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You searched for +publisher:"Penn State University" +contributor:("Patricia Mc Laughlin, Committee Member"). Showing records 1 – 3 of 3 total matches.

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Penn State University

1. Troy, Amanda Erin. Diet-induced modulation of vagal sensory signaling.

Degree: 2014, Penn State University

As obesity levels continue to rise in developed nations, it becomes increasingly important to determine the mechanisms underlying obesity. Ingested food induces the release of various neurohormones and neuropeptides, such as 5-HT, that activate the sensory vagus, which then relays the signal to the brain. These vagally-mediated satiety signals are capable of a substantial amount plasticity and modulation in response to physiological demands. The present work will investigate the effects of high fat diet (HFD) exposure on the ability of glucose to modulate the 5-HT-induced response of gastric projecting vagal afferent neurons. In response to changing circulating glucose levels, vagal afferent neurons are able to alter their membrane-associated 5-HT3 receptor profile and afferent nerve function centrally at the level of the nucleus of the tractus solitaries and peripherally at the level of the nodose ganglion. In several peripheral and central tissues, protein kinase C (PKC) activity is correlated with glucose level and, in the present study, the glucose-dependent modulation of 5-HT3 receptor density and function appears to be mediated via a PKC and/or PKC pathway. The rapid timescale of electrophysiological effects suggest that glucose may modulate vagal sensory signaling on a minute-to-minute basis. Therefore, by regulating the number of functional 5-HT3 receptors associated with the membrane of gastric vagal afferent neurons, extracellular glucose is able to adapt its own ‘perception’, allowing for amplification and prolongation of its own signaling. While exposure to a HFD does not affect either the proportion of gastric vagal afferent neurons that respond to 5-HT, or the magnitude of the 5-HT-induced response, the ability of glucose to modulate 5-HT3 receptor density and function is disrupted, even after relatively short periods of HFD exposure, well in advance of the development of obesity or dysregulation of blood glucose levels, suggesting that diet may profoundly affect vagal afferent responsiveness independent of obesity. While short periods of HFD exposure disrupt and attenuate the ability of glucose to modulate 5-HT-mediated vagal signaling, restoration of a normal diet permits recovery although the time-scale for recovery appears to be much longer than that required to induce the initial reduced sensitivity. This provides additional support for the concept that vago-vagal neurocircuits are sensitive to diet-induced modulation and adaptation. Furthermore, the reversibility of the adverse effects of HFD exposure suggests that peripheral vagal afferents may be a more readily accessible and attractive target for obesity research, potentially opening the door to new treatment options and preventative techniques. Advisors/Committee Members: Kirsteen Nairn Browning, Dissertation Advisor/Co-Advisor, Gregory Michael Holmes, Committee Member, Andras Hajnal, Committee Member, Patricia Mc Laughlin, Committee Member, Ann Ouyang, Committee Chair/Co-Chair.

Subjects/Keywords: vagus; vagal afferent; 5-HT; glucose; high fat diet; protein kinase C; electrophysiology; immunocytochemistry; 5-HT3 receptor

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

APA (6th Edition):

Troy, A. E. (2014). Diet-induced modulation of vagal sensory signaling. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/23416

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Troy, Amanda Erin. “Diet-induced modulation of vagal sensory signaling.” 2014. Thesis, Penn State University. Accessed March 03, 2021. https://submit-etda.libraries.psu.edu/catalog/23416.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Troy, Amanda Erin. “Diet-induced modulation of vagal sensory signaling.” 2014. Web. 03 Mar 2021.

Vancouver:

Troy AE. Diet-induced modulation of vagal sensory signaling. [Internet] [Thesis]. Penn State University; 2014. [cited 2021 Mar 03]. Available from: https://submit-etda.libraries.psu.edu/catalog/23416.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Troy AE. Diet-induced modulation of vagal sensory signaling. [Thesis]. Penn State University; 2014. Available from: https://submit-etda.libraries.psu.edu/catalog/23416

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Penn State University

2. McCarthy, Sarah Anne. A Role for TRPV6 Ion Channels in Prostate Cancer Bone Metastases.

Degree: 2012, Penn State University

There are currently no effective therapeutic treatments to prevent prostate cancer (PCa) bone metastases. Identifying mechanisms that facilitate favorable PCa cell to bone interactions will aid in the development of therapies to prevent bone metastases. The objective of this study was to identify a role for calcium and Transient Receptor Potential Vanilloid 6 (TRPV6) ion channels in the metastatic potential and early colonization of osteoblastic PCa cells to murine bone. We proposed that transient increases in serum calcium, following parathyroid hormone (PTH) 1-34 administration, confers a metastatic advantage to PCa cells in circulation, signaled partially via TRPV6 ion channels. To identify the effect of transient elevations in calcium on osteoblastic PCa cell metastatic potential, we employed heterotypic cell adhesion, transwell migration, and invasion assays. Observations from cell adhesion assays suggested that osteoblastic PCa cells increased adhesion to human bone marrow endothelial (hbmE) cells pre-treated with extracellular calcium. Studies suggested that increased extracellular calcium enhanced E-Selectin, VCAM-1 and ICAM-1 cell surface abundance on hbmE cells and that these molecules were partially responsible for increased heterotypic cell adhesion. Increased extracellular calcium also enhanced migration of osteoblastic PCa cell lines, in vitro. To identify the requirement for TRPV6 expression in osteoblastic PCa cell metastatic potential, we reduced TRPV6 expression in osteoblastic PCa cell lines. PCa cells with reduced levels of TRPV6 expression demonstrated slower proliferation rates and an impaired ability to adhere to and invade hbmE cells. Lastly, to identify a role for TRPV6 expression in early PCa cell colonization of murine bone, SCID/Beige mice were administered PTH 1-34 or vehicle, intermittently, then inoculated with PCa cells engineered to express reduced levels of TRPV6. Eight weeks post PCa cell inoculation, PCa cells were identified in long bones of 100% of animals administered PTH 1-34, relative to 20% of animals treated with vehicle. In contrast, PCa cells were identified in only 20% of the long bones of animals administered PTH 1-34, and then inoculated with PCa cells with reduced TRPV6 expression. Our observations support our hypothesis and suggest that calcium and TRPV6 may have a role in facilitating favorable PCa cell to bone interactions. Advisors/Committee Members: Ronald R Gomes Jr, Dissertation Advisor/Co-Advisor, Henry Joseph Donahue, Committee Member, Patricia Mc Laughlin, Committee Member, Andrea Manni, Committee Member, Andrea Marie Mastro, Committee Member.

Subjects/Keywords: Prostate cancer; TRPV6; parathyroid hormone; osteoblastic; calcium; bone metastases; invasion; adhesion

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

APA (6th Edition):

McCarthy, S. A. (2012). A Role for TRPV6 Ion Channels in Prostate Cancer Bone Metastases. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/13790

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

McCarthy, Sarah Anne. “A Role for TRPV6 Ion Channels in Prostate Cancer Bone Metastases.” 2012. Thesis, Penn State University. Accessed March 03, 2021. https://submit-etda.libraries.psu.edu/catalog/13790.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

McCarthy, Sarah Anne. “A Role for TRPV6 Ion Channels in Prostate Cancer Bone Metastases.” 2012. Web. 03 Mar 2021.

Vancouver:

McCarthy SA. A Role for TRPV6 Ion Channels in Prostate Cancer Bone Metastases. [Internet] [Thesis]. Penn State University; 2012. [cited 2021 Mar 03]. Available from: https://submit-etda.libraries.psu.edu/catalog/13790.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

McCarthy SA. A Role for TRPV6 Ion Channels in Prostate Cancer Bone Metastases. [Thesis]. Penn State University; 2012. Available from: https://submit-etda.libraries.psu.edu/catalog/13790

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Penn State University

3. Carroll, Melissa Anne. STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis .

Degree: 2011, Penn State University

The most well-known subsets of inflammatory bowel disease (IBD) are ulcerative colitis (UC) and Crohn’s Disease (CD). Currently, the etiology of CD is unknown but it is thought to result from excessive T helper (Th)1-cell mediated inflammation. There is no gender or age bias, but CD is most often detected between 15-30 years of age. Macrophages are tissue specific monocytes and are the first line of defense in innate immunity; once activated they produce interleukin (IL)-12, IL23 and tumor necrosis factor-alpha (TNFá), proinflammatory cytokines, which induce a Th1-cell mediated immune response. Th1-cells can synthesize several proinflammatory cytokines including IL6, TNFá and interferon-gamma (IFNã). Signal transducers and activators of transcription (STAT) proteins play an important role in mediating intestinal cytokine signaling and it is unknown if the loss of these proteins initiate severe downstream modifications that consequently result in CD. When compensating for a deficiency in STAT3, STAT1 levels increase, which leads to an increase in IFNã signaling, which promotes Th1-cell mediated inflammation. IL10, which is mediated through STAT3 signaling, is an anti-inflammatory cytokine that is secreted from activated macrophages. IL10 inhibits excessive macrophage activation which suppresses the macrophage induced synthesis of TNFá, and thus is responsible for down-regulating Th1-cell mediated immune responses. This suggests that STAT3 mediates mucosal immune tolerance during an innate immune response. Breeding a bone marrow (B)-TIE2 promoter driven Cre recombinase gene- targeted mouse with a STAT3 lox-P (F/F) mouse created a conditional (specific to bone marrow hematopoietic stem cells) STAT3 knock-out. This tissue specific STAT3 deficient mouse is suitable for in vivo studies because it exhibits a spontaneous Crohn’s-like pathogenesis in the small and large intestines, also characterized by an over production of pro-inflammatory cytokines and excessive macrophage infiltrations. In addition to these morphological changes, one functional change demonstrated a loss of NADPH oxidase activity, which is an important response induced by the innate immune system to kill phagocytosed materials (Welte et al., 2003). The overall goal of this project was to determine the role of STAT1 and STAT3 signaling in the development of inflammatory bowel disease. My working hypothesis was that defective innate immunity in Crohn’s disease may correlate with a loss in STAT3 activity. My specific hypothesis was that STAT3-deficiency in bone marrow hematopoietic stem cells results in dysfunctional macrophages and correlates with Crohn’s Disease-like pathogenesis. In conclusion, this study determined that STAT3 signaling is required for normal macrophage functions and that abnormal macrophages critical for the pathogenesis of a Crohn’s-like disease in these mice models. It was demonstrated that the role of STAT3 activity in monocyte development and function has a regulatory function, for differentiating numbers and… Advisors/Committee Members: Samuel Shaomin Zhang, Dissertation Advisor/Co-Advisor, Samuel Shaomin Zhang, Committee Chair/Co-Chair, Colin James Barnstable, Committee Member, Patricia Mc Laughlin, Committee Member, Lisa S Poritz, Committee Member.

Subjects/Keywords: macrophages

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

APA (6th Edition):

Carroll, M. A. (2011). STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/11611

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Carroll, Melissa Anne. “STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis .” 2011. Thesis, Penn State University. Accessed March 03, 2021. https://submit-etda.libraries.psu.edu/catalog/11611.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Carroll, Melissa Anne. “STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis .” 2011. Web. 03 Mar 2021.

Vancouver:

Carroll MA. STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis . [Internet] [Thesis]. Penn State University; 2011. [cited 2021 Mar 03]. Available from: https://submit-etda.libraries.psu.edu/catalog/11611.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Carroll MA. STAT3-Deficiency in Bone Marrow Hematopoietic Stem Cells results in Dysfunctional Macrophages and Correlates with Crohn's Disease-like Pathogenesis . [Thesis]. Penn State University; 2011. Available from: https://submit-etda.libraries.psu.edu/catalog/11611

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

.