The Temporal Relationship Between Faulty Gambling Cognitions and Gambling Severity in Young Adults.

Disordered gambling in young adults is hypothesized as being related to mistaken gambling-related cognitions. Few studies have examined the temporal order of this relationship using longitudinal data. The purpose of this study is to understand the directionality of the relationship between gambling cognitions and gambling severity in a longitudinal sample of young adults. Young adults (N = 578), initially aged 18-21 years, completed the Manitoba Longitudinal Survey of Young Adults at two time points approximately 2-3 years apart. Measures of beliefs about randomness related to gambling and gambling severity, as measured by the Problem Gambling Severity Index, were utilized. A cross-sectional relationship between gambling severity and gambling-related cognitions was observed with greater gambling severity being associated with increased endorsement of mistaken cognitions. Evidence for a bidirectional longitudinal relationship was observed with faulty gambling cognitions leading to later problematic gambling behaviors and vice versa when examining a total beliefs scale. When examining specific beliefs about randomness, initial gambling group membership predicted later endorsement of certain beliefs about randomness while initial belief ratings did not impact later gambling group membership. The results of this study suggest a bidirectional relationship between gambling severity and erroneous gambling-related cognitions. However, when examining specific beliefs about randomness, evidence was found for problem gambling behaviors leading to erroneous gambling beliefs. These findings suggest that prevention efforts targeting cognitions may not be as effective in impacting those not yet demonstrating disordered gambling behaviors.

Endogenous hypothalamic somatostatins differentially regulate growth hormone secretion from goldfish pituitary somatotropes in vitro.

Using Southern blot analysis of RT-PCR products, mRNA for three different somatostatin (SS) precursors (PSS-I, -II, and -III), which encode for SS(14), goldfish brain (gb)SS(28), and [Pro(2)]SS(14), respectively, were detected in goldfish hypothalamus. PSS-I and -II mRNA, but not PSS-III mRNA, were also detected in cultured pituitary cells. We subsequently examined the effects of the mature peptides, SS(14), gbSS(28), and [Pro(2)]SS(14), on somatotrope signaling and GH secretion. The gbSS(28) was more potent than either SS(14) or [Pro(2)]SS(14) in reducing basal GH release but was the least effective in reducing basal cellular cAMP. The ability of SS(14), [Pro(2)]SS(14), and gbSS(28) to attenuate GH responses to GnRH were comparable. However, gbSS(28) was less effective than SS(14) and [Pro(2)]SS(14) in diminishing dopamine- and pituitary adenylate cyclase-activating polypeptide-stimulated GH release, as well as GH release resulting from the activation of their underlying signaling cascades. In contrast, the actions of a different 28-amino-acid SS, mammalian SS(28), were more similar to those of SS(14) and [Pro(2)]SS(14). We conclude that, in goldfish, SSs differentially couple to the intracellular cascades regulating GH secretion from pituitary somatotropes. This raises the possibility that such differences may allow for the selective regulation of various aspects of somatotrope function by different SS peptides.