Miracle-dz/UniFAR-FTUs huggingface dataset:
Cytochrome P-450 pathway in acetylcholine-induced canine coronary microvascular vasodilation in vivo.

In the canine coronary microcirculation, acetylcholine (ACh)-induced vasodilation of large (≥100 μm) epicardial arterioles (LgA), but not small (<100 μm) epicardial arterioles (SmA), is blocked by nitric oxide (NO) synthase inhibitors in vivo. We hypothesized that the ACh-induced vasodilation of SmA is mediated by a cytochrome P-450 metabolite of arachidonic acid (AA). Epicardial coronary microvascular diameters in dogs were measured at baseline and after treatment with topically applied ACh (1, 10, and 100 μM), AA (1, 5, and 10 μM), or sodium nitroprusside (SNP; 10-100 μM). Coronary microvascular diameters were compared among control dogs ( group OO); dogs pretreated with N ω-nitro-l-arginine (l-NNA; 70 μM topically) ( group NO); dogs pretreated withl-NNA plus clotrimazole (Clo; 1.6 μM topically) or 17-octadecynoic acid (ODYA; 2 μM topically), cytochrome P-450 monooxygenase inhibitors ( groups NC and NY, respectively); dogs pretreated with Clo alone ( group OC); and dogs pretreated with l-NNA plus Clo with AA as the agonist ( group AA). ACh-induced vasodilation of LgA was abolished byl-NNA alone, whereas in SmA,l-NNA was without effect. Clo alone did not inhibit ACh-induced dilation in either SmA or LgA. However, the combinations ofl-NNA plus either Clo or ODYA abolished ACh- and AA-induced dilation of SmA (100 μM ACh: NC, 3 ± 5%; NY, 8 ± 2%; 10 μM AA: 6 ± 3%) but did not affect responses to SNP. These results suggest that the ACh-induced vasodilation of SmA is mediated in part by cytochrome P-450 metabolites of AA and provide the first evidence that the cytochrome P-450 pathway contributes to the regulation of coronary resistance vessels in vivo.
Biochemical and Molecular Actions of Nutrients VLDL Metabolism in Rats Is Affected by the Concentration and Source of Dietary Protein 1

The present study was designed to determine if changes in dietary protein level and source are related to changes in VLDL lipid concentrations and VLDL binding by hepatic membranes and isolated hepatocytes. Male Wistar rats were fed cholesterol-free diets containing 10, 20 or 30 g/100 g casein or highly puriﬁed soybean protein for 4 wk. Hepatic, plasma and VLDL lipids, VLDL apo B-100 and VLDL uptake by isolated hepatocytes and VLDL binding to hepatic membrane were determined. Increasing casein or soybean protein level (from 10 to 30 g/100 g) in the diet increased VLDL apo B-100, indicating an increase in the number of VLDL particles. VLDL uptake by isolated hepatocytes and VLDL binding to hepatic membrane increased when the protein level increased from 10 to 20 g/100 g in the diet and decreased with 30 g/100 g protein, regardless of protein type. The dietary protein source did not affect plasma total cholesterol concentrations at any protein level. Feeding 20 g/100 g soybean protein compared with casein lowered plasma triglyceride concentrations and VLDL number as measured by decreased VLDL-protein, -phospholipid, -triglyceride, -cholesterol and -apo B-100. VLDL uptake by isolated hepatocytes and VLDL binding to hepatic membrane were higher in rats fed soybean protein than those fed casein. The higher VLDL uptake could be responsible for the hypotriglyceridemia in rats fed soybean protein. J. Nutr. 133: 4102–4106, 2003.
Association of Anti–Transcription Intermediary Factor 1γ Antibodies With Paraneoplastic Rheumatic Syndromes Other Than Dermatomyositis

An association between cancer and dermatomyositis (DM) is well recognized. The high frequency of malignancies detected close to DM diagnosis suggest that DM can be a paraneoplastic syndrome. Recently, anti–transcription intermediary factor 1γ (anti‐TIF1γ) has been discovered to be associated with cancer and with DM. A meta‐analysis reported the pooled sensitivity of anti‐p155 for diagnosing cancer‐associated DM to be 78% and the specificity to be 89%. Thus, anti‐TIF1γ has shown promising results as a marker for cancer‐associated DM. However, none of the studies evaluated the association of anti‐TIF1γ with cancer with or without rheumatic diseases other than DM. To clarify the specificity of anti‐TIF1γ antibodies as a biomarker for cancer‐associated DM, we analyzed the frequency of anti‐TIF1γ antibodies in other cancer‐associated rheumatic syndromes, as well as in cancer patients and healthy controls.
Transgenic Expression of Nonclassically Secreted FGF Suppresses Kidney Repair

FGF1 is a signal peptide-less nonclassically released growth factor that is involved in angiogenesis, tissue repair, inflammation, and carcinogenesis. The effects of nonclassical FGF export in vivo are not sufficiently studied. We produced transgenic mice expressing FGF1 in endothelial cells (EC), which allowed the detection of FGF1 export to the vasculature, and studied the efficiency of postischemic kidney repair in these animals. Although FGF1 transgenic mice had a normal phenotype with unperturbed kidney structure, they showed a severely inhibited kidney repair after unilateral ischemia/reperfusion. This was manifested by a strong decrease of postischemic kidney size and weight, whereas the undamaged contralateral kidney exhibited an enhanced compensatory size increase. In addition, the postischemic kidneys of transgenic mice were characterized by hyperplasia of interstitial cells, paucity of epithelial tubular structures, increase of the areas occupied by connective tissue, and neutrophil and macrophage infiltration. The continuous treatment of transgenic mice with the cell membrane stabilizer, taurine, inhibited nonclassical FGF1 export and significantly rescued postischemic kidney repair. It was also found that similar to EC, the transgenic expression of FGF1 in monocytes and macrophages suppresses kidney repair. We suggest that nonclassical export may be used as a target for the treatment of pathologies involving signal peptide-less FGFs.
An endocrine and metabolic definition of the intermeal interval in humans: evidence for a role of leptin on the prandial pattern through fatty acid disposal.

BACKGROUND It has been proposed that leptin provides a hormonal link between adipose stores and food intake. OBJECTIVE This study investigated the role of leptin in the prandial pattern. DESIGN In experiment 1, a spontaneous prandial pattern was recreated in 6 young, normal-weight men who were deprived of time cues and had blood withdrawn continuously at a frequency of one tube every 5 min. Meals were consumed ad libitum and dinner was requested voluntarily. Data from a second experiment, conducted in 8 subjects, were used to confirm the changes in leptin during the intermeal interval (IMI). RESULTS Plasma leptin gradually rose to a peak (62 +/- 18% of the lunch concentration) during the IMI and declined before the dinner request (-21 +/- 4% of the peak concentration). This preprandial decline was confirmed in experiment 2 (-15 +/- 9%). The leptin concentration at lunch and fat-free mass were the only significant predictors of the IMI (both: r(2) = 0.91, P = 0.03). With fat intake at lunch, the leptin concentration at lunch was a positive predictor of the area under the curve of plasma fatty acids during the IMI (r(2) = 0.95, P = 0.01). Moreover, the leptin concentration at lunch was negatively correlated with energy intake in the first course of this meal (r = -0.95, P < 0.005). A similar result was found at dinner (r = -0.85, P < 0.05). Last, the change in leptin was predicted accurately by changes in glucose, triacylglycerol, and fatty acids (r(2) = 0.87, P < 10(-5)). CONCLUSION Plasma leptin concentrations increase during a spontaneous IMI and decline before the onset of a meal. The results argue for a role of leptin in the prandial pattern through fatty acid peripheral disposal.
TNF-α-induced endothelium-independent vasodilation: a role for phospholipase A2-dependent ceramide signaling.

Ceramide is a novel second messenger generated by hydrolysis of membrane sphingomyelin by a neutral sphingomyelinase (nSMase). Cytokines such as tumor necrosis factor-α (TNF-α) have been shown to increase intracellular ceramide through phospholipase A2(PLA2)-dependent activation of nSMase. TNF-α has been shown to cause endothelium-independent relaxation in isolated blood vessels. We have previously shown that exogenously applied sphingomyelinase and ceramide cause endothelium-independent vasodilation in rat thoracic aortas (D. G. Johns, H. Osborn, and R. C. Webb. Biochem. Biophys. Res. Commun. 237: 95-97, 1997). In the present study, we tested the hypothesis that ceramide mediates TNF-α-induced vasodilation. In phenylephrine-contracted rat thoracic aortic rings (no endothelium), TNF-α caused concentration-dependent relaxation in the presence of cyclooxygenase and lipoxygenase inhibitors. The phospholipase A2 antagonist 7,7-dimethyl-(5 Z,8 Z)-eicosadienoic acid (DEDA; 50 μM) and the nonselective PLA2 antagonist quinacrine (30 μM) inhibited TNF-α-induced relaxation. In cultured rat aortic vascular smooth muscle cells, TNF-α (10-7 g/ml) increased intracellular ceramide 1.5-fold over basal level (0.08 nmol/mg protein), which was blocked by the PLA2 antagonist DEDA (50 μM). We conclude that PLA2 activation and increased ceramide generation play a role in mediating TNF-α-induced endothelium-independent vasodilation.
Non-Hispanic white and Hispanic elementary school children's self-regulation of energy intake.

BACKGROUND Preschool-aged children consistently self-regulate energy intake by adjusting food intake to reflect the energy density of the diet. However, only select adults demonstrate self-regulation skills related to energy density cues. OBJECTIVE The objective was to examine the developmental characteristics of non-Hispanic white and Hispanic children's self-regulation of energy intake and to determine whether individual differences in the precision of food intake regulation were related to the children's anthropometric measures. DESIGN Three hundred forty-two 5-12-y-old children were recruited from 2 schools, one school that enrolled predominantly non-Hispanic white children (n = 148) and another school in a Hispanic neighborhood (n = 194). The children ate 2-part meals, which consisted of a preload and a main meal. The preloads were fruit-flavored drinks that were either high (625 kJ) or low (12.5 kJ) in energy density. The children's food intake at the meal was measured and energy intake was estimated. An eating Compensation Index (COMPX) score, which reflected the children's ability to regulate energy intake, was used to predict the children's adiposity. RESULTS Both non-Hispanic white and Hispanic children showed evidence of incomplete compensation, with a mean (+/-SEM) COMPX score of 48.6 +/- 6.4%. No significant ethnicity or sex differences in the children's overall COMPX scores were observed; however, the children's COMPX scores decreased with age (P < 0.05). Maternal body mass index was the best predictor of the children's weight status. CONCLUSION Children aged 5-12 y show individual variation in their responsiveness to energy density cues; the responsiveness declines with increasing age.
Differential Edit Distance: A Metric for Scene Segmentation Evaluation

In this paper, a novel approach to evaluating video temporal decomposition algorithms is presented. The evaluation measures typically used to this end are nonlinear combinations of precision-recall or coverage-overflow, which are not metrics and additionally possess undesirable properties, such as nonsymmetricity. To alleviate these drawbacks, we introduce a novel unidimensional measure that is proven to be metric and satisfies a number of qualitative prerequisites that previous measures do not. This measure is named differential edit distance (DED), since it can be seen as a variation of the well-known edit distance. After defining DED, we further introduce an algorithm that computes it in less than cubic time. Finally, DED is extensively compared with state-of-the-art measures, namely, the harmonic means (F-score) of precision-recall and coverage-overflow. The experiments include comparisons of qualitative properties, the time required for optimizing the parameters of scene segmentation algorithms with the help of these measures, and a user study gauging the agreement of these measures with the users' assessment of the segmentation results. The results confirm that the proposed measure is a unidimensional metric that is effective in evaluating scene segmentation techniques and in helping to optimize their parameters.
Moderate alcohol consumption lowers risk factors for cardiovascular disease in postmenopausal women fed a controlled diet.

BACKGROUND Moderate alcohol consumption (1-2 drinks/d) may decrease cardiovascular disease risk in postmenopausal women by improving lipid profiles. OBJECTIVE We measured the effect of moderate alcohol consumption on lipids and lipoproteins in postmenopausal women. DESIGN Postmenopausal women (n = 51) consumed 0 (control), 15 (1 drink), and 30 (2 drinks) g alcohol (ethanol)/d for 8 wk each as part of a controlled diet in a randomized crossover design. The control diet provided approximately 15%, 53%, and 32% of energy from protein, carbohydrate, and fat, respectively. The energy provided from alcohol in the 15- and 30-g alcohol diets was replaced with energy from carbohydrate. RESULTS Compared with concentrations after the control diet, plasma LDL cholesterol decreased from 3.45 to 3.34 mmol/L (P = 0.04) and triacylglycerol from 1.43 to 1.34 mmol/L (P = 0.05) after 15 g alcohol/d. There were no additional significant decreases in either lipid after an increase in alcohol intake from 15 to 30 g/d. Compared with concentrations after the control diet, plasma HDL cholesterol increased nonsignificantly from 1.40 to 1.43 mmol/L after 15 g alcohol/d but increased to 1.48 mmol/L after 30 g alcohol/d (P = 0.02). Apolipoprotein A-I increased significantly and apolipoprotein B decreased significantly after 30 g alcohol/d relative to the concentration after the control diet. CONCLUSIONS Consumption of 15-30 g alcohol/d by postmenopausal women apparently decreases cardiovascular disease risk by improving lipid profiles. Plasma LDL-cholesterol and triacylglycerol concentrations improve after 15 g alcohol/d; plasma HDL cholesterol improves only after 30 g alcohol/d.
Effects of zinc supplementation as adjunct therapy on the systemic immune responses in shigellosis.

BACKGROUND Zinc is lost during diarrheal diseases, and zinc deficiency induces intestinal morphology-altering inflammatory responses that zinc supplementation can correct. OBJECTIVE We assessed the in vivo effect of zinc supplementation on systemic and mucosal responses in mildly to moderately malnourished (defined as <-1 but >-2 and <-2 but >-3 weight-for-height z scores, respectively, based on the National Center for Health Statistics growth reference) children with shigellosis. DESIGN A double-blind placebo-controlled trial was conducted in Shigella flexneri-infected children aged 12-59 mo. Daily for 14 d, elemental zinc (20 mg) and multivitamins (vitamins A and D, thiamine, riboflavin, and nicotinamide) plus calcium were given at twice the US recommended dietary allowance to the zinc group (n=28), and multivitamins plus calcium were given to the control group (n=28). All subjects received standard antibiotic therapy. RESULTS There was no significant interaction between zinc supplementation and time, but zinc supplementation showed a significant effect on serum zinc concentrations. With a >or=4-fold increase in serum shigellacidal antibody titers from baseline used as the cutoff, the proportion of children with shigellacidal antibody response was greater in the zinc group than in the control group (P<0.03). There was a significant (P=0.02) treatment x time interaction for the proportions of circulating CD20+ and CD20+CD38+ cells, which were higher on day 7 in the zinc group than in the control group (P<0.007). No effect was seen on histopathologic features or the expression of innate and inflammatory mediators in the rectum. CONCLUSION Adjunct therapy with zinc during acute shigellosis significantly improved seroconversion to shigellacidal antibody response and increased the proportions of circulating B lymphocytes and plasma cells.
Muscle blood f low at onset of dynamic exercise in humans.

To evaluate the temporal relationship between blood flow, blood pressure, and muscle contractions, we continuously measured femoral arterial inflow with ultrasound Doppler at onset of passive exercise and voluntary, one-legged, dynamic knee-extensor exercise in humans. Blood velocity and inflow increased ( P < 0.006) with the first relaxation of passive and voluntary exercise, whereas the arterial-venous pressure difference was unaltered [ P = not significant (NS)]. During steady-state exercise, and with arterial pressure as a superimposed influence, blood velocity was affected by the muscle pump, peaking ( P < 0.001) at ∼2.5 ± 0.3 m/s as the relaxation coincided with peak systolic arterial blood pressure; blood velocity decreased ( P < 0.001) to 44.2 ± 8.6 and 28.5 ± 5.5% of peak velocity at the second dicrotic and diastolic blood pressure notches, respectively. Mechanical hindrance occurred ( P < 0.001) during the contraction phase at blood pressures less than or equal to that at the second dicrotic notch. The increase in blood flow (Q˙) was characterized by a one-component (∼15% of peak power output), two-component (∼40-70% of peak power output), or three-component exponential model (≥75% of peak power output), whereQ˙( t) =Q˙passive+ ΔQ˙1 ⋅ [1 - e -( t- TD1/τ1)] + ΔQ˙2 ⋅ [1 - e -( t - TD2/τ2)] + ΔQ˙3 ⋅ [1 - e -( t - TD3/τ3)]; Q˙passive, the blood flow during passive leg movement, equals 1.17 ± 0.11 l/min; TD is the onset latency; τ is the time constant; ΔQ˙ is the magnitude of blood flow rise; and subscripts 1-3 refer to the first, second, and third components of the exponential model, respectively. The time to reach 50% of the difference between passive and voluntary asymptotic blood flow was ∼2.2-8.9 s. The blood flow leveled off after ∼10-150 s, related to the power outputs. It is concluded that the elevation in blood flow with the first duty cycle(s) is due to muscle mechanical factors, but vasodilators initiate a more potent amplification within the second to fourth contraction.
Circulating oxidized LDL is associated with increased waist circumference independent of body mass index in men and women.

BACKGROUND Obesity is associated with oxidative stress, and the oxidation of LDL is thought to play a crucial role in the generation of atherosclerotic lesions. OBJECTIVE The objective was to describe the association of waist circumference (WC) and body mass index (BMI; in kg/m2) with plasma circulating oxidized LDL (ox-LDL) and C-reactive protein (CRP). DESIGN This cross-sectional study included data for circulating ox-LDL and CRP from a subpopulation of 586 men and women enrolled in a population-based survey conducted in 2000 in Girona, Spain. Multivariate analysis was performed to describe the independent association of WC and BMI with ox-LDL and CRP. RESULTS Multivariate logistic regression analysis adjusted for lifestyle, educational level, and dietary confounders showed a direct association of WC (quartile distribution) and BMI categories with ox-LDL (P for linear trend = 0.002) and CRP (P for linear trend = 0.004). Subjects in the top quartile of WC and with a BMI > 29.9 were at high risk of elevated circulating concentrations of ox-LDL and CRP. Further adjustment for cardiovascular disease risk factors did not substantially modify these associations. The risk of high ox-LDL concentrations in overweight (BMI = 25.0-29.9) or obese (BMI > or = 30) subjects with a WC < 102 cm (men) or < 88 cm (women) was not significantly different from that in normal-weight subjects with these WCs. In contrast, overweight or obese subjects with higher WCs (WC > or = 102 cm for men and > or = 88 cm for women) were at significantly higher risk of increased ox-LDL. CONCLUSION High WC was associated with high concentrations of ox-LDL independently of BMI in the study population.
Physical and Electrical Effects of the Dep-Anneal-Dep-Anneal (DADA) Process for HfO2 in High K/Metal Gate Stacks

The use of anneals between interspersed during hafnium oxide deposition to optimize electrical properties of the resulting films has recently been reported (1-4). In particular, Professor Toriumi’s group has reported anneals after every cycle (layer-by-layer deposition and anneal) to optimize ALD hafnium oxide films. We have extended this approach by performing multiple deposition cycles before each anneal to produce optimized hafnium oxide films in a process that is demonstrable and manufacturable on 300 mm wafers for advanced high K/metal gate stacks. The proposed mechanism for film growth on an SiO2 interlayer is illustrated in Figure 1. The electrical improvements observed in highly scaled gate first devices using this process have recently been reported (5,6).
A Phenomenological Approach for Real-Time Simulation of the Two-Way Shape Memory Effect in NiTi Alloys

A phenomenological model to simulate the two-way shape memory effect (TWSME) in nickel-titanium alloys (NiTi) is proposed. The model is based on the Prandtl–Ishlinksii operator and it is able to simulate the hysteretic behavior of the material in the straintemperature response. Starting from some experimental measurements of well known thermomechanical characteristics of NiTi alloys, the parameters of the phenomenological model are identified by simple and efficient numerical procedures. The model was developed in the commercial software package SIMULINK® and it is able to simulate the effects of applied stresses on the TWSME as well as partial thermal cycles, which generate incomplete martensitic transformations. A systematic comparison between experimental measurements, carried out under different values of applied stress, and numerical predictions are illustrated for both complete and incomplete phase transformations. The results are considered satisfactory both in accuracy and in computational time; therefore, the method is robust and suitable for use in real-time applications. DOI: 10.1115/1.2806264
Fat oxidation and its relation to serum parathyroid hormone in young women enrolled in a 1-y dairy calcium intervention.

BACKGROUND Increased dietary calcium is associated with changes in body composition. One proposed mechanism is that dietary calcium increases fat oxidation, potentially via regulation of serum parathyroid hormone (PTH) concentrations. OBJECTIVES The objectives of the study were to determine whether acute or chronic increased dairy calcium intakes alter postprandial whole-body fat oxidation and whether the increased intake is related to changes in PTH concentrations. DESIGN Normal-weight women aged 18-30 y were randomly assigned to a low (<800 mg/d, control; n = 10) or high (1000-1400 mg/d; n = 9) dietary calcium intake group for 1 y. Whole-body fat oxidation was assessed by measuring respiratory gas exchange after each subject consumed 2 isocaloric liquid meals containing 100 or 500 mg Ca at baseline and 1 y. Fasting serum PTH was measured at baseline and 1 y. RESULTS The mean 1-y change in fat oxidation was higher in the high-calcium group than in the low-calcium control group after a low-calcium meal (0.10 +/- 0.05 compared with 0.005 +/- 0.04 g/min; P < 0.001) and a high-calcium meal (0.06 +/- 0.05 compared with 0.03 +/- 0.04 g/min; P < 0.05). The 1-y change in serum log PTH was negatively associated with the 1-y change in postprandial fat oxidation after a high-calcium meal (partial r = -0.46, P < 0.04) when controlled for the1-y change in total body fat mass. CONCLUSIONS The results suggest that a chronic diet high in dairy calcium increases whole-body fat oxidation from a meal, and increases in fasting serum PTH relate to decreases in postprandial whole-body fat oxidation.