Thesis (Ph. D.)--University of Texas at Austin, 2001. / Vita. Includes bibliographical references. Available also from UMI/Dissertation Abstracts International.

Habilitationsschrift--Ruhr-Universität Bochum. / Bibliography: p. [457]-475.

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acase@tulane.edu / Sensitive parenting requires modulation of emotions in order to effectively organize and orient behavioral responses. There is considerable evidence that psychological distress is one of many factors that can negatively impact parenting practices. Difficulties in emotion regulation may be a pathway for the impact of psychological distress on parenting, as emotion regulation has been implicated in psychological distress; however, emotion regulation is not often examined in parenting models. The current study tested these relations in a low-income, community sample of caregivers of preschoolers (n = 64; age range 18-74 years). Results indicated that difficulties in emotion regulation mediated the relation between psychological distress and parenting sensitive engagement (b = -0.48, SE = 0.24, CI [-1.04, -0.07]). Difficulties in emotion regulation predicted decreased sensitive engagement, above and beyond the effect of psychological distress (b = -.69, SE = .33, t = -2.07, p = .044, CI [-1.35, -.20]). However, there was no total effect of psychological distress on sensitive engagement (b = -0.04, SE = 0.26, t = -0.13, p = .893, CI [-0.56, 0.49]). Acceptance of emotional responses (b = -0.34, SE = 0.15, p = .017, CI [-0.66, -0.11]) and clarity (b = -0.50, SE = 0.24, p = .025, CI [-0.97, -0.05]), or understanding of emotions, were found to predict sensitive engagement above and beyond the other dimensions of emotion regulation. Results suggest that emotion regulation is a process by which psychological distress affects parents’ sensitive engagement with their preschool-aged children. Additionally, acceptance and clarity are two dimensions of emotion regulation that may be more relevant for parents’ sensitive engagement than other dimensions. / 1 / Justin Thomas Carreras

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The regulatory mechanisms that govern heterocyst development in Anabaena sp. strain PCC 7120 have been continuously refined over the last two decades. In this work, we show that three of the sigma factor genes present in the Anabaena sp. strain PCC 7120 genome are developmentally regulated. Time-lapse microscopy of gfp reporter strains indicated that expression of sigC, sigG, and sigE is upregulated specifically in differentiating cells at 4 h, 9 h and 16 h, respectively, after induction of heterocyst development. We proposed that the sigma factors encoded by these genes are involved in regulation of heterocyst-specific genes whose expression is relatively coincident with that of sigC, sigG, or sigE. Indeed, inactivation of the sigC gene caused delayed and reduced expression of genes required for the early stages of heterocyst development, and caused delayed development. Inactivation of the sigE gene caused a considerable drop in expression of nifH, a late gene required for nitrogen fixation. We also provide evidence that c-di-GMP, a novel bacterial second messenger, is involved in regulating heterocyst development. The all2874 gene encodes a bona fide diguanylate cyclase, which synthesizes c-di-GMP, and the gene's inactivation resulted in a decreased tendency to form heterocysts; this phenotype was exacerbated by high light intensity. We hypothesize that the putative operon all2875-all2874 senses and relays information about light conditions and this information is integrated into the decision to form heterocysts. Finally, we identified the all0187 gene, which is expressed at 9 h, a time when cells that have initiated differentiation commit to complete the process. In nitrogen-free medium, all0187 mutant filaments formed abnormally long heterocysts and were unable to grow diazotrophically. Septum formation between heterocysts and their flanking vegetative cells was incomplete, leaving one or both poles of the heterocysts more opened and potentially more permeable to oxygen. Despite having nitrogenase activity, the all0187 mutant was unable to grow diazotrophically. We hypothesize that the diazotrophic growth defect is caused by the inability of the heterocysts to transport fixed nitrogen to the neighboring vegetative cells.

Thesis (Ph. D.) -- Lincoln University, 2009. / Also available via the World Wide Web.

Disequilibrium between coagulation and fibrinolysis can lead to severe haemostatic disorders such as thrombosis and hemophilia. Thrombin-activable fibrinolysis inhibitor (TAFI) is a carboxypeptidase B-like pro-enzyme that, once activated, attenuates fibrinolysis. TAFI may also mediate connections between coagulation and inflammation. Studies have associated high plasma TAFI levels with risk for thrombotic diseases. Interestingly, steroid hormones, such as estrogen and progestogens used in hormone replacement therapy or oral contraceptive preparations, have been shown to affect plasma TAFI levels. Regulation of the expression of the gene encoding TAFI, CBP2, is likely an important determinant of the role of the TAFI pathway in vivo; this concept motivated the investigations described in this thesis. In Chapter 2, the results of my research lead to the identification of key transcription factors regulating CPB2. Specifically, we described the binding of NF-Y and HNF-1 to the CPB2 promoter. NF-Y was shown to be an important factor for the basal CPB2 promoter activity. Binding of HNF-1 is essential for the activity of the promoter and is potentially responsible for the liver specific expression of CPB2. In Chapter 3, we set to investigate the effect of female sex hormone on hepatic expression of CPB2. We demonstrated that the levels of TAFI protein secreted from cultured hepatoma cells (HepG2) are decreased by 17beta-estradiol and progesterone. The change in protein expression was paralleled by decreases in CPB2 mRNA abundance and promoter activity. Deletion analysis of the CPB2 promoter indicated that the genomic effects of estrogen and progesterone are likely mediated via a non-classical mechanism. In Chapter 4, we evaluated the effects of various inflammatory mediators on expression of the gene encoding mouse TAFI (Cpb2). Our results showed that Cpb2 mRNA abundance and promoter activity are up-regulated by inflammatory mediators IL-1beta, IL-6, and TNFalpha. We also showed that TNFalpha mediates its effect via the binding of NFkB. Additionally, our results suggest that TNFalpha promotes the binding of NFkB to the promoter by increasing its translocation to the nucleus. The NFkB site is not conserved between human and mouse and may explained the different responses to inflammation observed in vivo. / Thesis (Ph.D, Biochemistry) -- Queen's University, 2009-09-25 16:56:46.043