Does Neck Strength in Male and Female Youth Soccer Players Affect Head Velocity During Goal-Directed Heading: A Proposal

Introduction: Head impact research in soccer (e.g., during heading) has increased recently, with the intent to reduce the risk of play-related injuries such as concussions. Low neck strength and head kinematics (e.g., velocity) in players have been proposed as risk factors for concussion1. However, previous research has primarily focused on collegiate athletes1, despite the possible increased risk for youth players due to crucial neurodevelopment occurring in this group2. Therefore, the purpose of this study is to determine neck strength differences between male and female youth soccer players, and to quantify the relationship between heading velocities and neck strength. Methods: Participants will include male and female youth soccer players (11 - 13 years old). Neck strength will be quantified while supine during lateral flexion, cervical flexion, and extension using a prone push test with a hand-held dynamometer. Participants will also complete five headers in the lab in each of three directions: balls tossed to them from their right, left, and in front. Three retroreflective markers on each participant’s head will be recorded using five GoPro Hero 9 cameras. ProAnalyst (Xcitex) motion capture analysis software will be used to determine head velocities. Pearson correlations will be completed to assess the strength of the relationship between neck strength and head velocities, and between sex and head velocities. Expected results: Youth with lower neck strength will have increased head velocities during purposeful heading. Moreover, females will have lower neck strength, and therefore, higher head velocities in comparison to their male counterparts. Keywords: youth soccer, neck strength, head velocities, sex differences References: Dezman, Z. D., Ledet, E. H., & Kerr, H. A. (2013). Neck strength imbalance correlates with increased head acceleration in soccer heading. Sports Health, 5(4), 320-326. Patel, D. R., Shivdasani, V., & Baker, R. J. (2005). Management of sport-related concussion in young athletes. Sports Medicine, 35(8), 671-84

Organ-on-a-chip: current gaps and future directions.

As an emerging hot topic of the last decade, Organ on Chip (OoC) is a new technology that is attracting interest from both basic and translational scientists. The Biochemical Society, with its mission of supporting the advancement of science, with addressing grand challenges that have societal impact, has included OoC into their agenda to review the current state of the art, bottlenecks and future directions. This conference brought together representatives of the main stakeholders in the OoC field including academics, end-users, regulators and technology developers to discuss and identify requirements for this new technology to deliver on par with the expectations and the key challenges and gaps that still need to be addressed to achieve robust human-relevant tools, able to positively impact decision making in the pharmaceutical industry and reduce overreliance on poorly predictive animal models

Application of Multi-SNP Approaches Bayesian LASSO and AUC-RF to Detect Main Effects of Inflammatory-Gene Variants Associated with Bladder Cancer Risk

The relationship between inflammation and cancer is well established in several tumor types, including bladder cancer. We performed an association study between 886 inflammatory-gene variants and bladder cancer risk in 1,047 cases and 988 controls from the Spanish Bladder Cancer (SBC)/EPICURO Study. A preliminary exploration with the widely used univariate logistic regression approach did not identify any significant SNP after correcting for multiple testing. We further applied two more comprehensive methods to capture the complexity of bladder cancer genetic susceptibility: Bayesian Threshold LASSO (BTL), a regularized regression method, and AUC-Random Forest, a machine-learning algorithm. Both approaches explore the joint effect of markers. BTL analysis identified a signature of 37 SNPs in 34 genes showing an association with bladder cancer. AUC-RF detected an optimal predictive subset of 56 SNPs. 13 SNPs were identified by both methods in the total population. Using resources from the Texas Bladder Cancer study we were able to replicate 30% of the SNPs assessed. The associations between inflammatory SNPs and bladder cancer were reexamined among non-smokers to eliminate the effect of tobacco, one of the strongest and most prevalent environmental risk factor for this tumor. A 9 SNP-signature was detected by BTL. Here we report, for the first time, a set of SNP in inflammatory genes jointly associated with bladder cancer risk. These results highlight the importance of the complex structure of genetic susceptibility associated with cancer risk.The work was partially supported by the Fondo de Investigacion Sanitaria, Instituto de Salud Carlos III (G03/174, 00/0745, PI051436, PI061614, PI09-02102, G03/174 and Sara Borrell fellowship to ELM) and Ministry of Science and Innovation (MTM2008-06747-C02-02 and FPU fellowship award to VU), Spain; AGAUR-Generalitat de Catalunya (Grant 2009SGR-581); Fundaciola Maratode TV3; Red Tematica de Investigacion Cooperativa en Cancer (RTICC); Asociacion Espanola Contra el Cancer (AECC); EU-FP7-201663; and RO1-CA089715 and CA34627; the Spanish National Institute for Bioinformatics (www.inab.org); and by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics, National Cancer Institute, USA. MD Anderson support for this project included U01 CA 127615 (XW); R01 CA 74880 (XW); P50 CA 91846 (XW, CPD); Betty B. Marcus Chair fund in Cancer Prevention (XW); UT Research Trust fund (XW) and R01 CA 131335 (JG)

Tumour necrosis factor-alpha mediates tumour promotion via a PKC alpha- and AP-1-dependent pathway

Tumour necrosis factor-alpha mediates tumour promotion via a PKC alpha- and AP-1-dependent pathway. Tumour necrosis factor-alpha (TNF-alpha) deficient mice (TNF-alpha(-/-) mice) are resistant to skin carcinogenesis. Cellular signalling via the transcription factor complex AP-1 is thought to play a key role in tumour promotion. The induction of a specific subset of AP-1 responsive genes thought to be important for tumour development, namely GM-CSF, MMP-9 and MMP-3, was suppressed in TNF-alpha(-/-) compared to wild-type mouse skin in response to the tumour promotor TPA. The differential induction of these genes correlated with a temporal shift in AP-1 activation and c-Jun expression in TNF-alpha(-/-) compared to wild-type epidermis. The major receptor for TPA-induced signalling in basal keratinocytes, PKCalpha, was also differentially regulated in wild-type compared with TNF-alpha(-/-) epidermis. A marked delay in TPA-induced intracellular translocation and downregulation of PKCalpha was observed in TNF-alpha(-/-) epidermis, which correlated with the deregulated TPA-induced AP-1 activation and c-Jun expression. The frequency of DNA adduct formation and c-Ha-ras mutations was the same in wild-type and TNF-alpha(-/-) epidermis after DMBA treatment, suggesting that TNF-alpha was not involved in tumour initiation. These data suggest that the pro-inflammatory cytokine TNF-alpha is a critical mediator of tumour promotion, acting via a PKCalpha- and AP-1-dependent pathway. This may be one mechanism by which chronic inflammation increases susceptibility to cancer