This meta-study analyzes the shift in research literature that focuses on the various shared causes of type 2 diabetes and Alzheimer’s disease from the years 2000 to 2022. Examining literature trends over the past two decades can offer valuable insight into the evolving emphasis on various topics. Altogether, a total of 154 publications were collected from the Pubmed and ResearchGate databases using a non-biased protocol and methodology. Each paper was then categorized by the topics it discussed. Visual representation of the data such as bar graphs and tables were created to comprehend the trends presented in the group of papers. The collection of publications were then differentiated into years of early (prior to 2005 or 2010) and late (after 2006 or 2011) periods to perform a statistical analysis of the patterns in the timeline. The increase in publications discussing Alzheimer’s disease, amyloid beta deposition, gut microbiota, mitochondrial dysfunction, type 2 diabetes, and tau hyperphosphorylation from the early to the late period were statistically significant. This means that the increase was not due to random chance, but rather supported by evidence. This can be attributed to researchers and physicians discovering more evidence that establishes a link between specific factors, type 2 diabetes, and Alzheimer’s disease. This reflects a genuine acknowledgment of the importance of understanding and addressing the relationship between these two pathologies. Research in the trends of literature can provide information in which areas of research are the most studied or understudied. Based on these findings, the identification of areas with limited knowledge and potential research directions can be inferred, ultimately leading to the enhancement of preventive measures and therapeutic approaches for these conditions.

Discussions of the nature of time can be enriched using insight from the field of biology. In the evolution of our species, biological timekeeping mechanisms have been honed to a fine point and can accurately adhere to a 24-hour cycle. When considering that these timekeeping mechanisms would only have evolved if they were reasonably accurate, it must be the case that our timekeeping systems are measuring a genuine feature of reality. This thesis explores this idea by discussing the veridicality of the circadian clock and contrasting it with the physiological origin of feelings of duration. As it turns out, duration can not be accounted for by the circadian clock, implying that the felt ‘flow’ of time is a cognitive illusion rather than a feature of objective reality. Given this, our knowledge of biology reconciles best with the Static View (B-theory) of time.

This project uses All of Us Data to analyze how well of a predictor APOE ε4 is in the Latinx community, a high grandparent care community. APOE is used as a predictor for Alzheimer’s disease, but it is unknown, due to the lack of studies, how strong of a predictor it will be for Latinx individuals. This project aims to understand if the increased risk of Alzheimer’s disease among Hispanics is associated with a different level of ε4 gene frequency.

In today's society, success is often associated with conventional norms and expectations. The pressure to conform to these norms can be daunting, especially for those who are aiming to succeed in highly competitive fields such as entrepreneurship or the healthcare field. However, to truly achieve success, it is important to think outside the box and push past one's comfort zone. Success in any career requires a combination of learning from others, embracing a growth mindset, developing discipline, harnessing the power of manifestation and visualization, and effectively handling negative criticism. This thesis and two podcast episodes linked at the end of the document will explore these topics in-depth, drawing upon personal experiences and anecdotes to illustrate the significance of these concepts. The thesis will also discuss the Dunning-Kruger effect and the Law of Attraction to provide a comprehensive understanding of the challenges and opportunities on the path to success.

Influenza virus A (IVA) poses a serious threat to human health, killing over 25,000 Americans in the 2022 flu season alone. In the past 10 years, vaccine efficacy has varied significantly, ranging from 20-60% each season. Because IVA is subject to high antigenic shift and strain cocirculation, more effective IVA vaccines are needed to reduce the incidence of disease. Herein we report the production of a recombinant immune complex (RIC) vaccine “4xM2e” in Nicotiana benthamiana plants using agroinfiltration for use as a potential universal IVA vaccine candidate. RICs fuse antigen to the C-terminus of an immunoglobulin heavy chain with an epitope tag cognate to the antibody, promoting immune complex formation to increase immunogenicity. IVA matrix protein 2 ectodomain (M2e) is selected to serve as vaccine antigen for its high sequence conservation, as only a small number of minor mutations have occurred since its discovery in 1981 in the human sequence. However, there is some divergence in zoonotic IVA strains, and to account for this, we designed a combination of human consensus, swine, and avian M2e variants, 4xM2e. This was fused to the C terminus of the RIC platform to improve M2e immunogenicity and IVA strain coverage. The 4xM2e RIC was produced in N. benthamiana and verified with SDS-PAGE and Western blot assays, along with an analysis of complex formation and the potential for complement activation via complement C1q ELISA. With this work, we demonstrate the potential of RICs and plant-expression systems to generate universal IVA vaccine candidates.

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.