA expression in elite MMA fighters compared to active controls. Global methylation differences between groups were assessed via a LINE-1 assay. At the same time, PCR arrays were used to estimate differential expression in samples of 21 fighters and 15 controls for 192 different miRNAs associated with inflammatory diseases. An Independent-Samples t-Test found no significant difference in LINE-1 methylation between groups. However, an Independent-Samples Mann-Whitney U Test revealed a significant upregulation in the expression of miR-155 in MMA fighter plasma. Since miR-155 has been recognized as an important regulator of neuroinflammation, this dysregulation suggests a possible epigenetic mechanism responsible for chronic inflammation associated with professional-level MMA training. Consistent with other published works, this study highlights the potential of miR-155 not only as a biomarker for monitoring long-term health risks linked to head trauma but also as a target to remediate the impact of chronic neuroinflammation.

Acute sleep deprivation disrupts emotion, cognition, inflammation, and cortisol in young healthy adults.

Chronic sleep deprivation has been demonstrated to diminish cognitive performance, alter mood states, and concomitantly dysregulate inflammation and stress hormones. At present, however, there is little understanding of how an acute sleep deprivation may collectively affect these factors and alter functioning. The present study aimed to determine the extent to which 24-h of sleep deprivation influences inflammatory cytokines, stress hormones, cognitive processing across domains, and emotion states. To that end, 23 participants (mean age = 20.78 years, SD = 2.87) filled out clinical health questionnaires measured by the Pittsburgh Sleep Quality Index, Morningness Eveningness Questionnaire, and Center for Epidemiological Studies Depression Scale. Actigraph was worn for seven days across testing to record sleep duration. At each session participants underwent a series of measures, including saliva and blood samples for quantification of leptin, ghrelin, IL-1ß, IL-6, CRP, and cortisol levels, they completed a cognitive battery using an iPad, and an emotion battery. We found that an acute sleep deprivation, limited to a 24 h period, increases negative emotion states such as anxiety, fatigue, confusion, and depression. In conjunction, sleep deprivation results in increased inflammation and decreased cortisol levels in the morning, that are accompanied by deficits in vigilance and impulsivity. Combined, these results suggest that individuals who undergo 24 h sleep deprivation will induce systemic alterations to inflammation and endocrine functioning, while concomitantly increasing negative emotions.

The Amphoteric Surfactant N,N-Dimethyldodecylamine N-Oxide Unfolds ß-Lactoglobulin above the Critical Micelle Concentration.

Understanding the interactions between surfactants and proteins is important for the formulation of consumer products as surfactant binding can alter protein activity and stability. Additionally, the structure of the protein-surfactant complex can influence surface activity, which is important for emulsion and foam development. N,N-Dimethyldodecylamine N-oxide (DDAO) is an amphoteric surfactant that is nonionic at high pH. It is often used as a foam booster in detergent formulations and for the extraction of membrane proteins. In this study, a variety of biophysical characterization methods was used to investigate the impact of DDAO at pH 8 on the structure of the globular protein ß-lactoglobulin (ßLG). Pyrene fluorescence and surface tension studies show that ßLG had minimal impact on the critical micelle concentration (CMC) of DDAO, while fluorescence and circular dichroism spectroscopy found unfolding of ßLG at concentrations of DDAO greater than the CMC. Small-angle X-ray scattering results confirm changes in the structure of ßLG at DDAO concentrations above the CMC. Taken together, DDAO behaves like nonionic and zwitterionic surfactants below its CMC with limited interaction with ßLG, while it induces protein unfolding at concentrations higher than the CMC, resulting in a protein-surfactant complex structure that resembles a protein-decorated micelle.

Sex Matters: Anxiety and Aggression Predict Cortisol Responsivity in Men but Not Women.

BACKGROUND: Sexual dimorphism in the hypothalamic pituitary adrenal (HPA) axis can influence sex-specific patterns of response to stressors. While a host of findings exist on sex differences in stress-induced activity of the HPA axis and associated mechanisms in rodents, less is known about the intricacies of sex differences in stress responsivity in humans. Accordingly, the overall aim of the present study was to investigate psychological variables that may account for differences in the cortisol stress response between men and women. METHODS: Eighty-six participants filled out self-report measures of anxiety (STA-Y), aggression (BPAQ), and happiness (SHS). We then exposed all participants to a one-minute Cold Pressor Test (CPT) that was maintained between 3-5° C. Cortisol and pain ratings were assessed. We focused on the 20-minute time point for cortisol since that is when cortisol is near its peak post-stress. RESULTS: Women reported higher pain ratings compared to men. Women also showed a positive relationship between pain ratings and cortisol. Aggression was significantly related to cortisol levels in men, but not in women. Similarly, trait anxiety was positively related to cortisol levels in men, but not in women. Happiness was unrelated to cortisol levels in women and men. Follow-up regressions were conducted separately for men and women. A significant model was found for cortisol in men only with trait anxiety, aggression, and the interaction between trait anxiety and aggression. CONCLUSIONS: The current study builds on previous reports by showing that aggression and anxiety differentially influence the cortisol response to an acute stress in men and women.

Advanced glycation end (AGE) product modification of laminin downregulates Kir4.1 in retinal Müller cells.

Diabetic retinopathy (DR) is a major cause of adult blindness. Retinal Müller cells maintain water homeostasis and potassium concentration via inwardly rectifying Kir4.1 channels. Accumulation of advanced glycation end products (AGEs) is a major pathologic event in DR. While diabetes leads to a decrease in the Kir4.1 channels, it remains unknown whether AGEs-linked to the basement membrane (BM) affect normal Kir4.1 channels. For this study, we hypothesized that AGE-modification of laminin is detrimental to Kir4.1 channels, therefore, disrupting Müller cell function. The AGE-modified laminin-coated substrates were prepared by incubating Petri-dishes with laminin and methylglyoxal for seven days. The rat Müller cells (rMC-1) were propagated on AGE-modified laminin, and Kir4.1 expression and function were evaluated. Quantification of AGEs using ELISA revealed a dose-dependent increase in methylglyoxal-hydro-imidazolone adducts. The rMC-1 propagated on AGE-modified laminin demonstrated a decrease in Kir4.1 levels in immunofluorescence and western blot studies and a decrease in the Kir4.1 channel function. Kir4.1 decrease on AGE-modified laminin resulted in a disorganization of an actin cytoskeleton and disruption of α-dystroglycan-syntrophin-dystrophin complexes. Our studies suggest that AGE-modification of laminin is detrimental to Kir4.1 channels. By studying the role of AGEs in Kir4.1 channels we have identified a novel mechanism of Müller cell dysfunction and its subsequent involvement in DR.