bluuebunny/crossref_metadata_2025_split huggingface dataset:
Metabolic response to feeding in weight-losing pancreatic cancer patients and its modulation by a fish-oil-enriched nutritional supplement
Authors: BARBER Matthew D. , MCMILLAN Donald C. , PRESTON Tom , ROSS James A. , FEARON Kenneth C. H. 
Published: August 2015

Weight-losing patients with advanced cancer often fail to gain weight with conventional nutritional support. This suboptimal response might be explained, in part, by an increased metabolic response to feeding. It has been suggested that eicosapentaenoic acid (EPA) can modify beneficially the metabolic response to cancer. The aim of the present study was to examine the metabolic response to feeding in cancer and the effects of an EPA-enriched oral food supplement on this response. A total of 16 weight-losing, non-diabetic patients with unresectable pancreatic adenocarcinoma and six healthy, weight-stable controls were studied by indirect calorimetry in the fasting and fed states. Body composition was estimated by bioimpedence analysis. Cancer patients were then given a fish-oil-enriched nutritional supplement providing 2 g of EPA and 2550 kJ daily, and underwent repeat metabolic study after 3 weeks of such supplementation. At baseline, resting energy expenditure whether expressed per kg body weight, lean body mass or body cell mass was significantly greater in the cancer patients compared with controls. Fat oxidation was significantly higher in the fasting state in cancer patients [median 1.26 g·kg-1·min-1 (interquartile range 0.95–1.38)] than in controls [0.76 g·kg-1·min-1 (0.62–0.92); P < 0.05]. Over the 4 h feeding period, changes in insulin and glucose concentrations in cancer patients suggested relative glucose intolerance. In response to oral meal feeding, the percentage change in the area under the curve of energy expenditure was significantly lower in the cancer patients [median 7.9% (interquartile range 3.4–9.0)] than in controls [12.6% (9.9–15.1); P < 0.01]. After 3 weeks of the EPA-enriched supplement, the body weight of the cancer patients had increased and the energy expenditure in response to feeding had risen significantly [9.6% (6.3–12.4)], such that it was no different from baseline healthy control values. Similarly, fasting fat oxidation fell to 1.02 g·kg-1·min-1 (0.8–1.18), again no longer significantly different from baseline healthy control values. While weight-losing patients with advanced pancreatic cancer have an increased resting energy expenditure and increased fat oxidation, the energy cost of feeding is, in fact, reduced. Provision of a fish-oil-enriched nutritional supplement results in some normalization of the metabolic response in both the fasted and fed states, in association with an improvement in nutritional status.
Splanchnic hyposensitivity to glypressin in a haemorrhage/transfused rat model of portal hypertension: role of nitric oxide and bradykinin
Authors: CHU Chi-Jen , WU Shwu-Ling , LEE Fa-Yauh , WANG Sun-Sang , CHANG Full-Young , LIN Han-Chieh , CHAN Che-Chang , LEE Shou-Dong 
Published: August 2015

Hyposensitivity to vasopressin is a well documented phenomenon in animals with portal hypertension and patients with cirrhosis subject to haemorrhage. Haemorrhage is associated with the endogenous release of bradykinin, which may subsequently stimulate the formation of nitric oxide (NO). The present study investigated the relative contribution of NO synthase (NOS) isoforms and the role of bradykinin in the pathogenesis of splanchnic hyposensitivity to a long-acting vasopressin analogue, glypressin, in rats with portal hypertension induced by partial portal vein ligation (PVL). At 14 days after the operation, systemic and portal haemodynamics were measured in stable or bleeding PVL rats receiving an intravenous infusion of glypressin (0.07 mg/kg). In the treatment groups, NG-nitro-L-arginine methyl ester (L-NAME; a non-selective NOS inhibitor), L-canavanine (a specific inhibitor of inducible NOS) or HOE 140 (a bradykinin B2 receptor antagonist) was administered 45 min before the infusion of glypressin. In rats with a hypotensive haemorrhage, 4.5 ml of blood was withdrawn and 50% of the withdrawn blood was re-infused before the administration of glypressin or various inhibitors. Splanchnic hyposensitivity to glypressin was demonstrated in the haemorrhage/transfused PVL rats. The infusion of L-NAME elevated the mean arterial pressure in the bleeding PVL rats without the modulation of portal pressure. The addition of L-NAME or HOE 140, but not L-canavanine, significantly and similarly potentiated the portal-hypotensive effects of glypressin. It is concluded that constitutive NOS and bradykinin are responsible, at least partly, for the splanchnic hyposensitivity to glypressin observed in the early stages of the haemorrhage/transfused rat model of portal hypertension.
Conjugated linoleic acid induces lipid peroxidation in men with abdominal obesity
Authors: BASU S. , RISÉRUS U. , TURPEINEN A. , VESSBY B. 
Published: August 2015

Conjugated linoleic acid (CLA) has been shown in experimental studies to have chemoprotective properties, and may decrease the deposition of body fat. CLA is prone to oxidation, and it has been suggested that increased lipid oxidation may contribute to the anti-tumorigenic effects of this agent. The present study investigates the urinary levels of 8-iso-prostaglandin F2α (8-iso-PGF2α), a major isoprostane, and of 15-oxo-dihydro-PGF2α, a major metabolite of PGF2α, as indicators of non-enzymic and enzymic arachidonic acid oxidation respectively after dietary supplementation with CLA in middle-aged men (mean age 53 years) with abdominal obesity for 1 month in a randomized controlled trial. Significant increases in the levels of both 8-iso-PGF2α and 15-oxo-dihydro-PGF2α in urine (P < 0.0001 and P = 0.0013 respectively) were observed after 1 month of daily CLA intake (4.2 g/day) as compared with the control group. The lipid peroxidation parameters had returned to their basal levels at 2 weeks after the cessation of CLA intake, and remained at the same levels for a further 2 weeks until the end of the study. CLA had no effect on serum α-tocopherol and γ-tocopherol levels, or on the urinary levels of 2,3-dinor-thromboxane B2. Thus CLA may induce both non-enzymic and enzymic lipid peroxidation in vivo in middle-aged men with abdominal obesity, without any side effects. The consequences of the increased lipid peroxidation after CLA supplementation are unknown.
The mechanism of resveratrol-induced vasorelaxation differs in the mesenteric resistance arteries of lean and obese rats
Authors: NADERALI Ebrahim K. , SMITH Sharon L. , DOYLE Patrick J. , WILLIAMS Gareth 
Published: August 2015

Resveratrol has been shown to induce vasorelaxation. In this study, we investigated the mechanism(s) of resveratrol-induced vasorelaxation in resistance mesenteric arteries from male lean and dietary-induced obese rats. Compared with lean rats, arteries from dietary-obese rats showed significant (P < 0.001) endothelial dysfunction, as indicated by a decrease (> 20%) in maximal acetylcholine-induced vasorelaxation. Resveratrol (5–35 µmol/l) induced concentration-dependent relaxation of mesenteric arteries preconstricted with noradrenaline (8 µmol/l) or KCl (125 mmol/l) from both lean and dietary-obese rats. There were no significant differences between the two groups, achieving a maximum relaxation of > 95% at a concentration of 35 µmol/l. In noradrenaline-preconstricted arteries from lean rats, NG-nitro-L-arginine methyl ester (L-NAME; 100 and 300 µmol/l) caused a significant (P < 0.01) concentration-dependent rightward shift in reseveratrol activity, with no effect on maximal responses. However, L-NAME (100 and 300 µmol/l) did not alter the effects of reseveratrol on arteries from dietary-obese rats, giving superimposed concentration–responses curves. Indomethacin was also ineffective in altering resveratrol activity in arteries from both lean and dietary-obese rats. In noradrenaline-precontracted arteries from dietary-obese rats, responses to resveratrol were not attenuated by endothelial denudation, indicating an action independent of the endothelium. This study indicates that: (a) the maximal effects of resveratrol on resistance arteries from lean and dietary-obese rats are not effected by endothelial dysfunction, and (b) the effects of resveratrol in lean animals (where endothelial function is not impaired), but not in dietary-obese rats, are mediated via NO.
Deterioration in peak systolic velocity is closely related to ischaemia during angioplasty: a vectorcardiographic and tissue Doppler imaging study
Authors: JENSEN Jens , BRODIN Lars-Åke , LIND Britta , ERIKSSON Sven V. , JENSEN-URSTAD Mats , SYLVÉN Christer 
Published: August 2015

We tested the hypothesis that the extent of signs of ischaemia detected by vectorcardiography (VCG) during elective coronary angioplasty (percutaneous transluminal coronary angioplasty; PTCA) is related to systolic and diastolic myocardial velocities, as determined by tissue Doppler echocardiography. A total of 15 patients undergoing PTCA (12 men/three women; age 61±9 years), without prior myocardial infarction and with an ejection fraction of &gt; 50%, were included. The balloon inflation was repeated three times, with minimum intervals of 2 min between inflations. Tissue Doppler echocardiography was performed, in an apical two- or four-chamber view, before and at the end of each inflation. Peak systolic velocity, time-to-peak systolic velocity (TTP), peak early (Em) and late (Am) diastolic velocities, the Em/Am ratio and isovolumic relaxation time were measured in the basal segments of the left ventricle. VCG recordings were carried out during the whole procedure. ST vector magnitude (ST-VM) and ST change vector magnitude (STC-VM) were monitored. The total duration and area of each VCG change during inflation were calculated for each patient. Isovolumic relaxation time, peak Em and Am values and the Em/Am ratio did not change significantly during inflation. Peak systolic velocity decreased (6.7±2.0 to 5.3±1.9 cm/s; P &lt; 0.001) and TTP increased (157±60 to 192±60 ms; P &lt; 0.01) during inflation. Both STC-VM time (r = -0.68, P &lt; 0.01) and STC-VM area (r = -0.68, P &lt; 0.01) were related to peak systolic velocity during inflation. STC-VM time was also related (r = 0.55, P &lt; 0.05) to the difference in peak systolic velocity during compared with before inflation. ST-VM was less closely related to peak systolic velocity. Thus the duration and degree of ischaemia, as measured by VCG, are related to peak systolic velocity in the basal segments of the left ventricle.
Water ingestion increases sympathetic vasoconstrictor discharge in normal human subjects
Authors: SCOTT Eleanor M. , GREENWOOD John P. , GILBEY Stephen G. , STOKER John B. , MARY David A. S. G. 
Published: August 2015

A marked pressor response to water drinking has been observed in patients with autonomic failure and in the elderly, and has been attributed to sympathetic vasoconstrictor activation, despite the absence of such a pressor response in healthy subjects with intact sympathetic mechanisms. We investigated whether water drinking in normal subjects affected peripheral sympathetic neural discharge and its effect on vascular resistance. In nine normal human subjects, we examined the effect of water ingestion on muscle sympathetic neural activity from the peroneal nerve, as multi-unit bursts (muscle sympathetic nerve activity; MSNA) and as single-unit impulses (s-MSNA) with vasoconstrictor function, and on calf vascular resistance for 120 min. In each subject, water ingestion caused increases in s-MSNA and MSNA which peaked at 30 min after ingestion; they increased respectively (mean±S.E.M.) from 42±4 to 58±5 impulses/100 beats (P < 0.01) and from 36±4 to 51±5 bursts/100 beats (P < 0.001). There were corresponding increases in calf vascular resistance and in plasma noradrenaline levels. A significant correlation occurred between all of these data. In conclusion, measurement of MSNA has provided direct evidence that water drinking in normal human subjects increases sympathetic nerve traffic, leading to peripheral vasoconstriction. This sympathetic activation was not accompanied by significant changes in arterial blood pressure.
Neurohormonal activation, the renal dopaminergic system and sodium handling in patients with severe heart failure under vasodilator therapy
Authors: FERREIRA António , BETTENCOURT Paulo , DIAS Paula , PESTANA Manuel , SERRÃO Paula , SOARES-DA-SILVA Patrício , CERQUEIRA-GOMES Mário 
Published: August 2015

The benefits of tailoring therapy with vasodilators in patients with severe heart failure are well documented, but this may lead to neurohormonal activation and sodium retention. Renal dopamine has local natriuretic actions and interacts with other hormones involved in renal sodium handling. The aim of the present work was to determine the effects of arterial underfilling induced by vasodilator therapy on renal sodium handling, neurohormonal activation and the activity of the renal dopaminergic system in patients with severe heart failure. For this purpose we monitored haemodynamic parameters, plasma levels of type B natriuretic peptide (BNP), catecholamines, aldosterone, renin activity (PRA), sodium and creatinine, and urinary excretion of sodium, creatinine, l-DOPA, dopamine and its metabolites, before initiation of sodium nitroprusside therapy and every 6 h thereafter (for 42 h), and again after 5 days of angiotensin-converting enzyme (ACE) inhibition, in 10 male patients with severe heart failure. The results of nitroprusside therapy were a marked increase in cardiac index and a substantial decrease in systemic vascular resistance index. Plasma levels of BNP decreased significantly, while PRA, noradrenaline and aldosterone showed marked increases, resulting in a substantial reduction in urinary sodium excretion. Creatinine clearance was not affected. Urinary dopamine and dopamine metabolites increased in response to nitroprusside therapy. After 5 days of ACE inhibition, urinary sodium returned to baseline values, while urinary dopamine was markedly reduced. These results suggest that the renal dopaminergic system is activated in patients with severe heart failure by stimuli leading to sodium renal reabsorption.
Association between serum values of C-reactive protein and cytokine production in whole blood of patients with Type 2 diabetes
Authors: Castoldi Giovanna , Galimberti Stefania , Riva Chiara , Papagna Ruggero , Querci Federico , Casati Marco , Zerbini Gianpaolo , Caccianiga Gianluigi , Ferrarese Carlo , Baldoni Marco , Valsecchi Maria Grazia , Stella Andrea 
Published: August 2015

Diabetes mellitus accelerates atherosclerotic processes, and it is known that inflammation plays a key role in atherosclerosis. The aim of the present study was to evaluate in patients with Type 2 diabetes whether serum levels of CRP (C-reactive protein) are associated with cytokine production in whole blood. A total of 89 outpatients with Type 2 diabetes were enrolled, and blood pressure, body mass index, fasting blood glucose, glycated haemoglobin, cholesterol, triacylglycerols (triglycerides) and hs-CRP (high-sensitivity CRP) were measured. IL-6 (interleukin-6), IL-1β (interleukin-1β) and TNF-α (tumour necrosis factor-α) were measured before and after 24 h of incubation of whole blood with LPS (lipopolysaccharide) or saline. The basal values of IL-1β, IL-6 and TNF-α were low and were not significantly related to hs-CRP levels. A univariate analysis showed that the level of IL-1β and IL-6, obtained after 24 h of incubation of whole blood with LPS, increased significantly with increasing levels of hs-CRP and, after adjusting for potential confounders, IL-1β still remained statistically significant. In our sample of patients with Type 2 diabetes, there was no association between serum hs-CRP levels and basal levels of IL-6, IL-1β and TNF-α. Conversely, a significant association was observed between serum hs-CRP levels and IL-1β and IL-6 production after 24 h of incubation of whole blood with LPS. In conclusion, our data suggest that patients with Type 2 diabetes and high hs-CRP levels may have an enhanced reactivity in response to specific stimuli that produce different interleukins, with possible implications in inflammatory atherosclerotic processes.
Urinary cortisol is inversely associated with capillary recruitment in women: a potential explanation for the cortisol–blood pressure relationship
Authors: de Jongh Renate T. , Ijzerman Richard G. , Serné Erik H. , van Weissenbruch Mirjam M. , Voordouw Jasper J. , Delemarre-van de Waal Henriette A. , Stehouwer Coen D. A. 
Published: August 2015

The relationships of cortisol with elevated blood pressure and insulin resistance are likely to be the result of a complex interplay of different mechanisms. We hypothesize that cortisol is associated with impaired microvascular function and that this contributes to cortisol-associated high blood pressure and insulin resistance. We examined 24 h urinary free cortisol excretion in 56 healthy adults (26 women). Blood pressure was assessed by 24 h ambulatory measurements. Insulin sensitivity was determined using the hyperinsulinaemic euglycaemic clamp technique. Skin capillary recruitment after arterial occlusion was visualized with videomicroscopy and endothelium-(in)dependent vasodilation was evaluated with iontophoresis of acetylcholine and sodium nitroprusside combined with laser Doppler fluxmetry. Men were characterized by higher urinary cortisol excretion [median (interquartile range), 162 (130–194) compared with 118 (99–156) nmol/24 h, P&lt;0.05]. In women, but not in men, urinary cortisol excretion was associated with impaired capillary recruitment (r=−0.66, P&lt;0.001), higher systolic blood pressure (r=0.64, P&lt;0.001) and lower insulin sensitivity (r=−0.43, P&lt;0.05). Urinary cortisol excretion was not associated with endothelium-(in)dependent vasodilation in men or women. Regression analysis demonstrated that capillary recruitment statistically explained 37% of the association between urinary cortisol and blood pressure in women. Capillary recruitment did not explain part of the association between urinary cortisol and insulin sensitivity. In conclusion, urinary cortisol excretion is inversely associated with capillary recruitment in women, but not in men, and capillary recruitment explains part of the cortisol–blood pressure relationship. These data suggest that, in women, impairment of capillary function mediates some of the adverse effects of cortisol and thus may provide a target to prevent such adverse effects.
Hydrothermal synthesis and tribological properties of MoSe2 nanoflowers
Authors: Zhang Xianghua , Xue Maoquan , Yang Xinghua , Luo Guangsi , Yang Feng 
Published: August 2015

Molybdenum selenide (MoSe2) nanoflowers have been favourably synthesised by a mild hydrothermal route using sodium molybdate and selenium powder at low temperatures. The gained crystallographic products were analysed by powder X‐ray powder diffraction (XRD), energy‐dispersive spectroscopy, scanning electron microscopy (SEM) and high‐resolution transmission electron microscopy. The XRD pattern of the product can be easily indexed to hexagonal MoSe2. SEM and transmission electron microscopy graphics of the products reveal that the MoSe2 nanoflowers with diameters of about 100 nm consist of nanosheets. The tribological behaviours of MoSe2 as oil additives were evaluated on a ball‐on‐disc tribometer. Under the given experimental conditions, the oil containing MoSe2 gave lower friction coefficients than that of the base oil. A smooth triboﬁlm formed on worn surfaces is believed to be responsible for the good lubricating effects of MoSe2 as additives.
Inference and analysis of population structure using genetic data and network theory
Authors: Greenbaum Gili , Templeton Alan R. , Bar-David Shirli 
Published: August 2015

AbstractClustering individuals to subpopulations based on genetic data has become commonplace in many genetic studies. Inference of population structure is most often done by applying model-based approaches, aided by visualization using distance-based approaches such as multidimensional scaling. While existing distance-based approaches suffer from lack of statistical rigor, model-based approaches entail assumptions of prior conditions such as that the subpopulations are at Hardy-Weinberg equilibria. Here we present a distance-based approach for inference of population structure using genetic data by defining population structure using network theory terminology and methods. A network is constructed from a pairwise genetic-similarity matrix of all sampled individuals. Thecommunity partition, a partition of a network to dense subgraphs, is equated with population structure, a partition of the population to genetically related groups. Community detection algorithms are used to partition the network into communities, interpreted as a partition of the population to subpopulations. The statistical significance of the structure can be estimated by using permutation tests to evaluate the significance of the partition’smodularity, a network theory measure indicating the quality of community partitions. In order to further characterize population structure, a new measure of the Strength of Association (SA) for an individual to its assigned community is presented. The Strength of Association Distribution (SAD) of the communities is analyzed to provide additional population structure characteristics, such as the relative amount of gene flow experienced by the different subpopulations and identification of hybrid individuals. Human genetic data and simulations are used to demonstrate the applicability of the analyses. The approach presented here provides a novel, computationally efficient, model-free method for inference of population structure which does not entail assumption of prior conditions. The method is implemented in the software NetStruct, available athttps://github.com/GiliG/NetStruct.
Change of mind
Authors: Ogawa Rodney T 
Published: August 2015

Purpose
– The purpose of this paper is for the author to recount how his use of organizational theory to understand educational reform in the USA led to a change of mind.

Design/methodology/approach
– My shift resulted from my conclusion, derived from the new institutionalism, that only marginal changes can be made in schools and, thus, fundamental change requires the design and construction of new systems.

Findings
– I moved from applying organization theory to find ways in which schools could improve academic outcomes for students, generally, and students from underserved communities, specifically to using organization theory to develop conditions that support efforts to design new systems to support learning.

Originality/value
– This paper’s contribution is that it encourages students of school organization to consider applying their theoretical perspectives to designing innovative social arrangements to foster learning and teaching.