bluuebunny/crossref_metadata_2025_split huggingface dataset:
Contribution of soluble aluminium species to absorption of aluminium from the rat gut in situ
Authors: Partridge Neil A. , Regnier Fred E. , Reed Willie M. , White Joe L. , Hem Stanley L. 
Published: August 2015

1. Rat gut perfusion studies in vivo at pH 4, 6 or 8 using aluminium chloride or equimolar aluminium chloride and sodium citrate showed that elevated plasma aluminium concentrations were associated with aluminium solubility in the perfusion. Elevated plasma aluminium levels and soluble aluminium in the perfusate occurred with perfusion of equimolar aluminium chloride and sodium citrate at all three pH values.
2. Partitioning studies in vitro, utilizing water and ethyl acetate, revealed that uncomplexed aluminium exhibited maximum partitioning into the ethyl acetate phase at pH 2.5. When complexed with citrate, aluminium exhibited partitioning over a much broader pH range, pH 2.5–8.0.
3. A direct linear relationship was observed between the soluble aluminium concentration of the perfusate and the increase in the plasma aluminium level, suggesting that soluble aluminium is absorbed by a passive diffusion mechanism.
Plasma concentrations of immunoreactive-endothelin in patients with chronic renal failure treated with recombinant human erythropoietin
Authors: Takahashi Kazuhiro , Totsune Kazuhito , Imai Yutaka , Sone Masahiko , Nozuki Mitsuru , Murakami Osamu , Sekino Hiroshi , Mouri Toraichi 
Published: August 2015

1. Elevation of blood pressure is one of the major side effects of recombinant human erythropoietin therapy in haemodialysis patients.
2. We investigated the possible involvement of endothelin in the pathogenesis of this recombinant human erythropoietin-induced blood pressure elevation in 51 patients undergoing maintenance haemodialysis.
3. Blood haemoglobin level increased from 7.1 ± 0.1 to 8.8 ± 0.1g/dl (means ± SEM) after 8 weeks of treatment with recombinant human erythropoietin (3000–4500 units/week). An increase in mean blood pressure was found in 19 patients (37%) (n = 9, by 0–10 mmHg; n = 10, by &gt; 10 mmHg).
4. Plasma immunoreactive-endothelin concentration significantly increased from 2.26 ± 0.18 to 3.14 ± 0.31 pmol/l in the 10 patients whose mean blood pressure increased by more than 10 mmHg (P &lt; 0.05), but not in the other patients. Moreover, the increase in plasma immunoreactive-endothelin concentration showed a significant positive correlation with the change in mean blood pressure in 19 patients with elevated mean blood pressure (r = 0.47, P &lt; 0.05).
5. There was no significant correlation between the change in plasma immunoreactive-endothelin concentration and the change in blood haemoglobin level or the change in body weight.
6. These results suggest the possibility that endothelin may contribute to the recombinant human erythropoietin-related rise in blood pressure in some haemodialysis patients.
Possible link between vitamin D and hyperoxaluria in patients with renal stone disease
Authors: Giannini Sandro , Nobile Martino , Castrignano Rocco , Pati Tecla , Tasca Andrea , Villi Giorgio , Pellegrini Federico , D'Angelo Angela 
Published: August 2015

1. Vitamin D seems to play an essential role in the pathogenesis of idiopathic hypercalciuria at least in part via intestinal hyperabsorption of calcium. Hyper-absorption of calcium, in turn, might enhance the intestinal uptake of free oxalate, thus leading to hyperoxaluria. To verify this hypothesis we studied 75 calcium-stone-formers subdivided as follows: group 1 (15 patients) with isolated hyperoxaluria; group 2 (25 patients) with hyperoxaluria and hypercalciuria; group 3 (22 patients) with isolated hypercalciuria; group 4 (12 patients) with no metabolic abnormalities.
2. As expected, urinary calcium excretion differed in the various groups (P &lt; 0.001), being highest in groups 2 and 3; urinary oxalate excretion, by definition highest in groups 1 and 2, was even more pronounced in group 2 than in group 1 (P &lt; 0.05). Although in the normal range, the serum 1,25-dihydroxyvitamin D concentration was higher (P &lt; 0.001) in the two hypercalciuric groups (2 and 3), showing peak levels in group 2.
3. When the data from the 75 stone-formers were pooled, there was a positive correlation between the serum concentration of 1,25-dihydroxyvitamin D and urinary calcium excretion (P &lt; 0.001) and urinary oxalate excretion (P &lt; 0.003), the latter relationship also being present when only the two hypercalciuric groups (groups 2 and 3) were considered together (P &lt; 0.05).
4. Our data seem to confirm a relevant role for the vitamin D system in the pathogenesis of calcium nephrolithiasis due to increased intestinal calcium absorption, but also because this in turn induces a greater intestinal absorption of oxalate, thus leading to the occurrence or exacerbation of hyperoxaluria.
Assessment of the mathematical issues involved in measuring the fractional synthesis rate of protein using the flooding dose technique
Authors: Chinkes David L. , Rosenblatt Judah , Wolfe Robert R. 
Published: August 2015

1. The fractional synthesis rate of protein is commonly measured by either the constant infusion method or the flooding dose method. The two methods often give different results.
2. An underlying assumption of the traditional flooding dose formula is that the protein synthesis rate is not stimulated by the flooding dose. A new formula for calculation of the fractional synthesis rate is derived with the alternative assumption that the protein synthesis rate is stimulated by an amount proportional to the change in the intracellular concentration of the infused amino acid. The alternative formula is:
where EB and EF are the enrichments of bound and free amino acid, respectively (atom per cent excess), and C=1-(EF/EI), where EI is the enrichment of the infusate. This approach defines the lowest possible value for the fractional synthesis rate. The traditional equation gives a maximal value for the fractional synthesis rate.
3. When data from the literature are considered, the fractional synthesis rate of muscle protein as calculated by the constant infusion technique falls between the values of fractional synthesis rate calculated by the two flooding dose formulae when leucine is the tracer, suggesting that a flooding dose of leucine exerts a stimulatory effect on the rate of protein synthesis, but that the increase is not as great as the increase in the intracellular concentration of leucine.
4. The precision of the formula for the calculation of fractional synthesis rate is limited by the accuracy of the underlying assumptions regarding the effect of the flooding dose on the fractional synthesis rate. At present, the best approach would appear to be the use of both equations to calculate the upper and lower bounds of the true fractional synthesis rate.
Elevated total body noradrenaline spillover in normotensive members of hypertensive families
Authors: Ferrier Claudia , Cox Helen , Esler Murray 
Published: August 2015

1. In prehypertension, abnormalities in cardiovascular control mechanisms have been described. It has been postulated that this may involve hereditary disturbances in the sympathetic regulation of blood pressure. Since the neurochemical methods used to test sympathetic nervous system activity have been rather imprecise, in the present study we have applied noradrenaline plasma kinetic methodology to evaluate sympathetic activity in normotensive subjects with a familial predisposition to essential hypertension.
2. Total body noradrenaline spillover to plasma, an index of integrated sympathetic nerve firing rates, was calculated during infusion of l-[7-3H] noradrenaline in 11 normotensive offspring of essential hypertensive parents and 11 age-, height- and weight-matched normotensive offspring of normotensive parents.
3. The resting arterial plasma noradrenaline concentration was higher in healthy subjects with a family history of essential hypertension (1.41 ± 0.15 nmol/l, mean ± SEM, P &lt; 0.002) than in normotensive subjects with no family history of essential hypertension (0.82 ± 0.07 nmol/l). The overall rate of spillover of noradrenaline to plasma was also elevated in the normotensive offspring of hypertensive parents (4.34 ± 0.54 nmol/min) compared with subjects with a negative family history of essential hypertension (2.02 ± 0.20 nmol/min). Similarly, the arterial plasma concentration of the noradrenaline precursor 3,4-dihydroxyphenylalanine was higher in subjects with a positive family history of essential hypertension (7.55 ± 0.24 nmol/l) than in normotensive control subjects (5.97 ± 0.30 nmol/l, P &lt; 0.001). Despite this apparent evidence of relative sympathetic nervous activation in the subjects with a positive family history of hypertension, their blood pressure and heart rate were only marginally, and non-significantly, higher.
4. Biochemical indices of sympathetic function in normotensive offspring of hypertensive parents suggest a familial disturbance in sympathetic nervous system activity, which may be a predictor for the development of hypertension in adult life.
Free-radical scavengers, thiol-containing reagents and endothelium-dependent relaxation in isolated rat and human resistance arteries
Authors: Sunman W. , Hughes A.D. , Sever P.S. 
Published: August 2015

1. Small arteries were isolated from either rat mesentery or human subcutaneous fat, and mounted in a myograph for the measurement of isometric force.
2. Superoxide dismutase, either in the presence or absence of catalase, relaxed noradrenaline-induced tone. This effect was abolished by removal of the endothelium or incubation with an inhibitor of NO synthase, N-ω-nitro-L-arginine methyl ester. Catalase alone had a negligible effect on noradrenaline-induced tone.
3. Captopril, an angiotensin-converting enzyme inhibitor and putative free-radical scavenger, did not relax pre-contracted isolated vessels. N-Acetylcysteine caused an endothelium-independent relaxation of rat vessels. Similar effects were observed in human vessels.
4. Acetylcholine induced a concentration-dependent relaxation of isolated resistance arteries, which was inhibited by removal of the endothelium or N-ω-nitro-L-arginine methyl ester, but unaffected by indomethacin. Preincubation with captopril, N-acetylcysteine or catalase alone did not alter the acetylcholine concentration-response relationship, but superoxide dismutase in combination with catalase enhanced responses to acetylcholine, causing a six-fold increase in potency.
5. Superoxide dismutase causes endothelium-dependent relaxation of resistance arteries and potentiates responses to acetylcholine. This action is probably due to the ability of the enzyme to scavenge superoxide anions which inhibit endothelium-dependent relaxation.
6. N-Acetylcysteine causes an endothelium-independent relaxation of resistance arteries which is probably unrelated to the putative ability of this compound to scavenge superoxide radicals and may reflect a direct action on vascular smooth muscle.
Assessment of Glomerular Charge Selectivity in Man by Differential Clearance of Isoamylases
Authors: Fox J. G. , Quin J. D. , O'reilly D. Stj. , Boulton-Jones J. M. 
Published: August 2015

1. Glomerular charge selectivity was assessed using the ratio of the clearance of pancreatic isoamylase to the clearance of the more anionic salivary isoamylase (CPAm/CSAm) in 30 normal subjects, 14 patients with minimal proteinuria and 23 patients with heavy proteinuria due to primary glomerulopathies. Seven patients with minimal change nephropathy were studied in relapse and remission.
2. CPAm/CSAm exceeded 2.0 (range 2.1-6.1) in all normal subjects, indicating that the normal glomerular capillary wall possesses charge selectivity at the molecular size of amylase (molecular mass 56 kDa). 3. CPAm/CSAm was significantly lower in patients with heavy proteinuria than in normal subjects or patients with minimal proteinuria. CPAm/CSAm was low in patients with minimal change nephropathy in relapse and rose into the normal range with steroid-induced remission.
4. These data suggest that heavy proteinuria in primary glomerulopathies is accompanied by loss of glomerular charge selectivity. Remission of minimal change nephropathy is associated with restoration of normal charge selectivity.
Intravenous Infusion of Tridihomo-γ-Linolenoyl-Glycerol Reduces Leukotriene B4 Production in the Rat and Rabbit
Authors: Nakamura Norio , Hamazaki Tomohito , Taki Hirofumi , Yamazaki Katsuya , Kobayashi Masashi 
Published: August 2015

1. We have formulated an infusible emulsion of 10% tridihomo-γ-linolenoyl-glycerol (94% pure) and investigated the effects of its infusion on leukotriene B4 production.
2. We infused the emulsion into the ear veins of two rabbits in a dose of 0.8 g of tridihomo-γ-linolenoyl-glycerol/kg. Polymorphonuclear leucocytes were obtained from rabbits before the infusion, and 6, 24, 72 and 168 h after. The ionophore-stimulated leukotriene B4 production by polymorphonuclear leucocytes was reduced to about 50% of baseline as early as 6 h after the infusion and remained reduced until 24 h after the infusion.
3. To closely investigate the changes in leukotriene B4 production at 6 h after the infusion, we infused 1.0 g of tridihomo-γ-linolenoyl-glycerol/kg into the tail veins of eight male Wistar rats. Six hours later, peritoneal macrophages were obtained from four rats for the analysis of ionophore-stimulated leukotriene B4 production. Peritoneal cells and blood samples were also obtained from the remaining rats for fatty acid analysis. Another eight rats were used without prior infusion for baseline determination.
4. The production of leukotriene B4 by macrophages was significantly reduced to 42% of baseline, and the plasma free dihomo-γ-linolenic acid was markedly increased from 0.26 to 4.82 mol%, in 6 h.
5. We conclude that the infusion of a tridihomo-γ-linolenoyl-glycerol emulsion is able to decrease leukotriene B4 production and to increase the dihomo-γ-linolenic acid concentrations in the plasma and peritoneal cells of rats in 6 h.
What is the Blood Flow to Resting Human Muscle?
Authors: Elia M. , Kurpad A. 
Published: August 2015

1. An investigation was carried out in five healthy lean adults to assess whether forearm and calf plethysmography largely reflect muscle blood flow as measured by 133Xe and whether there is substantial variability in the blood flow to muscles located at different sites in the body.
2. Blood flow to forearm and calf flexors and extensors, biceps, triceps and quadriceps was assessed using the 133Xe clearance technique. Blood flow to forearm skin and subcutaneous adipose tissue was also measured using the 133Xe clearance technique, whereas blood flow to the forearm and calf was measured using strain gauge plethysmography.
3. The mean blood flow to different muscles ranged from 1.4 ± 0.6 (gastrocnemius) to 1.8 ± 0.7 (forearm extensor) ml min−1 100 g−1 muscle (1.4 ± 0.6 and 1.9 ± 0.8 ml min−1 100 ml−1 muscle, respectively) but there were no significant differences between them. Forearm and calf blood flows (2.7 ± 0.3 and 3.0 ± 0.7 ml min−1 100 ml−1 limb tissue, respectively) were about 50% to more than 100% greater (P &lt;0.025) than blood flow to the muscles within them (1.7 ± 0.5 and 1.4 ± 0.5ml min−1 100g−1 muscle, respectively, or 1.8 ± 0.6 and 1.5 ± 0.5 ml min−1 100 ml−1 muscle, respectively). In contrast, the blood flows to 100 g of forearm skin (9.1 ± 2.6 ml min−1 100 g−1) and adipose tissue (3.8 ± 1.1 ml min−1 100 g−1) were higher than the blood flow to 100 g of forearm (P &lt;0.01 and not significant, respectively).
4. Although several possibilities can explain the discrepancy between muscle blood flow measured by 133Xe and blood flow to the distal limbs measured by plethysmography, the results suggest that non-muscular blood flow, especially that to skin, is substantially greater than muscular blood flow. Indeed, the overall blood flow to the forearm could be accounted for by summation of blood flows to individual constituent tissues, which were assumed to be present in proportions typical of lean subjects. The results have important implications in the use of arteriovenous catheterization studies for assessing flux of oxygen, carbon dioxide and metabolites across muscle.
Relationship between Serum Butyrylcholinesterase Activity, Hypertriglyceridaemia and Insulin Sensitivity in Diabetes Mellitus
Authors: Abbott C. A. , MacKness M. I. , Kumar S. , Olukoga A. O. , Gordon C. , Arrol S. , Bhatnagar D. , Boulton A. J. M. , Durrington P. N. 
Published: August 2015

1. The activity of serum butyrylcholinesterase (‘pseudocholinesterase’, EC3.1.1.8) was investigated in 56 patients with type 1 diabetes mellitus, 51 patients with type 2 diabetes mellitus and 101 healthy control subjects.
2. Butyrylcholinesterase activity was significantly elevated in both type 1 (8.10 ± 3.35 units/ml) and type 2 (7.22 ± 1.95 units/ml) diabetes compared with the control subjects (4.23 ± 1.89 units/ml) (P &lt;0.001).
3. In the patients with type 1 and type 2 diabetes, serum butyrylcholinesterase activity was correlated with log serum fasting triacylglycerol concentration (r = 0.41 and r = 0.43, respectively, P &lt;0.001). In the type 2 population serum butyrylcholinesterase activity was also correlated with insulin sensitivity (r = −0.51, P &lt;0.001).
4. Serum butyrylcholinesterase activity was unrelated to age, gender, serum γ-glutamyltranspeptidase activity, body mass index, or treatment for diabetes in both the diabetic populations.
5. In 37 non-diabetic patients with butyrylcholinesterase deficiency serum triacylglycerol levels were in the normal range.
6. These results are consistent with the view that butyrylcholinesterase may have a role in the altered lipoprotein metabolism in hypertriglyceridaemia associated with insulin insensitivity or insulin deficiency in diabetes mellitus.
Hyperproinsulinaemia in Impaired Glucose Tolerance
Authors: Krentz Andrew J. , Clark Penelope M. , Cox Lorna , Nattrass Malcolm 
Published: August 2015

1. Basal circulating concentrations of islet B cell products were measured using two-site monoclonal antibody-based immunoradiometric assays after a 10 h overnight fast in a group of non-obese subjects with recently diagnosed impaired glucose tolerance (World Health Organization criteria). A group of healthy subjects with normal oral glucose tolerance matched for age and body mass index served as normal controls.
2. Fasting blood glucose concentration was normal in all subjects with mean (±SEM) levels of 5.1 ± 0.2 and 4.8 ± 0.2 mmol/l (P &gt;0.1) for the group with impaired glucose tolerance and the healthy control group, respectively.
3. There was no significant difference (P &gt;0.1) in fasting plasma insulin or C-peptide concentrations between the groups.
4. By contrast, the fasting concentration of intact proinsulin was nearly four-fold higher in the subjects with impaired glucose tolerance than in the matched healthy control subjects (4.5 ± 1.0 versus 1.2 ± 0.2 pmol/l, P &lt;0.005).
5. Similarly, the fasting plasma concentration of 32–33 split proinsulin in the subjects with impaired glucose tolerance was almost twice that of the control subjects (7.4 ± 1.3 versus 3.9 ± 0.8 pmol/l, P &lt;0.02).
6. In conclusion, fasting concentrations of proinsulin-like molecules are elevated in non-obese subjects with newly diagnosed impaired glucose tolerance. This observation is consistent with defective islet B cell proinsulin processing in this syndrome.
A Novel Computer-Driven, Servo-Controlled Fluid Replacement Technique and Its Application to Renal Function Studies in Conscious Rats
Authors: Burgess W. J. , Shalmi M. , Petersen J. S. , Plange-Rhule J. , Balment R. J. , Atherton J. C. 
Published: August 2015

1. A new rat model has been developed allowing body fluid status to be accurately controlled and maintained throughout experimentation by computer-driven, servo-controlled replacement of spontaneous urinary fluid losses.
2. Experiments in vitro were performed to test the accuracy of the servo system, and experiments in vivo were carried out to re-assess basic renal function in servo-controlled vasopressin-replete Long Evans and vasopressin-deficient Brattleboro rats. The model was further evaluated in water-diuretic Wistar rats with or without administration of a vasopressin V2-receptor agonist, 1-desamino-8-d-arginine vasopressin.
3. The data gained from the present study indicate the suitability of the servo-controlled replacement system for conscious renal function studies in three different rat strains. Haemodynamic and renal function variables measured were demonstrated to be stable throughout a 5 h experimental procedure and reproducible between repeated experimental occasions over a 14 day post-operative period.
4. Using the servo-control technique, the expected action of 1-desamino-8-d-arginine vasopressin on renal water handling was demonstrated, but the natriuretic effect reported by some workers was not evident.
5. Since the servo-controlled fluid replacement technique maintains many of the inherent differences between vasopressin-replete Long Evans and vasopressin-deficient Brattleboro rats and eliminates the changes in body fluid volume during transition from a diuretic to an antidiuretic state, the model confers an advantage over previously employed constant infusion protocols.
Circulating Angiotensin II and Renal Sodium Handling in Man: A Dose-Response Study
Authors: Rahman A. R. A. , Motwani J. G. , Lang C. C. , Struthers A. D. 
Published: August 2015

1. Animal studies have shown that angiotensin II has a biphasic effect on urinary sodium excretion. To examine whether this is also true in man, we studied seven salt-replete male subjects in a single-blind placebo-controlled manner.
2. While undergoing maximum diuresis, subjects were infused with 0, 1, 2, 5 or 10 ng of angiotensin II min−1 kg−1 over 80 min. Subjects were studied while seated, and stood every 20 min for urine collection.
3. Angiotensin II produced a dose-dependent antidiuretic effect. The urine flow rate, in ml/min expressed as the change from baseline with increasing dose of angiotensin, was: + 3.4 ±1.77, −1.26 ±0.49 (P &lt;0.05), −2.75±1.23 (P &lt;0.05), −4.21 ± 0.82 (P &lt;0.05) and −6.51 ±1.07 (P &lt;0.01).
4. In contrast, the effect of angiotensin II on sodium excretion showed a flat dose-response curve beyond 5 ng min−1 kg−1. The urinary sodium excretion, in μmol/min expressed as the change from baseline with increasing dose of angiotensin, was: 9.5 ±21.2, −18.9± 29.6, −37.0±11.6 (P &lt;0.05), −67.7 ± 19.6 (P &lt;0.01) and −63.8±14.3 (P &lt;0.01).
5. The fractional distal reabsorption of sodium, determined by using the lithium clearance technique, showed a rise with all doses of angiotensin II used and reached statistical significance with the top two doses.
6. Unlike antidiuresis, antinatriuresis after graded doses of angiotensin II in human subjects showed a flat dose-response curve beyond 5 ng min−1 kg−1. Pressor doses of angiotensin II also have a significant effect on the distal tubule in promoting sodium reabsorption.