A collection of poems based on Elizabeth Barrett-Browning's Sonnets From The Portuguese.

Recent studies showed that GPR30, a seven-transmembrane G protein-coupled receptor, is a novel estrogen receptor (ER) that mediates some biological events elicited by estrogen in several types of cancer cells. However, its physiological or pathological role in vivo is unclear. For the first project of my dissertation, I investigated the physiological role(s) of GPR30 in energy metabolism by using transgenic mouse model as well as immortalized cell lines and primary stromal cells. We discovered for the first time that GPR30 knockout (GPRKO) female mice were protected from high-fat diet (HFD)-induced obesity, glucose intolerance, and insulin resistance. The decreased body weight gain in GPRKO female mice is due to the reduction in body fat mass. These effects occurred in the absence of significant changes in food intake, intestinal fat absorption, or triglyceride metabolism. However, GPR30 had no significant metabolic effects in male mice fed the HFD and both sexes of mice fed a chow diet. Further, GPR30 expression levels in fat tissues of WT obese female mice greatly increased, whereas ERα/β expression was not altered. Deletion of GPR30 reduced adipogenic differentiation of adipose tissue-derived stromal cells. Conversely, activation of GPR30 enhanced adipogenic differentiation of 3T3-L1 preadipocytes. For the second project, I explored whether estrogen acts through GPR30 to affect adiposity in female mice. For this study, I generated and examined three independent transgenic mouse models, aromatase (Ar) knockout (ArKO) mice, GPRKO, and GPR30 and Ar double knockout (DKO) mice. We discovered that GPR30 deficiency had limited effects on energy metabolism in mice fed a standard chow diet (STD). However, deletion of GPR30 promoted metabolic flexibility in both genders fed a HFD regardless of the presence of estrogen, suggesting that GPR30 may not solely act as an ER. Consistent with our previous findings, GPRKO mice had higher body temperature, indicating that GPR30 deficiency may promote thermogenesis and energy metabolism, resulting in the reduced fat depots and enhanced metabolic flexibility. For the third project, I further explored whether GPR30 is involved in regulating browning of adipose tissue and thermogenesis in mice. The results show that the expression of UCP-1, the key regulator of thermogenic browning, was higher in the adipose tissue of HFD-fed GPRKO female mice as compared with that of WT mice. Consistently, deletion of GPR30 enhanced mitochondrial respiration in brown adipose tissue (BAT), suggesting that GPR30 deficiency at least partially suppressed the fat accumulation by promoting thermogenesis and dissipating energy. Ex vivo, the expression of thermogenic genes and UCP-1 protein level were upregulated in beige adipocytes differentiated from GPR30-deficient stromal vascular fraction (SVF) cells. These findings provide evidence for the first time that deletion of GPR30 reduces adiposity, promotes white adipose beigeing and thermogenesis, therefore preventing the development of obesity in female mice exposed to excess energy. Further investigations elucidating the underlying mechanism by which GPR30 promotes obesity in females could provide a novel therapeutic target to fight obesity in females. / Doctor of Philosophy / Estrogen can elicit pleiotropic genomic and rapid nongenomic cellular responses via a diversity of estrogen receptors (ERs). Unlike the genomic responses, where the classical nuclear ERα and ERβ initiate gene transcription in estrogen target tissues, the nongenomic cellular responses to estrogen are believed to start at the plasma membrane, leading to rapid activation of second messengers-triggered cytoplasmic signal transduction cascades. The recently acknowledged ER, GPR30, was discovered in human breast cancer cells two decades ago and subsequently in many other cells. Since its discovery, it has been claimed that estrogen, ER antagonist fulvestrant, as well as some estrogenic compounds can directly bind to GPR30, and therefore initiate the rapid nongenomic cellular responses. We are interested to investigate the physiological role(s) of GPR30 in energy metabolism by using transgenic mouse model as well as immortalized cell lines and primary stromal cells. We discovered for the first time that deletion of GPR30 protects female mice from high fat-diet (HFD)-induced obesity and the expression of GPR30 increased in fat tissues of wild type (WT) obese mice, while no alterations of classical ERα/β observed. Consistently, activation of GPR30 by the selective agonist G-1 promotes adipogenic differentiation of 3T3-L1 preadipocytes. ERα is known to exert a protective effect against excess fat accumulation whereas GPR30 may acts as an “obesity gene” and counteracts the classical ERα’s action in regulating fat metabolism. We speculated that there might be a “Yin-Yang” relationship between GPR30 and ERα regarding their actions in the development of obesity. Therefore, we generated three independent transgenic mouse models, GPR30 and aromatase (Ar) double knockout (DKO), GPR30 knockout (GPRKO), and Ar knockout (ArKO) to test our hypothesis that the excess fat accumulation in HFD-fed WT mice could be, or at least partially, caused by the enhanced estrogen-GPR30 signaling. Ar is the key enzyme that catalyzes the biosynthesis of C18 estrogens from C19 androgens in men and postmenopausal women, thereby the ArKO and DKO mouse models allowed us to investigate the role of GPR30 in the absence of endogenous estrogen. We discovered that GPR30 deficiency had limited effects on energy metabolism in young mice fed a standard chow diet (STD). However, deletion of GPR30 promoted metabolic flexibility in both genders fed a HFD regardless of the presence of estrogen, suggesting GPR30 may not solely acts via the ligation of estrogen. Interestingly, consistent with our previous findings, GPRKO mice had higher body temperature, indicating that GPR30 deficiency may promote thermogenesis and energy metabolism, resulting in the reduced fat depots and enhanced metabolic flexibility. Hence, we explored that deletion of GPR30 exerted thermo-promoting effect via upregulation of the mitochondrial uncoupling protein-1 (UCP-1) and enhanced mitochondrial respiration in brown adipose tissue (BAT). Further, the expression of thermogenic genes were significantly higher in the stromal cells-differentiated beige adipocytes, suggesting that GPR30 deficiency suppressed fat accumulation by promoting thremogenic browning of white adipose tissue (WAT) and dissipating excess energy as heat. In summary, my dissertation work provide valuable insight regarding the role of GPR30 in energy metabolism. Further investigations testing whether GPR30 acts as a pro-obesity gene would facilitate our understanding of obesity development and provide a novel therapeutic target to fight obesity.

The effects of starch-based anti-caking agents on the browning of Mozzarella cheese were evaluated in this experiment. Six commercially available anti-caking agent treatments were examined and color measurements indicated that the starch-based anti-caking agents produced a baked cheese with a greater degree of browning than the samples treated with cellulose based anti-caking agents or no treatment (control). The cellulose-based treatments and the control also had a significantly greater moisture loss than the potato starch-based treatments. A negative correlation between percent moisture loss and the amount of browning was found (R2=0.51). The average surface temperature was at least 16 °C higher for the treatments containing potato starch than for the cellulose-based treatments. A significant relationship between average surface temperature and browning was also found (R2=0.67). These relationships suggest that the starch-based treatments impeded moisture loss, which decreased the amount of evaporative cooling. An increase in surface temperature resulted from the decrease in the amount of evaporative cooling and thus the Maillard reaction was accelerated leading to increased browning. The effects of the starch source were examined using starches from corn, rice and wheat. These starches were compared to commercially available potato starch and cellulose anti-caking agents. All starch sources were found to produce a greater degree of browning on the cheese sample compared to the cellulose treatment and control. Four adjuncts treatments, including dimethypolysiloxane, lactic acid, partially hydrogenated sunflower oil, and a combination of the dimethylpolysiloxane and sunflower oil were added to cheese treated with potato starch to determine if a reduction in the degree of browning could be achieved. No differences in browning between the potato starch treatment and those with added adjuncts were found. / Master of Science

By presenting the auditor as a unifying principle that links Browning's earliest works to his dramatic monologues, this dissertation enhances the importance of the ever-ignored experimental works in developing the dramatic monologue technique. An exploration of the emergence and development of the auditor has an additional, but never ancillary, effect of proclaiming the originality and inventiveness of Browning's dramatic technique.

This dissertation explores Elizabeth Barrett's dependency on the archetypal Victorian patriarch. Chapter I focuses on the psychological effects of this father-daughter relationship on Elizabeth Barrett. Chapter II addresses Barrett's acceptance of the conventional female role, which is suggested by the nature and the situation of the women she chooses to depict. These women are placed in situations where they can reveal their devotion to family, their capacity for passive endurance, and their wish to resist. Almost always, they choose death as an alternative to life where a powerful father figure is present. Chapter III concentrates on the highly sentimental images of women and children whom Barrett places in a divine order, where they exist untouched by the concerns of the social order of which they are a part. Chapter IV shows that the conventional ideologies of the time, society's commitment to the "angel in the house," and the small number of female role models before her increase her difficulty to find herself a place within this order. Chapter V discusses Aurora Leigh's mission to find herself an identity and to maintain the connection with her father or father substitute. Despite Elizabeth Barrett's desire to break away from her paternal ties and to establish herself as an independent woman and poet, her unconditional loyalty and love towards her father and her tremendous need for his affection, and the security he provides restrain her resistance and surface the child in her.

This thesis is concerned with the establishment of an underlying philosophy for Robert Browning's many themes. It asserts that a notion found in II Corinthians 3:6, "the letter killeth, but the spirit giveth life," is basic to ideas such as Browning's belief in the superiority of life over art, of the wisdom of the heart over the intellect, and of honest skepticism over unexamined belief. The sources used to establish this premise are mainly the poems themselves, grouped in categories by subject matter of art, love, and religion. Some of his correspondence is also examined to ascertain how relevant the philosophy was to his own life. The conclusion is that the concept is, indeed, pervasive throughout Browning's poetry and extremely important to the man himself.

Thesis (M.A.)--University of Montana, 2008. / Title from title screen. Description based on contents viewed Oct. 27, 2008. Includes bibliographical references (p. 73-75).

Thesis (Ph.D.)--Texas Christian University, 2007. / Includes abstract. Includes bibliographical references (p. 301-316). Also available in electronic form.

Thesis (Ph. D.)--University of Wisconsin, 1967. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliography.

Thesis (Ph.D.)--Texas Christian University, 2007. / Title from dissertation title page (viewed May. 15, 2007). Includes abstract. Includes bibliographical references.