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You searched for +publisher:"Texas A&M University" +contributor:("Weeks, Brad R"). Showing records 1 – 3 of 3 total matches.

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Texas A&M University

1. Jessen, Staci LeAnn. Computational and In Vitro Models to Analyze the Interactions of Ventricular Assist Devices and Thromboemboli.

Degree: PhD, Biomedical Engineering, 2016, Texas A&M University

Heart failure is consistently one of the top causes of death each year worldwide. Ventricular assist devices (VADs) have become common alternatives for patients with severe, end-stage heart failure; VADs take a significant load off of the heart and aid in perfusion of downstream organs by pumping blood from either or both ventricles to their corresponding great vessel. External VAD controllers track specific pump parameters such as estimated flow rates and device power consumption. Suspected thrombosis is a common clinical adverse event in VAD therapy. In this condition, a VAD controller will indicate periods of low flow or high power; clinicians suspect that this indicates that a thrombus is increasing friction between the moving components and/or obstructing the inflow or outflow. Suspected thrombosis typically results in device exchange surgery. A pathology evaluation of the explanted VAD can reveal if materials inside the pump at explant originated within or upstream from the device. VADs explanted after years of support often had an actively organizing thrombus along the inflow cannula or protruding from the insertion site in the ventricle. We hypothesize that these thrombi form over time due to regions of stagnation and recirculation of the blood in the ventricle. Moreover, as the VAD continues to take a load off of the heart, we suspect that the remodeling of the heart will change the flow dynamics within the ventricle and cause thrombi to dislodge and travel into the pump. As thrombi of different age and size pass into the device, we hypothesize that each VAD model will demonstrate a particular change in flow rate in response to the thrombus. Through the research in this dissertation, we have investigated these phenomena by creating a computational model of the ventricular insertion site before and after cardiac remodeling occurs, and an in vitro model that displays VAD response to thromboembolic particles. These computational and in vitro models show that over time, the presence of the VAD inflow cannula within the heart will change the potential for thrombi to form around the device, dislodge, and travel into the VAD, and result in changes of pump flow rate. This research is beneficial to VAD manufacturers and clinicians in the development of devices that will limit opportunity for thromboembolic complications, and provide direction for treatment of patients currently undergoing VAD therapy. Advisors/Committee Members: Clubb, Fred J (advisor), Criscione, John C (advisor), Weeks, Brad R (committee member), Moreno, Michael R (committee member).

Subjects/Keywords: ventricular assist devices; thrombosis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Jessen, S. L. (2016). Computational and In Vitro Models to Analyze the Interactions of Ventricular Assist Devices and Thromboemboli. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/157092

Chicago Manual of Style (16th Edition):

Jessen, Staci LeAnn. “Computational and In Vitro Models to Analyze the Interactions of Ventricular Assist Devices and Thromboemboli.” 2016. Doctoral Dissertation, Texas A&M University. Accessed February 26, 2021. http://hdl.handle.net/1969.1/157092.

MLA Handbook (7th Edition):

Jessen, Staci LeAnn. “Computational and In Vitro Models to Analyze the Interactions of Ventricular Assist Devices and Thromboemboli.” 2016. Web. 26 Feb 2021.

Vancouver:

Jessen SL. Computational and In Vitro Models to Analyze the Interactions of Ventricular Assist Devices and Thromboemboli. [Internet] [Doctoral dissertation]. Texas A&M University; 2016. [cited 2021 Feb 26]. Available from: http://hdl.handle.net/1969.1/157092.

Council of Science Editors:

Jessen SL. Computational and In Vitro Models to Analyze the Interactions of Ventricular Assist Devices and Thromboemboli. [Doctoral Dissertation]. Texas A&M University; 2016. Available from: http://hdl.handle.net/1969.1/157092


Texas A&M University

2. Yoo, Gyhye. Influence of Estradiol and Phytoestrogens on Colitis and Colon Cancer.

Degree: PhD, Nutrition, 2015, Texas A&M University

Estrogen is a female sex hormone that has a variety of biologic actions via modulation of gene expression through estrogen receptors (ERs). The protective effect of estradiol (E2) and estrogen signaling in colon cancer has been demonstrated in epidemiological and clinical data as well as animal experiments. The overall aim of this series of studies is to determine the protective mechanism of estrogen signaling activated by E2 and phytoestrogens on colitis and colon cancer. First, the estrogenic effect of novel phytoestrogens, trigonelline (Trig) and 3,3-diindolylmethane (DIM) was determined in non-malignant colonocytes (YAMCs). Both molecules decreased cell growth of YAMCs, but their mechanisms of action were distinct from E2. Trig increased apoptosis by functional ERs without direct binding to ERs while DIM altered the expression of target genes of ERs via increased ER transcriptional activity. These data suggest that phytoestrogens could activate estrogen signaling through unique mechanisms. Second, the protective effect of estrogen signaling on colitis and colitis associated colon cancer (CAC) was demonstrated in vitro and in vivo. In the in vitro study, IL-6 induced cell growth was observed, and E2 and genistein (GEN) treatment inhibited IL-6 actions via an increase of apoptosis and modulation of gene expression related to estrogen signaling. In the in vivo colitis experiment, chronic inflammation damaged the colon, but E2 treatment increased the recovery of the damaged colon via an increase of cell proliferation with modulation of cytokines. However, GEN treatment exacerbated the damage on chronic inflammation. In the CAC model, E2 and GEN treatment suppressed the formation of aberrant crypt foci (ACF), premalignant lesions. These data suggest that E2 protects the colon and colon epithelial cells, and the protective mechanism of estrogen signaling differs depending on the type of injury and local conditions. Lastly, the interaction of estrogen signaling and the p53 pathway was studied using intestinal epithelial cell-specific p53 knockout mice (Tp53^ΔIEC). The protective effect of E2 in Tp53^ΔIEC mice was observed, suggesting that the suppression of ACF by estrogen signaling is partially independent of the p53 pathway. Overall, estrogen signaling has a protective property against colitis and colon cancer but the protective mechanism of estrogen signaling could be changed from apoptosis to proliferation depending on the condition of the colon. In addition, each phytoestrogen has a distinct and unique way of influencing the colon. These data help clarify the role and the mechanism of estrogen signaling on colon cancer. Advisors/Committee Members: Allred, Clinton D (advisor), Chapkin, Robert S (committee member), Talcott, Stephen T (committee member), Weeks, Brad R (committee member).

Subjects/Keywords: Estrogen Signaling; Phytoestrogens; Colitis; Colon Cancer; IL-6; p53

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Yoo, G. (2015). Influence of Estradiol and Phytoestrogens on Colitis and Colon Cancer. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/156457

Chicago Manual of Style (16th Edition):

Yoo, Gyhye. “Influence of Estradiol and Phytoestrogens on Colitis and Colon Cancer.” 2015. Doctoral Dissertation, Texas A&M University. Accessed February 26, 2021. http://hdl.handle.net/1969.1/156457.

MLA Handbook (7th Edition):

Yoo, Gyhye. “Influence of Estradiol and Phytoestrogens on Colitis and Colon Cancer.” 2015. Web. 26 Feb 2021.

Vancouver:

Yoo G. Influence of Estradiol and Phytoestrogens on Colitis and Colon Cancer. [Internet] [Doctoral dissertation]. Texas A&M University; 2015. [cited 2021 Feb 26]. Available from: http://hdl.handle.net/1969.1/156457.

Council of Science Editors:

Yoo G. Influence of Estradiol and Phytoestrogens on Colitis and Colon Cancer. [Doctoral Dissertation]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/156457


Texas A&M University

3. Armstrong, Cameron Michelle. The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.

Degree: PhD, Nutrition, 2013, Texas A&M University

Epidemiological studies suggest pre-menopausal women have a reduced risk for sporadic and inflammation-associated colon cancer compared to post-menopausal women and men. The studies presented herein aim to determine the protective mechanisms of estradiol (E2) during sporadic and inflammation-associated colonic carcinogenesis. When investigating the role of E2 and fish oil at the earliest stage of sporadic colon cancer development, E2 had no effect on DNA adduct formation while dietary fish oil significantly reduced DNA adduct formation. Contrarily, E2 significantly induced apoptosis of damaged colonocytes while fish oil was not protective. In an in vivo model of inflammation-associated colon carcinogenesis with E2 administered following induction of DNA damage and initiation of inflammation, E2 treatment was associated with decreased colon tumor size and number in wild type (WT) but not estrogen receptor (ER) β knockout (ERβKO) mice. Interestingly, apoptosis was reduced and proliferation increased by E2 in these tumors in WT mice. This may be due to the altered ER expression in these tissues as the tumors developed, with ERβ expression decreasing concomitantly with ERα expression increasing. Contrary to the protective effect of E2 on inflammation-associated colon tumor formation, which was dependent on ERβ, during acute inflammation in the colon E2 was protective against inflammation in both WT and ERβKO mice and injury in ERβKO mice. The protection against inflammation is likely due to the reduction of pro-inflammatory cytokine expression by E2. Apoptosis and proliferation were decreased and increased in the proximal and distal colon respectively in ERβKO mice. In vitro studies further elucidated the roles of ERα and ERβ in colonocytes. E2 and ERβ, but not ERα, specific agonists reduced cell number and induce apoptosis in nonmalignant colonocytes. This effect was lost in the presence of mutated p53. In ERα overexpressed nonmalignant colonocytes, E2 had no effect on cell number while ERβ agonist and ERα agonists decreased and increased cell number respectively. These studies suggest that E2 is protective in the colon and ERβ is required for protection against carcinogenesis but not protection against inflammation. Additionally, the protection against colon carcinogenesis is likely p53 mediated. Advisors/Committee Members: Allred, Clinton D (advisor), Turner, Nancy D (committee member), Villalobos, Alice R (committee member), Weeks, Brad R (committee member).

Subjects/Keywords: colon cancer; estradiol; estrogen receptor; inflammation

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Armstrong, C. M. (2013). The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151883

Chicago Manual of Style (16th Edition):

Armstrong, Cameron Michelle. “The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.” 2013. Doctoral Dissertation, Texas A&M University. Accessed February 26, 2021. http://hdl.handle.net/1969.1/151883.

MLA Handbook (7th Edition):

Armstrong, Cameron Michelle. “The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer.” 2013. Web. 26 Feb 2021.

Vancouver:

Armstrong CM. The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Feb 26]. Available from: http://hdl.handle.net/1969.1/151883.

Council of Science Editors:

Armstrong CM. The Protective Effects of Estradiol on Sporadic and Inflammation-associated Colon Cancer. [Doctoral Dissertation]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151883

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