Miracle-dz/UniFAR-FTUs huggingface dataset:
Metabolic Complications of Chronic Kidney Failure and Hemodialysis

Chronic kidney disease is a very real and growing problem, as indicated by demographic trends. The total number of treated patients has markedly increased during the last 30 years, and chronic kidney disease currently affects approximately 19 million adult Americans, with an incidence that is still increasing (Snyder & Pendergraph, 2005). This trend is caused by a growing percentage of elderly people in the population as well as by technical progress and broader availability of dialysis therapy. An increasing number of diabetic patients is a further important factor. Chronic kidney disease is characterized by progressive deterioration of kidney function, which develops eventually into a terminal stage of chronic kidney failure. Chronic kidney failure has traditionally been categorized as mild, moderate, or severe. Other poorly defined terms like uremia and end-stage renal disease have commonly been applied. During the last few years, an international consensus has emerged categorizing chronic kidney failure into 5 stages according to the glomerular filtration rate (GFR) and presence of signs of kidney damage: stage 1: GFR > 90 ml/min and signs of kidney damage; stage 2: GFR = 60–89 ml/min and signs of kidney damage; stage 3: GFR = 30–59 ml/min; stage 4: GFR = 15–29 ml/min; and stage 5: GFR < 15 ml/min (Levey et al., 2005). RIFLE (from Risk, Injury, Failure, Loss, End Stage) is a modern classification of acute renal failure and it is noteworthy here (Van Biesen et al., 2006). Stage 5 of chronic kidney failure represents the total inability of kidneys to maintain homeostasis, and this metabolic state is without treatment incompatible with life. Thus, at this stage, it is necessary to use methods that substitute for kidney function to ensure patient survival; these methods include hemodialysis, peritoneal dialysis, and other extracorporeal purifying procedures, or kidney transplantation. Chronic kidney failure is associated with many kinds of metabolic changes caused by the kidney disease itself and also attributable to dialysis treatment. Phenomena such as accumulation or deficit of various substances and dysregulation of metabolic pathways participate and combine in the pathogenesis of these changes. In the process of accumulation, decreased urinary excretion plays a crucial role and leads to retention of metabolites in the organism (e.g., creatinine, urea, electrolytes, water, substances with middle molecular weight such as beta-2 microglobulin and other). The increased formation of metabolites through catabolic processes and alternative metabolic pathways also wields an influence. Regular dialysis treatment partly decreases this accumulation but cannot avert
Ferroelectric polymer thin films with high energy density and low loss

Dielectric materials with large electric energy density are actively pursued for many applications. Among commercially available polymer capacitor film, poly(vinylidene fluoride chlorotrifluoroethylene) P(VDF-CTFE) stands out due to its excellent capability to store electrical energy with relatively high efficiency. In this dissertation, we employed crosslinking approaches to improve energy density of the copolymer by concurrently reducing loss, enhancing permittivity, and improving breakdown strength of the copolymer. The fundamental idea of this effort is to introduce covalent bonding between the polymer chains to confine and destabilize the formation of ferroelectric domain. By carefully controlling of the process conditions and varying the polymer/crosslinking agents feeding ratios the copolymer structures were systematically tuned for optimized dielectric and electrical properties. The crosslinking method leads to the copolymer film with impressive 64% decreased of total loss, 24% improvement of polarization level (under 250 MV/m field) and 70 % improvement of breakdown strength compared to the pristine. All of above improvements have been synergized and consequently 315 % enhancement of energy density can be achieved in the crosslinked copolymers.
Metformin Inhibits N-Methyl-N-Nitrosourea Induced Gastric Tumorigenesis in db/db Mice

Abstract Aim Type 2 diabetes can elevate risk of gastric cancer and metformin, an anti-diabetic agent, has an inhibitory effect against gastric cancer cell in vitro. However, the effect of metformin on type 2 diabetes-related gastric tumorigenesis in vivo is still not clear. In the present study, we aim to detect whether metformin can inhibit increased risk of gastric cancer in diabetic db/db mice and which the potential anti-cancer mechanisms of metformin are. Methods 4-week-old mice were divided into 3 groups (2 db/db mice groups and one wild type mice group). All diabetic and non-diabetic mice were treated with N-Methyl-N-Nitrosourea (MNU) for 20 weeks to induce gastric tumorigenesis. At week 21, one db/db mice group were treated with metformin (5 mg/ml) for 10 weeks and the other 2 groups were treated with saline. Blood samples were collected for testing insulin and insulin-like growth factor (IGF)-1. Stomach tissues were collected for histopathological evaluation and mRNAs analysis. Results Metformin significantly decreased incidence of MNU-induced gastric dysplasia and cancer in diabetic db/db mice. Furthermore, metformin reduced serum insulin as well as IGF-1, and also suppressed expression of insulin receptor, IGF-1, IGF-1 receptor and several pro-inflammatory cytokines mRNAs in stomach of db/db mice, but did not significantly influence IGF-2 and IGF-2 receptor expressions. Conclusions The results show that metformin can prevent the risk of gastric cancer in type 2 diabetes and the protective mechanisms may involve in an inhibitory effect of metformin on insulin as well as IGF-1 signals and cancer related pro-inflammatory cytokines.
Experimental investigation and prediction of bonding strength of Oriental beech (Fagus orientalis Lipsky) bonded with polyvinyl acetate adhesive

Adhesive bond strength of solid wood plays a key role in the efficient use of wood in a large number of engineering applications. In this study, the effects of amount of adhesive, pressing pressure, and pressing time on bonding strength of beech wood bonded with polyvinyl acetate adhesive were investigated and predicted by developing an artificial neural network (ANN) model. Experimental results have showed that bonding strength of wood samples increased generally by increasing amount of adhesive, pressing pressure, and pressing time. Besides, ANN analysis has yielded highly satisfactory results. The designed neural network model allows predicting the bonding strength of wood samples with mean absolute percentage error of 2.454% and correlation coefficient of 97.8% for testing phase. It is clear from the results that the model has a good learning and generalization ability. This model therefore can be used to predict bonding strength of beech samples bonded with polyvinyl acetate adhesive under given conditions. Consequently, this study provides beneficial insights for practitioners in terms of the safe and efficient use of wood as an engineering material in applications related to the strength of the bond between wood and adhesive.
Mimicry of a constitutively active pre–B cell receptor in acute lymphoblastic leukemia cells

Pre–B cells undergo apoptosis unless they are rescued by pre–B cell receptor–dependent survival signals. We previously showed that the BCR-ABL1 kinase that is expressed in pre–B lymphoblastic leukemia bypasses selection for pre–B cell receptor–dependent survival signals. Investigating possible interference of BCR-ABL1 with pre–B cell receptor signaling, we found that neither SYK nor SLP65 can be phosphorylated in response to pre–B cell receptor engagement. Instead, Bruton's tyrosine kinase (BTK) is constitutively phosphorylated by BCR-ABL1. Activated BTK is essential for survival signals that otherwise would arise from the pre–B cell receptor, including activation of PLCγ1, autonomous Ca2+ signaling, STAT5-phosphorylation, and up-regulation of BCLX L. Inhibition of BTK activity specifically induces apoptosis in BCR-ABL1 + leukemia cells to a similar extent as inhibition of BCR-ABL1 kinase activity itself. However, BCR-ABL1 cannot directly bind to full-length BTK. Instead, BCR-ABL1 induces the expression of a truncated splice variant of BTK that acts as a linker between the two kinases. As opposed to full-length BTK, truncated BTK lacks kinase activity yet can bind to BCR-ABL1 through its SRC-homology domain 3. Acting as a linker, truncated BTK enables BCR-ABL1–dependent activation of full-length BTK, which initiates downstream survival signals and mimics a constitutively active pre–B cell receptor.
The RING-CH Ligase K5 Antagonizes Restriction of KSHV and HIV-1 Particle Release by Mediating Ubiquitin-Dependent Endosomal Degradation of Tetherin

Tetherin (CD317/BST2) is an interferon-induced membrane protein that inhibits the release of diverse enveloped viral particles. Several mammalian viruses have evolved countermeasures that inactivate tetherin, with the prototype being the HIV-1 Vpu protein. Here we show that the human herpesvirus Kaposi's sarcoma-associated herpesvirus (KSHV) is sensitive to tetherin restriction and its activity is counteracted by the KSHV encoded RING-CH E3 ubiquitin ligase K5. Tetherin expression in KSHV-infected cells inhibits viral particle release, as does depletion of K5 protein using RNA interference. K5 induces a species-specific downregulation of human tetherin from the cell surface followed by its endosomal degradation. We show that K5 targets a single lysine (K18) in the cytoplasmic tail of tetherin for ubiquitination, leading to relocalization of tetherin to CD63-positive endosomal compartments. Tetherin degradation is dependent on ESCRT-mediated endosomal sorting, but does not require a tyrosine-based sorting signal in the tetherin cytoplasmic tail. Importantly, we also show that the ability of K5 to substitute for Vpu in HIV-1 release is entirely dependent on K18 and the RING-CH domain of K5. By contrast, while Vpu induces ubiquitination of tetherin cytoplasmic tail lysine residues, mutation of these positions has no effect on its antagonism of tetherin function, and residual tetherin is associated with the trans-Golgi network (TGN) in Vpu-expressing cells. Taken together our results demonstrate that K5 is a mechanistically distinct viral countermeasure to tetherin-mediated restriction, and that herpesvirus particle release is sensitive to this mode of antiviral inhibition.
A class of multifrequency signals with low sidelobes in central zone of autocorrelation function

This paper is intended to introduce a class of signals based on frequency coding sequences that may be constructed by means of perfect difference sets. A regular algorithm for the construction of the frequency coding sequences is described. These sequences give rise to multifrequency signals having considerably lower sidelobes in the region surrounding the main lobe of the time autocorrelation function against those exhibited by conventional frequency-hopped signals. In addition, the signals exhibit a thumbtack ambiguity function with relatively low sidelobes over a wide region of the time-frequency plane.
Phospholipid flippases and Sfk1p, a novel regulator of phospholipid asymmetry, contribute to low permeability of the plasma membrane

Phospholipid flippase (type 4 P-type ATPase) plays a major role in the generation of phospholipid asymmetry in eukaryotic cell membranes. Loss of Lem3p-Dnf1/2p flippases leads to the exposure of phosphatidylserine (PS) and phosphatidylethanolamine (PE) on the cell surface in yeast, resulting in sensitivity to PS- or PE-binding peptides. We isolated Sfk1p, a conserved membrane protein in the TMEM150/FRAG1/DRAM family, as a multicopy suppressor of this sensitivity. Overexpression of SFK1 decreased PS/PE exposure in lem3Δ mutant cells. Consistent with this, lem3Δ sfk1Δ double mutant cells exposed more PS/PE than the lem3Δ mutant. Sfk1p was previously implicated in the regulation of the phosphatidylinositol-4 kinase Stt4p, but the effect of Sfk1p on PS/PE exposure in lem3Δ was independent of Stt4p. Surprisingly, Sfk1p did not facilitate phospholipid flipping but instead repressed it, even under ATP-depleted conditions. We propose that Sfk1p negatively regulates transbilayer movement of phospholipids irrespective of directions. In addition, we showed that the permeability of the plasma membrane was dramatically elevated in the lem3Δ sfk1Δ double mutant in comparison with the corresponding single mutants. Interestingly, total ergosterol was decreased in the lem3Δ sfk1Δ mutant. Our results suggest that phospholipid asymmetry is required for the maintenance of low plasma membrane permeability.
Recovery of linear local models of a system

The purpose of this paper is to locate and recovery linear behaviors of a nonlinear system. For this, we have used an ART2 neural network algorithm to a clustering process. In the simulation stage we have considered a system with three linear comportments. All system behaviors are present in a data file which is used to achieve a validation clustering step. A comparative study with three classification algorithms is then made.
Effect of Decentration on the Optical Quality of Two Intraocular Lenses

Purpose To analyze the effect of decentration on the optical quality of two diffractive-refractive intraocular lenses, a bifocal and a trifocal, when displaced laterally (horizontal direction) from the center. Methods The AT LISA 809M IOL (+3.75 D add) with two main foci and the AT LISA tri 839MP intraocular lens with three main foci (Carl Zeiss Meditec AG, Jena, Germany) were analyzed. The optical quality of the intraocular lenses was measured with the PMTF (power and modulation transfer function [MTF] measurement for refractive and diffractive intraocular lenses) optical bench (Lambda-X, Nivelles, Belgium). The optical quality of the lenses was evaluated by the MTF at different object vergences, the average modulation in the range of frequencies from 0 to 100 cycles/mm, and the through-focus MTF curves. All measures were recorded when the intraocular lenses were centered and decentered for 3.0- and 4.5-mm apertures. The Strehl ratio and the percentage of energy allocated at each focus at the centered position were also obtained. Results Our results showed a lower optical quality with increasing decentration. The MTFs for the diffractive-refractive intraocular lenses decreased when the intraocular lenses were decentered. Also, the relative percentages of light energy allocated at each object vergence, for both intraocular lenses, agreed well with theoretical specifications and were consistent with the overall design of each lens. Conclusions The optical quality of these diffractive-refractive multifocal intraocular lenses was slightly reduced when the induced decentration was less than 0.4 mm. For a decentration of 0.4 mm, the maximum difference in average modulation values was about 18% compared to the centered position.
Context Dependent Regulation of Human Phosphoenolpyruvate Carboxykinase Isoforms by DNA Promoter Methylation and RNA Stability

Cytoplasmic and mitochondrial isoforms of phosphoenolpyruvate carboxykinase (PEPCK‐C and PEPCK‐M) regulate hepatic gluconeogenesis to control systemic glucose homeostasis. Transcriptional and post‐transcriptional mechanisms may govern synthesis, maintenance and cooperative function of compartmentalized PEPCK enzymes. In a comparative analysis, we show that tumor cells consistently transcribe and translate higher levels of enzymatically active PEPCK‐C than PEPCK‐M and both the isoforms were present at lower levels in normal fibroblasts. Unlike in PEPCK‐M, absence of glucose reduced the PEPCK‐C mRNA and protein levels only in HepG2 cells. Interestingly, isoflavone genistein significantly increased PEPCK‐C mRNA and protein levels in normal fibroblasts indicating cell type specific control mechanisms. Genistein also significantly affected RNA stability of PEPCK‐C but not PEPCK‐M in HepG2 cells. This was due to the conserved and functional mRNA destabilizing AU rich sequences at the 3′‐UTR region of PEPCK‐C gene and was confirmed by luciferase reporter assays suggesting that glucose deprivation and genistein targets these sequences for mRNA degradation in HepG2 cells but not in fibroblasts. Analysis of promoter methylation by luciferase reporter assays and bisulfite DNA sequencing suggested that PEPCK‐C but not PEPCK‐M promoter was activated by 5‐aza‐2‐deoxycytidine by inducing cytosine demethylation at the specific CpG dinucleotides of 5′‐UTR region. Taken together, our data suggests stable PEPCK‐M activity and identifies intricate relationship between (1) mRNA stability and (2) promoter DNA methylation as two mechanisms of gene expression that distinguishes PEPCK‐C and PEPCK‐M enzyme activities in a context and cell type dependent manner during gluconeogenesis. J. Cell. Biochem. 117: 2506–2520, 2016. © 2016 Wiley Periodicals, Inc.
Re‐integrating earthworm juveniles into soil biodiversity studies: species identification through DNA barcoding

Species identification of earthworms is usually achieved by careful observation of morphological features, often sexual characters only present in adult specimens. Consequently, juveniles or cocoons are often impossible to identify, creating a possible bias in studies that aim to document species richness and abundance. DNA barcoding, the use of a short standardized DNA fragment for species identification, is a promising approach for species discrimination. When a reference library is available, DNA‐based identification is possible for all life stages. In this study, we show that DNA barcoding is an unrivaled tool for high volume identification of juvenile earthworms. To illustrate this advance, we generated DNA barcodes for specimens of Lumbricus collected from three temperate grasslands in western France. The analysis of genetic distances between individuals shows that juvenile sequences unequivocally match DNA barcode clusters of previously identified adult specimens, demonstrating the potential of DNA barcoding to provide exhaustive specimen identification for soil ecological research.
Marine reserves help coastal ecosystems cope with extreme weather

Natural ecosystems have experienced widespread degradation due to human activities. Consequently, enhancing resilience has become a primary objective for conservation. Nature reserves are a favored management tool, but we need clearer empirical tests of whether they can impart resilience. Catastrophic flooding in early 2011 impacted coastal ecosystems across eastern Australia. We demonstrate that marine reserves enhanced the capacity of coral reefs to withstand flood impacts. Reserve reefs resisted the impact of perturbation, whilst fished reefs did not. Changes on fished reefs were correlated with the magnitude of flood impact, whereas variation on reserve reefs was related to ecological variables. Herbivory and coral recruitment are critical ecological processes that underpin reef resilience, and were greater in reserves and further enhanced on reserve reefs near mangroves. The capacity of reserves to mitigate external disturbances and promote ecological resilience will be critical to resisting an increased frequency of climate‐related disturbance.
Developmental Stage, Phenotype, and Migration Distinguish Naive- and Effector/Memory-like CD4+ Regulatory T Cells

Regulatory T cells (Tregs) fulfill a central role in immune regulation. We reported previously that the integrin αEβ7 discriminates distinct subsets of murine CD4+ regulatory T cells. Use of this marker has now helped to unravel a fundamental dichotomy among regulatory T cells. αE −CD25+ cells expressed L-selectin and CCR7, enabling recirculation through lymphoid tissues. In contrast, αE-positive subsets (CD25+ and CD25−) displayed an effector/memory phenotype expressing high levels of E/P-selectin–binding ligands, multiple adhesion molecules as well as receptors for inflammatory chemokines, allowing efficient migration into inflamed sites. Accordingly, αE-expressing cells were found to be the most potent suppressors of inflammatory processes in disease models such as antigen-induced arthritis.
Bugs for a Bayesian Analysis of Stochastic Volatility Models

This paper reviews the general Bayesian approach to parameter estimation in stochastic volatility models with posterior computations performed by Gibbs sampling. The main purpose is to illustrate the ease with which the Bayesian stochastic volatility model can now be studied routinely via BUGS (Bayesian Inference Using Gibbs Sampling), a recently developed, user-friendly, and freely available software package. It is an ideal software tool for the exploratory phase of model building as any modifications of a model including changes of priors and sampling error distributions are readily realized with only minor changes of the code. BUGS automates the calculation of the full conditional posterior distributions using a model representation by directed acyclic graphs. It contains an expert system for choosing an efficient sampling method for each full conditional. Furthermore, software for convergence diagnostics and statistical summaries is available for the BUGS output. The BUGS implementation of a stochastic volatility model is illustrated using a time series of daily Pound/Dollar exchange rates.
Relationship Between Total Body Mass, Fat-Free Mass, Fat Mass, and Bone Mineral Density of the Hip In Middle-Age Women: The Roles of Diet, Physical Activity, and Menopause

Relationship Between Total Body Mass, Fat-Free Mass, Fat Mass, and Bone Mineral Density of the Hip in Middle-Age Women: The Roles of Diet, Physical Activity, and Menopause Elizabeth R. Fosson Department of Exercise Sciences, BYU Master of Science Objective: This study was conducted to investigate the relationship between hip bone mineral density (BMD), fat-free mass (FFM), fat mass (FM), and total body mass (TBM) and the extent to which these relationships were modified by various confounding factors. The cross-sectional analysis included 262 healthy females (mean age 41.6±3.0 years). Methods: BMD of the hip and body composition were assessed by the Hologic 4500W dual energy x-ray absorptiometry (DXA) system. Total and intensity of physical activity (PA) were objectively measured using an Actigraph accelerometer. Dietary calcium and vitamin D from food and beverages, as well as from supplements, were measured separately using the Block food frequency questionnaire. Menopause status and prescription bone drug use were measured by a questionnaire. Results: The relationship between FFM and hip BMD was strong and robust (F=24.5, P<0.0001). Using the pooled standard deviation revealed a large effect size of 1.2 when comparing hip BMD of women with low FFM and high FFM. Potentially confounding variables, considered individually and collectively, did not change this relationship. The association between FM and hip BMD was also substantial (F=9.9, P<0.0001) and remained significant when controlling for all potentially confounding variables, except differences in FFM. The relationship between TBM and hip BMD was also strong and dose-response (F=21.5, P<0.0001) and remained significant, except when differences in FFM were controlled. Conclusion: The relationships between body mass (total, fat, and fat-free) and BMD of the hip in middle-age women are strong and significant. The associations are not influenced by differences in age, height, menopause status, calcium or vitamin D intake, volume or intensity of PA, or the use of bone enhancing prescription drugs. The findings suggest that women with low body mass, particularly low FFM, tend to have low hip BMD and there is little that can be done to change this association.