Miracle-dz/UniFAR-FTUs huggingface dataset:
The Physical Activity Tracker Testing in Youth (P.A.T.T.Y.) Study: Content Analysis and Children’s Perceptions

Background Activity trackers are widely used by adults and several models are now marketed for children. Objective The aims of this study were to (1) perform a content analysis of behavioral change techniques (BCTs) used by three commercially available youth-oriented activity trackers and (2) obtain feedback describing children’s perception of these devices and the associated websites. Methods A content analysis recorded the presence of 36 possible BCTs for the MovBand (MB), Sqord (SQ), and Zamzee (ZZ) activity trackers. In addition, 16 participants (mean age 8.6 years [SD 1.6]; 50% female [8/16]) received all three trackers and were oriented to the devices and websites. Participants were instructed to wear the trackers on 4 consecutive days and spend ≥10 min/day on each website. A cognitive interview and survey were administered when the participant returned the devices. Qualitative data analysis was used to analyze the content of the cognitive interviews. Chi-square analyses were used to determine differences in behavioral monitoring and social interaction features between websites. Results The MB, SQ, and ZZ devices or websites included 8, 15, and 14 of the possible 36 BCTs, respectively. All of the websites had a behavioral monitoring feature (charts for tracking activity), but the percentage of participants indicating that they “liked” those features varied by website (MB: 8/16, 50%; SQ: 6/16, 38%; ZZ: 11/16, 69%). Two websites (SQ and ZZ) included an “avatar” that the user could create to represent themselves on the website. Participants reported that they “liked” creating and changing their avatar (SQ: 12/16, 75%, ZZ: 15/16, 94%), which was supported by the qualitative analyses of the cognitive interviews. Most participants (75%) indicated that they would want to wear the devices more if their friends were wearing a tracker. No significant differences were observed between SQ and ZZ devices in regards to liking or use of social support interaction features (P=.21 to .37). Conclusions The websites contained several BCTs consistent with previously identified strategies. Children “liked” the social aspects of the websites more than the activity tracking features. Developers of commercial activity trackers for youth may benefit from considering a theoretical perspective during the website design process.
Mycoplasma pneumoniae J‐domain protein required for terminal organelle function

The cell wall‐less prokaryote Mycoplasma pneumoniae causes tracheobronchitis and primary atypical pneumonia in humans. Colonization of the respiratory epithelium requires proper assembly of a complex, multifunctional, polar terminal organelle. Loss of a predicted J‐domain protein also having domains unique to mycoplasma terminal organelle proteins (TopJ) resulted in a non‐motile, adherence‐deficient phenotype. J‐domain proteins typically stimulate ATPase activity of Hsp70 chaperones to bind nascent peptides for proper folding, translocation or macromolecular assembly, or to resolve stress‐induced protein aggregates. By Western immunoblotting all defined terminal organelle proteins examined except protein P24 remained at wild‐type levels in the topJ mutant; previous studies established that P24 is required for normal initiation of terminal organelle formation. Nevertheless, terminal organelle proteins P1, P30, HMW1 and P41 failed to localize to a cell pole, and when evaluated quantitatively, P30 and HMW1 foci were undetectable in >40% of cells. Complementation of the topJ mutant with the recombinant wild‐type topJ allele largely restored terminal organelle development, gliding motility and cytadherence. We propose that this J‐domain protein, which localizes to the base of the terminal organelle in wild‐type M. pneumoniae, functions in the late stages of assembly, positioning, or both, of nascent terminal organelles.
Nuclear Respiratory Factor-1 (NRF-1) Regulates Transcription of the CXC Receptor 4 (CXCR4) in the Rat Retina.

Purpose The CXC receptor 4 (CXCR4) is required for various physiologic and pathologic processes in the eye, including stem cell trafficking, neuronal development, immune responses, and ocular neovascularization. Here, we used the rat retina models to determine the mechanisms driving CXCR4 transcription. Methods The expression pattern of CXCR4 and nuclear respiratory factor-1 (NRF-1) were profiled in the rat retina during the course of development. Chromatin immunoprecipitation (CHiP) assay determined the transcriptional mechanism of CXCR4 in rat retina. A rat model of oxygen-induced retinopathy (OIR) that mimics retinal ischemia-reperfusion injury was established. Under either normoxic or hypoxic conditions, CXCR4 and NRF-1 expression in rat retinas was tracked by RT-PCR and Western analysis. Immunofluorescence staining localized CXCR4 and NRF-1. Results Both CXCR4 and NRF-1 were highly expressed in the neonatal rat retina, down-regulated in parallel, and silenced in fully developed retinas (1 month of age). ChIP assays revealed that NRF-1 was required for CXCR4 promoter activity in rat retinas. In the OIR rat model, retinal hypoxia induced up-regulation of CXCR4 and NRF-1 concurrently. Conclusions Our findings suggest that NRF-1 regulates the expression of CXCR4 in normal retinal development and in pathologic processes of retinal hypoxia and neovascularization.
Blockade of GM-CSF pathway induced sustained suppression of myeloid and T cell activities in rheumatoid arthritis

Objectives Targeting the granulocyte-macrophage colony-stimulating factor (GM-CSF) pathway holds great potential in the treatment of inflammatory diseases. Mavrilimumab, a human monoclonal GM-CSF receptor-α antibody, has demonstrated clinical efficacy in RA. Our current study aimed to elucidate mechanisms of action and identify peripheral biomarkers associated with therapeutic responses of GM-CSF antagonism in RA. Methods A 24-week placebo (PBO)-controlled trial was conducted in 305 RA patients who received mavrilimumab (30, 100 or 150 mg) or PBO once every 2 weeks. Serum biomarkers and whole blood gene expression profiles were measured by protein immunoassay and whole genome microarray. Results Mavrilimumab treatment induced significant down-regulation of type IV collagen formation marker (P4NP 7S), macrophage-derived chemokine (CCL22), IL-2 receptor α and IL-6 compared with PBO. Both early and sustained reduction of P4NP 7S was associated with clinical response to 150 mg mavrilimumab treatment. Gene expression analyses demonstrated reduced expression of transcripts enriched in macrophage and IL-22/IL-17 signalling pathways after GM-CSF blockade therapy. Myeloid and T cell-associated transcripts were suppressed in mavrilimumab-treated ACR20 responders but not non-responders. While CCL22 and IL-6 down-regulation may reflect a direct effect of GM-CSFR blockade on the production of pro-inflammatory mediators by myeloid cells, the suppression of IL-2 receptor α and IL-17/IL-22 associated transcripts suggests an indirect suppressive effect of mavrilimumab on T cell activation. Conclusion Our results demonstrated association of peripheral biomarker changes with therapeutic response to mavrilimumab in RA patients. The sustained efficacy of mavrilimumab in RA may result from both direct effects on myeloid cells and indirect effects on T cell activation after GM-CSFR blockade.
(DEAD)-box RNA helicase 3 modulates NF-κB signal pathway by controlling the phosphorylation of PP2A-C subunit

Asp-Glu-Ala-Asp (DEAD)-box RNA helicase 3 (DDX3), an ATP-dependent RNA helicase, is associated with RNA splicing, mRNA export, transcription, translation, and RNA decay. Recent studies revealed that DDX3 participates in innate immune response during virus infection by interacting with TBK1 and regulating the production of IFN-β. In our studies, we demonstrated that DDX3 regulated NF-κB signal pathway. We found that DDX3 knockdown reduced the phosphorylation of p65 and IKK-β and ultimately attenuated the production of inflammatory cytokines induced by poly(I:C) or TNF-α stimulation. The regulatory effect of DDX3 on NF-κB signal pathway was not affected by the loss of its ATPase or helicase activity. We further identified PP2A C subunit (PP2A-C) as an interaction partner of DDX3 by co-immunoprecipitation and mass spectrum analysis. We confirmed that DDX3 formed the complex with PP2A-C/IKK-β and regulated the interaction between IKK-β and PP2A-C. Furthermore, we demonstrated that DDX3 modulated the activity of PP2A by controlling the phosphorylation of PP2A-C, which might enable PP2A-C to regulate NF-κB signal pathway by dephosphorylating IKK-β. All these findings suggested DDX3 plays multiple roles in modulating innate immune system.
Importance of Active Participation in Obesity Management Through Mobile Health Care Programs: Substudy of a Randomized Controlled Trial

Background Due to the prevalence of the westernized dietary pattern and lack of physical activity, the numbers of overweight or obese individuals are increasing, resulting in a growing health burden because of various related diseases. A lifestyle modification approach has additional advantages compared with pharmacological therapies or bariatric surgery. In our randomized controlled trial conducted in 2015, we successfully used a ubiquitous health care (SmartCare) service for patients with metabolic syndrome to achieve a significant weight loss effect. Various useful apps have been developed for the SmartCare Service, which involves using a mobile phone to manage chronic diseases, minimizing time and space restrictions. Many studies have demonstrated weight loss effects using a SmartCare service, but limited data are available regarding the effect of active participation in relation to weight loss. Objective We aimed to assess the weight loss effect achieved after using the SmartCare service in terms of adherence and participation. We divided the intervention group of the previous study according to participation level, and analyzed whether there was a significant difference in the outcome. Methods We classified participants into 3 groups according to their adherence. Within the intervention group using the SmartCare service, the active group comprised those transmitting anthropometric measurement data using a mobile phone 3 or more times per week or who had a health consultation 5 or more times during a 24-week period. The passive group comprised those who did not adhere to these levels of engagement. The control group comprised those who did not use the SmartCare service. We compared changes in body weight, body mass index (BMI), body fat percentage, waist circumference, and lipid profile among the 3 groups. Results We identified 422 participants and analyzed 405, excluding 17 who were missing necessary data for analysis. The active group consisted of 116 participants, compared with 80 in the passive group and 209 in the control group (without SmartCare service). There was a statistically significant difference in improvements to body weight, BMI, body fat percentage, and waist circumference among active participants compared with less active participants and the control group (P<.05). However, the lipid profile changes did not differ significantly between groups. Conclusions The level of participation may be related to improved weight-related outcomes, which may improve health outcomes. To maximize the effectiveness of the SmartCare service, encouraging active participation is important. Trial Registration Clinicaltrials.gov NCT01344811; https://clinicaltrials.gov/ct2/show/NCT01344811 (Archived by WebCite at http://www.webcitation.org/6alT2MmIB)
Clock gating methodologies and tools: a survey

Clock gating (CG) is a widely used design method for reducing the dynamic power consumption in digital circuits. Although it is a mature technique, theoretical work and tools for its application are still evolving and considered a matter of ongoing research, due to its significant effect in the overall power of the designs under study. This paper introduces a detailed review of the spectrum of CG approaches, theoretical and practical, from an architectural and register transfer level to synthesis, place and route, and testing issues. Furthermore, tools availability, limitations, and requirements concerning CG are examined for each design flow step. Conclusively, an evaluation of the presented techniques and literature is provided, estimating their usefulness and identifying areas for future research, exploration, and automation. Copyright © 2015 John Wiley & Sons, Ltd.
Melatonin: Pharmacology, Functions and Therapeutic Benefits

Abstract: Background: Melatonin synchronizes central but also peripheral oscillators (fetal adrenal gland, pancreas, liver, kidney, heart, lung, fat, gut, etc.), allowing temporal organization of biological functions through circadian rhythms (24-hour cycles) in relation to periodic environmental changes and therefore adaptation of the individual to his/her internal and external environment. Measures of melatonin are considered the best peripheral indices of human circadian timing based on an internal 24-hour clock. Methods: First, the pharmacology of melatonin (biosynthesis and circadian rhythms, pharmacokinetics and mechanisms of action) is described, allowing a better understanding of the short and long term effects of melatonin following its immediate or prolonged release. Then, research related to the physiological effects of melatonin is reviewed. Results: The physiological effects of melatonin are various and include detoxification of free radicals and antioxidant actions, bone formation and protection, reproduction, and cardiovascular, immune or body mass regulation. Also, protective and therapeutic effects of melatonin are reported, especially with regard to brain or gastrointestinal protection, psychiatric disorders, cardiovascular diseases and oncostatic effects. Conclusion: This review highlights the high number and diversity of major melatonin effects and opens important perspectives for measuring melatonin as a biomarker (biomarker of early identification of certain disorders and also biomarker of their follow-up) and using melatonin with clinical preventive and therapeutic applications in newborns, children and adults based on its physiological regulatory effects.
Automatic SVM Kernel Function Construction Based on Gene Expression Programming

Traditional support vector machine needs pre-assumed kernel functions. This paper proposes a method via gene expression programming to automatically construct the kernel. The contributions of this paper include: (1) proposing the concepts of GEP kernel and kernel tree; (2) proposing the properties of GEP kernel and the kernel relation theorem; (3) proposing GEP based support vector machine (KGEP-SVM), (4) decoding kernel individual algorithm (DKIA) and kernel operators operating algorithm (KOOA), and (5) extensive experiments show that the average accuracy of the method is increased by 4% and generation of GEP kernel is about 150.
Genetic Polymorphisms of 21 STR Loci in Hunan Province-based Han Population.

OBJECTIVES To investigate the genetic polymorphisms of 21 short tandem repeat （STR） loci （D3S1358, D13S317, D7S820, D16S539, Penta E, D2S441, TPOX, TH01, D2S1338, CSF1PO, Penta D, D10S1248, D19S433, vWA, D21S11, D18S51, D6S1043, D8S1179, D5S818, D12S391 and FGA）. METHODS A total of 560 blood samples were collected from unrelated healthy individuals of Han population in Hunan Province. Chelex-100 extraction method was applied to the extraction of genomic DNA, and an AGCU EX22 Kit and 9700 STR amplification was used in amplification reactions. The products were separated and analyzed on 310 Genetic Analyzer. RESULTS A total of 248 alleles were observed, the allelic frequencies ranging from 0.001 to 0.518. Observation of genotype distributions for each locus showed no deviations from Hardy-Weinberg equilibrium except Penta E （P=0.023）. The combined power of discrimination, combined power of exclusion, and combined matching probability of the 21 STR loci were approximately 0.999 999 999 999 999 999 999 999 8, 0.999 999 998, and 1.36×10⁻²⁵, respectively. CONCLUSIONS The 21 STR loci show high polymorphisms in the Han population, which can provide valuable data and a theoretical basis for forensic individual identification and paternity testing.
The epigenetic clock and physical development during childhood and adolescence: longitudinal analysis from a UK birth cohort

Abstract Background: Statistical models that use an individual’s DNA methylation levels to estimate their age (known as epigenetic clocks) have recently been developed, with 96% correlation found between epigenetic and chronological age. We postulate that differences between estimated and actual age [age acceleration (AA)] can be used as a measure of developmental age in early life. Methods: We obtained DNA methylation measures at three time points (birth, age 7 years and age 17 years) in 1018 children from the Avon Longitudinal Study of Parents and Children (ALSPAC). Using an online calculator, we estimated epigenetic age, and thus AA, for each child at each time point. We then investigated whether AA was prospectively associated with repeated measures of height, weight, body mass index (BMI), bone mineral density, bone mass, fat mass, lean mass and Tanner stage. Results: Positive AA at birth was associated with higher average fat mass [1321 g per year of AA, 95% confidence interval (CI) 386, 2256 g] from birth to adolescence (i.e. from age 0–17 years) and AA at age 7 was associated with higher average height (0.23 cm per year of AA, 95% CI 0.04, 0.41 cm). Conflicting evidence for the role of AA (at birth and in childhood) on changes during development was also found, with higher AA being positively associated with changes in weight, BMI and Tanner stage, but negatively with changes in height and fat mass. Conclusions: We found evidence that being ahead of one’s epigenetic age acceleration is related to developmental characteristics during childhood and adolescence. This demonstrates the potential for using AA as a measure of development in future research.
How Much Cache is Needed to Achieve Linear Capacity Scaling in Backhaul-Limited Dense Wireless Networks?

Dense wireless networks are a promising solution to meet the huge capacity demand in 5G wireless systems. However, there are two implementation issues, namely, the interference and backhaul issues. To resolve these issues, we propose a novel network architecture called the backhaul-limited cached dense wireless network (C-DWN), where a physical layer (PHY) caching scheme is employed at the base stations (BSs), but only a fraction of the BSs have wired payload backhauls. The PHY caching can replace the role of wired backhauls to achieve both the cache-induced multiple-input–multiple-output (MIMO) cooperation gain and cache-assisted multihopping gain. Two fundamental questions are addressed. Can we exploit the PHY caching to achieve linear capacity scaling with limited payload backhauls? If so, how much cache is needed? We show that the capacity of the backhaul-limited C-DWN indeed scales linearly with the number of BSs if the BS cache size is larger than a threshold that depends on the content popularity. We also quantify the throughput gain due to cache-induced MIMO cooperation over conventional caching schemes (which exploit purely the cached-assisted multihopping). Interestingly, the minimum BS cache size needed to achieve a significant cache-induced MIMO cooperation gain is the same as that needed to achieve the linear capacity scaling.
Changes in Systolic and Diastolic Function in a Mouse Model Overexpressing Cardiac Angiotensin II AT-1 Receptor

Angiotensin II (Ang II) is involved in various pathophysiological processes throughthe activation of angiotensin II AT-1 receptors. The purpose of this study was toassess in vivo and in vitro systolic and diastolic ventricular function in mice overexpressingthe cardiac-specific Ang II AT-1 receptor (AT1R). A second objective was todetermine whether ventricular function changes could be reversed with acute andchronic ATIR blockade.Mice were divided into four experimental groups. The first group included nontransgenicanimals (NTG, n=10), the second group consisted of transgenic mice (TG,n=7) with cardiac-specific AT1R overexpression and the third and fourth groupswere TG animals treated with losartan (L) for 7 (TG L7, n=9) and 30 days (TG L30,n=7), respectively. Transgenic animals exhibited left ventricular hypertrophy (LVH)which was only regressed with losartan treatment for 30 days. They also presented asignificant decrease in shortening fraction from 47.1±2.3% to 32.3±1.3% (p <0.05)and of +dP/dtmax from 7073 ± 674 to 3897.5 ± 209.7 mmHg/sec (p< 0.05). Systolicdysfunction recovered both with losartan treatment for 7 and 30 days.Isovolumic relaxation time and t1/2 were 24.1±1.3 and 5.1±0.5ms, respectively, inthe NTG group. These indexes increased to 33.1±2.2 and 8.4±0.4 ms, respectively,in TG mice (p<0.05). Diastolic dysfunction was completely reversed by losartantreatment for 7 and 30 days. In vitro ventricular function with controlled variablesconfirmed in vivo findings.In conclusion, cardiac-specific AT1R overexpression induces systolic and diastolicventricular dysfunction which is completely reversed by AT1R blockade. This beneficialeffect is independent of left ventricular mass changes.
Graft‐derived exosomes. When small vesicles play a big role in transplant rejection

Recipient pro-inflammatory T cells recognizing donor MHC molecules in a direct fashion trigger early acute rejection of cardiac allografts. In clinical settings, prevention of acute rejection is regularly achieved via continuous suppression of these T cells using immunosuppressive drugs, including calcineurin inhibitors. Nevertheless, within 5 years post-transplantation, up to 50% patients suffer late cardiac allograft failure whose major pathological manifestation is chronic allograft vasculopathy (CAV). CAV is characterized by intimal thickening, smooth muscle cell proliferation, and accumulation of extracellular matrix, which result in arterial narrowing and eventually graft ischemia and fibrosis. There is a body of evidence showing that CAV is initiated via a process involving cells of both innate and adaptive systems. However, the immunological mechanisms underlying CAV are still largely unknown. Gaining insights into this question is critical to the design of strategies for the prevention and/or treatment of late cardiac allograft failure and CAV. This article is protected by copyright. All rights reserved.