Miracle-dz/UniFAR-FTUs huggingface dataset:
THE INFLUENCE OF STORAGE TEMPERATURE AND TIME ON TOTAL PHENOLIC CONTENT IN A SOFT WHEAT CULTIVAR

The influence of storage temperature and time on Total Phenolic Content (TPC) in a soft wheat cultivar, was the purpose of this paper. The biological material was represented by soft wheat grains from which there were formed control and working samples (grains, flour and bran). The control samples were stored at 10°C, and the working ones at four thermal thresholds (40oC, 60oC, 120oC and 180oC) for 15 days. Aftet 5, 10 and 15 days, Total Phenolic Content (TPC) has been estimated by a colorimetric assay, by measuring the ability of phenols to reduce Folin-Ciocalteu reagent. In all analyzed samples, compared to controls (samples stored at 10oC), the largest decreases of Total Phenolic Content were registered after 15 days of storage, with significant percentage reductions at 180°C and 120°C, in flour type 480 (WF), and in whole-wheat flour (WWF). After 10 days of storage, significant percentage reductions of TPC were registered in flour type 480 (WF), and in whole-wheat flour (WWF), and after 5 days in WF (in all cases in samples stored at 180°C and 120°C). The percentage decrease of TPC values was emphasized more when the storage temperature increased from 120°C to 180°C, compared with the thresholds 40-60°C or 60-120°C. The keeping of soft wheat samples under high temperature conditions led to a greater reduction in the total content of phenolic compounds,as compared to grains or bran.
Are declines in physical performance associated with a reduction in skill-related performance during professional soccer match-play?

Abstract The aim of this study was to determine whether declines in physical performance in a professional soccer team during match-play were associated with reductions in skill-related performance. Computerized tracking of performance in midfield players (n = 11) showed that total distance and distance covered in high-speed running (>14.4 km · h−1) were greater in the first versus second half of games (both P < 0.001) and in the first versus the final 15 min of play (P < 0.05). Analysis of high-speed running across 5-min periods showed that more distance was covered in the first versus the final game period, and in the peak period of activity compared with the following period and game mean for other periods (all P < 0.05). Analysis of skill-related measures revealed no significant decline between halves, across 15-min intervals or in the 5-min period following that of peak high-speed activity compared with the game mean for other 5-min periods. In contrast, frequencies of passing, ball possessions, and duels were greater in the first 5-min than in the final 5-min period (P < 0.05). Neither physical nor skill-related performance was affected across three consecutive games within a period of ≤7 days. The results suggest that the players were generally able to maintain skill-related performance throughout games and when competing in successive matches within a short time.
A low-voltage fully-monolithic /spl Delta//spl Sigma/-based class-D audio amplifier

This paper presents a single-chip digital audio amplifier based on a delta-sigma (/spl Delta//spl Sigma/) modulator and a power efficient switching (class-D) output-stage without intermediate filtering. Fabricated in a 0.18/spl mu/m standard digital CMOS process, this audio amplifier can operate from a single power-supply of 1.8V down to 1V, without significant change in performance. It has a measured total-harmonic-distortion (THD) at the speaker terminals of less than 0.07%, with a dynamic range (DR) of 85 dB. An efficiency of 76% can be achieved with a 4.3-/spl Omega/ speaker. The maximum output power is 350mW (rms) from a single 1.8-V power-supply, and the stand-by power consumption is only 7.5mW (load connected). This work demonstrates the feasibility of implementing class-D amplifiers with a high-end audio performance in low-voltage environments.
Hypoglycemic events analysis via recurrent time-to-event (HEART) models

Abstract Diabetes affects an estimated 25.8 million people in the United States and is one of the leading causes of death. A major safety concern in treating diabetes is the occurrence of hypoglycemic events. Despite this concern, the current methods of analyzing hypoglycemic events, including the Wilcoxon rank sum test and negative binomial regression, are not satisfactory. The aim of this article is to propose a new model to analyze hypoglycemic events with the goal of making this model a standard method in industry. Our method is based on a gamma frailty recurrent event model. To make this method broadly accessible to practitioners, this article provides many details of how this method works and discusses practical issues with supporting theoretical proofs. In particular, we make efforts to translate conditions and theorems from abstract counting process and martingale theories to intuitive and clinical meaningful explanations. For example, we provide a simple proof and illustration of the coarsening at random condition so that the practitioner can easily verify this condition. Connections and differences with traditional methods are discussed, and we demonstrate that under certain scenarios the widely used Wilcoxon rank sum test and negative binomial regression cannot control type 1 error rates while our proposed method is robust in all these situations. The usefulness of our method is demonstrated through a diabetes dataset which provides new clinical insights on the hypoglycemic data.
Using Best's Ratings in Life Insurer Insolvency Prediction

This article examines the efficiency of Best's recommendations, Insurance Regulatory Information System (IRIS) ratios, and other financial measures in their statistical ability to classify solvent and insolvent life insurers by estimating classification models for a sample of insurers for 1969 through 1986 and applying the models to a holdout sample for 1987 through 1991. The financial variables and IRIS ratios outperformed Best's recommendations in distinguishing between the two groups in a logit model. However, combining all three types of predictors into one model provided the most accurate classification of solvent or insolvent life insurers.
Vasodilatation is obligatory for contraction‐induced hyperaemia in canine skeletal muscle

There is a rapid increase in blood flow to active skeletal muscle with the onset of exercise, but the mechanism(s) eliciting this increase remains elusive. We hypothesized that the rapid increase in blood flow to active skeletal muscle with the onset of exercise is attributable to vasodilatation as a consequence of smooth muscle hyperpolarization. To test this hypothesis we examined the blood flow response to a brief tetanic contraction in which potassium (K+) was infused intra‐arterially to elevate the [K+]o and clamp the smooth muscle membrane potential within the skeletal muscle vascular bed. In six anaesthetized beagle dogs control contractions increased hindlimb blood flow by 97 ± 14 ml min−1. During K+ infusion the hyperaemic response to contraction was 8 ± 3 ml min−1. Since the hindlimb blood flow was reduced during K+ infusion, a similar reduction in baseline blood flow was produced with phenylephrine infusion. During phenylephrine infusion the hyperaemic response to contraction was preserved (89 ± 23 ml min−1). Recovery contractions performed after the discontinuation of the K+ infusion elicited blood flow responses similar to control (100 ± 11 ml min−1). In a separate experimental protocol using the isolated gastrocnemius muscle of mongrel dogs (n= 6) K+ infusion did not alter force production by the skeletal muscle. Our data indicate that in the absence of vasodilatation, there is virtually no change in blood flow. One implication of this finding is that the muscle pump cannot be responsible for the initial contraction‐induced hyperaemia. We conclude that the increase in blood flow immediately following a single muscle contraction is due to vasodilatation, presumably as a consequence of smooth muscle hyperpolarization.
New Surfactant-based Dressing Product to Improve Wound Closure Rates of Nonhealing Wounds: A European Multicenter Study Including 1036 Patients.

OBJECTIVE A new surfactant-based biomaterial containing the antimicrobial 1% silver sulfadiazine (SSD) was developed at the University of Virginia (Charlottesville, VA) to improve outcomes for nonhealing wounds. This study's objective was to clinically test the wound care outcomes of the new surfactant-based antimicrobial wound dressing (SAWD) in a multicenter trial. METHODS AND MATERIALS This cohort study enrolled 1036 patients with any nonhealing wound of > 3 months duration not responding to standard-of-care treatments from 10 wound care centers in 7 European countries. The SAWD was used for all wound types at all stages of complexity, healing, and severity. Data collection ranged from 6 months to 2 years and measured the percentage of patients achieving wound closure and time to complete closure. RESULTS Of the 1036 patients, 70% achieved wound closure, 24.6% were still in treatment at data collection, and 5.4% had a therapy change. The majority (56%) of these non-healing wounds achieved wound closure within 11 weeks. Patients were treated with the SAWD for 3 weeks to more than 1 year with no complications or adverse effects from long-term SSD antimicrobial use. CONCLUSION Ten centers concluded that the new SAWD provided positive results (improved wound closure rates, reduction of inflammation, pain, and odor), improvements in clinical application (faster and easier dressing change), and improved patient compliance.
Inhibition of Cardiac Ca2+ Release Channels (RyR2) Determines Efficacy of Class I Antiarrhythmic Drugs in Catecholaminergic Polymorphic Ventricular Tachycardia

Background— Catecholaminergic polymorphic ventricular tachycardia (CPVT) is caused by mutations in the cardiac ryanodine receptor (RyR2) or calsequestrin (Casq2) and can be difficult to treat. The class Ic antiarrhythmic drug flecainide blocks RyR2 channels and prevents CPVT in mice and humans. It is not known whether other class I antiarrhythmic drugs also block RyR2 channels and to what extent RyR2 channel inhibition contributes to antiarrhythmic efficacy in CPVT. Methods and Results— We first measured the effect of all class I antiarrhythmic drugs marketed in the United States (quinidine, procainamide, disopyramide, lidocaine, mexiletine, flecainide, and propafenone) on single RyR2 channels incorporated into lipid bilayers. Only flecainide and propafenone inhibited RyR2 channels, with the S-enantiomer of propafenone having a significantly lower potency than R-propafenone or flecainide. In Casq2−/− myocytes, the propafenone enantiomers and flecainide significantly reduced arrhythmogenic Ca2+ waves at clinically relevant concentrations, whereas Na+ channel inhibitors without RyR2 blocking properties did not. In Casq2−/− mice, 5 mg/kg R-propafenone or 20 mg/kg S-propafenone prevented exercise-induced CPVT, whereas procainamide (20 mg/kg) or lidocaine (20 mg/kg) were ineffective (n=5 to 9 mice, P<0.05). QRS duration was not significantly different, indicating a similar degree of Na+ channel inhibition. Clinically, propafenone (900 mg/d) prevented ICD shocks in a 22-year-old CPVT patient who had been refractory to maximal standard drug therapy and bilateral stellate ganglionectomy. Conclusions— RyR2 cardiac Ca2+ release channel inhibition appears to determine efficacy of class I drugs for the prevention of CPVT in Casq2−/− mice. Propafenone may be an alternative to flecainide for CPVT patients symptomatic on &bgr;-blockers.
Choice and Threshold: A Further Experiment in Spatial Duopoly

A serious, often the principal, problem facing every firm in competition is how far to imitate, or to diverge from, decisions of competitors. Whether we prefer to think in terms of spatial, quality, price, or of any variety of competition, the firm's ability to choose between higher or lower degrees of imitation of its rivals is a prerequisite to the maximization of its general preference function. Traditional analysis has pointed to discontinuous and abrupt imitation, or "clustering", as the principal characteristics of oligopoly. The purpose of this paper is to show that such a view is not necessarily correct. It will be seen that an independent marketing policy, often encountered in practice, can be justified theoretically as long as threshold-sensitive market behaviouris taken into account. We shall choose an example in spatial duopoly, based on a recently developed theoretical mechanism, where threshold-sensitive consumer behaviour-as opposed to the hyper-sensitive human conduct which is traditionally postulated was introduced by assuming a minimum sensibile range of indifference for choice between comparable alternatives.2 The generally-shared view in the behavioural sciences that human conduct is best explained as threshold-sensitive response to environmental stimulation forms the basis of our theory. The device of the threshold is emphasized here because it is believed that it enables any desired amount of composite behavioural detail to be introduced consistently into the analysis.3 The traditional economic assumption of
Malaria antifolate resistance with contrasting Plasmodium falciparum dihydrofolate reductase (DHFR) polymorphisms in humans and Anopheles mosquitoes

Surveillance for drug-resistant parasites in human blood is a major effort in malaria control. Here we report contrasting antifolate resistance polymorphisms in Plasmodium falciparum when parasites in human blood were compared with parasites in Anopheles vector mosquitoes from sleeping huts in rural Zambia. DNA encoding P. falciparum dihydrofolate reductase (EC 1.5.1.3) was amplified by PCR with allele-specific restriction enzyme digestions. Markedly prevalent pyrimethamine-resistant mutants were evident in human P. falciparum infections—S108N (>90%), with N51I, C59R, and 108N+51I+59R triple mutants (30–80%). This resistance level may be from selection pressure due to decades of sulfadoxine/pyrimethamine use in the region. In contrast, cycloguanil-resistant mutants were detected in very low frequency in parasites from human blood samples—S108T (13%), with A16V and 108T+16V double mutants (∼4%). Surprisingly, pyrimethamine-resistant mutants were of very low prevalence (2–12%) in the midguts of Anopheles arabiensis vector mosquitoes, but cycloguanil-resistant mutants were highly prevalent—S108T (90%), with A16V and the 108T+16V double mutant (49–57%). Structural analysis of the dihydrofolate reductase by in silico modeling revealed a key difference in the enzyme within the NADPH binding pocket, predicting the S108N enzyme to have reduced stability but the S108T enzyme to have increased stability. We conclude that P. falciparum can bear highly host-specific drug-resistant polymorphisms, most likely reflecting different selective pressures found in humans and mosquitoes. Thus, it may be useful to sample both human and mosquito vector infections to accurately ascertain the epidemiological status of drug-resistant alleles.
Study of propagation over two ends of a vessel in VHF band

Channel characteristics and temporal variations associated with VHF waves propagation between the engine control room (ECR) and the bridge room on board a vessel is presented in this paper. Temporal variation associated with the signal-to-noise ratio (SNR), Rician K-factor as well as the root-mean-square (RMS) delay spread obtained from wideband sounding are studied and compared for two different transmitter positions. Better reception, i.e. higher SNR, higher K-factor is obtained for the transmitter at a position closer to the receiver, but temporal variation on the two mentioned parameters is more severe and lower maximum usable data rate is associated with that link due to engine rotations and human activities near the transmitter position.
Atorvastatin Coadministration May Increase Digoxin Concentrations by Inhibition of Intestinal P‐Glycoprotein‐Mediated Secretion

The effect of atorvastatin on digoxin pharmacokinetics was assessed in 24 healthy volunteers in two studies. Subjects received 0.25 mg digoxin daily for 20 days, administered alone for the first 10 days and concomitantly with 10 mg or 80 mg atorvastatin for the last 10 days. Mean steady‐state plasma digoxin concentrations were unchanged by administration of 10 mg atorvastatin. Mean steady‐state plasma digoxin concentrations following administration of digoxin with 80 mg atorvastatin were slightly higher than concentrations following administration of digoxin alone, resulting in 20% and 15% higher Cmax and AUC(0.24) values, respectively Since tmax and renal clearance were not significantly affected, the results are consistent with an increase in the extent of digoxin absorption in the presence of atorvastatin. Digoxin is known to undergo intestinal secretion mediated by P‐glycoprotein. Since atorvastatin is a CYP3A4 substrate and many CYP3A4 substrates are also substrates for P‐glycoprotein transport, the influence of atorvastatin and its metabolites on P‐glycoprotein‐mediated digoxin transport in monolayers of the human colon carcinoma (Caco‐2) cell line was investigated. In this model system, atorvastatin exhibited efflux or secretion kinetics with a Km of 110 μM. Atorvastatin (100 μM) inhibited digoxin secretion (transport from the basolateral to apical aspect of the monolayer) by 58%, equivalent to the extent of inhibition observed with verapamil, a known inhibitor of P‐glycoprotein transport. Thus, the increase in steady‐state digoxin concentrations produced by 80 mg atorvastatin coadministration may result from inhibition of digoxin secretion into the intestinal lumen.
Is Desensitization of Intestinal 5‐Hydroxytryptamine Receptors an In‐vitro Phenomenon?

Abstract— The responses of proximal jejunum and distal ileum to successive applications of 5‐hydroxytryptamine (5‐HT) were examined in‐vitro and in‐vivo by measuring the electrical changes that reflect the stimulation of Cl− secretion. In stripped intestinal sheets the second application of a maximal concentration of 5‐HT failed to elicit any response, indicating that complete desensitization had occurred. If submaximal concentrations were used, a second response was observed, although it was smaller than the first, indicating partial desensitization. Replacing the bathing solutions following application of a maximal 5‐HT concentration also reduced, but did not abolish, the degree of desensitization observed with a second application of 5‐HT. In an in‐vivo preparation, however, there was no diminution of the responses to four successive maximal doses of 5‐HT. This lack of desensitization was also evident in the cardiovascular responses to 5‐HT. It is concluded that desensitization to 5‐HT is a phenomenon that is readily observed only in‐vitro and which is probably related to the inability of a small amount of isolated tissue to eliminate 5‐HT.
Directed migration of mouse macrophages in vitro involves myristoylated alanine‐rich C‐kinase substrate (MARCKS) protein

A role for MARCKS protein in directed migration of macrophages toward a chemoattractant was investigated. A peptide identical to the N‐terminus of MARCKS (the MANS peptide), shown previously to inhibit the function of MARCKS in various cell types, was used. We investigated whether this MARCKS‐related peptide could affect migration of macrophages, using the mouse macrophage‐like J774A.1 cell line and primary murine macrophages. Both of these cell types migrated in response to the chemoattractants macrophage/MCPs, MCP‐1 (25–100 ng/ml) or C5a (5–20 ng/ml). Cells were preincubated (15 min) with MANS or a mis‐sense control peptide (RNS), both at 50 μM, and effects on migration determined 3 h after addition of chemoattractants. The movement and interactions of MARCKS and actin also were followed visually via confocal microscopy using a fluorescently labeled antibody to MARCKS and fluorescently tagged phalloidin to identify actin. MANS, but not RNS, attenuated migration of J774A.1 cells and primary macrophages in response to MCP‐1 or C5a, implicating MARCKS in the cellular mechanism of directed migration. Exposure of cells to MCP‐1 resulted in rapid phosphorylation and translocation of MARCKS from plasma membrane to cytosol, whereas actin appeared to spread through the cell and into cell protrusions; there was visual and biochemical evidence of a transient interaction between MARCKS and actin during the process of migration. These results suggest that MARCKS is involved in directed migration of macrophages via a process involving its phosphorylation, cytoplasmic translocation, and interaction with actin.
A continuous patient activity monitor: validation and relation to disability

The measurement of patient activity over prolonged periods has been attempted with accelerometer-based devices, but these summate total acceleration and deceleration over time periods, are difficult to relate to recognizable activities and are influenced by passive movement. We describe the development of a portable monitor of ambulation. This logs posture (sitting, standing and lying) and number and vigour of steps in real time over prolonged periods, usually 24 h. This is based on a system of position sensors and an accelerometer which is sampled when the subject is standing. Data are processed through an interface and stored on a Psion Series 3 `palm top' computer. The system has been validated against observation, and the relationship of activity to disability in rheumatoid arthritis explored. Keywords: monitoring, activity, disability
The Schizosaccharomyces pombe Map4 adhesin is a glycoprotein that can be extracted from the cell wall with alkali but not with β‐glucanases and requires the C‐terminal DIPSY domain for function

In fungi, cell adhesion is required for flocculation, mating and virulence, and it is mediated by covalently bound cell wall proteins termed adhesins. Map4, an adhesin required for mating in Schizosaccharomyces pombe, is N‐glycosylated and O‐glycosylated, and is an endogenous substrate for the mannosyl transferase Oma4p. Map4 has a modular structure with an N‐terminal signal peptide, a serine and threonine (S/T)‐rich domain that includes nine repeats of 36 amino acids (rich in serine and threonine residues, but lacking glutamines), and a C‐terminal DIPSY domain with no glycosylphosphatidyl inositol (GPI)‐anchor signal. Map4 can be extracted from cell walls with SDS/mercaptoethanol sample buffer or with mild alkali solutions. After extensive extraction with hot sample buffer, no more protein can be released by β‐glucanases or alkali. Additionally, none of the cysteine residues of the protein is required for its retention at the cell wall. These results show that Map4 is not directly bound to β‐glucans and point to the existence of alkali‐ and SDS/mercaptoethanol‐sensitive linkages between cell wall proteins. The N‐terminal S/T‐rich regions are required for cell wall attachment, but the C‐terminal DIPSY domain is required for agglutination and mating in liquid and solid media.
Stock Price Dynamics, Dividends, and Option Prices with Volatility Feedback

In this paper, we provide a new framework for stock and options valuations by characterizing the joint dynamics of stock price, dividends, and volatility with the volatility feedback effect in continuous-time. Within our framework, we consider the properties of stock price and its dynamics with volatility feedback casting light on the excess volatility and the correlation between volatility and stock price. Most importantly, we discover a channel through which the market price of return risk, or equity risk-premium, affects option prices. One implication is that an increase in squared return volatility can be unfavorable to the holder of in-the-money call options. Finally, we illustrate the use of our framework to identifying the risk-return relation using forward-looking option data.