Prevention Strategies of Traumatic Brain Injury in Football Players

In this project, we study the effects of the impact angle during a helmet-to-helmet collision on stress distribution and deacceleration values of the brain tissue in efforts to reduce brain injuries for football players. The overall goal is to provide sufficient information to improve the design of helmet technology. In addition, our study will be able to inform the athletes to avoid a helmet-to-helmet collision, such that, they can be trained to shift their heads in the horizontal direction to create a “glancing blow” effect. It is suggested that by avoiding a helmet-to-helmet collision, both rotational acceleration and stress can be reduced leading to a lower probability of receiving concussions and subsequent brain injuries [1].Cockrell School of Engineerin

Rehabilitation strategies to overcome quadriceps weakness for athletes with anterior cruciate ligament (ACL) reconstruction

This poster was presented at the Great Plains Honors Conference in Canyon, Texas.https://scholarworks.uttyler.edu/student_posters/1018/thumbnail.jp

Cupping Therapy: What is it and How is it Beneficial

This poster was presented at the National Collegiate Honors Conference in Atlanta, Georgia.https://scholarworks.uttyler.edu/student_posters/1007/thumbnail.jp

Comparison of Pitching from Flat Ground vs. 10-Inch Mound Regarding Elbow Varus Torque and Arm Speed

Purpose: The purpose of this study was to examine the effect of throwing surface and distance on varus elbow torque and arm speed. Methods: 11 male collegiate baseball pitchers (age = 20.73 ± 1.56 years, height = 175.26 ± 9.03 cm, mass = 70.31 ± 9.03 kg) participated in this study. Varus elbow torque and distance were measured using a 3D motion sensor housed in a spandex sleeve at the medial joint line of the elbow. Participants were instructed to complete their normal warmup routine as if they were about to pitch in a bullpen session or a game. Participants were then fitted with the sleeve and 3D motion sensor and then instructed to throw 5 maximum effort fastballs at both 60 feet 6 inches and 50 feet 6 inches from a 10-inch mound and 5 maximum effort fastballs at both 60 feet 6 inches and 50 feet 6 inches from flat ground. A two-way ANOVA with repeated measures was used to analyze the differences in elbow varus torque and arm speed when pitching from 60 feet 6 inches and 50 feet 6 inches from a 10-inch mound and from flat ground. Tests of significance were carried out at an alpha level p \u3c 0.05. Results: Significant differences in elbow varus torque were found when throwing from a 10-inch mound compared to flat ground (10-inch mound = 46.99 ± 2.36, Flat ground = 42.67 ± 3.14). No significant differences in elbow varus torque were found when throwing from 60 feet 6 inches compared to 50 feet 6 inches regardless of surface (60 feet 6 inches = 45.38 ± 2.96, 50 feet 6 inches = 44.28 ± 2.59). No significant differences in arm speed were found regardless of surface or distance. Conclusions: Throwing from a 10-inch mound appears to place more torque on the elbow than throwing from flat ground. Clinicians should be mindful of this fact when progressing patients through throwing programs

Decrease in Knee Flexion is observed in a Three Set Tennis Match on Knee Kinematics during the Tennis Serve

Tennis matches can be long, physically challenging affairs. The course of a match is often determined by the serving proficiency of both players. While the serve has been extensively studied, the relationship between the serve and match length specifically regarding knee kinematics is not well documented in a real time environment. The purpose of the current study was to determine the effect a three-set tennis match had on knee kinematics during the serve. Eleven male collegiate tennis players (age: 19.6±1.7) were recruited from The University of Texas at Tyler. All participants played a three-set match and digital video recordings of the first five serves and last five serves from each set were taken by placing reflective markers at hip, knee and ankle joints of all subjects. After digital videos were imported into a motion capture system (Vicon Motus), kinematic analyses were performed to calculate the knee flexion during the serve. Preliminary analyses showed a significant decrease in knee flexion from the beginning of the first set to the end of the third set. The average decrease was 6.13 degrees for all participants. Such results are consistent with previous studies which have shown that decreasing knee flexion has a detrimental effect on the serve and can cause a reduction in efficiency to occur as well. From this preliminary data a recommendation to coaches would be to cue the players in on their legs during the serve when a decrease in proficiency occurs during a match. Future study may use surface electromyography (EMG) to examine the contribution of muscle fatigue to the knee flexion during the serve in a three set tennis match

A Computational Method Based on the Integration of Heterogeneous Networks for Predicting Disease-Gene Associations

The identification of disease-causing genes is a fundamental challenge in human health and of great importance in improving medical care, and provides a better understanding of gene functions. Recent computational approaches based on the interactions among human proteins and disease similarities have shown their power in tackling the issue. In this paper, a novel systematic and global method that integrates two heterogeneous networks for prioritizing candidate disease-causing genes is provided, based on the observation that genes causing the same or similar diseases tend to lie close to one another in a network of protein-protein interactions. In this method, the association score function between a query disease and a candidate gene is defined as the weighted sum of all the association scores between similar diseases and neighbouring genes. Moreover, the topological correlation of these two heterogeneous networks can be incorporated into the definition of the score function, and finally an iterative algorithm is designed for this issue. This method was tested with 10-fold cross-validation on all 1,126 diseases that have at least a known causal gene, and it ranked the correct gene as one of the top ten in 622 of all the 1,428 cases, significantly outperforming a state-of-the-art method called PRINCE. The results brought about by this method were applied to study three multi-factorial disorders: breast cancer, Alzheimer disease and diabetes mellitus type 2, and some suggestions of novel causal genes and candidate disease-causing subnetworks were provided for further investigation

Extra-Nuclear Signalling of Estrogen Receptor to Breast Cancer Cytoskeletal Remodelling, Migration and Invasion

BACKGROUND: Estrogen is an established enhancer of breast cancer development, but less is known on its effect on local progression or metastasis. We studied the effect of estrogen receptor recruitment on actin cytoskeleton remodeling and breast cancer cell movement and invasion. Moreover, we characterized the signaling steps through which these actions are enacted. METHODOLOGY/PRINCIPAL FINDINGS: In estrogen receptor (ER) positive T47-D breast cancer cells ER activation with 17beta-estradiol induces rapid and dynamic actin cytoskeleton remodeling with the formation of specialized cell membrane structures like ruffles and pseudopodia. These effects depend on the rapid recruitment of the actin-binding protein moesin. Moesin activation by estradiol depends on the interaction of ER alpha with the G protein G alpha(13), which results in the recruitment of the small GTPase RhoA and in the subsequent activation of its downstream effector Rho-associated kinase-2 (ROCK-2). ROCK-2 is responsible for moesin phosphorylation. The G alpha(13)/RhoA/ROCK/moesin cascade is necessary for the cytoskeletal remodeling and for the enhancement of breast cancer cell horizontal migration and invasion of three-dimensional matrices induced by estrogen. In addition, human samples of normal breast tissue, fibroadenomas and invasive ductal carcinomas show that the expression of wild-type moesin as well as of its active form is deranged in cancers, with increased protein amounts and a loss of association with the cell membrane. CONCLUSIONS/SIGNIFICANCE: These results provide an original mechanism through which estrogen can facilitate breast cancer local and distant progression, identifying the extra-nuclear G alpha(13)/RhoA/ROCK/moesin signaling cascade as a target of ER alpha in breast cancer cells. This information helps to understand the effects of estrogen on breast cancer metastasis and may provide new targets for therapeutic interventions

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

HIV-1 assembly in macrophages

The molecular mechanisms involved in the assembly of newly synthesized Human Immunodeficiency Virus (HIV) particles are poorly understood. Most of the work on HIV-1 assembly has been performed in T cells in which viral particle budding and assembly take place at the plasma membrane. In contrast, few studies have been performed on macrophages, the other major target of HIV-1. Infected macrophages represent a viral reservoir and probably play a key role in HIV-1 physiopathology. Indeed macrophages retain infectious particles for long periods of time, keeping them protected from anti-viral immune response or drug treatments. Here, we present an overview of what is known about HIV-1 assembly in macrophages as compared to T lymphocytes or cell lines

Murine Leukemia Virus Spreading in Mice Impaired in the Biogenesis of Secretory Lysosomes and Ca2+-Regulated Exocytosis

Retroviruses have been observed to bud intracellularly into multivesicular bodies (MVB), in addition to the plasma membrane. Release from MVB is thought to occur by Ca(2+)-regulated fusion with the plasma membrane.To address the role of the MVB pathway in replication of the murine leukemia virus (MLV) we took advantage of mouse models for the Hermansky-Pudlak syndrome (HPS) and Griscelli syndrome. In humans, these disorders are characterized by hypopigmentation and immunological alterations that are caused by defects in the biogenesis and trafficking of MVBs and other lysosome related organelles. Neonatal mice for these disease models lacking functional AP-3, Rab27A and BLOC factors were infected with Moloney MLV and the spread of virus into bone marrow, spleen and thymus was monitored. We found a moderate reduction in MLV infection levels in most mutant mice, which differed by less than two-fold compared to wild-type mice. In vitro, MLV release form bone-marrow derived macrophages was slightly enhanced. Finally, we found no evidence for a Ca(2+)-regulated release pathway in vitro. Furthermore, MLV replication was only moderately affected in mice lacking Synaptotagmin VII, a Ca(2+)-sensor regulating lysosome fusion with the plasma membrane.Given that MLV spreading in mice depends on multiple rounds of replication even moderate reduction of virus release at the cellular level would accumulate and lead to a significant effect over time. Thus our in vivo and in vitro data collectively argue against an essential role for a MVB- and secretory lysosome-mediated pathway in the egress of MLV