Miracle-dz/UniFAR-FTUs huggingface dataset:
The Relationship Between Child and Parent Food Hedonics and Parent and Child Food Group Intake in Overweight/Obese Children

The manuscript copyediting, of the form. that during the production process errors may be discovered which could the content, and all legal disclaimers that apply to the Many factors influence children’s dietary intake, including children’s and parents’ food hedonics (liking), and parent intake. This secondary data analysis studied the relationship between child and parent liking (CL and PL), and parent and child intake (PI and CI) of fruits (F), vegetables (V), low-fat dairy (LFD), snack foods (SF), and sweetened beverages (SB) in four- to nine-year-old overweight/obese (body mass index (BMI) ≥ 85 th percentile) children presenting for obesity treatment (September 2005 to 2007) in Providence, RI. One-hundred thirty-five parent-child pairs, with complete baseline dietary (three-day food record) and food group hedonic data were included. Hedonic ratings were mean ratings using a five-point Likert scale (lower scores represented greater liking of a food group). Children were 7.2 ± 1.6 years, 63.0% female, 12.6% Black, 17.8% Hispanic, with a mean z-BMI of 2.3 ± 0.6. Total servings consumed by children over three days were: F: 2.7 ± 3.2; V: 3.4 ± 2.5; LFD: 2.4 ± 2.1; SF: 5.9 ± 4.2; SB: 2.7 ± 3.1. After demographic and anthropometric variables were controlled, PI was positively related (p < 0.05) to CI of all food groups except SB. CL was only significantly (p < 0.05) related to CI of V. In young overweight/obese children, PI was consistently related to CI. Changing PI may be important in aiding with changing young overweight/obese children’s dietary intake.
Immunogenicity and clinical protection against equine influenza by gene-based DNA vaccination of ponies

Equine influenza A (H3N8) virus is a leading cause of infectious respiratory disease in horses causing widespread morbidity and economic losses. As with influenza in other species, equine influenza strains continuously mutate, requiring constant re-evaluation of current vaccines and development of new vaccines. Current inactivated (killed) vaccines, while efficacious, only offer limited protection against multiple strains and require frequent boosts. Ongoing research into new vaccine technologies, including gene-based vaccines, aims to increase the neutralization potency, breadth, and duration of protective immunity of new or existing vaccines. In these hypothesis-generating experiments, we demonstrate that a DNA vaccine expressing the hemagglutinin protein of equine H3N8 influenza virus generates homologous and heterologous immune responses, and protects against clinical disease and viral replication following homologous H3N8 infection in horses. Furthermore, we demonstrate that a needle-free delivery device is as efficient and effective as conventional parenteral injection using a needle and syringe. The observed trends in this study drive the hypothesis that DNA vaccines offer a safe, effective, and promising alternative approach for veterinary vaccines against influenza, and applicable to combat equine influenza.
Molecules in focus: C-terminal tensin-like (CTEN): a promising biomarker and target for cancer

C-terminal tensin-like (cten, also known as tensin4, TNS4) is a member of the tensin family. Cten protein, like the other three tensin family members, localizes to focal adhesion sites but only shares sequence homology with other tensins at its C-terminal region, which contains the Src SH2 and PTB domains. Cten is abundantly expressed in normal prostate and placenta and is downregulated in prostate cancer. However, overexpression of cten frequently associates with tumors derived from breast, colon, lung, stomach, skin and pancreas. A variety of cancer-associated growth factors and cytokines induce cten expression. Up-regulated cten promotes cell motility, prolongs epidermal growth factor receptor signaling, and enhances tumorigenicity. Emerging findings suggest that cten is a promising biomarker and therapeutic target for various cancers.
Decentralized charging decisions for the smart grid

This thesis implements a decentralized smart charging strategy and V2G simulation for EVs and PHEVs within the large scale transport simulation framework MATSim [2]. The charging decisions of all vehicles aim to reach a maximum load flattening effect and can be completed with minimal information remotely in individual on-board processing units. This reduces the need for communication and infrastructure intensive systems. The decentralized smart charging algorithm relies on linear programming to optimize the charging durations for each parking interval and uses probability density functions, indicating the distribution of charging slots over the simulated day, to guide the exact time choices. In the V2G simulation, every vehicle estimates its required contribution to regulate the grid from the current total V2G need and an estimation of the number of connected vehicles available for V2G. Then, each vehicle makes an economic decision, if V2G regulation is provided dependent on the agent’s state, his next plans and the opportunity to reschedule. The decentralized smart charging algorithm proves to be a powerful method to shift charging times according to the distribution of free charging slots. Two suggestions to improve the methodology are made to mitigate grid violations completely. It is found that increases in battery size can significantly improve the performance of EVs and avoid CO2 emissions. The ratio of EVs in the system has no influence on the charging behaviour of agents and the gas price has only a small impact on the total charging costs. In the proposed V2G setup the maximum capacity of agents to provide regulation is relatively low and the potential revenues are unattractive. To make V2G regulation a feasible and economical concept, it is proposed to offer capacity payments and to limit V2G to PHEVs enforcing uneconomic but reliable V2G regulation decisions.
Association of the I g and I d Charge Movement with Calcium Release in Frog Skeletal Muscle

Charge movement and calcium transient were measured simultaneously in stretched frog cut twitch ﬁbers under voltage clamp, with the internal solution containing 20 mM EGTA plus added calcium and antipyrylazo III. When the nominal free [Ca 2 1 ] i was 10 nM, the shape of the broad I g hump in the ON segments of charge movement traces remained invariant when the calcium release rate was greatly diminished. When the nominal free [Ca 2 1 ] i was 50 nM, which was close to the physiological level, the I g humps were accelerated and a slow calcium-dependent I d component (or state) was generated. The peak of ON I d synchronized perfectly with the peak of the calcium release rate whereas the slow decay of ON I d followed the same time course as the decay of calcium release rate. Suppression of calcium release by TMB-8 reduced the amount of Q d concomitantly but not completely, and the effects were partially reversible. The same simultaneous suppression effects were achieved by depleting the sarcoplasmic reticulum calcium store with repetitive stimulation. The results suggest that the mobility of Q d needs to be primed by a physiological level of resting myoplasmic Ca 2 1 . Once the priming is completed, more I d is mobilized by the released Ca 2 1 during depolarization.
Targeted p21 WAF1/CIP1 Activation by RNAa Inhibits Hepatocellular Carcinoma Cells

RNA activation (RNAa) is a mechanism of gene activation triggered by promoter-targeted small double-stranded RNA (dsRNA), also known as small activating RNA (saRNA). p21 WAF1/CIP1 (p21) is a putative tumor suppressor gene due to its role as a key negative regulator of the cell cycle and cell proliferation. It is frequently downregulated in cancer including hepatocellular carcinoma (HCC), but is rarely mutated or deleted, making it an ideal target for RNAa-based overexpression to restore its tumor suppressor function. In the present study, we investigated the antigrowth effects of p21 RNAa in HCC cells. Transfection of a p21 saRNA (dsP21-322) into HepG2 and Hep3B cells signiﬁcantly induced the expression of p21 at both the mRNA and protein levels, and inhibited cell proliferation and survival. Further analysis of dsP21-322 transfected cells revealed that dsP21-322 arrested the cell cycle at the G 0 /G 1 phase in HepG2 cells but at G 2 /M phase in Hep3B cells which lack functional p53 and Rb genes, and induced both early and late stage apoptosis by activating caspase 3 in both cell lines. These results demonstrated that RNAa of p21 has in vitro antigrowth effects on HCC cells via impeding cell cycle progression and inducing apoptotic cell death. This study suggests that targeted activation of p21 by RNAa may be explored as a novel therapy for the treatment of HCC.
In Vivo Brain Glycine and Glutamate Concentrations in Patients with First-Episode Psychosis Measured by Echo-Time-Averaged Proton MR Spectroscopy at 4 Tesla

Background— Accumulating evidence suggests the involvement of abnormal glutamateric neurotransmission and N-methyl-D-aspartate receptor (NMDAR) hypofunction in the pathophysiology of psychotic disorders. The purpose of this study was to quantify in vivo glutamate (Glu) and glycine (Gly) levels in patients with first-episode psychosis as well as age-matched healthy controls with MR spectroscopy. Methods— The subjects were 46 patients with first-episode psychosis (20 schizophrenia-spectrum disorders (SZ), 26 bipolar disorder (BD)) and 50 age-matched healthy controls (HC). Glu and Gly levels were measured in vivo in the anterior cingulate cortex (ACC) and posterior cingulate cortex (PCC) of the subjects by using the echo-time (TE)-averaged proton MR spectroscopy technique ( 1 H-MRS) at 4 T (i.e., modified PRESS sequence: 24 TE steps with 20 ms increments). Metabolite levels were quantified using LCModel with simulated basis sets. Results— Significantly higher Glu and Gly levels were found in both the ACC and PCC of patients with first-episode psychosis as compared to healthy controls. Glu and Gly levels were positively correlated in patients. SZ and BD patients showed similar abnormalities. Conclusions— Our findings demonstrate abnormally elevated brain Glu and Gly levels in patients with first-episode psychosis by means of TE-averaged 1 H-MRS at 4 T. The findings implicate dysfunction of NMDAR and glutamatergic neurotransmission in the pathophysiology of the acute early phase of psychotic illnesses.
Mental Health Care Utilization and Unmet Needs for Health Care Among Lesbian and Bisexual Chinese-, Korean-, and Vietnamese-American Women

The extent to which sexual orientation is associated with receipt of mental health care, adequate mental health treatment, and unmet health care among Asian-American women is unknown. This study examined a relatively large sample of Chinese-, Korean-, and Vietnamese-American women (n=701) using Computer-Assisted Self-Interviews (CASI). After controlling for mental health status and other covariates, sexual minority women were more likely to have received any mental health services but still reported a greater unmet need for health care than their exclusively heterosexual counterparts. Among those who received mental health treatment, sexual minorities were no more likely to have received minimally adequate care. Given the high rates of mental health problems in Asian-American sexual minority women, efforts are needed to identify and overcome barriers to adequate mental health care and to minimize unmet health care needs.
Regional Adipose Distribution and Its Relationship to Exercise Intolerance in Older Obese HFpEF Patients

Background— Recent studies indicate that excess total body adipose contributes to exercise intolerance in heart failure with preserved ejection fraction (HFpEF). However, the impact of the pattern of regional (abdominal, cardiac, intermuscular) adipose deposition on exercise intolerance in HFpEF is unknown. Methods— We measured total body (dual-energy x-ray absorptiometry) and regional adipose (magnetic resonance imaging), peak oxygen uptake (peak VO 2 ), 6-minute walk distance (6MWD), short physical performance battery (SPPB), and leg press power in 100 older obese HFpEF patients and 61 healthy controls (HC), and adjusted for age, gender, race, and body surface area. Results— Peak VO 2 (15.7±0.4 vs. 23.0±0.6 ml/kg/min; p<0.001), 6MWD (427±7 vs. 538±10 m; p<0.001), SPPB (10.3±0.2 vs. 10.9±0.2; P<0.05) and leg power (117±5 vs. 152±9 watts, p=0.004) were significantly lower in HFpEF versus HC. Total fat mass, total percent fat, abdominal subcutaneous fat, intra-abdominal fat, and thigh intermuscular fat were significantly higher, while epicardial fat was significantly lower in HFpEF versus HC. After adjusting for total body fat, intra-abdominal fat remained significantly higher while epicardial fat remained significantly lower in HFpEF. Abdominal subcutaneous fat, thigh subcutaneous fat, and thigh intermuscular fat/skeletal muscle ratio were inversely associated, while epicardial fat was directly associated, with peak VO 2 , 6MWD, SPPB, and leg power. With multiple stepwise regression, intra-abdominal fat was the strongest independent predictor of peak VO 2 and 6MWD. Conclusions— In metabolic/obese HFpEF, the pattern of regional adipose deposition may have important adverse consequences beyond total body adipose. Interventions targeting intra-abdominal and intermuscular fat could potentially improve exercise intolerance. Clinical Trial www.clinicaltrials. gov DEXA and MRI, and multiple objective measures of physical function. Our study also has potential limitations. Although DEXA can potentially overestimate fat and lean mass in presence of edema, our HFpEF patients were well-compensated without overt fluid overload. Moreover, our MRI assessments confirm and extend our DEXA results by demonstrating regional differences in fat distribution between HFpEF and HC. Average BMI in the HC was lower than HFpEF, and even though we adjusted for body size, our data do not definitively prove that the pattern of regional fat distribution we identified is specific to obese HFpEF, which would require a control group matched for BMI and comorbidities.
Chronic cannabinoid CB 2 activation reverses paclitaxel neuropathy without tolerance or CB 1 -dependent withdrawal

Background— Mixed cannabinoid CB 1 /CB 2 agonists such as Δ 9 -tetrahydrocannabinol (Δ 9 -THC) can produce tolerance, physical withdrawal, and unwanted CB 1 -mediated central nervous system side effects. Whether repeated systemic administration of a CB 2 -preferring agonist engages CB 1 receptors or produces CB 1 -mediated side effects is unknown. Methods— We evaluated anti-allodynic efficacy, possible tolerance, and cannabimimetic side effects of repeated dosing with a CB 2 -preferring agonist AM1710 in a model of chemotherapy-induced neuropathy produced by paclitaxel using CB 1 KO, CB 2 KO, and WT mice. Comparisons were made with the prototypic classical cannabinoid Δ 9 -THC. We also explored the site and possible mechanism of action of AM1710. Results— Paclitaxel-induced mechanical and cold allodynia developed equivalently in CB 1 KO, CB 2 KO, and WT mice. Both AM1710 and Δ 9 -THC suppressed established paclitaxel-induced allodynia in WT mice. Unlike Δ 9 -THC, chronic AM1710 did not engage CB 1 activity or produce antinociceptive tolerance, CB 1 -mediated cannabinoid withdrawal, hypothermia, or motor dysfunction. Anti-allodynic efficacy of systemic AM1710 was absent in CB 2 KO mice or WT mice receiving the CB 2 antagonist AM630, administered either systemically chronic treatment with AM1710 decreased mRNA levels of tumor necrosis factor alpha and monocyte chemoattractant protein-1 in lumbar spinal cord of paclitaxel-treated WT mice. Conclusions— Our results highlight the potential of prolonged use of CB 2 agonists for managing chemotherapy-induced allodynia with a favorable therapeutic ratio marked by sustained efficacy and absence of tolerance, physical withdrawal, or CB 1 -mediated side effects. Here, we characterized antinociceptive efficacy of the CB 2 -preferring agonist AM1710 in a model of paclitaxel-induced neuropathy using CB 2 knockout (CB 2 KO), CB 1 knockout (CB 1 KO), and wildtype (WT) mice. We evaluated whether repeated administration of AM1710 would produce antinociceptive tolerance or CB 1 -mediated side effects (i.e. physical withdrawal, motor ataxia, and hypothermia). In addition, we investigated the site of action and the impact of AM1710 on mRNA levels of pro-inflammatory cytokines and chemokine in lumbar spinal cords of paclitaxel-treated mice.
Coronary Bioresorbable Scaffolds Bioresorbable Scaffolds

Percutaneous coronary intervention (PCI) has undergone major advances including the evolution in stent technology, from bare metal stents (BMS), to their drug eluting counterparts, to the development of bioresorbable scaffolds (BRS). The primary notion of BRS was to facilitate complete vascular healing and restore normal endothelial function following the resorption of stent scaffold while providing equivalent mechanical properties of a metallic drug eluting stents (DES) in the earlier stages. BRS provide attractive physiologic advancements over the existing DES and have shown promising results in initial clinical studies albeit with small sample sizes. Their use has been primarily restricted to patients recruited in clinical trials with limited real-world applicability. Thus, data from larger randomised control trials is awaited. The major objective of this article is to review the evidence on BRS and identify their clinical applicability in current interventional practice. of were met with disappointing results. The TVR rates were 39.7 % at four months and 45 % at 12 months due to both neointimal hyperplasia and recoil in the Clinical performance angiographic results of coronary stenting with absorbable metal stents (PROGRESS) paclitaxel-eluting
An additional function for bacteriophage A rex: The rexB product prevents degradation of the A 0 protein

The rex operon of bacteriophage A excludes the development of several unrelated bacteriophages. Here we present an additional A rexB function: it prevents degradation of the short-lived protein A 0 known to be involved in A DNA replication. We have shown that it is the productof rexB that is responsible for the stabilization of A 0: when a nonsense mutation is present in rexB, A 0 protein is labile; suppression of the mutation by the corresponding nonsense suppressor causes partial restabilization of A 0. A rexB also stabilizes A 0 in trans. We discuss our results in relation to the function of rexB in-A DNA replication and'its role in the protein degradation pathways of bacteriophage A. When phage A is in the lysogenic state in its host Escherichia coli, the only phage genes expressed are the adjacent genes cI and rex (1). The product of cI, the A repressor, prevents vegetative development of the prophage and also further infection by homologous phages (2). A rex expresses the Rex function, shown to exclude the development of several unrelated phages (3-11). The first-described Rex function was the exclusion by A prophage of the development of phage T4 rII mutants. Rex does not exclude wild-type T4 (3). The system for T4 ril exclusion (rex) is a landmark in the history of molecular biology: it was used for the first fine-structure analysis of a genetic region (T4rII) (3), for defining the cistron (12), and for elucidation
Benzodiazepine Oncogenesis as Mediated via Diminished Restorative Sleep Effected Sympathoadrenal Activation

documented and serious complication of this drug (and cocaine adulterant). Patients may present with a variety of neurologic symptoms related to multifocal white matter lesions that can be identified on magnetic resonance imaging. The lesions do not appear to be vasculitic and are often reversible with cessation of levamisole exposure. In the setting of cocaine abuse, the clinical and magnetic resonance imaging features can be confused with other complications of cocaine abuse and high-risk lifestyles.
γδ T Cell Subsets Play Opposing Roles in Regulating Experimental Autoimmune Encephalomyelitis1

γδ T cells are resident in cerebrospinal fluid and central nervous system (CNS) lesions of multiple sclerosis (MS) patients, but as multifaceted cells exhibiting innate and adaptive characteristics, their function remains unknown. Previous studies in experimental autoimmune encephalomyelitis (EAE) are contradictory and identified these cells as either promoting or suppressing disease pathogenesis. This study examines distinct γδ T cell subsets during EAE and indicates they mediate differential functions in CNS inflammation and demyelination resulting in pathogenesis or protection. We identified two γδ subsets in the CNS, Vγ1+ and Vγ4+, with distinct cytokine profiles and tissue specificity. Anti-γδ T cell receptor (TCR) monoclonal antibody (mAb) administration results in activation and downregulation of surface TCR, rendering the cells undetectable, but with opposing effects: anti-Vγ4 treatment exacerbates disease whereas anti-Vγ1 treatment is protective. The Vγ4+ subset produces multiple proinflammatory cytokines including high levels of IL-17, and accounts for 15-20% of the interleukin-17 (IL-17) producing cells in the CNS, but utilize a variant transcriptional program than CD4+ Th17 cells. In contrast, the Vγ1 subset produces CCR5 ligands, which may promote regulatory T cell differentiation. γδ T cell subsets thus play distinct and opposing roles during EAE, providing an explanation for previous reports and suggesting selective targeting to optimize regulation as a potential therapy for MS. © 2014 Elsevier Inc. All rights reserved. Corresponding Author: 6-718 Tarry Building, 303 E. Chicago Avenue, Chicago, IL 60611, Phone: 312-503-7674, FAX: 312-503-1154, s-d-miller@northwestern.edu. The authors declare no competing financial interests. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author Manuscript Cell Immunol. Author manuscript; available in PMC 2015 July 01. Published in final edited form as: Cell Immunol. 2014 July ; 290(1): 39–51. doi:10.1016/j.cellimm. 2014.04. 013. N IH -P A A uhor M anscript N IH -P A A uhor M anscript N IH -P A A uhor M anscript