Stigma associated with seeking help for psychological distress: how public and self-stigma, help-seeking attitudes and intent, self-compassion, and empathy relate

College and university students experience high levels of psychological distress and would likely benefit from accessing mental health services. However, the stigma associated with seeking help as well as the stigma associated with mental illness in general reduce one’s likelihood of seeking services and lead to other negative consequences such as lower self-esteem and loss of opportunities. This study was conducted in order to: (a) better understand the mental health difficulties, discrimination, and help-seeking patterns among university students, (b) elucidate the processes involved in stigma and help-seeking behaviour, and (c) investigate empathy and self-compassion as potential protective factors. Participants were university students who completed an online survey at two time points with an approximate 3-month interval in-between. Students demonstrated high rates of mental health difficulties and experiences of discrimination. Students sought help from informal sources more frequently than formal sources. Regarding the stigma process, endorsed stigma of mental illness predicted self-stigma of seeking help, which predicted attitudes toward help-seeking, which in turn, predicted intentions to seek counselling. Intentions did not predict help-seeking behaviour. Trait empathy did not demonstrate a moderating effect, but self-compassion demonstrated a potential buffering role in the relationship between public stigma of seeking help and anticipated self-stigma of seeking help. Based on these results, interventions seeking to promote mental health literacy and self-compassion may be helpful in promoting effective mental health support and reducing self-stigma, respectively, although future research is required. Limitations of the present research are outlined and other directions for future research are proposed

Antagonistic Regulation of Apoptosis and Differentiation by the Cut Transcription Factor Represents a Tumor-Suppressing Mechanism in Drosophila

Apoptosis is essential to prevent oncogenic transformation by triggering self-destruction of harmful cells, including those unable to differentiate. However, the mechanisms linking impaired cell differentiation and apoptosis during development and disease are not well understood. Here we report that the Drosophila transcription factor Cut coordinately controls differentiation and repression of apoptosis via direct regulation of the pro-apoptotic gene reaper. We also demonstrate that this regulatory circuit acts in diverse cell lineages to remove uncommitted precursor cells in status nascendi and thereby interferes with their potential to develop into cancer cells. Consistent with the role of Cut homologues in controlling cell death in vertebrates, we find repression of apoptosis regulators by Cux1 in human cancer cells. Finally, we present evidence that suggests that other lineage-restricted specification factors employ a similar mechanism to put the brakes on the oncogenic process

Inhibition of CLIC4 Enhances Autophagy and Triggers Mitochondrial and ER Stress-Induced Apoptosis in Human Glioma U251 Cells under Starvation

CLIC4/mtCLIC, a chloride intracellular channel protein, localizes to mitochondria, endoplasmic reticulum (ER), nucleus and cytoplasm, and participates in the apoptotic response to stress. Apoptosis and autophagy, the main types of the programmed cell death, seem interconnected under certain stress conditions. However, the role of CLIC4 in autophagy regulation has yet to be determined. In this study, we demonstrate upregulation and nuclear translocation of the CLIC4 protein following starvation in U251 cells. CLIC4 siRNA transfection enhanced autophagy with increased LC3-II protein and puncta accumulation in U251 cells under starvation conditions. In that condition, the interaction of the 14-3-3 epsilon isoform with CLIC4 was abolished and resulted in Beclin 1 overactivation, which further activated autophagy. Moreover, inhibiting the expression of CLIC4 triggered both mitochondrial apoptosis involved in Bax/Bcl-2 and cytochrome c release under starvation and endoplasmic reticulum stress-induced apoptosis with CHOP and caspase-4 upregulation. These results demonstrate that CLIC4 nuclear translocation is an integral part of the cellular response to starvation. Inhibiting the expression of CLIC4 enhances autophagy and contributes to mitochondrial and ER stress-induced apoptosis under starvation