bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bile salt transport in intestinal lymph of the rat
Authors: BECKETT GEOFFREY J. , PERCY‐ROBB IAIN W. 
Published: March 2008

Abstract. The concentrations of conjugated cholate and chenodeoxycholate have been measured in samples of rat thoracic duct lymph, portal and systemic blood. Both these bile salts were present in lymph. After administration of a corn oil meal the flux of both these bile salts in lymph increased significantly (P < 0.001; Student's t test), the cholate flux rising from 0.9 ± 0.6 nmol/h (mean ± SD) to 3.5 ± 1.1 nmol/h postprandially and the chenodeoxycholate flux rising from 2.5 ± 0.8 to 4.6 ± 1.6 nmol/h. This postprandial increase in bile salt flux was due to both an increase in bile salt concentration and an increased lymph flow which rose significantly (P= 0.007) from 0.5 ± 0.2 to 0.7 ± 0.2 ml/h.Biliary drainage significantly (P < 0.001) reduced the flux of cholate and chenodeoxycholate in lymph to 0.08 ± 0.05 and 0.17 ± 0.10 nmol/h respectively. These biliary drained animals produced no significant rise (P > 0.1) in bile salt flux when fed the corn oil meal.The ratio of the concentrations of conjugated cholate to chenodeoxycholate in systemic and portal blood was 1.9:1 and 3.3:1 respectively. In contrast, this bile salt ratio was only 0.44:1 in lymph.These studies show that bile salts, in particular chenodeoxycholate, can pass directly from the intestine into lymphatics thus establishing an enterolymphatic circulation of bile salts.
The value of plasma prolactin levels in the prediction of the responsiveness of growth hormone secretion to bromocriptine and TRH in acromegaly
Authors: LAMBERTS S. W. J. , LIUZZI A. , CHIODINI P. G. , VERDE S. , KLIJN J. G. M. , BIRKENHÁGER J. C. 
Published: March 2008

Abstract. The mechanism of the inhibition of growth hormone secretion in response to bromocriptine and the ability of thyrotropin releasing hormone to stimulate growth secretion in acromegaly is unknown. In the present study the relationship between the plasma prolactin concentration of untreated acromegalic patients and the reaction of growth hormone to thyrotropin releasing hormone and bromocriptine was investigated.Plasma prolactin levels were elevated in thirty‐three (42%) of seventy‐nine untreated acromegalic patients. Seventeen patients had mildly elevated prolactin levels, but in sixteen the plasma prolactin concentration was higher than 30 ng/ml. Bromocriptine (2.5 mg) inhibited growth hormone secretion by more than 50% in 22% of the normoprolactinaemic, in 53% of the mild hyperprolactinaemic and in 88% of the patients with a prolactin level above 30 ng/ml (P<0.01 v. normoprolactinaemic; P<0.01 v. mildly elevated prolactin levels). An increase of growth hormone secretion by more than 100% of the basal value in response to thyrotropin releasing hormone was observed in 44% of the normoprolactinaemic, in 59% of the mildly hyperprolactinaemic and in 75% of the clearly hyperprolactinaemic patients; (P<0.01 v. normo‐and mildly hyperprolactinaemic patients).Conclusion: An increased plasma prolactin concentration in patients with acromegaly is accompanied in most patients by a higher sensitivity of growth hormone secretion to bromocriptine.
The determination of aminopyrin elimination for control of the metabolic capacity of the liver in man
Authors: HAUSTEIN K.‐O. , HÜLLER G. , SENSING HELGA 
Published: March 2008

Abstract. The kinetics of plasma and breath elimination of aminopyrine after 14C‐aminopyrine given orally were studied using an open one‐compartment model and first order rates of elimination. The study comprises eight healthy volunteers and two groups with histologically verified chronic liver diseases (cirrhosis, n= 12, and chronic aggressive hepatitis, n= 12). Elimination rates from plasma and breath were significantly reduced in the group with cirrhosis, but only so in chronic aggressive hepatitis when they were expressed relative to each other.Monomethylaminopyrine was eliminated more rapidly compared to aminopyrine, and the rate of formaldehyde formation was positively correlated to the excretion rate of CO2 (r= 0.53, P<0.002). No correlation was found with clinical or other laboratory data in the groups of liver diseases studied.The test is a quantitative indicator of the drug metabolizing mixed function oxidases of the endoplasmatic reticulum of the liver, and may reflect the degree of damage to this system in chronic liver disease.
Effect of nitroglycerin on pulmonary perfusion distribution and gas exchange of normal subjects
Authors: NEMERY BENOÎT , VANDERLINDEN‐MAHIEU SONIA , PIRET LOUIS , BRASSEUR LUCIEN , FRANS ALBERT 
Published: March 2008

Abstract. In eight healthy subjects we assessed the effects of 3 mg sublingual nitroglycerin on lung distribution of ventilation and perfusion using 133Xe (sitting, supine and lateral decubitus) and on alveolo‐arterial O2 and CO2 partial pressure differences [(PAo2–Pao2), (Paco2–PAco2)] and physiological dead space to tidal volume ratio (VD/VT) (sitting).In all studied positions, nitroglycerin induced a significant decrease in uppermost perfusion indices, and a significant increase in dependent perfusion indices, without changing the distribution of ventilation. Significant increases in (Paco2–PAco2) and VD/VT were observed up to 60 min after nitroglycerin. No changes in (PAo2–Pao2) occurred, except for a transient decrease due to transient hyperventilation following nitroglycerin.The redistribution of pulmonary perfusion after nitroglycerin may be attributed to the passive effects of lowered pulmonary vascular pressures, and to possible action on extra‐alveolar vessels. The evolution of the indices of pulmonary gas exchange is compatible with the observed redistribution of ventilation/perfusion relationships.
Ammonia uptake by skeletal muscle in the hyperammonaemic rat
Authors: HOD G. , CHAOUAT M. , HASKEL Y. , LERNAU O. Z. , NISSAN S. , MAYER M. 
Published: March 2008

Abstract. A two‐stage surgical occlusion of the portal vein was employed to produce hyperammonaemia in the rat. The procedure resulted in a significant rise of arterial blood ammonia level from 70·5 ± 6·5 μmol/l (mean ± SEM, n= 10) to 214·0 ± 37·7 μmol/l and in a rise of venous blood ammonia from 65·0 ± 9·4 μmol/l to 122·2 ± 7·4 μmol/l during the first day following the complete vein occlusion. A marked increase of the arteriovenous difference of ammonia concentration from virtually zero in sham‐operated controls to 72 ± 9 (n= 8) μmol/l in rats 1 day after the surgical manipulation suggested uptake of ammonia by skeletal muscle. Rat muscle glutamine synthetase activity increased from 0·46 ± 0·06 u/mg (n= 7) in controls to 2·7 ± 0·3 u/mg (n= 7) on the fourth day following portal vein ligation, and muscle branched chain amino acids aminotransferase increased from 0·2 ± 0·05 u/mg in controls to 0·96 ± 0·1 u/mg (n= 7) during the first day of ligation. Glutamine dehydrogenase and aspartate aminotransferase activities were not affected by the surgical procedure. These observations suggest that ammonia trapping in skeletal muscle is coupled to glutamine formation via amination of glutamic acid. This conclusion was further supported by the finding that ammonia uptake correlated (r= 0·92) with enahnced release of glutamine from muscle and that treatment with methionine sulfoximine, a potent inhibitor of glutamine synthetase, changed the arteriovenous difference of glutamine from –0·92 ± 0·01 mmol/l in ligated animals (net release) to ± 0·12 ± 0·01 mmol/l (net uptake) in ligated and inhibitor‐treated animals. Similarly, the inhibitor also abolished the arterio‐venous difference of ammonia.Thus, the animal model of hyperammonaemia and the muscle enzyme assays reveal that skeletal muscle is involved in the regulation of blood ammonia level by conversion of ammonia, via glutamic acid, to glutamine.
Functionally inactive apolipoprotein E3 in a type III hyperlipoproteinaemic patient
Authors: HAVEKES LOUIS M. , LEUVEN JAN A. GEVERS , CORVEN EMILE VAN , WIT ELLY DE , EMEIS JEF J. 
Published: March 2008

Abstract. Type III hyperlipoproteinaemia (HLP) is, amongst others, characterized by the E2/2 phenotype as determined by isoelectric focusing of apolipoprotein E. However, one of our clinically symptomatic type III HLP patients showed a E3/3 phenotype.After complexation with phospholipid vesicles, apo E from this patient was, in contrast with apo E from a type IV HLP patient (E3/4 phenotype), unable to compete with low density lipoprotein (LDL) for binding to the specific LDL receptors on cultured human fibroblasts. This defect in binding to the LDL receptor was not due to an impaired lipid binding capability. The clinical symptomatic type III hyperlipoproteinaemia of our patient is probably due to a functionally inactive apo E3.
Quality control in parathyroid hormone radioimmunoassays: a multicentre study performed by the European Parathyroid Hormone Study Group
Authors: MINNE HELMUT W. 
Published: March 2008

Abstract. This paper reports the results of the second collaborative study of radioimmunological parathyroid hormone (PTH) determination in twenty‐two serum samples, performed by twenty‐four laboratories in the European PTH Study Group (EPSG). It demonstrates that radioimmunoassay systems can yield results that are clinically relevant in the differential diagnosis of hypercalcaemia. However, it also emphasizes, that numerical values, generated by a spectrum of different immunoassay systems cannot be compared directly. Numerical values can be compared, if the same reagents and method, provided as a kit, are used.Using their ‘in house’ reagents, fourteen out of twenty laboratories discriminated between low and normal iPTH serum, eleven of them between normal and marginal hyperparathyroid sera, seventeen of them between normal and grossly hyperparathyroid sera. Four laboratories agreed to a ranking order of serum samples, which was expected to cover all ranges on an average standard calibration curve, six were mistaking once, and ten two or more times.Using the kit, all participants but one discriminated between sera with low, normal, marginal and grossly elevated PTH and all agreed to the above ranking order of these sera.As far as these criteria are concerned, there was no relation between the quality of results, obtained with ‘in house’ reagents, and differences in antisera (but one, which was an anti human 1–34 PTH antiserum), methods of tracer preparation, and peptides used for tracer preparation. But only few laboratories, using bovine PTH standards were able to satisfy the above described conditions, whereas all of the laboratories, using human PTH standard preparations, did so with minor exceptions.
Infusion of cholecystokinin octapeptide in man: relation between plasma cholecystokinin concentrations and gallbladder emptying rates
Authors: MATON PAUL N. , SELDEN A. CLARE , FITZPATRICK MARGARET L. , CHADWICK VINTON S. 
Published: March 2008

Abstract. To establish the sensitivity of the gallbladder in relation to plasma concentrations of cholecystokinin, a dose‐response study was performed in five normal volunteers. Cholecystokinin octapeptide was infused in ascending incremental dose sequence, interval blood samples taken for estimation of plasma hormone concentrations and gallbladder emptying rates monitored continuously using 99mTc‐HIDA. In five other volunteers, gallbladder emptying rates following a liquid fat meal were measured. Infusion rates of 0·0, 0·75 ± 0·2, 6·8 ± 0·5, 23·8 ± 1·6 and 66·1 ± 2·5 pmol cholecystokinin kg‐1h‐1 produced plasma concentrations of <3·0 (undetectable), <3·0, 6·6 ± 1·8, 13·3 ± 1·5 and 26·9 ± 2·9 pmol l‐1 respectively and gallbladder emptying rates (% min‐1) of 0·0, 0·0, 0·14 ± 0·15, 1·57 ± 0·38 and 4·29 ± 1·12. Following the fat meal, peak plasma cholecystokinin concentrations reach 30 pmol l‐1 and gallbladder emptying rates (% min‐1) are 3·86 ± 1·01.We conclude that the threshold of the gallbladder to circulating cholecystokinin octapeptide is around 6 pmol l‐1, but that infusions which result in plasma levels of around 25 pmol l‐1 produce gallbladder emptying rates comparable with those seen after oral fat. This suggests that the gallbladder is equally sensitive to endogenous and exogenous cholecystokinin and that plasma concentrations observed after oral fat can entirely account for the gallbladder response.
Beta‐adrenergic regulation of cyclic adenosine 3‘,5’ monophosphate accumulation in human gastric epithelial glands. Inhibitory effect of somatostatin
Authors: BOIGE N. , DUPONT C. , CHENUT B. , GESPACH C. , ROSSELIN G. 
Published: March 2008

Abstract. The action of catecholamines and somatostatin on cyclic adenosine 3′,5′ monophosphate (cyclic AMP) formation in human isolated gastric glands is reported.We show that: (1) there is a beta 2 receptor‐mediated stimulation of cyclic AMP production in fundus. Catecholamines act with the order of potencies isoproterenol (ED50= 50 nmol l‐1) > epinephrine (ED50= 0·1 μmol l‐1) > norepinephrine (ED50= 5 μmol l‐1). Their action is completely reversed by propranolol at doses 103 times lower than practolol, while unaffected by phentolamine; (2) isoproterenol and Vasoactive Intestinal Peptide (VIP) have additive effects on cyclic AMP in fundic glands whereas no additivity is observed between histamine and isoproterenol; this, together with the absence of catecholamine effect in antral glands, suggests that the beta 2 receptor is located on parietal cells; (3) somatostatin (1 μmol l‐1) non‐competitively inhibits the stimulation by catecholamines but does not affect VIP and histamine stimulations.These results suggest a physiological stimulatory effect of catecholamines on gastric acid secretion in man, through a beta 2 receptor coupled to the cyclic AMP system, regulated by somatostatin.
Triglyceride metabolism in human liver: studies on hepatic phosphatidic‐acid phosphatase in obese and non‐obese subjects
Authors: BJÖRKHEM INGEMAR , ANGELIN BO , BACKMAN LARS , LILJEQVIST LARS , NILSELL KLAS , EINARSSON KURT 
Published: March 2008

Abstract. According to current concepts, soluble phosphatidic‐acid phosphatase, converting phosphatidic acid into a diglyceride, is a rate‐limiting enzyme in the hepatic biosynthesis of triglycerides. The present paper is the first report on this enzyme in human liver. The enzyme activity was assayed in ammonium sulphate precipitates of cytosol obtained from human liver biopsies. The activity was stimulated by preincubation with alkaline phosphatase and inhibited by Mg‐ATP, suggesting that phosphorylation‐dephosphorylation may be of some importance for the expression of the activity of the enzyme. When assayed under optimal conditions, the activity obtained in liver biopsies from normal‐weight gallstone patients averaged 12·8 ± 2·0 nmol min‐1 (mg protein)‐1 (mean ± SEM) (n= 17). The enzyme activity was slightly higher in liver biopsies from morbidly obese subjects 16·4 ± 2·8 nmol min‐1 (mg protein)‐1 (n= 14). The difference between the two groups of subjects was probably in part sex‐dependent and was not statistically significant. A similar small and insignificant difference between the two groups of subjects was found when the enzyme activity was assayed in the maximally stimulated state—i.e. after incubation with alkaline phosphate.These findings suggest that an increased capacity of the soluble phosphatidic‐acid phosphatase is not of major importance for the increased triglyceride synthesis known to occur in obesity. Other factors (i.e. availability of substrate and cofactors) may be of greater importance.
Early changes in sodium and water balances in patients with acute myocardial infarction: relationship to haemodynamics and creatine kinase
Authors: COL JACQUES , PETEIN MARC , EYLL CHRISTIAN VAN , CHERON PAUL , CHARLIER ANDRÉ A. , POULEUR HUBERT 
Published: March 2008

Abstract. The changes in sodium and water balances during the first 4 days after an uncomplicated transmural myocardial infarction (MI) were determined in forty patients. The sodium balance was positive 4 days after MI in 80% of the patients but negative in 20%. Neither in anterior (n= 23) nor in inferior (n= 17) MI were rank correlations found between the haemodynamic parameters (cardiac index, mean arterial pressure, mean right atrial or pulmonary capillary pressures, right or left ventricular work indices) and sodium balance. However, the sodium balances correlated with the total creatine kinase (CK) release in anterior MI after 1 day (r= 0·60; P < 0·002) and after 4 days (r= 0·65; P < 0·001) but not in inferior MI. Furthermore, in anterior and inferior MI matched for their CK release, the sodium handling was different both after 1 day (– 70 in anterior v.+ 44 mmol (24 h)‐1 in inferior MI; P < 0·001) and after 4 days (–36 v.+ 147 mmol (72 h)‐1; P < 0·01), a difference unexplained by differences in medical management or in sodium intake. Finally, sodium balance correlated with the changes in left ventricular stroke work index (LVSWI) observed during this period (r= 0·48, P < 0·001), LVSWI being more stable when sodium balance was more positive.In conclusion, sodium balance after uncomplicated acute MI is related to MI location, to the size of anterior MI, and cannot be predicted from initial haemodynamics. Finally, the relation between LVSWI stability and positive sodium balance suggests that arbitrary sodium restrictions or diuretics might be deleterious to the haemodynamics after uncomplicated myocardial infarction.
Blood acetaldehyde concentration gradient between hepatic and antecubital venous blood in ethanol‐intoxicated alcoholics and controls*
Authors: NUUTINEN H. U. , SALASPURO M. P. , VALLE M. , LINDROS K. O. 
Published: March 2008

Abstract. After ethanol (0·8 g kg‐1 body weight orally) significant concentrations of acetaldehyde (2–20 μmol l‐1) were found in hepatic venous blood of moderately intoxicated non‐alcoholic male Caucasians in spite of the absence of detectable levels (<2 μmol l‐1) in simultaneously taken antecubital blood. In thirteen chronic lcoholics the elevation of blood acetaldehyde was more constant in the hepatic than in the peripheral vein.Fructose infusion caused a marked elevation of acetaldehyde both in the hepatic and peripheral vein of four controls, but not of four alcoholics, who eliminated ethanol about 50% faster than controls. The rate of disappearance of acetaldehyde from sampled and in vitro incubated hepatic venous blood was similar to that observed after addition of acetaldehyde in vitro to ethanol‐free control blood (2 nmol ml‐1 min‐1 at 20 μmol l‐1 acetaldehyde; Km about 30 μmol l‐1). Uptake of acetaldehyde in blood was calculated to explain maximally 30–40% of the concentration gradient between central and peripheral blood.
Effects of physical exercise on serum calcium and parathyroid hormone
Authors: LJUNGHALL SVERKER , JOBORN HENRIK , BENSON LARS , FELLSTRÖM BENGT , WIDE LEIF , ÅKERSTROM GÖRAN 
Published: March 2008

Abstract. The effects of physical exercise on plasma ionized calcium, total serum calcium and parathyroid hormone (PTH) concentrations were evaluated in healthy subjects submitted to work on an ergometer bicycle.When the workload was increased stepwise there was a significant increase (P < 0·001) in the calcium concentrations (ionized calcium from 1·13 pL 0·03 (SD) to 1·24 pL 0·03 mmol l‐1 and total calcium from 2·35 pL 0·07 to 2·48 pL 0·07 mmol l‐1) when the workload exceeded approximately 65% of the estimated maximum—i.e. a load that caused accumulation in blood of lactic acid. The rise in plasma ionized calcium was, therefore, presumably largely attributed to the acidosis but reduction of plasma volume and influx from extracellular sources might also have contributed.Beta blockade (with oral intake of propranolol) reduced physical capacity, shortened the duration of work and caused less acidosis. These factors were probably responsible for a smaller rise in ionized calcium during beta blockade (7 pL 4%) than in control studies (21 pL 5%) without medication in subjects examined during short‐term maximal exercise.Long‐term (1 h) steady‐state work which caused fatigue without producing lactic acidosis did not affect the calcium concentrations.Despite the effects of work on calcium levels there was no discernible suppression of the PTH concentrations. This might have been due to a concomitant stimulation of PTH secretion by work.
Effect of carbamazepine on haem biosynthesis in man
Authors: RAPEPORT W. G. , CONNELL J. C. , THOMPSON G. G. , MOORE M. R. , BRODIE M. J. 
Published: March 2008

Summary. The effects of the enzyme‐inducing anticonvulsant carbamazepine on haem biosynthesis in healthy male subjects is reported. A dose‐dependent increase in the activity of leucocyte δ‐aminolaevulinicacid synthase, the rate‐limiting enzyme of haem biosynthesis, was noted following 400 and 600 mg carbamazepine daily in the same eight subjects. This rise was maximal after 1 week's treatment (400 mg:509%± 285 of baseline; 600 mg: 1062%± 170 of baseline; P < 0·01). Values fell from this peak during the second week despite continuing carbamazepine administration. This pattern was confirmed in a further six subjects taking carbamazepine 400 mg daily for 3 weeks in whom more frequent enzyme measurements were made. The activity of uroporphyrinogen‐1‐synthase in the erythrocyte fell by 10–15% during the treatment periods (P < 0·01). Uroporphyrin and penta‐, hexa‐ and hepta‐carboxylic porphyrins appeared in the urine of all subjects during CBZ therapy. Changes in daily urinary porphyrin and precursor excretion were inconsistent.CBZ is a porphyrinogenic drug which mimics the changes in enzyme activities and urinary porphyrin ester profile found in patients with latent acute intermittent porphyria, who have a genetic deficiency in uroporphyrinogen‐1‐synthase activity. Leucocyte δ‐aminolaevulinic‐acid synthase may provide a suitable in vivo system for testing the porphyrinogenicity of drags in man.
Defective renal water excretion in nephrotic syndrome: the relationship between renal water excretion and kidney function, arginine vasopressin, angiotensin II and aldosterone in plasma before and after oral water loading
Authors: PEDERSEN E. B. , DANIELSEN H. , MADSEN M. , JENSEN T. 
Published: March 2008

Abstract. An oral water load of 20 ml (kg body wt)‐1 was given to seventeen patients with the nephrotic syndrome and fifteen healthy control subjects. Diuresis (D), free water clearance (CH2O), plasma concentrations of arginine vasopressin (AVP), angiotensin II (AII) and aldosterone (Aldo) were determined before and 3 times during the first 4 h after loading. In the nephrotic syndrome D was significantly lower 1–2 h after loading than in the control subjects, predominantly due to a lower CH2O (2·61 and 7·01 ml min‐1 (medians), P < 0·01).Creatinine clearance and the maximum increase in CH2O were significantly correlated in patients with the nephrotic syndrome (ρ= 0·721, n= 17, P < 0·01) and the control subjects (ρ= 0·596, n= 15, P < 0·01). AVP was reduced in both groups during loading, but AVP was clearly elevated in the patients with the nephrotic syndrome when compared to the control subjects both before (3·0 and 1·9 pmol 1‐1, P < 0·01) and during loading. There was a significantly negative correlation between CH2O and AVP in both groups. AII and Aldo were reduced during loading, but the levels were the same in the patients and in the control group, and AII and Aldo were not correlated to CH2O. It is concluded that patients with the nephrotic syndrome excrete an oral water load more slowly than healthy control subjects, and that this phenomenon partly is due to reduced glomerular filtration rate and partly to increased AVP.