Miracle-dz/UniFAR-FTUs huggingface dataset:
Nutrient Requirements The Smallest Vertebrate , Teleost Fish , Can Utilize Synthetic Dipeptide-Based Diets 1

In vitro studies of brush-border intestinal transport of dipeptides and cytoplasmic hydrolysis in fish suggest that these processes could be key mechanisms in the absorption and utilization of nutrients for growth. However, in vivo experimentation to study the nutritional importance of these processes was needed. We compared three dietary formulations based on free, peptide and protein sources of amino acids. Our results were the first to show that a synthetic dipeptide (PP)-based diet could support growth in the early stages of ontogenesis of a teleost fish, rainbow trout (Oncorhynchus mykiss), whereas a free amino acid (FAA)-based diet failed. We found that fish fed an FAA-based diet had an increased rate of ammonia excretion [1.78 0.19 mmol NH3-N/(kg body wt h)], compared with fish fed a PP-based diet [1.25 0.07 mmol NH3-N/(kg body wt h)], suggesting that deamination is involved in the metabolism of dietary FAA. Teleost fish are known to obtain a high proportion of total energy from protein, compared with higher vertebrates. However, we found that feeding trout alevins a PP-based diet increased postprandial oxygen consumption for 2 to 24 h, whereas other treatments decreased 24-h postprandial metabolism. This may indicate that peptide metabolism is less efficient than protein metabolism. Juvenile rainbow trout differed from alevins in their response to FAAand PP-based diets. These observations strongly suggest that intestinal dietary peptide transport and hydrolysis could support protein synthesis and growth in vertebrates that respond poorly to FAA-based diets. We conclude that nutrient administration may be improved by manipulating dietary peptide composition and peptide/protein ratios, leading to better utilization of synthetic peptides, with nutritional and therapeutic implications for all vertebrates. J. Nutr. 133: 4225–4229, 2003.
Impact of Parallel Micro-Engineered Stent Grooves on Endothelial Cell Migration, Proliferation, and Function: An In Vivo Correlation Study of the Healing Response in the Coronary Swine Model

Background— Stent luminal surface characteristics influence surface endothelialization. We hypothesize that luminal stent microgrooves created in the direction of coronary flow accelerate endothelial cell migration, resulting in lower levels of neointimal formation. Methods and Results— Surface coverage efficiency was evaluated in vitro by allowing human aortic endothelial cells (HAEC) to migrate onto microgrooved (G) or smooth (NG) surfaces. HAEC functionality was assessed by proliferation rate, apoptosis rate, nitric oxide production, and inflammatory markers TNF-&agr; and VCAM-1 expression. Early endothelialization and restenosis studies were performed using the porcine coronary injury model. Stainless steel stents of identical design with (GS) and without (NGS) luminal microgrooves were used. The commercially available Multi-Link Vision (MLVS) stent of identical design was used as a control. The degree of GS and NGS surface endothelialization was compared at 3 days. Biocompatibility and tissue response outcomes were evaluated at 28 days. The in vitro study demonstrated that at 7 days the presence of surface microgrooves increased HAEC migration distance >2-fold. Cell proliferation rate and nitric oxide production were increased and apoptosis rate was decreased. There was no difference in inflammatory marker expression. At 3 days, coronary artery stent endothelialization was significantly increased in GS compared with NGS (81.3% versus 67.5%, P=0.0002). At 28 days, GS exhibited lower neointimal thickness compared with either NGS (21.1%, P=0.011) or MLVS (40.8%, P=0.014). Conclusion— Parallel microgrooves on coronary stent luminal surfaces promote endothelial cell migration and positively influence endothelial cell function, resulting in decreased neointimal formation in the porcine coronary injury model.
Combining Sgarbossa and Selvester ECG criteria to improve STEMI detection in the presence of LBBB

ECG detection of ST-segment Elevation Myocardial Infarction (STEMI) in the presence of left bundle-branch block (LBBB) has long been a challenge. The purpose of this study was to add Selvester criteria (the 10% rule) to Sgarbossa criteria for further improved detection of STEMI in LBBB and report the combined performance.
Adiponectin and Carotid Intima-Media Thickness in the Northern Manhattan Study

Background and Purpose— Adiponectin is an insulin-sensitizing plasma protein expressed in adipose tissue and suggested to play a role in atherosclerosis and cardiovascular disease. Data are lacking on the relationship between adiponectin and carotid intima-media thickness (IMT) in ethnically heterogeneous populations. We examined the relationship between adiponectin and IMT, a marker of atherosclerosis, in a multiethnic cohort study of stroke risk factors. Methods— Participants were from the Northern Manhattan Study (N=1522, mean age 66±9 years, 60% female, 20% black, 18% white, 60% Hispanic). Adiponectin was measured from baseline plasma samples and IMT was assessed by high-resolution B-mode carotid ultrasound. Regression models were used to examine the association between adiponectin, assessed continuously and in quartiles, and IMT controlling for demographics and vascular risk factors. Results— The mean adiponectin level was 10.3±5.2 &mgr;g/mL (median, 9.2 &mgr;g/mL; range, 2.3–53.3 &mgr;g/mL), and the mean IMT was 0.91±0.08 mm. Adiponectin was inversely associated with IMT, even after controlling for demographics and vascular risk factors. Individuals in the first quartile of adiponectin had mean IMT that was on average 0.02 mm greater than those in the top quartile. The relationship between adiponectin and IMT appeared to be stronger among those with diabetes. Conclusions— Our findings suggest that low adiponectin is associated with increased IMT in a multiethnic cohort and support a protective role for adiponectin in atherosclerosis.
Novel designs for thermally robust coplanar crossing in QCA

In this paper, different circuit arrangements of quantum-dot cellular automata (QCA) are proposed for the so-called coplanar crossing. These arrangements exploit the majority voting properties of QCA to allow a robust crossing of wires on the Cartesian plane. This is accomplished using enlarged lines and voting. Using a Bayesian network (BN) based simulator, new results are provided to evaluate the robustness to so-called kink of these arrangements to thermal variations. The BN simulator provides fast and reliable computation of the signal polarization versus normalized temperature. It is shown that by modifying the layout, a higher polarization level can be achieved in the routed signal by utilizing the proposed QCA arrangements
Neutrophil gelatinase-associated lipocalin--an emerging troponin for kidney injury.

NGAL as an AKI biomarker has successfully passed through the pre-clinical, assay development and initial clinical testing stages of the biomarker development process. It has now entered the prospective screening stage, facilitated by the development of commercial tools for the measurement of NGAL in large populations across different laboratories. But will any single biomarker such as NGAL suffice in AKI? In addition to early diagnosis and prediction, it would be desirable to identify biomarkers capable of discerning AKI subtypes, identifying etiologies, predicting clinical outcomes, allowing for risk stratification and monitoring the response to interventions. In order to obtain all of this desired information, a panel of validated biomarkers may be needed. The current status of NGAL as an AKI biomarker is shown in Table ​Table1.1. Other AKI panel candidates may include interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1), cystatin C and liver-type fatty acid binding protein (L-FABP), to name a few [4–6]. A brief comparison of the properties of NGAL versus other promising urinary biomarkers is shown in Tables ​Tables22 and ​and33. Table 1 NGAL as an AKI biomarker Table 2 Urinary biomarkers for the early prediction of AKI in various clinical settings Table 3 Urinary biomarkers for the early prediction of clinical outcomes in various AKI settings The availability of a panel of AKI biomarkers could revolutionize renal and critical care. However, such idealistic thinking must be tempered with the enormous technical and fiscal issues surrounding the identification, validation, commercial development and acceptance of multi-marker panels. Deriving from the recent cardiology literature, a clinically useful biomarker should (a) be easily measurable at a reasonable cost with short turnaround times; (b) provide information that is not already available from clinical assessment; and (c) aid in medical decision making [61]. In this respect, troponin as a stand-alone biomarker provides excellent diagnostic and prognostic information in acute coronary syndromes and acute decompensated heart failure [62], although the addition of brain natrituretic peptide does improve the risk stratification of death from cardiovascular causes [63]. If the current prospective multicenter studies of NGAL measurements with standardized laboratory platforms provide promising results, we may have already closed in on the ‘renal troponin’.
Aerobic Interval Training and Cardiometabolic Health in Patients with Type 2 Diabetes: A Meta-Analysis

Vigorous to maximal aerobic interval training (INT) has received remarkable interest in improving cardiometabolic outcomes for type 2 diabetes patients recently, yet with inconsistent findings. This meta-analysis was aimed to quantify its effectiveness in type 2 diabetes. Randomized controlled trials (RCTs) were identified by searches of 3 databases to October 2017, which evaluated the effects of INT with a minimal training duration of 8 weeks vs. moderate-intensity continuous training (MICT) or non-exercise training (NET) among type 2 diabetes patients on outcomes including cardiorespiratory fitness, glycemic control, body composition, blood pressure, and lipid profiles. Weighted mean differences with 95% confidence intervals (CIs) were calculated with the random-effects model. Nine datasets from 7 RCTs with 189 patients were included. Compared with MICT, INT improved maximal oxygen consumption (VO2max) by 2.60 ml/kg/min (95% CI: 1.32 to 3.88 ml/kg/min, P <0.001) and decreased hemoglobin A1c (HbA1c) by 0.26% (95% CI: −0.46% to −0.07%, P = 0.008). These outcomes for INT were also significant vs. energy expenditure-matched MICT, with VO2max increased by 2.18 ml/kg/min (P = 0.04) and HbA1c decreased by 0.28% (P = 0.01). Yet their magnitudes of changes were larger compared with NET, with VO2max increased by 6.38 ml/kg/min (P <0.001) and HbA1c reduced by 0.83% (P = 0.004). Systolic blood pressure could be lowered by INT compared with energy expenditure-matched MICT or NET (both P <0.05), but other cardiometabolic markers and body composition were not significantly altered in general. In conclusion, despite a limited number of studies, INT improves cardiometabolic health especially for VO2max and HbA1c among patients with type 2 diabetes, and might be considered an alternative to MICT. Yet the optimal training protocols still require to be established.
Why Do Manufacturers Issue Coupons? An Empirical Analysis of Breakfast Cereals

We explore the relationship between shelf prices and manufacturers' coupons for 25 ready-to-eat breakfast cereals. We find that shelf prices are lower during periods when coupons are available. This result is inconsistent with static monopoly price discrimination under a broad range of assumptions. We present evidence that is inconsistent with both dynamic theories of price discrimination and explanations of couponing based on the vertical relationship between manufacturers and retailers. We find support for models of price discrimination in oligopoly settings as well as suggestions that firmwide incentives may induce managers to use coupons and price cuts simultaneously. Finally, lagged coupons have a positive effect on current sales, suggesting that coupons are used to induce repurchase.
Mild hypothermia reduces expression of intercellular adhesion molecule‐1 (ICAM‐1) and the accumulation of neutrophils after acid‐induced lung injury in the rat

Background: The pathophysiology of the acute phase of acid‐induced lung injury (AILI) has been elucidated. However, once acute respiratory distress syndrome (ARDS) develops, the mortality rate remains high and there is, as yet, no effective therapy. There are reports that application of mild hypothermia is an effective treatment for ARDS. In this study, we hypothesize that mild hypothermia inhibits activation of neutrophils and expression of intercellular adhesion molecule‐1 (ICAM‐1) in an injured lung. We studied the effects of mild hypothermia on the expression of ICAM‐1 and the accumulation of neutrophils after AILI in the rat.
On average distortion of embedding metrics into the line and into L1

We introduce and study the notion of the average distortion of a nonexpanding embedding of one metric space into another. Less sensitive than the multiplicative metric distortion, the average distortion captures well the global picture, and, overall, is a quite interesting new measure of metric proximity, related to the concentration of measure phenomenon. We establish close mutual relations between the MinCut- MaxFlow gap in a uniform-demand multicommodity flow, and the average distortion of embedding the suitable (dual) metric into l1. These relations are exploited to show that the shortest-path metrics of special (e.g., planar, bounded treewidth, etc.) graphs embed into l1 with constant average distortion. The main result of the paper claims that this remains true even if l1 is replaced with the line. This result is further sharpened for graphs of a bounded treewidth.
Engineering neuronal growth cones to promote axon regeneration over inhibitory molecules

Neurons in the central nervous system (CNS) fail to regenerate axons after injuries due to the diminished intrinsic axon growth capacity of mature neurons and the hostile extrinsic environment composed of a milieu of inhibitory factors. Recent studies revealed that targeting a particular group of extracellular inhibitory factors is insufficient to trigger long-distance axon regeneration. Instead of antagonizing the growing list of impediments, tackling a common target that mediates axon growth inhibition offers an alternative strategy to promote axon regeneration. Neuronal growth cone, the machinery that derives axon extension, is the final converging target of most, if not all, growth impediments in the CNS. In this study, we aim to promote axon growth by directly targeting the growth cone. Here we report that pharmacological inhibition or genetic silencing of nonmuscle myosin II (NMII) markedly accelerates axon growth over permissive and nonpermissive substrates, including major CNS inhibitors such as chondroitin sulfate proteoglycans and myelin-associated inhibitors. We find that NMII inhibition leads to the reorganization of both actin and microtubules (MTs) in the growth cone, resulting in MT reorganization that allows rapid axon extension over inhibitory substrates. In addition to enhancing axon extension, we show that local blockade of NMII activity in axons is sufficient to trigger axons to grow across the permissive–inhibitory border. Together, our study proposes NMII and growth cone cytoskeletal components as effective targets for promoting axon regeneration.
The impact of galactic properties and environment on the quenching of central and satellite galaxies: A comparison between SDSS, Illustris and L-Galaxies

We quantify the impact that a variety of galactic and environmental properties have on the quenching of star formation. We collate a sample of ∼400 000 central and ∼100 000 satellite galaxies from the Sloan Digital Sky Survey Data Release 7 (SDSS DR7). Specifically, we consider central velocity dispersion (σc), stellar, halo, bulge and disc mass, local density, bulge-to-total ratio, groupcentric distance and galaxy–halo mass ratio. We develop and apply a new statistical technique to quantify the impact on the quenched fraction (ƒ_(Quench)) of varying one parameter, while keeping the remaining parameters fixed. For centrals, we find that the ƒ_(Quench)^(–σ)c relationship is tighter and steeper than for any other variable considered. We compare to the Illustris hydrodynamical simulation and the Munich semi-analytic model (L-Galaxies), finding that our results for centrals are qualitatively consistent with their predictions for quenching via radio-mode AGN feedback, hinting at the viability of this process in explaining our observational trends. However, we also find evidence that quenching in L-Galaxies is too efficient and quenching in Illustris is not efficient enough, compared to observations. For satellites, we find strong evidence that environment affects their quenched fraction at fixed central velocity dispersion, particularly at lower masses. At higher masses, satellites behave identically to centrals in their quenching. Of the environmental parameters considered, local density affects the quenched fraction of satellites the most at fixed central velocity dispersion.
Spontaneous mutations in the human immunodeficiency virus type 1 gag gene that affect viral replication in the presence of cyclosporins

Human immunodeficiency virus type 1 mutants that are resistant to inhibition by cyclosporins arise spontaneously in vitro during propagation in a HeLa-CD4+ cell line in the presence of a nonimmunosuppressive analog of cyclosporin A. Interestingly, the phenotype of all of the mutants examined is drug resistant and drug dependent, with both cyclosporin A and its analog. Four independently isolated mutants have been analyzed genetically by construction of recombinant proviruses in the NL4-3 parental strain background and subsequent testing of the chimeric viruses in HeLa cells. The cyclosporin-resistant, cyclosporin-dependent phenotype consistently transfers with a 1.3-kb fragment of gag, within which the four mutants share one of two possible single amino acid exchanges in a proline-rich stretch in the capsid domain of Pr55gag. These mutants provide the first evidence that mutations in human immunodeficiency virus type 1 gag confer resistance to cyclosporins; however, replication is conditional on the presence of the drug. In the T-cell line CEM, replication of the recombinant mutant viruses is also cyclosporin dependent. The drug-dependent replication in HeLa cells is stringent, and in the absence of cyclosporin only revertant viruses with the parental phenotype grow out of cultures infected with cyclosporin-dependent virus. In at least one isolate examined, the revertant phenotype appears to be due to suppressor mutations near the proline-rich region.
Woodchuck Hepatitis Virus Enhancer I and Enhancer II Are Both Involved in N-myc2 Activation in Woodchuck Liver Tumors

ABSTRACT Direct activation of the N-myc2 oncogene by insertion of woodchuck hepatitis virus (WHV) DNA is a major oncogenic step in woodchuck hepatocarcinogenesis. We previously reported that WHV enhancer II (We2), which controls expression of the core/pregenome RNA, can also activate the N-myc2 promoter in hepatoma cell lines. To better define the integrated WHV regulatory sequences responsible for N-myc2 promoter activation in woodchuck liver tumors, we analyzed the structure and enhancer activity of a single viral integrant found at the win locus in tumor 2260T1 and mapping approximately 175 kb 3′ of N-myc2. This viral insert was made of 11 concatemerized WHV fragments, 5 of which overlapped with We2 sequences and 1 with WHV sequence homologous to that of hepatitis B virus enhancer I (We1). In transient transfection assays in hepatoma-derived cells, the We2 activator was found to be fully effective only when inserted in close proximity to the N-myc2 promoter whereas the We1 element by itself was apparently devoid of activity. In contrast, the 2260T1 viral insert exhibited a potent enhancer capacity that depended both on multimerized We2 and on We1 sequences. In a survey of different woodchuck hepatomas, both elements were commonly found within integrated viral sequences involved in long-range N-myc2 activation.
Cannabinoids in Parkinson's Disease

Abstract The endocannabinoid system plays a regulatory role in a number of physiological processes and has been found altered in different pathological conditions, including movement disorders. The interactions between cannabinoids and dopamine in the basal ganglia are remarkably complex and involve both the modulation of other neurotransmitters (γ-aminobutyric acid, glutamate, opioids, peptides) and the activation of different receptors subtypes (cannabinoid receptor type 1 and 2). In the last years, experimental studies contributed to enrich this scenario reporting interactions between cannabinoids and other receptor systems (transient receptor potential vanilloid type 1 cation channel, adenosine receptors, 5-hydroxytryptamine receptors). The improved knowledge, adding new interpretation on the biochemical interaction between cannabinoids and other signaling pathways, may contribute to develop new pharmacological strategies. A number of preclinical studies in different experimental Parkinson's disease (PD) models demonstrated that modulating the cannabinoid system may be useful to treat some motor symptoms. Despite new cannabinoid-based medicines have been proposed for motor and nonmotor symptoms of PD, so far, results from clinical studies are controversial and inconclusive. Further clinical studies involving larger samples of patients, appropriate molecular targets, and specific clinical outcome measures are needed to clarify the effectiveness of cannabinoid-based therapies.
The CARD 8 p . C 10 X mutation associates with a low anti-glycans antibody response in patients with Crohn ’ s disease

Background: Crohn’s disease (CD) is associated with elevated anti-glycans antibody response in 60% of CD patients, and 25% of healthy first-degree relatives (HFDRs), suggesting a genetic influence for this humoral response. In mice, anti-glucan antibody response depends on the NLRP3 inflammasome. Here, we explored the effect of mutated CARD8, a component of the inflammasome, on anti-glycans antibody response in human. Methods: The association between p.C10X mutation (rs2043211) of the CARD8 gene and the levels of anti-glycans antibody response was examined in 39 CD families. The family-based QTDT association test was used to test for the genetic association between CARD8 p.C10X mutation and anti-glycan antibodies in the pedigrees. The difference in antibody responses determined by ELISA was tested in a subgroup of CD probands (one per family) and in a subgroup of HFDRs using the Wilcoxon Kruskal Wallis non-parametric test. Results: The QTDT familial transmission tests showed that the p.C10X mutation of CARD8 was significantly associated with lower levels of antibody to mannans and glucans but not chitin (p=0.024, p=0.0028 and p=0.577, for ASCA, ALCA and ACCA, respectively). These associations were independent of NOD2 and NOD1 genetic backgrounds. The p.C10X mutation significantly associated or displayed a trend toward lower ASCA and ALCA levels (p=0.038 and p=0.08, respectively) only in the subgroup of CD probands. Such associations were not significant for ACCA levels in both subgroups of CD probands and of HFDRs. Conclusion: Our results show that ASCA and ALCA but not ACCA levels are under the influence of CARD8 genotype. Alteration of CARD8, a component of inflammasome, is associated with lower levels of antibodies directed to mannans and glucans at least in CD patients.