bluuebunny/crossref_metadata_2025_split huggingface dataset:
IRON STORES IN ALCOHOL ABUSERS
Authors: Lundvall Ove , Weinfeld Aleksander , Lundin Per 
Published: August 2010

Abstract. Storage iron has been examined in aspiration liver biopsy specimens obtained from 41 alcohol abusers without cirrhosis of the liver and from 20 hematologically normal males with gall bladder disease who were otherwise healthy. No one had a history of hemorrhage or iron medication. Only male subjects were examined. The alcoholics consumed mainly distilled alcoholic beverages. Histochemical iron was estimated in parenchymal cells and in Kupffer cells and graded 0 to 4+. Stainable iron in parenchymal cells of grade 1+ or more was present in 15 of the 20 controls (75%) and in 25 of the 41 alcohol abusers (61%). In Kupffer cells stainable iron was present in three of the controls (15%) and in 15 of the alcohol abusers (37%). Two alcohol abusers had stainable iron in the Kupffer cells but not in the parenchymal cells. Thus, stainable iron of grade 1+ or more in either parenchymal cells or Kupffer cells was present in 27 of the 41 alcoholics (67%).In 37 alcoholics and in 20 controls non‐hemin iron in the liver was determined chemically. The mean non‐hemin iron concentration related to dry weight was significantly lower in the alcohol abusers (68.3±5.8 mg per 100 g dry weight) as compared with the controls (104.4±11.2 mg). With protein as reference the mean iron concentration in the liver was lower in the alcohol abusers (148.4±11.5 mg/100 g protein) as compared with the controls (185.7±20.6). The difference was, however, not significant. No alcoholic had a non‐hemin iron concentration above the range of the controls. Thus, the present study did not reveal increased iron stores in alcohol abusers. The results rather indicated diminished iron stores in alcohol abusers as compared with controls.
EXTENSIVE MUSCLE NECROSIS AFTER LONG‐TERM TREATMENT WITH AMINOCAPROIC ACID (EACA) IN A CASE OF HEREDITARY PERIODIC EDEMA
Authors: Korsan‐Bengtsen K. , Ysander L. , Blohmé G. , Tibblin E. 
Published: August 2010

Abstract. A 31‐year‐old man with hereditary periodic edema was treated with aminocaproic acid 30 g daily in two periods. After, respectively, five and seven weeks of treatment he complained of pain in the thighs and calves. The cell enzymes GOT, GPT and CPK increased to high levels in the serum. Myoglobin and an increased concentration of creatine were demonstrable in the urine. Microscopic examination of the material from a muscle biopsy showed Zenker's hyaline degeneration of the muscle cells.The patient regained muscle strength rapidly after the first incidence but slowly after the second.He has now been free from episodes of edema for eight months on methyltestosterone therapy.
ATRIAL FIBRILLATION
Authors: Åberg Hans 
Published: August 2010

Abstract. The amplitude of the f waves has previously been correlated to the etiology of the atrial fibrillation and to the size of the left atrium. This investigation has revealed coarse f waves to occur more frequently than fine f waves in rehumatic heart disease, which is in agreement with earlier reports. In arteriosclerotic heart disease, however, fine f waves occurred in only 21%, which is in opposition to the result of most earlier reports.No correlation between the amplitude of the f waves and the left atrial size was found.It is concluded that in the individual case no safe conclusions can be drawn from the size of the f waves in conventional ECG leads.
CHLORPROMAZINE‐INDUCED ANTINUCLEAR FACTORS
Authors: Berglund Stig , Gottfries C.‐G. , Gottfries Ingrid , Stormby Karin 
Published: August 2010

Abstract. A series consisting of 488 women admitted to a mental hospital have been studied for ANF. The material was divided into three diagnostic groups, viz. schizophrenia, other mental diseases, and senile dementia. From a therapeutic point of view the material was divided into four categories according to treatment with chlorpromazine. The four groups were: patients receiving chlorpromazine, patients who had previously received chlorpromazine, patients receiving other phenothiazine derivatives and a remaining group in which treatment had consisted of neuroleptics other than phenothiazines, antidepressives or sedatives. The frequency of ANF in the entire series was high. In the statistical analysis of the data only cases with a clearly positive ANF reaction were accepted as positive. The statistical analysis showed that treatment with chlorpromazine is an important inducing factor in the development of ANF. In the groups “receiving chlorpromazine” and “previous treatment with chlorpromazine” the frequency of ANF was significantly higher than in the other groups. The frequency of ANF does not appear to vary with the psychiatric diagnosis. High age may, however, be of some causal importance, the frequency of ANF appearing to be higher in the aged.The number of patients with a clearly positive ANF reaction was 77 (15.8%). They were examined clinically and with laboratory tests, mainly for autoimmune disease. The frequency of autoimmune disease in these patients was not found to be increased, but two of the patients showed serological abnormalities connected with a predisposition to autoimmune disease. Thus chlorpromazine, like methyldopa and isoniazid, appears to be able to induce antinuclear factors. Regular follow‐up of patients receiving treatment with chlorpromazine is recommended, particularly for antinuclear factors in the serum and with the possibility of latent SLE in mind.
DRUG‐INDUCED AGRANULOCYTOSIS, WITH SPECIAL REFERENCE TO AMINOPHENAZONE
Authors: Palva I. P. , Mustala O. O. 
Published: August 2010

Abstract. This is a report of 63 episodes of agranulocytosis in 51 patients during a period of 18.5 years (1950–68). In 54 cases (93%) there was a positive history of drug ingestion, most of those without such history being from the period before 1959. An “idiopathic” case of agranulocytosis is almost entirely a function of inadequate history‐taking. The frequency of agranulocytosis has greatly increased during the period, the increment being entirely in women. During the years 1950–59 the ratio of men to women was 4: 11, in 1960–68 4: 44. The mortality has decreased from the 83% of 1950–54 to 13% in 1960–68, being close to zero for patients under 50 years of age and in adequate treatment.As causative agents, sulphonamides and aminophenazone were the most commonly observed, the estimated incidence for the latter being 1 per 40,000 cures of the drug. A history of the use of chloramphenicol was rather common, but always in combination with other drugs known to cause agranulocytosis. The next most common agents were carbimazole, phenylbutazone and thioridazine, occasional cases being attributed to carbutamide, mephenytoin, thiamazole, phenobarbital, barbital, amithiozole, thiocarlide, metamizol natrium, tetracycline, chlorothiazide and chlorpromazine.
PLASMA LECITHIN‐CHOLESTEROL ACYLTRANSFERASE AND ERYTHROCYTE LIPIDS IN LIVER DISEASE
Authors: Gjone Egil , Norum Kaare R. 
Published: August 2010

Abstract. Plasma lecithin‐cholesterol acyltransferase (LCAT) activity was reduced to approximately one fourth of normal values in patients with chronic parenchymatous liver disease without marked jaundice (mean serum bilirubin 2.0 mg/dl). A significant increase in red cell cholesterol was concomitantly demonstrated with a highly significant correlation between red cell cholesterol content and the concentration of plasma‐free cholesterol.In patients with marked obstructive jaundice (mean serum bilirubin 14.6 mg/dl) the plasma LCAT activity was even lower and in some hardly detectable. This reduced activity could not be explained by LCAT inhibition in plasma. Erythrocyte cholesterol content was markedly increased up to twice the normal values. A significant increase in erythrocyte lecithin and significant decreases in sphingomyelin and phosphatidyl ethanolamine were also found. Erythrocyte cholesterol content was found to be normal in patients with hyperbetalipoproteinemia and marked elevation of plasma total cholesterol with normal plasma cholesterol esterification.
EXTREME PERSISTENT EOSINOPHILIA WITH HIGH SERUM B12 VALUES
Authors: Fledelius Hans 
Published: August 2010

Abstract. A report is given on two male patients—35 and 47 years old—with pronounced eosinophilia of long duration. The first patient is still alive after six years' observation, while the second patient—a diabetic—died after four years because of liver cirrhosis with portal hypertension and repeated haematemeses.In both cases, as well as in four cases of persistent eosinophilia reported by other authors, serum vitamin B12 was considerably elevated. It is discussed whether this finding may be interpreted as supporting a leukaemic nature of the diseases. To elucidate this theory further we made a pilot test on twenty cases of eosinophilia of wellknown origin, which all showed normal serum B12 concentrations.In the literature on eosinophilic leukaemia serum BJ2 determinations are mentioned only exceptionally. It therefore must be emphasized that serum B12 should be incorporated in the laboratory investigation programme when eosinophilia is present.
PLASMA LIPIDS AND LIPOPROTEINS IN PATIENTS WITH MYOCARDIAL INFARCTION AND IN A CONTROL MATERIAL
Authors: Dyerberg Jørn , Bang Hans Olaf , Nielsen John Allan 
Published: August 2010

Abstract. One hundred and eight patients with myocardial infarction have been investigated 1–1 1/2 year after the acute attack. As a control group 44 coaeval hospital patients with no known ischaemic heart disease and 65 healthy young subjects were examined.Significantly higher values were found for plasma total lipid, triglyceride, cholesterol, and phospholipids in the coronary patient group as compared with the coaeval hospital control group, and in the last mentioned group as compared with the young controls.Paper electrophoretic lipoprotein estimations were carried out in all cases. 15.9% of the hospital control group and 42.6% of the coronary patient group had Type II hyperlipoproteinaemia. Hyperlipoproteinaemia with increased pre‐β‐fraction was found in 34.1% and 35.2% respectively of the same groups. Analyses of the occurrence of pre‐β‐lipoprotein fractions in all three groups seem to suggest the existence of two different populations according to the metabolism of endogenous triglycerides. We think that this fact must be taken into consideration in future dietetic trials with the aim of preventing ischaemic heart disease.
CATECHOLAMINES AND METABOLISM OF HUMAN ADIPOSE TISSUE
Authors: Östman Jan , Efendić Suad 
Published: August 2010

Abstract. Human omental tissue was incubated in KrebsHenseleit bicarbonate medium containing 3% albumin and glucose with additions of noradrenaline, isopropylnoradrenaline, or theophylline. Glycerol release was measured and taken as the index of lipolytic activity.In the first series of experiments the effects of equimolar concentrations of noradrenaline and isopropylnoradrenaline were compared. At each concentration lsopropylnoradrenaline produced significantly higher glycerol release. Noradrenaline‐stimulated lipolysis was suppressed completely by the beta‐adrenergic blocking agent propranolol added at a concentration of 1 μg per ml of the incubation medium. At this concentration propranolol had no effect on basal glycerol release and that induced by theophylline (10‐2 M). The alpha‐adrenergic blocking agent phentolamine inhibited only in some experiments the glycerol release produced by noradrenaline and this occurred only when the agent was added at a high concentration (500 μg/ml) which also inhibited theophylline (10‐2 M) induced lipolysis. These data indicate that in human omental adipose tissue catecholamine‐induced lipolysis is mediated by beta‐adrenergic receptors. They also suggest that the antilipolytic action of high phentolamine concentrations is localized between the formation of cyclic adenosine‐3′,5′‐monophosphate (3′,5′‐AMP) and the induction of triglyceride lipase activity.In all experiments glycerol release produced by noradrenaline was further increased by addition of small concentrations (0.05–100 μg/ml) of phentolamine to the incubation medium. The stimulation of noradrenalineinduced lipolysis was negatively correlated with the effect of noradrenaline alone on basal lipolysis. These small concentrations of phentolamine did not significantly influence the glycerol release produced by theophylline or isopropylnoradrenaline. The maximal lipolytic responses to noradrenaline plus phentolamine were of similar magnitude to those produced either by theophylline or isopropylnoradrenaline alone. These results were interpreted as indicating that in human omental tissue there exist alpha‐adrenergic receptors which counteract the lipolytic effect of catecholamines by reducing the formation of 3′,5′‐AMP.
II. Development of an indirect LE factor test
Authors: LARSEN ROLF A. , BØYUM ARNE 
Published: August 2010

ABSTRACT:An indirect LE factor technique, including a simple method for separation of leucocytes, is described. In the test a standardized amount of serum reacts with a constant amount of damaged nuclei serving as antigen, and fagocytosis is secured by addition of a constant amount of freshly‐prepared leucocytes. It is possible to titrate LE sera. The titration of LE sera gives a regular succession of different phenomena associated with LE cell. This gradual change in the morphology has been described. Granulocyte‐ and lymphocyte‐specific LE factors are demonstrated.
FRUCTOSE METABOLISM IN ADIPOSE TISSUE
Authors: Froesch E. R. 
Published: August 2010

Abstract. The rate limiting step of fructose metabolism in adipose tissue is fructose transport into the cell. The step is accelerated by insulin only in the absence of glucose, so that insulin has no effect on fructose transport under physiologic conditions. The fructose carrier has a relatively high apparent Km for fructose transport so that significant quantities are transported only at relatively high concentrations of fructose in the blood.Fructose is the phosphorylated to fructose‐6‐phosphate by the enzyme hexokinase. Glucose does not compete because it is not present intracellularly in sufficiently high concentrations. This statement is correct only for adipose tissue.Fructose uptake by adipose tissue of diabetic animals is reduced as is glucose uptake, but to a lesser extent.In vivo, most of the C14‐incorporation of fructose‐C14 into triglycerides or C14O2 by adipose tissue occurs after hepatic conversion of C14‐fructose to C14‐glucose. Insulin is required for glucose transport into adipose tissue.
EFFECT OF FRUCTOSE ON CELLULAR RESPIRATION IN PERFUSED RAT LIVER
Authors: Hassinen I. E. , Ylikahri R. H. , Kähönen M. T. 
Published: August 2010

Abstract.

The regulation of energy metabolism is reviewed with special reference to the metabolism of fructose. Fructose metabolism in liver by‐passes the main regulatory step of glycolysis, the formation of fructose‐6‐phosphate. Therefore the overall regulation of energy metabolism is possibly adjusted in a new way. The by‐pass and the high activity of liver fructokinase cause metabolic alterations characterized by an accumulation of fructose‐1‐phosphate and depletion of inorganic phosphate and adenine nucleotides in the liver.
The effects of fructose on the redox state of nicotinamide nucleotides and mitochondrial flavoproteins and cytochromes were studied by surface fluorometry and transmission spectrophotometry in isolated perfused rat liver.

Oxygen consumption was inhibited and nicotinamide nucleotides were reduced concomitant with phosphate depletion. The spectrophotometry of intact tissue showed inhibition of electron transport at the first phosphorylation site of the mitochondrial respiratory chain.The fructose‐induced alterations in the cellular redox state can be interpreted as acceptor control for inorganic phosphate during the metabolism of fructose. The role of the metabolism of glyceraldehyde in these redox changes is discussed.
FRUCTOSE AND PURINE METABOLISM
Authors: Raivio K. O. , Kekomäki M. , Mäenpää P. 
Published: August 2010

Abstract.The interactions between fructose and purine metabolism are reviewed. Hyperuricemia and increased production of uric acid after fructose administration have been documented in man as well as in the rat. These effects appear to be dependent on the rapid phosphorylation of fructose, mainly in the liver. This results in a depletion of intracellular ATP and inorganic phosphate. As a consequence, the adenylate deaminase reaction is deinhibited and increased breakdown of adenine nucleotides to uric acid ensues.Some considerations of the hazards involved in the clinical use of fructose are presented, and other possible points of interaction between fructose and purine metabolism are discussed.
METABOLISM OF FRUCTOSE AND GLYCERALDEHYDE IN THE ISOLATED PERFUSED PIG LIVER
Authors: Sestoft L. , Damgaard S. , Tygstrup N. , Lundquist F. 
Published: August 2010

Abstract. Isolated pig livers were perfused under near physiological conditions, i.e. use of pigs blood, perfusion via both arterial and portal system, and constant pH (7.4). Fructose uptake and the production of a number of metabolites were measured in relation to the fructose concentration in the perfusion medium. A Michaelis type kinetics was found with Vm about 3 μmoles/g liver x min and Km about 5 mM. Fructose‐1‐phosphate was observed to accumulate as a consequence of the inhibition of the aldolase step, presumably by glyceraldehyde, AMP and IMP. Sorbitol formation is of small importance under our experimental condition.During continuous fructose infusion the concentration of glyceraldehyde was low (less than 0.5 mM). Therefore the metabolism of glyceraldehyde was studied separately. Measurement of the reaction products glycerol and glycerate as a function of the glyceraldehyde concentration support the assumption that glyceraldehyde is metabolized by several pathways.Measurement of acid production during metabolism of either fructose or D‐glyceraldehyde suggests that a considerable accumulation of acids occur in the liver, as only a minor part of the titration value is accounted for as the organic acids measured, of which lactic acid is the quantitatively most important.Only 20–30 % of the carbon of fructose and glyceraldehyde is accounted for through formation of lactate and glucose. The rest is oxidized or accumulates in some form in the liver.The oxygen consumption during fructose metabolism was increased about 30 %, and the lactate/pyruvate ratio showed small, but reproducible changes.
MODIFICATION OF METABOLIC EFFECTS OF ETHANOL BY FRUCTOSE
Authors: Ylikahri Reino H. , Kähönen Matti T. , Hassinen Ilmo 
Published: August 2010

Abstract. Present knowledge of the metabolic interactions between fructose and ethanol in man and laboratory animals is reviewed. The possible biochemical mechanisms of these interactions are considered. Some new data on the effects of fructose and ethanol on carbohydrate and lipid metabolism are included.Fructose increases the effects of ethanol on the hepatic lactate/pyruvate and a‐glycerophosphate/dihydroxyacetone phosphate ratios. Thus it augments the basic metabolic effect of ethanol, i.e. reduction of the hepatic redox state.The ethanol‐induced increase in hepatic a‐glycerophosphate concentration has been regarded as an important factor in the pathogenesis of the acute alcoholic fatty liver. But although fructose causes hypertriglyceridaemia and augments the effect of ethanol on hepatic a‐glycerophosphate concentration, it was found to diminish the ethanol‐induced accumulation of triglycerides in the liver. Glucose had a similar effect. The reason for this is uncertain, but the inhibition of peripheral lipolysis by fructose and glucose might be partly responsible.The most important effect of ethanol on carbohydrate metabolism is to inhibit hepatic gluconeogenesis by producing NADH in excess. Although the production of glucose from fructose is not directly dependent on the redox state of the liver, it is slightly inhibited by ethanol in vitro. However, in vivo fructose is effectively converted to glucose even during ethanol oxidation, and in ethanol‐induced hypoglycaemia it rapidly restores the blood glucose level.
METABOLISM OF FRUCTOSE IN DIABETES
Authors: Roch‐Norlund A. E. , Hultman E. , Nilsson L. H:son 
Published: August 2010

Abstract. Fructose and glucose (4 g/kg body‐weight during 4 hours) were given intravenously to normal subjects and to patients with diabetes without insulin treatment.Liver and muscle glycogen content was determined before and after the infusion. In normal subjects glucose and fructose gave similar increases in muscle glycogen stores, while the liver glycogen increased 4 times more after fructose infusion as compared to glucose. In the diabetics only fructose gave a liver glycogen increase and neither fructose nor glucose affected the muscle glycogen content.The mechanism for the glycogen increase in the liver of diabetics after fructose infusion could be due to allosteric activation of glycogen synthetase D and/or to availability of fructokinase.
EFFECT ON SERUM LIPIDS OF DIETARY SUCROSE AND FRUCTOSE
Authors: Macdonald Ian 
Published: August 2010

Abstract. Though the measurement of the concentration of substances in the serum may provide misleading evidence for metabolic studies, nevertheless findings of changes in the levels of various serum lipids have a high degree of association with vascular disease. Sucrose or one of its constituent monosaccharides, fructose, has been found to have an influence on serum triglyceride concentration — the effect on the serum cholesterol level being minimal — when compared with glucose or its polymers.After the acute ingestion of sucrose a less striking fall is found in the serum triglyceride level than after glucose ingestion. Experimental diets containing a large proportion of carbohydrate result in a level of triglyceride that is higher when the carbohydrate contained fructose than when it contained glucose. The effect of dietary fructose on the fasting level of serum triglyceride is modified by the sex of the consumer, the amount and type of fat accompanying the fructose, the type of protein in the diet, the frequency of intake, etc.The few studies on long term ingestion of fructose suggest that the rise in triglyceride concentration following fructose ingestion falls.There is some evidence that in vascular disease the fructose metabolism may be more disturbed than that of glucose.
EFFECTS OF DIETARY FRUCTOSE AND SUCROSE ON PLASMA TRIGLYCERIDE METABOLISM IN PATIENTS WITH ENDOGENOUS HYPERTRIGLYCERIDEMIA
Authors: Nikkilä Esko A. , Kekki Matti 
Published: August 2010

Abstract. Since fructose is now marketed as a nutrient a study has been initiated to compare the effects of fructose, sucrose and starch at a conventional dietary intake level on the plasma triglyceride concentration and turnover in patients with endogenous hypertriglyceridemia. Preliminary results are presented here.Fructose or sucrose in a daily amount of 75 to 80 grams were added to the diet in an isocaloric exchange for starch in twelve hyperglyceridemic patients under hospital conditions. Each dietary period lasted for 10 to 20 days and the triglyceride turnover was studied by endogenous glycerol labeling technique at the end of each period. Five of the patients had manifest diabetes managed by diet or oral antidiabetic drugs.Plasma triglyceride response to fructose was variable and the average change from the level observed during fructose‐free diet was not significant. However, in nondiabetic subjects a definite rising trend of triglyceride was noticeable. Sucrose caused a significant increase of triglyceride concentration above that measured during fructose and starch diets. Diabetics were not included into the sucrose group, however. The fractional removal rate of plasma triglycerides was identical during all three diets but the triglyceride production rate showed a rising trend during fructose and, particularly, during sucrose diet as compared to starch. Because of the limited number of subjects studied so far, these results do not justify any definite conclusions.