bluuebunny/crossref_metadata_2025_split huggingface dataset:
Recovery Kinetics After Speed-Endurance Training in Male Soccer Players
Authors: Tzatzakis Theofanis , Papanikolaou Konstantinos , Draganidis Dimitrios , Tsimeas Panagiotis , Kritikos Savvas , Poulios Athanasios , Laschou Vasiliki C. , Deli Chariklia K. , Chatzinikolaou Athanasios , Batrakoulis Alexios , Basdekis Georgios , Mohr Magni , Krustrup Peter , Jamurtas Athanasios Z. , Fatouros Ioannis G. 
Published: November 2019

Purpose: To determine the recovery kinetics of performance, muscle damage, and neuromuscular fatigue following 2 speed-endurance production training (SEPT) protocols in soccer. Methods: Ten well-trained, male soccer athletes randomly completed 3 trials: work-to-rest ratio (SEPT) 1:5, SEPT/1:8, and a control trial. Training load during SEPT was monitored using global positioning system and heart-rate monitors. Performance (isokinetic strength of knee extensors and flexors, speed, and countermovement jump) and muscle damage (delayed-onset muscle soreness [DOMS] and creatine kinase) were evaluated at baseline and at 0, 24, 48 and 72 h posttraining. Maximal voluntary contraction (fatigue index) of knee extensors and flexors was additionally assessed at 1, 2, and 3 h posttraining. Results: Fatigue increased (P < .05) in SEPT/1:5 (∼4–30%) for 3 h and in SEPT/1:8 (∼8–17%) for 2 h. Strength performance declined (P < .05) in both SEPT trials (∼5–20%) for 48 h. Speed decreased (∼4–18%; P < .05) for 72 h in SEPT/1:5 and for 48 h in SEPT/1:8. Countermovement-jump performance decreased (∼7–12%; P < .05) in both SEPT trials for 24 h. DOMS increased (P < .05) in SEPT/1:5 (∼2-fold) for 72 and in SEPT/1:8 (∼1- to 2-fold) for 48 h. Creatine kinase increased (∼1- to 2-fold, P < .05) in both SEPT trials for 72 h. Conclusions: SEPT induces short-term neuromuscular fatigue; provokes a prolonged deterioration of strength (48 h), speed (72 h), and jump performance (24 h); and is associated with a prolonged (72-h) rise of DOMS and creatine kinase. Time for recovery is reduced when longer work-to-rest ratios are applied. Fitness status may affect quality of SEPT and recovery kinetics.
Suppression of enteroendocrine cell glucagon-like peptide (GLP)-1 release by fat-induced small intestinal ketogenesis: a mechanism targeted by Roux-en-Y gastric bypass surgery but not by preoperative very-low-calorie diet
Authors: Wallenius Ville , Elias Erik , Elebring Erik , Haisma Bauke , Casselbrant Anna , Larraufie Pierre , Spak Emma , Reimann Frank , le Roux Carel W , Docherty Neil G , Gribble Fiona M , Fändriks Lars 
Published: November 2019

ObjectiveFood intake normally stimulates release of satiety and insulin-stimulating intestinal hormones, such as glucagon-like peptide (GLP)-1. This response is blunted in obese insulin resistant subjects, but is rapidly restored following Roux-en-Y gastric bypass (RYGB) surgery. We hypothesised this to be a result of the metabolic changes taking place in the small intestinal mucosa following the anatomical rearrangement after RYGB surgery, and aimed at identifying such mechanisms.DesignJejunal mucosa biopsies from patients undergoing RYGB surgery were retrieved before and after very-low calorie diet, at time of surgery and 6 months postoperatively. Samples were analysed by global protein expression analysis and Western blotting. Biological functionality of these findings was explored in mice and enteroendocrine cells (EECs) primary mouse jejunal cell cultures.ResultsThe most prominent change found after RYGB was decreased jejunal expression of the rate-limiting ketogenic enzyme mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase (mHMGCS), corroborated by decreased ketone body levels. In mice, prolonged high-fat feeding induced the expression of mHMGCS and functional ketogenesis in jejunum. The effect of ketone bodies on gut peptide secretion in EECs showed a ∼40% inhibition of GLP-1 release compared with baseline.ConclusionIntestinal ketogenesis is induced by high-fat diet and inhibited by RYGB surgery. In cell culture, ketone bodies inhibited GLP-1 release from EECs. Thus, we suggest that this may be a mechanism by which RYGB can remove the inhibitory effect of ketone bodies on EECs, thereby restituting the responsiveness of EECs resulting in increased meal-stimulated levels of GLP-1 after surgery.
Lepton flavor violation and collider searches in a type I + II seesaw model
Authors: Ferreira Manoel M. , de Melo Tessio B. , Kovalenko Sergey , Pinheiro Paulo R. D. , Queiroz Farinaldo S. 
Published: November 2019

AbstractNeutrinos are massless in the Standard Model. The most popular mechanism to generate neutrino masses are the type I and type II seesaw, where right-handed neutrinos and a scalar triplet are augmented to the Standard Model, respectively. In this work, we discuss a model where a type I + II seesaw mechanism naturally arises via spontaneous symmetry breaking of an enlarged gauge group. Lepton flavor violation is a common feature in such setup and for this reason, we compute the model contribution to the $$\mu \rightarrow e\gamma $$μ→eγ and $$\mu \rightarrow 3e$$μ→3e decays. Moreover, we explore the connection between the neutrino mass ordering and lepton flavor violation in perspective with the LHC, HL-LHC and HE-LHC sensitivities to the doubly charged scalar stemming from the Higgs triplet. Our results explicitly show the importance of searching for signs of lepton flavor violation in collider and muon decays. The conclusion about which probe yields stronger bounds depends strongly on the mass ordering adopted, the absolute neutrino masses and which much decay one considers. In the 1–5 TeV mass region of the doubly charged scalar, lepton flavor violation experiments and colliders offer orthogonal and complementary probes. Thus if a signal is observed in one of the two new physics searches, the other will be able to assess whether it stems from a seesaw framework.
Light Higgs bosons in the general NMSSM
Authors: Choi Kiwoon , Im Sang Hui , Jeong Kwang Sik , Park Chan Beom 
Published: November 2019

AbstractPhysics beyond the Standard Model (SM) may manifest itself as small deviations from the SM predictions for Higgs signal strengths at 125 GeV. Then, a plausible and interesting possibility is that the Higgs sector is extended and at the weak scale there appears an additional Higgs boson weakly coupled to the SM sector. Combined with the LEP excess in $$e^+e^-\rightarrow Z(h\rightarrow b\bar{b})$$e+e-→Z(h→bb¯), the diphoton excess around 96 GeV recently reported by CMS may suggest such a possibility. We examine if those LEP and CMS excesses can be explained simultaneously by a singlet-like Higgs boson in the general next-to-minimal supersymmetric Standard Model (NMSSM). Higgs mixing in the NMSSM relies on the singlet coupling to the MSSM Higgs doublets and the higgsino mass parameter, and thus is subject to the constraints on these supersymmetric parameters. We find that the NMSSM can account for both the LEP and CMS excesses at 96 GeV while accommodating the observed 125 GeV SM-like Higgs boson. Interestingly, the required mixing angles constrain the heavy doublet Higgs boson to be heavier than about 500 GeV. We also show that the viable region of mixing parameter space is considerably modified if the higgsino mass parameter is around the weak scale, mainly because of the Higgs coupling to photons induced by the charged higgsinos.
Spectrum of the $$uudc \bar{c}$$ hidden charm pentaquark with an SU(4) flavor-spin hyperfine interaction
Authors: Stancu Fl. 
Published: November 2019

AbstractWe study a few of the lowest states of the pentaquark $$uudc\overline{c}$$uudcc¯, of positive and negative parity, in a constituent quark model with an SU(4) flavor-spin hyperfine interaction. For positive parity we introduce space wave functions of appropriate permutation symmetry with one unit of orbital angular momentum in the internal motion of the four-quark subsystem or an orbital excitation between the antiquark and the four quark subsystem which remains in the ground state. We show that the lowest positive parity states $$1/2^+, 3/2^+$$1/2+,3/2+ are provided by the first alternative and are located below the $$1/2^-$$1/2- and the $$1/2^+$$1/2+ states with all quarks in the ground state. We compare our results with the LHCb three narrow pentaquark structures reported in 2019.
Accretion disk around the rotating Damour–Solodukhin wormhole
Authors: Karimov R. Kh. , Izmailov R. N. , Nandi K. K. 
Published: November 2019

AbstractA new rotating generalization of the Damour–Solodukhin wormhole (RDSWH), called Kerr-like wormhole, has recently been proposed and investigated by Bueno et al. for echoes in the gravitational wave signal. We show a novel feature of the RDSWH, viz., that the kinematic properties such as the ISCO or marginally stable radius $$r_{\mathrm{ms}}$$rms, efficiency $$\epsilon $$ϵ and the disk potential $$V_{\mathrm{eff}}$$Veff are independent of $$\lambda $$λ (which means they are identical to their KBH counterparts for any given spin). Differences however appear in the emissivity properties for higher values $$0.1<\lambda \le 1$$0.1<λ≤1 (say) and for the extreme spin $$a_{\star }=0.998$$a⋆=0.998. The kinematic and emissivity are generic properties as variations of the wormhole mass and the rate of accretion within the model preserve these properties. Specifically, the behavior of the luminosity peak is quite opposite to each other for the two objects, which could be useful from the viewpoint of observations. Apart from this, an estimate of the difference $$\varDelta _{\lambda }$$Δλ in the maxima of flux of radiation F(r) shows non-zero values but is too tiny to be observable at present for $$\lambda < 10^{-3}$$λ<10-3 permitted by the strong lensing bound. The broad conclusion is that RDSWH are experimentally indistinguishable from KBH by accretion characteristics.
GraVF-M
Authors: Engelhardt Nina , So Hayden K.-H. 
Published: November 2019

Due to the irregular nature of connections in most graph datasets, partitioning graph analysis algorithms across multiple computational nodes that do not share a common memory inevitably leads to large amounts of interconnect traffic. Previous research has shown that FPGAs can outcompete software-based graph processing in shared memory contexts, but it remains an open question if this advantage can be maintained in distributed systems.
In this work, we present GraVF-M, a framework designed to ease the implementation of FPGA-based graph processing accelerators for multi-FPGA platforms with distributed memory. Based on a lightweight description of the algorithm kernel, the framework automatically generates optimized RTL code for the whole multi-FPGA design. We exploit an aspect of the programming model to present a familiar message-passing paradigm to the user, while under the hood implementing a more efficient architecture that can reduce the necessary inter-FPGA network traffic by a factor equal to the average degree of the input graph. A performance model based on a theoretical analysis of the factors influencing performance serves to evaluate the efficiency of our implementation. With a throughput of up to 5.8GTEPS (billions of traversed edges per second) on a 4-FPGA system, the designs generated by GraVF-M compare favorably to state-of-the-art frameworks from the literature and reach 94% of the projected performance limit of the system.
Getting high school, college students interested in CS
Authors: Guzdial Mark , Hill Robin K. 
Published: November 2019

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Mark Guzdial considers how few U.S. high school students take computer science, while Robin K. Hill shares what she's learned in teaching first-year college computing students.
Right-to-left shunts in lowlanders with COPD traveling to altitude: a randomized controlled trial with dexamethasone
Authors: Lichtblau Mona , Furian Michael , Aeschbacher Sayaka S. , Bisang Maya , Sheraliev Ulan , Mademilov Maamed , Marazhapov Nuriddin H. , Ulrich Stefanie , Sooronbaev Talant , Bloch Konrad E. , Ulrich Silvia 
Published: November 2019

Right-to-left shunts (RLS) are prevalent in patients with chronic obstructive pulmonary disease (COPD) and might exaggerate oxygen desaturation, especially at altitude. The aim of this study was to describe the prevalence of RLS in patients with COPD traveling to altitude and the effect of preventive dexamethasone. Lowlanders with COPD [Global Initiative for Chronic Obstructive Lung Disease (GOLD) grades 1–2, oxygen saturation assessed by pulse oximetry ([Formula: see text]) >92%] were randomized to dexamethasone (4 mg bid) or placebo starting 24 h before ascent from 760 m and while staying at 3,100 m for 48 h. Saline-contrast echocardiography was performed at 760 m and after the first night at altitude. Of 87 patients (81 men, 6 women; mean ± SD age 57 ± 9 yr, forced expiratory volume in 1 s 89 ± 22% pred, [Formula: see text] 95 ± 2%), 39 were assigned to placebo and 48 to dexamethasone. In the placebo group, 19 patients (49%) had RLS, of which 13 were intracardiac. In the dexamethasone group 23 patients (48%) had RLS, of which 11 were intracardiac ( P = 1.0 vs. dexamethasone). Eleven patients receiving placebo and 13 receiving dexamethasone developed new RLS at altitude ( P = 0.011 for both changes, P = 0.411 between groups). RLS prevalence at 3,100 m was 30 (77%) in the placebo and 36 (75%) in the dexamethasone group ( P = not significant). Development of RLS at altitude could be predicted at lowland by a higher resting pulmonary artery pressure, a lower arterial partial pressure of oxygen, and a greater oxygen desaturation during exercise but not by treatment allocation. Almost half of lowlanders with COPD revealed RLS near sea level, and this proportion significantly increased to about three-fourths when traveling to 3,100 m irrespective of dexamethasone prophylaxis. NEW & NOTEWORTHY The prevalence of intracardiac and intrapulmonary right-to-left shunts (RLS) at altitude in patients with chronic obstructive pulmonary disease (COPD) has not been studied so far. In a large cohort of patients with moderate COPD, our randomized trial showed that the prevalence of RLS increased from 48% at 760 m to 75% at 3,100 m in patients taking placebo. Preventive treatment with dexamethasone did not significantly reduce the altitude-induced recruitment of RLS. Development of RLS at 3,100 m could be predicted at 760 m by a higher resting pulmonary artery pressure and arterial partial pressure of oxygen and a more pronounced oxygen desaturation during exercise. Dexamethasone did not modify the RLS prevalence at 3,100 m.
Peripheral microvascular serotoninergic signaling is dysregulated in young adults with major depressive disorder
Authors: Greaney Jody L. , Dillon Gabrielle A. , Saunders Erika F. H. , Alexander Lacy M. 
Published: November 2019

Dysfunction of the brain serotonergic system is implicated in the pathogenesis of major depressive disorder (MDD). Serotonin is also a vasoactive signaling molecule, the effects of which are modulated by both nitric oxide (NO) and the serotonin transporter [the primary target of selective serotonin reuptake inhibitors (SSRIs)]. Despite its role in the neurobiology of depression, serotoninergic signaling mechanisms in the microvasculature of adults with MDD are unknown. We hypothesized that 1) cutaneous microvascular responsiveness to serotonin would be attenuated in MDD and mediated by reductions in both 2) NO-dependent and 3) serotonin reuptake-dependent mechanisms. In 12 adults with MDD (nonmedicated) and 12 nondepressed adults, red cell flux (laser-Doppler flowmetry) was measured during graded intradermal microdialysis perfusion of 1) serotonin (10−10to 10−1mol/L) alone and in combination with a nonselective NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME; 15 mmol/L) and the SSRI paroxetine (10 μmol/L); and 2) paroxetine ( n = 6; 10−9to 10−2M) alone and in combination with l-NAME. Serotonin-induced vasodilation was preserved in MDD. The NO-dependent component of serotonin-induced vasodilation was not different between groups. Paroxetine augmented vasodilatory responsiveness to serotonin via NO-dependent mechanisms in both groups; however, the magnitude was blunted in MDD. The NO contribution to direct paroxetine-induced vasodilation was also reduced in adults with MDD. Collectively, these preliminary data suggest that cutaneous microvascular serotoninergic signaling is dysregulated in adults with MDD and mediated by NO-dependent and serotonin reuptake-dependent mechanisms, providing initial mechanistic insight to the purported vasculoprotective effect of chronic SSRI treatment.NEW & NOTEWORTHY Cutaneous microvascular vasodilatory responsiveness to serotonin was preserved in adults with major depressive disorder (MDD). However, the contribution of serotonin reuptake-dependent mechanisms to serotonin-induced dilation was reduced in MDD. Direct perfusion of the selective serotonin reuptake inhibitor (SSRI) paroxetine elicited vasodilation that is partially mediated by nitric oxide (NO)-dependent mechanisms, but these responses were blunted in MDD, reflective of a diminished contribution of NO to the direct effects of a SSRI on the cutaneous microvasculature.
Disparate kinetics of change in responses to electrical stimulation at the thoracic and lumbar level during fatiguing isometric knee extension
Authors: Brownstein Callum G. , Souron Robin , Royer Nicolas , Singh Benjamin , Lapole Thomas , Millet Guillaume Y. 
Published: November 2019

The present study compared the fatigue-induced change of matched-amplitude thoracic evoked potential (TMEP) and lumbar evoked potential (LEP) following electrical stimulation. Ten participants performed a 3 × 3 min isometric knee extension contraction separated by 4 min of recovery at the level of EMG required to produce 50% maximal voluntary contraction (MVC) force at baseline. The TMEP and LEP were evoked during the ongoing contraction at baseline and every minute into the fatiguing protocol and during recovery. Both responses were also assessed during a transcranial magnetic stimulation (TMS) evoked silent period to elicit a TMS-TMEP and TMS-LEP to assess responses without the confounding influence of descending drive. The results displayed disparate kinetics of the TMS-TMEP and TMS-LEP throughout the fatiguing protocol. The TMS-TMEP was reduced at all time points during exercise ( P < 0.001), whereas the TMS-LEP was reduced at 2 min into set 1 and 1 min into sets 2 and 3 ( P ≤ 0.04). TMS-LEPs were higher than the TMS-TMEPs at most time points ( P ≤ 0.04). No change was observed in the TMEP or LEP. When evoked during the silent period, the reduction in TMEP is greater than the LEP during fatiguing isometric exercise. The disparate kinetics of change suggest that differential mechanisms are responsible for evoked responses to thoracic and lumbar stimulation. More research is required to identify the mechanisms responsible for the TMEP and LEP before precise inferences can be made on what fatigue-induced changes in these variables reflect. NEW & NOTEWORTHY Assessing spinal excitability using lumbar stimulation when measuring responses in lower limbs has been suggested as an alternative method that could circumvent the issues associated with thoracic stimulation. The present study compared responses to the two types of stimuli throughout a fatiguing protocol and demonstrated that lumbar evoked responses differ substantially from thoracic responses when measured in the absence of voluntary drive. These findings suggest that different mechanisms are responsible for evoked responses to thoracic and lumbar stimuli.
Compartmental Analysis of T-cell Clonal Dynamics as a Function of Pathologic Response to Neoadjuvant PD-1 Blockade in Resectable Non–Small Cell Lung Cancer
Authors: Zhang Jiajia , Ji Zhicheng , Caushi Justina X. , El Asmar Margueritta , Anagnostou Valsamo , Cottrell Tricia R. , Chan Hok Yee , Suri Prerna , Guo Haidan , Merghoub Taha , Chaft Jamie E. , Reuss Joshua E. , Tam Ada J. , Blosser Richard L. , Abu-Akeel Mohsen , Sidhom John-William , Zhao Ni , Ha Jinny S. , Jones David R. , Marrone Kristen A. , Naidoo Jarushka , Gabrielson Edward , Taube Janis M. , Velculescu Victor E. , Brahmer Julie R. , Housseau Franck , Hellmann Matthew D. , Forde Patrick M. , Pardoll Drew M. , Ji Hongkai , Smith Kellie N. 
Published: November 2019

AbstractPurpose:Neoadjuvant PD-1 blockade is a promising treatment for resectable non–small cell lung cancer (NSCLC), yet immunologic mechanisms contributing to tumor regression and biomarkers of response are unknown. Using paired tumor/blood samples from a phase II clinical trial (NCT02259621), we explored whether the peripheral T-cell clonotypic dynamics can serve as a biomarker for response to neoadjuvant PD-1 blockade.Experimental Design:T-cell receptor (TCR) sequencing was performed on serial peripheral blood, tumor, and normal lung samples from resectable NSCLC patients treated with neoadjuvant PD-1 blockade. We explored the temporal dynamics of the T-cell repertoire in the peripheral and tumoral compartments in response to neoadjuvant PD-1 blockade by using the TCR as a molecular barcode.Results:Higher intratumoral TCR clonality was associated with reduced percent residual tumor at the time of surgery, and the TCR repertoire of tumors with major pathologic response (MPR; &lt;10% residual tumor after neoadjuvant therapy) had a higher clonality and greater sharing of tumor-infiltrating clonotypes with the peripheral blood relative to tumors without MPR. Additionally, the posttreatment tumor bed of patients with MPR was enriched with T-cell clones that had peripherally expanded between weeks 2 and 4 after anti–PD-1 initiation and the intratumoral space occupied by these clonotypes was inversely correlated with percent residual tumor.Conclusions:Our study suggests that exchange of T-cell clones between tumor and blood represents a key correlate of pathologic response to neoadjuvant immunotherapy and shows that the periphery may be a previously underappreciated originating compartment for effective antitumor immunity.See related commentary by Henick, p. 1205