Browsing by Author "Sotelo, Joseph"
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Item Biomechanical Markers of Lower Extremity Fatigue: A Literature Review(2024-03-21) Malhotra, Garima; Sotelo, Joseph; Ngo, Khang; Do, Khanh; Toledo, DavidPurpose: Lower-extremity (LE) muscular fatigue plays a pivotal role in injury occurrence across various domains, including sports, occupational settings, and daily activities. This is partly because fatigued muscles can absorb less energy before reaching the degree of stretch that causes injury. This review explores the significance of employing measurable biomechanical markers to assess lower extremity fatigue. Some studies have shown significant changes in post-fatigue functional tasks (vertical jump height), acceleration/velocity, postural stability (center of pressure), spatio-temporal gait metrics, and pressure distribution, but few reviews have compared these factors to identify the best predictors of fatigue. With the prevalence of musculoskeletal injuries, understanding the biomechanical changes associated with fatigue becomes imperative for predicting and preventing injury. Methods: PubMed, Google Scholar, and Scopus were searched using 20 distinct queries, which yielded 3,068 articles. The inclusion criteria used were: An experimental pre/post-test design, fatiguing protocol targeting lower extremities, recent studies after 2010, greater than 10 participants, data recorded via force plates or IMU, and a healthy adult population. In total, 44 articles met the inclusion criteria. Results: Of the included studies, CoP changes were dependent on the protocol used. High-intensity fatigue protocols were associated with significant increases in postural instability, measured by CoP displacement, velocity, and variability in both sagittal and coronal planes, but CoP measures were inconclusive in low-moderate intensity fatiguing protocols. When observing Spatio-Temporal gait metrics, the literature showed a strong positive correlation between increased ground contact time and fatigue. Stride length was negatively correlated with fatigue. Step width variability and single stance time were increased following fatigue. In terms of pressure distributions, increasing muscle fatigue was correlated with increases in plantar pressure. Peak pressure and force of metatarsals I - V were inconclusive, attributable to varying rear versus forefoot strike patterns, however, medial and lateral heel peak pressures consistently increased with muscle fatigue. In line with these findings, various studies demonstrated that increasing fatigue correlated with kinetic parameters such as increased stride cadence and, consequently, increased tibial acceleration. Prolonged or repetitive exposure to elevated tibial acceleration levels may be associated with greater impact forces and loading on the lower extremities, potentially contributing to muscle fatigue and elevating the risk of overuse injuries. Functional tests, such as jump height, showed a significant negative relationship with fatigue regardless of protocol intensity. A study comparing different jump height modalities and fatigue showed the highest repeatability and immediate/prolonged fatigue produced changes with CMJ, supported by its widespread use as an indicator for fatigue. Conclusions: We consistently found significant increases in sagittal plane CoP velocity, ground contact time, heel loading, and tibial acceleration with a significant decrease in CMJ height following LE fatigue. Limitations included variability in the fatigue protocols used and limited research that met inclusion criteria. In the future, these results can have implications for the development of wearables to track fatigue in athletes to decrease the incidence of injury.Item Comparing Methylation of CRP and IL-6 Associated Genes in Cognitively Impaired Mexican Americans to Non-Hispanic Whites(2024-03-21) Sotelo, Joseph; DeLeon, Justin; Housini, Mohammad; Phillips, Nicole; Barber, RobertPurpose: A large pool of literature shows that Alzheimer’s Disease (AD) results from inflammatory processes and neuronal loss via tau proteins and amyloid-β plaques. Mexican Americans are among those with the highest risk of developing Alzheimer’s and research into the epigenetics of this association is lacking. Methylation alterations are influenced by both genetic and lifestyle factors, which can help us identify the root cause of mild cognitive impairment, a precursor for Alzheimer’s Disease. C-reactive protein and interleukin 6 are well known for their roles in measuring systemic inflammation. This study seeks to explore if there is a significant difference between DNA methylation of CpG Islands for CRP and IL6-associated genes in Cognitively Impaired Mexican Americans (MA) and Non-Hispanic Whites (NHW). Methods: Participants were selected from the Texas Alzheimer’s Research and Care Consortium (TARCC) database. The final cohort (n = 551) consisted of 252 NHW (143 normal cognition (NC), and 109 cognitively impaired (CI)) and 299 MA participants (177 NC and 122 CI). Each participant underwent neurocognitive tests such as Clinical Dementia Rating (CDR) and Mini-Mental State Exam (MMSE) to determine cognitive status. Methylation at CpG sites was measured by array probes as beta values with 0=unmethylated, to 1=fully methylated site. CpG sites associated with CRP are cg06126421, cg10636246, cg18181703, cg19821297, and cg25325512. CpG sites associated with IL6 are cg12929678, cg17412005, cg19638572, cg20789595. Any differences between cognitively impaired participants and normal controls were assessed using the standard two-sample t-test assuming unequal variances in Rstudio. Linear Regression was performed in Rstudio, and covariates that were adjusted for include age, sex, education level (in years), APOE ɛ4 allele status, CD8 T-cells, CD4 T-cells, natural killer cells, B-cells, monocytes, and neutrophils. Results: In Mexican Americans, the CRP-associated sites showed: cg25325512 (gene FGD2) with significant hypomethylation in the CI group (p=0.0003). Cg19821297 (gene DNASE2) with significant hypomethylation in the CI group (p=0.015). Cg10636246 (genes AIM2 & IF116) had significant CI group hypomethylation (p=0.02). In Non-Hispanic Whites, one CRP-associated site showed significant hypermethylation in the CI group, cg06690548 (gene TUBB) (p=0.026). In Mexican Americans, the IL6-associated sites showed: cg17412005 (gene MUTYH & TOE1) with significant hypomethylation in the CI group (p=0.022). Cg19638572 (gene RASSF5) with significant hypermethylation in the CI group (p=0.013). Cg20789595 (gene ADCY5) with significant hypomethylation in the CI group (p<0.001). In Non-Hispanic Whites, zero IL6-associated sites showed any significant methylation between the CI and NC groups. Conclusion: Epigenetics related to AD is still being further investigated. This study suggests an association between hypomethylated CRP and IL6 genes and cognitive impairment in the Mexican American population. Limitations in this study include a limited number of CpG sites investigated, as well as possible comorbidities that should be adjusted for. There were also an unequal number of MA to NHW participants. Further studies should adjust for inflammatory comorbidities, such as metabolic syndrome, and further investigation is warranted into the FGD2 gene and ADCY5 gene as they were strongly correlated with hypomethylation in the cognitively impaired Mexican American population.Item Methylation of IL-6 & TNF-α Associated Genes in Cognitive Impairment: A Texas Alzheimer's Research & Care Consortium (TARCC) Study(2024-03-21) Deleon, Justin; Sotelo, Joseph; Housini, Mohammad; Phillips, Nicole; Barber, RobertPurpose: The Mexican American (MA) population poses one of the highest risk groups for the development of Alzheimer’s Disease (AD). Inflammatory biomarkers, such as IL-6 and TNF-a, have been associated with cognitive decline but most only in non-Hispanic Whites (NHWs). Epigenetic DNA methylation of CpG islands associated with inflammatory markers (IL-6 and TNF-a) have been studied and identified in other diseases but literature for its effects on cognitive impairment (CI), especially in MAs, is quite sparse. This study aims to determine if DNA methylation of CpG islands for IL-6 and TNF-a are associated with CI in a MA and NHW cohort. Methods: Utilizing the TARCC cohort (N = 551), participants within ethnic groups (N = 299 MAs, N = 252 NHWs) were stratified by cognitive status (normal cognition (NC) or CI). Methylation data at CpG sites were measured as beta values by array probes using the Illumina EPIC array. Linear regression analysis was performed in R comparing the beta value and cognitive diagnosis (NC or CI) for MA and NHW. Covariates include age, sex, education, CD8T cells, CD4T cells, B cells, monocytes, neutrophils, and the APOE gene. Result: The methylation sites cg04381957 and cg04583842 (both associated with IL-6) were significant within MAs. Those sites suggest hypomethylation and hypermethylation, respectively, in CI compared to the NC. Methylation site cg16411857 (associated with TNF-a) was not significant with CI in either MAs or NHWs. Conclusion: There was a stronger association with IL-6 related CpG sites and CI especially in MA at cg04381957 (p = 0.0035) within the RFTN1 gene. Future research plans to include inflammatory syndromes, such as diabetes, which could be a potential confounding variable affecting levels of IL-6 or TNF-a.