bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lack of correlation between endotoxaemia and renal hypoperfusion in cirrhotics without overt renal failure
Authors: GATTA A. , MILANI L. , MERKEL C. , ZUIN R. , AMODIO P. , CAREGARO L. , RUOL A. 
Published: March 2008

Abstract. Renal involvement in patients with liver cirrhosis is characterized by renal vasoconstriction, the aetiology of which remains obscure. Endotoxaemia, frequently found in patients with liver cirrhosis and renal failure, has been emphasized as a pathogenic factor.In fifty‐seven patients with liver cirrhosis without overt renal failure endotoxin plasma level (Limulus Lysate test), mean renal blood flow (MRBF) (133Xe washout technique), and effective renal plasma flow (ERPF) (p‐aminohippurate clearance) were determined.MRBF was decreased in nineteen out of twenty‐seven patients, averaging 1·88 ± 0·51 ml g‐1min‐1 (in fourteen controls 3·17 ± 0·51 ml g‐1ml‐1). ERPF was decreased in seventeen out of thirty patients, averaging 380±164 ml/min (in eighteen controls 624±127 ml/min). Systemic endotoxaemia was found in sixteen out of fifty‐seven patients, levels ranging from 0·62 to 200 ng/ml. No significant difference in renal blood flow values was found between patients with and without endotoxaemia (MRBF = 1·78 ± 0·51 and 1·93 ± 0·52 ml g‐1min‐1 respectively; ERPF = 429±119 and 365±175 ml/min respectively). No significant difference in the frequency of endotoxaemia was found between patients with impaired and unimpaired renal blood flow. Moreover no relation was found between endotoxin plasma levels and MRBF and ERPF respectively.In conclusion in patients with cirrhosis without overt renal failure renal vasoconstriction does not seem to be related to endotoxaemia.
Reversal of decreased hepatic lipase and lipoprotein lipase activities after treatment of hypothyroidism
Authors: VALDEMARSSON STIG , HEDNER PAVO , NILSSON‐EHLE PETER 
Published: March 2008

Abstract. Plasma lipoprotein concentrations, activities of hepatic lipase and lipoprotein lipase in post‐heparin plasma, and the removal rate of exogenous triglyceride were measured in fourteen patients with severe primary hypothyroidism before and after 4 months substitution therapy with 1‐thyroxine. Before treatment plasma LDL cholesterol concentrations were markedly increased while HDL cholesterol and plasma triglycerides were in the upper reference range. Thyroxine substitution led to a normalization of LDL cholesterol in all patients. Plasma triglycerides and HDL cholesterol decreased moderately. Hepatic lipase and lipoprotein lipase activities were initially reduced but increased significantly after treatment, by about 170% and 55%, respectively. The increase in hepatic lipase activities was significantly correlated to the increase in serum triiodothyronine levels and also to the reduction in LDL cholesterol concentrations. The decrease in LDL cholesterol was also significantly correlated to the increase in serum triiodothyronine concentration.In two patients initially treated with triiodothyronine, the activity of hepatic lipase, but not that of lipoprotein lipase, increased after 24 and 48 h, while LDL cholesterol levels decreased substantially.We suggest that the reduced activities of hepatic lipase as well as of lipoprotein lipase are important pathogenetic factors for the dyslipoproteinaemia occurring in hypothyroidism and that the low serum triiodothyronine concentration is of major importance for the alterations in lipid transport.
Plasma levels of false neurotransmitters across the brain in portal‐systemic encephalopathy
Authors: CANGIANO CARLO , FARBER MARK O. , CARDELLI‐CANGIANO PATRIZIA , ROSSI‐FANELLI FILIPPO , CASCINO ANTONIA , CAPOCACCIA LIVIO , COCKERILL EDWARD M. , MANFREDI FELICE 
Published: March 2008

Abstract. Arterial and internal jugular venous levels of false neurotransmitters (FNTs: octopamine, OCT, and phenylethanolamine, PEA), aromatic and branched‐chain amino acids, glutamine, ammonia, and pH were measured in patients with portal‐systemic encephalopathy (PSE) and in appropriate controls to define the role of these parameters in the pathogenesis of hepatic coma. The typical plasma patterns reported in the literature were observed: hyperammonaemia (59 ± 8 μmol/l v. controls 30 ± 4, P < 0.005), elevated OCT (19 ± 3 nmol/l v. 6 ± 1, P < 0.001) and PEA (64 ± 8 nmol/l v. 27 ± 3, P < 0.001), high ratio of aromatic to branched‐chain amino acids (0.92 ± 0.12 v. 0.32 ± 0.04, P < 0.005), and variable glutamine levels (216–734 μmol/l). No consistent net flux into or out of the brain could be demonstrated for any of these substances. The degree of encephalopathy correlated with the level of respiratory alkalosis (r= 0.325, P < 0.05) which, in turn, correlated with the degree of elevation of plasma OCT (r= 0.439, P < 0.05) and PEA (r= 0.489, P < 0.05) as well as with the excess of glutamine efflux from the brain (r= 0.927, P < 0.05).These findings support current views that hyperammonaemia, plasma amino acid imbalance, and elevated production of FNTs are interrelated disturbances which contribute to the pathogenesis of PSE. In addition, the data suggest that alkalosis accentuates the altered metabolism of these substances within the brain.
Stimulation of gastric mucus output by somatostatin in man
Authors: JOHANSSON C. , ALY A. 
Published: March 2008

Abstract. Effects of i.v. somatostatin on the gastric mucus output during a 60 min infusion of pentagastrin were examined in five healthy subjects. Experiments were also made with prior indomethacin administration to suppress the synthesis of endogenous prostaglandins. N‐acetyl neuraminic acid, a sialic acid, was measured in the gastric aspirates as an index of gastric mucus.Somatostatin increased significantly the gastric mucus output in a dose‐related way. The output increased to 158 ± 14% and 216 ± 24% of the control level by 1 and 2 μg kg‐1 h‐1 somatostatin, respectively. The increase induced by somatostatin was prevented by prior indomethacin. With indomethacin alone the mucus output was not different from in controls.Thus somatostatin has augmentory effects on the gastric mucus, which can be blocked by indomethacin, indicating that endogenous prostaglandins are involved in the augmentation.Somatostatin prevents stress ulcerations in the rat, assumedly by inhibiting the gastric acid secretion. This study suggests that additional mechanisms may contribute to the protective action of somatostatin on the gastric mucosa.
Fish eye disease: a new familial condition with massive corneal opacities and dyslipoproteinaemia Clinical and laboratory studies in two afflicted families
Authors: CARLSON LARS A. 
Published: March 2008

Abstract. Fish eye disease (FED) is characterized by severe corneal opacities, causing impaired vision, and dyslipoproteinaemia: hypertriglyceridaemia, raised levels of very low density lipoproteins (VLDL), triglyceride enrichment of low density liproteins (LDL) and reduction of high density lipoproteins (HDL). The disease is described in two unrelated families. In both there was a high proportion of low HDL in relatives without eye disease.VLDL, LDL and HDL had normal electrophoretic mobilities. The concentrations of VLDL cholesterol and triglycerides were increased fivefold. LDL cholesterol levels were normal but LDL triglycerides markedly increased. HDL cholesterol was reduced by 90% as were the levels of HDL apolipoproteins. The major part of HDL cholesterol was in the HDL3 fraction. FED HDL were smaller than normal with molecular weights of 115,000 daltons.Lecithin: cholesterol acyltransferase activity and amount of cholesterol esters in serum were normal. Postheparin lipoprotein and hepatic lipases showed normal or subnormal values.Clinically FED differs from other familial conditions with deficiency of HDL such as Tangier disease, LCAT‐deficiency and Milano‐AI‐apoprotein disease. In spite of the extremely low HDL cholesterol FED is not characterized by premature atherosclerosis. Mechanisms for the dyslipoproteinaemia are discussed.
The effect of oxprenolol and indomethacin on renin and aldosterone of normal subjects during low sodium diet
Authors: PEDRINELLI R. , MAGAGNA A. , SALVETTI A. 
Published: March 2008

Abstract. To study the mechanisms underlying renin and aldosterone increase during low sodium diet, eight normal subjects were studied during normal sodium diet (5 g of NaCl per day) for 5 days, after 4 days of low sodium diet, and, on continuing low sodium diet, after randomized treatment with oxprenolol (100 mg), indomethacin (200 mg) and oxprenolol + indomethacin (100 + 200 mg) each given for 24 h with a 48 h interval between each treatment.Renin (PRA) increased significantly after low sodium diet and the increase was inversely related to urinary sodium excretion.Both oxprenolol and indomethacin significantly reduced PRA to values similar to those during normal sodium intake, while the combination of the two drugs showed a net additive effect on PRA. PRA decrements after either oxprenolol or indomethacin were significantly related to PRA values after low sodium diet while no correlation was present between PRA values after oxprenolol and indomethacin.Aldosterone excretion showed a trend similar to that of PRA, being related to PRA on normal and low sodium diet, and to a lesser extent after drug treatment. These studies suggest that both the sympathetic nervous system and prostaglandins may play a permissive role in the regulation of renin and aldosterone of normal subjects on low sodium diet.
Serum thyroglobulin and its autoantibody following subtotal thyroid resection of Graves' disease
Authors: FELDT‐RASMUSSEN ULLA , BLICHERT‐TOFT M. , CHRISTIANSEN C. , DATE J. 
Published: March 2008

Abstract. Thyroid surgery leads to marked changes of the levels of serum thyroglobulin and its autoantibodies in the subsequent 3 postoperative weeks. Furthermore in Graves' disease progression of exophthalmos has sometimes been seen following thyroidectomy.Nineteen medically pretreated patients with Graves' disease and no signs of exophthalmos were studied systematically up to 6 months postoperatively. Nine patients had thyroglobulin antibodies. Mean values rose to 3·5 times pretreatment values within 2 months (P < 0·001) followed by a gradual fall below pretreatment level after 6 months. None of the antibody negative patients reverted to positive or vice versa. Serum thyroglobulin (n= 10) was elevated preoperatively (mean 309 μg/l, SD 251), their values being normalized within 1–2 months (mean 19·4 μg/l, SD 7·3). The preoperative serum thyroglobulin correlated to the weight of the removed thyroid tissue (r= 0·87, P < 0·01). Three patients showed elevated thyroid stimulating hormone after 1 month. Of these, two developed myxoedema, the third remained euthyroid with persistently elevated serum thyroglobulin. None showed recurrence or developed exophthalmos within the period of observation.In spite of rising levels of thyroglobulin antibodies in all patients with antibodies none developed exophthalmos and only one patient with thyroglobulin antibodies had clinical myxoedema.
Haemodynamics and myocardial metabolism of phosphorus depleted dogs: effects of catecholamines and angiotensin II
Authors: KREUSSER W. , VETTER H. O. , MITTMANN U. , HÖRL W. H. , RITZ E. 
Published: March 2008

Abstract. The responses of arterial pressure and myocardial contractile force (VPM) to infusion of angiotensin II, noradrenaline and orciprenaline were examined in twelve dogs during a control phase, after 30 days of dietary phosphorus deprivation and after 21 days of phosphorus repletion. In the phosphorus depletion period, animals had low skeletal and heart muscle Pi content, low magnesium, ATP and creatine phosphate in skeletal and heart muscle with no change of ADP, AMP or energy charge. In the basal state, VPM was diminished with no change of end‐diastolic and systolic pressure. Infusion of angiotensin II caused a significantly smaller rise of arterial pressure (angiotensin II resistance), and the stimulatory effect of noradrenaline and orciprenaline on VPM was diminished (catecholamine resistance). These effects were reversible with Pi repletion.In phosphorus depletion, arterial concentrations were increased for lactate, unchanged for FFA and decreased for acetoacetate/beta‐hydroxybutyrate. Unchanged myocardial extraction of lactate or beta‐hydroxybutyrate and preserved cell Pi uptake for glycogenolysis were observed. The initial rate of uptake of calcium and concentrating ability of myocardial sarcoplasmic reticulum were unchanged.
Diurnal metabolic profiles in hyperthyroidism
Authors: McCULLOCH A. J. , JOHNSTON D. G. , BURRIN J. M. , HODSON A. W. , CLARK F. , WAUGH C. , ALBERTI K. G. M. M. 
Published: March 2008

Abstract. Hormone and metabolite profiles during a 12 h period of normal meals and activity were examined in nine hyperthyroid subjects with Graves' disease and sixteen matched controls. Six hyperthyroid subjects were restudied when euthyroid on carbimazole and thyroxine. Thyrotoxic patients had mild fasting hyperglycaemia (mean pL SEM blood glucose, 5·5 pL 0·2 v. 4·8 pL 0·1 mmol/l, P < 0·01), elevated blood glycerol (0·15 pL 0·02 v. 0·08 pL 0·01 mmol/l, P < 0·001) and elevated plasma non‐esterified fatty acid (NEFA) concentrations (0·91 pL 0·06 v. 0·58 pL 0·03 mmol/l, P < 0·001) when compared to controls. Fasting blood concentrations of the gluconeogenic precursors lactate, pyruvate and alanine, blood ketone body concentrations and circulating insulin and growth hormone levels were similar in hyperthyroid and control subjects. Blood glucose responses to meals were exaggerated and the mean 12 h blood glucose was increased (6·1 pL 0·1 v. 5·5 pL 0·1 mmol/l, P < 0·01) in hyperthyroidism. Similarly, hyperlactataemia and hyperpyruvicaemia were observed after meals. Blood ketone body, blood glycerol and plasma NEFA levels showed exaggerated pre‐prandial peaks and the mean 12 h values for blood glycerol (0·12 pL 0·01 v. 0·08 pL 0·01 mmol/l, P < 0·01) and plasma NEFA (0·71 pL 0·03 v. 0·53 pL 0·04 mmol/l, P < 0·01) were increased. Concentrations of insulin and growth hormone remained similar to control values throughout the study period. Blocking therapy with carbimazole and thyroid hormone replacement with thyroxine for 5–10 months suppressed blood glycerol, plasma NEFA and blood ketone body levels to normal or subnormal values but had no effect on the elevated blood glucose, blood lactate or blood pyruvate profiles.Graves' disease with hyperthyroidism is thus associated with abnormalities of carbohydrate metabolism which are not restored to normal by 5–10 months oral antithyroid therapy. The changes in lipid metabolism in hyperthyroidism are normalized by this treatment.
The effect of respiratory and metabolic acid‐base changes on ionized calcium concentration: in vivo and in vitro experiments in man and rat
Authors: OBERLEITHNER HANS , GREGER RAINER , LANG FLORIAN 
Published: March 2008

Abstract. Correlation of ionized calcium concentration, [Ca2+] and blood pH has long been recognized. So far no distinction of the acid‐base changes, i.e. respiratory changes or metabolic changes seemed necessary. The present study, with the use of a recently developed system for in vivo analysis of [Ca2+], and with in vitro experiments reinvestigates this question.In a first series respiratory and metabolic changes were induced in rats. Changes of [Ca2+] (Δ[Ca2+]) and of plasma pH (ΔpH) were recorded continuously in vivo, plasma bicarbonate, [HCO‐3] was measured in vitro. In a second series respiratory and metabolic changes were induced in sixteen volunteers and, separately, in vitro in plasma and modified Ringer solution, and the same parameters were determined.In all experiments Δ[Ca2+] correlates negatively with ΔpH. However, the correlation in respiratory changes was significantly less as compared to that in metabolic changes. As expected, Δ[HCO‐3] correlates positively with pH in metabolic and negatively in respiratory changes. We conclude from these experiments that in metabolic changes the effects of calciumalbumin interaction and calcium complexation with bicarbonate are additive, whereas both effects oppose each other in respiratory changes. This might explain the blunted effect of pH changes on [Ca2+] in respiratory changes.
Effect of catecholamines on sterol synthesis in human mononuclear cells
Authors: KRONE W. , HILDEBRANDT F. , GRETEN H. 
Published: March 2008

Abstract. The effect of adrenaline, noradrenaline, isoproterenol and dibutyryl cyclic AMP on the rate of sterol synthesis was studied in freshly isolated human mononuclear cells.Incubation of cells in a medium containing lipid depleted serum led to a two‐fold rise in the rate of sterol synthesis from [14C]acetate. Adrenaline, noradrenaline and isoproterenol added in a concentration of 2 × 10‐5 mol/l at zero‐time resulted in an inhibition of 30% of this increase in sterol synthesis after 4 h, but had no effect when the hormones were given at 4 h. This indicates that the catecholamines require some time to exert their inhibitory action on sterol synthesis.The action of catecholamines on the incorporation of [14C]acetate into sterols could be mimicked by dibutyryl cyclic AMP. Propranolol added in increasing concentrations to the incubation medium diminished or totally prevented the inhibitory effect of adrenaline, noradrenaline and isoproterenol on sterol synthesis.The results indicate that cholesterol synthesis in extrahepatic human cells, regulated predominantly by low density lipoprotein derived from plasma, is under additional control of catecholamines which may act via cyclic AMP.
Adrenergic regulation of fat‐cell lipolysis in multiple symmetric lipomatosis
Authors: KATHER HORST , SCHRÖDER FRIEDHELM 
Published: March 2008

Abstract. The responsiveness towards catecholamines of normal and lipomatous fat cells of two male subjects suffering from multiple symmetric lipomatosis has been studied by means of a newly developed bioluminescent method for microdetermination of glycerol.In contrast to previous findings, lipomatous fat cells displayed normal α2– and β‐adrenergic responsiveness in both subjects studied. The apparent discrepancies between the results of the present study and those reported by others therefore support the contention that multiple symmetric lipomatosis is a symptom with various underlying causes rather than a nosological entity.
Effect of vitamin B6 administration on elevated plasma oxalic acid levels in haemodialysed patients
Authors: BALCKE P. , SCHMIDT P. , ZAZGORNIK J. , KOPSA H. , DEUTSCH E. 
Published: March 2008

Abstract. Accumulation of oxalic acid resulting in elevated plasma levels is a common finding in uraemic patients. Since vitamin B6 is an important coenzyme in oxalic acid metabolism the influence of vitamin B6 administration on plasma oxalic acid levels was investigated.Vitamin B6 was administered to eight chronic haemodialysis patients with secondary hyperoxalaemia. Mean plasma oxalic acid concentration decreased from 149·5 ± 67 μmol/l to 99·0 ± 36·4 μmol/l within 2 weeks and to 93·8 ± 33·1 μmol/l after 4 weeks of pyridoxine treatment (P<0·01) the mean reduction being 46% (32·0–56·1%). The decrease in plasma oxalic acid levels was most pronounced in patients with the highest pretreatment values. Two patients who received pyridoxine therapy prior to the beginning of the study had low initial values of plasma oxalic acid concentrations and showed no further decline.
Relationship between muscle morphology and metabolism in obese women: the effects of long‐term physical training
Authors: KROTKIEWSKI M. , BYLUND‐FALLENIUS A‐C. , HOLM J. , BJÖRNTORP P. , GRIMBY G. , MANDROUKAS K. 
Published: March 2008

Abstract. To evaluate the relationships between changes in muscle morphology and metabolic adaptation to physical training in obesity, twenty obese women were subjected to a physical training pro‐gramme with three sessions a week for 3 months. Physical training resulted in lowering of plasma insulin and improved glucose tolerance. Neither body weight nor body fat changed. With physical training the percentage distribution of fast twitch oxidative (FTa) muscle fibres (m vastus lateralis) increased (from 30.3±5.1% to 35.2±4.8%, P < 0.05) and that of fast twitch glycolytic fibres decreased (from 18.3±6.6 to 5.8±4.8%, P <0.05). The number of capillaries increased, mainly around slow twitch (ST) fibres (from 4.5±0.6 to 5.8±0.8, P < 0.01) and fast twitch oxidative (FTa) fibres (from 3.9±0.7 to 4.7±0.8, P <0.01). The activities of oxidative enzymes (cytochrome‐c‐oxidase and citrate synthase) increased (P<0.05) while those of glycolytic enzymes (phosphofructokinase and hexokinase) decreased after physical training (P<0.01).Significant negative correlations between plasma insulin and number of capillaries in contact with ST fibres (r=0.80, P<0.001) and FTa fibres (r= 0.62, P<0.001) were found before training. The capillary density around those fibres could predict 80% of the explained variance of plasma insulin levels (P<0.001). The changes of glucose concentration after training could be predicted by observed changes in enzyme activities. The strong associations between muscle morphology and capillarization and enzyme activities and glucose and insulin concentrations and their changes after training suggest an important regulatory role of muscle which warrants further studies.
The urinary excretion of prostaglandins E2 and F2α in essential hypertension
Authors: RATHAUS MAURO , KORZETS ZEEV , BERNHEIM JACQUES 
Published: March 2008

Abstract. The 24 h urinary excretions of prostaglandins E2 (E2/d) and F2α (F2α/d) were measured in twenty‐five normal subjects and in thirty‐five patients with essential hypertension [seventeen with low renin (LRH) and eighteen with normal renin (NRH) hypertension].E2/d was lower in patients with LRH than in normal subjects (P<0.01), whereas no difference was found between patients with NRH and the controls. F2α/d was similar in patients with LRH and in the normal subjects, but was significantly greater in patients with NRH (P<0.02). The ratio of prostaglandin E2 to prostaglandin F2α was decreased in hypertensive patients (P < 0.02), although in the NRH subgroup the difference was not statistically significant.It appears that LRH is associated with impaired production of prostaglandin E2, while a deranged relationship between the two prostaglandins exists in all the patients with essential hypertension. These changes in prostaglandin production could possibly contribute to the pathogenesis of hypertension, by increasing renal vascular resistance and decreasing sodium excretion. Alternatively, they might be a secondary phenomenon, reflecting changes in renal prostaglandin metabolism induced by the hypertensive state.
Peripheral blood cell changes in response to acute hypoglycaemia in man
Authors: FRIER B. M. , CORRALL R. J. M. , DAVIDSON N. McD. , WEBBER R. G. , DEWAR A. , FRENCH E. B. 
Published: March 2008

Abstract. Peripheral white and red blood cell changes were studied in response to acute insulin‐induced hypoglycaemia in six normal, six splenectomized and five sympathectomized (tetraplegic) subjects. The normal subjects were restudied during beta (propranolol) and beta1‐selective (metoprolol) adrenergic blockade.In the normal subjects a lymphocytosis immediately followed the acute hypoglycaemic reaction (R) with a neutrophilia 2 h later. The early lymphocytosis was absent in sympathectomized subjects (P<0.01) and reduced under beta blockade (P<0.02) in normal subjects, indicating mediation via an adrenergic mechanism. The later neutrophilia from R + 60 min was not abolished by adrenergic blockade or preceding sympathectomy; the enhanced response with propranolol was associated with an elevated plasma Cortisol.Haemoglobin, packed cell volume and total erythrocyte count rose maximally at R in all groups except the sympathectomized subjects in whom all parameters declined progressively from basal values. These peripheral erythrocyte changes appear to be mediated via an adrenergic mechanism which is unaffected by beta adrenergic blockade and which does not involve splenic contraction.