Matching Items (75)
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- All Subjects: Cancer
- All Subjects: Neuroscience
- Creators: School of Life Sciences
- Member of: Barrett, The Honors College Thesis/Creative Project Collection
Description
Parkinson’s disease (PD) is a debilitating neurodegenerative disease characterized primarily by physical impairments such as tremors, poor balance, and bradykinesia; however, some individuals with PD will additionally experience numerous nonmotor symptoms such as dementia, depression, and sleep disturbances amongst various other life-altering ailments. Two of the key pathological hallmarks of PD include the death of melanated dopaminergic neurons in the nigrostriatal pathway and the accumulation of Lewy bodies, which are primarily composed of aggregates of the protein α-synuclein (α-syn). Interestingly, members of the chitinase protein family, namely chitinase-3-like protein-1 (L1), have heightened concentrations in a number of neurodegenerative diseases other than PD. To investigate the specific role L1 plays in PD etiology, we evaluated if astrocytic L1 expression was elevated in postmortem brain tissue of PD patients as well as in an α-syn overexpression rat model, and further tested if manipulating astrocytic-specific L1 expression correlated with neuroinflammation and nigral neuronal degeneration in the model. Preliminary histological analysis has shown increased levels of L1 expression in the α-syn model before neuronal loss occurs, and in human tissue, L1 was found to be significantly increased in the postmortem tissue of individuals with PD versus non-diseased controls. Investigations in identifying an astrocytic-specific virus capsid and manipulating L1 expression in the α-syn model are ongoing. This preliminary data thus far supports that increased astrocytic expression of L1 is associated with PD pathology.
ContributorsPettigrew, Tiffany (Author) / Manfredsson, Fredric (Thesis director) / Sandoval, Ivette (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2023-12
Description
The Patient Guidance Project was created by a team of research assistants in the Arizona Cancer Evolution Center as a source of supplemental education and support for recently diagnosed cancer patients. Extensive background research in the form of literature reviews highlighted disparities between the information patients want and are receiving, as well as between average literacy levels of patients and the literacy levels at which cancer information is commonly provided. The Patient Guidance Project has published comprehensive guides for specific types of cancer, which so far include metastatic melanoma, glioblastoma, prostate cancer, oral cancer, kidney cancer, breast cancer, and colorectal cancer. The content of the guides is intended to bridge the gaps in information for patients with an emphasis on treatment options, treatment side effects, and psychological support resources, which surveys have identified as the topics patients want information on most. Written at a sixth-grade literacy level, which over half of adults in the U.S. read at, the guides are meant to be of benefit to as many people as possible. In the future, the team hopes to expand the Patient Guidance Project to include more cancer types, guides in different languages, and multimodal features to increase their effectiveness.
ContributorsWilliams, Erica (Author) / Maley, Carlo (Thesis director) / Baciu, Cristina (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2022-12
Description
Cancer is an ever-relevant disease with many genetic, social, environmental, and behavioral risk factors. One factor which has been garnering interest is the impact of nutrition on cancer. As a disease process, cancer is primarily driven by an accumulation of genetic aberrations. Recent epidemiological, pre-clinical, and clinical studies have demonstrated various impacts of bioactive food molecules on the promotion or prevention of these oncogenic mutations. This work explores several of these molecules and their relation to cancer prevention and provides a sample meal plan, which highlights many additional molecules that are currently being studied.
ContributorsCurtin, Elise (Author) / Don, Rachael (Thesis director) / Compton, Carolyn (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2022-05
Description
Obesity increases the risk for colorectal cancer. In mice, a pro-obesity high-fat-diet (HFD) leads to an intestinal phenotype characterized by enhanced proliferation, numbers, function and tumor-initiating capacity of stem cells, the cell-of-origin for many intestinal cancers. This phenotype is driven by a lipid metabolism program facilitated by an intrinsic Peroxisome Proliferator-Activated Receptor/Fatty Acid Oxidation (PPAR/FAO) axis that senses and utilizes cellular lipids. However, the microbiome is a known regulator of lipid metabolism in the gut, but little is understood about how the gut commensals affect access to the lipids and alter stem cell function. Here, we use the long term HFD-fed mouse model to analyze the phenotypic changes in the intestinal stem cells (ISCs) after depletion of the gut microbiota. We find that the loss of the gut microbiome after four weeks of antibiotic treatment imposes significant changes in ISC function leading to reduced HFD ISC regenerative potential. These results indicate that the gut microbiome plays a crucial role in the lipid metabolic process which regulates and maintains the HFD ISC phenotype, and further suggests that the gut microbiome may augment the diet-induced tumor initiating capacity by altering the stem cell function.
ContributorsSantos Molina, Pablo (Author) / Mana, Miyeko (Thesis director) / Whisner, Corrie (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor) / Historical, Philosophical & Religious Studies, Sch (Contributor)
Created2022-05
Description
Modified Salmonella strains and recombinant DNA in a plasmid are used to construct a
Salmonella strain that is dependent on the experimentally inserted plasmid. This construction
will be done via lab techniques such as polymerase chain reactions (PCR), transformation, and other means to create this construction. With future successful construction, the inhibition of flagella assembly, within the tumor environment, and increased synthesis of flagellin will be
possible. In the case that only assembly is prevented, then, the reliance on the lysis system to
release flagellin into the tumor microenvironment will be used as a means to induce immune
response. With the success of the self-lysis ability, these strains could be used to target these
tumor cells to deliver anticancer material as a vaccine delivery system.
ContributorsShagi, Agnel (Author) / Kong, Wei (Thesis director) / Fu, Lingchen (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2024-05