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Background: The relationship between an increasing elderly population and wide-ranging neurological conditions has led to heightened rates of cognitive function impairment. Some researchers have found that health literacy risk may be associated with cognitive impairment in older adults. Objectives: The purpose of this study was to delineate the difference in health literacy risk between older adults with mild cognitive impairment and those with normal cognitive function. Methods: We conducted a survey study to explore the health literacy risk in older adults with and without mild cognitive impairment. Data were collected from 412 subjects between 60 and 91 years of age (260 without and 152 with mild cognitive impairment) between June and December 2016 in China. Cognitive function was measured using the Mini-Mental Status Examination, Montreal Cognitive Assessment, Global Deterioration Scale, Activities of Daily Living, and Hamilton Depression Rating Scale. Health literacy was measured using the Chinese Citizen Health Literacy Questionnaire. Results: The scores of total health literacy and its three dimensions (basic health knowledge and mind, basic skills, and health lifestyle and behavior) were lower in those with mild cognitive impairment. Older adults with normal cognitive function had adequate or marginal health literacy levels, whereas those with mild cognitive impairment had marginal or inadequate health literacy levels. Using multiple logistic regression analysis, we found that health literacy risk, education level, age, marital status, and body mass index were independent risk factors for mild cognitive impairment. Discussion: These results suggest that low health literacy may be a predictor of mild cognitive impairment. Screening for lower health literacy risk should be included in multidimensional geriatric evaluation. [ABSTRACT FROM AUTHOR]

Background: Immunoglobulin E (IgE) belongs to a class of immunoglobulins involved in immune response to specific allergens. However, the roles of IgE and IgE receptor (FcεR1) in pathological cardiac remodeling and heart failure are unknown.Methods: Serum IgE levels and cardiac FcεR1 expression were assessed in diseased hearts from human and mouse. The role of FcεR1 signaling in pathological cardiac remodeling was explored in vivo by FcεR1 genetic depletion, anti-IgE antibodies, and bone marrow transplantation. The roles of the IgE-FcεR1 pathway were further evaluated in vitro in primary cultured rat cardiomyocytes and cardiac fibroblasts (CFs). RNA sequencing and bioinformatic analyses were used to identify biochemical changes and signaling pathways that are regulated by IgE/FcεR1.Results: Serum IgE levels were significantly elevated in patients with heart failure as well as in 2 mouse cardiac disease models induced by chronic pressure overload via transverse aortic constriction and chronic angiotensin II infusion. Interestingly, FcεR1 expression levels were also significantly upregulated in failing hearts from human and mouse. Blockade of the IgE-FcεR1 pathway by FcεR1 knockout alleviated transverse aortic constriction- or angiotensin II-induced pathological cardiac remodeling or dysfunction. Anti-IgE antibodies (including the clinical drug omalizumab) also significantly alleviated angiotensin II-induced cardiac remodeling. Bone marrow transplantation experiments indicated that IgE-induced cardiac remodeling was mediated through non-bone marrow-derived cells. FcεR1 was found to be expressed in both cardiomyocytes and CFs. In cultured rat cardiomyocytes, IgE-induced cardiomyocyte hypertrophy and hypertrophic marker expression were abolished by depleting FcεR1. In cultured rat CFs, IgE-induced CF activation and matrix protein production were also blocked by FcεR1 deficiency. RNA sequencing and signaling pathway analyses revealed that transforming growth factor-β may be a critical mediator, and blocking transforming growth factor-β indeed alleviated IgE-induced cardiomyocyte hypertrophy and cardiac fibroblast activation in vitro.Conclusions: Our findings suggest that IgE induction plays a causative role in pathological cardiac remodeling, at least partially via the activation of IgE-FcεR1 signaling in cardiomyocytes and CFs. Therapeutic strategies targeting the IgE-FcεR1 axis may be effective for managing IgE-mediated cardiac remodeling. [ABSTRACT FROM AUTHOR]

Objective: We aimed to quantify concentrations of inducible heme oxygenase (HO)-1 in the lungs of patients with acute respiratory distress syndrome (ARDS) and to investigate its role as a source of ferrous iron and as a signaling agent for iron regulation. Control of such processes by heme oxygenase has implications for the onset, progression, and resolution of ARDS.Design: Retrospective analysis of archived samples.Setting: Adult intensive care unit of a postgraduate teaching hospital.Patients: Patients admitted to the adult intensive care unit who fulfilled the American-European Consensus Conference criteria for ARDS.Interventions: Biochemical and immunohistochemical studies using bronchoalveolar lavage fluid or lung tissue were performed in patients with established ARDS and in those undergoing lung resection (controls).Measurements and Main Results: Concentrations of heme oxygenase protein were significantly elevated in lung tissue (193.7 +/- 13.27 vs. 81.0 +/- 16.0%, p < .01) and in bronchoalveolar lavage fluid (2.4 x 10(5) vs. 1.4 x 10(5) densitometric units, p = .047) taken from patients with ARDS compared with controls. Concentrations of heme oxygenase protein in bronchoalveolar lavage fluid from patients with ARDS correlated positively and significantly with changes in the concentrations of ferritin (r = .697, p = .02) and the iron saturation of transferrin (r = .8, p = .014) but correlated negatively and significantly with concentrations of bleomycin-detectable (redox-active) iron (r = -.73, p = .031). Significantly elevated (p < .05) concentrations of heme oxygenase staining in cell types expressing this protein were detected in patients with ARDS, compared with concentrations in the same cells taken from controls undergoing lung resection.Conclusions: Heme oxygenase protein is elevated in the lungs of patients with ARDS and may contribute to the changes in iron mobilization, signaling, and regulation seen in this condition. [ABSTRACT FROM AUTHOR]