bluuebunny/crossref_metadata_2025_split huggingface dataset:
Analysis of factors limiting maximal exercise performance in cystic fibrosis
Authors: Lands Larry C. , Heigenhauser George J. F. , Jones Norman L. 
Published: August 2015

1. Maximal exercise capacity in cystic fibrosis is influenced by both pulmonary and nutritional factors: lung disease by limiting maximal achievable ventilation, and malnutrition through a loss of muscle mass. The associated reduction in everyday activities may result in peripheral muscle deconditioning.
2. We studied 14 stable patients with cystic fibrosis (six males, eight females) and 14 healthy control subjects (seven males, seven females) in order to assess the influence of these factors on exercise performance. Subjects underwent anthropometry to estimate muscle mass, spirometry to assess ventilatory capacity, a 30 s sprint on an isokinetic cycle ergometer to assess maximal leg muscle performance, and progressive cycle ergometry to assess overall exercise capacity.
3. Compared with control subjects, the patients with cystic fibrosis were of similar age and height but weighed proportionately less [% ideal weight (mean ± sd): 94.3 ± 9.64 versus 109.5 ± 11.82] and showed evidence of airflow limitation [forced expiratory volume in 1.0s (FEV1.0) 72.5 ± 24.78 versus 112.6 ± 14.25% of predicted].
4. The patients with cystic fibrosis did less absolute (5.1 ± 1.89 versus 7.3 ± 1.97 kJ) but similar relative maximal (11.5 ± 3.41 versus 13.1 ± 3.55 kJ/kg lean body mass) sprint work. During progressive exercise, the group with cystic fibrosis achieved lower absolute [maximal O2 consumption (Vo2max.) 1.8 ± 0.527 versus 3.0 ± 0.655 litres/min] and relative (Vo2max./kg lean body mass: 40.5 ± 9.23 versus 53.0 ± 11.62 ml min−1kg−1) work levels.
5. Step-wise linear regression was carried out with Vo2max. as the dependent variable and lean body mass, FEV1.0 and 30 s sprint work as independent variables. Vo2max. was best accounted for by a two-factor equation with FEV1.0 and 30 s sprint work (r2 = 0.882), with FEV1.0 being relatively more important.
6. While noting the importance of lung disease as a limiting factor, these results suggest that peripheral muscle function is a more sensitive determinant of maximal performance than lean body mass. The 30 s sprint work results imply that the effects of mild malnutrition in cystic fibrosis are quantitative, affecting the size of the muscle mass but not the performance of the remaining muscle.
Ageing and the response of plasma insulin, glucose and C-peptide concentrations to intravenous glucose in postmenopausal women
Authors: Proudler Anthony J. , Felton Carl V. , Stevenson John C. 
Published: August 2015

1. Eighty-six apparently healthy postmenopausal women not receiving hormone replacement therapy were given an intravenous glucose tolerance test. Plasma glucose, insulin and C-peptide concentrations were determined in fasting and post-glucose challenge samples.
2. Using a multivariate regression model, with predictor variables of chronological age, menopausal age and body mass index, neither chronological age nor menopausal age correlated with fasting or post-challenge plasma glucose or C-peptide concentrations. In contrast, menopausal age was positively associated with fasting plasma insulin concentration (P = 0.038, model r2 = 0.107), insulin area (P = 0.01, model r2 = 0.236) and incremental insulin area (P = 0.024, model r2 = 0.243). This relationship could not be explained by differences in lifestyle variables of alcohol consumption, physical activity, previous duration of oral contraceptive usage, history of cigarette smoking or body mass index.
3. Our findings suggest that loss of ovarian function is associated with hyperinsulinaemia, possibly via alterations in the clearance of circulating insulin from the plasma. The hyperinsulinaemia observed may contribute to the increased risk of cardiovascular disease seen in postmenopausal women.
Effect of acute plasma volume expansion on peripheral arteriolar tone in healthy subjects
Authors: Calver Alison , Collier Joe , Green Daniel , Vallance Patrick 
Published: August 2015

1. Using venous occlusion plethysmography, we have investigated the forearm blood flow response in healthy subjects to the acute plasma volume expansion caused by a rapid intravenous infusion of saline. The contribution made to this response by nitric oxide has been investigated using local intra-arterial infusions of the nitric oxide synthase inhibitor NG-monomethyl-l-arginine.
2. The infusion of 1000 ml of saline over 25 min caused plasma volume to increase by about 7%, and resulted in a rise in forearm blood flow, with no change in arterial blood pressure. The onset of the blood flow response occurred within 10 min and blood flow remained elevated above baseline 20 mm after the end of the saline infusion.
3. Local intra-arterial infusion of NG-monomethyl-l-arginine alone caused a reduction in forearm blood flow which was maximal at the end of the infusion and gradually recovered to baseline levels over 40 min.
4. When local intra-arterial infusion of NG-monomethyl-l-arginine was followed by plasma volume expansion, the calculated effect of NG-monomethyl-l-arginine was such as to abolish the vasodilator response to saline.
5. The effect of local intra-arterial infusion of NG-monomethyl-l-arginine on forearm blood flow was greater when the drug was given after volume expansion had occurred, than when it was given before the administration of saline. However, in control experiments the vasoconstrictor response to noradrenaline was also enhanced after the administration of the volume load in comparison with the response to noradrenaline given alone.
6. These results are consistent with the possibility that increased local synthesis of nitric oxide contributes to the vasodilator response to volume expansion.
Long-term effects of a somatostatin analogue on renal haemodynamics and hypertrophy in diabetic rats
Authors: Muntzel Martin , Hannedouche Thierry , Niesor Roberte , Nöel Laure-Helène , Souberbielle Jean-Claude , Lacour Bernard , Drüeke Tilman 
Published: August 2015

1. To determine whether treatment with octreotide, a somatostatin analogue, may diminish or prevent long-term diabetic renal hypertrophy and nephropathy, uninephrectomized streptozotocin-diabetic rats maintained under moderate glycaemic control (∼300 mg/dl) were treated with either placebo (n = 10 rat/group) or octreotide for 14 weeks. Uninephrectomized non-diabetic rats given either placebo or octreotide served as controls.
2. Average body weight was diminished and kidney weight, daily urinary protein excretion, glomerular filtration rate and renal plasma flow were elevated in both diabetic groups relative to controls.
3. Administration of octreotide reduced average body weight and packed cell volume in non-diabetic and diabetic rats compared with their respective controls, but did not affect glomerular hyperfiltration or the increase in urinary protein excretion.
4. Histological examination at 14 weeks disclosed unequivocal glomerular hypertrophy and mild glomerular and tubulointerstitial lesions consistent with early diabetic renal alterations in all diabetic rats, but there was no independent effect of octreotide treatment
5. Thus, long-term treatment with octreotide did not afford protection against the development of renal hypertrophy-hyperfiltration and the evolution of early diabetic nephropathy in rats.
Serum sialic acid concentration in patients with hypertriglyceridaemia showing the Frederickson's IIB phenotype
Authors: Crook M. , Tutt P. 
Published: August 2015

1. Serum total sialic acid concentration, recently shown to be a cardiovascular risk factor, and also serum lipid-associated sialic acid concentration were measured in 15 patients with hypertriglyceridaemia (fasting serum triacylglycerol concentration &gt; 2.3 mmol/l) showing a Frederickson's type IIB phenotype, 15 patients with hypercholesterolaemia showing a IIA phenotype and 15 age- and sex-matched normal control subjects.
2. Total serum sialic acid concentration was significantly raised in the hypertriglyceridaemic group (84.9 ± 21.5 versus 64.9 ± 20.8 mg/dl, P&lt;0.03, Mann—Whitney U-test) compared with the normal control group, as was serum lipid-associated sialic acid concentration (23.0 ± 4.3 versus 12.0 ± 3.2 mg/dl, respectively, P&lt;0.001, Mann—Whitney U-test).
3. Serum total sialic acid concentration was also significantly elevated in the hypertriglyceridaemic group as compared with the IIA phenotype hypercholesterolaemic group (84.9 ± 21.5 versus 58.4 ± 11.7 mg/dl, P&lt;0.03, Mann—Whitney U-test), as was serum lipid-associated sialic acid concentration (23.0 ± 4.3 versus 14.9 ± 4.7 mg/dl, P&lt;0.001, Mann—Whitney U-test).
4. We suggest that serum concentrations of both total sialic acid and lipid-associated sialic acid may be useful markers of cardiovascular risk which could, in part, be related to hypertriglyceridaemia.
Impaired fatty-meal-stimulated gallbladder contractility in patients with Crohn's disease
Authors: Murray F. E. , McNicholas M. , Stack W. , O'Donoghue D. P. 
Published: August 2015

1. The incidence of gallstones in patients with Crohn's disease is increased compared with that in healthy control subjects. This is in part due to reduced terminal ileal bile salt absorption and consequent increased cholesterol saturation in bile. The aim of this study was to evaluate gallbladder contractility, a second important factor in the pathogenesis of gallstones, in Crohn's disease.
2. Thirty patients with Crohn's disease and no known biliary tract disease and nine healthy control subjects were studied. After an overnight fast, gallbladder volume was determined by real-time ultrasonography before and 10, 20, 30, 40, and 50 min after ingestion of a standard liquid fatty meal.
3. Compared with healthy control subjects, patients with Crohn's disease had similar fasting gallbladder volumes (control, 18.7 ± 2.3 ml; Crohn's disease, 18.2 ± 2.3 ml). Percentage emptying was significantly impaired at 30, 40 and 50 min in patients with Crohn's disease compared with control subjects. Patients with Crohn's disease limited to the small bowel had gallbladder contractility that was comparable with that of control subjects, whereas in those with large-bowel disease, minimum residual gallbladder volume was significantly smaller than in control subjects. Patients with both large- and small-bowel Crohn's disease demonstrated the most marked abnormalities, with gallbladder volumes significantly larger than those of control subjects at 30, 40 and 50 min. Likewise, patients with Crohn's disease who had undergone previous bowel resection had impaired emptying at 30, 40 and 50 min.
4. In summary, gallbladder contractility is significantly impaired in patients with Crohn's disease, an abnormality which is most marked in those patients who have undergone bowel resection or have both large- and small-bowel disease. Impaired gallbladder contractility may thus be a second factor contributing to gallstone formation in certain patients with Crohn's disease.
Glucocorticoid ameliorates altered gene expression of extracellular matrix components in kidneys of New Zealand Black/White F1 mice
Authors: Nakamura Tsukasa , Ebihara Isao , Tomino Yasuhiko , Koide Hikaru 
Published: August 2015

1. We examined the effects of methylprednisolone on the levels of messenger RNA encoding for extracellular matrix components, including α1(IV) collagen chain, laminin B1 and B2 chains, heparan sulphate proteoglycan and α1(I) and α1(III) collagen chains, and on the accumulation of these proteins in the renal cortex of New Zealand Black/White F1 mice.
2. At the onset of nephritis, at about 5 months of age, New Zealand Black/White F1 mice were divided in two groups that received either methylprednisolone or saline injections for 5 months.
3. The development of histological lesions and the glomerular deposition of IgG, IgM and C3 were suppressed by methylprednisolone treatment from 5 to 10 months of age.
4. The distribution and intensity of type IV collagen, laminin, heparan sulphate proteoglycan, type I collagen and type III collagen in renal cortex were decreased by the administration of methylprednisolone.
5. Levels of messenger RNA encoding for α1(IV) collagen chain, laminin B1 and B2 chains, heparan sulphate proteoglycan and α1(I) and α1(III) collagen chains in the renal cortex of New Zealand Black/White F1 mice were significantly ameliorated at 8–10 months of age by methylprednisolone administration.
6. These results indicate that methylprednisolone treatment can serve as an effective therapeutic approach to abnormal extracellular matrix regulation in murine lupus nephritis.
Influence of butter and of corn, coconut and fish oils on the effects of recombinant human tumour necrosis factor-α in rats
Authors: Mulrooney Hilda M. , Grimble Robert F. 
Published: August 2015

1. Tumour necrosis factor-α is produced in response to inflammatory stimuli. Fish oil can suppress the production and actions of cytokines. Little information is available on the effects of other fats on cytokine biology. We compared the effects of fats, with a wide range of fatty acid characteristics, on the effects of tumour necrosis factor-α on protein and zinc metabolism in rats.
2. Weanling rats were fed for 8 weeks on diets containing 10% fat in the form of corn, fish or coconut oils or butter before an intraperitoneal injection of recombinant human tumour necrosis factor-α was given. Measurements were made 24 h after the injection.
3. In rats fed corn oil, food intake was reduced by 62% and rates of protein synthesis were increased by 86, 32 and 39% in the liver, lung and kidney, respectively. Zinc concentrations increased by 23% in the liver but decreased by 10% in the kidney. Plasma caeruloplasmin and complement C3 levels increased by 25% and 28%, respectively, and plasma albumin level decreased by 24%.
4. Fish oil prevented the increase in hepatic protein synthesis and changed the response of protein synthesis in lung and kidney to a decrease. Changes in hepatic and renal zinc concentrations were prevented. The response of the plasma caeruloplasmin level was unaltered but those of the plasma complement C3 and albumin concentrations were prevented.
5. Coconut oil and butter, although similarly low in linoleic acid, differed in their modulatory effects. With the exception of the rise in the plasma complement C3 concentration, all responses were prevented or greatly inhibited in rats fed butter. In rats fed coconut oil the increase in liver protein synthesis was reduced but that in the lung and kidney was unaffected. Changes in hepatic zinc concentration were unaffected but those in renal zinc concentration were prevented.
6. Fish and coconut oils and butter reduced the intensity of anorexia caused by tumour necrosis factor-α. The extent to which fats rich in (n-3) polyunsaturates or poor in linoleic acid modulate the metabolic response to tumour necrosis factor-α depends upon additional fatty acid characteristics.
Splanchnic blood flow in man: evidence for mediation via a β-adrenergic mechanism
Authors: Braatvedt G. D. , Flynn M. D. , Stanners A. , Halliwell M. , Corrall R. J. M. 
Published: August 2015

1. Superior mesenteric artery blood flow was examined by Doppler ultrasound in six male subjects aged 19–23 years during the infusion of saline (control), 10 and 40 ng of adrenaline min−1 kg−1 for 30 min, or propranolol and 10 ng of adrenaline min−1kg−1 for 30 min, on four separate occasions.
2. Adrenaline infusion resulted in significant peak mean (SEM) rises in circulating adrenaline concentrations during the infusion period only [control, 0.20 (0.05) nmol/l; 10 ng of adrenaline min−1 kg−1, 1.37 (0.29) nmol/l; 40 ng of adrenaline min−1kg−1, 3.73 (0.40) nmol/l; 10 ng of adrenaline min−1kg−1 and propranolol, 1.48 (0.16) nmol/l, P &lt; 0.001 versus control]. These values are within the physiological range.
3. Superior mesenteric artery blood flow rose in a dose-dependent manner during the adrenaline infusions alone, but not during the infusion of adrenaline and propranolol [mean (95% confidence interval) area under the curve: control, −4.2 (−11 to +2.7)%; 10 ng of adrenaline min−1kg−1, +4 (−1 to 11.9)%; 40 ng of adrenaline min−1kg−1, +34 (+ 6.5 to + 61.5)%; 10 ng of adrenaline min−1kg−1 and propranolol, −8.4 (−23 to +6)%].
4. Superior mesenteric artery resistance fell during the adrenaline infusions alone and rose during the combined adrenaline and propranolol infusion [mean (SEM) area under the curve: control, 6.4 (2.7)%; 10 ng of adrenaline min−1kg−1, −2.9 (2.5)%; 40 ng of adrenaline min−1kg−1, −15 (1.4)%; 10 ng of adrenaline min−1kg−1 and propranolol, 16.9 (10)%].
5. These data suggest that splanchnic vasodilatation is mediated via a β-adrenergic mechanism.
Observations on the early renal uptake and later tubular metabolism of radiolabelled aprotinin (Trasylol) in man: theoretical and practical considerations
Authors: Rustom R. , Grime J. S. , Maltby P. , Stockdale H. R. , Critchley M. , Bone J. M. 
Published: August 2015

1. The novel method recently developed to measure renal tubular degradation of filtered proteins in man using radiolabelled aprotinin (Trasylol) has been modified to allow the fate and the significance of the renal catabolism of radiolabelled aprotinin to be determined beyond 24 h.
2. Ten renal patients with normal kidney function and variable proteinuria each received two separate intravenous injections of radiolabelled aprotinin, 5.0 mg of 99mTc-labelled aprotinin (40 MBq) and 0.5 mg of 131I-labelled aprotinin (5 MBq). Chromatography (Sephadex-G-25-M) was used to separate undegraded radiolabelled aprotinin from the free isotope in urine and plasma. Renal uptake from σ-camera images (24 h for 99mTc-Iabelled aprotinin and up to 96 h for 131I-labelled aprotinin) and urinary activity (48 and 96 h, respectively) were measured.
3. The renal handling of radiolabelled aprotinin was similar with the two isotopes. Chromatography showed that all plasma activity was undegraded radiolabelled aprotinin, and urine activity was only the free isotopic label.
4. Kidney uptake of 131I-labelled aprotinin was prompt, reaching a cumulative maximum of 37.1 ± 3.0% of dose at 24 h, but falling exponentially thereafter to 5.6 ± 1.0% of dose at 96 h.
5. The rate of excretion of the free label in urine, i.e. the metabolic rate of radiolabelled aprotinin, was relatively constant over the first 24 h (1.6 ± 0.09% of dose/h), but then fell in parallel with the diminishing activity over the kidney, i.e. to 1.0 ± 0.1% of dose/h over 24–48 h and to only 0.4 ± 0.08% of dose/h over 72–96 h.
6. Fractional renal degradation of radiolabelled aprotinin, derived from the mean rate of urinary excretion of the free isotope over a given interval divided by the mean cumulative kidney uptake over the same interval (h−1), fell steeply early and then more slowly to 0.05 ± 0.003 h−1 at 14.25h, and stabilized thereafter varying little between 0.04 ± 0.01 h−1 and 0.05 ± 0.01 h−1 over 36–84 h.
7. Thus, the maximum cumulative kidney uptake of radiolabelled aprotinin is achieved by 24 h, when the metabolic rate and fractional degradation are reliable indices of catabolism. The falling metabolic rate after 24 h, together with the constant rate of fractional degradation, suggests that there is a readily saturable step in the metabolic process. Hence, duplicate measurements of radiolabelled aprotinin uptake and metabolism around 24 h only (12–36 h) are sufficient and offer a simple and a reliable tool in clinical studies for determining the link between renal tubular protein degradation and renal disease progression.
Genetics of a multifactorial disease: Autoimmune type I diabetes mellitus
Authors: Cornall Richard John 
Published: August 2015

1. Three non-major histocompatability complex genes, Idd-3, Idd-4 and Idd-5, that influence the onset of autoimmune type 1 diabetes in the non-obese diabetic mouse have been located on chromosomes 3, 11 and 1.
2. In undertaking this study, a new map of the mouse genome has been created from polymerase chain reaction-analysable mouse microsatellite markers.
3. The homologues of these genes may reside on human chromosomes 1 or 4 (Idd-3), 17 (Idd-4) and 2q (Idd-5).
Effects of correcting arterial hypoxaemia on respiratory resistance in patients with chronic obstructive pulmonary disease
Authors: Coe C. I. , Pride N. B. 
Published: August 2015

1. We have re-examined the effects of breathing 100% O2 on airflow resistance in hypoxaemic patients with chronic obstructive pulmonary disease. We measured arterial O2 saturation with an ear oximeter and total respiratory resistance by imposing forced oscillations at the mouth over the range 6–26 Hz during tidal breathing. Six normal subjects (mean age, 27.3 years; forced expiratory volume in 1 s, 3.82 litres) and 18 patients with severe chronic obstructive pulmonary disease and hypoxaemia (mean age, 66.6 years; forced expiratory volume in 1 s, 0.61 litres; O2 saturation breathing air, 88.4%) were examined in the sitting position breathing air and 100% O2. Eleven of the patients with chronic obstructive pulmonary disease were also studied before and after treatment with nebulized salbutamol (2.5 mg).
2. In normal subjects total respiratory resistance at 8 Hz breathing air was 2.35(0.16) cmH2Ol−1 s [mean (SEM)]; after salbutamol there was a small decrease in total respiratory resistance to 1.99(0.12) cmH2Ol−1 s. Breathing 100% O2 had no effect on total respiratory resistance either before or after salbutamol treatment.
3. In the patients with chronic obstructive pulmonary disease, values of total respiratory resistance fell with increasing frequency of oscillation; at 8 Hz, total respiratory resistance was 4.53(0.35) cmH2Ol−1 s breathing air and 3.73(0.28) cmH2Ol−1 s breathing 100% O2 (paired t-test, P = 0.001). The reduction in total respiratory resistance with O2 breathing varied between patients but was not related to the severity of hypoxaemia breathing air. Inhaled salbutamol had no significant effect on total respiratory resistance breathing air or 100% O2.
4. These studies show that arterial hypoxaemia contributes to increased airflow resistance in patients with chronic obstructive pulmonary disease. Our results show that the airway response to correcting hypoxaemia is independent of the response to β-adrenoceptor agonists. Further studies are required to investigate the site and mechanism of the airway effects of hypoxaemia.
Enteric disease in Early Childhood Inhibits Microvillus Expression by Potential Stem Cells
Authors: Borg M. , Phillips A. D. , Smith M. W. , Brown D. 
Published: August 2015

1. Enterocyte development of microvillus structure has been measured in intestinal biopsies obtained from children suffering from coeliac disease, cow's milk protein intolerance and microvillus atrophy, and the results compared with similar measurements carried out in control children.
2. All types of enteric disease caused a significant 30% reduction in the length of microvilli present on undifferentiated basal crypt enterocytes, here referred to as potential stem cells.
3. Microvillus growth measured in control enterocytes took place mainly over the basal third of the villus. There was then little further change in structure during subsequent enterocyte migration to the villus tip.
4. Microvillus length in diseased tissue remained more or less constant during enterocyte migration to the crypt-villus junction. Microvillus length then decreased slightly during subsequent enterocyte migration over stunted villi.
5. The present results are discussed in relation to the supposed properties of potential stem cells. Comparisons are also made between profiles of microvillus development measured in healthy children and mature adults.