bluuebunny/crossref_metadata_2025_split huggingface dataset:
The repeated bout effect can occur without mechanical and neuromuscular changes after a bout of eccentric exercise
Authors: Pincheira P. A. , Hoffman B. W. , Cresswell A. G. , Carroll T. J. , Brown N. A. T. , Lichtwark G. A. 
Published: May 2018

Changes in muscle fascicle mechanics have been postulated to underpin the repeated bout effect (RBE) observed following exercise‐induced muscle damage (EIMD). However, in the medial gastrocnemius (MG), mixed evidence exists on whether fascicle stretch amplitude influences the level of EIMD, thus questioning whether changes in fascicle mechanics underpin the RBE. An alternative hypothesis is that neural adaptations contribute to the RBE in this muscle. The aim of this study was to investigate the neuromechanical adaptations during and after repeated bouts of a highly controlled muscle lengthening exercise that aimed to maximize EIMD in MG. In all, 20 subjects performed two bouts of 500 active lengthening contractions (70% of maximal activation) of the triceps surae, separated by 7 days. Ultrasound constructed fascicle length‐torque (L‐T) curves of MG, surface electromyography (EMG), maximum torque production, and muscle soreness were assessed before, 2 hours and 2 days after each exercise bout. The drop in maximum torque (4%) and the increase in muscle soreness (24%) following the repeated bout were significantly less than following the initial bout (8% and 59%, respectively), indicating a RBE. However, neither shift in the L‐T curve nor changes in EMG parameters were present. Furthermore, muscle properties during the exercise were not related to the EIMD or RBE. Our results show that there are no global changes in gastrocnemius mechanical behavior or neural activation that could explain the observed RBE in this muscle. We suggest that adaptations in the non‐contractile elements of the muscle are likely to explain the RBE in the triceps surae.
Effect of high‐intensity resistance circuit‐based training in hypoxia on aerobic performance and repeat sprint ability
Authors: Ramos‐Campo D. J. , Martínez‐Guardado I. , Olcina G. , Marín‐Pagán C. , Martínez‐Noguera F. J. , Carlos‐Vivas J. , Alcaraz P. E. , Rubio J. Á. 
Published: May 2018

AbstractRecent acute studies have shown that high‐intensity resistance circuit‐based (HRC) training in hypoxia increases metabolic stress. However, no intervention studies have yet proven their effectiveness. This study aimed to analyze the effect of 8 weeks of HRC in hypoxia on aerobic performance, resting energy expenditure (REE), repeat sprint ability (RSA) and hematological variables. Twenty‐eight subjects were assigned to hypoxia (FiO2 = 15%; HRChyp: n = 15; age: 24.6 ± 6.8 years; height: 177.4 ± 5.9 cm; weight: 74.9 ± 11.5 kg) and normoxia (FiO2 = 20.9%; HRCnorm: n = 13; age: 23.2 ± 5.2 years; height: 173.4 ± 6.2 cm; weight: 69.4 ± 7.4 kg) groups. Each training session consisted of two blocks of three exercises (Block 1: bench press, leg extension, front pull down; 2: deadlift, elbow flexion, ankle extension). Each exercise was performed at 6 repetitions maximum. Participants exercised twice weekly for 8 weeks and before and after the training program blood test, REE, RSA and treadmill running test were performed. Fatigue index in the RSA test was significantly decreased in the HRChyp (−0.9%; P < .01; ES = 2.75) but not in the HRCnorm. No changes were observed in REE and hematological variables. Absolute (4.5%; P = .014; ES = 0.42) and relative (5.2%; P = .008; ES = 0.43) maximal oxygen uptake (VO2max), speed at VO2max (4%; P = .010; ES = 0.25) and time to exhaustion (4.1%; P = .012; ES = 0.26) were significantly increased in HRChyp but not in the HRCnorm. No significant differences between groups were found. Compared with normoxic conditions, 8 weeks of HRC training under hypoxic conditions efficiently improves aerobic performance and RSA without changes in REE and red blood O2‐carrying capacity.
Detection of hydroquinone by Raman spectroscopy in patients with melasma before and after treatment
Authors: Cabrera‐Alonso R. , Guevara E. , Ramírez‐Elías M. G. , Moncada B. , González F. J. 
Published: May 2018

AbstractBackgroundMelasma is an acquired, facial hyperpigmentation without a specific origin. It is regularly associated with multiple etiologic factors such as pregnancy, genetic, racial, and from estrogen administration. Among the methods to treat skin hyperpigmentation a series of skin bleaching agents have been used. At present, the most commonly used agent is known as hydroquinone. Nowadays, it is known that hydroquinone can cause cancer in animals with unknown relevance to humans.Material and MethodsIn this work, Raman spectroscopy was used to observe the presence of hydroquinone in the skin of 18 patients who have been under treatment for melasma.ResultsA significant increase in the Raman signal was observed in the six bands associated with hydroquinone after melasma treatment.ConclusionThe authors believe that monitoring the presence of hydroquinone may be useful for an optimal personalized treatment of melasma and to provide the specialist a support tool to control the administration of this type of bleaching agents.
Split‐axilla comparison study of 0.5‐MHz, invasive, bipolar radiofrequency treatment using insulated microneedle electrodes for primary axillary hyperhidrosis
Authors: Cho S. B. , Park J. , Zheng Z. , Yoo K. H. , Kim H. 
Published: May 2018

AbstractBackgroundEnergy‐delivering devices can be used to induce thermal coagulation of the eccrine sweat glands for treating primary axillary hyperhidrosis (PAH).ObjectiveThe objective of this study was to compare the efficacy and safety of invasive, bipolar radiofrequency (RF) treatment for PAH.MethodsA split‐axilla study was performed to compare the clinical outcomes of 0.5 MHz, invasive, bipolar RF treatment with treatment settings of a longer conduction time and lower power (LC/LP) vs a shorter conduction time and higher power (SC/HP) for treating PAH.ResultsThe in vivo study revealed median hyperhidrosis disease severity scale scores of 1.5 (interquartile range [IQR], 1‐2) at 1 month and 1 (IQR, 1‐2) at 3 months after treatment with the LC/LP setting, compared to baseline. Meanwhile, the other side of the axillae treated with the SC/HP setting showed scores of 2 (IQR, 2‐2) at 1 month and 2 (IQR, 1.25‐2) at 3 months. Analysis via a linear mixed model revealed a significant interaction (group, P = .011; time, P < .001; and group × time, P = .048) between treatment group and time.ConclusionPAH can be effectively and safely treated with invasive, multilayered, multiple‐pass, 0.5‐MHz, bipolar RF treatment, particularly with LC/LP.
CTNNAL1 inhibits ozone‐induced epithelial–mesenchymal transition in human bronchial epithelial cells
Authors: Tan Meiling , Liu Caixia , Huang Wenjie , Deng Linhong , Qin Xiaoqun , Xiang Yang 
Published: May 2018

New Findings
What is the central question of this study?
What is the effect of catenin alpha‐like 1 (CTNNAL1), an asthma‐related epithelial adhesion molecule that plays a vital role in airway epithelial wound repair, on airway epithelial–mesenchymal transition?

What is the main finding and its importance?
CTNNAL1 inhibits ozone‐induced airway epithelial–mesenchymal transition features, mediated by repressing the expression of Twist1 mRNA and reducing TGF‐β1 levels. These findings contribute to our understanding of the pathology of airway EMT and may indicate a possible therapeutic target for airway remodelling in bronchial asthma.

AbstractEpithelial–mesenchymal transition (EMT), a crucial event occurring during epithelial and mesenchymal repair, was reported to be a possible mechanism for airway remodelling. Our previous work showed that the expression of catenin alpha‐like 1 (CTNNAL1) was down‐regulated in the bronchial epithelial cells of asthmatic models and played a vital role in airway epithelial wound repair. The aim of this study was to investigate the effect of CTNNAL1 on airway EMT. Overexpression or silencing of CTNNAL1 in human bronchial epithelial cells was induced by stable transfection. CTNNAL1 was silenced in primary mouse airway epithelial cells with an effective siRNA vector. Cells were stressed by ozone for 4 days at 30 min day−1 to induce EMT. EMT features, changes in the function of co‐cultured lung fibroblasts, changes in the expression of the transcriptional repressors Snail/Slug and Twist1/Twist2 and changes in the secretion of transforming growth factor β1 (TGF‐β1) were assayed in different cell lines with or without ozone exposure. Both ozone exposure and silencing of CTNNAL1 induced EMT features in airway epithelial cells. Functional changes in lung fibroblasts increased after co‐culture with (ozone‐stressed) CTNNAL1‐silenced cells. Snail and Twist1 expression increased, and the level of TGF‐β1 was enhanced. Conversely, CTNNAL1 overexpression reversed EMT features, repressed mRNA levels of Twist1 and reduced the secretion of TGF‐β1, both alone and in combination with ozone exposure. Our results indicate that ozone exposure induces airway EMT and that CTNNAL1 inhibits ozone‐induced airway EMT. CTNNAL1 may play a role in airway EMT by repressing the expression of Twist1 mRNA and reducing the level of TGF‐β1.
Attenuated nitric oxide bioavailability in systemic sclerosis: Evidence from the novel assessment of passive leg movement
Authors: Clifton Heather L. , Machin Daniel R. , Groot H. Jonathan , Frech Tracy M. , Donato Anthony J. , Richardson Russell S. , Wray D. Walter 
Published: May 2018

New Findings
What is the central question of this study?
Do systemic sclerosis patients exhibit impaired nitric oxide‐mediated vascular function of the lower limb and are these decrements correlated with plasma biomarkers for inflammation and oxidative stress?

What is the main finding and its importance?
Findings indicate impaired nitric oxide‐mediated vascular function, linked to the incidence of digital ulcers and a milieu of inflammation and oxidative stress. However, the absence of significant correlations between individual biomarkers and blood flow responses suggests that the vasculopathy observed in systemic sclerosis may not be solely the result of derangements in the redox balance or inflammatory signalling.

AbstractSystemic sclerosis (SSc) is an autoimmune disease characterized by vasculopathy, which may be the consequence of inflammation and oxidative stress that ultimately leads to a reduced nitric oxide (NO) bioavailability. Passive leg movement (PLM) is a novel methodology for assessing lower limb vascular function that is predominantly NO dependent. We combined this vascular assessment with a comprehensive panel of plasma biomarkers to assess the axis of inflammation, oxidative stress and NO in SSc patients (n = 12; 62 ± 11 years of age) compared with healthy control subjects (n = 17; 60 ± 16 years of age). The PLM‐induced changes in leg blood flow (LBF; 191 ± 104 versus 327 ± 217 ml min−1) and LBF area under the curve (39 ± 104 versus 125 ± 131 ml) were reduced in SSc compared with control subjects. Stratification of patients according to history of digital ulcer (DU) formation revealed a further reduction in LBF area under the curve in DU (−13 ± 83 ml) versus non‐DU (91 ± 102 ml) patients. Biomarkers of inflammation (C‐reactive protein) and oxidative stress (malondialdehyde and protein carbonyl) were all elevated in SSc (C‐reactive protein, 3299 ± 2372 versus 984 ± 565 ng ml−1; malondialdehyde, 3.2 ± 1.1 versus 1.1 ± 0.7 μm; and protein carbonyl, 0.15 ± 0.05 versus 0.12 ± 0.03 nmol mg−1), and C‐reactive protein was further elevated in patients with a history of DU (4551 ± 2752 versus 2047 ± 1019 ng ml−1) compared with non‐DU, although these were not individually correlated with changes in LBF. These findings of impaired NO‐mediated vascular function, linked to DU and a milieu of inflammation and oxidative stress, suggest that redox balance plays an important, but not necessarily deterministic, role in the vascular pathophysiology of SSc.
Neopterin/7,8‐dihydroneopterin is elevated in Duchenne muscular dystrophy patients and protects mdx skeletal muscle function
Authors: Lindsay Angus , Schmiechen Alexandra , Chamberlain Christopher M. , Ervasti James M. , Lowe Dawn A. 
Published: May 2018

New Findings
What is the central question of this study?
We examined whether the macrophage‐synthesized antioxidant 7,8‐dihydroneopterin was elevated in Duchenne muscular dystrophy (DMD) patients. We then examined whether 7,8‐dihydroneopterin could protect dystrophic skeletal mouse muscle from eccentric contraction‐induced force loss and improve recovery.

What is the main finding and its importance?
Urinary neopterin/creatinine and 7,8‐dihydroneopterin/creatinine were elevated in DMD patients. 7,8‐Dihydroneopterin attenuated eccentric contraction‐induced force loss of dystrophic skeletal mouse muscle and accelerated recovery of force. These results suggest that eccentric contraction‐induced force loss is mediated, in part, by an oxidative component and provides a potential protective role for 7,8‐dihydroneopterin in DMD.

AbstractMacrophage infiltration is a hallmark of dystrophin‐deficient muscle. We tested the hypothesis that Duchenne muscular dystrophy (DMD) patients would have elevated levels of the macrophage‐synthesized pterins, neopterin and 7,8‐dihydroneopterin, compared with unaffected age‐matched control subjects. Urinary neopterin/creatinine and 7,8‐dihydroneopterin/creatinine were elevated in DMD patients, and 7,8‐dihydroneopterin/creatinine was associated with patient age and ambulation. Urinary 7,8‐dihydroneopterin corrected for specific gravity was also elevated in DMD patients. Given that 7,8‐dihydroneopterin is an antioxidant, we then identified a potential role for 7,8‐dihydroneopterin in disease pathology. We assessed whether 7,8‐dihydroneopterin could: (i) protect against isometric force loss in wild‐type skeletal muscle exposed to various pro‐oxidants; and (ii) protect wild‐type and mdx muscle from eccentric contraction‐induced force loss, which has an oxidative component. Force loss was elicited in isolated extensor digitorum longus (EDL) muscles by 10 eccentric contractions, and recovery of force after the contractions was measured in the presence of exogenous 7,8‐dihydroneopterin. 7,8‐Dihydroneopterin attenuated isometric force loss by wild‐type EDL muscles when challenged by H2O2 and HOCl, but exacerbated force loss when challenged by SIN‐1 (NO•, O2•, ONOO−). 7,8‐Dihydroneopterin attenuated eccentric contraction‐induced force loss in mdx muscle. Isometric force production by EDL muscles of mdx mice also recovered to a greater degree after eccentric contractions in the presence of 7,8‐dihydroneopterin. The results corroborate macrophage activation in DMD patients, provide a potential protective role for 7,8‐dihydroneopterin in the susceptibility of dystrophic muscle to eccentric contractions and indicate that oxidative stress contributes to eccentric contraction‐induced force loss in mdx skeletal muscle.
Draft Genome Sequence of Rhizobium sophoriradicis H4, a Nitrogen-Fixing Bacterium Associated with the Leguminous Plant Phaseolus vulgaris on the Coast of Peru
Authors: Ormeño-Orrillo Ernesto , Aguilar-Cuba Yohana , Zúñiga-Dávila Doris 
Published: May 2018

ABSTRACT

The genome sequence of
Rhizobium sophoriradicis
H4, a nitrogen-fixing bacterium isolated from the common bean (
Phaseolus vulgaris
) in Peru, is reported here. The genome assembly revealed a 6.44-Mbp genome which was distributed into 95 contigs, with
N
50
and
L
50
values of 293 kbp and 9, respectively. The genome contained 6,312 coding sequence (CDS) genes and 52 RNA genes (49 tRNAs and 3 rRNAs).
Genome Sequence of PM2-Like Phage Cr39582, Induced from a Pseudoalteromonas sp. Isolated from the Gut of Ciona robusta
Authors: Leigh Brittany A. , Breitbart Mya , Oksanen Hanna M. , Bamford Dennis H. , Dishaw Larry J. 
Published: May 2018

ABSTRACT

Phage Cr39582 was induced by mitomycin C from
Pseudoalteromonas
sp. strain Cr6751, isolated from a marine invertebrate gut.
Pseudoalteromonas
phage Cr39582 has 85% pairwise nucleotide identity with phage PM2 but lacks sequence homology in the spike protein. This report supports previous bioinformatic identification of corticoviral sequences within aquatic bacterial genomes.
Complete Genome Sequences of Two Salmonella Viruses, VSe11 and VSe102 (Family
Myoviridae
, Subfamily
Ounavirinae
), with a Very High Degree of Similarity
Authors: Volozhantsev Nikolay V. , Denisenko Egor A. , Kislichkina Angelina A. , Myakinina Vera P. , Krasilnikova Valentina M. , Verevkin Vladimir V. , Kadnikova Lidiya A. , Maiskaya Nadezhda V. , Bogun Alexandr G. , Dyatlov Ivan A. 
Published: May 2018

ABSTRACT

Two lytic double-stranded DNA bacteriophages, VSe11 and VSe102, infecting broad-spectrum
Salmonella enterica
were isolated from the sewage of two different poultry farms. The phage genomes comprise 86,360 bp and 86,365 bp, respectively, with a G+C content of 39.0%, and both contain 129 putative coding sequences.
Draft Genome Sequence of the Plant Growth-Promoting Sphingobium sp. Strain AEW4, Isolated from the Rhizosphere of the Beachgrass Ammophila breviligulata
Authors: Wanees Abanoub E. , Zaslow Shari J. , Potter Savannah J. , Hsieh Brandon P. , Boss Brianna L. , Izquierdo Javier A. 
Published: May 2018

ABSTRACT

Sphingobium
sp. strain AEW4 is a novel isolate from rhizosphere soil attached to the root of the American beachgrass
Ammophila breviligulata
. The genomic sequence consisted of 4,678,518 bp and 4,428 protein-coding sequences. Here we report the draft genome sequence of this strain and some initial insights on its plant growth-promoting capabilities.
Single Passage of Human Metapneumovirus in LLC-MK2 Cells Does Not Affect Viral Protein-Coding Capacity
Authors: Loevenich Simon , Ianevski Aleksandr , Oitmaa Eneli , Kainov Denis E. , Anthonsen Marit W. 
Published: May 2018

ABSTRACT
Here, we report the complete genome sequences of human metapneumovirus (HMPV) prior to and after passaging in LLC-MK2 cells. Paired comparisons of the 13,335-nucleotide genomes revealed that the virus acquired the T10736C transition in its genome, which did not affect the amino acid sequences of HMPV proteins.
Draft Genome Sequence of Carbapenem-Resistant Klebsiella pneumoniae XPY20 Collected from a Bloodstream Infection Patient
Authors: Chen Qiong , Zhou Jia-wei , Wu Sheng-hai , Meng Xiao-hua , Yu Dao-jun , Wang Xian-jun 
Published: May 2018

ABSTRACT

Bloodstream infections caused by carbapenem-resistant
Klebsiella pneumoniae
(CRKP) strains have been a severe problem with high clinical costs and high mortality rates. The
bla
KPC-2
-producing CRKP strain XPY20 was collected from the blood of a patient. The genome characteristics and antimicrobial resistance mechanisms were determined using next-generation sequencing.
Complete Genome Sequence of Buffalopox Virus
Authors: Afrough Babak , Zafar Afia , Hasan Rumina , Hewson Roger 
Published: May 2018

ABSTRACT

The first complete genome assembly of buffalopox virus isolate Karachi 2005, with a length of 195,630 bp, is presented here. Phylogenetic analysis shows the virus to cluster within
Vaccinia
species, and the genome contains 177 protein-coding sequences.
Defining the Role of Stress Granules in Innate Immune Suppression by the Herpes Simplex Virus 1 Endoribonuclease VHS
Authors: Burgess Hannah M. , Mohr Ian 
Published: May 2018

ABSTRACT
In response to virus-induced shutoff host protein synthesis, dynamic aggregates containing mRNA, RNA-binding proteins and translation factors termed stress granules (SGs) often accumulate within the cytoplasm. SGs typically form following phosphorylation and inactivation of the eukaryotic translation initiation factor 2α (eIF2α), a substrate of the double-stranded RNA (dsRNA)-activated kinase protein kinase R (PKR). The detection of innate immune sensors and effectors like PKR at SGs suggests a role in pathogen nucleic acid sensing. However, the functional importance of SGs in host innate responses is unclear and has primarily been examined in response to infection with select RNA viruses. During infection with the DNA virus herpes simplex virus 1 (HSV-1), the virus-encoded virion host shutoff (VHS) endoribonuclease is required to restrict interferon production, PKR activation, and SG formation, although the relationship between these activities remains incompletely understood. Here, we show that in cells infected with a VHS-deficient HSV-1 (ΔVHS) dsRNA accumulated and localized to SGs. Surprisingly, formation of dsRNA and its concentration at SGs was not required for beta interferon mRNA induction, indicating that suppression of type I interferon induction by VHS does not stem from its control of dsRNA accumulation. Instead, STING signaling downstream of cGMP-AMP synthase (cGAS)-dependent DNA sensing is required for beta interferon induction. In contrast, significantly less PKR activation is observed when SG assembly is disrupted by ISRIB, an inhibitor of phosphorylated eIF2α-mediated translation repression, or depleting SG scaffolding proteins G3BP1 or TIA1. This demonstrates that PKR activation is intimately linked to SG formation and that SGs form important hubs to potentiate PKR activation during infection.

IMPORTANCE
Formation of cytoplasmic stress granules that are enriched for innate immune sensors and effectors is suppressed during many viral infections. It is unclear, however, to what extent this is a side effect of viral efforts to maintain protein synthesis or intentional disruption of a hub for innate immune sensing. In this study, we utilize a herpes simplex virus 1 mutant lacking the RNA nuclease VHS which upon infection induces SGs, PKR activation, and beta interferon to address this question. We show that dsRNA is localized to SGs and that SGs can function to promote PKR activation in the context of a DNA virus infection, but we find no evidence to support their importance for interferon induction during HSV-1 infection.
Financial disincentives? A three-armed randomised controlled trial of the effect of financial Incentives in Diabetic Eye Assessment by Screening (IDEAS) trial
Authors: Judah Gaby , Darzi Ara , Vlaev Ivo , Gunn Laura , King Derek , King Dominic , Valabhji Jonathan , Bicknell Colin 
Published: May 2018

ObjectiveConflicting evidence exists regarding the impact of financial incentives on encouraging attendance at medical screening appointments. The primary aim was to determine whether financial incentives increase attendance at diabetic eye screening in persistent non-attenders.Methods and analysisA three-armed randomised controlled trial was conducted in London in 2015. 1051 participants aged over 16 years, who had not attended eye screening appointments for 2 years or more, were randomised (1.4:1:1 randomisation ratio) to receive the usual invitation letter (control), an offer of £10 cash for attending screening (fixed incentive) or a 1 in 100 chance of winning £1000 (lottery incentive) if they attend. The primary outcome was the proportion of invitees attending screening, and a comparative analysis was performed to assess group differences. Pairwise comparisons of attendance rates were performed, using a conservative Bonferroni correction for independent comparisons.Results34/435 (7.8%) of control, 17/312 (5.5%) of fixed incentive and 10/304 (3.3%) of lottery incentive groups attended. Participants who received any incentive were significantly less likely to attend their appointment compared with controls (risk ratio (RR)=0.56; 95% CI 0.34 to 0.92). Those in the probabilistic incentive group (RR=0.42; 95% CI 0.18 to 0.98), but not the fixed incentive group (RR=1.66; 95% CI 0.65 to 4.21), were significantly less likely to attend than those in the control group.ConclusionFinancial incentives, particularly lottery-based incentives, attract fewer patients to diabetic eye screening than standard invites in this population. Financial incentives should not be used to promote screening unless tested in context, as they may negatively affect attendance rates.