Breaking Surface: Unearthing Meaning in Jenny Schwartz\u27s God\u27s Ear

I struggle with language. I don’t trust definitions or labels. Words elude me – articulating a thought becomes a painful exercise for my brain. I often adhere too strictly to meaning, and can pinpoint when an idea I’m mulling over doesn’t quite fit the word I’m using to describe it. My workaround habit is tacking on less definite, open-ended phrases (“This is kind of…” “This might be…”) – the enemies of someone training to be a clearer, well-spoken leader.I am intrigued by messy human stories that can’t be told through realism alone. I seek truth through a more imaginative theatrical lens – one in which time, space, and reality work differently than what we experience in day-to-day life

Beyond Good and Bad: The Linguistic Construction of Walter White’s Masculinity in Breaking Bad

Honors (Bachelor's)EnglishUniversity of Michiganhttp://deepblue.lib.umich.edu/bitstream/2027.42/112128/1/andypet.pd

The Assertive/Vulnerable Dimension of Dreaming Style

This study involved the exploration of the Assertive/Vulnerable dimension of dreaming style. Assertiveness and Vulnerability, as characteristics of dreaming experience, were measured using the Dreaming Style Questionnaire-Revised that was derived from a revision of Gruber\u27s 1988 Dreaming Style Questionnaire (DSQ.) For this study, the DSQ-R was administered to approximately 2500 participants. The structure, reliability, validity and waking correlates of the Assertive/Vulnerable scale of the DSQ-Revised was explored. Factor analysis replicated the Assertive/Vulnerable dreaming dimension, first uncovered by the original DSQ, as predicted, with the ten Assertive and Vulnerable items loading together to form one bi-polar factor. The exploration of sub-scales of the Assertive and Vulnerable dimensions were also replicated. The Assertive items formed sub-scales labeled Control, Power, Positive Emotion, and Success; while the Vulnerable items formed sub-scales labeled Lack of Control, Fear, Negative Emotion, and Failure. The results of test-retest procedures indicated a moderately high level of reliability (correlation\u27s between .81 and .85.) Additionally, Alpha coefficients indicated good internal consistency for both Assertive and Vulnerable scales (.81 and .86 respectively.) Finally, an investigation of waking personality traits of groups of Assertive and Vulnerable dreamers revealed very similar findings to that of Gruber (1988.) Discriminant analyses identified significant differences between groups of both men and women at p \u3c .0001. The resulting personality profiles provide support for the continuity of waking and dreaming experiences, as well as further supporting the validity of the Assertive/Vulnerable scale

Subtype-specific plasticity of inhibitory circuits in motor cortex during motor learning.

Motor skill learning induces long-lasting reorganization of dendritic spines, principal sites of excitatory synapses, in the motor cortex. However, mechanisms that regulate these excitatory synaptic changes remain poorly understood. Here, using in vivo two-photon imaging in awake mice, we found that learning-induced spine reorganization of layer (L) 2/3 excitatory neurons occurs in the distal branches of their apical dendrites in L1 but not in the perisomatic dendrites. This compartment-specific spine reorganization coincided with subtype-specific plasticity of local inhibitory circuits. Somatostatin-expressing inhibitory neurons (SOM-INs), which mainly inhibit distal dendrites of excitatory neurons, showed a decrease in axonal boutons immediately after the training began, whereas parvalbumin-expressing inhibitory neurons (PV-INs), which mainly inhibit perisomatic regions of excitatory neurons, exhibited a gradual increase in axonal boutons during training. Optogenetic enhancement and suppression of SOM-IN activity during training destabilized and hyperstabilized spines, respectively, and both manipulations impaired the learning of stereotyped movements. Our results identify SOM inhibition of distal dendrites as a key regulator of learning-related changes in excitatory synapses and the acquisition of motor skills

Pharmacologic and Genetic Manipulations of Angiotensin Signaling in Thoracic Aortic Disease Models

Thoracic aortic aneurysms and dissections (TAAD) are a major cause of morbidity and mortality in patients. Many different risk factors have been associated TAAD, but hypertension is the largest risk factor. Subsets of TAAD patients have identifiable syndromic genetic diseases, yet a number of genetic non-syndromic patients have been identified. Infusion of angiotensin II into mouse models causes aortic disease through inflammation and fibrosis. An angiotensin type I receptor (AT1R) blocker (ARB) or an angiotensin converting enzyme (ACE) inhibitor (ACEi) can reverse aortic pathology in some mouse models. I set out to better understand the relationship between angiotensin and TAAD in our mouse models, and hypothesized that angiotensin II signaling through the AT1R contributes to thoracic aortic aneurysm formation in multiple model systems of disease, and that blocking related receptors in addition to the AT1R, such as the AT2R and Mas receptor, may have negative consequences. Previously identified genetic variants in the gene encoding smooth muscle alpha-actin, ACTA2, were modeled with Acta2-/- mice. I found that the ascending aorta and aortic root in these mice become significantly dilated over time. Acta2-/- mice are hypotensive, and increasing the blood pressure with a pharmaceutical and diet based regimen significantly accelerated and worsened the aortic phenotype. Treatment with losartan, an ARB, attenuated the aortic dilation, but captopril, an ACEi, did not decrease aortic growth and worsened the disease. Transverse aortic constriction (TAC) was used to study the ascending aorta and aortic root in response to increased biomechanical forces. Losartan attenuated the histologic and inflammatory changes associated with TAC, but captopril was again unable to rescue the phenotype. To understand why, I investigated other receptors blocked by ACEis: the angiotensin II type 2 receptor (AT2R) and the Mas receptor, a receptor for the Ang1-7 peptide. I found that cotreatment with captopril and an agonist for the AT2R had similar physiologic effects as the AT1R blocker despite being unable to prevent the fibrotic and inflammatory remodeling. In contrast, cotreatment with captopril and an agonist for the Mas receptor blocked remodeling but did not rescue aneurysm formation. My results, coupled with clinical data, indicate that fibrosis may be beneficial in the aorta, and show we must expand our understanding of the angiotensin system in aortic disease