subject:(Transforming growth factor beta1)

1. Moore, Lakisha Dionne. Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis.

Degree: PhD, 2008, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,233

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Overexpresssion of transforming growth factor (TGF)-[beta] has been implicated in promoting immune suppression, tumor angiogenesis, tumor cell migration, and invasion in many cancers including carcinoma… (more)

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Overexpresssion of transforming growth factor (TGF)-[beta] has been implicated in promoting immune suppression, tumor angiogenesis, tumor cell migration, and invasion in many cancers including carcinoma of the breast. Thus, targeted downregulation of TGF-[beta]1 expression in breast cancer in situ and determination of its implications potentially could provide new treatment approaches for disease management. siRNA constructs targeting TGF-[beta]1 were validated and used to develop clonal derivatives of the MDA-MB-435 metastatic breast cancer cell line. Inhibition of TGF-[beta]1 expression in MDA-MB-435 cells showed decrease in migration and invasion in vitro with an increase in proliferation. In vivo analysis indicated a 90% decrease in the number of mice bearing macroscopic lung metastases. Analysis of TGF-[beta] signaling pathways in the clonal derivatives showed a decrease in Smad2 activation and an increase in AKT and ERK activation. Analysis of TGF-[beta] signaling in the tumor microenvironment was performed using co-culture assays consisting of both MDA-MB 435 tumor cells and fibroblasts. Early experiments involving analysis of gene expression in a breast cancer xenograft model showed an increase in TGF-[beta]1 and MMP expression in the tumor stroma over tumor progression. Co-culture experiments using Boyden chambers indicated increased expression of TGF-[beta]1, MMP-9, MMP-2, T[beta]R1 and T[beta]R2 in the tumor cells. Interestingly, there was a significant decrease in TGF-[beta]1, MMP-2, T[beta]R1 and T[beta]R2 expression in fibroblasts that were co-cultured with tumor cells. Experiments using conditioned media also showed a decrease in fibroblasts and tumor cell differentiation through decreases in alpha-smooth muscle actin and cytokeratin 18, respectively. Therapeutic efficacy was determined using rAAV to administer TGF-[beta]1 siRNA intra-tumorally. Results confirmed that the AAV6 serotype was effectively able to transduce the tumor cells both in vitro and in vivo. RT-PCR data confirmed that TGF-[beta]1, MMP-9 and MMP-2 were effectively decreased in the tumor injected with rAAV-TGF[beta]si when compared to the rAAV-GFP injected tumors. Macroscopic lung metastases were decreased in the treated group; however microscopic metastases were still present. Lung weights also show a decrease, however, the differences were not statistically significant. Better understanding of the molecular pathways involved in TGF-[beta] signaling will help to advance the development of targeted therapeutics along with improvements in delivery mechanics. Through our studies we have shown that inhibition of TGF-[beta] can effectively reduce cancer metastasis; we have identified secondary pathways active in mammary cancer neoplastic progression which may be targeted in combination to give a synergistic effect and tested alternative methods of delivery.

xi, 109 p. : ill., digital, PDF file

Joint Health Sciences

Transforming Growth Factor-beta Breast Cancer Metastasis Gene Therapy Adeno-Associated Virus …

Advisors/Committee Members: Ponnazhagan, Selvarangan, Chang, Chenbei <br>, Feng, Xu <br>, Serra, Rosa <br>, Siegal, Gene P. <br>, Thottassery, Jaideep.

Subjects/Keywords: Breast Neoplasms – genetics <; br>; Neoplasm Metastasis <; br>; RNA Interference <; br>; Transforming Growth Factor beta1 – genetics <; br>; Transforming Growth Factor beta1 – metabolism

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

APA (6^th Edition):

Moore, L. D. (2008). Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,233

Chicago Manual of Style (16^th Edition):

Moore, Lakisha Dionne. “Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 27, 2021. http://contentdm.mhsl.uab.edu/u?/etd,233.

MLA Handbook (7^th Edition):

Moore, Lakisha Dionne. “Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis.” 2008. Web. 27 Feb 2021.

Vancouver:

Moore LD. Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2021 Feb 27]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,233.

Council of Science Editors:

Moore LD. Modulation of Transforming Growth Factor (TGF)-[beta]1 and its implications in breast cancer metastasis. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,233

2. Liu, Jun. Snail1-mediated Gene Repression Links EMT to Enhanced Biliary Epithelial Cell Survival and Lung Epithelial Cancer Cell Migration.

Degree: PhD, Medical Microbiology and Immunology (graduate program), 2013, Creighton University

URL: http://hdl.handle.net/10504/42059

► Liver fibrosis and cancer metastasis remain significant health problems, with a mortality rate of nine million each year worldwide. Effective therapies for these problems are… (more)

▼ Liver fibrosis and cancer metastasis remain significant health problems, with a mortality rate of nine million each year worldwide. Effective therapies for these problems are very limited due to lack of a clear understanding of the underlying mechanisms. Epithelial-mesenchymal-transition (EMT) is a naturally occurring and strictly regulated trans-differentiation process essential for tissue morphogenesis during early embryonic development. Recent studies suggest that aberrant reactivation of EMT in adults may be a key event in both tissue fibrosis and cancer metastasis. Nevertheless, the pathological significance of EMT in the progression of fibrosis and tumor metastasis remains unclear. Despite the apparently different contributions of EMT in these processes, EMT seems to be induced by several common key regulators, including snail homolog 1 (Snail1). Understanding the role of this regulator in disease-associated processes (e.g. production of extracellular matrix proteins, apoptosis resistance and cell migration) is necessary to decipher the underlying mechanisms of tissue fibrosis and cancer metastasis. In this study, we utilized transforming growth factor-beta 1 (TGF-β1) to establish EMT in non-malignant murine biliary epithelial cells (cholangiocytes, 603B cells) and human lung epithelial carcinoma cells (A495 cells). We examined collagen production and cell survival in 603B cells and cell migration in A549 cells during TGF-β1-induced EMT. The involvement of Snail1 in mediating these disease-associated alterations was further evaluated to investigate the potential direct links between EMT and liver fibrosis as well as cancer metastasis. |We showed that TGF-β1 stimulation induced EMT-like alterations in 603B and A549 cells. TGF-β1-treated cells displayed EMT-associated morphological changes, and lost expression of epithelial marker E-cadherin (E-cad) and gained expression of mesenchymal marker N-cadherin (N-cad). In addition, TGF-β1 treatment induced a transient up-regulation of Snail1 in 603B cells and a persistent up-regulation of Snail1 in A549 cells. |We found that TGF-β1 transiently increased Collagen 1 alpha 1(Col1A1) production in 603B cells. Up-regulation of Snail1 following TGF-1 stimulation was required for EMT-associated changes in 603B cells. Interestingly, Snail1 induction was dispensable for TGF-β1 to enhance Col1A1 expression, arguing against the concept that cholangiocyte EMT is one of the major mechanisms of generating collagen-producing cells during liver fibrosis. TGF-β1 treatment protected 603B cells from tumor necrosis factor-alpha (TNF-α)-induced apoptosis. We demonstrated that Snail1 knockdown inhibited TGF-β1-induced apoptosis resistance in 603B cells. Moreover, Snail1 repressed the expression of multiple pro-apoptotic genes in 603B cells, suggesting the direct contributions of EMT to enhancing cell survival. Since the accumulation of cholangiocytes (ductular reactions) is a common feature of liver fibrosis, our data indicate a potential new mechanism of EMT to promote the development of… Advisors/Committee Members: Chen, Xian-Ming (advisor), Liu, Jun (cuauthor).

Subjects/Keywords: Epithelial-Mesenchymal Transition – genetics; Cell Movement; Liver Cirrhosis; Lung Neoplasm; Transforming Growth Factor beta1 – physiology

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

APA (6^th Edition):

Liu, J. (2013). Snail1-mediated Gene Repression Links EMT to Enhanced Biliary Epithelial Cell Survival and Lung Epithelial Cancer Cell Migration. (Doctoral Dissertation). Creighton University. Retrieved from http://hdl.handle.net/10504/42059

Chicago Manual of Style (16^th Edition):

Liu, Jun. “Snail1-mediated Gene Repression Links EMT to Enhanced Biliary Epithelial Cell Survival and Lung Epithelial Cancer Cell Migration.” 2013. Doctoral Dissertation, Creighton University. Accessed February 27, 2021. http://hdl.handle.net/10504/42059.

MLA Handbook (7^th Edition):

Liu, Jun. “Snail1-mediated Gene Repression Links EMT to Enhanced Biliary Epithelial Cell Survival and Lung Epithelial Cancer Cell Migration.” 2013. Web. 27 Feb 2021.

Vancouver:

Liu J. Snail1-mediated Gene Repression Links EMT to Enhanced Biliary Epithelial Cell Survival and Lung Epithelial Cancer Cell Migration. [Internet] [Doctoral dissertation]. Creighton University; 2013. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/10504/42059.

Council of Science Editors:

Liu J. Snail1-mediated Gene Repression Links EMT to Enhanced Biliary Epithelial Cell Survival and Lung Epithelial Cancer Cell Migration. [Doctoral Dissertation]. Creighton University; 2013. Available from: http://hdl.handle.net/10504/42059

North-West University

3. Campbell, Berenice. Pheroid technology for the topical delivery of depigmenting agents transforming growth factor–ß1 and tumor necrosis factor–a / Berenice Campbell .

Degree: 2010, North-West University

URL: http://hdl.handle.net/10394/4739

► Pigmentation disorders occur in multiple conditions (Hakozaki et al., 2006:105). Although many modalities of treatments are available, none are completely satisfactory (Briganti et al., 2003:101).… (more)

▼ Pigmentation disorders occur in multiple conditions (Hakozaki et al., 2006:105). Although many modalities of treatments are available, none are completely satisfactory (Briganti et al., 2003:101). Two cytokines normally present in the skin, transforming growth factor–beta1 (TGF–81) and tumour necrosis factor–alpha (TNF–9), have been shown to inhibit melanin synthesis (Martinez–Esparza, 2001:972). The stratum corneum has been commonly accepted as the main barrier to percutaneous absorption. Many techniques have been applied to overcome this barrier properties and to enhance penetration with varying success (Pellet et al., 1997:92). The objective of this study was to investigate the topical delivery of the above mentioned peptide drugs with aid of the Pheroid drug delivery system. Pheroid technology is a delivery system that promotes the absorption and increases the efficacy of dermatological, biological and oral medicines in various pharmacological groups (Grobler et al., 2008:4). Pheroid entraps drugs with high efficiency and delivers them with remarkable speed to target sites (Grobler, 2004:4). In order to avoid degradation of these peptides, bestatin hydrochloride (an aminopeptidase inhibitor), was used (Lkhagvaa et al., 2008:386). Topical drug delivery was achieved by means of vertical Franz cell diffusion studies performed over a 6 and 12 h period. ELISA (enzyme linked immunosorbent assay) detection was used to detect cytokine concentrations. Entrapped cytokine solutions were monitored by confocal laser scanning microscopy (CLSM). Upon removal of donor and receptor compartments, skin discs were subjected to tape stripping in order to establish the amount of active present within the stratum corneum and epidermis as well as the remaining dermis (Pellet et al., 1997:92). When comparing the two studies with each other, it is evident that the diffused concentration values obtained with PBS (phosphate buffer solution, pH 7.4) was lower than that obtained with the Pheroid drug delivery system. Both cytokine concentrations were successfully delivered topically as a minimum of concentrations for both actives were detected. This positive result was confirmed as well by the amount of active detected in stratum corneum–epidermis and epidermis–dermis solutions.

Subjects/Keywords: Pigmentation; Topical delivery; Pheroid; Transforming growth factor-beta1; Tumour necrosis factor-alpha; Bestatin; Tape stripping; Pigmentasie; Topikale aflewering; Transformerende groei faktor-beta1; Tumor nekrosis faktor-alpha; Bestatien; Bandstroping

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

APA (6^th Edition):

Campbell, B. (2010). Pheroid technology for the topical delivery of depigmenting agents transforming growth factor–ß1 and tumor necrosis factor–a / Berenice Campbell . (Thesis). North-West University. Retrieved from http://hdl.handle.net/10394/4739

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

Chicago Manual of Style (16^th Edition):

Campbell, Berenice. “Pheroid technology for the topical delivery of depigmenting agents transforming growth factor–ß1 and tumor necrosis factor–a / Berenice Campbell .” 2010. Thesis, North-West University. Accessed February 27, 2021. http://hdl.handle.net/10394/4739.

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

MLA Handbook (7^th Edition):

Campbell, Berenice. “Pheroid technology for the topical delivery of depigmenting agents transforming growth factor–ß1 and tumor necrosis factor–a / Berenice Campbell .” 2010. Web. 27 Feb 2021.

Vancouver:

Campbell B. Pheroid technology for the topical delivery of depigmenting agents transforming growth factor–ß1 and tumor necrosis factor–a / Berenice Campbell . [Internet] [Thesis]. North-West University; 2010. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/10394/4739.

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

Council of Science Editors:

Campbell B. Pheroid technology for the topical delivery of depigmenting agents transforming growth factor–ß1 and tumor necrosis factor–a / Berenice Campbell . [Thesis]. North-West University; 2010. Available from: http://hdl.handle.net/10394/4739

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

Universidade Estadual de Campinas

4. Bersaneti, Joseli Assem, 1964-. Eventos moleculares associados ao aumento gengival induzido por ciclosporina A são atenuados pela superexpressão de Smad7: Molecular events associated with cyclosporin A induced gingival overgrowth are attenuated by Smad 7 overexpression.

Degree: 2011, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/288719

► Abstract: Cyclosporin A (CsA)-induced gingival overgrowth is attributed to an exaggerated accumulation of extracellular matrix, which is mainly due to an increased expression of transforming… (more)

▼ Abstract: Cyclosporin A (CsA)-induced gingival overgrowth is attributed to an exaggerated accumulation of extracellular matrix, which is mainly due to an increased expression of transforming growth factor-beta1 (TGF-ß1). Herein the in vitro investigation of effects of overexpression of Smad7, a TGF-ß1 signaling inhibitor, in the events associated with CsA-induced extracellular matrix accumulation was performed. To assess the inhibitory effects of Smad7, we stably overexpressed Smad7 in fibroblasts from normal gingiva (NG). Smad7 overexpressing cells and controls were incubated with CsA and type I collagen synthesis, matrix metalloproteinase 2 (MMP-2) production and activity, and cellular proliferation were evaluated by ELISA, zymography, growth curve, BrdUincorporation assay and cell cycle analysis. CsA effects on cell viability and apoptosis of NG fibroblasts were also evaluated. Western blot and immunofluorescence for phospho-Smad2 were performed to measure the activation of TGF-ß1 signaling. Although the treatment with CsA stimulated TGF-ß1 production in both control and Smad7 overexpressing fibroblasts, its signaling was marked inhibited in Smad7 overexpressing cells as revealed by low levels of Smad2 phosphorylation. In Smad7 overexpressed cells, the effects of CsA on proliferation, synthesis of type I collagen and MMP-2 production and activity were significantly blocked. Smad7 overexpression blocked CsA-induced fibroblast proliferation via p27 regulation. Neither CsA nor Smad7 overexpression induced cell death. The data presented here confirm that TGF-ß1 expression is related to the molecular events associated with CsA-induced gingival overgrowth, and suggest that Smad7 overexpression is effective in the blockage of those events, including proliferation, type I collagen synthesis and MMP-2 activity Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Della Coletta, Ricardo, 1972- (advisor), Universidade Estadual de Campinas. Faculdade de Odontologia de Piracicaba (institution), Programa de Pós-Gaduação em Estomatopatologia (nameofprogram), Andrade, Clerverton Roberto de (committee member), Alves, Fabio de Abreu (committee member), Vargas, Pablo Agustin (committee member), Silva, Alan Roger dos Santos (committee member).

Subjects/Keywords: Proteínas smad; Fator de crescimento transformador beta1; Metaloproteinase 2 da matriz; Smad proteins; Transforming growth factor beta 1; Matrix metalloproteinase 2

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

APA (6^th Edition):

Bersaneti, Joseli Assem, 1. (2011). Eventos moleculares associados ao aumento gengival induzido por ciclosporina A são atenuados pela superexpressão de Smad7: Molecular events associated with cyclosporin A induced gingival overgrowth are attenuated by Smad 7 overexpression. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/288719

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

Chicago Manual of Style (16^th Edition):

Bersaneti, Joseli Assem, 1964-. “Eventos moleculares associados ao aumento gengival induzido por ciclosporina A são atenuados pela superexpressão de Smad7: Molecular events associated with cyclosporin A induced gingival overgrowth are attenuated by Smad 7 overexpression.” 2011. Thesis, Universidade Estadual de Campinas. Accessed February 27, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/288719.

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

MLA Handbook (7^th Edition):

Bersaneti, Joseli Assem, 1964-. “Eventos moleculares associados ao aumento gengival induzido por ciclosporina A são atenuados pela superexpressão de Smad7: Molecular events associated with cyclosporin A induced gingival overgrowth are attenuated by Smad 7 overexpression.” 2011. Web. 27 Feb 2021.

Vancouver:

Bersaneti, Joseli Assem 1. Eventos moleculares associados ao aumento gengival induzido por ciclosporina A são atenuados pela superexpressão de Smad7: Molecular events associated with cyclosporin A induced gingival overgrowth are attenuated by Smad 7 overexpression. [Internet] [Thesis]. Universidade Estadual de Campinas; 2011. [cited 2021 Feb 27]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/288719.

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

Council of Science Editors:

Bersaneti, Joseli Assem 1. Eventos moleculares associados ao aumento gengival induzido por ciclosporina A são atenuados pela superexpressão de Smad7: Molecular events associated with cyclosporin A induced gingival overgrowth are attenuated by Smad 7 overexpression. [Thesis]. Universidade Estadual de Campinas; 2011. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/288719

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

5. Rafael Braga Petito. Study of the effects of Mycobacterium leprae, and their lipid components of the TGF-b1 changes in extracellular matrix neural.

Degree: 2008, Fundação Oswaldo Cruz

URL: http://www.bdtd.cict.fiocruz.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=224

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Neural fibrosis is one of the causes of deformities during leprosy, which remains a major global health problem. Neural degeneration progresses after the patient healing… (more)

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Neural fibrosis is one of the causes of deformities during leprosy, which remains a major global health problem. Neural degeneration progresses after the patient healing and, as suggested by others, the Schwann cells (SC) are involved in the degeneration and regeneration of the nerve. Our group showed, in a human Schwannoma lineage (ST88-14), increased mRNA levels of the cytokine TGF-b1 and its receptors after Mycobacterium leprae (ML) stimulus. Since TGF-b1 neutralization reduces fibrosis, and this cytokine promotes transdifferentiation of the SC into myofibroblast, which in turn, overproduce extracellular matrix (ECM) components, resulting in neural degeneration, the aim of this study was to investigate the possible role of ML, PGL-I (lipidic component of ML cell wall) and TGF-b1 on the neural ECM expression. ST88-14 cells were stimulated with ML or PGL-I to evaluate TGF-b1, its mRNA and its receptor (TGFRII) expression. This cytokine levels were measured in these supernatants cultures. In order to evaluate myofibroblast transdifferentiation (a-actin smooth muscle; aSMA) and ECM secretion/deposition and proteins structural form, ST88-14 were stimulated with recombinant human TGF-b1, ML or PGL-I. TGF-b1 and SMA expression were analyzed in patients nerve biopsies without pathological changes or with varying degrees of fibrosis and inflammation. Our results showed that ML or PGL-I stimulation induced a rapid increase in TGF-b1 mRNA expression, followed by a decline that maintained until 6 hours. This cytokine secretion seems to accompany mRNA expression. However, after 6 hours of stimulation, TGF-b1 secretion seems gradually to return to baseline levels and to rise again after 7 days of stimulation. The intracellular cytokine expression increased in cells stimulated with ML, but the opposite took place when PGL-I was the stimulus. ML or PGL-I also up regulated the TGFRII expression. After 7 days of TGF-b1 stimulation, we noticed the increased expression of collagen IV, laminin, fibronectin and tenascin, and, in some cases, the modulation of their structural forms of some of these proteins. Moreover, TGF-b1 also induced transdifferentiation of SC into myofibroblasts. In leprosy biopsies patients, the TGF-b1 expression seems to pass from the axon to SC. For the first time, we showed the SMA expression in blood vessels, perineurium and some endoneurial cells in nerve biopsies with fibrosis presence. These results suggest a TGF-b1 involvement in cellular modulation response to ML and PGL-I, and SC-myofibroblastic transdifferentiation, which could contribute to fibrosis and, consequently, to neural degeneration.

A fibrose neural é uma das causas de deformidades durante o curso crônico da hanseníase, a qual ainda é um grande problema de saúde pública mundial. A degeneração neural progride mesmo depois da cura do paciente e as células de Schwann (CS) estão envolvidas na degeneração e regeneração neural. A produção de citocinas pela CS parece estar relacionada ao processo de degeneração e regeneração do nervo. Em trabalho…

Advisors/Committee Members: Euzenir Nunes Sarno.

Subjects/Keywords: BIOLOGIA MOLECULAR; Mycobacterium leprae; Fibrose/complicações; Hanseníase; Saúde Pública; Fator Transformador de Crescimento beta1/análise; Mycobacterium leprae; Fibrosis/Complications; Leprosy; Public Health; Transforming Growth Factor beta1/analysis

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

APA (6^th Edition):

Petito, R. B. (2008). Study of the effects of Mycobacterium leprae, and their lipid components of the TGF-b1 changes in extracellular matrix neural. (Thesis). Fundação Oswaldo Cruz. Retrieved from http://www.bdtd.cict.fiocruz.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=224

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

Chicago Manual of Style (16^th Edition):

Petito, Rafael Braga. “Study of the effects of Mycobacterium leprae, and their lipid components of the TGF-b1 changes in extracellular matrix neural.” 2008. Thesis, Fundação Oswaldo Cruz. Accessed February 27, 2021. http://www.bdtd.cict.fiocruz.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=224.

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

MLA Handbook (7^th Edition):

Petito, Rafael Braga. “Study of the effects of Mycobacterium leprae, and their lipid components of the TGF-b1 changes in extracellular matrix neural.” 2008. Web. 27 Feb 2021.

Vancouver:

Petito RB. Study of the effects of Mycobacterium leprae, and their lipid components of the TGF-b1 changes in extracellular matrix neural. [Internet] [Thesis]. Fundação Oswaldo Cruz; 2008. [cited 2021 Feb 27]. Available from: http://www.bdtd.cict.fiocruz.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=224.

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

Council of Science Editors:

Petito RB. Study of the effects of Mycobacterium leprae, and their lipid components of the TGF-b1 changes in extracellular matrix neural. [Thesis]. Fundação Oswaldo Cruz; 2008. Available from: http://www.bdtd.cict.fiocruz.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=224

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

6. Lopes, Roberto Iglesias. Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos.

Degree: PhD, Urologia, 2014, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5153/tde-29042014-101952/ ;

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Introdução: A alteração dos níveis normais de marcadores séricos e urinários ocorre na presença de dano renal associado à uropatia obstrutiva. Valores séricos e e… (more)

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Introdução: A alteração dos níveis normais de marcadores séricos e urinários ocorre na presença de dano renal associado à uropatia obstrutiva. Valores séricos e e urinários de TGF beta1 e CA 19-9 ainda não foram avaliados em modelo experimental de uropatia obstrutiva. Material e Métodos: Ratos foram divididos em sete grupos: referência, sham operation, nefrectomia unilateral, ligadura completa de ureter unilateral, obstrução parcial de ureter unilateral, obstrução parcial de ambos ureteres, nefrectomia unilateral associada à obstrução parcial do ureter contralateral. Morfometria renal e ureteral, concentrações séricas e urinárias de TGF beta1 e CA 19-9 e expressão tecidual renal de CA 19-9 foram analisadas. A correlação destes marcadores com os grupos submetidos a obstrução completa, obstrução parcial ou sem obstrução foi realizada. Resultados: Achados anatomopatológicos correlacionaram-se positivamente à intensidade da obstrução ureteral e negativamente aos níveis urinários de CA 19-9. Subexpressão acentuada do CA 19-9 foi observada em unidades renais com obstrução completa. Não foram encontradas diferenças estatisticamente significativas para os marcadores TGF beta1 urinário, TGF beta1 sérico e para o CA 19-9 sérico Conclusões: O CA 19-9 urinário correlacionou-se negativamente com o grau de obstrução ureteral. A análise imuno-histoquímica demonstrou a expressão do CA 19-9 no citoplasma das células epiteliais tubulares, sugerindo produção renal do marcador. O TGF beta1 sérico e urinário não apresentaram modificações de acordo com o grau de severidade e tempo de obstrução, o que pode estar relacionado a remodelamento renal menos intenso em resposta à uropatia obstrutiva nestes ratos

Introduction: Abnormal levels of serum and urinary markers occur in the presence of renal damage associated to obstructive uropathy. Urinary and serum TGFbeta1 and CA 19- 9 have not yet been evaluated in an experimental model of obstructive uropathy. Material and Methods: Rats were divided into seven groups: reference, sham operation, unilateral nephrectomy, complete unilateral ureteral obstruction, partial unilateral ureteral obstruction, partial bilateral ureteral obstruction, and unilateral nephrectomy with contralateral partial ureteral obstruction. Kidney and ureter morphometry, TGFbeta1 and CA 19-9 serum and urinary concentrations and CA 19-9 renal tissue expression were analysed. Correlation of these markers to complete, partial obstruction or unobstructed groups was performed. Results: Pathological findings correlated positively with the degree of ureteral obstruction, but negatively with urinary CA 19-9 levels. Marked underexpression of CA 19-9 was observed in kidneys with complete ureteral obstruction. No statistically significant differences were found for urinary and serum TGFbeta1 and also for serum CA 19-9. Conclusions: Urinary CA 19-9 correlated negatively with ureteral obstruction grade. Immunohistochemistry depicted CA 19-9 expression on epithelial tubular cells cytoplasm, suggesting renal origin. Serum and urinary…

Advisors/Committee Members: Denes, Francisco Tibor.

Subjects/Keywords: Antígeno CA 19-9; CA 19-9 antigen; Fator de crescimento transformador beta 1; Obstrução ureteral; Ratos Wistar; Transforming growth factor beta1; Ureter; Ureter; Ureteral obstruction; Wistar rats

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

APA (6^th Edition):

Lopes, R. I. (2014). Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5153/tde-29042014-101952/ ;

Chicago Manual of Style (16^th Edition):

Lopes, Roberto Iglesias. “Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos.” 2014. Doctoral Dissertation, University of São Paulo. Accessed February 27, 2021. http://www.teses.usp.br/teses/disponiveis/5/5153/tde-29042014-101952/ ;.

MLA Handbook (7^th Edition):

Lopes, Roberto Iglesias. “Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos.” 2014. Web. 27 Feb 2021.

Vancouver:

Lopes RI. Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos. [Internet] [Doctoral dissertation]. University of São Paulo; 2014. [cited 2021 Feb 27]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5153/tde-29042014-101952/ ;.

Council of Science Editors:

Lopes RI. Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos. [Doctoral Dissertation]. University of São Paulo; 2014. Available from: http://www.teses.usp.br/teses/disponiveis/5/5153/tde-29042014-101952/ ;

Universidade Estadual de Campinas

7. Nery-Diez, Ana Cláudia Coelho, 1980-. Avaliação da função da fibrilina-1 na trombogênese arterial: Evaluation of the role of fibrillin-1 in arterial thrombosis.

Degree: 2013, Universidade Estadual de Campinas

URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314064

► Abstract: Recent works show that an increased activation of the TGF-? is associated with most of the symptoms of the Marfan syndrome. Studies using mouse… (more)

▼ Abstract: Recent works show that an increased activation of the TGF-? is associated with most of the symptoms of the Marfan syndrome. Studies using mouse models of Marfan treated with losartan have been shown to prevent the degradation of the elastic matrix. Other investigators suggest that the metalloproteinases and the noncanonical ERK signaling are involved in the breakdown of the elastic fiber, which results in the aneurysm. In this study we investigated the role of fibrillin-1 in the arterial thrombosis model using mouse models of Marfan. We analyzed thrombus formation, platelet levels, APTT, PT and TT time, hemodynamic parameter, TGF-? levels, MMP activity as well as platelets, elastic fibers morphology and thrombus. This study demonstrated that Fbn1mg?/+ mice take about 120±21,07 minutes for the thrombus to be formed when compared with wild type, 58±7,16. When these Fbn1mg?/+ mice were treated with antihypertensive losartan and captopril the time taken for the thrombus formation was reduced in 57,5% and 67,5%, respectively. The activity of metalloproteinases and activity TGF-? was increased in the Fbn1mg?/+, however no significant difference between the hemodynamic parameters, levels of totals TGF-?, morphological platelets, elastic fiber and thrombus were observed. Finally, the results suggested that fibrillin-1 interferes with this process and antihypertensive affect the physiology of Fbn1mg?/+ mice. This study suggested that somehow drugs interfere with elastic matrix remodeling due to a decrease in the activity of matrix metalloproteinases which results in the recovery time of thrombus formation Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Werneck, Claudio Chrysostomo, 1966- (advisor), Universidade Estadual de Campinas. Instituto de Biologia (institution), Programa de Pós-Graduação em Biologia Funcional e Molecular (nameofprogram), Pimentel, Edson Rosa (committee member), Brocchi, Marcelo (committee member), Monteiro, Robson de Queiroz (committee member), Oliva, Maria Luiza Vilela (committee member).

Subjects/Keywords: Fibrilina-1; Matriz extracelular; Trombose; Agentes hipotensores; Fator de crescimento transformador beta; Fibrillin-1; Extracellular matrix; Thrombosis; Antihypertensive agents; Transforming growth factor beta1

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

APA (6^th Edition):

Nery-Diez, Ana Cláudia Coelho, 1. (2013). Avaliação da função da fibrilina-1 na trombogênese arterial: Evaluation of the role of fibrillin-1 in arterial thrombosis. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/314064

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

Chicago Manual of Style (16^th Edition):

Nery-Diez, Ana Cláudia Coelho, 1980-. “Avaliação da função da fibrilina-1 na trombogênese arterial: Evaluation of the role of fibrillin-1 in arterial thrombosis.” 2013. Thesis, Universidade Estadual de Campinas. Accessed February 27, 2021. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314064.

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

MLA Handbook (7^th Edition):

Nery-Diez, Ana Cláudia Coelho, 1980-. “Avaliação da função da fibrilina-1 na trombogênese arterial: Evaluation of the role of fibrillin-1 in arterial thrombosis.” 2013. Web. 27 Feb 2021.

Vancouver:

Nery-Diez, Ana Cláudia Coelho 1. Avaliação da função da fibrilina-1 na trombogênese arterial: Evaluation of the role of fibrillin-1 in arterial thrombosis. [Internet] [Thesis]. Universidade Estadual de Campinas; 2013. [cited 2021 Feb 27]. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314064.

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

Council of Science Editors:

Nery-Diez, Ana Cláudia Coelho 1. Avaliação da função da fibrilina-1 na trombogênese arterial: Evaluation of the role of fibrillin-1 in arterial thrombosis. [Thesis]. Universidade Estadual de Campinas; 2013. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/314064

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

8. Seo, Hwa-Seon. The role of TGF[beta] signaling in skeletal development.

Degree: PhD, 2008, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,338

►

Each skeletal element is essential for body movement along with the joints, muscles, tendons and ligaments. They also protect internal organs and serve as a… (more)

Subjects/Keywords: Bone and Bones – abnormalities <; br>; Homeodomain Proteins – genetics <; br>; Joints – abnormalities <; br>; Mesoderm – embryology <; br>; Protein-Serine-Threonine Kinases – Metabolism <; br>; Receptors, Transforming Growth Factor beta – metabolism <; br>; Transforming Growth Factor beta1 – physiology

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

APA (6^th Edition):

Seo, H. (2008). The role of TGF[beta] signaling in skeletal development. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,338

Chicago Manual of Style (16^th Edition):

Seo, Hwa-Seon. “The role of TGF[beta] signaling in skeletal development.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 27, 2021. http://contentdm.mhsl.uab.edu/u?/etd,338.

MLA Handbook (7^th Edition):

Seo, Hwa-Seon. “The role of TGF[beta] signaling in skeletal development.” 2008. Web. 27 Feb 2021.

Vancouver:

Seo H. The role of TGF[beta] signaling in skeletal development. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2021 Feb 27]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,338.

Council of Science Editors:

Seo H. The role of TGF[beta] signaling in skeletal development. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,338

IUPUI

9. Rhodes, Steven David. Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects.

Degree: 2014, IUPUI

URL: http://hdl.handle.net/1805/3793

►

Indiana University-Purdue University Indianapolis (IUPUI)

Skeletal manifestations including short stature, osteoporosis, kyphoscoliosis, and tibial dysplasia cumulatively affect approximately 70% of patients with neurofibromatosis type 1… (more)

▼

Indiana University-Purdue University Indianapolis (IUPUI)

Skeletal manifestations including short stature, osteoporosis, kyphoscoliosis, and tibial dysplasia cumulatively affect approximately 70% of patients with neurofibromatosis type 1 (NF1). Tibial pseudarthrosis, the chronic non-union of a spontaneous fracture, is a debilitating skeletal malady affecting young children with NF1. These non-healing fractures respond poorly to treatment and often require amputation of the affected limb due to limited understanding of the causative mechanisms. To better understand the cellular and molecular pathogenesis of these osseous defects, we have established a new mouse model which recapitulates a spectrum of skeletal pathologies frequently observed in patients with NF1. Nf1flox/-;Col2.3Cre mice, harboring Nf1 nullizygous osteoblasts on a Nf1+/- background, exhibit multiple osseous defects which are closely reminiscent of those found in NF1 patients, including runting (short stature), bone mass deficits, spinal deformities, and tibial fracture non-union. Through adoptive bone marrow transfer studies, we have demonstrated that the Nf1 haploinsufficient hematopoietic system pivotally mediates the pathogenesis of bone loss and fracture non-union in Nf1flox/-;Col2.3Cre mice. By genetic ablation of a single Nf1 allele in early myeloid development, under the control of LysMCre, we have further delineated that Nf1 haploinsufficient myeloid progenitors and osteoclasts are the culprit lineages mediating accelerated bone loss. Interestingly, conditional Nf1 haploinsufficiency in mature osteoclasts, induced by CtskCre, was insufficient to trigger enhanced lytic activity. These data provide direct genetic evidence for Nf1’s temporal significance as a gatekeeper of the osteoclast progenitor pool in primitive myelopoiesis. On the molecular level, we found that transforming growth factor-beta1 (TGF-β1), a primary mediator in the spatiotemporal coupling of bone remodeling, is pathologically overexpressed by five- to six- fold in both NF1 patients and in mice. Nf1 deficient osteoblasts, the principal source of TGF-β1 in the bone matrix, overexpress TGF-β1 in a gene dosage dependent fashion. Moreover, p21Ras dependent hyperactivation of the Smad pathway accentuates responses to pathological TGF-β1 signals in Nf1 deficient bone cells. As a proof of concept, we demonstrate that pharmacologic TβRI kinase inhibition can rescue bone mass defects and prevent tibial fracture non-union in Nf1flox/-;Col2.3Cre mice, suggesting that targeting TGF-β1 signaling in myeloid lineages may provide therapeutic benefit for treating NF1 skeletal defects.

Advisors/Committee Members: Yang, Feng-Chun, Clapp, D. Wade, Robling, Alexander G., Bidwell, Joseph P..

Subjects/Keywords: Neurofibromatosis type 1; Bone; Osteoporosis; Pseudarthrosis; Mouse model; Osteoclasts; Transforming growth factor-beta1; Neurofibromatosis – Research; Neurofibromatosis – Genetic aspects; Osteoporosis – Alternative treatment – Research – Methodology; Osteoporosis – Prevention; Pseudarthrosis – Research – Analysis; Mice – Diseases – Pathophysiology – Research; Osteoclasts – Research; Hematopoiesis – Research; Bone cells – Research; Bones – Growth; Spine – Abnormalities; Nervous system – Diseases; Bone marrow – Transplantation – Research; Transforming growth factors-beta – Research

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

APA (6^th Edition):

Rhodes, S. D. (2014). Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/3793

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

Chicago Manual of Style (16^th Edition):

Rhodes, Steven David. “Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects.” 2014. Thesis, IUPUI. Accessed February 27, 2021. http://hdl.handle.net/1805/3793.

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

MLA Handbook (7^th Edition):

Rhodes, Steven David. “Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects.” 2014. Web. 27 Feb 2021.

Vancouver:

Rhodes SD. Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects. [Internet] [Thesis]. IUPUI; 2014. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1805/3793.

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

Council of Science Editors:

Rhodes SD. Dissecting the cellular and molecular mechanisms mediating neurofibromatosis type 1 related bone defects. [Thesis]. IUPUI; 2014. Available from: http://hdl.handle.net/1805/3793

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

University of Western Ontario

10. Siraj, Sadia. A cross- sectional study of stress biomarkers and their associations with post-trauma complaints, and how those associations are moderated by early life adversity.

Degree: 2017, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/4856

► Chronic musculoskeletal pain results in significant personal, economic, and social burden. Early identification and intervention in those people with acute pain that are likely to… (more)

Subjects/Keywords: Chronic pain; acute musculoskeletal trauma; Hypothalamic-Pituitary-Adrenal axis (HPA axis); stress biomarkers; Cortisol; Brain-derived neurotrophic factor (BDNF); Transforming growth factor beta1 (TGFB1); early life adversity.; Physical Therapy; Preventive Medicine; Rehabilitation and Therapy; Trauma

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

APA (6^th Edition):

Siraj, S. (2017). A cross- sectional study of stress biomarkers and their associations with post-trauma complaints, and how those associations are moderated by early life adversity. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/4856

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

Chicago Manual of Style (16^th Edition):

Siraj, Sadia. “A cross- sectional study of stress biomarkers and their associations with post-trauma complaints, and how those associations are moderated by early life adversity.” 2017. Thesis, University of Western Ontario. Accessed February 27, 2021. https://ir.lib.uwo.ca/etd/4856.

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

MLA Handbook (7^th Edition):

Siraj, Sadia. “A cross- sectional study of stress biomarkers and their associations with post-trauma complaints, and how those associations are moderated by early life adversity.” 2017. Web. 27 Feb 2021.

Vancouver:

Siraj S. A cross- sectional study of stress biomarkers and their associations with post-trauma complaints, and how those associations are moderated by early life adversity. [Internet] [Thesis]. University of Western Ontario; 2017. [cited 2021 Feb 27]. Available from: https://ir.lib.uwo.ca/etd/4856.

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

Council of Science Editors:

Siraj S. A cross- sectional study of stress biomarkers and their associations with post-trauma complaints, and how those associations are moderated by early life adversity. [Thesis]. University of Western Ontario; 2017. Available from: https://ir.lib.uwo.ca/etd/4856

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

Texas A&M University

11. McMillin, Matthew Alexander. The Role of Transforming Growth Factor Beta in Hepatic Encephalopathy Pathogeneis.

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

URL: http://hdl.handle.net/1969.1/151843

► Hepatic encephalopathy (HE) is a neurological complication that arises due to liver dysfunction and is associated with increased circulating ammonia and a systemic immune response.… (more)

▼ Hepatic encephalopathy (HE) is a neurological complication that arises due to liver dysfunction and is associated with increased circulating ammonia and a systemic immune response. Treatment paradigms have attempted to minimize the metabolic and inflammatory consequences of liver failure. However, investigations into the specific cell signaling mechanisms between the liver and brain that induce these pathological processes are currently lacking. Both TGFβ1 and Shh are known to be upregulated in the liver and present in the circulation following liver damage. These studies employed the azoxymethane (AOM) model of acute liver failure in mice, the bile duct ligation (BDL) model of minimal HE in rats, and patients with liver cirrhosis who had HE to study cell signaling and pathological processes present during HE. Studies of specific cellular signaling mechanisms were performed in isolated primary neurons and immortalized brain endothelial cells. All pharmacological manipulations of hedgehog signaling, TGFβ signaling, and clodronate-liposome depletion of microglia were performed in AOM mice. Gli1 was upregulated in AOM, BDL, and HE patient cortices. Shh was upregulated in the liver and serum during HE, but had no effect on neurological decline. Liver TGFβ1 signaling was upregulated and had increased expression in cortical neurons. TGFβ1 suppressed neuronal Gli1 via SMAD3. The use of neutralizing antibodies against TGFβ generated neuroprotection during HE. The BBB was disrupted during AOM-induced HE and neutralizing antibodies against TGFβ significantly reduced permeability. Studies using bEnd.3 cells found that TGFβ1 suppressed Claudin-5 and increased MMP9 through a SMAD3-dependent mechanism. Depletion of microglia with clodronate liposomes in AOM mice was protective. Cortical CCL3/CCR1 axis signaling was elevated during HE and was reduced with neutralizing antibodies against TGFβ. Also, treatment with neutralizing antibodies against TGFβ reduced microgliosis and microglia activation. CCL3 KO mice had no changes in neurological decline compared to wild-type mice. Elevation of Gli1 or suppression of TGFβ1 was neuroprotective during HE. TGFβ1 increased BBB permeability and generated microglia activation and microgliosis during HE though this effect was not through the CCL3/CCR1 signaling axis. Gli1 or TGFβ1 may be therapeutic targets for the treatment and management of HE. Advisors/Committee Members: DeMorrow, Sharon (advisor), Di Patre, Pier L (committee member), Meininger, Cynthia (committee member), Sanchez, Russell (committee member).

Subjects/Keywords: Hepatic Encephalopathy; Transforming Growth Factor Beta

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

APA (6^th Edition):

McMillin, M. A. (2013). The Role of Transforming Growth Factor Beta in Hepatic Encephalopathy Pathogeneis. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151843

Chicago Manual of Style (16^th Edition):

McMillin, Matthew Alexander. “The Role of Transforming Growth Factor Beta in Hepatic Encephalopathy Pathogeneis.” 2013. Doctoral Dissertation, Texas A&M University. Accessed February 27, 2021. http://hdl.handle.net/1969.1/151843.

MLA Handbook (7^th Edition):

McMillin, Matthew Alexander. “The Role of Transforming Growth Factor Beta in Hepatic Encephalopathy Pathogeneis.” 2013. Web. 27 Feb 2021.

Vancouver:

McMillin MA. The Role of Transforming Growth Factor Beta in Hepatic Encephalopathy Pathogeneis. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/1969.1/151843.

Council of Science Editors:

McMillin MA. The Role of Transforming Growth Factor Beta in Hepatic Encephalopathy Pathogeneis. [Doctoral Dissertation]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151843

12. Roarty, Kevin Patrick. The role of TGF-[beta] and Wnt5a in mammary gland development and tumorigenesis.

Degree: PhD, 2008, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,337

►

Breast cancer is the second most common cancer worldwide behind lung cancer, affecting women of all ages, races, ethnicities, and socioeconomic strata. Concerted efforts have… (more)

Subjects/Keywords: Gene Expression Regulation, Developmental <; br>; Mammary Glands, Animal – growth & development <; br>; Mammary Glands, Animal – metabolism <; br>; Transforming Growth Factor beta1 – pharmacology <; br>; Wnt Proteins – metabolism

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

APA (6^th Edition):

Roarty, K. P. (2008). The role of TGF-[beta] and Wnt5a in mammary gland development and tumorigenesis. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,337

Chicago Manual of Style (16^th Edition):

Roarty, Kevin Patrick. “The role of TGF-[beta] and Wnt5a in mammary gland development and tumorigenesis.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 27, 2021. http://contentdm.mhsl.uab.edu/u?/etd,337.

MLA Handbook (7^th Edition):

Roarty, Kevin Patrick. “The role of TGF-[beta] and Wnt5a in mammary gland development and tumorigenesis.” 2008. Web. 27 Feb 2021.

Vancouver:

Roarty KP. The role of TGF-[beta] and Wnt5a in mammary gland development and tumorigenesis. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2021 Feb 27]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,337.

Council of Science Editors:

Roarty KP. The role of TGF-[beta] and Wnt5a in mammary gland development and tumorigenesis. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,337

NSYSU

13. Kao, Ying-hsien. Investigation on the Pathological Role of Hepatoma-Derived Growth Factor in Hepatic Fibrogenesis.

Degree: PhD, Biological Sciences, 2009, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-033053

► Liver fibrosis, a major medical problem with significant morbidity and mortality, is considered as a wound-healing response to a variety of chronic stimuli. It is… (more)

▼ Liver fibrosis, a major medical problem with significant morbidity and mortality, is considered as a wound-healing response to a variety of chronic stimuli. It is characterized by an excessive deposition of extracellular matrix (ECM) proteins, which disrupts the normal architecture of liver and ultimately leads to pathophysiological damage to liver. Hepatoma-derived growth factor (HDGF), a growth factor originally purified from hepatoma cells, is highly expressed in fetal hepatocytes and hepatoma. It is known to play multifunctional roles in mitogenesis, organogenesis, embryogenesis, and tumorigenesis. Its expression correlates with the proliferating state of hepatocellular carcinoma (HCC) and serves as a prognostic factor. Since liver fibrosis frequently occurs prior to HCC development, the specific aim of this study is to investigate the role of HDGF in the progression of liver fibrosis by using animal models of mice receiving either bile duct ligation surgery or carbon tetrachloride administration. Quantitative real-time PCR and Western blotting analysis showed a significant elevation of HDGF expression in both models. HDGF levels correlated with progression of liver fibrosis in a time-dependent manner as well as paralleled with the expression of other two fibrotic markers, transforming growth factor-b1 (TGF-b1) and pro-collagen type I, in fibrotic livers. Intriguingly, the over-expressed HDGF protein was localized mainly in perivenous hepatocytes of fibrotic livers. Besides, adenovirus-mediated HDGF gene delivery potentiated the production of TGF-b1 and pro-collagen type I, thereby enhancing the intrahepatic collagen matrix deposits as evidenced by Sirius red stain and morphometrical analysis. In cultured hepatocytes, TGF-b1 and HDGF mutually up-regulated their de novo synthesis only when grown on collagen-coated matrix, strongly suggesting that the TGF-b1- and/or HDGF-driven pro-fibrogenic signaling is collagen-dependent and a vicious circle may exist at the initial stage of hepatic fibrogenesis. Moreover, administration with recombinant HDGF stimulated BrdU uptake and synthesis of both a-smooth muscle actin and pro-collagen type I in cultured hepatic stellate cells, implicating that a mode of paracrinal action lies between these two cell types. In conclusion, HDGF plays a pro-fibrogenic role during liver fibrosis and blockade of HDGF pathway may potentially constitute the preventive or therapeutic strategies for chronic liver diseases. Advisors/Committee Members: Ming-hong Tai (committee member), Jiin-haur Chuang (chair), Tsung-hui Hu (chair), David Chao (committee member), Hung-tu Huang (chair).

Subjects/Keywords: hepatoma-derived growth factor; liver fibrosis; hepatocytes; transforming growth factor-beta

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

APA (6^th Edition):

Kao, Y. (2009). Investigation on the Pathological Role of Hepatoma-Derived Growth Factor in Hepatic Fibrogenesis. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-033053

Chicago Manual of Style (16^th Edition):

Kao, Ying-hsien. “Investigation on the Pathological Role of Hepatoma-Derived Growth Factor in Hepatic Fibrogenesis.” 2009. Doctoral Dissertation, NSYSU. Accessed February 27, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-033053.

MLA Handbook (7^th Edition):

Kao, Ying-hsien. “Investigation on the Pathological Role of Hepatoma-Derived Growth Factor in Hepatic Fibrogenesis.” 2009. Web. 27 Feb 2021.

Vancouver:

Kao Y. Investigation on the Pathological Role of Hepatoma-Derived Growth Factor in Hepatic Fibrogenesis. [Internet] [Doctoral dissertation]. NSYSU; 2009. [cited 2021 Feb 27]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-033053.

Council of Science Editors:

Kao Y. Investigation on the Pathological Role of Hepatoma-Derived Growth Factor in Hepatic Fibrogenesis. [Doctoral Dissertation]. NSYSU; 2009. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-033053

14. 윤, 영실. Transforming Growth Factor β1(TGF-β1)에 의해 유도된 세포노화 과정에서 미토콘드리아 기능의 중요성 연구.

Degree: 2005, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/2293 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000229

► PURPOSE: Normal cells enter a nondividing state after a finite number of population doubling, which is termed replicative senescence. Although the free radical theory has… (more)

▼ PURPOSE: Normal cells enter a nondividing state after a finite number of population doubling, which is termed replicative senescence. Although the free radical theory has long been implicated in the senescence, recent studies have emphasized mitochondrial DNA hypothesis because mitochondria is the major ROS generator in addition to its high vulnerability to oxidative damage. Transforming growth factor β1 (TGF β1) has well been known to suppress epithelial cell growth and recently been described to be involved in cellular senescence. The purpose of this study is to investigate how TGF β1 could induce senescence in Mv1Lu mink lung epithelial cells, whether and how mitochondrial defects are involved in the senescence. MATERIALS AND METHODS: Mink lung epithelial Mv1Lu cells were treated with TGF β1. Cell cycle, ROS generation, and mitochondrial membrane potential were analyzed by flow cytometric analysis. The activities of mitochondrial respiratory complex were analyzed by spectrophotometric analysis and cellular respiration. Expression pattern of proteins were analyzed by immunocytochemistry and immunoblotting. Mitochondrial morphology was examined by electron microscope. RESULTS: TGF β1 arrested mink lung epithelial Mv1Lu cells at G1 phase of the cell cycle with acquisition of senescent phenotypes in the presence of 10 % serum, whereas it gradually induced apoptosis with lower concentrations of serum. The senescent arrest was accompanied by prolonged generation of reactive oxygen species (ROS) and persistent disruption of mitochondrial membrane potential (ΔΨm). Therefore, we investigated the relationship between mitochondrial defect and the ROS production. Pretreatment of Mv1Lu cells with antioxidants effectively removed the generated ROS without preventing the ΔΨm disruption, and complete inhibition of respiratory chain activities with KCN or oligomycin totally blocked the ROS generation. In addition, the mitochondrial respiration rate gradually diminished upon treatment with TGF β1 and the decrease was accompanied by reduced complex IV activity. These data suggested that the mitochondrial respiratory defect via decreased complex IV activity was the cause of the prolonged ROS generation. The respiratory defect was also followed by mitochondrial oxidative stress, evidenced by oxidation of Prx III, and morphological change of mitochondria to highly elongated form. Finally, we demonstrated that hepatocyte growth factor released Mv1Lu cells from the arrest by protecting decrease of mitochondrial respiration, thereby preventing both the ΔΨm disruption and the ROS generation. CONCLUSIONS: Our results describe that TGF β1 induces senescence-like growth arrest in Mv1Lu cells in the presence of serum (higher than 5 %). During the arrest, ROS is persistently produced from the defective respiration, which is caused by decrease of mitochondrial complex IV activity. Moreover, HGF releases the arrest by preventing mitochondrial dysfunction. These results demonstrate that the mitochondrial defects are involved in the senescence… Advisors/Committee Members: 대학원 의학과, 200224342, 윤, 영실.

Subjects/Keywords: Transforming Growth Factor beta1 (TGF β1); senescence-like growth arrest; mitochondrial dysfunction; Reactive Oxygen Species (ROS); cellular respiration; Hepatocyte Growth Factor (HGF)

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APA (6^th Edition):

윤, �. (2005). Transforming Growth Factor β1(TGF-β1)에 의해 유도된 세포노화 과정에서 미토콘드리아 기능의 중요성 연구. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/2293 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000229

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

Chicago Manual of Style (16^th Edition):

윤, 영실. “Transforming Growth Factor β1(TGF-β1)에 의해 유도된 세포노화 과정에서 미토콘드리아 기능의 중요성 연구.” 2005. Thesis, Ajou University. Accessed February 27, 2021. http://repository.ajou.ac.kr/handle/201003/2293 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000229.

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

MLA Handbook (7^th Edition):

윤, 영실. “Transforming Growth Factor β1(TGF-β1)에 의해 유도된 세포노화 과정에서 미토콘드리아 기능의 중요성 연구.” 2005. Web. 27 Feb 2021.

Vancouver:

윤 �. Transforming Growth Factor β1(TGF-β1)에 의해 유도된 세포노화 과정에서 미토콘드리아 기능의 중요성 연구. [Internet] [Thesis]. Ajou University; 2005. [cited 2021 Feb 27]. Available from: http://repository.ajou.ac.kr/handle/201003/2293 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000229.

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

Council of Science Editors:

윤 �. Transforming Growth Factor β1(TGF-β1)에 의해 유도된 세포노화 과정에서 미토콘드리아 기능의 중요성 연구. [Thesis]. Ajou University; 2005. Available from: http://repository.ajou.ac.kr/handle/201003/2293 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000000229

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

University of Illinois – Urbana-Champaign

15. Xu, Jing. Characterization and modeling of cell activation upon TGF-??1 stimulation in a 3-D culture system.

Degree: MS, 0408, 2010, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/16963

► In this work, we explored a thick in vitro 3-D cell culture model with layered structure and applied transforming growth factor-beta1 (TGF-??1) on the top… (more)

Subjects/Keywords: myofibroblasts; transforming growth factor-beta1; alpha-smooth muscle actin; diffusion; confocal microscopy imaging; immunofluorescence staining

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

APA (6^th Edition):

Xu, J. (2010). Characterization and modeling of cell activation upon TGF-??1 stimulation in a 3-D culture system. (Thesis). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/16963

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

Chicago Manual of Style (16^th Edition):

Xu, Jing. “Characterization and modeling of cell activation upon TGF-??1 stimulation in a 3-D culture system.” 2010. Thesis, University of Illinois – Urbana-Champaign. Accessed February 27, 2021. http://hdl.handle.net/2142/16963.

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

MLA Handbook (7^th Edition):

Xu, Jing. “Characterization and modeling of cell activation upon TGF-??1 stimulation in a 3-D culture system.” 2010. Web. 27 Feb 2021.

Vancouver:

Xu J. Characterization and modeling of cell activation upon TGF-??1 stimulation in a 3-D culture system. [Internet] [Thesis]. University of Illinois – Urbana-Champaign; 2010. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2142/16963.

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

Council of Science Editors:

Xu J. Characterization and modeling of cell activation upon TGF-??1 stimulation in a 3-D culture system. [Thesis]. University of Illinois – Urbana-Champaign; 2010. Available from: http://hdl.handle.net/2142/16963

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

Florida International University

16. Stewart, Tiffanie S. Lifestyle and Biological Risk Factors for Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort: An HIV Infected and HIV/HCV Co-infected Population.

Degree: PhD, Dietetics and Nutrition, 2016, Florida International University

URL: https://digitalcommons.fiu.edu/etd/2459 ; 10.25148/etd.FIDC000286 ; FIDC000286

► Liver disease is now a leading cause of non-AIDS related morbidity and mortality in people living with HIV (PLWH). The present study investigated the… (more)

▼ Liver disease is now a leading cause of non-AIDS related morbidity and mortality in people living with HIV (PLWH). The present study investigated the interplay between adverse lifestyle factors that are prevalent in PLWH, biological mediators of liver pathogenesis, and a non-invasive measure of liver fibrosis (FIB-4 index) in HIV mono- and HIV/HCV co-infected individuals. The results of this investigation in the Miami Adult Studies of HIV (MASH) cohort show that the odds of liver fibrosis progression significantly increased over two years for HIV mono-infected participants who drank alcohol hazardously (OR 3.038, P=0.048), and had BMI ≥ 28kg/m² (OR 2.934, P=0.027). Cocaine use reduced the odds of advancing one stage of liver fibrosis (OR 0.228, P=0.038), but an interaction between high BMI and cocaine use slightly raised the odds by 4.8% of liver fibrosis progression (P=0.072). HIV/HCV co-infected participants showed interactions between cocaine use and high BMI with increased FIB-4 stage (OR 4.985, P= 0.034), however no lifestyle factors could independently predict FIB-4 stage in this group. Biological mediators previously associated with liver pathogenesis were associated with higher FIB-4 index over 2 years in a subset of (n=65) HIV mono-infected participants. Plasma measures of oxidative stress (% oxidized glutathione: OR 4.342, P= 0.046), hepatocyte-specific apoptosis (Cytokeratin-18 (CK-18): OR 1.008, P=0.021), and microbial endotoxin (lipopolysaccharide (LPS): OR 1.098, P= 0.097) were associated with having higher odds of progressing at least one stage of FIB-4 over 2 years. The same biological mediators were also associated with liver fibrosis within HIV infected people who also had a harmful lifestyle characteristic. FIB-4 index was significantly associated with % oxidized glutathione in obese subjects (β=0.563, P=0.018), TGF-β1 in cocaine users (β=0.858, P=0.027), and CK-18 in HIV infected individuals without any adverse lifestyle factors (β=0.435, P=0.015). Taken together, the findings of these studies describe interrelationships between HIV disease status, lifestyle, and biological mediators of liver fibrosis. The results show interactions between lifestyle conditions and the mediators of liver fibrosis may account for higher rates of liver disease in HIV infection. Research is warranted to develop personalized therapeutics for PLWH to curb the burden of liver disease. Advisors/Committee Members: Adriana Campa, Fatma Huffman, Marianna Baum, Juan Liuzzi, Wensong Wu.

Subjects/Keywords: HIV infection; HIV/HCV co-infection; liver fibrosis; alcohol; AUDIT; cocaine; body mass index; FIB-4 index; oxidative stress; hepatocyte apoptosis; transforming growth factor-beta1; microbial endotoxin; malondialdehyde; glutathione; MDA; GSH; TGF-β1; CK-18; LPS; Biochemical Phenomena, Metabolism, and Nutrition; Community Health and Preventive Medicine; Dietetics and Clinical Nutrition; Hepatology; Medical Biochemistry; Medical Immunology; Medical Nutrition; Other Medical Sciences

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

APA (6^th Edition):

Stewart, T. S. (2016). Lifestyle and Biological Risk Factors for Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort: An HIV Infected and HIV/HCV Co-infected Population. (Doctoral Dissertation). Florida International University. Retrieved from https://digitalcommons.fiu.edu/etd/2459 ; 10.25148/etd.FIDC000286 ; FIDC000286

Chicago Manual of Style (16^th Edition):

Stewart, Tiffanie S. “Lifestyle and Biological Risk Factors for Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort: An HIV Infected and HIV/HCV Co-infected Population.” 2016. Doctoral Dissertation, Florida International University. Accessed February 27, 2021. https://digitalcommons.fiu.edu/etd/2459 ; 10.25148/etd.FIDC000286 ; FIDC000286.

MLA Handbook (7^th Edition):

Stewart, Tiffanie S. “Lifestyle and Biological Risk Factors for Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort: An HIV Infected and HIV/HCV Co-infected Population.” 2016. Web. 27 Feb 2021.

Vancouver:

Stewart TS. Lifestyle and Biological Risk Factors for Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort: An HIV Infected and HIV/HCV Co-infected Population. [Internet] [Doctoral dissertation]. Florida International University; 2016. [cited 2021 Feb 27]. Available from: https://digitalcommons.fiu.edu/etd/2459 ; 10.25148/etd.FIDC000286 ; FIDC000286.

Council of Science Editors:

Stewart TS. Lifestyle and Biological Risk Factors for Liver Fibrosis in the Miami Adult Studies on HIV (MASH) Cohort: An HIV Infected and HIV/HCV Co-infected Population. [Doctoral Dissertation]. Florida International University; 2016. Available from: https://digitalcommons.fiu.edu/etd/2459 ; 10.25148/etd.FIDC000286 ; FIDC000286

NSYSU

17. Wu, Wei-Hao. The anti-neuroinflammatory effects of a synthetic marine-derived compound on STZ induced diabetic rats.

Degree: Master, Marine Biotechnology and Resources, 2013, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816113-115809

► Diabetes mellitus is a metabolic disease that can have long-term complications, including diabetic neuropathy pain. Base on preliminary screening, we had found that a marine-derived… (more)

Subjects/Keywords: neuroinflammation; immunohistochemistry; transforming growth factor-Î²; antinociceptive effects

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

APA (6^th Edition):

Wu, W. (2013). The anti-neuroinflammatory effects of a synthetic marine-derived compound on STZ induced diabetic rats. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816113-115809

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

Chicago Manual of Style (16^th Edition):

Wu, Wei-Hao. “The anti-neuroinflammatory effects of a synthetic marine-derived compound on STZ induced diabetic rats.” 2013. Thesis, NSYSU. Accessed February 27, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816113-115809.

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

MLA Handbook (7^th Edition):

Wu, Wei-Hao. “The anti-neuroinflammatory effects of a synthetic marine-derived compound on STZ induced diabetic rats.” 2013. Web. 27 Feb 2021.

Vancouver:

Wu W. The anti-neuroinflammatory effects of a synthetic marine-derived compound on STZ induced diabetic rats. [Internet] [Thesis]. NSYSU; 2013. [cited 2021 Feb 27]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816113-115809.

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

Council of Science Editors:

Wu W. The anti-neuroinflammatory effects of a synthetic marine-derived compound on STZ induced diabetic rats. [Thesis]. NSYSU; 2013. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816113-115809

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

NSYSU

18. Chen, Zhi-Cheng. The effects of skeleton extract obtained from marine organisms on wound healing.

Degree: PhD, Marine Biotechnology and Resources, 2017, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0120117-104748

► Shijueming (SJM) is a traditional Chinese medicine. Records from 1757, in the Qing dynasty, detail the use of SJM for treating skin injuries, particularly poorly… (more)

▼ Shijueming (SJM) is a traditional Chinese medicine. Records from 1757, in the Qing dynasty, detail the use of SJM for treating skin injuries, particularly poorly managed ulcers or traumatic wounds. However, no study has yet adopted an animal model to verify the phenomenon described in these records regarding the efficacy of SJM in promoting wound healing. In studies identifying novel bioactive materials in natural products that are useful for treating skin injuries, os sepiae (OS) extract has been reported to have a wound-healing effect. Therefore, this study used in vitro and in vivo models and performed tissue section analysis and Western blotting to evaluate the effect of SJM and OS on wound healing. RAW264.7 cells were used in antiinflammatory activity and phagocytic assays. Male Wistar rats were used to evaluate the effect of SJM and OS on burn and excision wound healing. The results were analyzed through hematoxylin and eosin staining, picrosirius red staining, and Western blotting. The results revealed that in the in vitro model, SJM promoted the phagocytic activity of RAW264.7 cells and OS promoted EA. hy 926 endothelial cell migration. Both SJM and OS reduced inducible nitric oxide synthase (iNOS) expression and enhanced macrophage phagocytosis in vitro. Compared with vehicle-treated rats, both SJM and OS significantly promoted wound healing in the rat burn injury model. Furthermore, SJM reduced neutrophil infiltration and promoted transforming growth factor-beta 1 (TGF-Î²1) protein expression, thus increasing the collagen I content. We suggest that the mechanism through which SJM and OS promote wound healing is related to macrophage activation and angiogenesis enhancement, respectively. In the inflammatory phase, both SJM and OS alleviate inflammation by inhibiting iNOS expression and removing neutrophils through phagocytosis. Furthermore, SJM induces TGF-Î²1 secretion, converting collagen during the tissue remodeling phase. These findings indicate that SJM is a promising therapeutic option for treating burn injury. Advisors/Committee Members: Ming-Hong Tai (chair), Wen-Sheng Liu (chair), Hui-Min Wang (chair), Zhi-Hong Wen (committee member), Hsiu-Chin Lin (chair), Yao-Chang Chen (chair), Chien-Chih Chiu (chair).

Subjects/Keywords: wound healing; Shijueming; os sepiae; macrophage; transforming growth factor-beta

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

APA (6^th Edition):

Chen, Z. (2017). The effects of skeleton extract obtained from marine organisms on wound healing. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0120117-104748

Chicago Manual of Style (16^th Edition):

Chen, Zhi-Cheng. “The effects of skeleton extract obtained from marine organisms on wound healing.” 2017. Doctoral Dissertation, NSYSU. Accessed February 27, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0120117-104748.

MLA Handbook (7^th Edition):

Chen, Zhi-Cheng. “The effects of skeleton extract obtained from marine organisms on wound healing.” 2017. Web. 27 Feb 2021.

Vancouver:

Chen Z. The effects of skeleton extract obtained from marine organisms on wound healing. [Internet] [Doctoral dissertation]. NSYSU; 2017. [cited 2021 Feb 27]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0120117-104748.

Council of Science Editors:

Chen Z. The effects of skeleton extract obtained from marine organisms on wound healing. [Doctoral Dissertation]. NSYSU; 2017. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0120117-104748

Ruhr Universität Bochum

19. Beck, Lars Hendrik. Bestimmung der Frequenz TGF-β-produzierender T-Lymphozyten gesunder Kinder verschiedener Altersklassen.

Degree: 2009, Ruhr Universität Bochum

URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-25629

► Problem: Um detailliertere Einblicke in die regelrechte Entwicklung regulatorisch bedeutsamer Immunkomponenten gewinnen zu können, wurde hier erstmals die Frequenz und der Charakter TGF-β-produzierender T-Lymphozyten gesunder… (more)

Subjects/Keywords: Transforming Growth Factor beta; T-Lymphozyt; Helferzelle; Immunologie

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APA (6^th Edition):

Beck, L. H. (2009). Bestimmung der Frequenz TGF-β-produzierender T-Lymphozyten gesunder Kinder verschiedener Altersklassen. (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-25629

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

Chicago Manual of Style (16^th Edition):

Beck, Lars Hendrik. “Bestimmung der Frequenz TGF-β-produzierender T-Lymphozyten gesunder Kinder verschiedener Altersklassen.” 2009. Thesis, Ruhr Universität Bochum. Accessed February 27, 2021. http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-25629.

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

MLA Handbook (7^th Edition):

Beck, Lars Hendrik. “Bestimmung der Frequenz TGF-β-produzierender T-Lymphozyten gesunder Kinder verschiedener Altersklassen.” 2009. Web. 27 Feb 2021.

Vancouver:

Beck LH. Bestimmung der Frequenz TGF-β-produzierender T-Lymphozyten gesunder Kinder verschiedener Altersklassen. [Internet] [Thesis]. Ruhr Universität Bochum; 2009. [cited 2021 Feb 27]. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-25629.

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

Council of Science Editors:

Beck LH. Bestimmung der Frequenz TGF-β-produzierender T-Lymphozyten gesunder Kinder verschiedener Altersklassen. [Thesis]. Ruhr Universität Bochum; 2009. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-25629

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

Ruhr Universität Bochum

20. Pennartz, Christian. Untersuchungen zur Modulation der intestinalen Epithelrestitution in vitro durch Vascular endothelian growth factor.

Degree: 2009, Ruhr Universität Bochum

URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-27034

► Chronisch entzündliche Darmerkrankungen sind geprägt durch destruierende Entzündungs-reaktionen der Darmschleimhaut. Bei intakter Basalmembran werden kleinere Epitheldefekte mittels der Epithelzellrestitution unabhängig von der Proliferation repariert. Ziel… (more)

Subjects/Keywords: Migration (Biologie); Proliferation; Transforming Growth Factor beta; Chronische Darmentzündung

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

APA (6^th Edition):

Pennartz, C. (2009). Untersuchungen zur Modulation der intestinalen Epithelrestitution in vitro durch Vascular endothelian growth factor. (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-27034

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

Chicago Manual of Style (16^th Edition):

Pennartz, Christian. “Untersuchungen zur Modulation der intestinalen Epithelrestitution in vitro durch Vascular endothelian growth factor.” 2009. Thesis, Ruhr Universität Bochum. Accessed February 27, 2021. http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-27034.

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

MLA Handbook (7^th Edition):

Pennartz, Christian. “Untersuchungen zur Modulation der intestinalen Epithelrestitution in vitro durch Vascular endothelian growth factor.” 2009. Web. 27 Feb 2021.

Vancouver:

Pennartz C. Untersuchungen zur Modulation der intestinalen Epithelrestitution in vitro durch Vascular endothelian growth factor. [Internet] [Thesis]. Ruhr Universität Bochum; 2009. [cited 2021 Feb 27]. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-27034.

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

Council of Science Editors:

Pennartz C. Untersuchungen zur Modulation der intestinalen Epithelrestitution in vitro durch Vascular endothelian growth factor. [Thesis]. Ruhr Universität Bochum; 2009. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-27034

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

Ruhr Universität Bochum

21. Horstkemper, Marita. Abortive Replikation des Respiratory Syncytial Virus in Langerhanszell-ähnlichen dendritischen Zellen nach Differenzierung mit Transforming-growth-factor-β.

Degree: 2010, Ruhr Universität Bochum

URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-29941

► Es wurden zwei Gruppen dendritischer Zellen mit dem Respiratory Syncytial Virus infiziert. TGF-beta-Zellen entsprechen langerhansähnlichen dendritischen Zellen des Lungenepithels und IL-4-Zellen sind monozytenähnliche dendritische Zellen.… (more)

Subjects/Keywords: RS-Virusinfektion; Dendritische Zelle; Langerhans-Zelle; Transforming Growth Factor beta; Atemwege

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

APA (6^th Edition):

Horstkemper, M. (2010). Abortive Replikation des Respiratory Syncytial Virus in Langerhanszell-ähnlichen dendritischen Zellen nach Differenzierung mit Transforming-growth-factor-β. (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-29941

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

Chicago Manual of Style (16^th Edition):

Horstkemper, Marita. “Abortive Replikation des Respiratory Syncytial Virus in Langerhanszell-ähnlichen dendritischen Zellen nach Differenzierung mit Transforming-growth-factor-β.” 2010. Thesis, Ruhr Universität Bochum. Accessed February 27, 2021. http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-29941.

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

MLA Handbook (7^th Edition):

Horstkemper, Marita. “Abortive Replikation des Respiratory Syncytial Virus in Langerhanszell-ähnlichen dendritischen Zellen nach Differenzierung mit Transforming-growth-factor-β.” 2010. Web. 27 Feb 2021.

Vancouver:

Horstkemper M. Abortive Replikation des Respiratory Syncytial Virus in Langerhanszell-ähnlichen dendritischen Zellen nach Differenzierung mit Transforming-growth-factor-β. [Internet] [Thesis]. Ruhr Universität Bochum; 2010. [cited 2021 Feb 27]. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-29941.

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

Council of Science Editors:

Horstkemper M. Abortive Replikation des Respiratory Syncytial Virus in Langerhanszell-ähnlichen dendritischen Zellen nach Differenzierung mit Transforming-growth-factor-β. [Thesis]. Ruhr Universität Bochum; 2010. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-29941

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

Ruhr Universität Bochum

22. Özdemir, Semih. Prognostische Relevanz von Frameshift-Mutationen der Gene TGFβ-R-II, ACVR-II und BAX bei Lynch-Syndrom-assoziierten kolorektalen Karzinomen.

Degree: 2013, Ruhr Universität Bochum

URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-37069

► Einleitung: Mutationshäufigkeiten sowie prognostisch relevante Marker beim Lynch-Syndrom assoziierten KRK sind, im Gegensatz zu Veränderungen bei sporadischen KRK, kaum untersucht. Methode: 81 HNPCC Patienten wurden… (more)

Subjects/Keywords: Lynch-Syndrom; Transforming Growth Factor beta; Dickdarmkrebs; Chemotherapie; Marker

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APA (6^th Edition):

Özdemir, S. (2013). Prognostische Relevanz von Frameshift-Mutationen der Gene TGFβ-R-II, ACVR-II und BAX bei Lynch-Syndrom-assoziierten kolorektalen Karzinomen. (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-37069

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

Chicago Manual of Style (16^th Edition):

Özdemir, Semih. “Prognostische Relevanz von Frameshift-Mutationen der Gene TGFβ-R-II, ACVR-II und BAX bei Lynch-Syndrom-assoziierten kolorektalen Karzinomen.” 2013. Thesis, Ruhr Universität Bochum. Accessed February 27, 2021. http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-37069.

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

MLA Handbook (7^th Edition):

Özdemir, Semih. “Prognostische Relevanz von Frameshift-Mutationen der Gene TGFβ-R-II, ACVR-II und BAX bei Lynch-Syndrom-assoziierten kolorektalen Karzinomen.” 2013. Web. 27 Feb 2021.

Vancouver:

Özdemir S. Prognostische Relevanz von Frameshift-Mutationen der Gene TGFβ-R-II, ACVR-II und BAX bei Lynch-Syndrom-assoziierten kolorektalen Karzinomen. [Internet] [Thesis]. Ruhr Universität Bochum; 2013. [cited 2021 Feb 27]. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-37069.

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

Council of Science Editors:

Özdemir S. Prognostische Relevanz von Frameshift-Mutationen der Gene TGFβ-R-II, ACVR-II und BAX bei Lynch-Syndrom-assoziierten kolorektalen Karzinomen. [Thesis]. Ruhr Universität Bochum; 2013. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-37069

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

23. 岡, 宏亮. Inhibitory effects of pitavastatin on fibrogenic mediator production by human lung fibroblasts.

Degree: 博士(医学), 2016, Oita University / 大分大学

URL: http://hdl.handle.net/10559/15611

►

AIMS: Idiopathic pulmonary fibrosis continues to be a devastating clinical disorder for which there are few therapeutic options, and the pathogenesis of this disease remains… (more)

Subjects/Keywords: Pulmonary fibrosis; Statin; Mevalonate; Transforming growth factor-β

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APA (6^th Edition):

岡, �. (2016). Inhibitory effects of pitavastatin on fibrogenic mediator production by human lung fibroblasts. (Thesis). Oita University / 大分大学. Retrieved from http://hdl.handle.net/10559/15611

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

Chicago Manual of Style (16^th Edition):

岡, 宏亮. “Inhibitory effects of pitavastatin on fibrogenic mediator production by human lung fibroblasts.” 2016. Thesis, Oita University / 大分大学. Accessed February 27, 2021. http://hdl.handle.net/10559/15611.

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

MLA Handbook (7^th Edition):

岡, 宏亮. “Inhibitory effects of pitavastatin on fibrogenic mediator production by human lung fibroblasts.” 2016. Web. 27 Feb 2021.

Vancouver:

岡 �. Inhibitory effects of pitavastatin on fibrogenic mediator production by human lung fibroblasts. [Internet] [Thesis]. Oita University / 大分大学; 2016. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/10559/15611.

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

Council of Science Editors:

岡 �. Inhibitory effects of pitavastatin on fibrogenic mediator production by human lung fibroblasts. [Thesis]. Oita University / 大分大学; 2016. Available from: http://hdl.handle.net/10559/15611

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

24. Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, Hiroyuki. Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin.

Degree: 博士（歯学）, 2014, Fukuoka Dental College / 福岡歯科大学

URL: http://id.nii.ac.jp/1167/00000003/

►

Transforming growth factor-β1 (TGF-β1) reportedly causes the differentiation of fibroblasts to myofibroblasts during wound healing. We investigated the mechanism underlying the activation of latent TGF-β1… (more)

Subjects/Keywords: keratinocyte; fibroblast; transforming growth factor-β1; αv-integrin; matrix metalloproteinase

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APA (6^th Edition):

Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, H. (2014). Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. (Thesis). Fukuoka Dental College / 福岡歯科大学. Retrieved from http://id.nii.ac.jp/1167/00000003/

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

Chicago Manual of Style (16^th Edition):

Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, Hiroyuki. “Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin.” 2014. Thesis, Fukuoka Dental College / 福岡歯科大学. Accessed February 27, 2021. http://id.nii.ac.jp/1167/00000003/.

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

MLA Handbook (7^th Edition):

Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa, Hiroyuki. “Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin.” 2014. Web. 27 Feb 2021.

Vancouver:

Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa H. Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. [Internet] [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2014. [cited 2021 Feb 27]. Available from: http://id.nii.ac.jp/1167/00000003/.

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

Council of Science Editors:

Hata, Shozaburo; Okamura, Kazuhiko; Hatta, Mitsutoki; Ishikawa H. Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. : Proteolytic and non-proteolytic activation of keratinocyte-derived latent TGF-β1 induces fibroblast differentiation in a wound-healing model using rat skin. [Thesis]. Fukuoka Dental College / 福岡歯科大学; 2014. Available from: http://id.nii.ac.jp/1167/00000003/

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

25. Kourtis, Nikolaos. Πολυμορφισμός του γονιδίου του TGF-β στο χρόνιο απλό γλαύκωμα.

Degree: 2015, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/42444

►

Primary open-angle glaucoma is a chronic ,progressive, anterior optic neuropathy with apathophysiologic mechanism that hasn’t been fully elucidated yet.The only factor related to thedevelopment of… (more)

▼

Primary open-angle glaucoma is a chronic ,progressive, anterior optic neuropathy with apathophysiologic mechanism that hasn’t been fully elucidated yet.The only factor related to thedevelopment of this neuropathy that could be modified with a medical intervention is intraocularpressure.It is believed that the trabeculum of the anterior chamber angle of the eye bulb is theanatomical site , the disturbance of which contributes to the increased resistance to the aqueousoutflow and as a consequence to the elevated intraocular pressure and the damage to the retinalganglion cells.A significant number of microscopic alterations have been found in the trabeculum anddifferent biological factors are thought to be responsible for them.One of these factors is TransformingGrowth Factor beta (TGF-beta) , a cytokine which is a member of a superfamily of polypeptides withvariable activity in tissue reformation, in immune response regulation and in blood cell production.Ofspecial interest is its action on extracellular matrix production which is thought to be related to damageto the trabeculum.Considering this and the fact that several TGF-beta gene polymorphisms are underinvestigation in relation to various diseases , we tried , in this study , to establish a possible connectionbetween rs1800471 (G915C, Arg25Pro) polymorphism of the TGF-beta1 gene and primary open-angleglaucoma.In order to prove it we studied two groups , the first of primary open-angle glaucoma patientsand the other of normal controls.We used the PCR method to investigate the aforementionedpolymorphism in the DNA of peripheral blood cells from individuals included in the two groups.Statistical analysis of the laboratory results didn’t reveal a statistically significant difference in Arg25Pro(GC) genotype’s prevalence between primary open-angle glaucoma patients and controlsubjects.Similar studies could help elucidate possible relation between TGF-beta polymorphisms andprimary open-angle glaucoma and implementation of these relationships in disease prevention and,even, disease management.

Το Χρόνιο Απλό Γλαύκωμα (ΧΑΓ) είναι μια χρόνια,προοδευτική πρόσθια οπτική νευροπάθεια , της οποίας ο παθοφυσιολογικός μηχανισμός δεν έχει αποσαφηνισθεί πλήρως ακόμη.Η μοναδική παράμετρος που συσχετίζεται με την ανάπτυξη αυτής της νευροπάθειας και η οποία μπορεί να μεταβληθεί με κάποια θεραπευτική παρέμβαση είναι η ενδοφθάλμια πίεση.Θεωρείται ότι ο διηθητικός ηθμός στην γωνία του προσθίου θαλάμου του οφθαλμικού βολβού αποτελεί την ανατομική δομή, η διαταραχή της οποίας συμβάλει στην αύξηση της αντίστασης στην αποχέτευση του υδατοειδούς υγρού και στη συνέχεια στην αύξηση της ενδοφθάλμιας πίεσης και στην πρόκληση βλάβης στα γαγγλιακά κύτταρα του αμφιβληστροειδούς.Έχουν ανευρεθεί ποικίλες μικροσκοπικές βλάβες στον διηθητικό ηθμό και ποικίλοι παράγοντες που ενοχοποιούνται για αυτές.Ένας από αυτούς είναι ο Τροποποιητικός Αυξητικός Παράγοντας-βήτα ο οποίος είναι μια κυτοκίνη που ανήκει σε μια υπεροικογένεια πολυπεπτιδικών παραγόντων με δράση στην αναγέννηση των ιστών,την…

Subjects/Keywords: Πολυμορφισμός; Γλαύκωμα; Τροποποιητικός αυξητικός παράγοντας; Polymorphism; Glaucoma; Transforming growth factor

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APA (6^th Edition):

Kourtis, N. (2015). Πολυμορφισμός του γονιδίου του TGF-β στο χρόνιο απλό γλαύκωμα. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/42444

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

Chicago Manual of Style (16^th Edition):

Kourtis, Nikolaos. “Πολυμορφισμός του γονιδίου του TGF-β στο χρόνιο απλό γλαύκωμα.” 2015. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed February 27, 2021. http://hdl.handle.net/10442/hedi/42444.

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

MLA Handbook (7^th Edition):

Kourtis, Nikolaos. “Πολυμορφισμός του γονιδίου του TGF-β στο χρόνιο απλό γλαύκωμα.” 2015. Web. 27 Feb 2021.

Vancouver:

Kourtis N. Πολυμορφισμός του γονιδίου του TGF-β στο χρόνιο απλό γλαύκωμα. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2015. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/10442/hedi/42444.

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

Council of Science Editors:

Kourtis N. Πολυμορφισμός του γονιδίου του TGF-β στο χρόνιο απλό γλαύκωμα. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2015. Available from: http://hdl.handle.net/10442/hedi/42444

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

26. Warsinske, Hayley. Understanding the Role of TGF-b1 in Interstitial Lung Disease Using A Multi-Scale Systems Biology Approach.

Degree: PhD, Microbiology & Immunology, 2017, University of Michigan

URL: http://hdl.handle.net/2027.42/137147

► Pulmonary diseases are a major global health burden affecting approximately one billion people every year. They result from many types of insults including but not… (more)

▼ Pulmonary diseases are a major global health burden affecting approximately one billion people every year. They result from many types of insults including but not limited to infections, such as tuberculosis (TB), and dysregulations of the lung physiology, such as idiopathic pulmonary fibrosis. (IPF) The key to producing better therapeutics to treat pulmonary diseases is in understanding the role of immune mediators in these diseases. Transforming growth factor-β1 (TGF-β1) is an immune mediator that has been implicated in the exacerbation of both TB and IPF. TGF-β1 is traditionally described as and anti-inflammatory cytokine, thought to restrict the immune response. TGF-β1 affects a variety of cellular processes including proliferation, cytokine secretion, and even apoptosis. These effects are very cell type specific and often concentration dependent. Effective modulation of the immune response through TGF-β1 requires understanding which cells are being regulated, what are the specific results of TGF-β1 regulation, and through what mechanisms TGF-β1 is acting on the cells. To answer these questions it is necessary to look across biological scales at TGF-β1 signaling on a molecular scale, a cellular scale, and a tissue scale. The role of TGF-β1 across multiple biologic scales has not been well characterized in the context of pulmonary disease. In this work I took a multi-scale systems biology approach to understanding the mechanistic role of TGF-β1 in pulmonary disease across molecular, cellular, and tissue scales. I constructed a novel ordinary differential equation (ODE) model of TGF-β1 receptor ligand signaling in a single fibroblast and from that model, identified the necessity for simultaneous TGF-β1 and prostaglandin E2 signaling to maintain homeostatic fibroblast response during injury. I then combined this ODE model with a novel in silico agent based model (ABM) of fibroblasts and epithelial cells in co-culture in order to evaluate the effects of molecular scale signaling dynamics of cellular scale outputs such as cell proliferation, differentiation, and survival. With this model I identified a need for differential therapeutic treatment of fibroblasts and epithelial cells in order to prevent exacerbation of fibrotic disease. I then introduced TGF-β1 signaling into the existing in silico ABM model of TB induced granuloma formation in the lung (GranSim). Using this updated version of GranSim in combination with studies performed in non-human primates, I demonstrate the inhibition of TGF-β1 in the granuloma increases bacterial killing and promotes lesion sterilization by enabling increased effector functions from cytotoxic T cells. I also show that macrophages and cytotoxic T cells are differentially regulated in the granuloma by interleukin-10 and TGF-β1 respectively. Finally, I combine work on fibrosis and granuloma formation by introducing fibroblasts with an ODE model defining TGF-β1 receptor-ligand signaling dynamics into GranSim in order to characterize the formation of fibrotic granulomas. In this… Advisors/Committee Members: Kirschner, Denise E (committee member), Garikipati, Krishnakumar R (committee member), Laouar, Yasmina (committee member), Luker, Gary D (committee member), Moore, Bethany B (committee member).

Subjects/Keywords: Transforming growth factor-beta; Microbiology and Immunology; Science

11 more images…

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

APA (6^th Edition):

Warsinske, H. (2017). Understanding the Role of TGF-b1 in Interstitial Lung Disease Using A Multi-Scale Systems Biology Approach. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/137147

Chicago Manual of Style (16^th Edition):

Warsinske, Hayley. “Understanding the Role of TGF-b1 in Interstitial Lung Disease Using A Multi-Scale Systems Biology Approach.” 2017. Doctoral Dissertation, University of Michigan. Accessed February 27, 2021. http://hdl.handle.net/2027.42/137147.

MLA Handbook (7^th Edition):

Warsinske, Hayley. “Understanding the Role of TGF-b1 in Interstitial Lung Disease Using A Multi-Scale Systems Biology Approach.” 2017. Web. 27 Feb 2021.

Vancouver:

Warsinske H. Understanding the Role of TGF-b1 in Interstitial Lung Disease Using A Multi-Scale Systems Biology Approach. [Internet] [Doctoral dissertation]. University of Michigan; 2017. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2027.42/137147.

Council of Science Editors:

Warsinske H. Understanding the Role of TGF-b1 in Interstitial Lung Disease Using A Multi-Scale Systems Biology Approach. [Doctoral Dissertation]. University of Michigan; 2017. Available from: http://hdl.handle.net/2027.42/137147

University of Guelph

27. Zours, Sonja Charlotte. The Characterization of Endothelial-Mesenchymal-Transition in Response to TGF-beta and its Potential Role in Angiogenesis.

Degree: MS, Department of Biomedical Sciences, 2012, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3986

► Angiogenesis is the formation of new blood vessels by sprouting from pre-existing ones. Transforming growth factor-beta (TGFβ) promotes angiogenesis and is a known inducer of… (more)

Subjects/Keywords: Endothelial-mesenchymal transition; EndMT; transforming growth factor-beta; TGFβ; angiogenesis

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APA (6^th Edition):

Zours, S. C. (2012). The Characterization of Endothelial-Mesenchymal-Transition in Response to TGF-beta and its Potential Role in Angiogenesis. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3986

Chicago Manual of Style (16^th Edition):

Zours, Sonja Charlotte. “The Characterization of Endothelial-Mesenchymal-Transition in Response to TGF-beta and its Potential Role in Angiogenesis.” 2012. Masters Thesis, University of Guelph. Accessed February 27, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3986.

MLA Handbook (7^th Edition):

Zours, Sonja Charlotte. “The Characterization of Endothelial-Mesenchymal-Transition in Response to TGF-beta and its Potential Role in Angiogenesis.” 2012. Web. 27 Feb 2021.

Vancouver:

Zours SC. The Characterization of Endothelial-Mesenchymal-Transition in Response to TGF-beta and its Potential Role in Angiogenesis. [Internet] [Masters thesis]. University of Guelph; 2012. [cited 2021 Feb 27]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3986.

Council of Science Editors:

Zours SC. The Characterization of Endothelial-Mesenchymal-Transition in Response to TGF-beta and its Potential Role in Angiogenesis. [Masters Thesis]. University of Guelph; 2012. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3986

University of Guelph

28. Richard, Amy. Investigating the dose-dependent signalling of Transforming Growth Factor-Beta in bovine aortic endothelial cells.

Degree: MS, Department of Biomedical Sciences, 2012, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/4043

► Transforming growth factor-beta (TGFβ) is an important signaling molecule that regulates several cellular processes including angiogenesis. However, its effects on angiogenesis are complex, with it… (more)

Subjects/Keywords: Cancer; Angiogenesis; Transforming Growth Factor-Beta; Endothelial cells

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

APA (6^th Edition):

Richard, A. (2012). Investigating the dose-dependent signalling of Transforming Growth Factor-Beta in bovine aortic endothelial cells. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/4043

Chicago Manual of Style (16^th Edition):

Richard, Amy. “Investigating the dose-dependent signalling of Transforming Growth Factor-Beta in bovine aortic endothelial cells.” 2012. Masters Thesis, University of Guelph. Accessed February 27, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/4043.

MLA Handbook (7^th Edition):

Richard, Amy. “Investigating the dose-dependent signalling of Transforming Growth Factor-Beta in bovine aortic endothelial cells.” 2012. Web. 27 Feb 2021.

Vancouver:

Richard A. Investigating the dose-dependent signalling of Transforming Growth Factor-Beta in bovine aortic endothelial cells. [Internet] [Masters thesis]. University of Guelph; 2012. [cited 2021 Feb 27]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/4043.

Council of Science Editors:

Richard A. Investigating the dose-dependent signalling of Transforming Growth Factor-Beta in bovine aortic endothelial cells. [Masters Thesis]. University of Guelph; 2012. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/4043

University of Texas Southwestern Medical Center

29. Coster, Adam D. Quantitative Single-Cell Imaging Reveals Insulation of Morphogenic Signal Transduction.

Degree: 2014, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/3586

► How cells integrate external cues in order to make behavioral decisions is a central problem of cell biology. In development and in tissue-homeostasis, cell-fate decisions… (more)

Subjects/Keywords: Bone Morphogenetic Proteins; Signal Transduction; Transforming Growth Factor beta; Wnt Proteins

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APA (6^th Edition):

Coster, A. D. (2014). Quantitative Single-Cell Imaging Reveals Insulation of Morphogenic Signal Transduction. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/3586

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

Chicago Manual of Style (16^th Edition):

Coster, Adam D. “Quantitative Single-Cell Imaging Reveals Insulation of Morphogenic Signal Transduction.” 2014. Thesis, University of Texas Southwestern Medical Center. Accessed February 27, 2021. http://hdl.handle.net/2152.5/3586.

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

MLA Handbook (7^th Edition):

Coster, Adam D. “Quantitative Single-Cell Imaging Reveals Insulation of Morphogenic Signal Transduction.” 2014. Web. 27 Feb 2021.

Vancouver:

Coster AD. Quantitative Single-Cell Imaging Reveals Insulation of Morphogenic Signal Transduction. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2014. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152.5/3586.

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

Council of Science Editors:

Coster AD. Quantitative Single-Cell Imaging Reveals Insulation of Morphogenic Signal Transduction. [Thesis]. University of Texas Southwestern Medical Center; 2014. Available from: http://hdl.handle.net/2152.5/3586

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

University of Texas Southwestern Medical Center

30. Hooks, Jared Cole. Regulation of the Tumor Suppressor ARF by TGFβ in Human Cancer Cells.

Degree: 2016, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/6143

► Since its discovery, p14ARF (p19Arf in mice) has been shown to be an important regulator of the cell cycle, carrying out this function through p53-dependent… (more)

Subjects/Keywords: Gene Expression Regulation; Transforming Growth Factor beta; Tumor Suppressor Protein p14ARF

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APA (6^th Edition):

Hooks, J. C. (2016). Regulation of the Tumor Suppressor ARF by TGFβ in Human Cancer Cells. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/6143

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

Chicago Manual of Style (16^th Edition):

Hooks, Jared Cole. “Regulation of the Tumor Suppressor ARF by TGFβ in Human Cancer Cells.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed February 27, 2021. http://hdl.handle.net/2152.5/6143.

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

MLA Handbook (7^th Edition):

Hooks, Jared Cole. “Regulation of the Tumor Suppressor ARF by TGFβ in Human Cancer Cells.” 2016. Web. 27 Feb 2021.

Vancouver:

Hooks JC. Regulation of the Tumor Suppressor ARF by TGFβ in Human Cancer Cells. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2021 Feb 27]. Available from: http://hdl.handle.net/2152.5/6143.

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

Council of Science Editors:

Hooks JC. Regulation of the Tumor Suppressor ARF by TGFβ in Human Cancer Cells. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/6143

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

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Open Access Theses and Dissertations