bluuebunny/crossref_metadata_2025_split huggingface dataset:
HEREDITARY ABNORMAL MUSCLE METABOLISM WITH HYPERKINETIC CIRCULATION DURING EXERCISE
Authors: Linderholm H. , MüllerT R. , Ringqvist T. , Sörnäs R. 
Published: August 2010

Abstract.Patients with a hereditary myopathy with paroxysmal myoglobinuria were studied in the chronic state of the disease. They were characterized by muscle contractions of fairly normal strength and quite good endurance in exercise with small muscle groups, but a poor physical performance in exercise of some duration with large muscle groups.Several facts indicate that it was not muscular weakness, but the circulatory capacity that was a main factor limiting the physical working capacity in exercise of some duration with large muscle groups. The oxygen uptake was largely normal in relation to the work performed. However, even light exercise on a bicycle ergometer caused tachycardia (approaching maximum heart rate), a high cardiac output (approaching, for the size of the individual, maximum values in the normal range) and an abundant blood flow through the exercising legs. Thus, there were no signs of insufficient heart function, but the utilization of the oxygen of the blood in the exercising limbs was low.The concentration of lactate, and particularly of pyruvate, in the blood, and the lactate and pyruvate production increased more than in the controls for the slight work performed. During exercise the lactate/pyruvate ratio decreased and the calculated “excess of lactate” was negative, while it increased in normal subjects. After exercise the excess lactate was higher in the patients than in the controls. This indicates an abnormal muscle metabolism, probably a decreased capacity for pyruvate oxidation.It is suggested that a metabolic disturbance caused an abnormally large production of metabolites in the working muscles, resulting in muscular vessel dilatation by a local humoral effect. The muscles acted almost like a‐v shunts and, as a consequence, the patients had a hyperkinetic circulation, i.e. a low O2uptake in relation to cardiac output, a low a‐v O2difference for mixed venous blood and for the venous blood of the exercising limbs.
EFFECTS OF HYPERVENTILATION ON ECG IN PATIENTS WITH CIRCULATORY DISTURBANCES
Authors: Furberg Curt , Linderholm Håkan 
Published: August 2010

Abstract.The ECG has been recorded in patients with vasoregulatory asthenia, coronary insufficiency and arterial hypertension, as well as in healthy controls at rest, after hyperventilation, during an orthostatic test and a work test.S‐T and T depressions, usually of sympathicotonic type, appeared or were accentuated after hyperventilation, particularly in patients with vasoregulatory asthenia, who also showed similar changes during an orthostatic test. Such ECG changes were uncommon in the other groups.The results sustain the concept that an increased sympathetic autonomic nervous tone provoked by hyperventilation causes the S‐T and T depressions, particularly in patients with vasoregulatory asthenia.The diagnostic value of the hyperventilation ECG for analysing functional S‐T and T depressions is emphasized, as well as the diagnostic difficulties in the evaluation of ECG changes in patients who hyperventilate, for instance during a hypoxia test.
LIPID CHANGES AFTER INCUBATION OF NORMAL PLASMA
Authors: Berlin Ragnar , Oldfelt Carl Olof , Vikrot Olle 
Published: August 2010

Abstract. The individual phospholipids as well as the triglycerides, free fatty acids, total cholesterol and its non‐esterified fraction have been determined on a normal material comprising 37 men and women of different age groups. Young men exhibited significantly higher values of lysolecithin in comparison with elderly men and women irrespective of age.Incubation studies revealed a lecithin splitting activity with subsequent formation of lysolecithin and release of fatty acids. Simultaneously the well‐known lipase activity was found, splitting also the triglycerides and releasing further amounts of free fatty acids. Free cholesterol decreased to a significant extent, probably by transesterification of fatty acids released during the incubation from lecithin and probably also to a lesser degree from triglycerides. No change of sphingomyelin was noted and phosphatidylethanolamine also remained unchanged during the incubation. The reported lysolecithin increase in incubated plasma probably explains the previously reported reduced sedimentation rate of red cells added to such a plasma. The increment of free fatty acids may also contribute to the same result to a lesser extent.
EFFECT OF ALUMINIUM HYDROXIDE (ALUDROX) UPON SERUM CALCIUM, SERUM PHOSPHORUS, AND CALCIUM47 TURNOVER IN URAEMIC PATIENTS
Authors: Friis Th. , Weeke E. 
Published: August 2010

Abstract. In 11 normal persons and 16 uraemic patients serum calcium, serum phosphorus, and calcium pool (exchangeable calcium) were determined (Heaney and Whedon (9)). Among the 16 uraemic patients eight had inulin clearance < 20 ml/min, five between 20 and 40 ml/min, and three > 40 ml/min. Nine of the uraemic patients had serum calcium levels below normal (inulin clearance <40 ml/min) and six serum phosphorus above the normal range (inulin clearance <20 ml/min). Ten had abnormal X‐ray appearances of the spine and skull (halisteresis, fractures). Fourteen had chronic pyelonephritis, one renal tubular acidosis, and one polycystic kidneys. The exchangeable calcium was 59.9 ±13.9 mg/kg in the normals and 77.6 ±39.4 mg/kg in the uraemic patients; this difference is not significant. The patients with severe halisteresis had the highest exchangeable calcium.In four normals and 14 uraemics the effect of 6% mangesiumfree aluminium hydroxide (Aludrox) was studied, 90 ml being given daily for 1–8 months, mean period for the normals 3.5 months, for the uraemics 4.8 months. During the treatment the serum phosphorus decreased; there was a correlation between this decrease and the original level (r = ‐ 0.540). Serum calcium rose when it had originally been reduced.Exchangeable calcium increased in all the normals and in all uraemics with inulin clearance > 20 ml/min. In four of the uraemic patients with inulin clearance < 20 ml/min exchangeable calcium decreased. In patients who showed an increase the exchangeable calcium again declined towards the initial values at the end of some months.The bone formation rate was determined in 12 of the uraemic patients (mean = 14.5 ± 8.6 mg/kg, in normals 12.2 ± 2.3 mg/kg; this difference is not significant). Here, too, the highest values were found in patients with severe bone complications. In 11 of these patients the effect of aluminium hydroxide was studied (seven with inulin clearance <20 ml/min, three with inulin clearance between 20 and 40 ml/min, and one with inulin clearance above 40 ml/min). The values rose in all patients with inulin clearance above 20 ml/min and in five with inulin clearance below 20 ml/min. After some time, the bone formation rate declined towards the initial values.There was a correlation between exchangeable calcium and bone formation rate (r = 0.740) and between the fall in serum phosphorus and the increase in bone formation rate (r = ‐0.531).
HEMODYNAMIC CHANGES IN LONG‐TERM DIURETIC THERAPY OF ESSENTIAL HYPERTENSION
Authors: Lund‐Johansen Per 
Published: August 2010

Abstract. Thirty‐eight men with untreated essential hypertension in WHO stage 1 or II, aged 19–57 years, all working, have been studied ambulatorily. Oxygen consumption, heart rate, cardiac output (Cardiogreen) and intra‐arterial brachial pressure were recorded at rest in supine, sitting and standing position and during steady state work. At rest plasma volume and serum electrolytes were measured. The subjects were divided into four groups: I, untreated 7; II, chlorthalidone 100 mg every second day 9; III, polythiazide 1 mg every second day 7; and IV, hydrochlorothiazide 50 mg twice daily 15.The subjects were restudied after 8–12 months. In the untreated group none of the results at the second examination were significantly different from those at the first. In the treated groups the causal resting blood pressure and intra‐arterial pressure at rest and during work were significantly lower after treatment than before. At rest when sitting, the mean arterial pressure was reduced 21, 15 and 18% in groups II, III and IV and during work a little less. Serum‐K dropped significantly in all groups, the mean drop being about 0.7 mEq/1 in all groups. Plasma volume (hydrochlorothiazide group only) was 0.24 1 lower after therapy, but the difference was not significant. In the thiazide groups the pressure drop was usually associated with a drop in peripheral resistance, both at rest and during exercise. In the chlorothalidone group the pressure drop was usually caused by a reduction in cardiac index, with little or no effect on the peripheral resistance.
BLOOD FLOW IN VASCULAR DISORDERS
Authors: Hillestad Ixif 
Published: August 2010

Leif HillestadAbstract. The peripheral cutaneous vessels have been studied at various ambient temperatures and at local temperatures ranging from 40 to 6°C. At the higher local temperatures sympathetic stimuli exerted a strong effect upon the blood flow. By applying local cooling of increasing strength the influence of sympathetic stimuli upon the vascular tone was successively abolished. From around 15°C of local temperature and down to zero vessels were unresponsive to sympathetic nerve influence. It appears that the local cold stimulus is the major determinant of the vascular tone of the skin when man is exposed to cold. Studies of the cutaneous circulation under the same conditions were carried out in patients suffering from various peripheral vascular disorders. Local cold was again found to be the determinant factor for producing the abnormal vasoconstriction. Abolition of sympathetic tone did not prevent the occurrence of spasmodic attacks. The hemodynamic difference between cold‐sensitivity in vasospastic and in obstructive arterial disease of the hands is demonstrated. The findings are discussed in the light of presently applied criteria for treatment of cold‐sensitive peripheral vascular disorders.
I. A proband material from central eastern Norway
Authors: LARSEN ROLF A. 
Published: August 2010

ABSTRACT:A survey of SLE in an area from central eastern Norway is given, together with clinical and laboratory data on the 72 patients diagnosed as SLE in this area during the years 1959–1963. The main proportion of these cases would have been classified as definite SLE according to diagnostic criteria given in the literature. Annual incidence and prevalence rates were lower than rates presented from other countries. The frequency of various clinical manifestations is consistent with previous reports. The SLE patients were classified according to syndromes they exhibited during the active stages of their disease, and the manifestations in various syndromes were compared.The SLE material serves as a proband material for family studies, and sub‐grouping of SLE cases is the basis for comparison of the findings in relatives of these various groups of SLE probands.
INTESTINAL ABSORPTION OF SUCROSE
Authors: Dahlqvist Arne 
Published: August 2010

Abstract: Sucrose in synthetized in the green leaves of plants. With increasing economical status the sucrose from sugar cane and beets, like fat, supplies an increasing fraction of our food. Sucrose is easily metabolized and utilized. Too high consumption is, however, not desirable from nutritional point of view, since this highly refined product contains calories but no essential nutrients.The general concept is that animals (and humans) do not synthesize sucrose. A single report of a sucrose‐synthesizing patient needs confirmation from other sources before it can be accepted.The intestinal absorption of sucrose can only occur if the hydrolyzing enzyme, invertase (sucrase), is present in the mucosal cells. Acid hydrolysis in the stomach has been suggested, but does not occur. The intestinal invertase is an a‐glucosidase.In the human intestine invertase, as well as the other a‐glucosidases, is developed very early in fetal life — much earlier than lactase. In the animals studied so far, in contrast, intestinal invertase and other a‐glucosidases are weak until the weaning period, when lactase disappears and the a‐glucosidase develops. The reason for these species differences is yet unexplained.Human populations with low sucrose consumption have approximately equally high intestinal invertase activity as those in countries with high sucrose consumption. In Greenland Eskimos the adults have for a very long period of time (probably thousands of years) consumed nearly no carbohydrates at all. The average intestinal activity of invertase and the other a‐glucosidases in the Greenland Eskimos is nevertheless nearly the same as ours. Specific enzyme defects, which among us occur only as very rare cases of «inborn errors of metabolism« are, however, rather frequent in the Greenland Eskimos.
ASPECTS OF FRUCTOSE METABOLISM IN NORMAL MAN
Authors: Bergström J. , Fürst P. , Gallyas F. , Hultman E. , Nilsson L. H:son , Roch‐Norlund A. E. , Vinnars E. 
Published: August 2010

Abstract.In normal subjects infusion of fructose (1 g/kg/hr) for 4 hrs resulted in an increase in the glycogen content of them. quadriceps femorisof 3.3 g/kg wet muscle (muscle samples obtained by needle biopsy). This was equal to the amount of glycogen formed after a glucose infusion of the same magnitude. In muscle depleted of glycogen by exercise, infusion of glucose resulted in twice as much glycogen formed, as did a fructose infusion. Formation of liver glycogen was much higher after fructose than after glucose infusion (liver samples obtained by Menghini biopsy). Studies by hepatic vein catheterization indicated that glucose formation by the liver was insufficient to account for the synthesis of muscle glycogen, which presumably occurred directly from fructose taken up by the muscle.The occurrence of high lactic acid concentrations in blood resulting from infusion of fructose could be partly abolished by simultaneous infusion of amino acids, thus lessening the risk of lactic acidosis.
DOES DIETARY FRUCTOSE AFFECT THE CONTROL OF DIABETES IN CHILDREN?
Authors: Äkerblom H. K. , Siltanen Irmeli , Kallio Anna‐Kaarina 
Published: August 2010

Abstract. The purpose of the study was to find out whether fructose can be used as a dietetic sweetener for diabetic children.Acute effects of ingested fructose were studied in 26 hospitalized diabetic children by giving fructose, 1.0 g/kg, at breakfast, and by comparing 3 hours postcibal blood glucose to that of control days, when a corresponding amount of calories was given as a regular breakfast. Postcibal hyperglycemia from 30 to 120 min was significantly less on fructose days as compared with control days. The differences between blood glucose on control and fructose days were significantly greater from 30 to 120 min than the chance variations on two control days.The effects of more prolonged use of dietary fructose on diabetes were studied in 16 patients at home for four weeks by alternating between one week periods on diets which included 1.5 g/kg/day of fructose and control weeks of regular isocaloric sugar‐free diets. Glucosuria, recorded twice daily by Clinitest®, and once a week by measuring 24‐hour glucose excretion, was similar during control and fructose weeks. Ketonuria was infrequent during either diet. Fructose did not elevate serum triglycerides.Because dietary fructose, given in substantially larger amounts did not impair the control of diabetes, it is concluded that fructose can be used by diabetic children at a rate of 0.5 g/kg/day without negative effect so long as the patient otherwise adheres to a quantitative diet, includes fructose on an isocaloric basis, and only patient's mother administers the compound.
THE OPHTHALMOSCOPIC AND FLUORESCEIN ANGIOGRAPHIC PICTURE OF DIABETIC RETINOPATHY
Authors: Larsen Hans‐Walther 
Published: August 2010

Abstract. The ophthalmoscopic and fluorescein angiographic findings in diabetic retinopathy are reviewed. It is pointed out that the fundus lesions seen in diabetic retinopathy are characteristic, but not specific for diabetes.It is still not settled which role alterations in the microcirculation, alterations in the tissue metabolism, hypoxia or defects in the oxygen delivery system may play as provoking factors in the development of the diabetic retinopathy.Future investigations should concentrate on early diabetes and must include studies on the retinal blood‐flow, electroretinographic and histopathologic changes.
DYNAMIC CHANGES IN THE MICROCIRCULATION OF DIABETICS AS RELATED TO DIABETIC MICROANGIOPATHY
Authors: Kohner Eva M. 
Published: August 2010

Abstract. Reversible abnormalities of many vascular beds have been observed in early diabetes, before irreversible structural changes of diabetic microangiopathy became apparent.In the bulbar conjenctiva and in the kidney the changes are associated with vascular dysfunction and may be due to autonomic neuropathy. The role of autoregulation in these vascular beds is not clear.In the limb muscles and in the retina the functional abnormality in early diabetes and in those with only mild retionopathy is increased blood flow. This increase in blood flow is probably the result of autoregulatory adaptation to hypoxia induced by 2,3 diphosphoglycerate deficiency. Lactic acid accumulation may also contribute.Breakdown of the autoregulation in the retina results in the development of diabetic retinopathy. The late stages of retinopathy, new vessel formation, are an attempt at revascularisation of areas of capillary non‐perfusion.
THE PROBLEM OF TISSUE OXYGENATION IN DIABETES MELLITUS
Authors: Ditzel Jørn 
Published: August 2010

Abstract. Evidence for a causative relationship between prolonged tissue hypoxia and diabetic retinopathy and glomerulosclerosis are presented. Based on the assumption that one of the most fundamental requirements for optimal cellular metabolism is a constant cellular oxygen tension, the “three‐in‐one concept” for the development of diabetic microangiopathy is formulated. The term “three‐in‐one” is employed because this concept partly or completely includes “the glycoprotein‐”, “the hypoxia‐”, and “the growth hormone hypothesis”. Diabetics show evidence of variability in the tissue oxygen availability/demand ratio which is compensated by three self‐regulating factors: 1) an increase in local flow, 2) an increase in red cell 2,3‐DPG leading to a shift to the right of the oxyhaemoglobin dissociation curve, and 3) an increase in the oxygen‐binding capacity or the haemoglobin concentration. The level of plasma inorganic phosphate (Pi) is of importance in maintaining high 2,3‐DPG levels. However, since Pi fluctuates depending upon changes in the control of diabetes, the regulatory mechanism of the 2,3‐DPG modulated unloading of oxygen from the erythrocytes often becomes insufficient, and therefore in poorly regulated diabetics with less than optimal 2,3‐DPG levels, the main load of compensation against tissue hypoxia is placed on an adjustment in the microcirculation of the organ involved. However, in order for the microvascular dilatation to occur, the cells must experience a hypoxic stimulus. The summation of the infinite number of discrete and occasionally pronounced hypoxic injuries to the tissue cells in association with the adverse effect of local vasodilatation with increased plasma permeation through the vessel walls might over the years lead to diabetic microangiopathy.Based on this theory the high level of Pi in diabetes becomes of particular significance. Our experience with a high phosphate diabetes diet in the treatment of diabetics is presented. This dietary regimen leads to a significant increase in the oxygen release capacity of the erythrocytes, suggesting an improvement in tissue oxygenation, and may therefore become of value in the prophylaxis of diabetic microangiopathy.
Studies of the Mode of Action of Erucic Acid on Heart Metabolism
Authors: HEIJKENSKJÖLD LOLO , ERNSTER LARS 
Published: August 2010

AbstractThe effects of erucic acid on the oxidative metabolism of rat‐heart mitochondria have been investigated using intact animals, perfused beating heart, isolated mitochondria and mitochondrial extracts. Feeding rats with a diet containing erucic acid was found to lead to a diminished ability of the isolated heart mitochondria to oxidize various substrates, in accordance with previous reports (Houtsmuller et al., Biochim. Biophys. Acta 218 (1970) 564). This effect was most pronounced with palmitylcarnitine as substrate, in which case the rate of oxidation was decreased by more than 50 % at such a low erucic acid content in the diet as 1.4 % given over 2–4 weeks. Oxidation of palmitylcarnitine was also found to be inhibited when erucylcarnitine was added to isolated heart mitochondria from control animals, in agreement with earlier observations (Christophersen and Bremer, FEES Lett. 23 (1972) 230; Biochim. Biophys. Acta 280 (1972) 506). The inhibition was accompanied by a decrease in the rate and extent of reduction of mitochondrial flavoprotein. Experiments with perfused beating rat‐heart likewise revealed an inhibition of flavoprotein reduction, as well as nicotinamide nucleotide reduction, when erucate was added to the perfusing medium of the beating heart respiring with oleate ‐ but not with octanoate ‐ as substrate. These data together with those earlier published in the literature indicate that erucic acid may interfere with the enzyme system involved in the mitochondrial oxidation of long‐chain fatty acids, probably at the level of acyl‐CoA dehydrogenase. Kinetic data supporting this conclusion, obtained with extracts of rat‐heart mitochondria containing the acyl‐CoA dehydrogenase and electron‐transferring flavoprotein system, are presented. The possible implications of these results for the known effect of dietary erucic acid in causing an accumulation of fat in the heart are discussed.
Treatment of Hypertension in a Swedish Community—the Problem of Borderline Hypertension
Authors: WILHELMSEN LARS 
Published: August 2010

Summary. In a multifactor primary preventive trial currently in progress in Gothenburg, one‐third of men born between 1915–1922 and 1924–1925 were examined. The remaining two‐thirds acted as controls. Coronary heart disease (CHD) and stroke account for a considerable part of fatal and non‐fatal serious events in this population. In the intervention group the mortality was considerably higher among the non‐participants than among the participants.Hypertension is the main risk factor for stroke and is important in addition to hypercholesterolemia and smoking in CHD.The experiences concerning hypertension in the present population samale have been that:

Between 10% and iO% of men aged 47–55 years need treatment for high blood pressure.
At least 50% of these men do not know that they have hypertension and only 15% were on adequate treatment at the screening examination.
With the provision of information and use of calling system the drop‐out rate during the first year of follow‐up was only 1–2%.
Adverse drug reactions have not been a serious problem.
A major problem is the difficulty in controlling BP during the whole day including stressful events.
Another problem is to find simple additional tests which can reveal the prognosis in “borderline hypertension”.