bluuebunny/crossref_metadata_2025_split huggingface dataset:
Atrial Natriuretic Peptide, Altitude and Acute Mountain Sickness
Authors: Milledge J. S. , Beeley J. M. , McArthur S. , Morice A. H. 
Published: August 2015

1. To investigate the mechanisms of acute mountain sickness, 22 subjects travelled to 3100 m by road and the following day walked to 4300 m on Mount Kenya. Control measurements were made over 2 days at 1300 m before ascent and for 2 days after arrival at 4300 m. These included body weight, 24 h urine volume, 24 h sodium and potassium excretion, blood haemoglobin, packed cell volume, and symptom score for acute mountain sickness. In 15 subjects blood samples were taken for assay of plasma aldosterone and atrial natriuretic peptide.
2. Altitude and the exercise in ascent resulted in a marked decrease in 24 h urine volume and sodium excretion. Aldosterone levels were elevated on the first day and atrial natriuretic peptide levels were higher on both altitude days compared with control.
3. Acute mountain sickness symptom scores showed a significant negative correlation with 24 h urinary sodium excretion on the first altitude day. Aldosterone levels tended to be lowest in subjects with low symptom scores and higher sodium excretion. No correlation was found between changes in haemoglobin concentration, packed cell volume, 24 h urine volume or body weight and acute mountain sickness symptom score.
4. Atrial natriuretic peptide levels at low altitude showed a significant inverse correlation with acute mountain sickness symptom scores on ascent.
Genetic Factors in the Development of Nephropathy in Diabetic Lewis and Da Rats
Authors: Payton Colin D. , Boulton-Jones J. M. 
Published: August 2015

1. Streptozotocin was used to induce diabetes in two inbred strains of rats, Lewis and DA, known to have different glomerular properties.
2. Dietary protein intake, weight and plasma glucose were monitored during the course of the experiment, and, at regular intervals, urine collections were made utilizing metabolic cages.
3. No significant differences were found in protein intake or plasma glucose between the two strains.
4. Proteinuria was higher in the diabetic Lewis rats than in the diabetic DA rats, and the difference became progressively greater with the passage of time. After 6 months of diabetes, the median values for proteinuria were 19.9 mg/24 h in the Lewis rats and 9.0 mg/24 h in the DA rats.
5. Electron microscopic examination revealed a greater degree of mesangial expansion in the glomeruli of the Lewis rats than in those of the DA rats after 6 months of diabetes. The median fractional mesangial area was 44.8% in the diabetic Lewis rats and 31.4% in the diabetic DA rats.
6. These results suggest that Lewis rats possess an inherited susceptibility to diabetic nephropathy, and that DA rats are relatively resistant. These differences in susceptibilities support the hypothesis that inherited glomerular properties determine an individual's susceptibility to diabetic nephropathy.
Plasma levels of the Lyso-Derivative of Platelet-Activating Factor in Acute Severe Systemic Illness
Authors: Leonelli Fabio M. , Leong Lillian L. , Sturm Marian J. , Strophair Julie A. , Clarke Geoffrey M. , Taylor Roger R. 
Published: August 2015

1. Evidence suggests that activation of phospholipase A2 and production of eicosanoids and platelet-activating factor (PAF) are involved in various responses associated with severe tissue damage and shock. It was postulated that the plasma level of the precursor and degradation product of PAF, lyso-platelet-activating factor (lyso-PAF), might be increased in acute severe illness.
2. After plasma extraction, lyso-PAF was acetylated in vitro to PAF, which was measured by bioassay using 5-[14C]hydroxytryptamine-labelled rabbit platelets. Measurements were made in 18 severely ill patients (five with cardiogenic shock; five with severe infection, five after repair of abdominal aortic aneurysm, two with acute pancreatitis; 13 males, five females). Plasma lyso-PAF in these patients was 33 ± 15 (sd) ng/ml (range 5–111 ng/ml), whereas values in normal males (40–65 years) ranged from 102 to 253 ng/ml (n = 15) and in females from 74 to 174 ng/ml (n = 10). Depression of plasma lyso-PAF did not relate closely to the patient group nor to specific therapy, but repeated measurements in each of 10 patients showed an increase in plasma lyso-PAF (P &lt; 0.002), associated with clinical improvement.
3. Evidence was obtained indicating that neither the presence of an inhibitor in the assay system nor reconversion of PAF to lyso-PAF in vitro produced the unexpected depression of plasma lyso-PAF.
4. The mechanisms responsible, which may have therapeutic implications, remain to be elucidated.
Immunoreactive N-terminal Pro-Atrial Natriuretic Peptide in Human Plasma: Plasma Levels and Comparisons with α-Human Atrial Natriuretic Peptide in Normal Subjects, Patients with Essential Hypertension, Cardiac Transplant and Chronic Renal Failure
Authors: Buckley M. G. , Sagnella G. A. , Markandu N. D. , Singer D. R. J. , MacGregor G. A. 
Published: August 2015

1. Plasma levels of immunoreactive N-terminal pro-atrial natriuretic peptide (N-terminal ANP) have been measured in 25 normal subjects, 29 patients with essential hypertension, six cardiac transplant recipients, seven patients with dialysis-independent chronic renal failure and 11 patients with haemodialysis-dependent chronic renal failure. Plasma was extracted on Sep-Pak cartridges and N-terminal ANP immunoreactivity was measured using an antibody directed against pro-ANP (1–30).
2. Plasma levels of TV-terminal ANP (means ± sem) were 235.3 ± 19.2 pg/ml in normal subjects and were significantly raised in patients with essential hypertension (363.6 ± 36.3 pg/ml), in cardiac transplant recipients (1240.0 ± 196.2 pg/ml), in patients with chronic renal failure not requiring dialysis (1636.6 ± 488.4 pg/ml) and patients with chronic renal failure on maintenance haemodialysis (10 336.1 ± 2043.7 pg/ml).
3. There were positive and significant correlations between the plasma levels of TV-terminal ANP and α-human ANP (α-hANP) with individual correlation coefficients of 0.68 within the normal subjects, 0.47 in patients with essential hypertension, 0.78 in patients with dialysis-independent chronic renal failure and 0.68 in patients with haemodialysis-dependent chronic renal failure (P &lt; 0.05 in every case).
4. Gel filtration behaviour on Sephadex G-50 of the immunoreactive N-terminal ANP from Sep-Pak extracts of plasma from normal subjects or patients was consistent with a single peak having an elution volume corresponding to that of human pro-ANP (1–67) standard.
5. These studies demonstrate that the N-terminal pro-ANP peptide is co-secreted with α-hANP in both normal subjects and patients with cardiovascular/renal disease. The higher levels of the N-terminal ANP may reflect differences in the rate of elimination from the circulation but the exact structure and functional significance of the circulating N-terminal ANP remains to be established.
Anaesthetic Agents and Their Effect on Tissue Protein Synthesis in the Rat
Authors: Heys S. D. , Norton A. C. , Dundas C. R. , Eremin O. , Ferguson K. , Garlick P. J. 
Published: August 2015

1. Rates of protein synthesis were measured, in vivo, in lung, liver, heart and skeletal muscle of young male rats. Groups of rats were exposed for 1 h duration to one of the following anaesthetic regimens: 1.4% halothane, 2.2% halothane, 1.4% halothane in 66% nitrous oxide, intravenous pentobarbitone (20 mg/kg) and intravenous midazolam (18 mg/kg) combined with fentanyl (2 μg/kg). Fractional rates of protein synthesis were determined by injecting [3H]phenylalanine (150 μmol/100 g body weight)
2. Liver protein synthesis was depressed significantly by all regimens, except midazolam/fentanyl, by up to 37.7% of control values. Lung protein synthesis was significantly reduced by all the anaesthetic agents by up to 30% of control rates
3. The effects of the anaesthetic agents on skeletal muscle and heart were small and not statistically significant
4. There was no evidence of ventilatory depression as manifested by changes in arterial blood gas partial pressures of CO2 and O2, except in the group treated with 2.2% halothane.
Age-related changes in the circulating levels of congeners of vitamin K2, menaquinone-7 and menaquinone-8
Authors: Hodges S. J. , Pilkington M. J. , Shearer M. J. , Bitensky Lucille , Chayen J. 
Published: August 2015

1. Through the vitamin K1 cycle, phylloquinone is now known to play an active role, not only in relation to prothrombin, but also in the synthesis of bone peptides.
2. The recent development of a sensitive method allowed the demonstration of a deficit of vitamin K1 in the circulation of osteoporotic subjects.
3. Vitamin K2, namely the menaquinones of various chain-lengths, has been shown by others to be more effective than vitamin K1 in the curative rat bioassay.
4. Earlier reports had shown that the concentration of menaquinones in human liver may exceed that of vitamin K1. But previous methods were too insensitive for testing the normal circulating levels of menaquinones in the human.
5. The new sensitive method has now been applied to measuring the circulating levels of vitamin K1 and of two of the menaquinones, namely menaquinone-7 and menaquinone-8.
6. In normal individuals, the circulating levels of vitamin K1 were the same, irrespective of age.
7. In young normal subjects, the combined levels of menaquinone-7 and menaquinone-8 were at least the same as the level of vitamin K1. In elderly normal subjects, there was a marked deficit of menaquinone-8.
Decreased natural killer cell activity in late-onset hypogammaglobulinaemia
Authors: Aparicio-Pagés M. N. , den Hartog G. , Verspaget H. W. , Peña A. S. , van der Meer J. W. M. , van Furth R. , Lamers C. B. H. W. 
Published: August 2015

1. Natural killer cell activity and monocyte cytotoxicity was evaluated in three subgroups of patients with primary hypogammaglobulinaemia (ten patients with late-onset, eight with X-linked and five with early-onset disease) and in two patients with secondary late-onset hypogammaglobulinaemia against the K-562 erythro-leukaemia, the CaCo-2 colon carcinoma and the HGT-1 gastric carcinoma cell lines and compared with the results found in healthy control subjects.
2. The natural killer cell activity, both spontaneous and after stimulation with recombinant γ-interferon, was found to be decreased in patients with late-onset hypogammaglobulinaemia. The natural killer cell activity in this subgroup was found to be impaired in 60% of the patients (P &lt; 0.05). Within the other forms of primary hypogammaglobulinaemia a decreased natural killer cell activity was found to be less frequent (33%).
3. The lectin-mediated cytotoxicity by phytohaem-agglutinin resulted in a similar maximal cytotoxicity in patients and control subjects.
4. The cytotoxicity of monocytes, spontaneous and after recombinant γ-interferon stimulation, was found to be normal in all patients with hypogammaglobulinaemia.
5. The impaired natural killer cell activity which was found in patients with late-onset hypogammaglobulinaemia may contribute to the increased susceptibility to infections and to the increased incidence of malignancies in this subgroup of patients with primary hypogammaglobulinaemia.
Increased density of peripheral benzodiazepine-binding sites in ovarian carcinomas as compared with benign ovarian tumours and normal ovaries
Authors: Katz Yeshayahu , Ben-Baruch Gilad , Kloog Yoel , Menczer Joseph , Gavish Moshe 
Published: August 2015

1. Benzodiazepines are involved in the control of proliferation and differentiation of normal and malignant cells in vitro. This regulatory ability is probably mediated via peripheral benzodiazepine-binding sites.
2. In the present study we compared the binding characteristics of peripheral benzodiazepine-binding sites in human epithelial ovarian carcinoma with those in benign ovarian tumours and normal ovaries.
3. The affinity and density of peripheral benzodiazepine-binding sites in homogenate preparations of ovarian carcinoma as compared with benign ovarian tumours and with normal tissues (used as controls) were determined using a ligand specific for peripheral benzodiazepine-binding sites, [3H]PK 11195, an isoquinoline carboxamide derivative.
4. We observed a robust (three-to five-fold) increase in the neoplasm compared with benign ovarian tumours and normal tissues, without a concomitant change in affinity values.
5. This finding may reflect a change in the metabolic rates of ovarian cancer which is expressed as the alteration in the density of peripheral benzodiazepine-binding sites.
Effects of circulating endogenous catecholamines on plasma glucose, potassium and magnesium
Authors: Corr L. A. , Grounds R. M. , Beacham J. L. , Whitwam J. G. , Brown M. J. 
Published: August 2015

1. To examine the metabolic effects of increases in circulating endogenous plasma catecholamines, we measured plasma glucose, potassium and magnesium in 14 patients undergoing elective coronary artery bypass grafting. The patients were randomized into two groups and received either sodium nitroprusside (a direct-acting vasodilator) or trimetaphan camsylate (a ganglion-blocking agent) for routine control of blood pressure during the operation.
2. There were significant differences between the two groups in the levels of all three metabolic variables studied. Plasma glucose levels rose in both groups, but were significantly higher in the sodium nitroprusside group [peak levels 9.14 (sem 0.72)mmol/l compared with 6.71 (0.88) mmol/l, P&lt; 0.001, analysis of variance]. The cardioplegia solution caused a large increase in plasma magnesium in both groups but in the sodium nitroprusside group the level rose higher [to 1.59 (0.12)mmol/l compared with 1.34 (0.06)mmol/l] and fell faster (P &lt; 0.05, analysis of variance). In the group receiving sodium nitroprusside, plasma potassium fell, by a mean of 0.34 mmol/l, as plasma catecholamine levels rose; no such fall was seen in the group receiving trimetaphan camsylate (P &lt; 0.05, analysis of variance).
3. It is concluded that the sympathoadrenal system is important in causing metabolic changes during cardiopulmonary bypass and may be relevant in other conditions such as acute myocardial infarction.
Regulation of nicotinamide–adenine dinucleotide synthesis in erythrocytes of patients with hypoxanthine–guanine phosphoribosyltransferase deficiency and a patient with phosphoribosylpyrophosphate synthetase superactivity
Authors: Micheli Vanna , Simmonds H. Anne , Ricci Carlo 
Published: August 2015

1. The synthesis of nicotinamide–adenine dinucleotide from nicotinamide and nicotinic acid was compared over different time scales at both physiological (0.7 μmol/l) and high (0.2–3 mmol/l) substrate concentrations in erythrocytes from three patients with hypoxanthine–guanine phosphoribosyltransferase (hypoxanthine phosphoribosyltransferase, EC 2.4.2.8) deficiency (including one Lesch–Nyhan patient) and from one patient with phosphoribosylpyrophosphate synthetase superactivity. The above disorders are associated with grossly altered erythrocyte nicotinamide-adenine dinucleotide levels.
2. At the physiological substrate concentration and incubation times up to 2 h, nicotinamide proved the most efficient nicotinamide–adenine dinucleotide precursor for erythrocytes from both patients and control subjects. The conversion of nicotinamide to its mononucleotide, but not further metabolism, was impaired in phosphoribosylpyrophosphate synthetase-mutant cells. The Lesch–Nyhan and phosphoribosylpyrophosphate synthetase-mutant cells were unusual in that both showed no further stimulation of nucleotide synthesis at 18 mmol/l Pi compared with 1 mmol/l.
3. At the high substrate concentrations, using 18 mmol/l Pi, nicotinamide was a poor precursor in all instances. Using nicotinic acid, nucleotide formation was 30-fold that from nicotinamide, reaching its maximum at 0.2 mmol/l. Conversion of nicotinic acid to nicotinamide–adenine dinucleotide in the phosphoribosylpyrophosphate synthetase-mutant cells was again grossly impaired.
4. There was no evidence for increased nicotinamide–adenine dinucleotide breakdown in the phosphoribosylpyrophosphate synthetase-mutant cells under any of the above conditions.
5. These results suggest that the differing nicotinamide–adenine dinucleotide levels in the two disorders cannot be related directly to the altered phosphoribosylpyrophosphate levels. The problem appears to be one of decreased synthesis in the phosphoribosylpyrophosphate synthetase-mutant cells, whereas the synthetic capacity in intact hypoxanthine–guanine phosphoribosyltransferase-deficient cells is neither enhanced nor inhibited by the raised nicotinamide–adenine dinucleotide levels.
Electrocardiographic changes induced by inhaled salbutamol after treatment with bendrofluazide: Effects of replacement therapy with potassium, magnesium and triamterene
Authors: Lipworth B. J. , McDevitt D. G. , Struthers A. D. 
Published: August 2015

1. Twelve normal subjects were given 5 days' treatment with (a) placebo; (b) 5 mg of bendrofluazide; (c) 5 mg of bendrofluazide plus 24 mmol of potassium; (d) 5 mg of bendrofluazide plus 24 mmol of magnesium; (e) 5 mg of bendrofluazide plus 24 mmol of potassium plus 24 mmol of magnesium; (f) 5 mg of bendrofluazide plus 50 mg of triamterene.
2. After each treatment period, subjects were given two doses of inhaled salbutamol (each of 1 mg), and measurements were made 25 min after each dose.
3. Treatment with bendrofluazide plus salbutamol produced a lower absolute level of plasma potassium than salbutamol alone, although the addition of potassium, magnesium or triamterene did not attenuate this effect. Plasma magnesium was unchanged by salbutamol.
4. Salbutamol was associated with significant electrocardiographic effects, including T-wave flattening, Q-Tc interval prolongation and, in some subjects, U-waves and S-T segment depression.
5. Prior treatment with bendrofluazide potentiated the electrocardiographic effects of salbutamol. Supplementation with potassium and magnesium had no effect on electrocardiographic changes, and the addition of triamterene to bendrofluazide only attenuated electrocardiographic responses in some subjects.
Total-body potassium in insulin-dependent diabetes mellitus
Authors: Goodship T. H. J. , Butler P. C. , Rodham D. , Clayton B. , Home P. D. , Alberti K. G. M. M. 
Published: August 2015

1. Total-body potassium and fat-free mass have been measured in 31 insulin-dependent diabetic patients and 31 age- and sex-matched normal volunteers.
2. Body mass index was significantly higher in the insulin-dependent diabetic patients (24.7 ± .5 vs 23.3 ± 0.4 kg/m2; P = 0.05).
3. Total-body potassium, uncorrected and corrected for weight and for fat-free mass, was not significantly different in the two groups (3281 ± 141 mmol, 47.3 ± 1.3 mmol/kg body weight, 60.9 ± 1.0 mmol/kg fat-free mass, and 3315 ± 143 mmol, 48.6 ± 1.0 mmol/kg body weight, 60.4 ± 0.8 mmol/kg fat-free mass, respectively, in diabetic patients and non-diabetic subjects). There was no relationship between blood glucose control, as assessed by glycated haemoglobin concentrations, and total-body potassium.
4. These results suggest, by contrast with previous reports, that in insulin-dependent diabetic patients, showing varying degrees of glycaemic control (glycated haemoglobin range 6.1–15.3%, mean 9.0%) that: (a) there is no significant abnormality of body potassium homoeostasis, and (b) there is no relation between total-body potassium and glycaemic control.
Abnormal arterial flow pattern in untreated essential hypertension: Possible link with the development of atherosclerosis
Authors: Jones Christopher J. H. , Singer Donald R. J. , Watkins Nicholas V. , MacGregor Graham A. , Caro Colin G. 
Published: August 2015

1. We compared the velocity waveforms in the superficial femoral artery measured by multichannel Doppler ultrasound in 45 subjects: 21 patients with untreated essential hypertension and 24 normal subjects of similar age and sex.
2. The pattern of arterial flow was abnormal in hypertensive patients, with the acceleration time, the duration of reverse flow and the time to maximum flow reversal being abbreviated. The internal arterial diameter, calculated from the velocity profile, was reduced despite raised pressure, suggesting altered arterial wall mechanics in essential hypertension.
3. These abnormalities will influence the wall shear stress, a major determinant of arterial function. The abnormal arterial wall mechanics and abnormal blood flow pattern may contribute to the increased risk of arterial disease in patients with untreated hypertension.
Overall renal and tubular function during infusion of amino acids in normal man
Authors: Olsen N. V. , Hansen J. M. , Ladefoged S. D. , Fogh-Andersen N. , Nielsen S. Levin , Leyssac P. P. 
Published: August 2015

1. Amino acids have been used to test renal reserve filtration capacity. Previous studies suggest that amino acids increase glomerular filtration rate (GFR) by reducing distal tubular flow and tubuloglomerular feedback activity.
2. Glomerular function and the renal tubular handling of sodium during infusion of amino acids was studied in 12 normal volunteers.
3. Clearance of sodium (CNa) was unchanged. Effective renal plasma flow increased slightly, but significantly, by 9% (P &lt;0.05). GFR was increased by 13% (P &lt;0.001). Clearance of lithium (CLi) (used as an index of proximal tubular outflow) increased by 38% (P &lt;0.001). Calculated absolute proximal reabsorption (GFR-CLi) remained unchanged. Fractional proximal reabsorption [1-(CLi/GFR)] was decreased by 10% (P &lt;0.001). Calculated absolute distal sodium reabsorption [(CLi–CNa) × PNa, where PNa is plasma sodium concentration] increased by 40% (P &lt;0.001). Plasma renin concentration did not change significantly.
4. The results suggest that amino acids increase GFR by a primary effect on renal haemodynamics or, less likely, by reducing the signal to the tubuloglomerular feedback mechanism. The increase in proximal tubular outflow was compensated for in the distal tubules, so that the sodium excretion rate remained unchanged.
Attenuation of the low-density-lipoprotein-activated phosphoinositide signalling system by calcium blockers in human lymphocytes
Authors: Locher Rudolf , Sachinidis Agapios , Steiner Albert , Vetter Wilhelm 
Published: August 2015

1. The capacity of low-density lipoprotein-cholesterol (40 μg/ml) to stimulate both the phosphoinositide cycle and the dislocation of the phospholipid- and calcium-dependent protein kinase C activity from the cytosolic to the membranous compartment in human circulating lymphocytes has been studied.
2. Pretreatment of lymphocytes with pertussis toxin inhibited significantly the low-density-lipoprotein-induced formation of inositol trisphosphate.
3. The calcium-channel blockers verapamil, nifedipine and diltiazem, each in a concentration range from 1 μmol/l to 1 nmol/l, attenuated the low-density lipoprotein-induced formation of inositol trisphosphate in a dose-dependent manner. Similar results were observed when so-called non-specific calcium antagonists, such as flunarizine and molsidomine, were used.
4. The results suggest that low-density lipoprotein activates the phosphoinositide cycle in circulating lymphocytes through mechanisms sensitive to calcium blockers and pertussis toxin.