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You searched for +publisher:"University of Miami" +contributor:("Si M. Pham"). Showing records 1 – 3 of 3 total matches.

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University of Miami

1. Montero, Ramon B. Design of Electrospun Gelatin Based Scaffolds with Controlled Biological and Architectural Cues for Therapeutic Angiogenesis.

Degree: PhD, Biomedical Engineering (Engineering), 2012, University of Miami

Current therapeutic angiogenesis strategies are focused on the development of biologically responsive scaffolds that can deliver multiple angiogenic cytokines and/or cells in ischemic regions. Herein, we report on a novel electrospinning approach to fabricate cytokine-containing nanofibrous scaffolds with tunable architecture to promote angiogenesis. Fiber diameter and uniformity were controlled by varying the concentration of the polymeric (i.e. gelatin) solution, the feed rate, needle to collector distance, and electric field potential between the collector plate and injection needle. Scaffold fiber orientation (random vs. aligned) was achieved by alternating the polarity of two parallel electrodes placed on the collector plate thus dictating fiber deposition patterns. Basic fibroblast growth factor (bFGF) was physically immobilized within the gelatin scaffolds at variable concentrations and human umbilical vein endothelial cells (HUVEC) were seeded on the top of the scaffolds. Cell proliferation and migration was assessed as a function of growth factor loading and scaffold architecture. HUVECs successfully adhered onto gelatin B scaffolds and cell proliferation was directly proportional to the loading concentrations of the growth factor (0–100 bFGF ng/mL). Fiber orientation had a pronounced effect on cell morphology and orientation. Cells were spread along the fibers of the electrospun scaffolds with the aligned orientation and developed a spindle-like morphology parallel to the scaffold’s fibers. In contrast, cells seeded onto the scaffolds with random fiber orientation, did not demonstrate any directionality and appeared to have a rounder shape. Capillary formation (i.e. sprouts length and number of sprouts per bead), assessed in a 3-D in vitro angiogenesis assay, was a function of bFGF loading concentration (0 ng, 50 ng and 100 ng per scaffold) for both types of electrospun scaffolds (i.e. with aligned or random fiber orientation). In addition, a murine ischemic hind limb model was utilized to assess the reperfusion potential of such scaffolds, both aligned and randomly deposited, and with or without bFGF. Assessment of the treatment groups included LDPI imaging at 5, 7, 10, 14, and 21 days post-surgery, and DiL vessel staining on day 21 visualized with a confocal microscope. Aligned scaffolds achieved 70% reperfusion of the ischemic leg within 21 days and the DiL stained vessel architecture demonstrated significant alignment compared to randomly deposited scaffolds. Hence, this evidence suggest that the herein developed treatment group consisting of aligned bFGF loaded gelatin B electrospun scaffolds successfully enhanced the angiogenic process and had a pronounced effect on the newly formed vessel bed architecture. Advisors/Committee Members: Fotios M. Andreopoulos, Si M. Pham, Jorge E. Bohorquez, Alicia R. Jackson, Roberto I. Vazquez-Padron.

Subjects/Keywords: Electrospinning; Angiogenesis; Scaffolds

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

APA (6th Edition):

Montero, R. B. (2012). Design of Electrospun Gelatin Based Scaffolds with Controlled Biological and Architectural Cues for Therapeutic Angiogenesis. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/882

Chicago Manual of Style (16th Edition):

Montero, Ramon B. “Design of Electrospun Gelatin Based Scaffolds with Controlled Biological and Architectural Cues for Therapeutic Angiogenesis.” 2012. Doctoral Dissertation, University of Miami. Accessed June 24, 2019. https://scholarlyrepository.miami.edu/oa_dissertations/882.

MLA Handbook (7th Edition):

Montero, Ramon B. “Design of Electrospun Gelatin Based Scaffolds with Controlled Biological and Architectural Cues for Therapeutic Angiogenesis.” 2012. Web. 24 Jun 2019.

Vancouver:

Montero RB. Design of Electrospun Gelatin Based Scaffolds with Controlled Biological and Architectural Cues for Therapeutic Angiogenesis. [Internet] [Doctoral dissertation]. University of Miami; 2012. [cited 2019 Jun 24]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/882.

Council of Science Editors:

Montero RB. Design of Electrospun Gelatin Based Scaffolds with Controlled Biological and Architectural Cues for Therapeutic Angiogenesis. [Doctoral Dissertation]. University of Miami; 2012. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/882


University of Miami

2. Layman, Hans Richard William. Tissue Engineering Strategies for the Treatment of Peripheral Vascular Diseases.

Degree: PhD, Biomedical Engineering (Engineering), 2010, University of Miami

Peripheral vascular diseases such as peripheral artery disease (PAD) and critical limb ischemia (CLI) are growing at an ever-increasing rate in the Western world due to an aging population and the incidence of type II diabetes. A growing economic burden continues because these diseases are common indicators of future heart attack or stroke. Common therapies are generally limited to pharmacologic agents or endovascular therapies which have had mixed results still ending in necrosis or limb loss. Therapeutic angiogenic strategies have become welcome options for patients suffering from PAD due to the restoration of blood flow in the extremities. Capillary sprouting and a return to normoxic tissue states are also demonstrated by the use of angiogenic cytokines in conjunction with bone marrow cell populations. To this point, it has been determined that spatial and temporal controlled release of growth factors from vehicles provides a greater therapeutic and angiogenic effect than growth factors delivered intramuscularly, intravenously, or intraarterialy due to rapid metabolization of the cytokine, and non-targeted release. Furthermore, bone marrow cells have been implicated to enhance angiogenesis in numerous ischemic diseases due to their ability to secrete angiogenic cytokines and their numerous cell fractions present which are implicated to promote mature vessel formation. Use of angiogenic peptides, in conjunction with bone marrow cells, has been hypothesized in EPC mobilization from the periphery and marrow tissues to facilitate neovessel formation. For this purpose, controlled release of angiogenic peptides basic fibroblast growth factor (FGF-2) and granulocyte-colony stimulating factor (G-CSF) was performed using tunable ionic gelatin hydrogels or fibrin scaffolds with ionic albumin microspheres. The proliferation of endothelial cell culture was determined to have an enhanced effect based on altering concentrations of growth factors and method of release: co-delivery versus sequential. Scaffolds with these angiogenic peptides were implanted in young balb/c mice that underwent unilateral hindlimb ischemia by ligation and excision of the femoral artery. Endpoints for hindlimb reperfusion and angiogenesis were determined by Laser Doppler Perfusion Imaging and immunohistochemical staining for capillaries (CD-31) and smooth muscle cells (alpha-SMA). In addition to controlled release of angiogenic peptides, further studies combined the use of a fibrin co-delivery scaffold with FGF-2 and G-CSF with bone marrow stem cell transplantation to enhance vessel formation following CLI. Endpoints also included lipophilic vascular painting to evaluate the extent of angiogenesis and arteriogenesis in an ischemic hindlimb. Tissue engineering strategies utilizing bone marrow cells and angiogenic peptides demonstrate improved hindlimb blood flow compared to BM cells or cytokines alone, as well as enhanced angiogenesis based on immunohistochemical staining and vessel densities. Advisors/Committee Members: Fotios M. Andreopoulos - Committee Chair, Si M. Pham - Committee Member, Weiyong Gu - Committee Member, Herman Cheung - Committee Member, Cherie Stabler - Mentor.

Subjects/Keywords: Critical Limb Ischemia; Peripheral Artery Disease; Microsphere; Albumin; Fibrin; Gelatin; G-CSF; BFGF; Bone Marrow Cells; Angiogenesis; Biomaterial; Controlled Release

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

APA (6th Edition):

Layman, H. R. W. (2010). Tissue Engineering Strategies for the Treatment of Peripheral Vascular Diseases. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/461

Chicago Manual of Style (16th Edition):

Layman, Hans Richard William. “Tissue Engineering Strategies for the Treatment of Peripheral Vascular Diseases.” 2010. Doctoral Dissertation, University of Miami. Accessed June 24, 2019. https://scholarlyrepository.miami.edu/oa_dissertations/461.

MLA Handbook (7th Edition):

Layman, Hans Richard William. “Tissue Engineering Strategies for the Treatment of Peripheral Vascular Diseases.” 2010. Web. 24 Jun 2019.

Vancouver:

Layman HRW. Tissue Engineering Strategies for the Treatment of Peripheral Vascular Diseases. [Internet] [Doctoral dissertation]. University of Miami; 2010. [cited 2019 Jun 24]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/461.

Council of Science Editors:

Layman HRW. Tissue Engineering Strategies for the Treatment of Peripheral Vascular Diseases. [Doctoral Dissertation]. University of Miami; 2010. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/461


University of Miami

3. Thompson, John William. DNA Fragmentation and Histone Hyperacetylation in the Hypoxic-Acidotic Cardiomyocyte.

Degree: PhD, Molecular and Cellular Pharmacology (Medicine), 2008, University of Miami

Bnip3 is a BH3-only member of the Bcl-2 family of apoptotic proteins. Our laboratory has previously shown that Bnip3 induces a unique pathway of cardiac myocyte cell death, characterized by mitochondrial dysfunction, cytochrome c release and DNA fragmentation. Bnip3 is induced by hypoxia and the death pathway is activated by concurrent acidosis. We have shown that hypoxia-acidosis creates an environment that is permissive to calpain but not caspase activation and is characterized by enhanced DNase(s) activity as evidenced by genomic DNA fragmentation. This dissertation describes the nuclear consequences of Bnip3 activation by hypoxia-acidosis. Chapter 3 presents my evidence that hypoxia with progressive acidosis in cardiac myocytes results in a biphasic activation of DNases. In phase 1, [pH]o 6.9-6.7, apoptosis-inducing factor (AIF) is released from the mitochondria and translocates to the nucleus. AIF release coincided with the loss of mitochondrial membrane potential and with the release of cytochrome c from the mitochondria. In Phase II, [pH]o 6.3-6.0, DNase II translocates from the cytoplasm to the nuclear compartment. Nuclear localization of DNase II was associated with the collapse of endosomal pH gradients, indicated by diffuse Lysotracker Red staining and with single strand DNA nicks. Both phases of DNase release were independent of Bnip3, the mPTP and calpains. Neither phase involved activation of caspase-dependent DNases. Chapter 4 describes a unique role for Bnip3 in the modulation of histone acetylation. I found that hypoxia with acidosis in cardiac myocytes but not hypoxia alone stimulated a global increase in the acetylation of histones H3 and H4. Acetylation was initiated at [pH]o ~ 6.8 and increased as the pH declined. Histone hyperacetylation was associated with an increase in histone acetyltransferase (HAT) activity but no change in deacetylase (HDAC) activity. Knockdown of Bnip3 protein expression with siRNA dramatically reduced both histone H3 and H4 acetylation levels and HAT activity indicating an essential role for Bnip3 in this process. Components of the hypoxia-acidosis death pathway including the mPTP and calpains are not required for Bnip3-mediated histone hyperacetylation. These results reveal a novel role for Bnip3 in regulating HAT activity and histone acetylation which may lead to altered cardiac gene expression. Advisors/Committee Members: Sandra K. Lemmon - Committee Chair, Si M. Pham - Committee Member, James D. Potter - Committee Member, Keith A. Webster - Mentor, Rakesh C. Kukreja - Outside Committee Member.

Subjects/Keywords: Bnip3; Hypoxia; Cardiac Myocytes; Apoptosis; Gene Regulation; Histone Acetylation; DNA Fragmentation; Apoptosis Inducing Factor; Dnase II; Caspase Activted DNase

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

APA (6th Edition):

Thompson, J. W. (2008). DNA Fragmentation and Histone Hyperacetylation in the Hypoxic-Acidotic Cardiomyocyte. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/169

Chicago Manual of Style (16th Edition):

Thompson, John William. “DNA Fragmentation and Histone Hyperacetylation in the Hypoxic-Acidotic Cardiomyocyte.” 2008. Doctoral Dissertation, University of Miami. Accessed June 24, 2019. https://scholarlyrepository.miami.edu/oa_dissertations/169.

MLA Handbook (7th Edition):

Thompson, John William. “DNA Fragmentation and Histone Hyperacetylation in the Hypoxic-Acidotic Cardiomyocyte.” 2008. Web. 24 Jun 2019.

Vancouver:

Thompson JW. DNA Fragmentation and Histone Hyperacetylation in the Hypoxic-Acidotic Cardiomyocyte. [Internet] [Doctoral dissertation]. University of Miami; 2008. [cited 2019 Jun 24]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/169.

Council of Science Editors:

Thompson JW. DNA Fragmentation and Histone Hyperacetylation in the Hypoxic-Acidotic Cardiomyocyte. [Doctoral Dissertation]. University of Miami; 2008. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/169

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