Miracle-dz/UniFAR-FTUs huggingface dataset:
Proinflammatory cytokines depress cardiac efficiency by a nitric oxide-dependent mechanism.

Proinflammatory cytokines (interleukin-1β, tumor necrosis factor-α, and interferon-γ; Cytomix) depress myocardial contractile work partially by stimulating expression of inducible nitric oxide (NO) synthase (iNOS). Because NO and peroxynitrite inhibit myocardial O2 consumption (MV˙o 2), we examined whether this mechanism contributes to reduced cardiac work. In control isolated working rat hearts, cardiac work was stable for 60 min, followed by a decline from 60 to 120 min, without change in MV˙o 2. Cardiac efficiency (work/MV˙o 2) was therefore reduced from 60 to 120 min. Cytomix shortened the onset (within 20-40 min) and enhanced the depression in cardiac work and efficiency and inhibited MV˙o 2 after 80 min. Mercaptoethylguanidine (MEG), an iNOS inhibitor and peroxynitrite scavenger, or the glucocorticoid dexamethasone (Dex) abolished the effects of Cytomix. iNOS expression was increased 10-fold by Cytomix and abolished by Dex but not MEG. That cytokine-induced depression in cardiac work precedes the reduction in MV˙o 2 suggests, at least in the early response, that NO and/or peroxynitrite may not impair heart function by inhibiting mitochondrial respiration but reduce the heart's ability to utilize ATP for contractile work.
Differential regulation of NHE isoforms by sodium depletion in proximal and distal segments of rat colon.

Dietary sodium depletion has multiple diverse effects on ion transport in the rat colon, including both the induction and inhibition of electroneutral NaCl absorption in proximal and distal colon of rat, respectively. To establish the mechanism of the differential regulation of Na+ absorption by sodium depletion, this study utilized 1) HOE-694, a dose-dependent inhibitor of Na+/H+exchanger (NHE) isoforms, in studies of proton gradient-driven22Na uptake (i.e., Na+/H+exchange) by apical membrane vesicles (AMV); 2) Northern blot analyses of NHE isoform-specific mRNA abundance; and 3) Western blot analyses of NHE isoform-specific protein expression. HOE-694 inhibition studies establish that 25 μM HOE-694-sensitive (NHE2) and 25 μM HOE-694-insensitive (NHE3) Na+/H+exchange activities are present in AMV of both proximal and distal colon of normal rats. In proximal colon, dietary sodium depletion enhanced both NHE2 and NHE3 isoform-specific Na+/H+exchange activities, protein expression, and mRNA abundance. In contrast, in distal colon both NHE2 and NHE3 isoform-specific Na+/H+exchange activities, protein expression, and mRNA abundance were inhibited by sodium depletion. NHE1 isoform-specific mRNA abundance in proximal or distal colon was not altered by sodium depletion. Differential effects by sodium depletion on Na+/H+exchange in rat colon are tissue specific and isoform specific; sodium depletion both induces and inhibits apical Na+/H+exchange at a pretranslational level.
Child / Computer interaction : Observation in classroom setting

Background in music education: The relationship between new technology and learning is gaining more relevance in the field of music education (Webster 2002). The present study deals with an area still under-studied, that of interactive musical systems, in an attempt to understand in what way it can affect the learning and the musical creativity of children. In particular, we chose to study young children, 3/5 years old, because at this age the problem of the interaction between child and machine takes on a fundamental role in the learning process. Imberty (2002), in accordance with the psychologist Daniel Stern (1977), describes the musical development of young children as based on the vocal play between child and mother (lallation, baby-talk), characterised by the mechanism of repetition and variation. The point of interest is to verify what type of music development arises when this interaction takes place not between two human subjects, but rather between a child and a machine.
Pressure-dependent renin release: effects of sodium intake and changes of total body sodium.

The impact of sodium intake and changes in total body sodium (TBS) for the setting of pressure-dependent renin release (PDRR) was studied in freely moving dogs. An aortic cuff allowed servo control of renal perfusion pressure (RPP) at preset values. Protocols were 1) high sodium intake (HSI), 2) low sodium intake (LSI), 3) TBS moderately increased (+3.1 mmol Na/kg body wt) by 20% reduction of RPP for 2-4 days, 4) large increase of TBS (+8.2) by combining protocol 3 with aldosterone infusion, and 5) TBS reduced (-3.1) by peritoneal dialyses. Twenty-four-hour time courses of arterial plasma renin activity (PRA) revealed that LSI increased PRA for the first 10 h only; afterward PRA did not differ between LSI and HSI. Reduced TBS increased PRA constantly, and the large increase of TBS constantly reduced PRA. PDRR stimulus-response curves (assessed 20 h after last sodium intake) revealed an exponential relationship in each protocol. PDRR was not changed by different sodium intake. Conversely, reduced TBS increased PDRR markedly, whereas the large increase of TBS suppressed it. Thus an inverse relationship between TBS and PRA, i.e., a TBS-dependent renin release, was found. This relationship was enhanced by decreasing RPP. This interplay between TBS-dependent renin release and PDRR allows the organism a differentiated reaction to changes in TBS and arterial pressure.
Deep transcriptome annotation enables the discovery and functional characterization of cryptic small proteins

Recent functional, proteomic and ribosome profiling studies in eukaryotes have concurrently demonstrated the translation of alternative open-reading frames (altORFs) in addition to annotated protein coding sequences (CDSs). We show that a large number of small proteins could in fact be coded by these altORFs. The putative alternative proteins translated from altORFs have orthologs in many species and contain functional domains. Evolutionary analyses indicate that altORFs often show more extreme conservation patterns than their CDSs. Thousands of alternative proteins are detected in proteomic datasets by reanalysis using a database containing predicted alternative proteins. This is illustrated with specific examples, including altMiD51, a 70 amino acid mitochondrial fission-promoting protein encoded in MiD51/Mief1/SMCR7L, a gene encoding an annotated protein promoting mitochondrial fission. Our results suggest that many genes are multicoding genes and code for a large protein and one or several small proteins.
A systematic screening of total antioxidants in dietary plants.

A predominantly plant-based diet reduces the risk for development of several chronic diseases. It is often assumed that antioxidants contribute to this protection, but results from intervention trials with single antioxidants administered as supplements quite consistently do not support any benefit. Because dietary plants contain several hundred different antioxidants, it would be useful to know the total concentration of electron-donating antioxidants (i.e., reductants) in individual items. Such data might be useful in the identification of the most beneficial dietary plants. We have assessed systematically total antioxidants in a variety of dietary plants used worldwide, including various fruits, berries, vegetables, cereals, nuts and pulses. When possible, we analyzed three or more samples of dietary plants from three different geographic regions in the world. Total antioxidants was assessed by the reduction of Fe(3+) to Fe(2+) (i.e., the FRAP assay), which occurred rapidly with all reductants with half-reaction reduction potentials above that of Fe(3+)/Fe(2+). The values, therefore, expressed the corresponding concentration of electron-donating antioxidants. Our results demonstrated that there is more than a 1000-fold difference among total antioxidants in various dietary plants. Plants that contain most antioxidants included members of several families, such as Rosaceae (dog rose, sour cherry, blackberry, strawberry, raspberry), Empetraceae (crowberry), Ericaceae (blueberry), Grossulariaceae (black currant), Juglandaceae (walnut), Asteraceae (sunflower seed), Punicaceae (pomegranate) and Zingiberaceae (ginger). In a Norwegian diet, fruits, berries and cereals contributed 43.6%, 27.1% and 11.7%, respectively, of the total intake of plant antioxidants. Vegetables contributed only 8.9%. The systematic analysis presented here will facilitate research into the nutritional role of the combined effect of antioxidants in dietary plants.
Intracellular pH shifts in cultured kidney (A6) cells: effects on apical Na+ transport.

We report, for the epithelial Na+ channel (ENaC) in A6 cells, the modulation by cell pH (pHc) of the transepithelial Na+ current ( I Na), the current through the individual Na+channel ( i), the open Na+ channel density ( N o), and the kinetic parameters of the relationship between I Na and the apical Na+ concentration. The i and N o were evaluated from the Lorentzian I Na noise induced by the apical Na+ channel blocker 6-chloro-3,5-diaminopyrazine-2-carboxamide. pHc shifts were induced, under strict and volume-controlled experimental conditions, by apical/basolateral NH4Cl pulses or basolateral arrest of the Na+/H+exchanger (Na+ removal; block by ethylisopropylamiloride) and were measured with the pH-sensitive probe 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. The changes in pHc were positively correlated to changes in I Na and the apically dominated transepithelial conductance. The sole pHc-sensitive parameter underlying I Na was N o. Only the saturation value of the I Na kinetics was subject to changes in pHc. pHc-dependent changes in N o may be caused by influencing P o, the ENaC open probability, or/and the total channel number, N T = N o/ P o.
Visible-light photon migration through myocardium in vivo.

Empirical data between 510 and 590 nm of diffuse reflected light from the pig heart in vivo have shown that myoglobin and cytochrome c absorption peaks with little apparent contribution of red blood cell (RBC) Hb. Monte Carlo simulations of photon migration in tissue were performed to compare the effects of myoglobin and cytochromes with those of blood Hb on photon pathlengths and diffuse reflectance of visible wavelengths (450-600 nm) from the pig heart in vivo. Wavelength dependence of the input parameters, including the transport-corrected scattering coefficients (1.1-1.2 mm-1) and the absorption coefficients of blood-free solubilized heart tissue (0.43-1.47 mm-1), as well as the absorption coefficients of Hb, were determined by an integrating sphere method and standard spectrophotometry, respectively. The Monte Carlo simulations indicate that in the 510- to 590-nm range the mean path length within the myocardium for diffusely reflected light varies from 1.4 to 1.2 mm, whereas their mean penetration depth within the epicardium is only 330-400 μm for blood-free heart tissue. Analysis shows that the blood Hb absorption extrema are only observable between 510 and 590 nm when RBC concentration in tissue is >0.5%. Blood within vessels much larger than capillaries does not contribute significantly to the spectral features, because virtually all light in this spectral range is absorbed during transit through large vessels (>100 μm). This analysis suggests that diffuse reflected light in the 510- to 590-nm region will show spectral features uniquely associated with myoglobin and cytochrome c oxygenation states within 400 μm of the surface of the heart in situ as long as the capillary RBC concentration remains <0.5%.
Influence of methylenetetrahydrofolate reductase genotype, age, vitamin B-12, and folate status on plasma homocysteine in children.

BACKGROUND Several studies have examined the association of the methylenetetrahydrofolate reductase (MTHFR) genotype with plasma homocysteine in adults, but few studies have been performed in children. OBJECTIVE We measured the concentrations of plasma total homocysteine, folate, and vitamin B-12 in a group of healthy fasting children and related these to MTHFR genotype. DESIGN After the subjects fasted, blood samples were collected into EDTA-containing tubes. Plasma, red blood cells, and the buffy coat were immediately stored at -80 degrees C for biochemical and molecular analyses. Plasma total homocysteine was determined by HPLC. Folate and vitamin B-12 were measured by a double-labeled radioimmunoassay, and the genotypic analysis was performed by polymerase chain reaction amplification of genomic DNA extracted from blood leukocytes. RESULTS Plasma homocysteine concentrations correlated negatively with folate and vitamin B-12(,) but positively with age (P: < 0. 0001). Whereas folate and vitamin B-12 accounted for 27% and 19% of the variation in homocysteine, respectively, age accounted for 48% of the variation. When the cohort was divided into older (>10 y) and younger (</=10 y) individuals, folate was significantly lower in the older individuals who were homozygous for the mutation (T/T) than in those who were homozygous for the wild-type allele (C/C). Homocysteine was higher in the T/T group than in both the C/C and C/T subgroups aged >10 y. CONCLUSION Our data show that in a healthy pediatric population, MTHFR genotype played a significant role in determining homocysteine concentrations in older (>10 y), nutritionally stressed children.
Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance.

BACKGROUND Exercise practitioners often take vitamin C supplements because intense muscular contractile activity can result in oxidative stress, as indicated by altered muscle and blood glutathione concentrations and increases in protein, DNA, and lipid peroxidation. There is, however, considerable debate regarding the beneficial health effects of vitamin C supplementation. OBJECTIVE This study was designed to study the effect of vitamin C on training efficiency in rats and in humans. DESIGN The human study was double-blind and randomized. Fourteen men (27-36 y old) were trained for 8 wk. Five of the men were supplemented daily with an oral dose of 1 g vitamin C. In the animal study, 24 male Wistar rats were exercised under 2 different protocols for 3 and 6 wk. Twelve of the rats were treated with a daily dose of vitamin C (0.24 mg/cm2 body surface area). RESULTS The administration of vitamin C significantly (P=0.014) hampered endurance capacity. The adverse effects of vitamin C may result from its capacity to reduce the exercise-induced expression of key transcription factors involved in mitochondrial biogenesis. These factors are peroxisome proliferator-activated receptor co-activator 1, nuclear respiratory factor 1, and mitochondrial transcription factor A. Vitamin C also prevented the exercise-induced expression of cytochrome C (a marker of mitochondrial content) and of the antioxidant enzymes superoxide dismutase and glutathione peroxidase. CONCLUSION Vitamin C supplementation decreases training efficiency because it prevents some cellular adaptations to exercise.
Abnormal platelet Ca2+handling accompanied by increased cytosolic free Mg2+ in essential hypertension.

To test the hypothesis that abnormal platelet Ca2+ handling in essential hypertension results from cellular Mg2+ deficiency, cytosolic free Mg2+ concentration ([Mg2+]i) and Ca2+ metabolism were studied in mag-fura 2 and fura 2-loaded platelets from 30 essential hypertensive patients and 30 sex- and age-matched normotensive controls. Basal cytosolic free Ca2+ concentration ([Ca2+]i) and intracellular Ca2+ discharge capacity were higher in hypertensives than in normotensives (22 ± 5 vs. 18 ± 5 nM, P < 0.05; 743 ± 250 vs. 624 ± 144 nM, P < 0.05, respectively). The thrombin (0.03-1.0 U/ml)-evoked [Ca2+]iresponse was also enhanced in platelets from hypertensives in both the absence and presence of extracellular Ca2+. However, basal [Mg2+]iwas higher in hypertensives than in normotensives (437 ± 110 vs. 353 ± 85 μM, P < 0.05), whereas serum Mg2+ was similar in the two groups. These results oppose the Mg2+ deficiency hypothesis in platelets in essential hypertension.
Detecting Copy-Move Forgeries in Scanned Text Documents

The detection of copy–move forgeries has been studied extensively, however all known methods were designed and evaluated for digital images depicting natural scenes. In this paper, we address the problem of detecting and localizing copy–move forgeries in images of scanned text documents. The purpose of our analysis is to study how block-based detection of near-duplicates performs in this application scenario considering that even authentic scanned text contains multiple, similar-looking glyphs (letters, numbers, and punctuation marks). A series of experiments on scanned documents is carried out to examine the operation of some feature representations proposed in the literature with respect to the correct detection of copied image segments and the minimization of false positives. Our findings indicate that, subject to specific threshold and parameter values, the block-based methods show modest performance in detecting copy–move forgery from scanned documents. We explore strategies to further adapt block-based copy–move forgery detection approaches to this relevant application scenario.
Differential protective effects of Bcl-xL and Bcl-2 on apoptotic liver injury in transgenic mice.

Fas ligand (CD95L) and tumor necrosis factor-α (TNF-α) are pivotal inducers of hepatocyte apoptosis. Uncontrolled activation of these two systems is involved in several forms of liver injury. Although the broad antiapoptotic action of Bcl-2 and Bcl-xL has been clearly established in various apoptotic pathways, their ability to inhibit the Fas/CD95- and TNF-α-mediated apoptotic signal has remained controversial. We have demonstrated that the expression of BCL-2 in hepatocytes protects them against Fas-induced fulminant hepatitis in transgenic mice. The present study shows that transgenic mice overexpressing[Formula: see text]in hepatocytes are also protected from Fas-induced apoptosis in a dose-dependent manner. Bcl-xL and Bcl-2 were protective without any change in the level of endogenous[Formula: see text]or Bax and inhibited hepatic caspase-3-like activity. In vivo injection of TNF-α caused massive apoptosis and death only when transcription was inhibited. Under these conditions,[Formula: see text]mice were partially protected from liver injury and death but PK-BCL-2 mice were not. A similar differential protective effect of Bcl-xL and Bcl-2 transgenes was observed when Fas/CD95 was activated and transcription blocked. These results suggest that apoptosis triggered by activation of both Fas/CD95 and TNF-α receptors is to some extent counteracted by the transcription-dependent protective effects, which are essential for the antiapoptotic activity of Bcl-2 but not of Bcl-xL. Therefore, Bcl-xL and Bcl-2 appear to have different antiapoptotic effects in the liver whose characterization could facilitate their use to prevent the uncontrolled apoptosis of hepatocytes.
Texture Virtualization for Terrain Rendering

Virtual texturing is a technique that allows the use of arbitrarily large textures within the limited physical video memory. Through a paging and streaming system, only the currently visible parts of a mipmap chain are stored in the video memory while the rest of the data may reside in any other memory or storage device. Not only does this enable the use of unique and very detailed textures, but makes high resolution images such as satellite or aerial photography data usable in real-time applications without further modiﬁcations or downsampling. This work sketches the virtual texturing pipeline and discusses the beneﬁts and limitations of it. Due to the nature of terrains in real-time applications, the discussed methods are of particular importance for performant and photorealistic terrain rendering and are thus viewed with regard to these properties and needs. Special emphasis is devoted to recent developments in virtual texturing and possible future ﬁelds of application as well as acceleration techniques.
Stimulated mechanisms of Ca2+entry into vascular smooth muscle during NO synthesis inhibition in pregnant rats.

We have previously found that the vascular responsiveness to α1-adrenergic agonists is reduced in pregnant rats and enhanced in a rat model of pregnancy-induced hypertension produced by chronic treatment of pregnant rats with the nitric oxide (NO) synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME). The purpose of this study was to investigate whether the observed changes in vascular reactivity during normal pregnancy and during pregnancy-induced hypertension reflect changes in the mechanisms of Ca2+ entry into vascular smooth muscle.45Ca2+influx and active stress during α1-adrenergic stimulation by phenylephrine and membrane depolarization by 96 mM KCl were measured in deendothelialized aortic strips isolated from virgin and pregnant Sprague-Dawley rats untreated or treated with 1 mg/dayl-NAME for 4-6 days and incubated in Krebs solution containing increasing concentrations of extracellular Ca2+([Ca2+]e). In all groups of rats, both phenylephrine and 96 mM KCl caused [Ca2+]e-dependent increases in active stress and45Ca2+influx. The phenylephrine- and 96 mM KCl-induced active stress and Ca2+ influx were significantly reduced in pregnant rats but significantly enhanced in pregnant rats treated with l-NAME. The phenylephrine-induced Ca2+influx-stress relationship was significantly greater than that induced by 96 mM KCl in pregnant rats treated withl-NAME. The phenylephrine-induced Ca2+influx-stress relationship was reduced in pregnant rats but enhanced in pregnant rats treated withl-NAME. Chronic treatment withl-NAME had minimal effect on active stress, Ca2+ influx, and the Ca2+ influx-stress relationship in virgin rats. These results provide evidence that the mechanisms of Ca2+ entry into vascular smooth muscle are inhibited during pregnancy but enhanced during inhibition of NO synthesis in late pregnancy. The enhancement of the phenylephrine-induced Ca2+influx-stress relationship in pregnant rats treated withl-NAME suggests activation of other contractile mechanisms in addition to stimulation of Ca2+ entry. These mechanisms appear to be inhibited during normal pregnancy.
Acclimation to humid heat lowers resting core temperature.

The purpose of this study was to test the hypothesis that a reduction in resting rectal temperature (Tre) is partially responsible for the attenuation in the rise of core temperature during heat exposure following acclimation to humid heat. Nine male volunteers completed 7 days of acclimation, performing 2 h of exercise per day in a hot, humid environment (35°C, 75% relative humidity). Mean (±SD) ending Tre significantly ( P < 0.05) decreased from 38.9 ± 0.5°C on day 1 to 38.3 ± 0.4°C on day 7. Likewise, mean (±SD) resting Tre significantly ( P < 0.05) decreased from 37.0 ± 0.3 to 36.7 ± 0.4°C. In fact, all nine men showed a decrease in resting Tre from day 1to day 7, ranging from -0.1 to -0.5°C. In addition, resting Tre and ending Tre were significantly correlated ( r = 0.68). However, the mean increases in Tre (ending Tre minus resting Tre) and heat storage that occurred on each of the 7 acclimation days were not significantly different. These results support the hypothesis that a reduction in resting Tre is partially responsible for the attenuation in ending Tre during heat exposure following short-term acclimation to humid heat.