bluuebunny/crossref_metadata_2025_split huggingface dataset:
Uptake of a Series of Neutral Dipeptides Including l-Alanyl-l-Alanine, Glycylglycine and Glycylsarcosine by Hamster Jejunum in Vitro
Authors: Matthews D. M. , Burston D. 
Published: August 2015

1. This paper is the last of a set reporting an investigation of the kinetics of jejunal uptake and inhibitory ability of a series of neutral dipeptides, glycylglycine, l-ananyl-l-alanine, l-valyl-l-valine and l-leucyl-l-leucine, with progressively longer and more lipophilic side chains.
2. The results suggested that at pH 5, uptake of l-alanyl-l-alanine, like that of l-valyl-l-valine and l-leucyl-l-leucine, was the result of two processes, uptake of intact peptide and uptake of free amino acid released extracellularly. On the other hand, uptake of glycylglycine was entirely in the form of intact peptide. In contrast to uptake of l-valyl-l-valine and l-leucyl-l-leucine, the proportion of intact l-alanyl-l-alanine taken up by mediated transport was greatest at the lowest concentration studied and smallest at the highest concentration.
3. Taking the series of results as a whole, whereas the corresponding series of amino acids, glycine, l-alanine, l-valine and l-leucine, showed a progressive increase in apparent affinity for uptake and a decrease in Vmax., we could find no such regular progression with the peptides.
4. The results of work on inhibition of uptake of one dipeptide by another were unexpectedly complex. Examples were the very powerful inhibitory effect of l-valyl-l-valine on uptake of glycylsarcosine, not suggested by the Kt of the former peptide, and the failure of glycylsarcosine to cause complete inhibition of uptake of l-alanyl-l-alanine and l-leucyl-l-leucine, though it could completely inhibit uptake of l-valyl-l-valine. There may be more than one uptake system for intact peptides, but we cannot yet suggest an explanation for all the results on inhibitions of uptake.
Thyroid Status in Patients after Acute Myocardial Infarction
Authors: Franklyn J. A. , Gammage M. D. , Ramsden D. B. , Sheppard M. C. 
Published: August 2015

1. Subjects followed serially after acute myocardial infarction demonstrated a rapid and sustained fall in serum total tri-iodothyronine (T3) concentration and a rise in reverse tri-iodothyronine (rT3) concentration. There was a transient fall in total thyroxine (T4) concentration.
2. Thyroxine binding globulin (TBG) levels were unchanged after acute myocardial infarction but prolonged falls were observed in thyroxine binding prealbumin (TBPA) and albumin concentrations.
3. In contrast to the fall in total T4, both measured and calculated free T4 concentrations were unchanged but measured and calculated free T3 concentrations fell as did total T3.
4. Despite the observed fall in T3, basal thyrotrophin (TSH) concentrations did not rise.
5. The reduction in circulating T3 levels after acute myocardial infarction suggests that a hypothyroid state exists. Until tissue thyroid status can be assessed directly, however, this conclusion must remain in doubt.
Comparison of Atrial Pacing and the Cold Pressor Test in Patients with Angina Pectoris
Authors: Emanuelsson H. , Caidahl K. , Hjalmarson Å. , Holmberg S. , Svensson S.-E. , Waagstein F. , Waldenström A. 
Published: August 2015

1. A haemodynamic and myocardial metabolic study was performed to compare effects of maximal atrial pacing and the cold pressor test (CPT) in patients with angina pectoris. Twelve patients (group I) had angiographically severe coronary artery disease, while 16 patients (group II) had normal coronary angiograms.
2. At maximal pacing, angina developed in all patients in group I, and myocardial lactate production was found in eight of 12 patients. In group II, 12 out of 16 patients experienced chest pain, but only two patients had myocardial lactate production. Neither angina nor myocardial lactate production was present in any patient in either group during CPT.
3. Coronary sinus flow increased and coronary vascular resistance decreased significantly in both groups at maximal pacing (P&lt;0.001). At CPT, coronary flow decreased (P&lt;0.05) and coronary resistance increased (P&lt;0.001) in group I, while individual response was more variable in group II.
4. In conclusion, maximal pacing was a more effective method of provocation of angina pectoris than CPT. The reactions of coronary sinus flow and coronary vascular resistance were different in group I than in group II. However, because of the variability of response in patients with normal coronary arteries, CPT cannot be used to distinguish patients with coronary artery disease from patients with no such disease.
Prostacyclin and Thromboxane in Non-Insulin Dependent Diabetes: The Chlorpropamide Alcohol Flush Reaction Revisited
Authors: Johnston Colin , Carey Frank , Forder Robert A. , Haworth Duncan 
Published: August 2015

1. Levels of immunoreactive 6-oxo-prostaglandin F1α (6-oxo-PGF1α) and thromboxane B2 (TXB2) were measured in peripheral venous plasma in a group of volunteers and non-insulin dependent diabetic patients (NIDDS). Levels of these eicosanoids were close to the limit of sensitivity of the radioimmunoassays and consequently data are reported as maximal values. Basal plasma levels of 6-oxo-PGF1α did not exceed 5 pg/ml in either group and maximal levels of immunoreactive TXB2 were 125 ± 14 and 128 ± 8 pg/ml for volunteers and NIDDS respectively.
2. Attempts to elicit peripheral vascular prostacyclin biosynthesis in volunteers by using forearm ischaemia produced no increase in plasma 6-oxo-PGF1α levels. Measurement of the combined plasma levels of 6-oxo-PGF1α, 13,14-dihydro-6-oxo-PGF1α, 13,14-dihydro-6,15-dioxo-PGF1α and 6-oxo-PGE1 indicated that these were also low (less than 5 pg/ml) and that failure to demonstrate increased 6-oxo-PGF1α levels was unlikely to have arisen from metabolism of prostacyclin to one or more of these metabolites.
3. Measurement of 6-oxo-PGF1α and TXB2 in peripheral venous plasma before and during chloropropamide alcohol flushing (CPAF) did not provide evidence for a role for these eicosanoids in the etiology of this phenomenon.
4. These findings point to the need for a reappraisal of studies that have described altered plasma levels of 6-oxo-PGF1α and TXB2 in CPAF and other pathophysiological conditions in man.
Dexamethasone Inhibits the Production of Thromboxane B2 and Leukotriene B4 by Human Alveolar and Peritoneal Macrophages in Culture
Authors: Fuller Richard W. , Kelsey Christopher R. , Cole Peter J. , Dollery Colin T. , MacDermot John 
Published: August 2015

1. Cultured human alveolar and peritoneal macrophages have been shown to release thromboxane B2 and leukotriene B4.
2. The release was facilitated by stimulation of the macrophages with opsonized zymosan A (1.2 mg/ml).
3. The release was inhibited in a concentration-dependent manner by incubation of the cells with dexamethasone (1 nmol/l to 1 μmol/l).
Gas Transfer for Carbon Monoxide in Polycythaemia Secondary to Hypoxic Lung Disease
Authors: Wedzicha J. A. , Cotter F. E. , Wallis P. J. W. , Newland A. C. , Empey D. W. 
Published: August 2015

1. The transfer factor for carbon monoxide and its subdivisions, the membrane diffusing capacity (Dm) and the pulmonary capillary blood volume (Vc), were measured in 16 patients with polycythaemia secondary to chronic hypoxic lung disease and in ten hypoxic non-polycythaemic control subjects.
2. The mean pulmonary capillary blood volume was significantly lower in the polycythaemic patients (31.6 ml, sd 11.2) compared with the control group (65.2 ml, sd 22.5) (P&lt;0.001).
3. Erythrapheresis, as a method of isovolaemic haemodilution, was performed in 15 of the polycythaemic patients. The mean packed cell volume fell from 58 (sd 5)% to 47 (sd 5)% after treatment, with significant reductions in blood viscosity at both high and lower shear rates (P&lt;0.001).
4. The mean pulmonary capillary blood volume increased from 32.3 ml (sd 11.3) before treatment to 48.7 ml (sd 18.7) after erythrapheresis (P&lt;0.01), with no significant change in membrane diffusing capacity.
5. The rise in pulmonary capillary blood volume is another potential physiological advantage of the reduction of packed cell volume in patients with polycythaemia secondary to hypoxic lung disease.
Enhancement of the Urinary Excretion of Non-Sulphated and Sulphated Radioactive Bile Acids by Sodium Acetate in the Bile Duct Obstructed Rat
Authors: Chitranukroh A. , Taggart G. , Billing B. H. 
Published: August 2015

1. The renal clearances of [14C]glycocholate, [14C]taurocholate and [3H]glycochenodeoxycholate-3-sulphate were determined in bile duct obstructed rats.
2. Comparisons of the bile acid clearances with glomerular filtration rates (GFR) indicate that most of the filtered bile acids are reabsorbed.
3. Inhibition studies with p-aminohippurate (PAH) and probenecid suggest that a proportion of the bile acids in urine is secreted.
4. Attempts were made to increase the renal clearance of the bile acids by the administration of pharmacological agents.
5. An infusion of sodium acetate (0.3 mol/l) increased the clearance of the radioactive bile acids and augmented the urinary excretion of endogenous 3α-hydroxy bile acids and reduced their concentration in plasma.
Plasma Catecholamine Responses to Change of Posture in Alcoholics during Withdrawal and after Continued Abstinence from Alcohol
Authors: Eisenhofer G. , Whiteside E. A. , Johnson R. H. 
Published: August 2015

1. Plasma catecholamine, blood pressure and heart rate responses to standing were measured in ten alcoholics during withdrawal, ten alcoholics after 2–7 weeks of abstinence from alcohol, six abstinent alcoholics with orthostatic hypotension and ten normal control subjects.
2. Withdrawing alcoholics had supine and standing heart rates and plasma noradrenaline and adrenaline concentrations that were higher than in abstinent alcoholics or control subjects. Supine blood pressures were also higher in withdrawing alcoholics than in abstinent alcoholics or control subjects, but on standing blood pressures in withdrawing alcoholics fell, four patients having a fall of more than 30/5 mmHg.
3. Abstinent alcoholics without orthostatic hypotension had higher basal and standing concentrations of noradrenaline than control subjects but normal heart rates and adrenaline concentrations.
4. Abstinent alcoholics with orthostatic hypotension showed a wide range of basal plasma noradrenaline concentrations and were found to have variable plasma noradrenaline responses to standing, three subjects having normal responses and three subjects having no or little increase in plasma noradrenaline on standing.
5. It is concluded that alcohol withdrawal is associated with increased sympathetic nervous activity, as reflected by raised supine and standing plasma concentrations of catecholamines, and that even after 2–7 weeks of abstinence from alcohol plasma noradrenaline concentrations may be higher than in control subjects. Despite increased sympathetic nervous responses to standing, alcoholics during withdrawal have impaired blood pressure control and some may exhibit orthostatic hypotension. Orthostatic hypotension may also be observed in alcoholics during continuing abstinence from alcohol; in some of these patients failure of reflex noradrenaline release in response to standing may contribute to orthostatic hypotension.
Selective Inhibition of Renal Thromboxane Biosynthesis Increased Sodium Excretion Rate in Normal and Saline-Loaded Rats
Authors: Papanicolaou N. , Gkika E.-L. , Gkikas G. , Bariety J. 
Published: August 2015

1. The excretion rates of renal thromboxane B2 (TXB2) and 6-ketoPGF1α, the stable chemical metabolites of thromboxane A2(TXA2) and prostaglandin I2 (PGI2) respectively, PGE2 and sodium were determined in normal and saline-loaded rats treated with the thromboxane synthetase inhibitor imidazole.
2. In normal rats the administration of imidazole in doses which did not affect renal 6-keto-PGF1α and PGE2 excretion but selectively inhibited renal TXB2 excretion, significantly increased the sodium excretion rate.
3. Volume expansion with saline increased renal PGE2 and 6-ketoPGF1α excretion but did not alter renal TXB2 excretion. The increase in renal prostaglandin excretion was accompanied by an increased sodium excretion rate.
4. The administration of imidazole to saline-loaded animals also decreased renal TXB2 excretion but did not alter the increased excretion of renal PGE2 and 6-ketoPGF1α. This reduction in renal thromboxane biosynthesis by imidazole further increased the sodium excretion rate.
5. We suggest that TXA2 is a potent anti-natriuretic factor as well as the most potent vasoconstrictor agent known.
Effect of Bicarbonate Feeding on Intestinal Absorption of Calcium and Vitamin D Metabolism in Rats
Authors: Gafter U. , Edelstein S. , Levi J. 
Published: August 2015

1. The effect of bicarbonate (NaHCO3) feeding on intestinal absorption of calcium and phosphorus and vitamin D metabolism was investigated. Gut sac uptake of 45Ca and [32P]phosphate in vitro, as well as the plasma level of vitamin D metabolites, was determined in rats fed with NaHCO3 for 9 days and their pair-fed controls.
2. Duodenal uptake of 45Ca and [32P]phosphate by alkalotic rats was less than duodenal uptake by controls. 1,25(OH)2D plasma level was much higher in alkalotic rats than in their controls, and 25(OH)D slightly higher than in controls.
3. These data suggest that NaHCO3 feeding causes a substantial increase in 1,25(OH)2D plasma level, but interferes with calcium and phosphorus absorption in the duodenum.
Liver-Specific Autoantibodies in Chronic Hepatitis B Virus Infection
Authors: Meliconi R. , Facchini A. , Miglio F. , Trevisan A. , Alberti A. , Realdi G. , Baraldini M. , Gasbarrini G. 
Published: August 2015

1. Anti-liver-specific protein (LSP) antibody and liver membrane autoantibody (LMA) have been evaluated in 88 patients with hepatitis B virus (HBV)-induced chronic liver disease by means of radioimmunoprecipitation and immunofluorescence. Among our patients, 38 presented circulating HBe antigen while 43 had HBe antibody and seven were negative for both.
2. Anti-LSP was mainly found in HBeAg positive chronic active hepatitis (CAH), anti-HBe in positive CAH and in anti-HBe positive chronic persistent hepatitis (CPH).
3. Similar prevalences of LMA (range 13-33%) were detected in the various groups studied.
4. Taking into account the histological diagnosis of disease activity (periportal inflammation and piecemeal necrosis) no significant differences were found between active and inactive patients.
5. Taking into account the HBeAg/anti-HBe status, no significant differences were found between the patients positive for ‘e’ antigen or ‘e’ antibody.
6. Humoral autoimmune reactions may also play a role in HBV-induced chronic (active) liver disease irrespective of HBeAg/anti-HBe status and hence of the viral replication activity of the patients.
Vitamin D Metabolism in Patients Intoxicated with Ergocalciferol
Authors: Mawer E. Barbara , Hann J. T. , Berry Jacqueline L. , Davies M. 
Published: August 2015

1. Vitamin D metabolites were measured on admission in eight patients intoxicated with ergocalciferol (serum calcium 3.01-4.05 mmol/l) and also during the subsequent 2 months in six of the eight.
2. Serum concentrations of 25-hydroxyergocalciferol, on admission, were grossly elevated in all patients (range 583-1843 nmol/l).
3. Serum calcium concentration was related significantly only to the concentration of 25-hydroxyergocalciferol (P = 0.003).
4. Concentrations of 25-hydroxyergocalciferol in serum were significantly related to those of calciferol (P = 0.004).
5. Elevated initial concentrations of 1,25-dihydroxycalciferol, mainly as 1,25-dihydroxyergocalciferol, were found in seven of the eight patients (range 179-313 pmol/l).
6. It is suggested that the hypercalcaemia in these patients may be explained by the action of 25-hydroxyergocalciferol at high concentration in competing for 1,25-dihydroxycalciferol receptors, thus exerting a biological effect per se, and also by increasing the synthesis of 1,25-dihydroxycalciferol through a mass-action effect on the renal 1α-hydroxylase.
Abnormal Regulation of Venous Alanine after Glucose Ingestion in Myotonic Dystrophy
Authors: Moxley Richard T. , Kingston William , Griggs Robert C. 
Published: August 2015

1. The concentration of amino acids in whole blood was measured before and during standard 5 h oral glucose tolerance testing in six male patients with myotonic dystrophy and five normal males. The plasma levels of insulin and glucose were also determined.
2. From 90 to 240 min after glucose ingestion there was a striking decline in venous alanine concentration in the patients with myotonic dystrophy in contrast to a slight rise in alanine in the normal group.
3. The patients displayed normal glucose tolerance, and there was a sustained fall in the venous concentration of the insulin-sensitive amino acids comparable with that seen in the normal controls. However, the patients showed a threefold increase of plasma insulin after glucose.
4. These data indicate an abnormal regulation of alanine in myotonic dystrophy which may be the result of an alteration in muscle synthesis of this amino acid. This defect in alanine synthesis may be due to a decreased availability of intracellular pyruvate caused by the insulin resistance that exists in these patients.
The Contribution of Endogenous urea to Faecal Ammonia in man, Determined by 15N Labelling of Plasma Urea
Authors: Wrong O. M. , Vince A. J. , Waterlow J. C. 
Published: August 2015

1. To establish the role of endogenous urea as a source of faecal ammonia, the plasma urea of two healthy men was labelled with 15N at a constant level for several days and its 15N enrichment was compared with that of faecal ammonia and total nitrogen.
2. Faeces collected after one complete gastrointestinal transit from the onset of plasma labelling had ammonia 15N enrichments which were only 8.5 ± 1.2% and total nitrogen enrichments which were 6.8 ± 0.7% of the plasma urea 15N enrichment.
3. These results show that endogenous urea is not the main precursor of faecal ammonia, which is probably derived by bacterial deamination from the protein of dietary residues, intestinal secretions and shed epithelial cells. The minor contribution of endogenous urea to faecal ammonia suggests that the lumen of the large bowel is not the main site of endogenous urea hydrolysis. The similar labelling of faecal total nitrogen and ammonia nitrogen supports other evidence that these faecal nitrogen fractions are in a constant state of exchange.
Amyloid ‘degrading factor activity': a non-specific calcium-mediated effect
Authors: Scott D. L. , Bracken P. , Bacon P. A. , Husby G. 
Published: August 2015

1. The clarification of turbid AA-amyloidfibril-containing agarose gels by serum has been ascribed to degradation of the fibrils and designated as ‘amyloid degrading factor'. In the present study, sera of 32 healthy blood donors and 32 patients with rheumatoid arthritis all showed ‘degrading factor activity’ against both AA amyloid fibrils and a non-fibrillar reticulin preparation of normal liver in an agarose plate assay. AL amyloid fibrils were not affected.
2. The ‘degrading activity’ of serum was correlated with the serum albumin concentration, and the effect was also given by purified human and bovine serum albumin, although it was not seen with other serum proteins.
3. The ‘degrading activity’ of serum against AA amyloid and reticulin was significantly correlated: both substrates showed low levels in a chronic disease such as rheumatoid arthritis, and reticulin inhibited ‘degrading activity’ against AA amyloid and vice versa. These results suggest the same process involves both substrates.
4. ‘Degrading activity’ was also given by EDTA and a specific calcium chelator, and was inhibited by calcium and magnesium.
5. An enzyme inhibitor showed only partial inhibition of the ‘degrading activity’ of serum, purified albumin, and EDTA.
6. These results suggest that serum ‘degrading factor activity’ is a non-specific calcium-mediated effect against AA amyloid and reticulin preparations dispersed in agarose. It may represent a change in the degree of aggregation of these proteins rather than being an effect of proteolytic degradation. This confirms the conclusions of other workers that amyloid ‘degrading factor activity’ is an phenomenon in vitro of doubtful pathophysiological significance.
Total body potassium and water, and exchangeable sodium, in muscular dystrophy
Authors: Edmonds C. J. , Smith T. , Griffiths R. D. , Mackenzie J. , Edwards R. H. T. 
Published: August 2015

1. Total body potassium (40K method) and total body water and exchangeable sodium (both by isotope dilution) were determined in 26 boys, aged 5-17 years, with muscular dystrophy. Total body potassium values were compared with measurements in a large series of normal boys on the basis of height.
2. Total body potassium was reduced even in the youngest patients and was only slightly higher in the older boys, despite their considerably greater height. Exchangeable sodium increased with increasing height in a way similar to that of normal boys. Total body water was also reduced but increased with growth, although to a lesser extent than expected for normal boys. The total body water measurements indicated that many of the affected boys were very obese, despite an apparently normal body weight.
3. An intravenous bolus of 22Na distributed at a similar rate in boys with muscular dystrophy to that in normal males.
4. In relation to the predicted values, total body potassium and 24 h urinary creatinine excretion of the affected boys both declined at a rate of 4% per year.
Interaction of renal prostaglandins with the renin-angiotensin and renal adrenergic nervous systems in healthy subjects during dietary changes in sodium intake
Authors: Kramer Herbert J. , Stinnesbeck Bruno , Klautke Georg , Kipnowski Jochen , Klingmueller Dietrich , Glaenzer Kilian , Duesing Rainer 
Published: August 2015

1. In six healthy subjects the role of renal prostaglandins (PG) in modulating the actions of the renin-angiotensin and renal adrenergic nervous systems on renal function was investigated.
2. During high dietary sodium intake (350 mmol/day) for 4 days no changes in urinary excretion of PGE2, PGF2α, noradrenaline or adrenaline were noted, whereas plasma renin activity (PRA) and urinary aldosterone excretion were suppressed.
3. After 4 days of low sodium intake (35 mmol/day) urinary excretion of PGE2, aldosterone and noradrenaline, as well as PRA, had significantly increased.
4. Inhibition of PG synthesis with indomethacin (2 mg/kg body weight) had no effects on renal function on day 5 of high sodium intake. Despite suppression of PRA and urinary aldosterone, indomethacin significantly reduced p-aminohippurate (PAH) clearance, glomerular filtration rate (GFR) and urinary sodium excretion on day 5 of low sodium intake, when urinary noradrenaline excretion remained high.
5. The results point to the crucial role of the renal adrenergic nervous system in controlling renal vascular resistance and sodium conservation in healthy subjects during low sodium intake, which is unmasked when renal PG synthesis is blocked by indomethacin. Enhanced renal PG synthesis during sodium restriction therefore not only attenuates the vascular and tubular effects of the renin-angiotensin system but, more importantly, also those of the highly stimulated renal adrenergic nervous system.