Does endurance fatigue increase the risk of injury when performing drop jumps?

Although from an athletic performance perspective it may be beneficial to undertake drop jump training when fatigued (principle of "specificity" of training), such endur-ance fatigue may expose the body to a greater risk of injury if it causes an increase in peak impact accelerations. This study aimed to determine if endurance fatigue resulted in an increase in tibial peak impact acceleration and an associated change in knee kinematics when completing plyometric drop jumps. Fifteen females performed drop jumps from 3 heights (15, 30, and 45 cm) when fatigued and nonfatigued. Treadmill running was used to induce endurance fatigue. The following variables were assessed: tibial peak impact acceleration, knee angle at initial ground contact, maximum angle of flexion, range of flexion, and peak knee angular velocity. Fatigue resulted in significantly greater (p < 0.05) tibial peak impact acceleration and knee flexion peak angular velocity in drop jumps from 15 and 30 cm, but not from 45 cm. Fatigue had no effect on any of the knee angles assessed. The neuromuscular system was affected negatively by endurance fatigue at 15 and 30 cm, indicating that coaches should be aware of a potential increased risk of injury in performing drop jumps when fatigued. Because from the greater drop height of 45 cm the neuromuscular system had a reduced capacity to attenuate the impact accelerations per se, whether nonfatigued or fatigued, this would suggest that this height may have been too great for the athletes examined

The risk of secondary traumatic stress in the qualitative transcription process: A research note.

Kiyimba, N. & O'Reilly, M., The risk of secondary traumatic stress in the qualitative transcription process: a research note, Qualitative Research (16:4) pp. 468-476. Copyright © Nikki Kiyimba & Michelle O'Reilly, 2015. Reprinted by permission of SAGE Publications.It is recognised that transcribing is not merely a neutral and mechanical process, but is active and requires careful engagement with the qualitative data. Whether the researcher transcribes their own data or employs professional transcriptionists the process requires repeated listening to participants’ personal narratives. This repetition has a cumulative effect on the transcriptionist and hearing the participants’ personal narratives of a sensitive or distressing nature, can have an emotional impact. However, this potential emotional impact is often not something which is accounted for in the planning stages of research. In this article we critically discuss the importance of considering the effects on transcriptionists who engage with qualitative data

The Relationship between Youth Inactivity and Health

As technology advances, youth engage in the sedentary lifestyle of playing computer games, leaving no time for physical activities. The purpose of this study is to prove the relationship between youth inactivity and health. The inactive behavior of adolescents has contributed to increased health issues. Among them are cardiovascular diseases, obesity, depression, type 2 diabetes, and hypertension. The research data was collected in the form of secondary data from a literature review, where credible peer reviewed articles published between 2013 to 2020, and government websites were used for the study. By studying the connection of physical inactivity and the health of adolescents, researchers seek to reduce cases of health conditions experienced. This research is important because it proves a relationship between youth inactivity and health issues. It can spread awareness to improve the health of the youth and teach them how to actively improve their health. The study enhances cost-effectiveness on both individual and government levels. The research will promote engagement in physical activities leading to health benefits like improved muscles and cardiovascular fitness, improved bones, reduced risk of hypertension and cardiovascular illnesses, fundamental to energy balance, and several others

Proclaiming Jubilee: Preaching that Sets Women Free

In Luke 4, Jesus outlines his mission: to proclaim the year of the Lord’s favor and free the oppressed. Yet the marginalization and oppression of women have been structurally normalized throughout history, both in secular society as well as Christian culture. Through historical, cultural, biblical, exegetical, hermeneutical, and homiletical analysis, this study posits that a jubilee homiletic is a crucial part of embodying liberation from textual interpretations that have prioritized those who are privileged, so that women may reclaim scripture as a source of freedom

The Candida albicans transcription factor Cas5 couples stress responses, drug resistance and cell cycle regulation

We thank Cowen lab members for helpful discussions. We also thank David Rogers (University of Tennessee) for sharing microarray analysis of the CAS5 homozygous mutant, and Li Ang (University of Macau) for assistance in optimizing the ChIP-Seq experiments. J.L.X. is supported by a Canadian Institutes of Health Research Doctoral award and M.D.L. is supported by a Sir Henry Wellcome Postdoctoral Fellowship (Wellcome Trust 096072). B.T.G. holds an Ontario Graduate Scholarship. C.B. and B.J.A. are supported by the Canadian Institutes of Health Research Foundation Grants (FDN-143264 and -143265). D.J.K. is supported by a National Institute of Allergy and Infectious Diseases grant (1R01AI098450) and J.D.L.C.D. is supported by the University of Rochester School of Dentistry and Medicine PREP program (R25 GM064133). A.S. is supported by the Creighton University and the Nebraska Department of Health and Human Services (LB506-2017-55). K.H.W. is supported by the Science and Technology Development Fund of Macau S.A.R. (FDCT; 085/2014/A2). L.E.C. is supported by the Canadian Institutes of Health Research Operating Grants (MOP-86452 and MOP-119520), the Natural Sciences and Engineering Council (NSERC) of Canada Discovery Grants (06261 and 462167), and an NSERC E.W.R. Steacie Memorial Fellowship (477598).Peer reviewedPublisher PD

Advancing Alternative Analysis: Integration of Decision Science.

Decision analysis-a systematic approach to solving complex problems-offers tools and frameworks to support decision making that are increasingly being applied to environmental challenges. Alternatives analysis is a method used in regulation and product design to identify, compare, and evaluate the safety and viability of potential substitutes for hazardous chemicals.Assess whether decision science may assist the alternatives analysis decision maker in comparing alternatives across a range of metrics.A workshop was convened that included representatives from government, academia, business, and civil society and included experts in toxicology, decision science, alternatives assessment, engineering, and law and policy. Participants were divided into two groups and prompted with targeted questions. Throughout the workshop, the groups periodically came together in plenary sessions to reflect on other groups' findings.We conclude the further incorporation of decision science into alternatives analysis would advance the ability of companies and regulators to select alternatives to harmful ingredients, and would also advance the science of decision analysis.We advance four recommendations: (1) engaging the systematic development and evaluation of decision approaches and tools; (2) using case studies to advance the integration of decision analysis into alternatives analysis; (3) supporting transdisciplinary research; and (4) supporting education and outreach efforts

Scene-selective coding by single neurons in the human parahippocampal cortex

Imaging, electrophysiological, and lesion studies have shown a relationship between the parahippocampal cortex (PHC) and the processing of spatial scenes. Our present knowledge of PHC, however, is restricted to the macroscopic properties and dynamics of bulk tissue; the behavior and selectivity of single parahippocampal neurons remains largely unknown. In this study, we analyzed responses from 630 parahippocampal neurons in 24 neurosurgical patients during visual stimulus presentation. We found a spatially clustered subpopulation of scene-selective units with an associated event-related field potential. These units form a population code that is more distributed for scenes than for other stimulus categories, and less sparse than elsewhere in the medial temporal lobe. Our electrophysiological findings provide insight into how individual units give rise to the population response observed with functional imaging in the parahippocampal place area

A novel albumin gene mutation (R222I) in familial dysalbuminemic hyperthyroxinemia.

CONTEXT: Familial dysalbuminemic hyperthyroxinemia, characterized by abnormal circulating albumin with increased T4 affinity, causes artefactual elevation of free T4 concentrations in euthyroid individuals. OBJECTIVE: Four unrelated index cases with discordant thyroid function tests in different assay platforms were investigated. DESIGN AND RESULTS: Laboratory biochemical assessment, radiolabeled T4 binding studies, and ALB sequencing were undertaken. (125)I-T4 binding to both serum and albumin in affected individuals was markedly increased, comparable with known familial dysalbuminemic hyperthyroxinemia cases. Sequencing showed heterozygosity for a novel ALB mutation (arginine to isoleucine at codon 222, R222I) in all four cases and segregation of the genetic defect with abnormal biochemical phenotype in one family. Molecular modeling indicates that arginine 222 is located within a high-affinity T4 binding site in albumin, with substitution by isoleucine, which has a smaller side chain predicted to reduce steric hindrance, thereby facilitating T4 and rT3 binding. When tested in current immunoassays, serum free T4 values from R222I heterozygotes were more measurably abnormal in one-step vs two-step assay architectures. Total rT3 measurements were also abnormally elevated. CONCLUSIONS: A novel mutation (R222I) in the ALB gene mediates dominantly inherited dysalbuminemic hyperthyroxinemia. Susceptibility of current free T4 immunoassays to interference by this mutant albumin suggests likely future identification of individuals with this variant binding protein.This work was supported by funding from the Wellcome Trust (Grant 100585/Z/12/Z, to N.S., Grant 095564/Z/11/Z, to K.C.) and National Institute for Health Research Cambridge Biomedical Research Centre (to C.M., and M.G.).This is the final published version of the article. It was originally published in The Journal of Clinical Endocrinology & Metabolism (Nadia Schoenmakers, Carla Moran, Irene Campi, Maura Agostini, Olivia Bacon, Odelia Rajanayagam, John Schwabe, Sonia Bradbury, Timothy Barrett, Frank Geoghegan, Maralyn Druce, Paolo Beck-Peccoz, Angela O'Toole, Penelope Clark, Michelle Bignell, Greta Lyons, David Halsall, Mark Gurnell, Krishna Chatterjee. J Clin Endocrinol Metab 2014 Jul 19;99(7):E1381-6. Epub 2014 Mar 19. http://dx.doi.org/10.1210/jc.2013-4077). A correction to this article was issued because the CC-BY licence was not present on the final published paper (http://dx.doi.org/10.1210/jc.2015-1656)

CYLD Proteolysis Protects Macrophages from TNF-Mediated Auto-necroptosis Induced by LPS and Licensed by Type I IFN

SummaryTumor necrosis factor (TNF) induces necroptosis, a RIPK3/MLKL-dependent form of inflammatory cell death. In response to infection by Gram-negative bacteria, multiple receptors on macrophages, including TLR4, TNF, and type I IFN receptors, are concurrently activated, but it is unclear how they crosstalk to regulate necroptosis. We report that TLR4 activates CASPASE-8 to cleave and remove the deubiquitinase cylindromatosis (CYLD) in a TRIF- and RIPK1-dependent manner to disable necroptosis in macrophages. Inhibiting CASPASE-8 leads to CYLD-dependent necroptosis caused by the TNF produced in response to TLR4 ligation. While lipopolysaccharides (LPS)-induced necroptosis was abrogated in Tnf−/− macrophages, a soluble TNF antagonist was not able to do so in Tnf+/+ macrophages, indicating that necroptosis occurs in a cell-autonomous manner. Surprisingly, TNF-mediated auto-necroptosis of macrophages requires type I IFN, which primes the expression of key necroptosis-signaling molecules, including TNFR2 and MLKL. Thus, the TNF necroptosis pathway is regulated by both negative and positive crosstalk