The Effects of Increasing Running Speed on vGRF and Asymmetry

Biomechanical and physiological parameters related to running performance are usually studied separately. However, evaluating both aspects together could be beneficial in improving athletic performance. The purpose of this study was to observe the change in peak vGRF and asymmetry as speed increases, while observing physiological responses during a O2maxtest. Data from athlete monitoring of 12 cross-country and triathlon athletes were analyzed. The athlete monitoring protocol included three unweighted countermovement jumps and a O2maxtest performed by the athletes. The athletes had an average O2maxof 53.4 ± 7.7 mL/kg/min, while their average vGRF asymmetry throughout the O2maxtestwas 1.38 ± 0.68%. A strong, positive correlation was found between average vGRF and average blood lactate (r=0.93), indicating that as vGRF increased so did blood lactate. It was concluded that physiological and biomechanical parameters are related in athletic performance. Therefore, athlete monitoring should include analysis of both physiological and biomechanical parameters in order to form a more well-rounded analysis of athlete performance

Distance Labs

This capstone paper is a compilation of the information we discovered during our research on the topic of distance lab environments for online computing courses. We provide our research, our findings, and our supporting evidence to answer the following question: How can La Salle University deliver a comparable hands-on learning experience for its online student population without requiring the students to attend on-campus? Initially, our research suggests a solution for the Economic Crime Forensics (ECF) courses; however, it will benefit all lab related computing courses at La Salle University. This paper will show: (a) that the goal of using a distance lab for the Economic Crime Forensics (ECF) courses is obtainable, and how it will benefit students by completing the lab assignments in the computing courses; (b) our literature review; (c) and our research findings from several sources. Our research includes discussions with La Salle University Faculty; sample sessions with three public cloud computing services: CloudShare ProPlus, Skytap, and Amazon Web Services (AWS); and implementations from schools using a private cloud service on-campus with the IBM Virtual Computing Lab Initiative (VCL) Model including how Higher Education is using commercially available virtualization software from VMWare (VCloud) on top of their own architecture

Update on the LLRF operations status at the European XFEL

The European XFEL (EuXFEL) is a free-electron laser in the X-ray range for users. Its high availability is one of the key aspects of the machine. In 2022, it entered in the sixth year of operation. The EuXFEL linac is based on the TESLA superconducting RF technology, operating at 1.3 GHz with an RF pulse length of 650 $\mu$s and a repetition rate of 10 Hz. The LLRF system is based on the MicroTCA standard and relies on a high level of automation. In this contribution, we review the LLRF operation at the EuXFEL and the development of new tools and features to improve the monitoring and extend the usability of the LLRF system.Comment: Talk presented at LLRF Workshop 2022 (LLRF2022, arXiv:2208.13680

A long noncoding RNA influences the choice of the X chromosome to be inactivated

X chromosome inactivation (XCI) is the process of silencing one of the X chromosomes in cells of the female mammal which ensures dosage compensation between the sexes. Although theoretically random in somatic tissues, the choice of which X chromosome is chosen to be inactivated can be biased in mice by genetic element(s) associated with the so-called X-controlling element (Xce). Although the Xce was first described and genetically localized nearly 40 y ago, its mode of action remains elusive. In the approach presented here, we identify a single long noncoding RNA (lncRNA) within the Xce locus, Lppnx, which may be the driving factor in the choice of which X chromosome will be inactivated in the developing female mouse embryo. Comparing weak and strong Xce alleles we show that Lppnx modulates the expression of Xist lncRNA, one of the key factors in XCI, by controlling the occupancy of pluripotency factors at Intron1 of Xist. This effect is counteracted by enhanced binding of Rex1 in DxPas34, another key element in XCI regulating the activity of Tsix lncRNA, the main antagonist of Xist, in the strong but not in the weak Xce allele. These results suggest that the different susceptibility for XCI observed in weak and strong Xce alleles results from differential transcription factor binding of Xist Intron 1 and DxPas34, and that Lppnx represents a decisive factor in explaining the action of the Xce

IL-6-Mediated Activation of Stat3α Prevents Trauma/Hemorrhagic Shock-Induced Liver Inflammation

Trauma complicated by hemorrhagic shock (T/HS) is the leading cause of morbidity and mortality in the United States for individuals under the age of 44 years. Initial survivors are susceptible to developing multiple organ failure (MOF), which is thought to be caused, at least in part, by excessive or maladaptive activation of inflammatory pathways. We previously demonstrated in rodents that T/HS results in liver injury that can be prevented by IL-6 administration at the start of resuscitation; however, the contribution of the severity of HS to the extent of liver injury, whether or not resuscitation is required, and the mechanism(s) for the IL-6 protective effect have not been reported. In the experiments described here, we demonstrated that the extent of liver inflammation induced by T/HS depends on the duration of hypotension and requires resuscitation. We established that IL-6 administration at the start of resuscitation is capable of completely reversing liver inflammation and is associated with increased Stat3 activation. Global assessment of the livers showed that the main effect of IL-6 was to normalize the T/HS-induced inflammation transcriptome. Pharmacological inhibition of Stat3 activity within the liver blocked the ability of IL-6 to prevent liver inflammation and to normalize the T/HS-induced liver inflammation transcriptome. Genetic deletion of a Stat3β, a naturally occurring, dominant-negative isoform of the Stat3, attenuated T/HS-induced liver inflammation, confirming a role for Stat3, especially Stat3α, in preventing T/HS-mediated liver inflammation. Thus, T/HS-induced liver inflammation depends on the duration of hypotension and requires resuscitation; IL-6 administration at the start of resuscitation reverses T/HS-induced liver inflammation, through activation of Stat3α, which normalized the T/HS-induced liver inflammation transcriptome

Quantifying the improvement of surrogate indices of hepatic insulin resistance using complex measurement techniques

We evaluated the ability of simple and complex surrogate-indices to identify individuals from an overweight/obese cohort with hepatic insulin-resistance (HEP-IR). Five indices, one previously defined and four newly generated through step-wise linear regression, were created against a single-cohort sample of 77 extensively characterised participants with the metabolic syndrome (age 55.6±1.0 years, BMI 31.5±0.4 kg/m2; 30 males). HEP-IR was defined by measuring endogenous-glucose-production (EGP) with [6–62H2] glucose during fasting and euglycemic-hyperinsulinemic clamps and expressed as EGP*fasting plasma insulin. Complex measures were incorporated into the model, including various non-standard biomarkers and the measurement of body-fat distribution and liver-fat, to further improve the predictive capability of the index. Validation was performed against a data set of the same subjects after an isoenergetic dietary intervention (4 arms, diets varying in protein and fiber content versus control). All five indices produced comparable prediction of HEP-IR, explaining 39–56% of the variance, depending on regression variable combination. The validation of the regression equations showed little variation between the different proposed indices (r2 = 27–32%) on a matched dataset. New complex indices encompassing advanced measurement techniques offered an improved correlation (r = 0.75, P<0.001). However, when validated against the alternative dataset all indices performed comparably with the standard homeostasis model assessment for insulin resistance (HOMA-IR) (r = 0.54, P<0.001). Thus, simple estimates of HEP-IR performed comparable to more complex indices and could be an efficient and cost effective approach in large epidemiological investigations

Genome sequences of Human Adenovirus 14 isolates from mild respiratory cases and a fatal pneumonia, isolated during 2006-2007 epidemics in North America

<p>Abstract</p> <p>Background</p> <p>Human adenovirus 14 (HAdV-14) is a recognized causative agent of epidemic febrile respiratory illness (FRI). Last reported in Eurasia in 1963, this virus has since been conspicuously absent in broad surveys, and was never isolated in North America despite inclusion of specific tests for this serotype in surveillance methods. In 2006 and 2007, this virus suddenly emerged in North America, causing high attack rate epidemics of FRI and, in some cases, severe pneumonias and occasional fatalities. Some outbreaks have been relatively mild, with low rates of progression beyond uncomplicated FRI, while other outbreaks have involved high rates of more serious outcomes.</p> <p>Methodology and Findings</p> <p>In this paper we present the complete genomic sequence of this emerging pathogen, and compare genomic sequences of isolates from both mild and severe outbreaks. We also compare the genome sequences of the recent isolates with those of the prototype HAdV-14 that circulated in Eurasia 30 years ago and the closely related sequence of HAdV-11a, which has been circulating in southeast Asia.</p> <p>Conclusions</p> <p>The data suggest that the currently circulating strain of HAdV-14 is closely related to the historically recognized prototype throughout its genome, though it does display a couple of potentially functional mutations in the fiber knob and E1A genes. There are no polymorphisms that suggest an obvious explanation for the divergence in severity between outbreak events, suggesting that differences in outcome are more likely environmental or host determined rather than viral genetics.</p