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Previous research has indicated that the path-goal theory is an effective way to study leadership behavior; however, a gap exists in the literature with respect to its achievement-oriented and participative leadership dimensions in high-tech organizations. In this quantitative study, the effects of a core values intervention on the four leadership dimensions of House's path-goal theory were evaluated at a semiconductor manufacturer with a focus on the differences between supervisors and non-supervisory personnel. Data were gathered from the validated, company-developed Corporate Culture Survey that was administered pre and post intervention. Data were also gathered from a categorization task that sorted the Corporate Culture Survey items into leadership dimensions to form the dependent measures. ANOVA was used to determine whether significant changes in perceptions of leadership behavior by supervisors and non-supervisory personnel occurred on House's four leadership dimensions as a result of the values intervention. Results of a two-way ANOVA on the directive supervision subscale show an interaction between the pre-post intervention factor and supervisors/non-supervisory factor in addition to a main effect for the pre-post intervention factor. Analysis of the simple effects for directive leadership shows a significant pre-post intervention gain on mean score for non-supervisory personnel. Implications for social change include recognizing perceptions of enhanced directive leadership that can help remove manufacturing interruptions to increase productivity and decrease costs.

Risky alcohol use is a major health concern among college students, with 40.1% reporting binge drinking (5 or more drinks in one occasion) and 14.4% reporting heavy drinking (binge drinking on 5 or more occasions) in the past month. Risky alcohol use is thought to be the result of a complex interplay between genes, biological processes, and other phenotypic characteristics. Understanding this complex relationship is further complicated by known phenotypic heterogeneity in the development of alcohol use. Developmental studies have suggested two pathways to risky alcohol use, characterized by externalizing and internalizing characteristics, respectively. However, the underlying biological processes that differentiate these pathways are not fully understood. Neuroimaging studies have assessed reward sensitivity, emotion reactivity, and behavioral inhibition using fMRI and separately demonstrate associations in externalizing and internalizing disorders more broadly. In addition, previous genetic studies have found associations between specific polymorphisms and these externalizing and internalizing subtypes. Therefore, we sought further characterize the biological influences on binge drinking subtypes through the following specific aims: 1) determine the genetic relationship between externalizing and internalizing characteristics in binge drinkers, 2) test whether externalizing and internalizing binge drinkers show differences in brain activation in response to tasks measuring emotion reactivity, reward sensitivity, and behavioral inhibition. In order to achieve these aims, we conducted a series of genetic analyses assessing differences in overall SNP-based heritability and specific associated variants between the externalizing and internalizing subtypes. There were a few variants that reached genome-wide significance, the most notable being a cluster of SNPs associated with internalizing characteristics that were located in the RP3AL gene. In a subset of these binge drinking young adults, brain activation was measured on tasks assessing behavioral inhibition, reward sensitivity, and emotion reactivity. We found some preliminary differences with regard to emotion reactivity, that suggest internalizing binge drinkers are more reactive to faces overall but have blunted reaction to sad faces compared to externalizers. These findings provide an initial step to better understanding the underlying biology between the classic externalizing and internalizing alcohol use subtypes, which has the potential to elucidate new subtype specific targets for prevention and intervention.

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A significant number of individuals begin drinking alcohol early in life during adolescence, a period in which their brain is developing. Drinking alcohol at an early age is linked to a greater likelihood that a person will become an alcoholic later in life. Levels of Glutamate (GLU), a major neurotransmitter, in the medial prefrontal cortex (mPFC) has been directly linked to the expression of alcohol-use disorders. Thus, a better understanding of how childhood drinking produces alterations in the brain, thereby contributing to alcoholism, is needed. The current research utilized an animal model of alcoholism to examine the long range consequences of alcohol consumption during adolescence on GLU functioning within the mPFC in adulthood. It was hypothesized, adolescent drinking would lead to a higher levels of GLU in the mPFC in adulthood. Two groups of alcohol-preferring (P) rats received either free-access to alcohol (15% v/v) and water or water alone in their home cage (24 hrs a day; 7 days a week) during their adolescent period. At the end of the adolescent period, alcohol was removed and all animals were provided only water to drink for approximately 21 days. Next, animals were implanted with guide cannula aimed at infralimbic and prelimbic regions of the mPFC and provided one-week to recover before undergoing quantitative microdialysis, a method that allows for the direct sampling of GLU from brain tissue. During testing, samples were collected every 10 minutes and animals were first exposed to artificial cerebral spinal fluid (aCSF) followed by aCSF containing three GLU concentrations (1 µM, 5 µM , and 10 µM; presented in randomized order across rats). By exposing the animals to different levels of GLU, the average brain level of GLU can be established as well as how fast the brain is removing/clearing GLU. Samples were analyzed using high-pressure liquid chromatography a method that quantifies GLU levels in each sample. Analyses revealed a significantly lower level of GLU removal/clearance in the prelimbic region of the mPFC of the alcohol-drinking group compared to the water group. Analyses also revealed a significantly higher average level of GLU in the alcohol-drinking group compared to the water drinking control group. There were no differences between groups in average GLU levels or GLU clearance in the infralimbic region of the mPFC. Overall, the data from the current study suggest that the consumption of alcohol during adolescence may produce a long-lasting reduction of GLU removal/clearance thereby resulting in increased GLU levels within the prelimbic region of the mPFC. The current findings may represent a long-lasting change that happens in the brain when an individual consumes alcohol during adolescence which could then contribute to the development of an alcohol-use disorder later in life.

A placebo effect is a real and beneficial psychobiological phenomenon following the administration of a substance or procedure that has no inherent power to produce an effect. Nocebo effects, on the other hand are genuine and detrimental psychobiological phenomenon following the administration of and inert substance or procedure. These effects have been extensively studied but are not well understood. Central to the development of a placebo effect is the anticipation of benefit or the anticipation of harm. Indeed, expectancy and conditioning are thought to be the two primary mechanisms involved in the acquisition of the placebo effect. The neurotransmitter Dopamine (DA) is integral to expectancy and reward and as such has recently been considered a key player in the mechanisms of the placebo effect. Based on this line of inquiry this study sought to investigate the role DA might have in the development of the placebo effect as observed in pain using an animal (mouse) model. It was proposed that DA is involved in the acquisition and maintenance of the placebo effect. Specifically it was proposed that the DA agonist cocaine would enhance the magnitude and duration of the placebo analgesia and that the DA antagonists SCH23390 and eticlopride would together or separately block the acquisition of the placebo analgesia. These proposals were assessed by utilizing supra-spinal (hotplate) and spinal (tail flick latency) protocols. Results indicated that cocaine enhanced placebo analgesia in spinal but not supra-spinal measures and that the DA antagonists SCH23390 and eticlopride each contributed to the acquisition, rather than the blockade, of placebo analgesia in both spinal and supra-spinal models. In fact, the most profound effect was observed when both antagonists were administered together rather than separately on supra-spinal measures but not spinal measures resulting in an enduring nocebo effect contradicting all predictions. The novel results presented in this study raises more questions than they answer, warranting more detailed exploration of the mechanisms of DA and its relationship with placebo effects.

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