Auburn Research Day 2022

B i omed i ca l Resea rch | Med i ca l St udent Evaluating The Effect of Creep and Cyclic Loading on Human Tendons

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Nathan Pool; Gavin Husted; Beth Birchfield; Kashan Mahmood Center for Occupational Safety, Ergonomics, and Injury Prevention at Auburn University; VCOM-Auburn

Fatigue failure theory explains how materials incur damage, rupture, or break from repeated loading. All known materials fail via this process. Recently, Auburn University has developed three ergonomic assessment tools based on fatigue failure. While much is known about materials such as steel, the fatigue properties of human tissues are less well-known. The purpose of this research is to better characterize the impact of repeated loading on human tissues relevant to ergonomics. Therefore, this study is focusing on the properties of human tendons and their response to both cyclic (intermittent, repeated) and creep (steady, constant) loading via different levels of stress. This information is directly relevant to

models such as the Distal Upper Extremity Tool (DUET) and can serve to improve the algorithms on which it is based. Preliminary results from the related tests indicate cycles to failure for 12 flexor digitorum profundus and flexor digitorum superficialis tendons ranging from 0 to 21,498 cycles. Tendons exposed to creep loading had a time to failure ranging from .8 to 73561s.

B i omed i ca l Resea rch | Gr adua te/Undergr adua te St udent Gut Metabolite Trimethylamine Oxide Induces ER Stress and Neuronal Dysfunction

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Christopher Purvis; Victoria Jiminez; Manoj Govindarajulu; Priyanka Pinky Das; Ian M. Steinke; Sieun Yoo; Vishnu Suppiramaniam; Rajesh H. Amin Drug Discovery and Development, Harrison School of Pharmacy

Background: Dysbiosis of gut microbiota is associated with metabolic diseases including diabetes, obesity, and cardiovascular disease. Recent studies indicate that Trimethylamine N-oxide (TMAO), a gut microbe-dependent metabolite is implicated in the development of age-related cognitive decline. Methods: We therefore investigated the association between TMAO and deficits in neuronal function in an Alzheimer’s model (3×Tg-AD) and insulin resistance (Leptin deficient db/db) mouse by measuring levels of TMAO in the plasma and brain.

Results: Our findings indicate that TMAO levels increase in the plasma and brain of both db/db and 3×Tg-AD mice when compared to age matched wild-type mice. Further observed deficiencies in neuronal function, in the form of reduced long-term potentiation (LTP), in both groups of mice when compared to wild-type mice. To explain these observations we further observed that TMAO induced the ER stress in TMAO treated ex-vivo slices as well as in both db/db and 3×Tg-AD mice. Lastly, we also observed reduced postsynaptic receptor expression. Conclusion: Our findings suggest that TMAO induce deficits in neuronal function through ER stress.

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