You searched for subject:(Genetic Processes).
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University of Texas Southwestern Medical Center
1.
Steininger, Robert Joseph, III.
Investigating Roles for Cellular Heterogeneity in Cancer.
Degree: 2014, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/3589 
► Cell populations, even those derived from a single clone, can exhibit a high degree of phenotypic variability. However, most biological studies take measurements as averages…
(more)
▼ Cell populations, even those derived from a single clone, can exhibit a high degree of phenotypic variability. However, most biological studies take measurements as averages of entire populations without consideration for the underlying distribution of cellular phenotypes. Though there is growing evidence that variability within cellular populations has some functional consequences, the significance of cell to cell heterogeneity is still poorly understood. Here, we present an analytical platform that represents heterogeneity of cell populations as mixtures of distinct cell phenotypes, or subpopulations, based on immunofluorescent images. These "subpopulation profiles" make the heterogeneity of cell populations more tractable and comparable. We go on to demonstrate that subpopulation profiles can be predictive of clonal populations' drug responses. This separation is shown to be independent of the population's cell-cycle distribution. The subpopulation profiles are then shown to be robust population readouts and used to classify diverse cell lines. We show that, in diverse panels of cell populations, the relationship between basal state heterogeneity and drug response tends to break down. We also show, however, that the subpopulation profiles of diverse cell lines can be useful for identifying independently informative biomarkers. Taken together, these results demonstrate that a subpopulation level reduction of heterogeneity can be a useful readout of cell populations with many potential applications.
Advisors/Committee Members: Pearson, Gray W., Ranganathan, Rama, White, Michael A., Altschuler, Steven J., Wu, Lani.
Subjects/Keywords: Genetic Heterogeneity; Neoplasms; Physiological Processes
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APA (6th Edition):
Steininger, Robert Joseph, I. (2014). Investigating Roles for Cellular Heterogeneity in Cancer. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/3589
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Steininger, Robert Joseph, III. “Investigating Roles for Cellular Heterogeneity in Cancer.” 2014. Thesis, University of Texas Southwestern Medical Center. Accessed February 27, 2021.
http://hdl.handle.net/2152.5/3589.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Steininger, Robert Joseph, III. “Investigating Roles for Cellular Heterogeneity in Cancer.” 2014. Web. 27 Feb 2021.
Vancouver:
Steininger, Robert Joseph I. Investigating Roles for Cellular Heterogeneity in Cancer. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2014. [cited 2021 Feb 27].
Available from: http://hdl.handle.net/2152.5/3589.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Steininger, Robert Joseph I. Investigating Roles for Cellular Heterogeneity in Cancer. [Thesis]. University of Texas Southwestern Medical Center; 2014. Available from: http://hdl.handle.net/2152.5/3589
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Drexel University
2.
Huang, Yu-Hung.
Role of HuR in Mediating Ovarian Cancer Treatment.
Degree: 2016, Drexel University
URL: http://hdl.handle.net/1860/idea:7154
► An mRNA-binding protein, HuR (Human antigen R, aka ELAVL1), is highly elevated in many cancers, and is a master regulator of gene expression. HuR-regulated genes…
(more)
▼ An mRNA-binding protein, HuR (Human antigen R, aka ELAVL1), is highly elevated in many cancers, and is a master regulator of gene expression. HuR-regulated genes are involved in cancer cell survival, growth, and metastasis. In ovarian cancer, cytoplasmic accumulation of HuR is associated with poor prognosis. High HuR expression in ovarian cancer cells provides a rationale for targeting HuR as a therapeutic strategy. Here, we found that silencing HuR in ovarian cancer cells in culture by transient transfection of small interfering RNA (siHuR) or by stable expression of short hairpin RNA (shHuR) significantly decreased cell proliferation and anchorage-independent growth, and impaired migration and invasion. Furthermore, systemic administration of siHuR-conjugated folic acid (FA) – derivatized DNA dendrimer nanocarrier (3DNA®) to ovarian tumor-bearing mice suppressed tumor growth and ascites development, and significantly prolonged lifespan. Using NanoString gene expression analysis, we showed that suppression of HuR disrupts multiple essential cellular molecular pathways needed by ovarian tumor cells to survive, a finding that sets this therapeutic approach apart from other therapies that target a single gene. These results are the first to demonstrate the versatility of the 3DNA nanocarrier for in vivo targeted delivery of a cancer therapeutic, support the notion that HuR is a promising target, and support the potential use of FA-derivatized 3DNA dendrimer for siHuR targeted delivery to ovarian tumor cells for treatment of advanced ovarian cancer patients. Given that HuR serves as a predictive marker for gemcitabine efficacy in pancreatic cancer, we performed a retrospective study of ovarian cancer patients aiming to investigate the role that HuR plays in the response of high-grade serous ovarian tumors to chemotherapeutics. We found that there is no correlation between HuR intracellular localization and progression free survival (PFS) following second-line therapy with gemcitabine, usually administered in combination with carboplatin. We further performed ribonucleoprotein immunoprecipitation (RNP-IP) on ovarian cancer cells in culture to determine if HuR regulates deoxycytidine kinase, a metabolic enzyme that activates gemcitabine. We also examined the effects of carboplatin treatment on expression of HuR and the mitotic inhibitor WEE1, and on cell cycle kinetics. Treatment of cells with gemcitabine upregulated deoxycytidine kinase (dCK), while treatment with carboplatin upregulated both HuR and WEE1 expression. One would expect enhancement of gemcitabine activation and efficacy resulting from elevated dCK to be impeded by elevated WEE1 expression. This may explain why HuR cytoplasmic localization is not predictive of therapeutic response to combination gemcitabine/carboplatin therapy and PFS. These results suggest combination treatment of recurrent ovarian tumors with gemcitabine, carboplatin, and a WEE1 inhibitor may be potentially advantageous as compared to current clinical practices.
Ph.D., Molecular and Cell…
Advisors/Committee Members: Reginato, Mauricio, College of Medicine.
Subjects/Keywords: Molecular biology; Cytology; Genetics; Biochemical Phenomena; Genetic Phenomena; Genetic Processes
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APA (6th Edition):
Huang, Y. (2016). Role of HuR in Mediating Ovarian Cancer Treatment. (Thesis). Drexel University. Retrieved from http://hdl.handle.net/1860/idea:7154
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Huang, Yu-Hung. “Role of HuR in Mediating Ovarian Cancer Treatment.” 2016. Thesis, Drexel University. Accessed February 27, 2021.
http://hdl.handle.net/1860/idea:7154.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Huang, Yu-Hung. “Role of HuR in Mediating Ovarian Cancer Treatment.” 2016. Web. 27 Feb 2021.
Vancouver:
Huang Y. Role of HuR in Mediating Ovarian Cancer Treatment. [Internet] [Thesis]. Drexel University; 2016. [cited 2021 Feb 27].
Available from: http://hdl.handle.net/1860/idea:7154.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Huang Y. Role of HuR in Mediating Ovarian Cancer Treatment. [Thesis]. Drexel University; 2016. Available from: http://hdl.handle.net/1860/idea:7154
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Drexel University
3.
Tuyishime, Marina.
Investigation into the mechanism of a novel HIV-1 fusion inhibitor, SC12.
Degree: 2016, Drexel University
URL: http://hdl.handle.net/1860/idea:7177
► Due to the emergence of drug-resistant viruses and problems with drug side effects, new drugs and drug targets are constantly required in the battle against…
(more)
▼ Due to the emergence of drug-resistant viruses and problems with drug side effects, new drugs and drug targets are constantly required in the battle against HIV-1/AIDS. The entry of the virus into host cells and the molecular machine that facilitates this process, the Env glycoproteins, are extremely attractive and underexploited therapeutic targets. Env glycoproteins, gp120 and gp41, are assembled into trimeric complexes on the virion surface. The attachment of virus to target cells triggers conformational changes within viral Env that ultimately leads to the fusion of the viral and cell membranes, completing the viral entry process. Using a combination of high-content pharmacophore in silico screening, chemical syntheses, bioisosteric replacement, and antiviral testing, we have developed a novel entry inhibitor, SC12, which inhibits the entry of HIV-1 into susceptible cells in the nanomolar range. Direct binding of SC12 to HIV-1 Env did not block Env interaction with the host cellular receptors, thereby allowing Env attachment to the host target cell. Additionally, differential scanning calorimetry indicates that interaction of SC12 with the soluble cleaved trimeric SOSIP.664 gp140 thermally stabilizes the protein. Moreover, binding of SC12 to HIV-1 Env did not alter recognition of epitopes on Env surface by broadly neutralizing and non-neutralizing antibodies. Furthermore, SC12-induced resistance mutations were located away from the CD4-binding site. Envs from SC12-resistant viruses have conformations closely resembling the post-engagement “prefusogenic” state exposing the conserved MPER region, therefore, making these viruses more susceptible to neutralization by MPER-specific antibodies. Taken together, SC12 functions as a novel allosteric HIV-1 fusion inhibitor, binding to Env and preventing conformational changes downstream of receptor engagement that lead to viral and cell membrane fusion.
Ph.D., Molecular and Cell Biology and Genetics – Drexel University, 2016
Advisors/Committee Members: Cocklin, Simon, College of Medicine.
Subjects/Keywords: Molecular biology; Cytology; Genetics; Biochemical Phenomena; Genetic Phenomena; Genetic Processes
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APA ·
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APA (6th Edition):
Tuyishime, M. (2016). Investigation into the mechanism of a novel HIV-1 fusion inhibitor, SC12. (Thesis). Drexel University. Retrieved from http://hdl.handle.net/1860/idea:7177
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Tuyishime, Marina. “Investigation into the mechanism of a novel HIV-1 fusion inhibitor, SC12.” 2016. Thesis, Drexel University. Accessed February 27, 2021.
http://hdl.handle.net/1860/idea:7177.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Tuyishime, Marina. “Investigation into the mechanism of a novel HIV-1 fusion inhibitor, SC12.” 2016. Web. 27 Feb 2021.
Vancouver:
Tuyishime M. Investigation into the mechanism of a novel HIV-1 fusion inhibitor, SC12. [Internet] [Thesis]. Drexel University; 2016. [cited 2021 Feb 27].
Available from: http://hdl.handle.net/1860/idea:7177.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Tuyishime M. Investigation into the mechanism of a novel HIV-1 fusion inhibitor, SC12. [Thesis]. Drexel University; 2016. Available from: http://hdl.handle.net/1860/idea:7177
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Drexel University
4.
Sodi, Valerie.
Regulation of O-GlcNAc Transferase in breast cancer and its role in regulating lipid metabolism.
Degree: 2016, Drexel University
URL: http://hdl.handle.net/1860/idea:7176
► Cancer cells exhibit altered metabolism characterized by increased glucose and glutamine uptake. Altered utilization of these substrates directly contributes to O-linked-[beta]-N-acetylglucosamine (O-GlcNAc) modifications on intracellular…
(more)
▼ Cancer cells exhibit altered metabolism characterized by increased glucose and glutamine uptake. Altered utilization of these substrates directly contributes to O-linked-[beta]-N-acetylglucosamine (O-GlcNAc) modifications on intracellular proteins. Multiple cancers contain elevated total O-GlcNAcylation, in part, by increasing O-GlcNAc transferase (OGT) levels, the enzyme that catalyzes this modification. Although cancer cells require OGT for oncogenesis, it is not clear how tumor cells regulate OGT expression and O-GlcNAcylation. Here, we show that the PI3K/mTOR/MYC pathway is required for elevation of OGT and O-GlcNAcylation in breast cancer cells as treatment with PI3K and mTOR inhibitors reduced OGT protein expression and decreased levels of overall O-GlcNAcylation. Downstream of mTOR, the oncogenic transcription factor c-MYC is required and sufficient for increased OGT protein expression in an RNA-independent manner and c-MYC regulation of OGT in cancer cells requires the expression of c-MYC target HSP90A. Mammary tumor epithelial cells derived from MMTV-c-myc transgenic mice contain elevated OGT and O-GlcNAcylation and OGT inhibition in these tumor cells induces apoptosis. In an attempt to further address consequences of elevated O-GlcNAcylation in breast cancer, we performed comprehensive metabolomics. Metabolomics analysis revealed that reducing OGT levels in breast cancer cells altered a number of metabolic pathways including amino acids and nucleotides, however, the largest change was seen in fatty acid metabolism. We show that O-GlcNAcylation regulates the transcription factor sterol regulatory element binding protein 1 (SREBP-1) and its transcriptional targets, critical enzymes involved in lipid synthesis. OGT regulates SREBP-1 protein expression and stability/degradation via AMP Activated protein kinase (AMPK). SREBP-1 is critical for OGT-mediated regulation of cell survival and of lipid synthesis, as overexpression of SREBP-1 rescues lipogenic defects associated with OGT suppression, and tumor growth in vitro and in vivo. We also find that OGT regulates these factors in lactating mammary glands, highly lipogenic normal tissue. These results unravel a previously unidentified link between O-GlcNAcylation, lipid metabolism and the regulation of SREBP-1 in cancer. These finding suggests OGT may be a novel therapeutic target for the treatment of lipid-dependent cancers.
Ph.D., Molecular and Cell Biology and Genetics – Drexel University, 2016
Advisors/Committee Members: Reginato, Mauricio, College of Medicine.
Subjects/Keywords: Molecular biology; Cytology; Genetics; Biochemical Phenomena; Genetic Phenomena; Genetic Processes
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Sodi, V. (2016). Regulation of O-GlcNAc Transferase in breast cancer and its role in regulating lipid metabolism. (Thesis). Drexel University. Retrieved from http://hdl.handle.net/1860/idea:7176
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Sodi, Valerie. “Regulation of O-GlcNAc Transferase in breast cancer and its role in regulating lipid metabolism.” 2016. Thesis, Drexel University. Accessed February 27, 2021.
http://hdl.handle.net/1860/idea:7176.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Sodi, Valerie. “Regulation of O-GlcNAc Transferase in breast cancer and its role in regulating lipid metabolism.” 2016. Web. 27 Feb 2021.
Vancouver:
Sodi V. Regulation of O-GlcNAc Transferase in breast cancer and its role in regulating lipid metabolism. [Internet] [Thesis]. Drexel University; 2016. [cited 2021 Feb 27].
Available from: http://hdl.handle.net/1860/idea:7176.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Sodi V. Regulation of O-GlcNAc Transferase in breast cancer and its role in regulating lipid metabolism. [Thesis]. Drexel University; 2016. Available from: http://hdl.handle.net/1860/idea:7176
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Drexel University
5.
Sowash Molinari, Aislinn Rebecca.
Transcription Factor Specificity Protein 1 (Sp1) Regulates the Centrochromatin Landscape and Centromeric Transcription During Mitosis.
Degree: 2016, Drexel University
URL: http://hdl.handle.net/1860/idea:7146
► Chromosomal instability (CIN) is a dynamic and continual gain or loss of whole chromosomes, or parts of chromosomes, during cell division. It is associated with…
(more)
▼ Chromosomal instability (CIN) is a dynamic and continual gain or loss of whole chromosomes, or parts of chromosomes, during cell division. It is associated with poor patient outcome in multiple cancer types, as well as tumor heterogeneity and resistance to multiple chemotherapeutics, underscoring its clinical importance. Despite its prevalence and clinical significance, the exact mechanisms that lead to CIN remain to be determined. The transcription factor Specificity Protein 1 (Sp1) regulates the transcription of genes involved with many cellular processes, including differentiation, cell cycle progression, DNA repair, apoptosis, and senescence. Sp1 binds to specific GC-rich elements through its highly conserved carboxy-terminal zinc finger DNA binding domain, and recruits various factors to chromatin to influence transcription. Our previous work shows that Sp1 is important for maintaining chromosomal stability during mitosis. We have shown that loss of Sp1 results in abnormal chromosome alignment along the metaphase plate, creation of micronuclei, and aneuploidy, as well as lagging chromosomes and anaphase bridges, all of which are phenotypes consistent with CIN. We now show that Sp1 localizes and binds to centromeres during mitosis. Rapid localization is dependent on ATM (ataxia telangiectasia mutated) activity, and does not require the Sp1 DNA binding domain. Loss of Sp1 results in disrupted centrochromatin, including changes in histone modifications and transcription of α-satellite arrays. Further, loss of Sp1 results in defects in centromeric cohesion, as well as a decrease in Centromeric Protein C (CENP-C) and Centromeric Protein A (CENP-A) binding at centromeres. These data suggest that Sp1 may be an important factor for maintaining the structure, function, and identity of centromeres, thereby maintaining chromosomal stability.
Ph.D., Molecular and Cell Biology and Genetics – Drexel University, 2016
Advisors/Committee Members: Clifford, Jane, College of Medicine.
Subjects/Keywords: Molecular biology; Cytology; Genetics; Biochemical Phenomena; Genetic Phenomena; Genetic Processes
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APA ·
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APA (6th Edition):
Sowash Molinari, A. R. (2016). Transcription Factor Specificity Protein 1 (Sp1) Regulates the Centrochromatin Landscape and Centromeric Transcription During Mitosis. (Thesis). Drexel University. Retrieved from http://hdl.handle.net/1860/idea:7146
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Sowash Molinari, Aislinn Rebecca. “Transcription Factor Specificity Protein 1 (Sp1) Regulates the Centrochromatin Landscape and Centromeric Transcription During Mitosis.” 2016. Thesis, Drexel University. Accessed February 27, 2021.
http://hdl.handle.net/1860/idea:7146.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Sowash Molinari, Aislinn Rebecca. “Transcription Factor Specificity Protein 1 (Sp1) Regulates the Centrochromatin Landscape and Centromeric Transcription During Mitosis.” 2016. Web. 27 Feb 2021.
Vancouver:
Sowash Molinari AR. Transcription Factor Specificity Protein 1 (Sp1) Regulates the Centrochromatin Landscape and Centromeric Transcription During Mitosis. [Internet] [Thesis]. Drexel University; 2016. [cited 2021 Feb 27].
Available from: http://hdl.handle.net/1860/idea:7146.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Sowash Molinari AR. Transcription Factor Specificity Protein 1 (Sp1) Regulates the Centrochromatin Landscape and Centromeric Transcription During Mitosis. [Thesis]. Drexel University; 2016. Available from: http://hdl.handle.net/1860/idea:7146
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Drexel University
6.
Klee, Nicole Siobhan.
Type II diabetes and detrusor muscle function: Compensated and decompensated states.
Degree: 2016, Drexel University
URL: http://hdl.handle.net/1860/idea:7159
► Bladder smooth muscle (detrusor muscle) undergoes temporal changes in response to diabetes, resulting in diabetic bladder dysfunction (DBD). DBD induces a compensated state of bladder…
(more)
▼ Bladder smooth muscle (detrusor muscle) undergoes temporal changes in response to diabetes, resulting in diabetic bladder dysfunction (DBD). DBD induces a compensated state of bladder function exhibiting detrusor muscle remodeling and a hypercontractile phenotype progressing into a decompensated state of bladder function and a hypocontractile phenotype. While the majority of DBD studies have been performed in type I diabetes, there are relatively few in type II diabetes; in these studies none have characterized the two states of DBD. Our studies utilized a type II diabetic model induced by a high-fat diet, to induce insulin resistance, and low-dose streptozotocin (HFD/STZ), to induce hyperglycemia and compromised ß-cell function. The goal of this study was to investigate the timeline of DBD development, detrusor muscle contractility, and underlying mechanisms during the two states of DBD. The compensated state was characterized by increased volume per void, detrusor muscle hypertrophy, and increased contractility to carbachol and ATP. These results indicated that the enhanced contractility to carbachol was due to increased levels of M2 expression, without corresponding changes in myosin light chain (MLC) phosphorylation. The decompensated state was characterized by increased volume per void and number of voids, detrusor hypertrophy, and increased contractility to ATP but not carbachol. This suggested that progression of DBD involves decreased contractility to muscarinic stimulation. In addition, proteins involved with calcium sensitization and MLC demonstrated decreased phosphorylation levels. Decompensated detrusor also exhibited enhanced purinergic neurogenic force. The underlying increase in purinergic component of detrusor contractility is a possible therapeutic target for DBD.
Ph.D., Molecular and Cell Biology and Genetics – Drexel University, 2016
Advisors/Committee Members: Moreland, Robert S., College of Medicine.
Subjects/Keywords: Molecular biology; Cytology; Genetics; Biochemical Phenomena; Genetic Phenomena; Genetic Processes
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APA ·
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Export
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Manager
APA (6th Edition):
Klee, N. S. (2016). Type II diabetes and detrusor muscle function: Compensated and decompensated states. (Thesis). Drexel University. Retrieved from http://hdl.handle.net/1860/idea:7159
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Klee, Nicole Siobhan. “Type II diabetes and detrusor muscle function: Compensated and decompensated states.” 2016. Thesis, Drexel University. Accessed February 27, 2021.
http://hdl.handle.net/1860/idea:7159.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Klee, Nicole Siobhan. “Type II diabetes and detrusor muscle function: Compensated and decompensated states.” 2016. Web. 27 Feb 2021.
Vancouver:
Klee NS. Type II diabetes and detrusor muscle function: Compensated and decompensated states. [Internet] [Thesis]. Drexel University; 2016. [cited 2021 Feb 27].
Available from: http://hdl.handle.net/1860/idea:7159.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Klee NS. Type II diabetes and detrusor muscle function: Compensated and decompensated states. [Thesis]. Drexel University; 2016. Available from: http://hdl.handle.net/1860/idea:7159
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Drexel University
7.
Pershing, April M.
Genetic exploration of the ATP synthase complex in Plasmodium falciparum.
Degree: 2016, Drexel University
URL: http://hdl.handle.net/1860/idea:7148
► During the blood stages of its life cycle, P. falciparum relies on glycolysis as its major source of ATP rather than oxidative phosphorylation. Yet, we…
(more)
▼ During the blood stages of its life cycle, P. falciparum relies on glycolysis as its major source of ATP rather than oxidative phosphorylation. Yet, we have been unable to disrupt the genes encoding the [beta] and [gamma] subunits of the ATP synthase complex in P. falciparum blood stages. To address the essential nature of ATP synthase we generated a merodiploid line expressing a tagged mutated [beta] subunit from an ectopic site. This should reduce the overall ATP synthase activity. Although the mutant subunit was correctly trafficked to the mitochondrion, the transgenic parasites grew at the same rate as the parental lines, indicating that the ectopically expressed mutant subunits did not have a dominant negative effect. Furthermore, we generated a transgenic parasite line that permitted conditional knockdown of the [beta] subunit through the use of a regulated ribozyme. Knockdown of the [beta] subunit showed no growth phenotype, indicating >80% reduction in its expression was not detrimental to the parasites. These knockdown parasite lines allowed us to revisit a hypothesis regarding the target of proguanil, a drug shown to work synergistically with atovaquone to kill the parasite, and which is a component of the registered antimalarial drug combination Malarone®. Earlier work from our laboratory led to a hypothesis that proguanil targets a secondary pathway for generating mitochondrial membrane potential ([delta psi] m), and that this pathway becomes essential when the primary pathway of mitochondrial electron transport chain (mtETC) is inhibited by atovaquone. We monitored the effects of the merodiploid catalytic knockdown line and the ribozyme knockdown line for their sensitivity to atovaquone as well as another mtETC inhibitor, ELQ300. We also reengineered the ribozyme conditional knockdown line to become mtETC independent and thus resistant to atovaquone. This provided a means to examine the secondary pathway of [delta psi]-m generation in absence of mtETC. Through the use of these transgenic parasite lines we were able to provide strong evidence that the alternate pathway to generate the [delta psi]-m is likely to be the ATP hydrolase activity of the parasite ATP synthase. These findings now solve a decades long mystery regarding the nature of proguanil synergy with atovaquone.
Ph.D., Molecular and Cell Biology and Genetics – Drexel University, 2016
Advisors/Committee Members: Vaidya, Akhil, College of Medicine.
Subjects/Keywords: Molecular biology; Cytology; Genetics; Biochemical Phenomena; Genetic Phenomena; Genetic Processes
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APA ·
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APA (6th Edition):
Pershing, A. M. (2016). Genetic exploration of the ATP synthase complex in Plasmodium falciparum. (Thesis). Drexel University. Retrieved from http://hdl.handle.net/1860/idea:7148
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Pershing, April M. “Genetic exploration of the ATP synthase complex in Plasmodium falciparum.” 2016. Thesis, Drexel University. Accessed February 27, 2021.
http://hdl.handle.net/1860/idea:7148.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Pershing, April M. “Genetic exploration of the ATP synthase complex in Plasmodium falciparum.” 2016. Web. 27 Feb 2021.
Vancouver:
Pershing AM. Genetic exploration of the ATP synthase complex in Plasmodium falciparum. [Internet] [Thesis]. Drexel University; 2016. [cited 2021 Feb 27].
Available from: http://hdl.handle.net/1860/idea:7148.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Pershing AM. Genetic exploration of the ATP synthase complex in Plasmodium falciparum. [Thesis]. Drexel University; 2016. Available from: http://hdl.handle.net/1860/idea:7148
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Drexel University
8.
Chen, Natalie Cheng.
Age-like Phenotype of Microglia During HIV-1 Infection.
Degree: 2016, Drexel University
URL: http://hdl.handle.net/1860/idea:7160
► HIV Associated Neurocognitive Disorder (HAND) persists in 50% of infected patients despite treatments. Moreover, HAND potentiates aging-associated neurocognitive decline as the infected population grow older.…
(more)
▼ HIV Associated Neurocognitive Disorder (HAND) persists in 50% of infected patients despite treatments. Moreover, HAND potentiates aging-associated neurocognitive decline as the infected population grow older. Microglia cells support productive HIV-1 infection in the brain and elevated senescence markers including p53 and p21 have been detected in microglia in HAND tissues. We hypothesize that HIV-1 induces age-like phenotypes in microglia. In an in vitro model of primary human microglia infected with HIV-1 pseudotype, we examined various markers of aging including the expression of cell cycle inhibitors (p53, p21 and p16), DNA damage associated p53 binding protein 1 (53BP1) foci formation, senescence associated [beta]-galactosidase (SA-[beta]-gal) activity, and the development of Senescence Associated Secretory Phenotype (SASP). Finally, we examined mitochondrial reactive oxygen species (ROS) and mitochondrial respiration, which are known to be altered during organismal aging. We detected elevated expression of p53 and p21, increased percentage of cells expressing 53BP1 foci and [beta]-gal, as well as significantly elevated levels of various cytokines including IL8 and IL6 post infection. The development of age-like phenotype is accompanied by increased mitochondrial ROS production and altered mitochondrial respiratory activity. Finally, exposure to the supernatant of infected microglia results in elevated p21 and caveolin-1 protein expression. Overall, we have demonstrated for the first time age-like phenotypes in human microglia during HIV-1 infection. HIV-1 induced microglial age-like phenotype could play a role in the development of HAND.
Ph.D., Molecular and Cell Biology and Genetics – Drexel University, 2016
Advisors/Committee Members: Martin-Garcia, Julio, College of Medicine.
Subjects/Keywords: Molecular biology; Cytology; Genetics; Biochemical Phenomena; Genetic Phenomena; Genetic Processes; Molecular biology; Cytology; Genetics
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APA (6th Edition):
Chen, N. C. (2016). Age-like Phenotype of Microglia During HIV-1 Infection. (Thesis). Drexel University. Retrieved from http://hdl.handle.net/1860/idea:7160
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Chen, Natalie Cheng. “Age-like Phenotype of Microglia During HIV-1 Infection.” 2016. Thesis, Drexel University. Accessed February 27, 2021.
http://hdl.handle.net/1860/idea:7160.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chen, Natalie Cheng. “Age-like Phenotype of Microglia During HIV-1 Infection.” 2016. Web. 27 Feb 2021.
Vancouver:
Chen NC. Age-like Phenotype of Microglia During HIV-1 Infection. [Internet] [Thesis]. Drexel University; 2016. [cited 2021 Feb 27].
Available from: http://hdl.handle.net/1860/idea:7160.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chen NC. Age-like Phenotype of Microglia During HIV-1 Infection. [Thesis]. Drexel University; 2016. Available from: http://hdl.handle.net/1860/idea:7160
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Western Kentucky University
9.
Ravipati, Dhatri.
Activity of Analogs of Anticancer Drugs on the Serine Protease Enzymes Subtilisin and Chymotrypsin.
Degree: MS, Department of Chemistry, 2011, Western Kentucky University
URL: https://digitalcommons.wku.edu/theses/1134
► The anticancer activity of several platinum compounds is due to the formation of complexes with DNA. We hypothesize that the size and shape of…
(more)
▼ The anticancer activity of several platinum compounds is due to the formation of complexes with DNA. We hypothesize that the size and shape of the platinum compounds would impact interaction with proteins, and these interactions may be partly responsible for the anticancer activity. Chymotrypsin and subtilisin are serine proteases that have a histidine residue in the active site. We are investigating the inhibition of the digestive enzymes chymotrypsin and subtilisin by analogs of the anticancer drug cisplatin and trying to discern trends in the inhibition as the active site residues vary. In our research, we found that the enzyme subtilisin did not show any significant inhibition with different platinum compounds we used, while chymotrypsin showed inhibition only with the potassium tetrachloroplatinate and this inhibition is concentration dependent
Advisors/Committee Members: Dr. Kevin Williams (Director), Dr. Bangbo Yan,Dr. Eric Conte.
Subjects/Keywords: platinum compounds; serine proteases; digestive enzymes; Genetic Processes; Medicinal-Pharmaceutical Chemistry
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APA (6th Edition):
Ravipati, D. (2011). Activity of Analogs of Anticancer Drugs on the Serine Protease Enzymes Subtilisin and Chymotrypsin. (Masters Thesis). Western Kentucky University. Retrieved from https://digitalcommons.wku.edu/theses/1134
Chicago Manual of Style (16th Edition):
Ravipati, Dhatri. “Activity of Analogs of Anticancer Drugs on the Serine Protease Enzymes Subtilisin and Chymotrypsin.” 2011. Masters Thesis, Western Kentucky University. Accessed February 27, 2021.
https://digitalcommons.wku.edu/theses/1134.
MLA Handbook (7th Edition):
Ravipati, Dhatri. “Activity of Analogs of Anticancer Drugs on the Serine Protease Enzymes Subtilisin and Chymotrypsin.” 2011. Web. 27 Feb 2021.
Vancouver:
Ravipati D. Activity of Analogs of Anticancer Drugs on the Serine Protease Enzymes Subtilisin and Chymotrypsin. [Internet] [Masters thesis]. Western Kentucky University; 2011. [cited 2021 Feb 27].
Available from: https://digitalcommons.wku.edu/theses/1134.
Council of Science Editors:
Ravipati D. Activity of Analogs of Anticancer Drugs on the Serine Protease Enzymes Subtilisin and Chymotrypsin. [Masters Thesis]. Western Kentucky University; 2011. Available from: https://digitalcommons.wku.edu/theses/1134
University of Western Ontario
10.
Baktash, Navid.
The Differential Expression of EGFL7 Transcripts during Angiogenesis in Human Fibrosarcoma.
Degree: 2012, University of Western Ontario
URL: https://ir.lib.uwo.ca/etd/753
► The growth of a tumor depends on de novo angiogenesis, which involves multiple signaling cascades and is also a target for many anti-angiogenic therapies. Epidermal…
(more)
▼ The growth of a tumor depends on de novo angiogenesis, which involves multiple signaling cascades and is also a target for many anti-angiogenic therapies. Epidermal growth factor like (EGFL7), is a protein that is exclusively expressed by endothelial cells during angiogenesis and is necessary for the proper assembly of a sprout. However, EGFL7 is also upregulated in many tumors such as glioma and non-small cell lung cancer, associated with poor patient prognosis. We have previously shown that EGFL7 expression by tumor cells inhibits tumor angiogenesis, which is contrary to its requirement for angiogenesis when expressed by endothelial cells. As a result, the objective of this research is to understand the basis of this differential regulation. We hypothesize that the differential effects of EGFL7 on angiogenesis is due to the presence of alternative transcripts in HT1080 tumor cells. Here, I demonstrate that endothelial cells express two families of transcripts, TSS1 and TSS2 families, which are transcribed from two different transcriptional start sites. In HT1080 tumor cells however, only TSS2 families of transcripts are produced. Importantly, a novel non-coding transcripts in both TSS1 and TSS2 family is identified. Knocking down TSS2 transcripts in tumor cells resulted in enhanced angiogenesis. Result from this thesis; identify novel differential EGFL7 transcripts expressed in HT1080 tumor cells, which inhibits angiogenesis.
Subjects/Keywords: EGFL7; Transcripts; Angiogenesis; Differential Regulation; Tumor; Genetic Processes; Medical Biochemistry
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APA (6th Edition):
Baktash, N. (2012). The Differential Expression of EGFL7 Transcripts during Angiogenesis in Human Fibrosarcoma. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/753
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Baktash, Navid. “The Differential Expression of EGFL7 Transcripts during Angiogenesis in Human Fibrosarcoma.” 2012. Thesis, University of Western Ontario. Accessed February 27, 2021.
https://ir.lib.uwo.ca/etd/753.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Baktash, Navid. “The Differential Expression of EGFL7 Transcripts during Angiogenesis in Human Fibrosarcoma.” 2012. Web. 27 Feb 2021.
Vancouver:
Baktash N. The Differential Expression of EGFL7 Transcripts during Angiogenesis in Human Fibrosarcoma. [Internet] [Thesis]. University of Western Ontario; 2012. [cited 2021 Feb 27].
Available from: https://ir.lib.uwo.ca/etd/753.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Baktash N. The Differential Expression of EGFL7 Transcripts during Angiogenesis in Human Fibrosarcoma. [Thesis]. University of Western Ontario; 2012. Available from: https://ir.lib.uwo.ca/etd/753
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Georgia Tech
11.
Meddin, Mona.
Genetic algorithms :
a markov chain and detail balance approach.
Degree: PhD, Mathematics, 1995, Georgia Tech
URL: http://hdl.handle.net/1853/29196
Subjects/Keywords: Genetic algorithms; Markov processes
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APA (6th Edition):
Meddin, M. (1995). Genetic algorithms :
a markov chain and detail balance approach. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/29196
Chicago Manual of Style (16th Edition):
Meddin, Mona. “Genetic algorithms :
a markov chain and detail balance approach.” 1995. Doctoral Dissertation, Georgia Tech. Accessed February 27, 2021.
http://hdl.handle.net/1853/29196.
MLA Handbook (7th Edition):
Meddin, Mona. “Genetic algorithms :
a markov chain and detail balance approach.” 1995. Web. 27 Feb 2021.
Vancouver:
Meddin M. Genetic algorithms :
a markov chain and detail balance approach. [Internet] [Doctoral dissertation]. Georgia Tech; 1995. [cited 2021 Feb 27].
Available from: http://hdl.handle.net/1853/29196.
Council of Science Editors:
Meddin M. Genetic algorithms :
a markov chain and detail balance approach. [Doctoral Dissertation]. Georgia Tech; 1995. Available from: http://hdl.handle.net/1853/29196
University of Montana
12.
Zheng, Cuixiu.
Using Markov chain model to compare a steady-state and a generational GA.
Degree: MS, 2000, University of Montana
URL: https://scholarworks.umt.edu/etd/8349
Subjects/Keywords: Genetic algorithms.; Markov processes Numerical solutions.; Markov processes.
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Manager
APA (6th Edition):
Zheng, C. (2000). Using Markov chain model to compare a steady-state and a generational GA. (Masters Thesis). University of Montana. Retrieved from https://scholarworks.umt.edu/etd/8349
Chicago Manual of Style (16th Edition):
Zheng, Cuixiu. “Using Markov chain model to compare a steady-state and a generational GA.” 2000. Masters Thesis, University of Montana. Accessed February 27, 2021.
https://scholarworks.umt.edu/etd/8349.
MLA Handbook (7th Edition):
Zheng, Cuixiu. “Using Markov chain model to compare a steady-state and a generational GA.” 2000. Web. 27 Feb 2021.
Vancouver:
Zheng C. Using Markov chain model to compare a steady-state and a generational GA. [Internet] [Masters thesis]. University of Montana; 2000. [cited 2021 Feb 27].
Available from: https://scholarworks.umt.edu/etd/8349.
Council of Science Editors:
Zheng C. Using Markov chain model to compare a steady-state and a generational GA. [Masters Thesis]. University of Montana; 2000. Available from: https://scholarworks.umt.edu/etd/8349
West Virginia University
13.
Sundar, Jesse C.
Alternative Splicing in Vertebrate Photoreceptors and Mechanisms Underlying Retinitis Pigmentosa.
Degree: PhD, Biochemistry, 2019, West Virginia University
URL: https://doi.org/10.33915/etd.7661
;
https://researchrepository.wvu.edu/etd/7661
► RNA binding proteins (RBPs) have emerged as important regulators of gene expression. RBPs typically contain RNA binding domains that recognize a specific sequence and/or…
(more)
▼ RNA binding proteins (RBPs) have emerged as important regulators of gene expression. RBPs typically contain RNA binding domains that recognize a specific sequence and/or structural motifs within the RNA. This allows them to modulate metabolism of RNAs in several possible ways including regulation of alternative splicing and processing, polyadenylation, translocation, localization, modification, stability, or translation. Previous studies have shown the Musashi (MSI) RBP family to be highly expressed in the retina, and more specifically, photoreceptors, but the importance of this expression remains largely unknown. We identified the MSI proteins as potential regulators of alternative exon splicing in murine photoreceptors. We hypothesized that the MSI proteins are essential splicing factors needed to produce photoreceptor-specific transcripts and that inactivation of the Msi genes would lead to decreased photoreceptor function and survival subsequent to aberrant splicing. We also predicted that the MSI proteins were regulating splicing of transcripts involved in ciliogenesis and outer segment morphogenesis.
To test our hypothesis, I generated Cre-LoxP conditional knockout mice to inactivate the
Msi genes either in the entire retina and ventral forebrain or specifically rod photoreceptors. I found that both rod and cone photoreceptor function was completely absent after pan-retinal inactivation of both
Msi genes. I also discovered alterations in retinal progenitor cell proliferation and decreased retinal cell survival at later ages in the absence of the MSI proteins. When analyzing the morphology of the outer segment and connecting cilium in the absence of MSI, I found defects only in outer segment morphology. Furthermore, I found that the MSI proteins regulate the photoreceptor-specific splicing of several outer segment and cilia-related transcripts including Bbs8, Cc2d2a, Cep290, and Prom1. Lastly, we found that deletion of these photoreceptor-specific exons in
C57BL6/J mice did not significantly affect photoreceptor function.
Advisors/Committee Members: Visvanathan Ramamurthy, Ronald Gross.
Subjects/Keywords: Alternative Splicing; Musashi; RNA Binding Protein; BBS8; Retina; Photoreceptor; Outer Segment; Rhodopsin; Transducin; Retinitis Pigmentosa; Genetic Phenomena; Genetic Processes
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APA (6th Edition):
Sundar, J. C. (2019). Alternative Splicing in Vertebrate Photoreceptors and Mechanisms Underlying Retinitis Pigmentosa. (Doctoral Dissertation). West Virginia University. Retrieved from https://doi.org/10.33915/etd.7661 ; https://researchrepository.wvu.edu/etd/7661
Chicago Manual of Style (16th Edition):
Sundar, Jesse C. “Alternative Splicing in Vertebrate Photoreceptors and Mechanisms Underlying Retinitis Pigmentosa.” 2019. Doctoral Dissertation, West Virginia University. Accessed February 27, 2021.
https://doi.org/10.33915/etd.7661 ; https://researchrepository.wvu.edu/etd/7661.
MLA Handbook (7th Edition):
Sundar, Jesse C. “Alternative Splicing in Vertebrate Photoreceptors and Mechanisms Underlying Retinitis Pigmentosa.” 2019. Web. 27 Feb 2021.
Vancouver:
Sundar JC. Alternative Splicing in Vertebrate Photoreceptors and Mechanisms Underlying Retinitis Pigmentosa. [Internet] [Doctoral dissertation]. West Virginia University; 2019. [cited 2021 Feb 27].
Available from: https://doi.org/10.33915/etd.7661 ; https://researchrepository.wvu.edu/etd/7661.
Council of Science Editors:
Sundar JC. Alternative Splicing in Vertebrate Photoreceptors and Mechanisms Underlying Retinitis Pigmentosa. [Doctoral Dissertation]. West Virginia University; 2019. Available from: https://doi.org/10.33915/etd.7661 ; https://researchrepository.wvu.edu/etd/7661
University of South Carolina
14.
Spencer, Christopher Michael.
Spiritual Care in Cancer Genetic Counseling: Patient Perceptions of Methods.
Degree: MS, Genetic Counseling, 2018, University of South Carolina
URL: https://scholarcommons.sc.edu/etd/4745
► The integration of spirituality into medical care is a growing area of debate among professionals, involving a delicate balance between serving patients who may…
(more)
▼ The integration of spirituality into medical care is a growing area of debate among professionals, involving a delicate balance between serving patients who may benefit from this without alienating those who would not. To date, little research has targeted spirituality in cancer
genetic counseling, particularly concerning the various methods a
genetic counselor can use to address spirituality with their patients. A paper questionnaire was created and distributed to patients following their cancer
genetic counseling appointments to gain insight on their perception of these methods. Fifty-two participants completed this questionnaire. The eight different spiritual integration methods presented each showed positive responses by the participant group on average, though opinions varied between participants. The method with the highest approval involved a
genetic counselor informing patients that spirituality was a welcome topic of discussion during their appointment. Overall, 78.9% viewed this as a positive action by the counselor, while 11.5% viewed this negatively. Higher participant approval was typically seen for more indirect methods of addressing spirituality, and some methods were more beneficial for Christians compared to Non-Christians. Interestingly, 48.1% of patients indicated that they did not desire the
genetic counselor to address their spiritual needs, with only 23% responding that they did. The fact that this item was presented before the potential methods may indicate a misconception that spirituality and genetics are incompatible. This study highlights the many opportunities for further research into this topic
Advisors/Committee Members: Janice Edwards.
Subjects/Keywords: Genetic Processes; Medical Sciences; Medicine and Health Sciences; Spiritual Care; Cancer; Genetic Counseling; Patient; Perceptions; Methods
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APA (6th Edition):
Spencer, C. M. (2018). Spiritual Care in Cancer Genetic Counseling: Patient Perceptions of Methods. (Masters Thesis). University of South Carolina. Retrieved from https://scholarcommons.sc.edu/etd/4745
Chicago Manual of Style (16th Edition):
Spencer, Christopher Michael. “Spiritual Care in Cancer Genetic Counseling: Patient Perceptions of Methods.” 2018. Masters Thesis, University of South Carolina. Accessed February 27, 2021.
https://scholarcommons.sc.edu/etd/4745.
MLA Handbook (7th Edition):
Spencer, Christopher Michael. “Spiritual Care in Cancer Genetic Counseling: Patient Perceptions of Methods.” 2018. Web. 27 Feb 2021.
Vancouver:
Spencer CM. Spiritual Care in Cancer Genetic Counseling: Patient Perceptions of Methods. [Internet] [Masters thesis]. University of South Carolina; 2018. [cited 2021 Feb 27].
Available from: https://scholarcommons.sc.edu/etd/4745.
Council of Science Editors:
Spencer CM. Spiritual Care in Cancer Genetic Counseling: Patient Perceptions of Methods. [Masters Thesis]. University of South Carolina; 2018. Available from: https://scholarcommons.sc.edu/etd/4745
Universidade do Rio Grande do Sul
15.
Oliveira, Lauro César Pecktor de.
Doppelgänger : da ideia à obra.
Degree: 2014, Universidade do Rio Grande do Sul
URL: http://hdl.handle.net/10183/103499
► Este memorial trata da investigação do processo criativo de Doppelgänger, para dois pianos. Com suporte nos pressupostos metodológicos da crítica genética expandidos para o campo…
(more)
▼ Este memorial trata da investigação do processo criativo de Doppelgänger, para dois pianos. Com suporte nos pressupostos metodológicos da crítica genética expandidos para o campo da música, o olhar investigativo procurou elos entre as operações que, nos níveis de decisão, colocaram o processo criativo em movimento. A expansão da crítica genética para a música fez com que se tornasse imprescindível restituir aos documentos de processo a sua realidade sonora e temporal, considerando-a como parte do estatuto genético da obra em investigação. A pesquisa sobre a gênese do processo criativo de Doppelgänger revelou uma série de decisões tomadas e operações empreendidas, permitindo reconstruir o caminho da ideia à obra.
The creative process in Doppelgänger for two pianos is investigated in this paper. With genetic criticism as its methodology, it attempts to recreate the compositional process that has transformed an idea into a finished work through a web of creative operations. In music, genetic criticism has to take into account the sonic and temporal reality of the avant-textes, as they are integral to the construction of the genetic dossier of a particular work. The genetic investigation on Doppelgänger has brought to light a series of decisions and operations, which, in their written and sonic representations, chart the creative trail that led to the finished piece.
Advisors/Committee Members: Chaves, Celso Giannetti Loureiro.
Subjects/Keywords: Composição musical; Musical composition; Crítica genética; Genetic criticism; Processo criativo; Creative processes
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APA (6th Edition):
Oliveira, L. C. P. d. (2014). Doppelgänger : da ideia à obra. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/103499
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Oliveira, Lauro César Pecktor de. “Doppelgänger : da ideia à obra.” 2014. Thesis, Universidade do Rio Grande do Sul. Accessed February 27, 2021.
http://hdl.handle.net/10183/103499.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Oliveira, Lauro César Pecktor de. “Doppelgänger : da ideia à obra.” 2014. Web. 27 Feb 2021.
Vancouver:
Oliveira LCPd. Doppelgänger : da ideia à obra. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2014. [cited 2021 Feb 27].
Available from: http://hdl.handle.net/10183/103499.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Oliveira LCPd. Doppelgänger : da ideia à obra. [Thesis]. Universidade do Rio Grande do Sul; 2014. Available from: http://hdl.handle.net/10183/103499
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
McMaster University
16.
Sarin, Sanjay.
β-catenin overexpression within the metanephric mesenchyme causes renal dysplasia via upregulation of the Gdnf signalling axis.
Degree: MSc, 2013, McMaster University
URL: http://hdl.handle.net/11375/12888
► Renal dysplasia, a developmental disorder characterized by defective nephrogenesis and branching morphogenesis, ranks as one of the major causes of renal failure among the…
(more)
▼ Renal dysplasia, a developmental disorder characterized by defective nephrogenesis and branching morphogenesis, ranks as one of the major causes of renal failure among the pediatric population. The molecular mechanisms underlying the pathogenesis of renal dysplasia are not well understood; however, changes in gene expression are a major contributing factor. In this study, we demonstrate that the levels of activated β-catenin, a transcriptional co-regulator, are elevated in the nuclei of ureteric, stromal, and mesenchymal cells within dysplastic human kidney tissue. To determine the mechanisms by which mesenchymal β-catenin over-expression leads to renal dysplasia, we generated a conditional mouse model in which β-catenin was stabilized exclusively in the metanephric mesenchyme. Kidneys from these mutant mice are remarkably similar to dysplastic human kidneys. In addition, these mutant mice also demonstrate the formation of 4 to 6 ectopic kidneys. While nephrogenesis appeared normal, investigation of ureteric branch pattern revealed ectopic ureteric budding off the Wolffian duct, ectopic branching off the initial ureteric bud stalk and a disorganization of branch patterning. In-situ hybridization of mutant kidneys revealed increased expression of Gdnf, Cret, and Wnt11, key factors that regulate ureteric branch patterning. We further demonstrate that β-catenin directly binds to TCF consensus binding sites within the Gdnf promoter region located 4.9kb, 2.25kb and 2.1kb upstream of the Gdnf transcriptional start site. Molecular cloning of the 4.9kb fragment upstream of a luciferase gene revealed that ß-catenin regulates gene transcription from the 4.9kb consensus site. Consistent with these findings, genetic deletion of β-catenin from the metanephric mesenchyme cell lineage lead to decreased Gdnf expression and a reduction in ureteric branching morphogenesis resulting in renal hypoplasia. Taken together, our findings establish that β-catenin is an essential regulator of Gdnf expression within the metanephric mesenchyme. Furthermore, we have identified a novel disrupted signalling pathway that contributes to the pathogenesis of renal dysplasia. In this pathway, an over-expression of β-catenin directly leads to an over-expression of Gdnf, causing ectopic and disorganized branching morphogenesis and, consequently, renal dysplasia.
Master of Health Sciences (MSc)
Advisors/Committee Members: Bridgewater, Darren, Medical Sciences.
Subjects/Keywords: Kidney development; branching morphogenesis; Developmental Biology; Genetic Processes; Medical Sciences; Developmental Biology
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APA (6th Edition):
Sarin, S. (2013). β-catenin overexpression within the metanephric mesenchyme causes renal dysplasia via upregulation of the Gdnf signalling axis. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/12888
Chicago Manual of Style (16th Edition):
Sarin, Sanjay. “β-catenin overexpression within the metanephric mesenchyme causes renal dysplasia via upregulation of the Gdnf signalling axis.” 2013. Masters Thesis, McMaster University. Accessed February 27, 2021.
http://hdl.handle.net/11375/12888.
MLA Handbook (7th Edition):
Sarin, Sanjay. “β-catenin overexpression within the metanephric mesenchyme causes renal dysplasia via upregulation of the Gdnf signalling axis.” 2013. Web. 27 Feb 2021.
Vancouver:
Sarin S. β-catenin overexpression within the metanephric mesenchyme causes renal dysplasia via upregulation of the Gdnf signalling axis. [Internet] [Masters thesis]. McMaster University; 2013. [cited 2021 Feb 27].
Available from: http://hdl.handle.net/11375/12888.
Council of Science Editors:
Sarin S. β-catenin overexpression within the metanephric mesenchyme causes renal dysplasia via upregulation of the Gdnf signalling axis. [Masters Thesis]. McMaster University; 2013. Available from: http://hdl.handle.net/11375/12888
Texas Medical Center
17.
Schoberle, Taylor J.
NOVEL INDUCERS OF GLIOTOXIN PRODUCTION IN ASPERGILLUS FUMIGATUS.
Degree: PhD, 2013, Texas Medical Center
URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/379
► Secondary metabolites are produced by numerous organisms and can either be benign to humans or harmful. Genes involved in the synthesis and transport of…
(more)
▼ Secondary metabolites are produced by numerous organisms and can either be benign to humans or harmful. Genes involved in the synthesis and transport of these secondary metabolites are frequently found in gene clusters, which are often located in subtelomeric regions of the chromosome. These clusters are often coordinately regulated, being almost exclusively dependent on transcription factors that are located within the clusters themselves. Secondary metabolites are also regulated by a variety of factors, including nutritional factors, environmental factors and developmental
processes. Gliotoxin, which is produced by a variety of
Aspergillus species,
Trichoderma species, and
Penicillium species, exhibits immunosuppressive properties and has therefore been the
subject of research for many laboratories. There have been a few proteins shown to regulate the gliotoxin cluster, most notably GliZ, a Zn
2Cys
6 binuclear finger transcription factor that lies within the cluster, and LaeA, a putative methyltransferase that globally regulates secondary metabolism clusters within numerous fungal organisms, although no study has demonstrated the direct binding of any protein to a promoter region in the gliotoxin cluster.
I report here two novel proteins, GipA, a C
2H
2 transcription factor and GipB, a hybrid sensor kinase, which are involved in regulating the gliotoxin biosynthetic cluster. GipA plays an important role in gliotoxin production, as high-copy expression of
gipA induces gliotoxin biosynthesis and loss of
gipA reduces gliotoxin biosynthesis by 50%. GipB is also involved in regulating gliotoxin production, as high-copy expression of
gipB induces gliotoxin biosynthesis, but only during certain stages of asexual development. Furthermore, loss of
gipB reduces gliotoxin biosynthesis by 10%. Based on data obtained from this project, I propose a model for the regulation of
gliA, the efflux pump of the gliotoxin cluster, which involves GipB signaling through both GliZ and GipA. I propose that GliZ and GipA are interdependent, as mutation of the GipA DNA binding site in the
gliA promoter negatively affects both GliZ-mediated and GipA-mediated induction of
gliA. This is further supported by the fact that GliZ cannot fully induce
gliA in the absence of GipA and vice versa. This is the first time that anyone has shown evidence of a protein directly binding to the gliotoxin cluster. Even though biosynthetic clusters are often coordinately regulated, my model raises the possibility that
gliA is independently regulated, as the layout of the binding site in the
gliA promoter is not present upstream of any other genes in the gliotoxin cluster, except for
gliZ.
Advisors/Committee Members: Dr. Gregory May, Dr. Michelle Barton, Dr. Kevin Morano.
Subjects/Keywords: Gliotoxin; Gene Transcription; Fungal genetics; Fungi; Genetic Processes; Medicine and Health Sciences
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APA (6th Edition):
Schoberle, T. J. (2013). NOVEL INDUCERS OF GLIOTOXIN PRODUCTION IN ASPERGILLUS FUMIGATUS. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/379
Chicago Manual of Style (16th Edition):
Schoberle, Taylor J. “NOVEL INDUCERS OF GLIOTOXIN PRODUCTION IN ASPERGILLUS FUMIGATUS.” 2013. Doctoral Dissertation, Texas Medical Center. Accessed February 27, 2021.
https://digitalcommons.library.tmc.edu/utgsbs_dissertations/379.
MLA Handbook (7th Edition):
Schoberle, Taylor J. “NOVEL INDUCERS OF GLIOTOXIN PRODUCTION IN ASPERGILLUS FUMIGATUS.” 2013. Web. 27 Feb 2021.
Vancouver:
Schoberle TJ. NOVEL INDUCERS OF GLIOTOXIN PRODUCTION IN ASPERGILLUS FUMIGATUS. [Internet] [Doctoral dissertation]. Texas Medical Center; 2013. [cited 2021 Feb 27].
Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/379.
Council of Science Editors:
Schoberle TJ. NOVEL INDUCERS OF GLIOTOXIN PRODUCTION IN ASPERGILLUS FUMIGATUS. [Doctoral Dissertation]. Texas Medical Center; 2013. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/379
Hong Kong University of Science and Technology
18.
Pardo Avila, Fátima Alejandra.
Dynamics of the transcription elongation process of RNA polymerase elucidated at atomic resolution by molecular dynamics and Markov state models.
Degree: 2015, Hong Kong University of Science and Technology
URL: http://repository.ust.hk/ir/Record/1783.1-87361
;
https://doi.org/10.14711/thesis-b1514965
;
http://repository.ust.hk/ir/bitstream/1783.1-87361/1/th_redirect.html
► RNA polymerase is central in gene transcription. During transcription elongation stage, the RNA polymerase processively adds nucleotides to a nascent RNA transcript based on a…
(more)
▼ RNA polymerase is central in gene transcription. During transcription elongation stage, the RNA polymerase processively adds nucleotides to a nascent RNA transcript based on a DNA template. The series of steps required to add a nucleotide are known as the nucleotide addition cycle (NAC). Multiple structural studies have provided static snapshots of the different steps of the NAC, however, the dynamical mechanisms connecting the steps remain elusive or controversial. Molecular Dynamics simulations are useful to study the function of biological molecules at atomic resolution, and in combination with Markov State Models (MSM), it is possible to reach long timescale dynamics, which are necessary to study the relevant steps of transcription elongation. This thesis presents the results obtained from extensive MD simulations and MSMs for: Trigger Loop Motion, Backtracking, Translocation (in eukaryotes) and Pyrophosphate Ion release (in a bacteria). A chapter is included regarding the construction of system that contains the full transcription bubble and the investigation of the possible NTP entry pathways. All these projects, taken together, provide a working model of the complete NAC at atomic resolution and at the millisecond timescale.
Subjects/Keywords: RNA polymerases
; Genetics
; Mathematical models
; Genetic transcription
; Nucleotides
; Analysis
; Molecular dynamics
; Markov processes
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APA (6th Edition):
Pardo Avila, F. A. (2015). Dynamics of the transcription elongation process of RNA polymerase elucidated at atomic resolution by molecular dynamics and Markov state models. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-87361 ; https://doi.org/10.14711/thesis-b1514965 ; http://repository.ust.hk/ir/bitstream/1783.1-87361/1/th_redirect.html
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Pardo Avila, Fátima Alejandra. “Dynamics of the transcription elongation process of RNA polymerase elucidated at atomic resolution by molecular dynamics and Markov state models.” 2015. Thesis, Hong Kong University of Science and Technology. Accessed February 27, 2021.
http://repository.ust.hk/ir/Record/1783.1-87361 ; https://doi.org/10.14711/thesis-b1514965 ; http://repository.ust.hk/ir/bitstream/1783.1-87361/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Pardo Avila, Fátima Alejandra. “Dynamics of the transcription elongation process of RNA polymerase elucidated at atomic resolution by molecular dynamics and Markov state models.” 2015. Web. 27 Feb 2021.
Vancouver:
Pardo Avila FA. Dynamics of the transcription elongation process of RNA polymerase elucidated at atomic resolution by molecular dynamics and Markov state models. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2015. [cited 2021 Feb 27].
Available from: http://repository.ust.hk/ir/Record/1783.1-87361 ; https://doi.org/10.14711/thesis-b1514965 ; http://repository.ust.hk/ir/bitstream/1783.1-87361/1/th_redirect.html.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Pardo Avila FA. Dynamics of the transcription elongation process of RNA polymerase elucidated at atomic resolution by molecular dynamics and Markov state models. [Thesis]. Hong Kong University of Science and Technology; 2015. Available from: http://repository.ust.hk/ir/Record/1783.1-87361 ; https://doi.org/10.14711/thesis-b1514965 ; http://repository.ust.hk/ir/bitstream/1783.1-87361/1/th_redirect.html
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Florida Atlantic University
19.
Santos, Radleigh G.
A novel optimization algorithm and other techniques in medicinal chemistry.
Degree: PhD, 2012, Florida Atlantic University
URL: http://purl.flvc.org/FAU/3352830
► Summary: In this dissertation we will present a stochastic optimization algorithm and use it and other mathematical techniques to tackle problems arising in medicinal chemistry.…
(more)
▼ Summary: In this dissertation we will present a stochastic optimization algorithm and use it and other mathematical techniques to tackle problems arising in medicinal chemistry. In Chapter 1, we present some background about stochastic optimization and the Accelerated Random Search (ARS) algorithm. We then present a novel improvement of the ARS algorithm, DIrected Accelerated Random Search (DARS), motivated by some theoretical results, and demonstrate through numerical results that it improves upon ARS. In Chapter 2, we use DARS and other methods to address issues arising from the use of mixture-based combinatorial libraries in drug discovery. In particular, we look at models associated with the biological activity of these mixtures and use them to answer questions about sensitivity and robustness, and also present a novel method for determining the integrity of the synthesis. Finally, in Chapter 3 we present an in-depth analysis of some statistical and mathematical techniques in combinatorial chemistry, including a novel probabilistic approach to using structural similarity to predict the activity landscape.
Electronic reproduction. Boca Raton, Fla., 2012.
Subjects/Keywords: Drugs – Design – Mathematical models; Combinatorial optimization; Combinatorial chemistry; Genetic algorithms; Mathematical optimization; Stochastic processes
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APA (6th Edition):
Santos, R. G. (2012). A novel optimization algorithm and other techniques in medicinal chemistry. (Doctoral Dissertation). Florida Atlantic University. Retrieved from http://purl.flvc.org/FAU/3352830
Chicago Manual of Style (16th Edition):
Santos, Radleigh G. “A novel optimization algorithm and other techniques in medicinal chemistry.” 2012. Doctoral Dissertation, Florida Atlantic University. Accessed February 27, 2021.
http://purl.flvc.org/FAU/3352830.
MLA Handbook (7th Edition):
Santos, Radleigh G. “A novel optimization algorithm and other techniques in medicinal chemistry.” 2012. Web. 27 Feb 2021.
Vancouver:
Santos RG. A novel optimization algorithm and other techniques in medicinal chemistry. [Internet] [Doctoral dissertation]. Florida Atlantic University; 2012. [cited 2021 Feb 27].
Available from: http://purl.flvc.org/FAU/3352830.
Council of Science Editors:
Santos RG. A novel optimization algorithm and other techniques in medicinal chemistry. [Doctoral Dissertation]. Florida Atlantic University; 2012. Available from: http://purl.flvc.org/FAU/3352830
University of Western Ontario
20.
Abbas, Ali.
Transcriptional regulation of peptidylarginine deiminase type IV: implications for rheumatoid arthritis.
Degree: 2014, University of Western Ontario
URL: https://ir.lib.uwo.ca/etd/2189
► High titers of anti-citrullinated protein antibodies have been detected in sera of rheumatoid arthritis (RA) patients, implicating citrullinating enzymes in the pathogenesis of RA. Peptidylarginine…
(more)
▼ High titers of anti-citrullinated protein antibodies have been detected in sera of rheumatoid arthritis (RA) patients, implicating citrullinating enzymes in the pathogenesis of RA. Peptidylarginine deiminase type IV (PAD4) is a member of the PAD family of enzymes that catalyze the post- translational modification of arginine to citrulline and has been linked with RA. However, little is known about its transcriptional regulation. Therefore, our aim was to determine how transcription of PAD4 is activated in the myeloid lineage. Using bioinformatics, a potential nuclear factor kappa B (NF-kB) binding site was identified on the PAD4 promoter. Luciferase assays were used to test promoter activity in human and murine myeloid cells. Interestingly, mutation of the NF-κB binding site significantly lowered promoter activity in WEHI-3B cells but significantly increased it in both HL-60 and THP-1 cell lines. In addition, PAD4 mRNA was significantly lowered in response to TNF-α treatment in HL-60 cells but increased in WEHI-3B cells. Finally, chromatin immunoprecipitation (ChIP) using anti-p50 and anti-p65 antibodies revealed that there was a significant increase in p50 enrichment at the PAD4 promoter, but not p65 in cells treated with TNF-α. Our results suggest that NF-κB may play an important role in the transcriptional regulation of PAD4 in human and murine immune systems.
Subjects/Keywords: PAD4; NF-κB; Rheumatoid Arthritis; Autoimmunity; Transcription; Citrullination; Genetic Processes; Immunity; Medical Immunology
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Export
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APA (6th Edition):
Abbas, A. (2014). Transcriptional regulation of peptidylarginine deiminase type IV: implications for rheumatoid arthritis. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/2189
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Abbas, Ali. “Transcriptional regulation of peptidylarginine deiminase type IV: implications for rheumatoid arthritis.” 2014. Thesis, University of Western Ontario. Accessed February 27, 2021.
https://ir.lib.uwo.ca/etd/2189.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Abbas, Ali. “Transcriptional regulation of peptidylarginine deiminase type IV: implications for rheumatoid arthritis.” 2014. Web. 27 Feb 2021.
Vancouver:
Abbas A. Transcriptional regulation of peptidylarginine deiminase type IV: implications for rheumatoid arthritis. [Internet] [Thesis]. University of Western Ontario; 2014. [cited 2021 Feb 27].
Available from: https://ir.lib.uwo.ca/etd/2189.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Abbas A. Transcriptional regulation of peptidylarginine deiminase type IV: implications for rheumatoid arthritis. [Thesis]. University of Western Ontario; 2014. Available from: https://ir.lib.uwo.ca/etd/2189
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Grand Valley State University
21.
Regenold, Miranda M.
The Determination of Phosphorylation of Nato3 by PKA.
Degree: 2020, Grand Valley State University
URL: https://scholarworks.gvsu.edu/theses/974
► One of the leading regulators of neuronal cell differentiation in the CNS is the family of basic helix–loop–helix (bHLH) transcription factors. One of these proteins,…
(more)
▼ One of the leading regulators of neuronal cell differentiation in the CNS is the family of basic helix–loop–helix (bHLH) transcription factors. One of these proteins, Nato3, is associated with the formation of dopaminergic neurons. Transcription factors can be regulated by kinase activity, and in order to detect the associated change of phosphorylation of Nato3, we have generated Nato3 with specific epitope tags that allow for the detection and isolation of the Nato3 protein. Through subcloning techniques and a successful transformation of the Nato3 gene with the sequences of the 3X-Flag epitope and the Myc epitope into the pcDNA3.0 vector, we were able to begin testing the phosphorylation status of Nato3. In particular, these epitopes attached to Nato3 allowed us to better detect the phosphorylation status and migration patterns in SDS-PAGE gels. We were able to see significant mobility shifts on the gels consistent with a phosphorylation event. This type of phosphorylation of the Nato3 protein will allow us to continue forward to determine the specific residue within Nato3 that is phosphorylated. Understanding the post-translational modification of Nato3 may help lead to better understanding of dopamine neurogenesis.
Subjects/Keywords: Nato3; epitope-tagged; phosphorylation; SDS-PAGE; PKA; dopamine; Genetic Processes; Medical Biochemistry
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APA (6th Edition):
Regenold, M. M. (2020). The Determination of Phosphorylation of Nato3 by PKA. (Thesis). Grand Valley State University. Retrieved from https://scholarworks.gvsu.edu/theses/974
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Regenold, Miranda M. “The Determination of Phosphorylation of Nato3 by PKA.” 2020. Thesis, Grand Valley State University. Accessed February 27, 2021.
https://scholarworks.gvsu.edu/theses/974.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Regenold, Miranda M. “The Determination of Phosphorylation of Nato3 by PKA.” 2020. Web. 27 Feb 2021.
Vancouver:
Regenold MM. The Determination of Phosphorylation of Nato3 by PKA. [Internet] [Thesis]. Grand Valley State University; 2020. [cited 2021 Feb 27].
Available from: https://scholarworks.gvsu.edu/theses/974.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Regenold MM. The Determination of Phosphorylation of Nato3 by PKA. [Thesis]. Grand Valley State University; 2020. Available from: https://scholarworks.gvsu.edu/theses/974
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of South Carolina
22.
Hickey, Rachel Elizabeth.
Assessment of Patient Satisfaction with the Provision of Fertility Information in Women with Lynch Syndrome.
Degree: MS, Genetic Counseling, 2017, University of South Carolina
URL: https://scholarcommons.sc.edu/etd/4111
► Lynch Syndrome (LS), one of the most common hereditary cancer syndromes, is primarily known for its substantially increased risks for colorectal cancer. The incidence…
(more)
▼ Lynch Syndrome (LS), one of the most common hereditary cancer syndromes, is primarily known for its substantially increased risks for colorectal cancer. The incidence of gynecologic cancers (endometrial and ovarian cancers) equals or exceeds the incidence of colorectal cancers in female patients with LS. The prevention and treatment methods for these cancers can drastically affect fertility and reproduction. Previous studies with cancer patients have revealed challenges in acquiring information related to these topics; thus far, no research has assessed whether there is an informational gap regarding fertility information for women in the LS population. The purpose of this study was to identify the amount of information received related to fertility and reproduction, assess patient satisfaction, and characterize current practices of this information delivery within our target patient population.
Data was collected from 154 women with LS. Likert scales were used to quantify the amount of information provided about major themes pertaining to fertility in LS: effects of cancer treatment, risk-reducing surgeries, fertility preservation and family planning. Overall, participants were more satisfied when they received more information about certain topics within these themes. There was a distinct lack of individualization in patient care, and lack of uniformity regarding the provision of this information among healthcare providers. Participant opinions indicate that
genetic counselors may be an untapped resource in the provision of fertility and reproduction information to this population.
Advisors/Committee Members: Emily Jordon.
Subjects/Keywords: Genetic Processes; Medical Sciences; Medicine and Health Sciences; Patient; Fertility; Information; Lynch; Syndrome; Women
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APA (6th Edition):
Hickey, R. E. (2017). Assessment of Patient Satisfaction with the Provision of Fertility Information in Women with Lynch Syndrome. (Masters Thesis). University of South Carolina. Retrieved from https://scholarcommons.sc.edu/etd/4111
Chicago Manual of Style (16th Edition):
Hickey, Rachel Elizabeth. “Assessment of Patient Satisfaction with the Provision of Fertility Information in Women with Lynch Syndrome.” 2017. Masters Thesis, University of South Carolina. Accessed February 27, 2021.
https://scholarcommons.sc.edu/etd/4111.
MLA Handbook (7th Edition):
Hickey, Rachel Elizabeth. “Assessment of Patient Satisfaction with the Provision of Fertility Information in Women with Lynch Syndrome.” 2017. Web. 27 Feb 2021.
Vancouver:
Hickey RE. Assessment of Patient Satisfaction with the Provision of Fertility Information in Women with Lynch Syndrome. [Internet] [Masters thesis]. University of South Carolina; 2017. [cited 2021 Feb 27].
Available from: https://scholarcommons.sc.edu/etd/4111.
Council of Science Editors:
Hickey RE. Assessment of Patient Satisfaction with the Provision of Fertility Information in Women with Lynch Syndrome. [Masters Thesis]. University of South Carolina; 2017. Available from: https://scholarcommons.sc.edu/etd/4111
23.
Peacock, Danielle L.
Identification of Novel HIF1A Target Genes That Regulate Tumor Progression and Metastasis.
Degree: PhD, Biomedical Sciences, 2013, University of Tennessee Health Science Center
URL: https://dc.uthsc.edu/dissertations/358
► Hypoxia is a hallmark of most solid tumors. In response to hypoxic stress tumor cells adapt by regulating survival, metabolism and angiogenesis. The heterodimeric…
(more)
▼ Hypoxia is a hallmark of most solid tumors. In response to hypoxic stress tumor cells adapt by regulating survival, metabolism and angiogenesis. The heterodimeric HypoxiaInducible Factor (HIF) transcription factors are the master regulators of this response. HIFs play key roles in many critical aspects of cancer biology including angiogenesis, stem cell maintenance, metabolic reprogramming, invasion, metastasis and resistance to radiation therapy and chemotherapy. Overexpression of HIF-1α and HIF-2α has been documented in multiple human cancers and HIF-1 protein is over-expressed in ~30% of primary breast tumors and ~70% of metastases, which independently correlates with poor prognosis and decreased survival in patients. A precise role for HIF-2 in breast cancer is still being elucidated.
Our lab has established primary mammary tumor epithelial cells (MTECs) from late stage carcinomas originating in PyMT+; Hif1a floxed mice. These MTECs were exposed to either Adenovirus-beta-gal or -Cre to create wild-type (WT) and knockout (KO) cells, respectively. Deletion of HIF-1 activity reduced primary tumor growth by ~60% and the formation of lung macrometastases originating from mammary fat pad tumors by >90%. In addition, deletion of Hif1a reduced mammary tumorsphere formation efficiency (TSE) in vitro and tumor initiating cell (TIC) frequency in vivo. In contrast, in triple negative models of breast cancer, knockdown of HIF1A had the opposite phenotype, increasing TSE in vitro and increased primary mammary tumor growth in vivo. ITGA6 (CD49f) was identified as one HIF-1α-dependent cancer stem cell marker that enriches for both primary mammary tumor growth and metastasis to the lung. Microarray profiling conducted to identify genes differentially expressed between PyMT WT and KO cells and end-stage WT and KO tumors revealed several genes that were down-regulated in both data sets in response to deletion of Hif1a. One mRNA of particular interest, creatine kinase brain isoform (Ckb) was down-regulated in KO cells >100 fold and >2 fold in end-stage tumors. Transplantation of Ckb knockdown (KD) PyMT cells to the mammary fat pad delayed initiation of palpable tumors by >30 days. When cells were introduced into the circulation via tail vein injection, 20% of mice injected with Ckb KD cells developed lung metastases whereas 100% of mice injected with WT cells developed metastases. Likewise, when mice injected with WT PyMT cells were treated daily with a CKB chemical inhibitor, cyclocreatine (cCr), lungs of vehicle treated (saline) mice were almost completely covered with surface metastases, while lungs of cCr treated mice contained very few metastases.
Overall, our data show that HIF-1α strongly promotes mammary tumor initiation, progression and metastasis, in part through regulation of TIC activity. Metastasis is the major cause of mortality in breast cancer patients. Further characterization of the distinct roles of HIF- 1α versus HIF-2α in breast cancer and metastasis, and genes downstream of the HIFs, such as…
Advisors/Committee Members: Tiffany N. Seagroves, Ph.D..
Subjects/Keywords: Breast Cancer; Metastasis; HIF1A; Hypoxia; Diseases; Genetic Processes; Medical Sciences; Medicine and Health Sciences; Neoplasms
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Peacock, D. L. (2013). Identification of Novel HIF1A Target Genes That Regulate Tumor Progression and Metastasis. (Doctoral Dissertation). University of Tennessee Health Science Center. Retrieved from https://dc.uthsc.edu/dissertations/358
Chicago Manual of Style (16th Edition):
Peacock, Danielle L. “Identification of Novel HIF1A Target Genes That Regulate Tumor Progression and Metastasis.” 2013. Doctoral Dissertation, University of Tennessee Health Science Center. Accessed February 27, 2021.
https://dc.uthsc.edu/dissertations/358.
MLA Handbook (7th Edition):
Peacock, Danielle L. “Identification of Novel HIF1A Target Genes That Regulate Tumor Progression and Metastasis.” 2013. Web. 27 Feb 2021.
Vancouver:
Peacock DL. Identification of Novel HIF1A Target Genes That Regulate Tumor Progression and Metastasis. [Internet] [Doctoral dissertation]. University of Tennessee Health Science Center; 2013. [cited 2021 Feb 27].
Available from: https://dc.uthsc.edu/dissertations/358.
Council of Science Editors:
Peacock DL. Identification of Novel HIF1A Target Genes That Regulate Tumor Progression and Metastasis. [Doctoral Dissertation]. University of Tennessee Health Science Center; 2013. Available from: https://dc.uthsc.edu/dissertations/358
24.
Gadson, Sean.
The Hormonal Regulation of the Claudin Genes in the Ovary.
Degree: MS, Biology, 2016, Central Washington University
URL: https://digitalcommons.cwu.edu/etd/540
► The ovary is a dynamic organ that responds to many hormonal signals. When these hormonal signals are disrupted, ovarian dysfunction can occur. One such example…
(more)
▼ The ovary is a dynamic organ that responds to many hormonal signals. When these hormonal signals are disrupted, ovarian dysfunction can occur. One such example is Polycystic Ovarian Syndrome (PCOS). PCOS patients suffer from high levels of testosterone. Excess testosterone may misregulate genes in the ovary and disrupt ovarian function. The Claudin (
Cldn) 3 and
Cldn11 genes have been shown to be regulated by androgens in the testis, while studies in ovarian cancer cells suggests a coregulatory mechanism for the expressions of
Cldn3 and
Cldn4 in the ovary. The objective of this study was to characterize the hormonal regulation of
Claudin gene expression in the ovary. The ovaries of estrogen receptor alpha knockout (αERKO) mice have high serum testosterone concentrations, therefore
Claudin expression was measured in these ovaries. Experiments were conducted using Quantitative Real Time PCR (QRT-PCR) to monitor the expression of
Cldn3,
4, and
11 in wild-type (WT) and αERKO mouse ovaries. These experiments indicated that
Cldn3,
4, and
11 were more highly expressed in αERKO mice than their wild-type counterparts (p < 0.05, n = 5). Further experiments characterized Claudin
expression in the ovaries of mice treated with Dihydrotestosterone (DHT) for 90 days which serve as a common mouse model of PCOS. DHT treated mice were found to express
Cldn3 and
Cldn11 significantly higher than control mice.
Cldn4 expression decreased in DHT treated mice when compared to the controls (p < 0.05, n = 4 for control and DHT groups). These findings indicated that
Cldn3 and
Cldn11 are upregulated by testosterone in the ovary. The data also indicates
Cldn4 is regulated via different mechanisms than the other Claudin genes in the mouse ovary. DHT reduces expression of
Cldn4, while increases are observed in the absence of ERα. Claudin expression was also evaluated in the ovaries of mice that were treated with testosterone propionate (TP) for three or six days. No expression of
Cldn3 or
Cldn11 was found, however
Cldn4 steadily increased in conjunction with the duration of the testosterone propionate treatment. Western blot analysis for the presence of CLDN3 in the ovaries of control and TP treated mice yielded no detectable signal for either group.
Studies done in cell lines found that
CLDN4 expression decreased when BG-1 ovarian epithelial cells were treated with testosterone. These findings provide a first consider the regulation of the Claudin genes in the ovary, while providing a basis for future research to explore how they may contribute to PCOS.
Advisors/Committee Members: April K. Binder, Lucinda Carnell, Holly Pinkart.
Subjects/Keywords: PCOS; Polycystic Ovarian Syndrome; Claudin; Expression; Endocrine System Diseases; Female Urogenital Diseases and Pregnancy Complications; Genetic Processes; Medical Pathology; Physiological Processes; Reproductive and Urinary Physiology
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APA (6th Edition):
Gadson, S. (2016). The Hormonal Regulation of the Claudin Genes in the Ovary. (Masters Thesis). Central Washington University. Retrieved from https://digitalcommons.cwu.edu/etd/540
Chicago Manual of Style (16th Edition):
Gadson, Sean. “The Hormonal Regulation of the Claudin Genes in the Ovary.” 2016. Masters Thesis, Central Washington University. Accessed February 27, 2021.
https://digitalcommons.cwu.edu/etd/540.
MLA Handbook (7th Edition):
Gadson, Sean. “The Hormonal Regulation of the Claudin Genes in the Ovary.” 2016. Web. 27 Feb 2021.
Vancouver:
Gadson S. The Hormonal Regulation of the Claudin Genes in the Ovary. [Internet] [Masters thesis]. Central Washington University; 2016. [cited 2021 Feb 27].
Available from: https://digitalcommons.cwu.edu/etd/540.
Council of Science Editors:
Gadson S. The Hormonal Regulation of the Claudin Genes in the Ovary. [Masters Thesis]. Central Washington University; 2016. Available from: https://digitalcommons.cwu.edu/etd/540
University of Kentucky
25.
Englund, Davis A.
DETERMINING THE ROLE OF SATELLITE CELLS DURING SKELETAL MUSCLE ADAPTATION.
Degree: 2020, University of Kentucky
URL: https://uknowledge.uky.edu/rehabsci_etds/69
► Physical inactivity, advancing age, limb immobilization, degenerative diseases and various systemic diseases (many cancers, sepsis, HIV, COPD, kidney disease) all lead to skeletal muscle wasting.…
(more)
▼ Physical inactivity, advancing age, limb immobilization, degenerative diseases and various systemic diseases (many cancers, sepsis, HIV, COPD, kidney disease) all lead to skeletal muscle wasting. The loss of muscle mass is of major clinical importance because it leads to an increased risk for morbidity, disability, and the loss of independence; collectively contributing to a substantive increase in healthcare utilization and cost. The prevalence of cachexia (disease-induced muscle wasting) can reach as high as 80% in certain patient populations and the average cost per hospital stay is 4,641 more than in non-cachectic patients. Direct healthcare costs attributable to sarcopenia were estimated to be 18.5 billion in 2002. Therefore, developing effective skeletal muscle restoration therapies is critical to improve quality of life and prolong functional independence in the broad patient population afflicted by the loss of muscle mass.
There are few promising strategies emerging to treat loss of muscle mass. Currently, exercise (e.g., resistance training) is the most effective lifestyle intervention used to promote muscle growth, and testosterone is a well-known pharmacological intervention used to increase muscle mass. A greater understanding of the underlying cellular mechanisms that promote muscle growth and adaptation in response to exercise and pharmacological agents will enable the design of more targeted and effective interventions. Moreover, identifying the mechanisms that regulate muscle growth provides an opportunity to discover novel therapeutic targets for those who cannot or are unwilling to participate in exercise. In particular, a fundamental understanding of the role of muscle stem cells (satellite cells) during regeneration and recovery from volumetric muscle loss made targeting and improving satellite cell function and restorative capacity during these conditions possible. Gaining an in depth understanding for the function of satellite cells during muscle growth may likewise allow them to be targeted and increase their ability to promote muscle growth.
Our lab previously showed that while a lack of satellite cells does not limit short-term muscle growth, satellite cells are required to support sustained growth, at least in the plantaris (100% type 2 fibers). As myonuclear accretion and satellite cell abundance are tightly associated with growth in satellite cell replete muscle, the compensatory pathways activated in the absence of satellite cell fusion to enable short-term muscle growth are of interest. In line with this, the mechanism precipitating a shift in the requirement for satellite cells during sustained muscle growth remains to be elucidated. Due to the method of mechanical overload (synergist ablation) used to induce muscle growth in previous studies, our understanding for satellite cell-mediated muscle growth in adult mice is currently restricted to the plantaris. Emerging evidence suggests that these findings may not extend to muscles with a more oxidative phenotype, like the soleus (50%…
Subjects/Keywords: Satellite Cells; Stem Cells; Skeletal Muscle; Hypertrophy; Exercise; Testosterone; Biochemical Phenomena, Metabolism, and Nutrition; Biological Phenomena, Cell Phenomena, and Immunity; Genetic Processes; Medical Biochemistry; Physiological Processes
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APA (6th Edition):
Englund, D. A. (2020). DETERMINING THE ROLE OF SATELLITE CELLS DURING SKELETAL MUSCLE ADAPTATION. (Doctoral Dissertation). University of Kentucky. Retrieved from https://uknowledge.uky.edu/rehabsci_etds/69
Chicago Manual of Style (16th Edition):
Englund, Davis A. “DETERMINING THE ROLE OF SATELLITE CELLS DURING SKELETAL MUSCLE ADAPTATION.” 2020. Doctoral Dissertation, University of Kentucky. Accessed February 27, 2021.
https://uknowledge.uky.edu/rehabsci_etds/69.
MLA Handbook (7th Edition):
Englund, Davis A. “DETERMINING THE ROLE OF SATELLITE CELLS DURING SKELETAL MUSCLE ADAPTATION.” 2020. Web. 27 Feb 2021.
Vancouver:
Englund DA. DETERMINING THE ROLE OF SATELLITE CELLS DURING SKELETAL MUSCLE ADAPTATION. [Internet] [Doctoral dissertation]. University of Kentucky; 2020. [cited 2021 Feb 27].
Available from: https://uknowledge.uky.edu/rehabsci_etds/69.
Council of Science Editors:
Englund DA. DETERMINING THE ROLE OF SATELLITE CELLS DURING SKELETAL MUSCLE ADAPTATION. [Doctoral Dissertation]. University of Kentucky; 2020. Available from: https://uknowledge.uky.edu/rehabsci_etds/69
Universidade do Rio Grande do Sul
26.
Ferretti, Cláudio.
Processo cognitivo e objetos interativos de aprendizagem : a construção do equilíbrio físico.
Degree: 2007, Universidade do Rio Grande do Sul
URL: http://hdl.handle.net/10183/13750
► Os objetos de aprendizagem digitais, quando empregados para reconhecer e analisar processos cognitivos, podem contribuir para o desenvolvimento de uma didática voltada ao aprendizado. Esta…
(more)
▼ Os objetos de aprendizagem digitais, quando empregados para reconhecer e analisar processos cognitivos, podem contribuir para o desenvolvimento de uma didática voltada ao aprendizado. Esta pesquisa investiga em que medida os objetos digitais de aprendizagem contribuem para identificar os processos cognitivos em desenvolvimento durante a formação do conceito do equilíbrio físico na balança. Tais conhecimentos permitem desenhar objetos digitais de aprendizagem interativos, viabilizando aos professores organizarem estratégias que possibilitem a formação de operações lógicas em seus alunos, indispensáveis ao raciocínio formal. Na Epistemologia Genética de Piaget, encontramos tanto a explicação teórica (Equilibração das Estruturas Cognitivas) como os métodos que permitem conhecer tais processos em desenvolvimento (Método Clínico Piagetiano).
The physical concepts are considered on difficult understanding for some students of the Basic School, directed only to people endowed with special talents. Such difficulty can come from the teaching method employed in Physics Education. The knowledge of the cognitive processes that grow during the formation of those concepts can contribute for the development of a teaching method aimed at learning. However, education professionals with knowledge on epistemology and specific concepts in this subject, need a thorough, interdisciplinary and permanent formation. Analyzing the cognitive processes and developing tools for their identification, we will be making available to the educators, resources capable to aid them in his/her task of discovering their students' difficulties. This research investigates in which way the digital objects of learning contribute to identify the cognitive processes in development, during the formation of the concept of the physical balance, using a scale. Such knowledge permits to design interactive digital learning objects, allowing the teachers to organize methods that make possible the formation of logical operations in their students, necessary to a formal reasoning. In the Genetic Epistemology of Piaget, we found the theoretical explanation (Cognitive Structures Equilibration) as well as the methods allowing to know the development of these processes (Piaget’s Clinical Method).
Advisors/Committee Members: Zaro, Milton Antonio.
Subjects/Keywords: Conceptualization processes; Epistemologia genética; Genetic epistemology; Objeto de aprendizagem; Logical systems; Informática na educação; Technology and education; Learning objects
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APA (6th Edition):
Ferretti, C. (2007). Processo cognitivo e objetos interativos de aprendizagem : a construção do equilíbrio físico. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/13750
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Ferretti, Cláudio. “Processo cognitivo e objetos interativos de aprendizagem : a construção do equilíbrio físico.” 2007. Thesis, Universidade do Rio Grande do Sul. Accessed February 27, 2021.
http://hdl.handle.net/10183/13750.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ferretti, Cláudio. “Processo cognitivo e objetos interativos de aprendizagem : a construção do equilíbrio físico.” 2007. Web. 27 Feb 2021.
Vancouver:
Ferretti C. Processo cognitivo e objetos interativos de aprendizagem : a construção do equilíbrio físico. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2007. [cited 2021 Feb 27].
Available from: http://hdl.handle.net/10183/13750.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ferretti C. Processo cognitivo e objetos interativos de aprendizagem : a construção do equilíbrio físico. [Thesis]. Universidade do Rio Grande do Sul; 2007. Available from: http://hdl.handle.net/10183/13750
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
27.
Guhasarkar, Dwijit.
A Walk on the Fine Line Between Reward and Risk: AAV-IFNβ Gene Therapy for Glioblastoma: A Dissertation.
Degree: Interdisciplinary Graduate Program, Neurology, 2016, U of Massachusetts : Med
URL: http://escholarship.umassmed.edu/gsbs_diss/843
► Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor. The current standard-of-care treatment including surgery, radiation and temozolomide (TMZ) chemotherapy does…
(more)
▼ Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor. The current standard-of-care treatment including surgery, radiation and temozolomide (TMZ) chemotherapy does not prolong the survival satisfactorily. Here we have tested the feasibility, efficacy and safety of a potential gene therapy approach using AAV as gene delivery vehicle for treatment of GBM.
Interferon-beta (IFNβ) is a cytokine molecule also having pleiotropic anticancerous properties. Previously it has been shown by our group that AAV mediated local (intracranial) gene delivery of human IFNβ (hIFNβ) could be an effective treatment for non-invasive human glioblastoma (U87) in orthotopic xenograft mouse model.But as one of the major challenges to treat GBM effectively in clinics is its highly invasive property, in the current study we first sought to test the efficacy of our therapeutic model in a highly invasive human GBM (GBM8) xenograft mouse model.
One major limitation of using the xenograft mouse model is that these mice are immune-compromised. Moreover, as IFNβ does not interact with cross-species receptors, the influence of immune systems on GBM remains largely untested. Therefore to test the therapeutic approach in an immune-competent mouse model, we next treated a syngeneic mouse GBM model (GL261) in an immune-competent mouse (C57B6) with the gene encoding the species-matched IFNβ (mIFNβ). We also tested if combination of this IFNβ gene therapy with the current standard chemotherapeutic drug (TMZ) is more effective than any one of the therapeutic modes alone. Finally, we tested the long term safety of the AAV-mIFNβ local gene therapy in healthy C57B6 mice.
Next, we hypothesized that global
genetic engineering of brain cells expressing secretory therapeutic protein like hIFNβ could be more beneficial for treatment of invasive, migratory and distal multifocal GBM. We tested this hypothesis using systemic delivery of AAV9 vectors encoding hIFNβ gene for treatment of GBM8 tumor in nude mice.
Using in vivo bioluminescence imaging of tumor associated firefly luciferase activity, long term survival assay and histological analysis of the brains we have shown that local treatment of AAV-hIFNβ for highly invasive human GBM8 is therapeutically beneficial at an early growth phase of tumor. However, systemic delivery route treatment is far superior for treating multifocal distal GBM8 tumors. Nonetheless, for both delivery routes, treatment efficacy is significantly reduced when treated at a later growth phase of the tumor.
In syngeneic GL261 tumor model study, we show that local AAV-mIFNβ gene therapy alone or in combination with TMZ treatment can provide significant survival benefit over control or only TMZ treatment, respectively. However, the animals eventually succumb to the tumor. Safety study in the healthy animals shows significant body weight loss in some treatment groups, whereas one group shows long term survival without any weight loss or any noticeable changes in the external…
Advisors/Committee Members: Miguel Sena-Esteves, Ph.D..
Subjects/Keywords: Glioblastoma multiforme (GBM); gene therapy; AAV; adeno-associated
virus; gene delivery; Interferon-beta; Genetic Processes; Genetics and Genomics; Neoplasms; Therapeutics
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APA ·
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Export
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APA (6th Edition):
Guhasarkar, D. (2016). A Walk on the Fine Line Between Reward and Risk: AAV-IFNβ Gene Therapy for Glioblastoma: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/843
Chicago Manual of Style (16th Edition):
Guhasarkar, Dwijit. “A Walk on the Fine Line Between Reward and Risk: AAV-IFNβ Gene Therapy for Glioblastoma: A Dissertation.” 2016. Doctoral Dissertation, U of Massachusetts : Med. Accessed February 27, 2021.
http://escholarship.umassmed.edu/gsbs_diss/843.
MLA Handbook (7th Edition):
Guhasarkar, Dwijit. “A Walk on the Fine Line Between Reward and Risk: AAV-IFNβ Gene Therapy for Glioblastoma: A Dissertation.” 2016. Web. 27 Feb 2021.
Vancouver:
Guhasarkar D. A Walk on the Fine Line Between Reward and Risk: AAV-IFNβ Gene Therapy for Glioblastoma: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2016. [cited 2021 Feb 27].
Available from: http://escholarship.umassmed.edu/gsbs_diss/843.
Council of Science Editors:
Guhasarkar D. A Walk on the Fine Line Between Reward and Risk: AAV-IFNβ Gene Therapy for Glioblastoma: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2016. Available from: http://escholarship.umassmed.edu/gsbs_diss/843
Anna University
28.
Janakiraman V.
Concurrent optimization of operating parameters and
tolerances for CNC machining processes;.
Degree: 2013, Anna University
URL: http://shodhganga.inflibnet.ac.in/handle/10603/11430
► This research work is concerned with the concurrent optimization of CNC machining process parameters and tolerances for manufacturing of various engineering products in order to…
(more)
▼ This research work is concerned with the concurrent
optimization of CNC machining process parameters and tolerances for
manufacturing of various engineering products in order to enhance
the manufacturability, reliability, quality and field performance.
The stringent specification of tolerances on the dimensions of
manufactured parts has a significant impact on final production
cost. Considering these significances, the research work was
carried out. The objective is to minimize the manufacturing cost or
time for CNC machining processes without satisfying quality and to
develop the concurrent optimization procedure for the manufacture
of a particular component. Machining process Optimization procedure
has been developed based on three popular algorithms: Nelder-Mead
Simplex (NMS) method, Simulated Annealing Algorithm (SAA) and
Genetic Algorithm (GA). A Mathematical model was also developed to
find the tolerance level through response surface (Central
Composite Rotatable Design) methodology using MiniTAB Statistical
tool. Applying this model, the range of the dimension deviations
for external finish grinding of the piston material spheriodal cast
iron (SG 600/3) was determined. Predicated tolerance was used to
calculate the Quality Loss Cost. The results clearly show that a
30% reduction in total manufacturing cost was achieved in milling
process and a minimum of 10.2% reduction in machining time was
achieved in turning process. The resulting operating parameters
have been accepted for implementation by the industries in which
the case study was conducted. For concurrent optimization process,
the cutting speed, feed rate and depth-of-cut were the parameters
analyzed for eight different machining processes. The actual
convergence to the optimum value was at the 403rd iteration. The
results obtained in this research work clearly indicate that
reduction in manufacturing cost / time is achievable using GA for
solving the single stage, multi-stage CNC machining and concurrent
optimization problems. newline newline newline
Appendices 1 to 8; pp.126-197
Advisors/Committee Members: Saravanan, R..
Subjects/Keywords: Operating parameters; tolerances; CNC machining
processes; Nelder-Mead Simplex(NMS); Simulated Annealing
Algorithm(SAA); Genetic Algorithm(GA); MiniTAB
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Manager
APA (6th Edition):
V, J. (2013). Concurrent optimization of operating parameters and
tolerances for CNC machining processes;. (Thesis). Anna University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/11430
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
V, Janakiraman. “Concurrent optimization of operating parameters and
tolerances for CNC machining processes;.” 2013. Thesis, Anna University. Accessed February 27, 2021.
http://shodhganga.inflibnet.ac.in/handle/10603/11430.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
V, Janakiraman. “Concurrent optimization of operating parameters and
tolerances for CNC machining processes;.” 2013. Web. 27 Feb 2021.
Vancouver:
V J. Concurrent optimization of operating parameters and
tolerances for CNC machining processes;. [Internet] [Thesis]. Anna University; 2013. [cited 2021 Feb 27].
Available from: http://shodhganga.inflibnet.ac.in/handle/10603/11430.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
V J. Concurrent optimization of operating parameters and
tolerances for CNC machining processes;. [Thesis]. Anna University; 2013. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/11430
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Virginia Commonwealth University
29.
Lind, Mackenzie J.
Sleep disturbances and depression: the role of genes and trauma.
Degree: PhD, Clinical and Translational Sciences, 2017, Virginia Commonwealth University
URL: https://doi.org/10.25772/PBQR-9887
;
https://scholarscompass.vcu.edu/etd/4858
► Sleep disturbances and insomnia are prevalent, with around 33% of adults indicating that they experience at least one main symptom of insomnia, and bidirectional…
(more)
▼ Sleep disturbances and insomnia are prevalent, with around 33% of adults indicating that they experience at least one main symptom of insomnia, and bidirectional relationships exist with common psychopathology, particularly major depressive disorder (MDD). However,
genetic and environmental (e.g., traumatic event exposure) contributions to the etiology of these phenotypes are not yet well understood. A genetically informative sample of approximately 12,000 Han Chinese women aged 30-60 (50% with recurrent MDD) was used to address several gaps within the sleep literature. Sleep disturbances were assessed in all individuals using a general item addressing sleeplessness (GS). A sleep within depression sum score (SDS) was also created in MDD cases, combining information from the GS and two insomnia items within MDD. A total of 11 traumatic events were assessed and additional information on childhood sexual abuse (CSA) was also obtained. First, factor analyses were conducted to determine trauma factor structure. The best-fit solution included 3 factors: interpersonal, child interpersonal, and non-assaultive, and composite variables were constructed accordingly. A series of hierarchical regressions were run to examine differential effects of trauma type and timing on sleeplessness. All traumatic events predicted sleeplessness at similar magnitudes, although population models indicated that childhood interpersonal trauma may be particularly potent. An association between CSA and sleeplessness was also replicated. A series of
genetic analyses demonstrated that the single nucleotide polymorphism-based heritability of sleep phenotypes did not differ significantly from zero. Further, association analyses did not identify any genome-wide significant loci. However, using a liberal false discovery rate threshold of 0.5, two genes of interest,
KCNK9 and
ALDH1A2, emerged for the SDS. Polygenic risk score (PRS) analyses demonstrated
genetic overlap between the SDS in MDD cases and GS in MDD controls, with PRSs explaining 0.2-0.3% of the variance. A final combined model of both
genetic and environmental risk indicated that both PRS and traumatic events were significant predictors of sleeplessness. While
genetic results should be interpreted with caution given the lack of heritability, additional research into the
genetic and environmental contributions to insomnia, utilizing more standardized phenotypes and properly ascertained samples, is clearly warranted.
Advisors/Committee Members: Ananda B Amstadter, Kenneth S Kendler.
Subjects/Keywords: sleep disturbances; insomnia; depression; traumatic events; genome-wide association study; polygenic risk scores; Genetic Processes; Mental Disorders
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APA ·
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APA (6th Edition):
Lind, M. J. (2017). Sleep disturbances and depression: the role of genes and trauma. (Doctoral Dissertation). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/PBQR-9887 ; https://scholarscompass.vcu.edu/etd/4858
Chicago Manual of Style (16th Edition):
Lind, Mackenzie J. “Sleep disturbances and depression: the role of genes and trauma.” 2017. Doctoral Dissertation, Virginia Commonwealth University. Accessed February 27, 2021.
https://doi.org/10.25772/PBQR-9887 ; https://scholarscompass.vcu.edu/etd/4858.
MLA Handbook (7th Edition):
Lind, Mackenzie J. “Sleep disturbances and depression: the role of genes and trauma.” 2017. Web. 27 Feb 2021.
Vancouver:
Lind MJ. Sleep disturbances and depression: the role of genes and trauma. [Internet] [Doctoral dissertation]. Virginia Commonwealth University; 2017. [cited 2021 Feb 27].
Available from: https://doi.org/10.25772/PBQR-9887 ; https://scholarscompass.vcu.edu/etd/4858.
Council of Science Editors:
Lind MJ. Sleep disturbances and depression: the role of genes and trauma. [Doctoral Dissertation]. Virginia Commonwealth University; 2017. Available from: https://doi.org/10.25772/PBQR-9887 ; https://scholarscompass.vcu.edu/etd/4858
30.
Makowski, Mateusz.
High-Throughput Data Analysis: Application to Micronuclei Frequency and T-cell Receptor Sequencing.
Degree: PhD, Biostatistics, 2015, Virginia Commonwealth University
URL: https://doi.org/10.25772/4CY7-PH72
;
https://scholarscompass.vcu.edu/etd/3923
► The advent of high-throughput sequencing has brought about the creation of an unprecedented amount of research data. Analytical methodology has not been able to…
(more)
▼ The advent of high-throughput sequencing has brought about the creation of an unprecedented amount of research data. Analytical methodology has not been able to keep pace with the plethora of data being produced. Two assays, ImmunoSEQ and the cytokinesisblock micronucleus (CBMN), that both produce count data and have few methods available to analyze them are considered.
ImmunoSEQ is a sequencing assay that measures the beta T-cell receptor (TCR) repertoire. The ImmunoSEQ assay was used to describe the TCR repertoires of patients that have undergone hematopoietic stem cell transplantation (HSCT). Several different methods for spectratype analysis were extended to the TCR sequencing setting then applied to these data to demonstrate different ways the data set can be analyzed. The different methods include CDR3 distribution perturbation, Oligoscores, Simpson's diversity, Shannon diversity, Kullback-Liebler divergence, a non-parametric method and a proportion logit transformation method. Herein we also demonstrate adapting compositional data analysis methods to the TCR sequencing setting. The various methods were compared when analyzing a set of 13 subjects who underwent hematopoietic stem cell transplantation. The eight subjects who developed graft versus host disease were compared to the five who did not. There was no little overlap in the results of the different methods showing that researchers must choose the appropriate method for their research question of interest.
The CBMN assay measures the rate of micronuclei (MN) formation in a sample of cells and can be paired with gene expression or methylation assays to determine association between MN formation and other
genetic markers. Herein we extended the generalized monotone incremental forward stagewise (GMIFS) method to the situation where the response is count data and there are more independent variables than there are samples. Our Poisson GMIFS method was compared to a popular alternative, glmpath, by using simulations and applying both to real data. Simulations showed that both methods perform similarly in accurately choosing truly significant variables. However, glmpath appears to overfit compared to our GMIFS method. Finally, when both methods were applied to two data sets GMIFS appeared to be more stable than glmpath.
Advisors/Committee Members: Kellie J. Archer.
Subjects/Keywords: GMIFS; Micronuclei; high-throughput sequencing; TCR; hematopoietic stem cell transplantation; gene expression; Biostatistics; Genetic Processes; Other Immunology and Infectious Disease
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APA ·
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MLA ·
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Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Makowski, M. (2015). High-Throughput Data Analysis: Application to Micronuclei Frequency and T-cell Receptor Sequencing. (Doctoral Dissertation). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/4CY7-PH72 ; https://scholarscompass.vcu.edu/etd/3923
Chicago Manual of Style (16th Edition):
Makowski, Mateusz. “High-Throughput Data Analysis: Application to Micronuclei Frequency and T-cell Receptor Sequencing.” 2015. Doctoral Dissertation, Virginia Commonwealth University. Accessed February 27, 2021.
https://doi.org/10.25772/4CY7-PH72 ; https://scholarscompass.vcu.edu/etd/3923.
MLA Handbook (7th Edition):
Makowski, Mateusz. “High-Throughput Data Analysis: Application to Micronuclei Frequency and T-cell Receptor Sequencing.” 2015. Web. 27 Feb 2021.
Vancouver:
Makowski M. High-Throughput Data Analysis: Application to Micronuclei Frequency and T-cell Receptor Sequencing. [Internet] [Doctoral dissertation]. Virginia Commonwealth University; 2015. [cited 2021 Feb 27].
Available from: https://doi.org/10.25772/4CY7-PH72 ; https://scholarscompass.vcu.edu/etd/3923.
Council of Science Editors:
Makowski M. High-Throughput Data Analysis: Application to Micronuclei Frequency and T-cell Receptor Sequencing. [Doctoral Dissertation]. Virginia Commonwealth University; 2015. Available from: https://doi.org/10.25772/4CY7-PH72 ; https://scholarscompass.vcu.edu/etd/3923
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Open Access Theses and Dissertations
