ABSTRACT
To address the gap of lacking research on the association between coping self-efficacy and loneliness, this study examined this relationship to inform future research and intervention on loneliness. Using data from 151 community-dwelling older adults ages 65 and older, we estimated multivariate logistic regression models with age, race/ethnicity, sex, body mass index, chronic disease composite score, social support, coping self-efficacy, and depression symptoms. Loneliness was reported in 32.1% of participants and negatively associated with coping self-efficacy (OR = 0.68, 95% CI: 0.50-0.93) while controlling for age, race, sex, chronic disease composite score, and body mass index. Our findings suggest that coping self-efficacy may be a target for intervention involving loneliness in future research; however, the causal relationship between coping self-efficacy and loneliness should be explored further.
Subject(s)
Loneliness , Self Efficacy , Humans , Aged , Adaptation, Psychological , Social Support , Chronic DiseaseABSTRACT
PURPOSE: Corneal neovascularization (CNV) is associated with Chlamydia trachomatis. The minimal components of bacterial cell walls are recognized by nucleotide-binding oligomerization domain-containing protein (Nod), which is important for host defense--a mechanism manifested in human corneal cells. We aimed to examine whether Nod stimulation is associated with CNV. METHODS: Three groups of mice with alkali-induced CNV were topically treated with tripeptide L-Ala-γ-D-Glu-meso-diaminopimelic acid (Tri-DAP, a Nod1 agonist), muramyl dipeptide (a Nod2 agonist), or phosphate-buffered saline twice daily for 8 days. The time course responses were quantified using biomicroscopic examinations and immunohistochemistry. Angiogenic factor expression was evaluated by quantitative real-time reverse transcription-polymerase chain reaction. To confirm the involvement of Nod1 signaling in CNV, RICK (an essential molecule in Nod signaling)-knockout mice treated with Tri-DAP were examined biomicroscopically and immunohistochemically 8 days after injury. RESULTS: According to the biomicroscopic camera images and histology, Tri-DAP and muramyl dipeptide promoted CNV. Significantly, Tri-DAP increased the number and size of the neovascularized areas. The messenger RNA expression level of vascular endothelial growth factor was elevated in the Tri-DAP-treated mice after alkali injury. Compared with wild-type mice, CNV was attenuated in RICK-deficient mice treated with Tri-DAP. CONCLUSIONS: These data suggest that Nod1 stimulation is an important inducer of CNV and that Nod1 might be useful in the development of CNV therapies.
Subject(s)
Corneal Neovascularization/metabolism , Disease Models, Animal , Nod1 Signaling Adaptor Protein/physiology , Acetylmuramyl-Alanyl-Isoglutamine/therapeutic use , Animals , Corneal Neovascularization/drug therapy , Diaminopimelic Acid/analogs & derivatives , Diaminopimelic Acid/therapeutic use , Gene Expression , Immunohistochemistry , Mice , Mice, Inbred C57BL , Mice, Knockout , Nod1 Signaling Adaptor Protein/agonists , Nod2 Signaling Adaptor Protein/agonists , Nod2 Signaling Adaptor Protein/physiology , Oligopeptides/therapeutic use , Real-Time Polymerase Chain Reaction , Receptor-Interacting Protein Serine-Threonine Kinase 2 , Receptor-Interacting Protein Serine-Threonine Kinases/genetics , Vascular Endothelial Growth Factor A/geneticsABSTRACT
OBJECTIVE: Chemerin, a recently discovered adipocytokine, may be linked to obesity and obesity-associated metabolic complications. However, the relationship between visceral fat accumulation and chemerin is still unknown. Therefore, we investigated the relationship between serum chemerin levels and body composition as measured by computed tomography (CT). PATIENTS: We recruited 173 men and women without histories of diabetes or cardiovascular disease. MEASUREMENTS: Biomarkers of metabolic risk factors and body composition by computed tomography were assessed. Serum chemerin levels were measured by enzyme-linked immunosorbent assay. RESULTS: Chemerin levels correlated with body mass index (BMI), waist circumference, abdominal visceral fat area, blood pressure, fasting insulin, homoeostasis model of assessment-insulin resistance, total cholesterol, triglyceride, creatinine, aspartate aminotransferase and alanine aminotransferase. By stepwise multiple regression analysis, abdominal visceral fat area, blood pressure and total cholesterol levels independently affected chemerin levels. CONCLUSIONS: Abdominal visceral fat accumulation, blood pressure and lipid profile were significantly associated with serum chemerin levels. Our findings suggest that chemerin may be a mediator that links visceral obesity to cardiovascular risk factors.
