Creatures of Play

This thesis explores my practice as an artist and my work’s cultural, theoretical and social contexts, such carnival theory, feminist studies and film studies, as well as references to mythology and my own biography. I discuss forms of representation of gendered identities through my work in drawing, performance, animation, video and installation. The masks we wear become as real as our bare face. Through the act of doubling the representation, my thesis work BECOMING/a fine line situates the mask as the mediator between reflections, mirroring the identity and the notion of performativity. Embracing a certain incompleteness and embodying the theoretical idea of becoming, my work relies on the ill-defined and immediate drawing quality to reflect the perpetually unrealized performance of a stable and fixed identity

Identifying Communication Barriers and Trust Issues of Black Women Seeking Preventive Health Services in Houston, Texas

Black women mortality rates are perceived to be impacted by communication barriers, trust issues, and the lack of quality preventive health services. The purpose of this phenomenological study was to explore communication barriers and trust issues perceived by Black women when seeking preventive health services. HMB was used to identify public attitudes around receiving preventive health services and to construct each question based on perceived susceptibility and perceived severity of communication barriers and trust issues. An ecological model of the communication process was used as a framework to identify fundamental relationships between the Black female patients and health care providers. Data were collected using open-ended interview questions from Black women in public health and health care professions in southeast Texas (N=10). Results were coded and evaluated by thematic analysis. NVivo 10 software was used to store and manage data. Study findings showed 4 participants voiced their beliefs that their healthcare provider was somewhat apathetic when it came to addressing their health care needs, and 3 of the participants who visited a doctor\u27s office within the last 12 months reportedly expressed having poor communication and trust issues with their health care provider. Emerged themes included lack of attentiveness from health care providers and lack of a comfortable atmosphere or bedside manner when receiving preventive health care services from their healthcare provider. This research has implications for social change if the health inequalities of Black women are identified and addressed, then Black women may have a reduction in health disparities when receiving preventive health services and an increase healthier outcomes

Epithelial cell-directed efferocytosis in the post-partum mammary gland is necessary for tissue homeostasis and future lactation

<p>Abstract</p> <p>Background</p> <p>Mammary glands harbor a profound burden of apoptotic cells (ACs) during post-lactational involution, but little is known regarding mechanisms by which ACs are cleared from the mammary gland, or consequences if this process is interrupted. We investigated AC clearance, also termed efferocytosis, during post-lactational remodeling, using mice deficient for MerTK, Axl, and Tyro3, three related receptor tyrosine kinases (RTKs) regulating macrophage-mediated efferocytosis in monocytes. MerTK expression, apoptosis and the accumulation of apoptotic debris were examined in histological sections of MerTK-deficient, Axl/Tyro3-deficient, and wild-type mammary glands harvested at specific time points during lactation and synchronized involution. The ability of primary mammary epithelial cells (MECs) to engulf ACs was assessed in culture. Transplant of MerTK-deficient mammary epithelium into cleared WT mammary fat pads was used to assess the contribution of WT mammary macrophages to post-lactational efferocytosis.</p> <p>Results</p> <p>ACs induced MerTK expression in MECs, resulting in elevated MerTK levels at the earliest stages of involution. Loss of MerTK resulted in AC accumulation in post-lactational MerTK-deficient mammary glands, but not in Axl and Tyro3-deficient mammary glands. Increased vascularization, fibrosis, and epithelial hyperproliferation were observed in MerTK-deficient mammary glands through at least 60 days post-weaning, due to failed efferocytosis after lactation, but did not manifest in nulliparous mice. WT host-derived macrophages failed to rescue efferocytosis in transplanted MerTK-deficient mammary epithelium.</p> <p>Conclusion</p> <p>Efferocytosis by MECs through MerTK is crucial for mammary gland homeostasis and function during the post-lactational period. Efferocytosis by MECs thus limits pathologic consequences associated with the apoptotic load following lactation.</p

Randomized Clinical Trial of Distraction for Infant Immunization Pain

Distraction has been shown to be an effective technique for managing pain in children; however, few investigations have examined the utility of this technique with infants. The goal of the current study was to investigate the effectiveness of movie distraction in reducing infants’ immunization distress. Participants were 136 infants (range = 1 to 21 months; M = 7.6 months, SD = 5.0 months) and their parents, all of whom were recruited when presenting for routine vaccinations. The parent-child dyads were randomly assigned to either a Distraction or Typical Care control condition. Infant and adult behaviors were assessed using a visual analog scale and a behavioral observation rating scale. Results indicated parents in the Distraction group engaged in higher rates of distraction than those in the Typical Care group, whereas there was no difference in the behavior of nurses in the Distraction and Typical Care groups. In addition, infants in the Distraction group displayed fewer distress behaviors than infants in the Typical Care group both prior to and during recovery from the injection. Findings suggest that a simple and practical distraction intervention can provide some distress relief to infants during routine injections

Adrenal Demedullation and Oxygen Supplementation Independently Increase Glucose-Stimulated Insulin Concentrations in Fetal Sheep With Intrauterine Growth Restriction

In pregnancies complicated by placental insufficiency and intrauterine growth restriction (IUGR), fetal glucose and oxygen concentrations are reduced, whereas plasma norepinephrine and epinephrine concentrations are elevated throughout the final third of gestation. Here we study the effects of chronic hypoxemia and hypercatecholaminemia on β-cell function in fetal sheep with placental insufficiency-induced IUGR that is produced by maternal hyperthermia. IUGR and control fetuses underwent a sham (intact) or bilateral adrenal demedullation (AD) surgical procedure at 0.65 gestation. As expected, AD-IUGR fetuses had lower norepinephrine concentrations than intact-IUGR fetuses despite being hypoxemic and hypoglycemic. Placental insufficiency reduced fetal weights, but the severity of IUGR was less with AD. Although 2 basal plasma insulin concentrations were lower in intact-IUGR and AD-IUGR fetuses compared with intact-controls, glucose-stimulated insulin concentrations were greater in AD-IUGR fetuses compared with intact-IUGR fetuses. Interestingly, AD-controls had lower glucose- and arginine-stimulated insulin concentrations than intact-controls, but AD-IUGR and AD-control insulin responses were not different. To investigate chronic hypoxemia in the IUGR fetus, arterial oxygen tension was increased to normal levels by increasing the maternal inspired oxygen fraction. Oxygenation of IUGR fetuses enhanced glucose-stimulated insulin concentrations 3.3-fold in intact-IUGR and 1.7-fold in AD-IUGR fetuses but did not lower norepinephrine and epinephrine concentrations. Together these findings show that chronic hypoxemia and hypercatecholaminemia have distinct but complementary roles in the suppression of β-cell responsiveness in IUGR fetuses. Placental insufficiency restricts the supply of oxygen and nutrients to the fetus and causes intrauterine growth restriction (IUGR) (1, 2). The resulting fetal hypoxemia and hypoglycemia provoke endocrine responses that lower plasma insulin concentrations (3,–5). High norepinephrine and epinephrine concentrations are a hallmark of both human and animal IUGR fetuses (6,–11). These high concentrations of catecholamines inhibit insulin secretion from pancreatic β-cells and may contribute to very low insulin concentrations in the IUGR fetus (12, 13). In addition, chronic elevation of norepinephrine has been shown to slow fetal growth and induce asymmetric growth of fetal tissues (14, 15)

Molecular Analysis of Mutations Induced at the hisD3052 Allele of Salmonella by Single Chemicals and Complex Mixtures

More single chemicals and complex environmental mixtures have been evaluated for mutagenicity at the hisD3052 allele of Salmonella, primarily in strain TA98, than in any other mutation assay. The development of colony probe hybridization procedures and the application of the polymerase chain reaction and direct DNA sequencing has permitted rapid molecular access to this allele. We discuss these techniques and the resulting mutation spectra that have been induced by a variety of environmental mutagens and complex mixtures. A common GC or CG deletion within a hot-spot region of the sequence dominates most of the spectra. In addition to this two-base deletion, we have recovered about 200 other types of mutations within the 72-base target for reversion of the hisD3052 allele. These include a variety of deletions (as large as 35 bases), duplications (as large as 46 bases), and complex mutations involving base substitutions. The quasipalindromic nature of the target sequence and its potential to form DNA secondary structures and slippage mismatches appear to be an important basis for the mutability of this allele

Exome sequencing reveals independent SGCD deletions causing limb girdle muscular dystrophy in Boston terriers

Background: Limb-girdle muscular dystrophies (LGMDs) are a heterogeneous group of inherited autosomal myopathies that preferentially affect voluntary muscles of the shoulders and hips. LGMD has been clinically described in several breeds of dogs, but the responsible mutations are unknown. The clinical presentation in dogs is characterized by marked muscle weakness and atrophy in the shoulder and hips during puppyhood. Methods: Following clinical evaluation, the identification of the dystrophic histological phenotype on muscle histology, and demonstration of the absence of sarcoglycan-sarcospan complex by immunostaining, whole exome sequencing was performed on five Boston terriers: one affected dog and its three family members and one unrelated affected dog. Results: Within sarcoglycan-delta (SGCD), a two base pair deletion segregating with LGMD in the family was discovered, and a deletion encompassing exons 7 and 8 was found in the unrelated dog. Both mutations are predicted to cause an absence of SGCD protein, confirmed by immunohistochemistry. The mutations are private to each family. Conclusions: Here, we describe the first cases of canine LGMD characterized at the molecular level with the classification of LGMD2F.Peer reviewe

Imprints, Vol. 3

Imprints, Vol. 3 Laura Lundgren, Stephen F Austin State UniversitySandra L. Standley, Stephen F Austin State UniversityMelissa Miller, Stephen F Austin State UniversityCurtis Simmons, Stephen F Austin State UniversityVaughn Hamilton, Stephen F Austin State UniversitySteve Geissen, Stephen F Austin State UniversityEdward Shelton, Stephen F Austin State UniversityJames L. Choron, Stephen F Austin State UniversityAnderson Kelley, Stephen F Austin State UniversityAndrew J. Urbanus, Stephen F Austin State UniversityGordon Garrett Conner, Stephen F Austin State UniversityJames Chionsini Jr., Stephen F Austin State UniversityPaul M. Thomason, Stephen F Austin State UniversityCarol McBrayerJessica Anton, Stephen F Austin State University Download Download Full Text (5.7 MB) Description Imprints is the official publication for Sigma Tau Delta, the honorary English fraternity. The editors welcome creative works submitted by contributors and also publish winners of the annual T. E. Ferguson Writing Contest. Especially welcom are poems, fiction pieces and essays of no more than 5,000 words in length. At this time, we would like to express our gratitude to David Whitescarver, Sigma Tau Delta faculty advisor, for his unrelenting optimism and valuable help in the preparation of this journal

HER4 D-Box Sequences Regulate Mitotic Progression and Degradation of the Nuclear HER4 Cleavage Product s80HER4

Heregulin-mediated activation of HER4 initiates receptor cleavage (releasing an 80-kDa HER4 intracellular domain, s80HER4, containing nuclear localization sequences) and results in G2/M delay by unknown signaling mechanisms. We report herein that s80HER4 contains a functional cyclin B-like sequence known as a D-box, which targets proteins for degradation by APC/C, a multisubunit ubiquitin ligase. s80HER4 ubiquitination and ptoteosomal degradation occurred during mitosis but not during S-phase. Inhibition of an APC subunit (APC2) using siRNA knock-down impaired s80HER4 degradation. Mutation of the s80HER4 D-box sequence stabilized s80HER4 during mitosis, and s80HER4-dependent growth inhibition via G2/M delay was significantly greater with the D-box mutant. Polyomvirus middle-T antigen-transformed HC11 cells expressing s80HER4 resulted in smaller, less proliferative, more differentiated tumors in vivo than those expressing kinase-dead s80HER4 or the empty vector. Cells expressing s80HER4 with a disrupted D-box did not form tumors, instead forming differentiated ductal structures. These results suggest that cell cycle-dependent degradation of s80HER4 limits its growth inhibitory action, and stabilization of s80HER4 enhances tumor suppression, thus providing a link between HER4-mediated growth inhibition and cell cycle control