bluuebunny/crossref_metadata_2025_split huggingface dataset:
Validity of Fitbit’s active minutes as compared with a research-grade accelerometer and self-reported measures
Authors: Brewer Wayne , Swanson Brian T , Ortiz Alexis 
Published: September 2017

ObjectivesThe main purpose of the study was to assess the validity between the Fitbit and ActiGraph GT3X+ accelerometer. The specific aims were to determine the: (1) concurrent validity between the various models of the Fitbit and the GTX3+ accelerometer as the criterion measure for: number of steps and active minutes averaged over a single-day and 7-day period; (2) validity of the two devices with the International Physical Activity Questionnaire (IPAQ) for the number of daily active minutes performed.MethodsFifty-three subjects wore a Fitbit and ActiGraph concurrently for 7 days. Data were analysed using correlation coefficients, t-tests to assess mean comparisons and Bland-Altman plots to determine agreement between the Fitbit and the ActiGraph.ResultsThe correlations between the Fitbit and ActiGraph for steps per day and per 7 days were r=0.862 and 0.820, respectively with significant mean differences between both devices. Bland-Altman analyses revealed agreement between the Fitbit and the ActiGraph for 7-day active minutes only. The correlations between the Fitbit and ActiGraph for active minutes per day and per 7 days were r=0.695 and r=0.658, respectively, with no significant mean differences between both devices. No significant correlations were found between the IPAQ and the other two devices.ConclusionsThe data produced by the Fitbit were consistent with the ActiGraph when the means of each device were compared over the 1-day and 7-day time periods. However, Bland-Altman analyses revealed that the Fitbit agreed with the ActiGraph when used to measure physical activity levels over a 7-day span only.
Vitamin D supplementation to palliative cancer patients: protocol of a double-blind, randomised controlled trial ‘Palliative-D’
Authors: Helde-Frankling Maria , Bergqvist Jenny , Klasson Caritha , Nordström Marie , Höijer Jonas , Bergman Peter , Björkhem-Bergman Linda 
Published: September 2017

BackgroundAccording to a small pilot study on palliative cancer patients at our ward, vitamin D supplementation had beneficial effects on pain (measured as opioid consumption), infections and quality of life (QoL) without having any significant side effects.ObjectiveThe primary objective of the ‘Palliative-D’ study is to test the hypothesis that vitamin D supplementation for 12 weeks reduces opioid consumption. The secondary objectives are to study if reduction of antibiotic consumption and fatigue as well as improvement in QoL assessments can be observed. Effect on the 25-hydroxy vitamin D (25-OHD) levels in serum after 12 weeks of treatment will be studied, as well as the change in opioid dose in relation to genetic polymorphism in genes involved in the effect and metabolism of vitamin D.MethodA randomised, double-blind placebo-controlled multicentre trial has been designed. The trial will include 254 adult palliative cancer patients with 25-OHD levels <50 nmol/L and a life expectancy of more than 3 months recruited from two advanced palliative home care centres in Stockholm. Included patients will be randomly assigned to 12 weeks of treatment with cholecalciferol (vitamin D3) 4000 IU/day or placebo. The study will start in November 2017 and will finish in December 2019. The study is approved by the Regional Ethical Committee, Dnr2017/405-31/1, by the Swedish Medical Products Agency, EudraCT: 2017-000268-14, and is registered at Clinicaltrial.gov:NCT03038516. The study is financed with research grants from the Swedish Cancer Society and the Stockholm County Council.
Diversity in spatial scope of contrast adaptation among mouse retinal ganglion cells
Authors: Khani Mohammad Hossein , Gollisch Tim 
Published: September 2017

Retinal ganglion cells adapt to changes in visual contrast by adjusting their response kinetics and sensitivity. While much work has focused on the time scales of these adaptation processes, less is known about the spatial scale of contrast adaptation. For example, do small, localized contrast changes affect a cell’s signal processing across its entire receptive field? Previous investigations have provided conflicting evidence, suggesting that contrast adaptation occurs either locally within subregions of a ganglion cell’s receptive field or globally over the receptive field in its entirety. Here, we investigated the spatial extent of contrast adaptation in ganglion cells of the isolated mouse retina through multielectrode-array recordings. We applied visual stimuli so that ganglion cell receptive fields contained regions where the average contrast level changed periodically as well as regions with constant average contrast level. This allowed us to analyze temporal stimulus integration and sensitivity separately for stimulus regions with and without contrast changes. We found that the spatial scope of contrast adaptation depends strongly on cell identity, with some ganglion cells displaying clear local adaptation, whereas others, in particular large transient ganglion cells, adapted globally to contrast changes. Thus, the spatial scope of contrast adaptation in mouse retinal ganglion cells appears to be cell-type specific. This could reflect differences in mechanisms of contrast adaptation and may contribute to the functional diversity of different ganglion cell types.NEW & NOTEWORTHY Understanding whether adaptation of a neuron in a sensory system can occur locally inside the receptive field or whether it always globally affects the entire receptive field is important for understanding how the neuron processes complex sensory stimuli. For mouse retinal ganglion cells, we here show that both local and global contrast adaptation exist and that this diversity in spatial scope can contribute to the functional diversity of retinal ganglion cell types.
Comparison of three models of saccade disconjugacy in strabismus
Authors: Walton Mark M. G. , Mustari Michael J. 
Published: September 2017

In pattern strabismus the horizontal and vertical misalignments vary with eye position along the orthogonal axis. The disorder is typically described in terms of overaction or underaction of oblique muscles. Recent behavioral studies in humans and monkeys, however, have reported that such actions are insufficient to fully explain the patterns of directional and amplitude disconjugacy of saccades. There is mounting evidence that the oculomotor abnormalities associated with strabismus are at least partially attributable to neurophysiological abnormalities. A number of control systems models have been developed to simulate the kinematic characteristics of saccades in normal primates. In the present study we sought to determine whether these models could simulate the abnormalities of saccades in strabismus by making two assumptions: 1) in strabismus the burst generator gains differ for the two eyes and 2) abnormal crosstalk exists between the horizontal and vertical saccadic circuits in the brain stem. We tested three models, distinguished by the location of the horizontal-vertical crosstalk. All three models were able to simulate amplitude and directional saccade disconjugacy, postsaccadic drift, and a pattern strabismus for static fixation, but they made different predictions about the dynamics of saccades. By assuming that crosstalk occurs at multiple nodes, the Distributed Crosstalk Model correctly predicted the dynamics of saccades. These new models make additional predictions that can be tested with future neurophysiological experiments.NEW & NOTEWORTHY Over the past several decades, numerous control systems models have been devised to simulate the known kinematic features of saccades in normal primates. These models have proven valuable to neurophysiology, as a means of generating testable predictions. The present manuscript, as far as we are aware, is the first to present control systems models to simulate the known abnormalities of saccades in strabismus.
CCR5-Dependent Homing of T Regulatory Cells to the Tumor Microenvironment Contributes to Skin Squamous Cell Carcinoma Development
Authors: de Oliveira Carine Ervolino , Gasparoto Thaís Helena , Pinheiro Claudia Ramos , Amôr Nádia Ghinelli , Nogueira Maria Renata Sales , Kaneno Ramon , Garlet Gustavo Pompermaier , Lara Vanessa Soares , Silva João Santana , Cavassani Karen Angélica , Campanelli Ana Paula 
Published: September 2017

Abstract
Squamous cell carcinoma (SCC) is one of the most common human cancers worldwide. Recent studies show that regulatory T cells (Treg) have a critical role in the modulation of an antitumor immune response, and consequently the SCC development. Because the accumulation of Tregs at the tumor site is, in part, due to selective recruitment through CCR5- and CCR5-associated chemokines, we investigated the role of CCR5 in the SCC development. Our findings showed that CCR5-deficient mice (CCR5KO) were efficient in controlling papilloma's incidence when compared with wild-type mice. Analysis of tumor lesions in wild-type (WT) and CCR5KO mice revealed that lack of CCR5 lead to significant reduction in frequency of Tregs and increased of CD4 T cells into the tumors. Moreover, the adoptive transfer of naturally occurring Tregs CD4+CD25+CCR5+, CD4+CD25−CCR5+ or CD8+CCR5+ conventional T cells to CCR5KO mice resulted in an increased papilloma incidence. Interestingly, adoptive transfer of WT CD4+CD25+CCR5+ cells to CCR5KO mice induced more undifferentiated SCC lesions, characterized by higher infiltration of macrophages and dendritic cells. In this study, we also demonstrated that Treg migration to the tumor microenvironment is mediated by CCR5, and these cells are promoting tumor growth via inhibition of antitumor cells such as cytotoxic CD8+ T cells. Our findings reinforce the therapeutic potential of CCR5 inhibition for cancer treatment, and indicate an attractive approach for SCC treatment. Mol Cancer Ther; 16(12); 2871–80. ©2017 AACR.
Superior Properties of Fc-comprising scTRAIL Fusion Proteins
Authors: Hutt Meike , Marquardt Lisa , Seifert Oliver , Siegemund Martin , Müller Ines , Kulms Dagmar , Pfizenmaier Klaus , Kontermann Roland E. 
Published: September 2017

Abstract
The TNF-related apoptosis-inducing ligand (TRAIL) has been considered as a promising molecule for cancer treatment. However, clinical studies with soluble TRAIL failed to show therapeutic activity, which resulted in subsequent development of more potent TRAIL-based therapeutics. In this study, we applied defined oligomerization and tumor targeting as strategies to further improve the activity of a single-chain version of TRAIL (scTRAIL). We compared three different formats of EGF receptor (EGFR)-targeting dimeric scTRAIL fusion proteins [Diabody (Db)-scTRAIL, scFv-IgE heavy chain domain 2 (EHD2)-scTRAIL, scFv-Fc-scTRAIL] as well as two nontargeted dimeric scTRAIL molecules (EHD2-scTRAIL, Fc-scTRAIL) to reveal the influence of targeting and protein format on antitumor activity. All EGFR-targeted dimeric scTRAIL molecules showed similar binding properties and comparable cell death induction in vitro, exceeding the activity of the respective nontargeted dimeric format and monomeric scTRAIL. Superior properties were observed for the Fc fusion proteins with respect to production and in vivo half-life. In vivo studies using a Colo205 xenograft model revealed potent antitumor activity of all EGFR-targeting formats and Fc-scTRAIL and furthermore highlighted the higher efficacy of fusion proteins comprising an Fc part. Despite enhanced in vitro cell death induction of targeted scTRAIL molecules, however, comparable antitumor activities were found for the EGFR-targeting scFv-Fc-scTRAIL and the nontargeting Fc-scTRAIL in vivo. Mol Cancer Ther; 16(12); 2792–802. ©2017 AACR.
Gene Methylation Biomarkers in Sputum and Plasma as Predictors for Lung Cancer Recurrence
Authors: Belinsky Steven A. , Leng Shuguang , Wu Guodong , Thomas Cynthia L. , Picchi Maria A. , Lee Sandra J. , Aisner Seena , Ramalingam Suresh , Khuri Fadlo R. , Karp Daniel D. 
Published: September 2017

Abstract
Detection of methylated genes in exfoliated cells from the lungs of smokers provides an assessment of the extent of field cancerization, is a validated biomarker for predicting lung cancer, and provides some discrimination when interrogated in blood. The potential utility of this 8-gene methylation panel for predicting tumor recurrence has not been assessed. The Eastern Cooperative Oncology Group initiated a prevention trial (ECOG-ACRIN5597) that enrolled resected stage I non–small cell lung cancer patients who were randomized 2:1 to receive selenized yeast versus placebo for 4 years. We conducted a correlative biomarker study to assess prevalence for methylation of the 8-gene panel in longitudinally collected sputum and blood after tumor resection to determine whether selenium alters their methylation profile and whether this panel predicts local and/or distant recurrence. Patients (N = 1,561) were enrolled into the prevention trial; 565 participated in the biomarker study with 122 recurrences among that group. Assessing the association between recurrence and risk of gene methylation longitudinally for up to 48 months showed a 1.4-fold increase in OR for methylation in sputum in the placebo group independent of location (local or distant). Kaplan–Meier curves evaluating the association between number of methylated genes and time to recurrence showed no increased risk in sputum, while a significant HR of 1.5 was seen in plasma. Methylation detection in sputum and blood is associated with risk for recurrence. Cancer Prev Res; 10(11); 635–40. ©2017 AACR.
Venous Stasis and Cerebrovascular Complications in Cerebral Venous Sinus Thrombosis
Authors: Sato Takeo , Terasawa Yuka , Mitsumura Hidetaka , Komatsu Teppei , Sakuta Kenichi , Sakai Kenichiro , Matsushima Satoshi , Iguchi Yasuyuki 
Published: September 2017

<b><i>Background/Aims:</i></b> The factors related to cerebrovascular complications in cerebral venous sinus thrombosis (CVST) are controversial. We focused on venous stasis and investigated its relationship with cerebrovascular complications in CVST. <b><i>Methods:</i></b> CVST patients between June 2013 and October 2016 were enrolled. Relationships between cerebrovascular complications, defined as cerebral venous infarction, intracerebral hemorrhage, or subarachnoid hemorrhage, and cerebrum venous stasis and other clinical information were retrospectively analyzed. Venous stasis was evaluated by the prominence of the veins on susceptibility-weighted imaging (SWI). The cerebrum was divided into 10 regions according to the venous drainage territories, and venous stasis was quantified by adding one point for venous prominence on SWI for each region (CVST SWI score). <b><i>Results:</i></b> All 5 cases in the noncomplicated group had a CVST SWI score of 0. The 3 patients with CVST SWI scores higher than 0 had cerebrovascular complications. The CVST SWI scores were higher in the complicated group than in the noncomplicated group (3.0 vs. 0, <i>p</i> = 0.010). Seizures were seen in all patients with complications and in none of the patients without complications (3 vs. 0, <i>p</i> = 0.018). <b><i>Conclusion:</i></b> Venous stasis evaluated by SWI can help predict cerebrovascular complications in CVST. A seizure is an important initial symptom that suggests cerebrovascular complications in CVST.
Ivabradine in Heart Failure
Authors: Das Debraj , Savarese Gianluigi , Dahlström Ulf , Fu Michael , Howlett Jonathan , Ezekowitz Justin A. , Lund Lars H. 
Published: September 2017

Background:
The sinus node inhibitor ivabradine was approved for patients with heart failure (HF) after the ivabradine and outcomes in chronic HF (SHIFT [Systolic Heart Failure Treatment With the IF Inhibitor Ivabradine Trial]) trial. Our objective was to characterize the proportion of patients with HF eligible for ivabradine and the representativeness of the SHIFT trial enrollees compared with those in the Swedish Heart Failure Registry.

Methods and Results:

We examined 26 404 patients with clinical HF from the Swedish Heart Failure Registry and divided them into SHIFT type (left ventricular ejection fraction <40%, New York Heart Association class II–IV, sinus rhythm, and heart rate ≥70 beats per minute) and non-SHIFT type. Baseline characteristics and medication use were compared and change in eligibility over time was reported at 6 months and 1 year in a subset of patients. Overall, 14.2% (n=3741) of patients were SHIFT type. These patients were more likely to be younger, men, have diabetes mellitus, ischemic heart disease, lower left ventricular ejection fraction, and more recent onset HF (<6 months; all,
P
<0.001). Although 88.9% of SHIFT type and 88.5% of non-SHIFT type (
P
=0.421) were receiving selected β-blockers, only 58.8% and 67.3% (
P
<0.001) were on >50% of target dose. From those patients who had repeated visits within 6 months (n=5420) and 1 year (n=6840), respectively, 10.2% (n=555) and 10.6% (n=724) of SHIFT-type patients became ineligible, 77.3% (n=4188) and 77.3% (n=5287) remained ineligible, and 4.6% (n=252) and 4.9% (n=335) of non-SHIFT–type patients became eligible for initiation of ivabradine.

Conclusions:
From the Swedish Heart Failure Registry, 14.2% of patients with HF were eligible for ivabradine. These patients more commonly were not receiving target β-blocker dose. Over time, a minority of patients became ineligible and an even smaller minority became eligible.
Association Between Living in Food Deserts and Cardiovascular Risk
Authors: Kelli Heval M. , Hammadah Muhammad , Ahmed Hina , Ko Yi-An , Topel Matthew , Samman-Tahhan Ayman , Awad Mossab , Patel Keyur , Mohammed Kareem , Sperling Laurence S. , Pemu Priscilla , Vaccarino Viola , Lewis Tene , Taylor Herman , Martin Greg , Gibbons Gary H. , Quyyumi Arshed A. 
Published: September 2017

Background—
Food deserts (FD), neighborhoods defined as low-income areas with low access to healthy food, are a public health concern. We evaluated the impact of living in FD on cardiovascular risk factors and subclinical cardiovascular disease (CVD) with the hypothesis that people living in FD will have an unfavorable CVD risk profile. We further assessed whether the impact of FD on these measures is driven by area income, individual household income, or area access to healthy food.

Methods and Results—

We studied 1421 subjects residing in the Atlanta metropolitan area who participated in the META-Health study (Morehouse and Emory Team up to Eliminate Health Disparities; n=712) and the Predictive Health study (n=709). Participants’ zip codes were entered into the United States Food Access Research Atlas for FD status. Demographic data, metabolic profiles, hs-CRP (high-sensitivity C-reactive protein) levels, oxidative stress markers (glutathione and cystine), and arterial stiffness were evaluated. Mean age was 49.4 years, 38.5% male and 36.6% black. Compared with those not living in FD, subjects living in FD (n=187, 13.2%) had a higher prevalence of hypertension and smoking, higher body mass index, fasting glucose, and 10-year risk for CVD. They also had higher hs-CRP (
P
=0.014), higher central augmentation index (
P
=0.015), and lower glutathione level (
P
=0.003), indicative of increased oxidative stress. Area income and individual income, rather than food access, were associated with CVD risk measures. In a multivariate analysis that included food access, area income and individual income, both low-income area and low individual household income, were independent predictors of a higher 10-year risk for CVD. Only low individual income was an independent predictor of higher hs-CRP and augmentation index.

Conclusions—
Although living in FD is associated with a higher burden of cardiovascular risk factors and preclinical indices of CVD, these associations are mainly driven by area income and individual income rather than access to healthy food.
Interactions Between the Corticospinal Tract and Premotor–Motor Pathways for Residual Motor Output After Stroke
Authors: Schulz Robert , Park Eunhee , Lee Jungsoo , Chang Won Hyuk , Lee Ahee , Kim Yun-Hee , Hummel Friedhelm C. 
Published: September 2017

Background and Purpose—
Brain imaging has continuously enhanced our understanding how different brain networks contribute to motor recovery after stroke. However, the present models are still incomplete and do not fit for every patient. The interaction between the degree of damage of the corticospinal tract (CST) and of corticocortical motor connections, that is, the influence of the microstructural state of one connection on the importance of another has been largely neglected.

Methods—
Applying diffusion–weighted imaging and probabilistic tractography, we investigated cross-network interactions between the integrity of ipsilesional CST and ipsilesional corticocortical motor pathways for variance in residual motor outcome in 53 patients with subacute stroke.

Results—
The main finding was a significant interaction between the CST and corticocortical connections between the primary motor and ventral premotor cortex in relation to residual motor output. More specifically, the data indicate that the microstructural state of the connection primary motor–ventral premotor cortex plays only a role in patients with significant damage to the CST. In patients with slightly affected CST, this connection did not explain a relevant amount of variance in motor outcome.

Conclusions—
The present data show that patients with stroke with different degree of CST disruption differ in their dependency on structural premotor–motor connections for residual motor output. This finding might have important implications for future research on recovery prediction models and on responses to treatment strategies.
Hemorrhagic Transformation After Large Cerebral Infarction in Rats Pretreated With Dabigatran or Warfarin
Authors: Kwon Il , An Sunho , Kim Jayoung , Yang Seung-Hee , Yoo Joonsang , Baek Jang-Hyun , Nam Hyo Suk , Kim Young Dae , Lee Hye Sun , Choi Hyun-Jung , Heo Ji Hoe 
Published: September 2017

Background and Purpose—
It is uncertain whether hemorrhagic transformation (HT) after large cerebral infarction is less frequent in dabigatran users than warfarin users. We compared the occurrence of HT after large cerebral infarction among rats pretreated with dabigatran, warfarin, or placebo.

Methods—
This was a triple-blind, randomized, and placebo-controlled experiment. After treatment with warfarin (0.2 mg/kg), dabigatran (20 mg/kg), or saline for 7 days, Wistar rats were subjected to transient middle cerebral artery occlusion. As the primary outcome, HT was determined by gradient-recalled echo imaging. For the secondary outcome, intracranial hemorrhage was assessed via gradient-recalled echo imaging in surviving rats and via autopsy for dead rats.

Results—

Of 62 rats, there were 33 deaths (53.2%, 17 technical reasons). Of the intention-to-treat population, 33 rats underwent brain imaging. HT was less frequent in the dabigatran group than the warfarin group (placebo 2/14 [14%], dabigatran 0/10 [0%], and warfarin 9/9 [100%]; dabigatran versus warfarin;
P
<0.001). In all 62 rats, compared with the placebo (2/14 [14.3%]), the incidence of intracranial hemorrhage was significantly higher in the warfarin group (19/29 [65.5%];
P
=0.003), but not in the dabigatran group (6/19 [31.6%];
P
=0.420). Mortality was significantly higher in the warfarin group than the dabigatran group (79.3% versus 47.4%;
P
=0.022), but not related to the hemorrhage frequency.

Conclusions—
The risk of HT after a large cerebral infarction was significantly increased in rats pretreated with warfarin than those with dabigatran. However, the results here may not have an exact clinical translation.