Aarupwinstead1796

Ethnic identity is an important protective factor for various ethnic groups and developmental periods. Although existing measures assessing ethnic identity are well known, less is known about the measurement invariance of the Multigroup Ethnic Identity Measure (MEIM) across adolescent ethnic groups. The present study evaluates the factor structure of MEIM (Roberts et al., 1999) and tests the measurement invariance across early and middle adolescence and ethnic background (N=4940).

Data from an ethnic minority sample of youth (54% girls; M

=13.88, grades 6th - 12th; 60% African American, 22% multi-ethnic, 8% Latinx, 5% Asian, 5% American Indian) in the United States of America were examined using confirmatory factor analysis (CFA) and multi-group measurement invariance via a structural equation modeling (SEM) framework. Models for invariance were tested using full information maximum likelihood-robust (FIML-R) estimation in Mplus.

CFA supported a three-factor solution (i.e., cognitive clarity, behavioral engagement, and affective pride). The model indicated scalar invariance across early and middle adolescence and partial scalar invariance across the five self-identified racial/ethnic minority groups. There were no grade differences on the ethnic identity factors. Among the racial/ethnic groups, multi-ethnic youth reported the lowest levels on all three ethnic identity factors compared to the other groups.

Results of this study point to the validity of using the MEIM for meaningful comparisons of ethnic identity across ethnic groups and across early and middle adolescence. Implications for the interpretation and use of this measure with diverse adolescents are discussed.

Results of this study point to the validity of using the MEIM for meaningful comparisons of ethnic identity across ethnic groups and across early and middle adolescence. Implications for the interpretation and use of this measure with diverse adolescents are discussed.Ovarian aging occurs due to the reduction of the quality and quantity of the oocytes, and is regulated by mitochondrial survival and apoptotic signals. Reactive Oxygen Species (ROS) are one of those signals considered detrimental to cellular homeostasis. Nowadays, ROS are regarded as a regulatory factor at low levels as it induces the stress resistance which in turn increases the longevity. It is believed that the main mechanism for the life-promoting role of the ROS mediated by the 5' Adenosine Monophosphate-activated Protein Kinase (AMPK). N1-Methylnicotinamide (MNAM) is well known for its anti-diabetic, anti-thrombotic, and anti-inflammatory activity. Aldehyde oxidase 1 (AOX1) is a detoxifying enzyme, which metabolizes the MNAM and produces two metabolites including N1-methyl-2-pyridone-5- carboxamide (2py) and N1-methyl-4-pyridone-3-carboxamide (4py). The activity of AOX1 enhances the production of ROS and improves the longevity. It has been reported that the MNAM could postpone the aging through the induction of low-level stress. It has been documented that the production of MNAM is significantly higher in the cumulus cells of the patients with Polycystic Ovary Syndrome (PCOS) and its administration on the rat model of PCOS has been shown to alleviate the hyperandrogenism and successfully activate the ovarian AMPK. Therefore, it can be hypothesized that the anti-ovarian aging effects of the MNAM are possibly based on the activation of AMPK through transient elevation of the ROS.Musculoskeletal disorders related to ageing are one of the most common causes of mortality and morbidity among elderly individuals worldwide. The typical constitutive components of the musculoskeletal system, including bone, muscle, and joints, gradually undergo a process of tissue loss and degeneration as a result of life-long mechanical and biological stress, ultimately leading to the onset of a series of age-related musculoskeletal diseases, including osteoporosis (OP), sarcopenia, and osteoarthritis (OA). Dehydroepiandrosterone (DHEA), a precursor of androgen secreted mainly by the adrenal gland, has attracted much attention as a marker for senescence due to its unique age-related changes. This pre-hormone has been publicly regarded as an "antidote for ageing" because of its favourable effect against a wide range of age-related diseases, such as Alzheimer disease, cardiovascular diseases, immunosenescence and skin senescence, though its effect on age-related musculoskeletal diseases has been explored to a lesser extent. In the present review, we summarized the action of DHEA against OP, sarcopenia and OA. Extensive detailed descriptions of the pathogenesis of each of these musculoskeletal disorders are beyond the scope of this review; instead, we aim to highlight the association of changes in DHEA with the processes of OP, sarcopenia and OA. buy Volasertib A special focus will also be placed on the overlapping pathogeneses among these three diseases, and the molecular mechanisms underlying the action of DHEA against these diseases are discussed or postulated.Mitophagy serves as a cardinal regulator in the maintenance of mitochondrial integrity, function, and cardiovascular homeostasis, through the fine control and governance of cellular metabolism, ATP production, redox balance, and mitochondrial quality and quantity control. As a unique form of selective autophagy, mitophagy specifically recognizes and engulfs long-lived or damaged (depolarized) mitochondria through formation of the double-membraned intracellular organelles - mitophagosomes, ultimately resulting in lysosomal degradation. Levels of mitophagy are reported to be altered in pathological settings including cardiovascular diseases and biological ageing although the precise nature of mitophagy change in ageing and ageing-associated cardiovascular deterioration remains poorly defined. Ample clinical and experimental evidence has depicted a convincing tie between cardiovascular ageing and altered mitophagy. In particular, ageing perturbs multiple enigmatic various signal machineries governing mitophagy, mitochondrial quality, and mitochondrial function, contributing to ageing-elicited anomalies in the cardiovascular system. This review will update novel regulatory mechanisms of mitophagy especially in the perspective of advanced ageing, and discuss how mitophagy dysregulation may be linked to cardiovascular abnormalities in ageing. We hope to pave the way for development of new therapeutic strategies against the growing health and socieconomical issue of cardiovascular ageing through targeting mitophagy.