bluuebunny/crossref_metadata_2025_split huggingface dataset:
Basal fuel homoeostasis in symptomatic human immunodeficiency virus infection
Authors: Hommes M. J. T. , Romijn J. A. , Endert E. , Schattenkerk J. K. M. Eeftinck , Sauerwein H. P. 
Published: August 2015

1. In eight clinically stable symptomatic human-immunodeficiency-virus-infected patients and in seven healthy control subjects, glucose and fat metabolism were studied, using indirect calorimetry and primed continuous infusions of [3-3H]glucose and [14C]palmitate.
2. Studies were performed in the post-absorptive state (16 h of overnight fasting) and again after 22 h of overnight fasting.
3. In the post-absorptive state, net fat oxidation and triacylglycerol (‘triglyceride’) concentrations were significantly higher in the patients, but concentrations and turnover of free fatty acids were not significantly different between patients and control subjects. After 22 h of overnight fasting, free fatty acid turnover in the patients rose to significantly higher levels when compared with the control subjects.
4. Post-absorptive glucose oxidation, glucose turnover and glucose clearance did not differ between patients and control subjects. Although fasting induced a significantly greater decline in glucose turnover in the patients, plasma glucose concentrations decreased comparably in patients and control subjects.
5. No differences were found in plasma concentrations of insulin or of the counter-regulatory hormones between patients and control subjects.
6. It is concluded that the metabolic adaptation to short-term starvation in clinically stable human-immunodeficiency-virus-infected patients differs from that in healthy control subjects. Short-term starvation results in a significantly greater fall in glucose turnover, whereas fat metabolism is clearly stimulated. These alterations cannot be explained by differences in the concentrations of insulin or of the counter-regulatory hormones.
Effects of contractile activity on muscle damage in the dystrophin-deficient mdx mouse
Authors: McArdle A. , Edwards R. H. T. , Jackson M. J. 
Published: August 2015

1. Isolated extensor digitorum longus muscles from control C57BL/10 and mutant dystrophin-deficient C57BL/10 mdx mice have been studied in vitro to determine whether dystrophin deficiency influences the susceptibility of muscle to contractile activity-induced damage.
2. mdx muscles were found to release reduced amounts of intracellular creatine kinase compared with control tissue in response to excessive contractile activity with or without simultaneous stretching of the muscle to 130% of its resting length.
3. In contrast, prostaglandin E2 release from mdx muscle was elevated compared with control tissue in response to either form of contractile activity or to treatment with the calcium ionophore A23187.
4. These results do not support the hypothesis that dystrophin-deficient muscle is more susceptible to damage induced by contractile activity, but suggest that dystrophin deficiency influences the activity of muscle membrane phospholipase enzymes.
Influence of the plasma protein concentration on renal function
Authors: Cumming Allan D. , Linton Adam 
Published: August 2015

1. The effect of the plasma protein concentration on renal function remains controversial. Most, but not all, experimental studies suggest that a reduced plasma protein concentration perfusing the kidney may reduce tubular sodium reabsorption. Hypoproteinaemic disease states are usually associated with sodium retention, which is not always volume-dependent.
2. We induced a 21% and 24% reduction in plasma total protein and plasma albumin, respectively, in unanaesthetized sheep by acute extracorporeal plasmapheresis. Arterial pressure did not change, and changes in circulatory volume were minimised by infusion of crystalloid to maintain pulmonary artery occlusion pressure, measured using a Swann-Ganz pulmonary artery catheter.
3. After plasmapheresis, there was no significant change in creatinine clearance, sodium excretion, plasma renin activity or urinary kallikrein excretion.
4. After plasmapheresis, there was a significant reduction in plasma osmolality, increase in urine osmolality and fall in free water clearance.
5. The results suggest that in the absence of detectable changes in circulating volume or arterial pressure, acute hypoproteinaemia is associated with significant changes in renal water handling, but has no direct effect on sodium excretion or on renal release of renin and kallikrein.
Effect of α-ketoglutarate infusions on organ balances of glutamine and glutamate in anaesthetized dogs in the catabolic state
Authors: Roth E. , Karner J. , Roth-Merten A. , Winkler S. , Valentini L. , Schaupp K. 
Published: August 2015

1. The salt complex of l-(+)-ornithine and α-ketoglutarate (2-oxoglutarate) has recently been proposed for the treatment of patients in the catabolic state. As yet, it is unclear which of the two substrates (ornithine or α-ketoglutarate) is responsible for the anticatabolic effect. We infused α-ketoglutarate into anaesthetized postoperative dogs in order to investigate whether infusion of α-ketoglutarate affects the flux of glutamine and glutamate between skeletal muscle and the splanchnic bed. We used three infusion rates: 3, 10 and 20 μmol min−1 kg−1. A steady state of α-ketoglutarate concentration in arterial whole-blood was attained only when the infusion rate was 3 μmol min−1 kg−1.
2. Arterial whole-blood concentrations of α-ketoglutarate were 8.8 ± 1.2 μmol/l in the basal period and rose to 208 ± 41, 344 ± 61 and 1418 ± 315 μmol/l after 60 min infusions of α-ketoglutarate at 3, 10 and 20 μmol min−1 kg−1, respectively.
3. α-Ketoglutarate uptake was measured in skeletal muscle, liver, gut and kidneys in the basal period and during the infusion of α-ketoglutarate. The net uptake of infused α-ketoglutarate was highest in the skeletal muscle, followed by kidneys, liver and gut.
4. The α-ketoglutarate load increased the muscular tissue content of α-ketoglutarate from 49.5 ± 5 to 142 ± 15 nmol/g of dry substance (P &lt; 0.001), but did not alter the muscular glutamate or glutamine contents.
5. Infusion of α-ketoglutarate had no effect on the plasma glutamine concentration, nor on the glutamine and glutamate balances across the skeletal muscle, liver and gut. However, α-ketoglutarate infusion significantly reduced the renal extraction of glutamine (P &lt; 0.05) and enhanced the renal production of glutamate (P &lt; 0.05).
6. We conclude that an intravenous α-ketoglutarate load affects the renal balances of glutamine and glutamate, but does not alter the nitrogen flux of glutamine and glutamate between skeletal muscle, liver and gut.
Ketone infusion lowers hormonal responses to hypoglycaemia: Evidence for acute cerebral utilization of a non-glucose fuel
Authors: Amiel Stephanie A. , Archibald Helen R. , Chusney Gary , Williams Alistair J. K. , Gale Edwin A. M. 
Published: August 2015

1. The effect of hyperketonaemia on counter-regulatory hormone responses to hypoglycaemia has been examined in six healthy subjects.
2. A controlled, step-wise reduction in blood glucose concentration was achieved by adjusting the rate of glucose infusion during a primed-continuous infusion of soluble insulin (1.5 m-units min−1 kg−1 body weight, plasma insulin concentration approximately 90 m-units/l). Simultaneous infusion of either saline or β-hydroxybutyrate (3 mg min−1 kg−1 body weight) was administered in a single-blind fashion, in random order. Despite a need for 40% more glucose during the ketone infusion, an identical fall in blood glucose concentration was achieved in each study.
3. The glycaemic threshold for stimulating an adrenaline response of 0.41 nmol/l was reduced from 3.1 to 2.8 mmol/l (P &lt; 0.05) during ketone infusion, and that for stimulating a response of more than 50% of basal from 3.6 to 3.1 mmol/l (P &lt; 0.001). The peak adrenaline response fell from 7.97 to 2.6 nmol/l (P &lt; 0.04). Peak noradrenaline, cortisol and growth hormone responses were also significantly lower during ketone infusion (P = 0.04, 0.001 and 0.006, respectively). Glucagon responses alone were unaffected by hyperketonaemia.
4. The provision of an alternate metabolic fuel thus produced immediate changes in the neurohumoral responses to hypoglycaemia. This is consistent with the hypothesis that human nervous tissue can metabolize ketones acutely.
Altered small-intestinal permeability associated with diarrhoea in human-immunodeficiency-virus-infected Caucasian and African subjects
Authors: Kapembwa M. S. , Fleming S. C. , Sewankambo N. , Serwadda D. , Lucas S. , Moody A. , Griffin G. E. 
Published: August 2015

1. Small-intestine integrity in Caucasian and African patients infected with human immunodeficiency virus was determined by measuring the permeation across the mucosa of two sugars, lactulose and mannitol.
2. The sugars were assayed by h.p.l.c. and pulsed amperometric detection in 6 h urine samples. Stool microscopy for enteropathogens was performed in all patients.
3. The ratio of lactulose to mannitol recovered in urine was increased in Caucasian and African patients with advanced human immunodeficiency virus infection. Asymptomatic human-immunodeficiency-virus-infected subjects had a normal lactulose/mannitol ratio. African patients with diarrhoea showed a twofold reduction in mannitol excretion. Such a change in mannitol absorption was not detected in Caucasian patients and occurred regardless of the presence of enteropathogens.
4. Altered small-intestinal permeability is associated with symptomatic diarrhoea in human immunodeficiency virus infection in both Caucasian and African patients.
Heparin and heparan sulphate are inhibitors of human leucocyte elastase
Authors: Walsh R. L. , Dillon T. J. , Scicchitano R. , McLennan G. 
Published: August 2015

1. Heparin and heparan sulphate strongly inhibited human leucocyte elastase activity in an automated assay using the soluble substrate, n-succinyl-(l-alanine)3-p-nitroanilide (50% inhibition of 250 μl of 10 μg of human leucocyte elastase/ml was obtained with 80 μl of 2.8 μg of heparin/ml and 8 μg of heparan sulphate/ml). Less significant inhibition at the same concentrations was seen with the other glycosaminoglycans tested: hyaluronic acid and chondroitin sulphates A–C.
2. Heparin and heparan sulphate also strongly inhibited human leucocyte elastase activity towards insoluble human lung elastin, as determined by an e.l.i.s.a. for soluble elastin-derived peptides released by elastolytic activity on the elastin. This inhibition was shown not to be due to a direct interference of the glycosaminoglycans in the e.l.i.s.a. nor to the inhibition causing a change in the size of the elastin-derived peptides. However, unlike the chromogenic assay with n-succinyl-(l-alanine)3-p-nitroanilide as substrate, where heparin was the more effective inhibitor, in this assay system heparan sulphate was the more effective inhibitor (50% inhibition of 100 μl of 50 ng of human leucocyte elastase/ml was obtained with 100 μl of 4.5 μg of heparin/ml and 0.8 μg of heparan sulphate/ml). These results suggest that heparin and heparan sulphate, as components of cellular and basement membranes, are likely to have a role in protecting structural proteins, such as elastin, from the proteolytic activity of human leucocyte elastase.
3. The degree of inhibition by heparin was independent of pH within the range of pH studied (pH 6–9) and was almost immediate in the automated chromogenic assay system where a 10 s preincubation step was used. The inhibitory effect of heparin could be prevented by the addition of protamine sulphate or by the removal of heparin by an ion-exchange resin.
4. Low Mr preparations of heparin were also found to inhibit human leucocyte elastase, although preparations with Mr of 2000 or less did not inhibit the enzyme to the same extent as commercial preparations.
5. Heparin at the same concentrations did not inhibit other leucocyte enzymes, such as cathepsin G and myeloperoxidase, nor the pancreatic enzymes, pancreatic elastase, trypsin and chymotrypsin.
Non-diabetic microalbuminuria in clinical practice and its relationship to posture, exercise and blood pressure
Authors: West J. N. W. , Gosling P. , Dimmitt S. B. , Littler W. A. 
Published: August 2015

1. The effects of posture and exercise on the relationship between low-level urinary albumin excretion (microalbuminuria) and blood pressure was investigated in two groups of non-diabetic patients at increased cardiovascular risk: 21 otherwise healthy patients with untreated essential hypertension (blood pressure &gt; 160/90 mmHg), and 14 age-matched patients with blood pressure at presentation within the normotensive range (&lt; 160/90 mmHg) attending a cardiovascular clinic for assessment of chest pain.
2. A significant linear relationship between logarithmically transformed ‘spot’ urinary albumin/creatinine ratio and simultaneous clinic blood pressure existed when data from both groups of patients were analysed (r = 0.58, P &lt; 0.05). The relationship between the scatter plot of blood pressure and the albumin/creatinine ratio appeared most marked when the mean blood pressure exceeded 120 mmHg.
3. In patients with essential hypertension, clinic systolic blood pressure was related to the albumin/creatinine ratio in simultaneous ‘spot’ urine samples (r = 0.69, P &lt; 0.05) and also to the albumin/creatinine ratio in early-morning urine samples (r = 0.51, P &lt; 0.05). However, the relationship between clinic blood pressure and simultaneous ‘spot’ urinary albumin/creatinine ratio in the patients with chest pain did not achieve significance when analysed independently.
4. Hourly averaged ambulatory intra-arterial blood pressure was recorded in four of the patients with essential hypertension during normal daytime activity, and a significant correlation with the simultaneous hourly daytime urinary albumin/creatinine ratio was found (r = 0.65, P &lt; 0.01).
5. Low-level albumin excretion increased in both groups after exercise: peak systolic blood pressure during exercise was related to the rise in albumin excretion (hypertensive patients, r = 0.68, P &lt; 0.01; normotensive patients, r = 0.66, P &lt; 0.05).
Effects of continuous infusion of atrial natriuretic peptide on the pulmonary hypertension induced by chronic hypoxia in rats
Authors: Zhao L. , Winter R. J. D. , Krausz T. , Hughes J. M. B. 
Published: August 2015

1. The effects of the continuous infusion of atrial natriuretic peptide on the development of pulmonary hypertension were studied in rats exposed to chronic hypoxia.
2. Continuous intravenous infusion of two doses of synthetic rat atrial natriuretic peptide, 300 ng/h per rat (0.10 pmol/h per rat) and 800 ng/h per rat (0.28 pmol/h per rat), attenuated the development of pulmonary hypertension in rats exposed to chronic hypoxia (fractional concentration of oxygen in inspired air = 10%) for 7 days: (i) the pulmonary artery pressure (mean ± sd) in the vehicle-treated hypoxic group was 45 ± 6 mmHg compared with 28 ± 6 mmHg in the vehicle-treated normotoxic group (n = 8, P &lt; 0.001); (ii) treatment with atrial natriuretic peptide in normoxia did not alter the pulmonary artery pressure, systemic blood pressure or heart rate; (iii) treatment with atrial natriuretic peptide in hypoxia resulted in a lower pulmonary artery pressure in the group treated with 800 ng of atrial natriuretic peptide/h per rat (38 ± 8 mmHg, P &lt; 0.05 compared with the vehicle-treated hypoxic group) without affecting the systemic blood pressure or heart rate.
3. Chronic hypoxia resulted in an extension of vascular smooth muscle towards the periphery of the lung with the development of muscle in normally non-muscularized vessels (remodelling). Quantitative assessment of the small pulmonary vessels (external diameter 25–55 μm) showed that atrial natriuretic peptide treatment reduced pulmonary vascular remodelling in hypoxia (the percentage of thick-walled vessels in the peripheral lung hypoxic vehicle-treated group was 25 ± 6 compared with 19 ± 4 in the group given 300 ng of atrial natriuretic peptide/h per rat and 17 ± 7 in the group given 800 ng of atrial natriuretic peptide/h per rat, means ± sd, both P &lt; 0.01 compared with the vehicle-treated normoxic group).
4. These data show that infusion of synthetic atrial natriuretic peptide attenuated the pulmonary vascular remodelling and associated pulmonary hypertension produced by chronic hypoxia.
Peripheral triacylglycerol extraction in the fasting and post-prandial states
Authors: Potts Jennifer L. , Fisher Rachel M. , Humphreys Sandy M. , Coppack Simon W. , Gibbons Geoffrey F. , Frayn Keith N. 
Published: August 2015

1. Triacylglycerol extraction by subcutaneous adipose tissue and forearm muscle was studied in nine normal subjects after an overnight fast and after the consumption of a mixed meal.
2. There was an inverse correlation between the total plasma fractional triacylglycerol extraction across the adipose tissue and the fasting arterial plasma triacylglycerol concentration. In contrast, there was no correlation between the lower fractional triacylglycerol extraction across the forearm muscle and the fasting plasma triacylglycerol concentration.
3. Chylomicron-triacylglycerol concentrations in arterial(ized) plasma increased post-prandially and peaked at 240–300 min. There was a comparable increase in the very-low-density lipoprotein-triacylglycerol concentration, peaking at 300 min.
4. Clearance of chylomicron-triacylglycerol by adipose tissue increased after the meal (P &lt;0.05). In contrast, the clearance of very-low-density lipoprotein-triacylglycerol by adipose tissue decreased post-prandially (P &lt;0.05).
5. Although there was significant uptake of chylomicron-triacylglycerol by the forearm muscle post-prandially, this was less than by the adipose tissue. Very-low-density lipoprotein-triacylglycerol was unaffected by passage through the forearm muscle at any time.
6. We conclude that the extraction of lipoprotein-triacylglycerol by human adipose tissue is important in determining the fasting plasma triacylglycerol concentration. Chylomicron-triacylglycerol, appearing in the plasma post-prandially, may compete with very-low-density lipoprotein-triacylglycerol for clearance by adipose tissue lipoprotein lipase, and this mechanism may explain, at least in part, the post-prandial rise in very-low-density lipoprotein-triacylglycerol. Forearm muscle, in contrast, appears to play a much smaller role in the extraction of plasma triacylglycerol, especially that in the very-low-density lipoprotein fraction.
Sternomastoid muscle twitch maximum relaxation rate: prolonged slowing with fatigue and post-tetanic acceleration
Authors: Mak V. H. F. , Chapman F. , James C. , Spiro S. G. 
Published: August 2015

1. The maximum rate of relaxation of stimulated twitches (twitch maximum relaxation rate) of the sternomastoid muscle was compared with its frequency-force curve (expressed as the ratio of force produced at a stimulation frequency of 20 Hz to that produced at 50 Hz, the 20:50 ratio) before and after fatiguing exercise of the sternomastoid muscle in 10 normal subjects. The mean (±) fresh state twitch maximum relaxation rate was 9.51 (± 0.64)% force loss/10 ms and the mean (± sem) 20:50 ratio was 73.4 (± 2.6)%.
2. The mean twitch maximum relaxation rate fell to 71.5 (± 2.2)% of the pre-fatigue value at 2 min after exercise, recovering to 73.1 (± 1.6)% by 5 min, 78.4 (± 2.34)% by 10 min and 80.6 (± 2.70)% by 60 min. The 20:50 ratio fell to 72.3 (± 3.56)% of pre-fatigue levels at 10 min after exercise and recovered to 78.8 (± 3.16)% by 60 min. There was no significant difference in the percentage falls between the two techniques.
3. Further studies were performed to determine the response of the twitch maximum relaxation rate to a prior brief tetanic stimulus or a brief maximal voluntary contraction of the muscle. Both tetanic stimulation and maximal voluntary contraction accelerated the twitch maximum relaxation rate to over 140% of the fresh state value. Both manoeuvres temporarily returned the slowed twitch maximum relaxation rate after fatiguing exercise back to the fresh state value.
4. The effect of fatiguing exercise on the time course of recovery of quadriceps twitch maximum relaxation rate was also studied in two subjects. The twitch maximum relaxation rate had not recovered to fresh state levels by 5 min after exercise in both subjects. At 10 min, one subject had recovered to the fresh state value, but the other had recovered to only 85% of the fresh state value. Both recovered to fresh state values by 1 h.
5. We conclude that the twitch maximum relaxation rate of the sternomastoid as measured from a twitch contraction has a prolonged time course of recovery after fatiguing exercise, and may follow the same time course of recovery as low-frequency fatigue. Tetanic stimulation and voluntary contractions may temporarily accelerate the relaxation rate, and therefore a distinction should be made between relaxation rates measured after a twitch contraction (twitch maximum relaxation rate) and those after tetanic stimulation or a maximum voluntary contraction (maximum relaxation rate).
Anti-oxidants show an anti-hypertensive effect in diabetic and hypertensive subjects
Authors: Ceriello Antonio , Giugliano Dario , Quatraro Antonio , Lefebvre Pierre J. 
Published: August 2015

1. In this study an acute anti-hypertensive effect of three anti-oxidant agents (vitamin C, thiopronine and glutathione) in hypertensive subjects and in both hypertensive and non-hypertensive diabetic patients is reported.
2. The anti-oxidants had no effect on blood pressure in healthy normal subjects at a dose of 6 mmol, but thiopronine and glutathione produced a significant hypotensive effect at a dose of 12 mmol.
3. These data suggest that anti-oxidants might have a dilatatory effect and that an imbalance of the nitric oxide-free radical interaction might facilitate the development of hypertension in humans.