Perilous and unaccountable: The positive relationship between dominance and moral hazard behaviors.

Moral hazard involves a context where decision-makers engage in behaviors that prioritize self-interest while allowing the associated risk to be primarily borne by others. Such decision making can lead to catastrophic consequences, as seen in the 2008 global financial crisis after hedge fund managers indiscriminately invested their clients' money in subprime mortgages. This research examines which decision-makers are most likely to engage in moral hazard decision making and the psychological mechanism driving this behavior. Drawing on the dual model of social influence, we posit that individuals associated with dominance, but not prestige, will engage in greater moral hazard behaviors. We further contend that these behaviors are driven by dominant decision-makers' enhanced focus on end goals (outcomes) rather than the means (process) that they use to pursue such goals. We find support for our hypotheses across 13 studies (NObservations = 26,880; of which eight were preregistered and six studies are reported in the Supplemental Materials), using both correlational and experimental designs. Additionally, we vary the moral hazard context (e.g., a financial setting, a health and safety issue, etc.) and capture both behavioral intentions and actual behaviors, while also ruling out several alternative explanations. These findings demonstrate that dominant decision-makers engage in moral hazard behaviors because of their tendency to prioritize outcomes over processes. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Meh, whatever: The effects of indifference expressions on cooperation in social conflict.

Conflicts are inherently emotional, yet parties in conflict may choose to explicitly express indifference. It is unclear, however, whether this represents an effective strategy. Drawing on emotions as social information (EASI) theory, we examined the interpersonal effects of indifference expressions in conflict and the processes that underlie these effects. Study 1 indicated that people believe indifference expressions constitute a neutral emotional signal. However, Study 2 demonstrated experimentally that counterparts' indifference expressions reduce focal negotiators' cooperative intentions through both affective (negative affective reactions) and inferential (decreased expected collaboration) processes when compared to negative (anger, contempt), positive (hope), and neutral (no emotion) expressions. Study 3 revealed negative effects of indifference (vs. neutral) expressions on cooperative intentions, expected collaboration, and heart rate variability as a physiological indicator of affective responding. Results further showed an indirect effect through expected collaboration, but not through affective reactions. Study 4 established the negative effects of indifference expressions on a behavioral measure of cooperation through expected collaboration. Studies 5 and 6 (preregistered) demonstrated that the impact of indifference expressions on cooperative intentions (Study 5) and actual cooperation (Study 6) via counterpart's expected collaboration is reduced when a counterpart explicitly indicates cooperative intentions, reducing the diagnostic value of indifference expressions. Across studies (N = 2,447), multiple expressive modalities of indifference were used, including verbal and nonverbal expressions. Findings demonstrate that explicit expressions of indifference have qualitatively different interpersonal effects than other emotional expressions, including neutral expressions, and cast doubt on the effectiveness of expressing indifference in negotiating social conflict. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

IGF-I protects human oral buccal mucosal epithelial cells from sodium nitroprusside-induced apoptosis via PI3-kinase.

OBJECTIVE: Cancers of the head and neck account for the vast majority of all malignancies of the oral cavity. The insulin-like growth factor (IGF) family of proteins is well documented to have an important role in rescuing cells from apoptosis. While it is known the IGF proteins are present in normal oral epithelial and cancer cells its role is not fully understood. Our aim was to study the ability of IGFs to rescue sodium nitroprusside (SNP)-induced apoptotic normal oral epithelial cells in vitro. DESIGN: Cultured normal human oral keratinocytes (NOKs) or epithelial cells were used. Apoptosis was induced by SNP then cells were exposed to IGF-I or IGF-II to rescue them. Cell viability was assessed by ELISA (for cell death and caspase 3) and FACS analysis; post receptor effects of IGF-I or IGF-II were assessed by [(3)H] thymidine incorporation. Cell signaling events were measured by western blotting using antibodies against phosphorylated Akt or p42/p44 MAPK, and measuring PI3-K activity by ELISA. RESULTS: SNP induced apoptosis of NOKs and activated the PI3-K/Akt survival pathway. Exposing cells to IGF proteins prevented their apoptosis. IGF-I and -II caused significant increases in PI3-K, but not MAPK, activity. SNP and LY294002, a PI3-K inhibitor, both caused a significant rise in caspase 3 release from NOKs which was reduced in the presence of IGFs. CONCLUSIONS: The data establishes the importance of IGF-activated PI3-K in rescuing cells from apoptosis. It lends further evidence to the significance of IGF proteins in the possible development of oral cancer.

Resolution of obstructive sleep apnoea after resection of a pleomorphic salivary adenoma.

We describe a 54-year-old man whose obstructive sleep apnoea was cured by resection of a pleomorphic salivary adenoma, and emphasise the importance of a full examination of the upper airway in the assessment of a patient with symptoms of sleep apnoea.

Upregulation of IGF-2 and IGF-1 receptor expression in oral cancer cell lines.

The insulin-like growth factors (IGFs) are a family of mitogenic proteins involved in the regulation of cell growth and differentiation. The presence and role of the IGF system in oral mucosal epithelium is not clear but could influence our understanding of the pathogenesis of oral cancer. We characterised the expression and function of IGF-1, IGF-2 and IGF receptor in human oral squamous carcinoma cell lines and normal oral epithelial cells as well as normal oral and squamous cell carcinoma tissues. Using reverse transcription followed by PCR, IGF-1 mRNA was only detected in normal cells, whereas IGF-2 and IGF-1R mRNA transcripts were highly expressed in tumour cell lines and tissues. Similar observations were seen by Western blot analysis and immunohistochemistry. Exogenous IGF-2, but not IGF-1, caused significant increases in DNA synthesis in the cell lines. IGF-2 also increased cell proliferation which was significantly attenuated in the presence of an IGF-2 neutralizing antibody or one which blocked IGF-1R. Taken together, these studies suggest that autocrine production of IGF-2, together with over-expression of IGF-1R, may be important components controlling the proliferation of oral carcinoma cells.