bluuebunny/crossref_metadata_2025_split huggingface dataset:
Human gastric mucosal adenylate cyclase activity: effects of various cytoprotective prostaglandins
Authors: SIMON BERND , KATHER HORST 
Published: March 2008

Abstract. Several prostaglandins prevent ulcer formation (called cytoprotection) by a mechanism other than inhibition of gastric acid secretion. One suggestion is that they increase cyclic AMP in non‐parietal cells.A variety of prostaglandins with potent cytoprotective properties were tested for their capacity to modulate adenylate cyclase activity in homogenates of human gastric mucosa. Prostaglandin E2, prostacyclin (PGI2) and 15(S)‐methyl‐PGE2 stimulated the cyclase in human gastric mucosal biopsy specimens in a dose‐dependent manner. Cytoprotective prostaglandins without antisecretory properties such as PGF2 β were also able to activate the enzyme system dose‐depen‐dently. In contrast, cytoprotective prostaglandins such as PGD2, the PGE1‐analogue, SC‐29333, and the pro‐staglandin‐like compound C83 did not stimulate human gastric adenylate cyclase. Whereas PGD2 did not modulate enzyme activity at all, SC‐29333 and C83, at concentrations greater than 10 µmol/l, inhibited basal and PGE2‐stimulated enzyme activities. These studies suggest that cyclic AMP is not directly related to the cytoprotective effect of prostaglandins, at least in human gastric mucosa.
Effects of hypothyroidism and cholesterol feeding on the clearance of chylomicron remnants in vivo and by rat hepatocyte monolayers
Authors: FLORÉN CLAES HENRIK , NILSSON ÅKE 
Published: March 2008

Abstract. The hepatic catabolism of chylomicron remnants in normal rats and in hypothyroid rats which were either normocholesterolaemic or made hypercholesterolaemic by feeding cholesterol and cholic acid was studied in vivo and in hepatocyte monolayers. In vivo, the clearance of injected chylomicron remnants labelled with either cholesteryl‐ or retinyl ester was delayed in the hypercholesterolaemic hypothyroid rats, but not in normocholesterolaemic hypothyroid rats.Cholesteryl‐ester‐rich hepatocytes from hypercholesterolaemic hypothyroid rats took up remnants less efficiently than did normal hepatocytes. Hepatocytes from normocholesterolaemic hypothyroid rats had a lower cholesteryl ester content and took up remant particles to a greater degree than did normal hepatocytes. When normal hepatocytes were incubated with hypercholesterolaemic serum or with mevalonolactone, which increased cell cholesteryl ester content, there was a slight suppression of remnant uptake. Also, addition of triiodothyronine to hepatocyte monolayers suppressed rather than increased uptake of chylomicron remants in hepatocytes.Thus, the study suggests that chylomicron remnant uptake by the liver is not inhibited by hypothyroidism per se but by the cholesterol accumulation in hepatocytes that is the consequence of cholesterol and bile acid feeding of the rats. Although the cholesteryl ester content in hepatocytes seems to determine remnant uptake, the regulation of uptake does not seem to be as effective as that of the LDL receptor in extrahepatic cells.
Influence of previous diuretic intake on the humoral and hormonal profile of idiopathic oedema
Authors: THIBONNIER M. J. , MARCHETTI J. P. , CORVOL P. L. , MENARD J. E. , SIRE O. G. , MILLIEZ P. L. 
Published: March 2008

Abstract. Three groups of women underwent water loading tests: normal subjects, idiopathic oedema patients who had taken no medication for at least 3 months, and a second oedema group with recent diuretic intake.Idiopathic oedema in drug‐free patients was characterized by an abnormal capillary permeability, lower basal protein values, a dramatic drop in urinary output in the upright position due to reduced glomerular filtration, enhanced reabsorption of sodium and water and stimulation of aldosterone and antidiuretic hormone (AVP) secretions. In these idiopathic oedema cases, osmolar AVP regulation was disrupted but AVP control by plasma volume was maintained.In the basal state, patients with recent diuretic intake were characterized by a gain in body weight and by depletion of plasma volume and plasma potassium. In these subjects, urinary output in the upright posture was as insufficient as in drug‐free patients but was due to higher sodium reabsorption. Renal insensitivity to AVP action was also observed. Osmolar regulation and volume regulation of AVP were both disrupted in these cases with recent diuretic intake.
Development of bone mineral loss in insulin‐treated diabetes: a 1 1/2 years follow‐up study in sixty patients
Authors: McNAIR P. , CHRISTIANSEN C. , CHRISTENSEN M. S. , MADSBAD S. , FABER O. K. , BINDER C. , TRANSBØL I. 
Published: March 2008

Abstract. The change in bone mass during 1 1/2 years was determined in a longitudinal study of sixty adult insulin‐treated diabetic out‐patients. During the study period the mean bone mass decreased by 1.30 ± 0.28 (SEM) % (P < 0.001), to a mean value of 91.0 ± 1.7% of normal (P < 0.001). The rate of bone loss was significantly higher in patients with 1–6 years of diabetes (n= 29, bone loss: 1.96 ± 0.32%/1 1/2 years) than in patients with longer duration of the disease (n= 31, bone loss: 0.61 ± 0.44%/l 1/2 years, P < 0.02). The endogenous insulin secretion estimated with the glucagonstimulated serum C‐peptide concentration decreased during the observation period in 58.6% of the patients with 1–6 years of diabetes compared to 16.1% among patients with 7–11 years of diabetes (P < 0.002). The rate of bone mineral loss was almost 3 times higher in the twenty‐two patients in whom endogenous insulin secretion had deteriorated (2.12 ± 0.30%/l 1/2 years) than in the thirty‐eight patients without as well as with unchanged or increased insulin secretion (0.78 ± 0.39%/l 1/2 years, P < 0.01). In twenty patients with an increased insulin dose during the study period the mean bone mineral loss was 2.05 ± 0.36%/l 1/2 years compared to a mean bone mineral loss of 0.91 ± 0.38%/l 1/2 years in the forty patients with unchanged or decreased insulin dosage (P < 0.05).This longitudinal study further supports the hypothesis that the bone mineral loss in insulin‐treated diabetic patients begins with the onset of clinical diabetes and that its development is associated with the deterioration of the beta‐cell function and with the increment in insulin dosage. The rate of bone mineral loss is high during the first few years of clinical diabetes, but levels off with increasing duration of the disease.
Role of the liver in the degradation of very low density lipoproteins: a study of lipolysis by heparin releasable liver lipase and uptake during isolated rat liver perfusion
Authors: BERRY E. M. , ALDINI R. , BARON H. , EISENBERG S. 
Published: March 2008

Abstract. The role of the liver and of a heparin‐releas‐able liver lipase in the metabolism of very low density lipoprotein (VLDL) was investigated in vitro and during recycling rat liver perfusion. Rat plasma VLDL and nascent hepatic VLDL were labelled biosyntheti‐cally in their lipid moieties. Incubation in vitro of VLDL with the lipase caused hydrolysis of VLDL‐tri‐glycerides (>80%) and VLDL‐phosphatidylcholine (> 30%). Nascent VLDL was a better substrate for the enzyme. The hydrolytic activities were inhibited by 70–90% when rat plasma (10–30 vol%) was added to the incubation mixture.VLDL‐triglycerides and cholesterol esters were taken up by the liver during 180 min recycling perfusion. The rate of disappearance of nascent VLDL was faster than that of plasma VLDL (half‐life times of 56.2 ±13.9 and 125.0±24.8 min respectively). Injection of heparin into the perfusion medium caused accelerated uptake of the hydrolysed VLDL‐triglycer‐ide by the liver. Addition of plasma (d> 1.006 g/ml) to the perfusion at a concentration of 10 vol% delayed the rate of disappearance of VLDL from the perfusate by about 50–75%.These studies have established the capacity of the hepatic lipase to hydrolyse VLDL‐lipids and the ability of the liver to degrade nascent and plasma VLDL particles. These two activities, however, are depressed by plasma and therefore previous studies of VLDL metabolism may have to be re‐examined when based on incubations or perfusions in the absence of plasma.
Clofibrate treatment and bile cholesterol saturation: short‐term and long‐term effects and influence of combination with chenodeoxycholic acid
Authors: ANGELIN BO , EINARSSON KURT , LEIJD BARBRO 
Published: March 2008

Abstract. In order to determine whether the clofibrate‐induced increase in bile cholesterol saturation is transitory, duodenal bile samples were analysed from sixteen hyperlipoproteinaemic patients before and after 6 months to 2 years treatment with clofibrate, 2 g daily. Standardized dietary and weight conditions were obtained. In all but two subjects cholesterol saturation remained elevated (150 ± 7%, mean ± SEM) compared to pretreatment values (112 ± 6%, P < 0.01).In nine of the patients, duodenal bile was obtained also after 6 weeks of treatment. Although two patients with increased saturation at 6 weeks displayed a return to basal values at 2 years, the majority showed no consistent changes between these two occasions.Addition of chenodeoxycholic acid to clofibrate medication led to a normalization of cholesterol saturation (from 145 ± 9 to 89 ± 18%, P < 0.01) in eight out of nine patients studied. The serum levels of total cholesterol and triglycerides, very low density lipopro‐tein and high density lipoprotein cholesterol were not significantly changed. However, the low density lipoprotein (LDL) cholesterol concentration was increased by 15–20% (from 4.8 ±0.3 to 5.7 ± 0.4 mmol/l, P <0.01).It is concluded that clofibrate induces changes in biliary lipid composition which are consistent over at least 2 years of treatment. Possible measures to avoid these effects must therefore also be taken over a prolonged time. Chenodeoxycholic acid prevents the lithogenic effect of clofibrate but it cannot presently be recommended as an adjunct to clofibrate treatment since it simultaneously causes a rise in the serum concentration of LDL‐cholesterol.
Gastro‐entero‐pancreatic hormones in normal pregnancy: response to a protein rich meal
Authors: HORNNES PETER J. , KÜHL CLAUS , LAURITSEN KELD B. 
Published: March 2008

Abstract. The plasma concentrations of gastrin, gastric inhibitory polypeptide (GIP), gut glucagon‐like‐immunoreactivity (gut GLI), insulin, glucagon, and pancreatic polypeptide (PP) were studied following the ingestion of a protein rich meal in late pregnancy and postpartum in 11 normal women. In pregnancy, the fasting plasma concentrations of glucose (mean ± SEM in pregnancy: 4.1 ± 0.1 mmol1‐1, postpartum: 4.7 ± 0.1 mmol1‐1, p<0.01), gut GLI (25± 3 v. 33± 2 pmol‐eqv 1‐1, P<0.01) and PP (7.9 ± 1.0 v. 13.0± 1.2 pmol 11, P<0.01) were decreased, gastrin and GIP unaltered, and insulin (90± 9 v. 72 ± 5 pmol 11, P<005) and glucagon (17±1 v. 13 ± 1 pmol 1‐1, P<0.01) increased.The gastrin, GIP and glucagon responses to the meal were unaffected by pregnancy, whereas the responses of gut GLI (integrated responses in pregnancy: 1217 ± 325 pmol‐eqv 1‐1 postpartum 2223± 404 pmol‐eqv 1‐1, P<005) and PP (9801 &± 1440 v. 14,078 ± 1543 pmol 1‐1, P<001) were impaired and the insulin response enhanced (27,973 ± 6814 v. 11,409 ± 3102 pmol 1‐1, P<001) in pregnancy.The physiological implications of these findings are at present not known in detail. They may, however, be important for the altered carbohydrate metabolism in pregnancy and also for the changes occurring during gestation in gastrointestinal physiology.
Biochemical and histological changes in pulmonary fibrosis induced in rabbits with intratracheal bleomycin
Authors: LAURENT GEOFFREY J. , McANULTY ROBIN J. , CORRIN BRYAN , COCKERILL PETER 
Published: March 2008

Abstract. Pulmonary fibrosis was induced in rabbits by an intratracheal instillation of bleomycin. Histologi‐cally, at 2 weeks there was inflammation but only limited evidence of increased collagen deposition; at 8 weeks the inflammatory response had subsided and increased collagen deposition, characteristic of early interstitial fibrosis, was observed. Biochemical analyses showed bleomycin treatment caused marked increases in the total amounts of RNA, DNA, mixed protein, collagen and elastin when compared to controls (P < 0.001 in all cases). Furthermore the increases were essentially complete by 2 weeks where the contents had increased by 110±13%, 60±%, 148±12%, 94±15% and 89±% respectively (P < 0.001 in all cases). When collagen and elastin were expressed as concentrations with respect to wet weight, total protein or DNA content, the changes were not statistically significant. No changes were observed in the relative amounts of type I and type III collagen.It is concluded that: (1) compared to biochemical analysis, histology is relatively insensitive in detecting the early increases in connective tissue proteins; (2) measurements of lung collagen and elastin should be expressed as total lung contents wherever possible; the concentration of these proteins may remain unchanged, especially in the early stages of fibrosis, due to concomitant increases in other lung constituents; (3) changes in the relative amounts of types I and III collagens do not play a major role in the pathology of this form of pulmonary fibrosis.
Adrenoceptor of the alpha2‐subtype mediating inhibition of the human fat cell adenylate cyclase
Authors: KATHER HORST , SIMON BERND 
Published: March 2008

Abstract. In an attempt to characterize the adenylate cyclase‐coupled alpha‐adrenoceptors of human fat cells the effects of various alpha‐adrenergic agonists and antagonists were examined in the presence of 0.05 mmol/1 of propranolol.The order of agonist potencies with respect to alpha‐adrenergic inhibition was (—)‐adrenaline > alpha‐methyl‐(‐)‐noradrenaline » (—)‐phenylephrine with half‐maximal inhibition occurring at 2 μmol/1 of (‐)‐adrenaline and 7 μmol/l of alpha‐methyl‐(‐)‐noradrenaline respectively.The inhibition of adenylate cyclase induced by 005 mmol/1 of (—)‐adrenaline was reversed by the alpha‐blocking agents yohimbine and prazosin, with the alphai‐site‐directed antagonist yohimbine being more than 100‐times more potent than prazosin which is more active at alphai‐sites.The results show that the cyclase‐coupled alpha‐adrenoceptors of human fat cells, which probably represent the physiologically relevant target of antili‐polytic catecholamine effects, display characteristic features of the alpha2‐adrenoceptor subtype.
On the diabetogenic effect of growth hormone in man: effects of growth hormone on glucagon and insulin secretion
Authors: ADAMSON ULF 
Published: March 2008

Abstract. The effects of human growth hormone (GH) on glucose homeostasis and the secretion of insulin and glucagon was investigated in eighteen healthy subjects. GH (40 μg/kg) was given as a 30 min i.v. infusion and was followed immediately, or after 60 min, by either a glucose infusion, or an i.v. L‐arginine infusion or i.v. insulin (005 IU/kg).An insulin‐like effect of GH was seen about 15 min after the start of the GH infusion, and became a diabetogenic action 90 min later. Basal and glucose stimulated insulin secretion were suppressed 60 min after the start of the GH infusion, while insulin response to i.v. L‐arginine, on the whole, was uninfluenced. Basal glucagon as well as glucagon response to arginine or hypoglycaemia were uninfluenced by GH. GH did not alter the degree of hypoglycaemia reached after i.v. insulin, whereas the rapidity of blood glucose fall was significantly decreased. The restitution of blood glucose after its nadir was not modified by the hormone.These results demonstrate that the diabetogenic action of GH is not mediated by GH effects on glucagon secretion, and that GH is of little importance in the acute counter‐regulation of insulin‐induced hypoglycaemia.
The metabolism of fibrinogen and plasminogen related to diabetic retinopathy in man
Authors: CEDERHOLM‐WILLIAMS S. A. , DORNAN T. L. , TURNER R. C. 
Published: March 2008

Abstract. Metabolic turnover of fibrinogen and plasminogen were studied in thirty insulin‐treated diabetics and ten non‐diabetic controls. 131‐iodine labelled fibrinogen and 125‐iodine labelled plasminogen were injected intravenously and the plasma clearance of the two proteins measured simultaneously over a period of 8 days. The diabetics were selected to represent three grades of severity of diabetic retinopathy assessed by ophthalmoscopy and fiuorescein angiography; ten patients had no significant retinopathy, ten background and ten proliferative retinopathy. Subjects were matched as closely as possible for body weight, age and duration of diabetes.Plasma fibrinogen concentrations were higher in diabetics (3–24 g/1) than controls (2–65 g/1; P<0.025); the patients with the severest retinopathy had the highest fibrinogen concentrations (3.75 g/1). As a direct consequence of the elevation of plasma fibrinogen the catabolic rate was higher in diabetics (20.9 mg kg‐1 day‐1) than controls (140 mg kg‐1 day‐1; P < 0.025) and higher in patients with background retinopathy (24.1 mg kg‐1 day‐1) and proliferative retinopathy (22.4 mg kg‐1 day‐1) than diabetics without retinopathy (16.3 mg kg‐1 day‐1; P= 0.05). Fibrin(ogen) degradation products were detectable in all diabetics but in only one‐third of controls.Plasminogen metabolism was normal in all groups of diabetics.It is concluded that fibrinogen metabolism is increased in diabetes and bears a relationship to diabetic retinopathy but is not accompanied by significant alterations of plasminogen metabolism.
In vitro inhibition of protein synthesis by dialysates of plasma from uraemic patients
Authors: DELAPORTE C. , GROS F. 
Published: March 2008

Abstract. An in vitro technique was devised to test the effects on protein synthesis of plasma dialysate from control and uraemic subjects. Each plasma was dia‐lysed for 24 h to extract the molecules having molecular weight less than 12,000 and the dialysate was lyophilized. Protein synthesis was studied in vitro, using a cell‐free system form mouse Krebs II ascites cells. The cells were lysed, and the 30,000 g supernatant (‘S‐30 lysate’) was used to test the protein‐synthesizing activity of dialysates of control and uraemic plasma. The rate of protein synthesis was monitored by measuring the incorporation of [14C]leucine into tri‐chloracetic acid‐precipitable material in the presence of various amounts of plasma dialysate.The presence of normal plasma dialysate increased the [14C]leucine incorporation rate which went through a maximum for 20–22 μl of added plasma dialysate. In contrast, in the presence of uraemic plasma dialysate, the incorporation rate of the radiolabel decreased as the amount of uraemic dialysate was raised. The ratio of incorporation in the presence of these two kinds of plasma dialysates significantly differed (P < 001) in the range of 15–25 μl of added plasma dialysate. Heating the uraemic plasma dialysate at 100 C for 1 h prior to incubation almost restored the ratio of [14C]leucine incorporation to control values.Therefore it is concluded that: (1) uraemic plasma inhibits protein synthesis, (2) a significant part of this inhibitory effect is related to thermosensitive molecules, (3) the total inhibition appears to be the results of combined effects of ionic and organic compounds accumulated in uraemic plasma.
Hormonal and substrate responses during recovery from hypoglycaemia in man during beta1‐selective and non‐selective beta‐adrenergic blockade
Authors: CORRALL R.J.M. , FRIER B. M. , DAVIDSON N. McD. , FRENCH E. B. 
Published: March 2008

Abstract. recovery from acute hypoglycaemia induced by the injection of insulin has been examined in six human subjects under control conditions, under nonselective beta blockade (propranolol) and under selective beta] blockade (metoprolol). The normal blood glucose recovery was biphasic with an initial rapid and a slower subsequent phase of recovery. The early recovery mechanism was unaffected by either form of beta blockade, but with propranolol the late phase of recovery was significantly prolonged. Rises in blood lactate and plasma free fatty acids following hypoglycaemia were markedly reduced by propranolol but to a much lesser degree with metoprolol. The counterregulatory hormonal responses of glucagon, cortisol and growth hormone were augmented appropriately for the prolonged hypoglycaemia associated with propranolol.Non‐selective beta adrenergic blockade with propranolol is associated with an impairment of the late phase of blood glucose recovery from hypoglycaemia. The possible mechanisms of this impairment are discussed.
Myocardial perfusion imaging with thallium‐201 to assess left ventricular hypertrophy and regional ischaemia in hypertensive patients
Authors: FOLMER S. C. C. REINDERS , WIELING W. , DUNNING A. J. 
Published: March 2008

Abstract. The increase in mortality from cardiovascular disease in the presence of electrocardiographic signs of left ventricular hypertrophy (LVH) has been ascribed to ischaemic changes in the hypertrophied left ventricle even in the absence of overt coronary artery disease.To test this hypothesis and to investigate the usefulness in the detection of LVH myocardial perfusion scintigraphy with thallium‐201 and echocardiography was performed in thirty‐three hypertensive patients. Sixteen had had electrocardiographic signs of left ventricular hypertrophy. Twelve patients had symptoms of cardiovascular disease. In twenty‐six subjects the scintigraphic procedure consisted of a combined restexercise study, in the other seven only resting images were obtained. Measurement of septa1 wall thickness on the scintiscans correlated fairly well with echographic dimensions and allowed separation of a group of patients with LVH from a group without. In individual patients, however, the perfusion scan was not a reliable tool to affirm the presence of LVH. A total of eight patients, six with LVH on the echocardiogram, had an abnormal rest‐exercise perfusion scan, either with a new perfusion defect after exercise and/or with a resting defect alone. In nine other patients with echocardiographic LVH, on the other hand, no abnormal perfusion was found. Thus, perfusion abnormalities did not correlate with the presence of LVH. The presence of such abnormalities in relation to increasing age and symptomatic cardiovascular disease could well be the expression of anatomic coronary artery disease and cannot be differentiated from the possible ischaemia of the hypertrophied left ventricle.
Effect of 1,25‐dihydroxy ‐ vitamin D3 in itself or combined with hormone treatment in preventing postmenopausal osteoporosis
Authors: CHRISTIANSEN C. , CHRISTENSEN M.S. , RØDBRO P. , HAGEN C. , TRANSBØL I. 
Published: March 2008

Abstract. Eighty‐four normal women, 2.5‐5 years after their natural menopause, participated in a controlled double‐blind trial. The effect of various therapeutic regimens on postmenopausal bone mineral loss was measured by photonabsorptiometric determination of the bone mineral content of both forearms. The women were randomized into four treatment groups: 1,25‐dihydroxycholecalciferol (1,25(OH)2D3) alone in a daily dose of 0.25 μg, oestrogens/gestagen alone or combined with 1,25(OH)2D3, and placebo. The groups treated with oestrogens/gestagen (without and with 1,25(OH)2D3) showed a similar increase in bone mineral content of about 1% during one year of treatment. In contrast, both the placebo group and the 1,25(OH)2D3 group demonstrated a decrease of 1.9% and 2.1%, respectively, within the same period of time. While 1,25(OH)2D3 did not alter the rate of bone loss, it caused the characteristic and pronounced increase in urinary calcium excretion (15%).It is concluded that 1,25(OH)2D3 neither serves as an alternative nor as an additive to gonadal hormones in the prevention of postmenopausal osteoporosis.