Emerging Adulthood Attributes, Discrimination, Mental Health, and Substance Use in a Sample of Asian, Native Hawaiian/Pacific Islander, and White College Students.

Although Asian/Pacific Islanders are considered a single ethnic/racial category in national studies, Native Hawaiians/other Pacific Islanders (NHOPIs) and Asians show marked disparities in health outcomes and risk behaviors, including substance use. Currently, knowledge regarding the psychosocial mechanisms by which NHOPI ethnicity is associated with increased substance use, compared with Asian or White, is limited, especially among emerging adults. The present study tested a model in which the relationship between NHOPI ethnicity and higher substance use (i.e., current tobacco, alcohol, marijuana, and illicit drug use) was hypothesized to be mediated through higher emerging adulthood stress (e.g., feeling "in-between," instability), higher self-reported racial/ethnic discrimination, substance use in one's social networks, and poorer mental health symptomology (i.e., depression, anxiety). Data collected at a single time-point from 2,344 college students (M age = 21.2 [SD = 2.1]; 54% Women; 24% NHOPI, 49% Asian, 27% White) were analyzed by employing structural equation modeling. NHOPI and Asian ethnicity were dummy coded with reference to White, and separate analyses were run for NHOPI and Asian groups, with White as the reference group. Results indicated that the association between NHOPI ethnicity and higher substance use was mediated in two steps, via higher racial/ethnic discrimination and poorer mental health symptomatology. NHOPI ethnicity, but not Asian, was associated with higher identification with emerging adulthood attributes, which in turn was associated with increased substance use. Implications are discussed in the context of reducing health disparities faced by NHOPIs.

Frequency of social media use and exposure to tobacco or nicotine-related content in association with E-cigarette use among youth: A cross-sectional and longitudinal survey analysis.

Exposure to social media and its content featuring tobacco products is associated with e-cigarette use among adolescents. This study measured the association between frequency of Instagram, TikTok and YouTube use and exposure to tobacco-related content on each of these platforms with e-cigarette ever-use, current (past 30-day) use and initiation among adolescents. A cross-sectional and longitudinal analyses were used based on a self-reported survey conducted online in January - May 2021-2022 among socioeconomically- and racially-diverse Los Angeles, California high school students (N = 2,036). Adolescents had higher odds of e-cigarette ever-use (adjusted odds ratio [AOR] = 2.16; CI: 1.20;3.90) and current (past 30-day) use (AOR = 3.11; CI: 1.64;5.89) if they used TikTok several times per day, compared to adolescents who used TikTok less frequently or not at all. Adolescents also had higher odds of e-cigarette initiation (AOR = 2.97; CI: 1.53;5.77) if they used TikTok daily or several times per day, compared to adolescents who used TikTok less frequently or not at all. Adolescents had higher odds of e-cigarette ever-use (AOR = 2.60; CI: 2.02;3.35) and current use (AOR = 3.11; CI: 1.64;5.89) if they reported seeing tobacco or nicotine posts, including e-cigarettes, on TikTok at least weekly. Frequent use of and frequent exposure to tobacco content on TikTok is associated with increased risk of e-cigarette use and initiation among adolescents. Tobacco-related content on social media popular among youth, especially on TikTok, requires stronger regulation and better enforcement by platforms of their policies restricting tobacco content.

Accelerated thymic atrophy as a result of elevated homeostatic expression of the genes encoded by the TNF/lymphotoxin cytokine locus.

TNF, lymphotoxin (LT)-alpha, LT-beta and LIGHT are members of a larger superfamily of TNF-related cytokines that can cross-utilize several receptors. Although LIGHT has been implicated in thymic development and function, the role of TNF and LT remains incompletely defined. To address this, we created a model of modest homeostatic overexpression of TNF/LT cytokines using the genomic human TNF/LT locus as a low copy number Tg. Strikingly, expression of Tg TNF/LT gene products led to profound early thymic atrophy characterized by decreased numbers of thymocytes and cortical thymic epithelial cells, partial block of thymocyte proliferation at double negative (DN) 1 stage, increased apoptosis of DN2 thymocytes and severe decline of T-cell numbers in the periphery. Results of backcrossing to TNFR1-, LTbetaR- or TNF/LT-deficient backgrounds and of reciprocal bone marrow transfers implicated both LT-alpha/LT-beta to LTbetaR and TNF/LT-alpha to TNFR1 signaling in accelerated thymus degeneration. We hypothesize that chronic infections can promote thymic atrophy by upregulating LT and TNF production.