bluuebunny/crossref_metadata_2025_split huggingface dataset:
Plasma profiles and removal rates of inorganic sulphate, and their influence on serum ionized calcium, in patients on maintenance haemodialysis
Authors: Marangella M. , Petrarulo M. , Cosseddu D. , Vitale C. , Linari F. 
Published: August 2015

1. Regular dialysis treatment is reported to remove inorganic sulphate, but not to restore its level to normal. To evaluate the adequacy of modern dialysis techniques in maintaining the sulphate balance, intra- and inter-dialysis plasma profiles and removal rates of sulphate were studied in 20 stable patients on maintenance haemodialysis. The influence of sulphate levels on the distribution of calcium-complex species was also investigated.
2. Sulphate was determined by ion-exchange chromatography of both serum ultrafiltrates, taken at the start of, during, at the end of, and at 24 h and 48 h after a dialysis session, and whole diffusate collections. Dialyser clearances of sulphate were assessed by two independent procedures and compared with those of urea and creatinine, on two different methods of dialysis, i.e. traditional haemodialysis with Cuprophan hollow fibre filters, and haemodiafiltration with high-flux Polysulphone or polyacrylonitrile dialysers. Concentrations of the main serum ions were determined before and after dialysis and used to solve a multiple mass balance equation system by which concentrations of the calcium-complex species were calculated.
3. Before dialysis, sulphate levels were eight times those determined in 17 control subjects and remained higher than normal at the end of dialysis. These changes were independent of the dialysis procedure. There was a close correlation between serum levels of sulphate and creatinine. Dialyser clearances of sulphate were comparable with those of creatinine, but lower than those of urea. Clearances of all solutes were higher on haemodiafiltration.
4. The mean removal of sulphate during a single session was about 30 mmol; the estimated removal rate averaged 15 mmol/day and was closely related to the protein catabolic rate as derived by urea kinetic modelling. Removal rates were slightly lower than rates of sulphate excretion in 40 control subjects. Because serum sulphate levels were quite stable over time this decrease was accounted for by a reduction in the net generation of sulphate, due to either altered catabolism of sulphur-containing amino acids or reduced intakes of animal protein.
5. The distribution of calcium-complex species demonstrated that the calcium-sulphate complex concentration in pre-dialysis samples was similar to that of calcium-phosphate complex and both were markedly increased as compared with normal subjects. Dialysis minimized but did not cancel out these abnormalities, which were responsible for significant decreases in free calcium concentration.
6. It is concluded that, although dialysis efficiently removes newly generated inorganic sulphate, it does not prevent chronic increases in this anion. Inadequate control of plasma sulphate levels by dialysis or through the diet may adversely affect the clinical state of uraemic patients and induce pervasive changes in calcium homoeostasis.
Noradrenaline release in skeletal muscle and in adipose tissue studied by microdialysis
Authors: Grønlund Bo , Astrup Arne , Bie Peter , Christensen Niels Juel 
Published: August 2015

1. In adipose tissue and in skeletal muscle the extracellular noradrenaline levels were studied by microdialysis in the conscious dog and compared with the noradrenaline concentration in arterial plasma.
2. The experiments were performed with and without tyramine added to the perfusion medium, and noradrenaline was measured by a sensitive radioenzymic assay.
3. In the absence of tyramine, the interstitial noradrenaline levels in adipose tissue and skeletal muscles were similar to arterial blood concentrations, provided that the former were corrected for recovery. The recovery estimated from experiments in vitro averaged 16% at room temperature.
4. With tyramine added to the perfusates, noradrenaline levels increased 10-fold. Arterial noradrenaline concentrations did not change, indicating that noradrenaline was released only locally in the tissue.
5. Our results indicate that the microdialysis technique combined with a sensitive assay for measuring noradrenaline may be applicable to the assessment of local noradrenaline release in adipose tissue and in skeletal muscle. This may be of interest, especially in adipose tissue during physiological stimulation in which sympathetic activity is difficult to evaluate by other techniques.
Cigarette smoking and urinary excretion of markers for platelet/vessel wall interaction in healthy women
Authors: Rångemark C. , Wennmalm Å. 
Published: August 2015

1. Cigarette smoking is known to increase the risk of cardiovascular disease in both men and women. Experimental and epidemiological studies have demonstrated that cigarette smoking is associated with several indices of increased platelet activation and platelet/vessel wall interaction in men. The aim of the present study was to test the hypothesis that cigarette smoking is linked to an increased platelet activity in women also.
2. In 26 healthy smoking and non-smoking women (age 21–49 years) the urinary excretion of the thromboxane A2 metabolite 2,3-dinor-thromboxane B2 (an index of platelet activation) and of the prostacyclin metabolite 2,3-dinor-6-keto-prostaglandin F1α (an index of platelet/vessel wall interaction) were analysed by g.c.-m.s. in samples collected on days 3, 10 and 20 of their respective menstrual cycles.
3. The urinary excretion of 2,3-dinor-thromboxane B2 did not vary significantly during the menstrual cycle, either in the smokers or in the non-smokers. It was consistently higher (P &lt; 0.004) in the group of smokers (average of days 3, 10 and 20, 395 ± 61 pg/mg of creatinine; mean ± sem) than in the group of non-smokers (average 188 ± 22 pg/mg of creatinine).
4. The urinary excretion of 2,3-dinor-6-keto-prostaglandin F1α did not differ between the groups on any of the days studied (average on days 3, 10 and 20 in the smokers and non-smokers was 281 ± 50 and 227 ± 30 pg/mg of creatinine, respectively).
5. These data demonstrate that smoking fertile women excrete more of the thromboxane A2 metabolite than do non-smokers, thereby supporting the hypothesis that cigarette smoking elicits platelet activation in healthy women. In contrast, platelet/vessel wall interaction does not appear to be facilitated in smoking compared with non-smoking women. The data suggest that platelet activation is not a major haemostatic mechanism during menstruation.
Increased plasma cholecystokinin levels and small gall bladders in adult patients with cystic fibrosis
Authors: van Haren E. H. J. , Hopman W. P. M. , Jansen J. B. M. J. , Rosenbusch G. , Lamers C. B. H. W. , van Herwaarden C. L. A. 
Published: August 2015

1. In patients with cystic fibrosis, abnormalities in plasma cholecystokinin level and gall-bladder emptying may contribute to the development of maldigestion and gall-stones.
2. Therefore, we have measured plasma cholecystokinin levels and gall-bladder volumes before and after ingestion of a standard breakfast in eight adult patients with cystic fibrosis and in eight normal control subjects.
3. In the patients with cystic fibrosis basal (2.8 ± 0.4 pmol/l; P &lt; 0.05, t-test) and maximum post-prandial (5.7 ± 0.5 pmol/l; P &lt; 0.05, t-test) plasma cholecystokinin levels were significantly higher than those in the control subjects (1.9 ± 0.1 pmol/l, and 4.5 ± 0.2 pmol/l, respectively). On the other hand, integrated plasma cholecystokinin secretion in response to the meal was similar (t-test, P = 0.4 versus control subjects). The increased plasma cholecystokinin levels in the patients with cystic fibrosis were accompanied by reduced gallbladder volumes in both the basal (7.8 ± 2.1 cm3 versus 20.9 ± 2.3 cm3 in control subjects; P &lt; 0.005, t-test) and the post-prandial state (2.2 ± 1.0 cm3 versus 4.8 ± 0.8 cm3 in control subjects; P = 0.06, t-test). Gall-bladder emptying in the patients with cystic fibrosis was well preserved (70 ± 7% versus 78 ± 9% in control subjects; P = 0.4, t-test).
4. In comparison with normal control subjects, patients with cystic fibrosis have an increased basal plasma cholecystokinin level and a reduced gall-bladder volume, whereas post-prandial gall-bladder emptying and plasma cholecystokinin secretion are not significantly different. In cystic fibrosis, neither impaired cholecystokinin release nor impaired gall-bladder emptying appear to play a role in the pathogenesis of either gall-stones or maldigestion.
A defect in insulin release in women at risk of future non-insulin-dependent diabetes
Authors: Dornhorst Anne , Edwards Simon G. M. , Nicholls Jonathan S. D. , Anyaoku Victor , Mclaren Duncan , Heslop Kirsten E. , Elkeles Robert S. , Beard Richard W. , Johnston Desmond G. 
Published: August 2015

1. A study on seven Caucasian glucose-tolerant women with previous gestational diabetes and seven matched control subjects is presented. The insulin response to oral glucose, insulin sensitivity and fasting glucose production rates were measured by using a 75 g oral glucose tolerance test, an insulin tolerance test and a non-radioactive tracer, [6,6-2H]glucose, respectively.
2. Fasting plasma glucose levels were similar between the women with previous gestational diabetes and the control subjects (4.8 ± 0.3 versus 4.7 ± 0.2 mmol/l), as were fasting plasma insulin levels (median 4 m-units/l, range 1–13 m-units/l versus median 4 m-units/l, range 1–24 m-units/l). After oral glucose the 60 min plasma glucose levels in the women with previous gestational diabetes were significantly higher (8.5 ± 0.6 versus 6.7 ± 0.8 mmol/l, P &lt; 0.05), whereas the plasma insulin level was significantly lower at both 30 min (median 23 m-units/l, range 4–47 m-units/l versus median 55 m-units/l, range 23–100 m-units/l, P &lt; 0.02) and at 60 min (median 23 m-units/l, range 4–43 m-units/l versus median 60 m-units/l, range 16–126 m-units/l, P&lt; 0.02).
3. Insulin sensitivity, expressed as the slope of the regression line of plasma glucose level against time after intravenous infusion of insulin (0.05 unit/kg), was similar in the women with previous gestational diabetes and the control subjects (mean slope, −0.17 ± 0.01 versus −0.17 ± 0.01).
4. Fasting glucose production rates were similar in the women with previous gestational diabetes and the control subjects (2.2 ± 0.3 versus 1.9 ± 0.1 mg min−1 kg−1).
5. Women with previous gestational diabetes, a group at risk of future non-insulin-dependent diabetes, have abnormalities of insulin release at a time when insulin sensitivity and fasting glucose production are normal.
Metalloproteinases in degenerative aortic disease
Authors: Vine N. , Powell Janet T. 
Published: August 2015

1. Atherosclerosis and aneurysm of the abdominal aorta are associated with thinning of the medial connective tissue. We have investigated the presence of the connective-tissue-degrading metalloproteinases in homogenates prepared from atherosclerotic, aneurysmal and control aortic media.
2. Gelatinase activity was much increased in homogenates from atherosclerotic and aneurysmal aorta [10.911.8 and 13.3 ± 3.3 μg of gelatin hydrolysed h−1 (mg of protein)−1 respectively]. This gelatinase activity was highest at the luminal aspect of the aortic media, where the activity increased three-to five-fold after the destruction of α2-macroglobulin. Zymograms demonstrated the principal gelatinase in atherosclerotic aorta to have a molecular mass of about 92 kDa, whereas in aneurysmal aorta there was a spectrum of gelatinase activity from 92 to 55 kDa.
3. Collagenase and stromelysin (proteoglycanase) could be detected by immunoblotting in homogenates of aneurysmal aorta, but rarely in atherosclerotic aorta and never in control aorta. Collagenase and stromelysin activities were low, but increased two-to three-fold after the destruction of tissue inhibitor of metalloproteinases. Collagenase and stromelysin activities were highest at the adventitial aspect of aneurysmal media.
4. The secretion of gelatinase by inflammatory cells at the intima of diseased aorta could have a pathological role in establishing atherosclerotic plaques and medial thinning. Secretion of collagenase, gelatinase and stromelysin from the adventitia could accelerate connective tissue degradation in the media of aneurysmal aorta.
Spectrum of orthostatic disorders: Classification based on an analysis of the short-term circulatory response upon standing
Authors: Wieling W. , ten Harkel A. D. J. , van Lieshout J. J. 
Published: August 2015

1. In 31 consecutively referred patients (20 females, 11 males) with overt or suspected orthostatic disorders, the changes in blood pressure and heart rate that occur in the first 2 min of standing were analysed.
2. Blood pressure was measured continuously by Finapres. The blood pressure and heart rate responses after 1–2 min of standing (early steady-state response) were used to classify the patients as follows: group I (n = 17, age 42 ± 17 years), normal early steady-state blood pressure and heart rate responses; group II (n = 5, age 40 ± 14 years), combination of normal early steady-state blood pressure and postural tachycardia; group III (n = 9, age 51 ± 14 years), hypotensive orthostatic response with (4/9) or without (5/9) postural tachycardia. We examined whether additional information could be obtained by beat-to-beat analysis of the initial circulatory response (first 30 s). It was quantified by identifying the blood pressure trough and overshoot and the maximum heart rate and relative bradycardia.
3. The initial drop in systolic and diastolic blood pressures did not differ between the three groups. A recovery of blood pressure with a systolic and/or diastolic blood pressure overshoot was present in all group I and II patients, but was absent in all except two patients in group III. The initial maximum heart rate increase did not differ between the three groups. The relative bradycardia was less in groups II and III than in group I.
4. We conclude that analysis of the beat-to-beat blood pressure changes in the first 30 s after the onset of standing provides almost all the information that is necessary to determine abnormalities in orthostatic circulatory control.
Influence of nifedipine on cyclosporin A nephrotoxicity after unilateral nephrectomy in the spontaneously hypertensive rat
Authors: McNally P. G. , Baker F. , Mistry N. , Walls J. , Feehally J. 
Published: August 2015

1. Nifedipine ameliorates cyclosporin A-induced renal impairment in surgically intact (two-kidney) rats. This study investigates the effect of nifedipine on cyclosporin A nephrotoxicity in spontaneously hypertensive rats after either uninephrectomy or uninephrectomy with contralateral renal denervation.
2. Fourteen days after uninephrectomy pair-fed rats were injected for 14 days with cyclosporin A (25 mg/kg body weight) via the subcutaneous route and with nifedipine (0.1 mg/kg body weight) via the intraperitoneal route. Renal and systemic haemodynamics were measured in conscious unrestrained rats.
3. Whole-blood levels of cyclosporin A did not differ between groups (overall 352 ± 22 ng/ml, means ± sem). After uninephrectomy, cyclosporin A decreased the glomerular filtration rate (olive oil versus cyclosporin A: 0.96 ± 0.04 versus 0.70 ± 0.06 ml min−1 100 g body weight, P &lt; 0.02) and effective renal plasma flow (1.94 ± 0.10 versus 1.38 ± 0.13, P &lt; 0.01), and increased renal vascular resistance {(20.2 ± 1.8) × 104 versus (31.6 ± 3.3) × 104 kPa l−1 s [(20.2 ± 1.8) × 103 versus (31.6 ± 3.3) × 103 dyn s cm−5], P &lt; 0.02} and mean arterial pressure (146.7 ± 6.7 versus 167.3 ± 2.9 mmHg, P &lt; 0.05). Neither renal denervation nor nifedipine prevented the reduction in glomerular filtration rate or effective renal plasma flow induced by cyclosporin A.
4. This study infers that the sympathetic nervous system does not play an active role in cyclosporin A nephrotoxicity and demonstrates that the concomitant administration of nifedipine to rats with reduced renal mass does not ameliorate cyclosporin A-induced renal impairment.
Effects of diuretics on stroke development in Kyoto–Wistar stroke-prone spontaneously hypertensive rats
Authors: Smeda John S. , Tkachenko Olexa 
Published: August 2015

1. Previous studies have indicated that increases in dietary K+ promote diuresis and retard stroke development in stroke-prone spontaneously hypertensive rats (spSHR) fed a Japanese-style diet containing 4% NaCl.
2. It is possible that elevations in dietary K+ retard stroke development by inducing natriuresis and facilitating the clearance of Na+, and that diuretics associated with natriuresis might also be capable of retarding stroke development in spSHR. To test if this was the case, the onset of stroke development in spSHR fed a low (0.75%) K+ diet containing 4% NaCl (controls) was monitored and compared with that in spSHR treated with (a) frusemide, (b) chlorothiazide, (c) amiloride or (d) acetazolamide, and with (e) untreated spSHR fed a high (2.11%) K+ diet.
3. The onset of stroke, as well as death resulting from stroke, occurred at a significantly later age in spSHR fed a high K+ diet than in spSHR fed a low-K+ diet, despite the fact that both groups of spSHR rats had comparable blood pressures.
4. Treatment of spSHR with the above-named diuretics before stroke development did not alter the blood pressure of the rats. The onset of stroke development and death in spSHR treated with chlorothiazide, amiloride or acetazolamide was comparable with that observed in untreated control spSHR. In spSHR treated with frusemide, the onset of stroke was comparable with that of untreated control spSHR, whereas the onset of death after stroke development was accelerated.
5. Post mortems performed on spSHR that developed stroke indicated the presence of haemorrhagic stroke of comparable severity in the six groups of spSHR studied.
6. The results indicate that treatment of spSHR with diuretics at levels which do not alter the animals’ blood pressure does not alter the timing or incidence of stroke development, and does not prolong the lifespan of the animals after stroke has developed.
Plasma ascorbate levels and inhibition of the antioxidant activity of caeruloplasmin
Authors: Gutteridge John M. C. 
Published: August 2015

1. The copper-containing protein caeruloplasmin has several oxidase activities.
2. Its ability to catalyse the oxidation of ferrous ions to the ferric state (ferroxidase activity) makes it an important antioxidant in vivo.
3. Recent reports have suggested that oral supplementation with vitamin C can inhibit the oxidase activities of caeruloplasmin.
4. As expected, damage to DNA and membrane lipids was stimulated by mixtures of iron salt and ascorbate, and this damage could be inhibited by caeruloplasmin provided the molar ratio of ascorbate to caeruloplasmin was kept sufficiently low.
5. When the molar ratio of ascorbate to caeruloplasmin was greater than 200 substantial loss of ferroxidase antioxidant activity occurred.
6. It is unlikely, however, that oral supplementation with vitamin C can raise plasma levels sufficiently to inhibit caeruloplasmin activity in vivo.
Zinc improves the filterability of sickle erythrocytes at intermediate oxygen partial pressures
Authors: Taylor J. A. , Acharya J. , Pearson T. C. , Thompson R. P. H. 
Published: August 2015

1. The deformability of erythrocytes from patients with sickle-cell anaemia was measured with a St George's blood filtrometer at a range of oxygen partial pressures and at four levels of zinc loading.
2. When incubated in buffered saline containing zinc and the chelator ethyl maltol, erythrocytes rapidly accumulated zinc and thus their oxygen affinity was increased.
3. Neither the oxygen partial pressure nor zinc loading affected the filtration of normal erythrocytes.
4. Deoxygenation of sickle erythrocytes greatly impaired filtration, although the initial filtration rate declined sharply at different oxygen partial pressures (between 70 and 35 mmHg) in different patients.
5. Low levels of zinc (0.03 ± 0.003 mol of zinc/mol of haemoglobin tetramer) were without effect on sickle cells, but at zinc/haemoglobin ratios of 0.6:1 and above, the sharp fall in filtration rate occurred at oxygen partial pressures 8–25 mmHg below the oxygen partial pressure that impaired filtration of untreated cells.
6. Hence, the deformability of sickle erythrocytes in vitro can be improved by increasing the intracellular content of zinc to 20-fold above normal. Further studies are now required to examine the stability of zinc in erythrocytes, the effects of high intracellular zinc concentrations on erythrocyte viability, and the toxicity of zinc released from zinc-laden cells.
Changes in blood pressure during the normal menstrual cycle
Authors: Dunne F. P. , Barry D. G. , Ferriss J. B. , Grealy G. , Murphy D. 
Published: August 2015

1. Changes in blood pressure during the normal menstrual cycle are not well documented, and previous studies have given conflicting results.
2. Thirty normotensive women and ten mildly hypertensive women measured their blood pressure at home each morning for 6 weeks, under standardized conditions, using a UA-751 semi-automatic sphygmomanometer. All had normal menstrual cycles and subjects entered the study at difference phases of the cycle.
3. Blood pressure was higher at the onset of menstruation than at most other phases of the cycle (systolic blood pressure, P &lt; 0.05; diastolic blood pressure, P &lt; 0.001). Adjusted diastolic blood pressure was higher in the follicular than in the luteal phase (mean difference 1.23 mmHg, P &lt; 0.001). Similarly, blood pressure was lower during days 17–26 than during the remainder of the cycle (adjusted mean difference in systolic blood pressure −0.65 mmHg, P = 0.07; adjusted mean difference in diastolic blood pressure − 1.19 mmHg, P &lt; 0.001).
4. Similar patterns were seen in normotensive and hypertensive subjects, and changes in plasma 17β-oestradiol and progesterone concentrations were also similar in the two groups.
Cardiovascular effects of growth hormone treatment in growth-hormone-deficient adults: stimulation of the renin-aldosterone system
Authors: Cuneo Ross C. , Salomon Franco , Wilmshurst Peter , Byrne Chris , Wiles C. Mark , Hesp Richard , Sönksen Peter H. 
Published: August 2015

1. In adult humans with growth hormone deficiency, treatment with growth hormone has recently been shown to have major anabolic effects and to improve exercise performance. The cardiovascular effects of growth hormone in adults with growth hormone deficiency were examined in 24 patients treated with recombinant human growth hormone (0.07 units/kg at night) in a double-blind, placebo-controlled trial lasting 6 months.
2. Compared with placebo, resting M-mode echocardiography showed increases in left ventricular end-diastolic dimension and stroke volume in the group treated with recombinant human growth hormone. No differences were noted between the groups with respect to left ventricular end-systolic dimension, fractional shortening, wall thicknesses or mean arterial blood pressure. Left ventricular myocardial mass increased in the group given recombinant human growth hormone.
3. The supine plasma renin activity was increased and remained elevated over the 6 months, whereas the plasma aldosterone concentration was unchanged, after treatment with recombinant human growth hormone. Clinical signs of sodium retention were evident during the first 3 months of treatment with recombinant human growth hormone.
4. We conclude that treatment with recombinant human growth hormone in adults with growth hormone deficiency resulted in small increases in left ventricular pre-load, due to the sodium-retaining action of growth hormone. Activation of the renin-aldosterone system was involved in such changes. Myocardial hypertrophy was observed without changes in mean arterial pressure, reflecting the anabolic action of growth hormone.