The following paper explores the various effects of stress on the endocrine system. Many understand that being stressed can jeopardize maintaining adequate health, but what specifically happens when humans are stressed? Why does stress affect human health? This paper delves into background information, previous research, and the depths to which stress negatively affects the body. The effects stress has on the endocrine system, specifically on the hypothalamic-pituitary-thyroid axis (HPT) and hypothalamic-pituitary-adrenal axis (HPA), is discussed, and additionally, at home de-stressing methods are researched. The study included a set of participants at Arizona State University. The method took place over the course of 2 weeks: one normal week, and the other with the implementation of a de-stressing method. The normal week involved the participants living their daily lives with the addition of a stress-measuring survey, while the second week involved implementing a de-stressing method and stress-measuring survey. The purpose of this study was to discover if there was a correlation between performing these relaxation activities and decreasing stress levels in ASU students. The results found that students reported they felt more relaxed and calm after the activities. Overall, this thesis provides information and first hand research on the effects of stress and stress-reducing activities and discusses the importance of maintaining lower stress levels throughout everyday life.

Exploration of a mouse model (C57BL/6J) capable of demonstrating behavioral changes after adolescent social isolation that are consistent with prior findings may prove beneficial in later research. This study examined 2 proposed long-term effects of isolated housing (one mouse/cage), when compared to group housing (two mice/cage) during adolescence. Mice were placed in their respective housing conditions after weaning (PND 21) and remained in those conditions until PND 60. The same cohorts were used in both phases of the experiment. Phase 1 sought to confirm previous findings that showed increases in ethanol intake after adolescent social isolation using a 2-bottle preference Drinking-in-the-Dark (DID) design over a 4-day period (PND 64-PND 67.). Phase 2 sought to elucidate the effects present after adolescent social isolation, as measured using response inhibition capabilities demonstrated during fixed-minimum interval (FMI) trials (PND 81-PND 111). Findings in phase 1 of the experiment were non-significant, save a strong tendency for female mice in both housing conditions to drink more as a proportion of their bodyweight (g/kg). However, a trend of lower bodyweight in single housed mice did exist, which does suggest that detrimental stress was applied via the used of adolescent isolation in that housing condition. Findings in phase 2 showed little effect of adolescent social isolation on mean inter-response time (IRT) at any criterion used (FMI-0, FMI-4, FMI-6). Evaluation of mean interquartile range (IQR) of IRTs showed a significantly greater amount of variation in IRT responses within single housed mice at the highest criterion (FMI-6), and a trend in the same direction when FMI-4 and FMI-6 were tested concurrently. Taken as a whole, the findings of this experiment suggest that the effect of adolescent social isolation on ethanol intake is far less robust than the effect of sex and may be difficult to replicate in a low-power study. Additionally, adolescent social isolation may interfere with the ability of mice to show consistent accuracy during FMI tasks or a delay in recognition of FMI criterion change.

Down syndrome (DS) is a common genetic developmental disorder characterized by the trisomy of chromosome 21 (Hsa21). All individuals with DS have some kind of intellectual disability, associated with dysfunction in cognition-related structures, including the frontal cortex. Studies have examined developmental changes in the frontal cortex during prenatal stages in DS, however little is known about cortical lamination and neuronal differentiation in postnatal periods in this neurodevelopmental disorder. Therefore, we examined the quantitative and qualitative distribution of neuronal profiles containing the neuronal migration protein doublecortin (DCX), the non-phosphorylated high-molecular-weight neurofilament SMI-32, the calcium-binding proteins calbindin D-28K (Calb), calretinin (Calr), and parvalbumin (Parv), as well as human β-amyloid and APP (6E10), Aβ1-42, and phospho-tau (CP-13) in the supragranular (SG, II/III) and infragranular (IG, V/VI) layers in the DS postnatal frontal cortex compared to neurotypically developing (NTD) controls from ages 28 weeks to 196.4 weeks using immunohistochemistry. Furthermore, cortical lamination was evaluated using thionin, a Nissl stain. We found DCX-immunoreactive (-ir) cells in both the SG and IG layers in younger cases, but not in the oldest cases in both groups. Strong expression of SMI-32 immunoreactivity was observed in pyramidal cells in layers III and V in the oldest cases in both groups, however SMI-32-ir cells appeared much earlier in NTD compared to DS. We found small and fusiform Calb-ir cells in the younger cases (28 to 44 weeks), while in the oldest cases, Calb immunoreactivity was also found in pyramidal cells. Calr-ir cells appeared earlier in DS at 32 weeks compared to NTD at 44 weeks, however both groups showed large bipolar fusiform-shaped Calr-ir cells in the oldest cases. Diffuse APP/Aβ-ir plaque-like accumulations were found in the frontal cortex grey and white matter at all ages, but no Aβ1-42 immunoreactivity was detected in any case. Furthermore, neuropil (but not cellular) granular CP-13 immunostaining was seen in layer I only at 41 weeks NTD and 33 weeks DS. Cell counts show a significantly higher cell number in SG compared to IG for all the neuronal markers in both groups, except in Calb and SMI-32. In NTD, age and brain weight showed the strongest correlations with all cellular counts, except in thionin where DS had a stronger negative correlation with age and brain weight compared to NTD. In addition, height and body weight showed a strong negative correlation in NTD with the migration and neurogenesis marker DCX. These findings suggest that trisomy 21 affects the postnatal frontal cortex lamination, neuronal migration<br/>eurogenesis, and differentiation of projection pyramidal cells and interneurons, which contribute to the disruption of the local and projection inhibitory and excitatory circuitries that may underlie the cognitive disabilities in DS.