bluuebunny/crossref_metadata_2025_split huggingface dataset:
Glucose-Induced Thermogenesis in Splanchnic and Leg Tissues in Man
Authors: Simonsen Lene , Ryge Camilla , Bülow Jens 
Published: August 2015

1. Fourteen healthy subjects were investigated before and for 4 hours after oral intake of 75 g of glucose (n = 8) or tap water (n = 6). Whole-body energy expenditure was measured by an open-circuit ventilated hood system. Blood samples for determination of oxygen, carbon dioxide, glucose and lactate were taken from an artery, a hepatic vein and a femoral vein. Blood flow in the splanchnic region was measured by constant infusion of Indocyanine Green. Leg blood flow was measured by venous occlusion strain-gauge plethysmography. Oxygen uptake and carbon dioxide output in the splanchnic and leg tissues were calculated as the product of blood flow and arteriovenous differences in oxygen or carbon dioxide concentrations. Net exchanges of glucose and lactate across the splanchnic and leg tissues were calculated as the product of blood flow and arteriovenous differences in whole-blood glucose or lactate concentrations.
2. Splanchnic oxygen uptake had a biphasic course with an initial increase from 2.35 ± 0.88 (SD) mmol/min to 2.85 ± 1.20 mmol/min 30 min after the glucose intake (P &lt; 0.005) and a later decrease below the basal value to around 2.02 mmol/min 90–180 min after the glucose intake (P &lt; 0.05). The integrated increase in the splanchnic oxygen uptake during the 4 h after the glucose intake was −32.6 ± 49.7 mmol/240 min. Leg oxygen uptake increased from 4.3 ± 1.4 μmol min−1 100 g−1 to 7.0 ± 3.2 μmol min−1 100 g−1 90 min after the glucose intake (P &lt; 0.01). The integrated increase in leg oxygen uptake was 305.1 ± 394.3 μmol 240 min−1 100 g−1. Assuming leg oxygen uptake mainly represents average skeletal muscle, the skeletal muscle mass can explain around 45% of the whole-body glucose-induced thermogenesis.
3. It is concluded that the splanchnic tissues do not contribute to the integrated glucose-induced thermogenesis owing to a biphasic response in oxygen uptake, with an initial increase and a later decrease. Measurements across a leg give the same information as measurements across a forearm with respect to estimation of glucose-induced thermogenesis in skeletal muscle.
Microalbuminuria Reflects a Generalized Transvascular Albumin Leakiness in Clinically Healthy Subjects
Authors: Jensen Jan Skov , Borch-Johnsen Knut , Jensen Gorm , Feldt-Rasmussen BO 
Published: August 2015

1. In epidemiological studies microalbuminuria, i.e. slightly elevated urinary albumin excretion rate, predicts increased atherosclerotic vascular morbidity and mortality. This study aimed to test the hypothesis that microalbuminuria in clinically healthy subjects is associated with a systemic transvascular albumin leakiness. In animal experiments the outflux of albumin and lipids to the arterial wall are highly correlated, and both are elevated in atherosclerosis.
2. All participants were recruited at random from a population-based epidemiological study, where the upper decile of urinary albumin excretion rate was 6.6 μg/min. Twenty-seven patients with persistent microalbuminuria (urinary albumin excretion rate 6.6–150 μg/min), and 56 age- and sex-matched control subjects with persistent normoalbuminuria (UAER ≤ 6.6 μg/min) were studied.
3. The systemic transvascular albumin leakage was measured as the fractional disappearance rate of 125I-labelled albumin from the total plasma compartment in 1 h after intravenous injection.
4. The fractional disappearance rate of albumin from the plasma compartment was higher in the microalbuminuric than in the normoalbuminuric group [5.8 (95% confidence interval 5.3–6.2; n = 27) versus 5.0 (4.6–5.5; n = 56)%/h, P &lt; 0.05]. The positive correlation between urinary albumin excretion rate on continuous scale (logarithmically transformed) and the fractional disappearance rate of albumin from the plasma compartment [slope 0.4 (95% confidence interval 0.1–0.7; n = 83), r = 0.29, P &lt; 0.005] was independent of age, sex, smoking status, blood pressure, body size, plasma volume, plasma albumin concentration and concentrations of blood glucose, serum insulin and serum lipids.
5. In conclusion, microalbuminuria is an independent marker of systemic transvascular albumin leakiness in clinically healthy subjects. This finding may partly explain the increased atherosclerotic vascular morbidity and mortality in microalbuminuric subjects. It is suggested that the observed transvascular leakiness, in addition, may cause increased lipid insudation to the arterial walls.
Plasma-Mediated Neutrophil Activation during Acute Myocardial Infarction: Role of Platelet-Activating Factor
Authors: Siminiak Tomasz , Egdell Robin M. , O'Gorman Daniel J. , Dye Julian F. , Sheridan Desmond J. 
Published: August 2015

1. Polymorphonuclear neutrophils are involved in the development of myocardial injury during ischaemia through the release of free oxygen radicals and by adhesion of activated polymorphonuclear neutrophils to endothelium, resulting in plugging of coronary capillaries. Polymorphonuclear neutrophil activation may be a result of contact with ligands expressed by endothelial cells and/or a response to soluble stimuli released from ischaemic tissue to the plasma.
2. To investigate this we studied plasma-mediated polymorphonuclear neutrophil activation in vitro using plasma samples collected from 14 patients with acute myocardial infarction at time of admission and 6 h and 1, 2, 5 and 7 days later. Plasma samples were incubated with washed polymorphonuclear neutrophils isolated from healthy donors. Expression of adhesion molecules CD18/CD11b integrin and L-selectin (Leu-8) were measured by flow cytometry and superoxide anion production in polymorphonuclear neutrophils was measured by chemiluminescence.
3. Plasma samples obtained 6 h and 1 day after admission were capable of inducing CD18/CD11b antigen expression, superoxide anion production and L-selectin shedding in the washed polymorphonuclear neutrophils, and this effect was significant when compared with plasma taken at 5 and 7 days after admission.
4. The plasma-mediated polymorphonuclear neutrophil stimulation was prevented when the PMN were pretreated with platelet-activating factor receptor antagonists BN52021 or BN50739. The platelet-activating factor concentrations detected in the plasma samples were not higher than those detected in plasma from healthy subjects.
5. These findings suggest that during acute myocardial infarction peripheral plasma contains soluble stimuli capable of inducing polymorphonuclear neutrophil integrin expression, L-selectin shedding and oxygen free radical production and that platelet-activating factor appears to act as an autocrine polymorphonuclear neutrophil stimulus.
Comparison of Bio-Impedance Spectroscopy and Multi-Frequency Bio-Impedance Analysis for the Assessment of Extracellular and Total Body Water in Surgical Patients
Authors: Hannan W. J. , Cowen S. J. , Plester C. E. , Fearon K. C. H. , Debeau A. 
Published: August 2015

1. Measurements of extracellular and total body water provide useful information on the nutritional status of surgical patients and may be estimated from whole-body bio-impedance measurements at different frequencies.
2. Resistance and reactance were measured at 50 frequencies from 5 kHz to 1 MHz in 29 surgical patients (17 males, 12 females) with a wide range of extracellular to total body water ratios.
3. A fit to the spectrum of reactance versus resistance data gave predicted resistances at frequencies zero and infinity. Values of extracellular and total body water determined by this bio-impedance spectroscopy technique were regressed against values obtained from radioisotope dilution. The standard errors of the estimate were 1.893l and 3.259l respectively.
4. Resistance indices (height2/resistance) at selected frequencies gave the highest correlations with extracellular and total body water at 5 kHz and 200 kHz respectively, and prediction equations derived from multiple stepwise regressions also showed these to be the optimum frequencies. The standard errors of the estimate for this multi-frequency bio-impedance analysis method were 1.937l and 2.606l for extracellular and total body water respectively.
5. To assess the ability of the two methods to measure changes in extracellular and total body water, reproducibility was assessed from repeat measurements 10 min apart in a subgroup of 15 patients. Bio-impedance spectroscopy gave mean coefficients of variation for extracellular and total body water of 0.9% and 3.0% respectively. For multi-frequency bio-impedance analysis the corresponding coefficients of variation were 0.9% and 0.6%.
6. It is concluded that a simple impedance analyser operating at only two frequencies compares favourably with the more complex spectroscopy technique for the determination of extracellular and total body water in surgical patients.
Effects of Intermittent Pressure-Induced Strain on the Electrophysiology of Cultured Human Chondrocytes: Evidence for the Presence of Stretch-Activated Membrane Ion Channels
Authors: Wright Malcolm , Jobanputra Paresh , Bavington Charles , Salter Donald M. , Nuki George 
Published: August 2015

1. Cyclical pressurization of cultured chondrocytes results in increases in cyclic AMP and in the rate of proteoglycan synthesis. Intermittent increases in hydrostatic pressure are also associated with hyperpolarization of chondrocyte cell membranes and activation of Ca2+-dependent K+-ion channels but the physiological basis for this response to mechanical stimulation is unclear.
2. Experiments have been undertaken to better define the types of ion channels involved and to explore the possibility that the hyperpolarization response associated with cyclical pressurization of chondrocytes follows activation of stretch-activated ion channels.
3. The mean membrane potential of chondrocytes in non-confluent monolayer cell culture rose from −15.3 ± 0.24 mV to −21.1 ± 0.28 mV (n = 60, P &lt; 0.0001) after intermittent pressurization (0.33 Hz, 16 kPa, 20 min).
4. Strain gauge measurements showed that cyclical pressurization was associated with strain on the base of the culture plate. The amplitude of the hyperpolarization response was proportional to the microstrain to which cells were subjected.
5. Membrane hyperpolarization did not occur when chondrocytes were subjected to cyclical pressurization in rigid glass culture dishes or plastic dishes positioned in the pressurization chamber so as to avoid bending of the base of the culture dish.
6. Indirect evidence that the hyperpolarization response after intermittent pressure-induced strain was associated with stimulation of stretch-activated ion channels was obtained from experiments with gadolinium, amiloride and hexamethylene amiloride, each of which abolished hyperpolarization.
7. Experiments with apamin, charybdotoxin and iberiotoxin showed that the Ca2+-activated K+ channels involved in the hyperpolarization response are apamin-sensitive, charybdotoxin- and iberiotoxin-resistant, low-conductance channels.
8. Somatostatin and cadmium chloride, which block L-type calcium channels, abolished strain-induced chondrocyte hyperpolarization. EGTA, which chelates extracellular Ca2+, reduced the response to 48% of control values, and thapsigargin, which raises intracellular Ca2+ by inhibition of Ca2+—ATPase in endoplasmic reticulum, caused hyperpolarization independently with further hyperpolarization after pressure-induced strain. These data indicate that chondrocyte hyperpolarization was dependent on intracellular Ca2+ concentrations.
9. Further work is required to determine whether stretch-activated ion channels shown to be associated with chondrocyte hyperpolarization after cyclical pressure-induced strain are also involved in the signal transduction process that leads to increases in proteoglycan synthesis.
Effects of Dobutamine on the Relationship between Oxygen Consumption and Delivery in Healthy Volunteers: Comparison with Sodium Nitroprusside
Authors: De Backer Daniel , Berre Jacques , Moraine Jean Jacques , Melot Christian , Vanfraechem Jacques , Vincent Jean-Louis 
Published: August 2015

1. Dobutamine has been used to study the relationship between oxygen consumption (VO2) and oxygen delivery (DO2) in critically ill patients, but this has led to concerns that it could consistently increase VO2 in all patients. Although a direct thermogenic effect of the catecholamine has been primarily implicated in this increase in VO2, an increase in blood flow may contribute significantly by increasing the oxygen requirements of the heart and other organs such as the kidney and the liver. If this mechanism is predominant, it should also be observed when blood flow increases during the infusion of non-adrenergic agents. To separate the two mechanisms, we compared the effects of dobutamine with those of sodium nitroprusside on VO2/DO2 relationships in healthy volunteers.
2. Eight healthy volunteers received infusions of dobutamine at doses of 2, 4 and 6 μg min−1 kg−1 and nitroprusside at doses of 0.5, 1 and 2 μg min−1 kg−1 in an alternate order.
3. VO2 was determined by indirect calorimetry and cardiac output by electrical bioimpedance. Data were analysed by analysis of variance for repeated measurements and individual VO2/DO2 slopes were determined by linear regression.
4. VO2 increased more with dobutamine than with nitroprusside (from 138 ± 14 to 149 ± 20 ml min−1 m−2, P &lt; 0.001, and from 131 ± 14 to 138 ± 17 ml min−1 m−2, P &lt; 0.001, respectively). However, DO2 also increased more with dobutamine than with nitroprusside (from 531 ± 186 to 702 ± 274 ml min−1 m−2, P &lt; 0.001, and from 523 ± 107 to 610 ± 122 ml min−1 m−2, P &lt; 0.001, respectively). Individual VO2/DO2 slopes were similar with dobutamine and nitroprusside (6.5 ± 3.5 compared with 7.1 ± 4.6%, P not significant).
5. At the doses used, DO2 and VO2 increased more with dobutamine than with nitroprusside in healthy volunteers. However, the VO2/DO2 slopes were similar for both substances. Thus, an increase in VO2 is not exclusively observed with catecholamines. Studies of the effects of therapeutic interventions on oxygen-derived variables should report not only changes in VO2 but also VO2/DO2 slopes.
Autonomic Control of Skin Microvessels: Assessment by Power Spectrum of Photoplethysmographic Waves
Authors: Bernardi Luciano , Radaelli Alberto , Solda Pier Luigi , Coats Andrew J. S. , Reeder Martin , Calciati Alessandro , Garrard Christopher S. , Sleight Peter 
Published: August 2015

1. Although it is well known that the microvessels of the skin constantly undergo spontaneous variations in volume, the significance of these rhythmic changes remains uncertain.
2. In 10 healthy males and in 15 patients in intensive care, we assessed the origin of the autonomic influences on spontaneous fluctuations in the microcirculation of the skin, obtained by an infra-red photoplethysmographic device; we used spectral analysis techniques to compare these fluctuations (which were recorded simultaneously in two sites) with those of blood pressure, in order to test the presence of autonomic control of any synchronous fluctuations in these different measurements from the cardiovascular system. In order to minimize mechanical fluctuations caused by occasional slow breaths, rather than nervously mediated fluctuations in skin blood flow, respiration was controlled at 15 breaths/min (0.25 Hz).
3. Spontaneous infra-red photoplethysmographic fluctuations were observed in different body areas (left index finger and left ear lobe, right and left index finger), and all were evident at 0.1 Hz, as well as respiration-related components at 0.25 Hz. Active standing increased the power of the 0.1 Hz fluctuations (sympathetic activity) in both blood pressure (from 62.7 ± 7.1 to 79.2 ± 3.7 normalized units, P&lt;0.05) and IRP (finger: from 68.5 ± 6.4 to 86.9 ± 3.4 normalized units, P&lt;0.05; ear: from 59.0 ± 5.9 to 88.1 ± 2.0, P&lt;0.01). There was a high (&gt;0.5) coherence between the fluctuations obtained in blood pressure, in IRP signals obtained simultaneously at the finger and at the ear, and in R—R interval. This synchronization between the oscillations in all these signals, which were unrelated to the respiratory frequency or to the pulse rate, suggests a common neural, non-local origin. The phase between IRP and blood pressure was positive in the 0.1 Hz region (+ 1.65 ± 0.41 radians, i.e. IRP was leading blood pressure, showing that 0.1 Hz fluctuations were not passively transmitted to the skin microvessels from large arteries) and negative in the 0.25 Hz region (−0.74 ± 0.19 radians, P&lt;0.01 compared with phase in the 0.1 Hz region, i.e. IRP was lagging behind blood pressure, suggesting possible passive transmission to the skin microvessels of blood pressure fluctuations caused by respiration). Fluctuations at lower frequency were observed in all IRP recordings, suggesting a local origin for these. Intra-arterial and IRP fluctuations were compared in the 15 intensive care patients and gave similar results.
4. The skin microcirculation is thus not only under local control, but also reflects changes in sympathetic activity; the effect of these changes on the skin microcirculation can be easily evaluated by the spectral analysis of the IRP signal obtained simultaneously in multiple areas, in conjunction with the spectra of R—R interval and blood pressure.
Modulation of Multidrug Resistance Gene (mdr-1) with Antisense Oligodeoxynucleotides
Authors: Liu Chao , Qureshi Imran Ahmad , Ding Xun-Jie , Shan Yi-Fei , Huang Yi-Wei , Xie YI , Ji Mei-Rong 
Published: August 2015

1. Multidrug resistance is the major obstacle to successful cancer chemotherapy. Circumventing multidrug resistance therefore represents a high priority for clinical anti-cancer treatment. Among many reversal strategies, antisense oligodeoxynucleotides may offer a molecular targeting tool for overcoming cellular multidrug resistance.
2. Two 17-mer phosphorothioate antisense oligomers, complementary to the 5′ end of the ATG initiator codon-containing region and loop-forming site (located at nucleotides 991–1007 from the first ATG codon) in mdr-1 cDNA sequence, were synthesized. The purpose was to study their effects on the function and expression of P-glycoprotein and mdr-1 gene.
3. The results showed that 10 μmol/l antisense oligomers could significantly inhibit the growth of multidrug resistant K562/Adm cells cultured in adriamycin-containing medium. No such effect was observed for parental (sensitive) K562/S cells. Intracellular daunorubicin accumulation increased greatly in the K562/Adm cells after they were treated with oligomers for 48 h and P-glycoprotein synthesis was strikingly reduced.
4. Further investigation with [α-32P]dCTP incorporation by the reverse transcriptase—polymerase chain reaction method revealed that antisense oligomers could result in a reduction in the level of mdr-1 mRNA, probably through hindering mdr-1 gene transcription.
5. The high reversal efficiency and specificity of antisense oligomers in regulating mdr-1 gene expression suggest a potential clinical application in gene therapy for drug resistant malignancies.
Neutrophil Adhesion Molecule Expression and Response to Stimulation with Bacterial Wall Products in Humans is Unaffected by Parenteral Nutrition
Authors: Plusa Mr S. M. , Webster N. , Primrose J. N. 
Published: August 2015

1. Total parenteral nutrition is associated with a high incidence of septic complications. This may be partly due to neutrophil dysfunction induced by the parenteral nutrition.
2. Neutrophil adhesion molecule expression and the expression of CD11b in response to stimulation with formylmethionyl-leucyl-phenylalanine and lipopolysaccharide were determined before and after 24 h of lipid-containing parenteral nutrition. Eighteen adult patients referred for parenteral nutrition were studied.
3. There was no change in the expression of neutrophil l-selectin (CD62L), CD11a, CDllb, CD11c or CD15. Neutrophil response to stimulation with formylmethionyl-leucyl-phenylalanine and lipopolysaccharide as determined by CD11b expression was unaffected by parenteral nutrition.
4. This study has shown no evidence of parenteral nutrition-induced neutrophil dysfunction.
Negative Association between Erythrocyte Reduced Glutathione Concentration and Diabetic Complications
Authors: Thornalley P. J. , McLellan A. C. , Lo T. W. C. , Benn J. , Sönksen P. H. 
Published: August 2015

1. Multiple logistic regression analysis of biochemical and clinical variables in diabetic patients was performed to identify those associated with the presence of diabetic complications (retinopathy, neuropathy and nephropathy).
2. The presence of diabetic complications correlated positively with duration of diabetes and patient age and negatively with the concentration of reduced glutathione in erythrocytes. Individually, retinopathy, neuropathy and nephropathy correlated with duration of diabetes, but retinopathy also correlated positively with haemoglobin A1c in diabetic patients. In insulin-dependent patients, the concentration of methylglyoxal was also in the logistic model for retinopathy and diabetic complications, but the logistic regression coefficient was not significant.
3. Multiple linear regression analysis indicated that erythrocyte reduced glutathione concentration correlated negatively with d-lactate concentration and positively with duration of diabetes in insulin-dependent patients and correlated negatively with glucose concentration in non-insulin-dependent diabetic patients.
4. In non-diabetic subjects, erythrocyte glyoxalase I activity correlated positively with methylglyoxal concentration. There was no similar correlation in diabetic patients. In insulin-dependent patients, methylglyoxal concentration correlated positively with duration of diabetes.
5. Glyoxal and methylglyoxal are detoxified by the glyoxalase system with reduced glutathione as co-factor. The concentration of reduced glutathione may be decreased by oxidative stress and by decreased in situ glutathione reductase activity in diabetes mellitus. A reduced concentration of reduced glutathione may predispose diabetic patients to oxidative damage and to α-oxoaldehyde-mediated glycation by decreasing the in situ glyoxalase I activity. Recent studies of vascular endothelial cells in vitro have suggested that α-oxoaldehydes detoxified by glyoxalase I are the major precursors of advanced glycation end products implicated in the development of diabetic complications. The role of these factors in the development of diabetic complications and the prospective prevention of diabetic complications by supplementation of reduced glutathione and/or α-oxoaldehyde-scavenging agents now deserve investigation.
Chromatographic Method for the Determination of Non-Transferrin-Bound Iron Suitable for Use on the Plasma and Bronchoalveolar Lavage Fluid of Preterm Babies
Authors: Kime Robert , Gibson Alan , Yong Wiston , Hider Robert , Powers Hilary 
Published: August 2015

1. Non-protein-bound iron has been implicated in the aetiology of chronic lung disease of prematurity.
2. The modification of a method for the measurement of non-transferrin-bound iron in small volumes of plasma and bronchoalveolar lavage fluid from preterm babies is described.
3. The assay runs with a good degree of precision and a lower limit of detection of 0.02 μmol/l.
4. Non-transferrin-bound iron was detected in 50% of plasma samples and 11% of bronchoalveolar lavage fluid samples collected over the first week of life from babies born prematurely.