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Biomedical subjects

P Lund

Publications and source records attributed to P Lund.

At least 127 records · Page 7Linked to original sources
PubMed1979

Cervico-facial actinomycosis. A retrospective study.

A retrospective investigation of 25 cases of verified cervico-facial actinomycosis recorded in the period 1971--76 is presented. The results have been compared with the findings from a previous examination carried out by one of the authors during 1955--64. A marked increase of cervico-facial actinomycosis was noted. The clinical picture seems to be changing to a more alarming appearance, in agreement with the classical description of this entity. According to this agreement with the classical description of this entity. According to this a prolongation of the period of treatment was found. Other aspects of the disease are discussed based on the present results. The recommended treatment is still a combination of antibiotic medication and surgical removal of infectious foci.

Actinomycosis, Cervicofacial↗
PubMed1978

Sources of ammonia for mammalian urea synthesis.

The initial rate of incorporation of [15N]alanine into the 6-amino group of the adenine nucleotides in rat hepatocytes was about one-eighteenth of the rate of incorporation into urea. Thus the purine nucleotide cycle cannot provide most of the ammonia needed in urea synthesis for the carbamoyl phosphate synthase reaction (EC 2.7.2.5). On the other hand, contrary to the view expressed by McGivan & Chappell [(1975) FEBS Lett. 52, 1--7], the experiments support the view that hepatic glutamate dehydrogenase can supply the required ammonia.

Adenine Nucleotides↗
PubMed1977

Skin perfusion pressure measured as the external pressure required to stop isotope washout. Methodological considerations and normal values on the legs.

The skin perfusion pressure was measured as the external pressure required to stop blood flow, as evidenced by cessation of the washout of an intracutaneous depot of [131I-]antipyrine mixed with histamine. The external pressure on the skin was measured by an 11 x 11 cm slack air-filled plastic cushion connected to a mercury manometer and interposed between the labelled area and a blood pressure cuff. The 'flow cessation external pressure' (FCEP) varied parallel to the intra-arterial femoral mean blood pressure, but was on the average 10.8 mmHg (SD 6.4) lower. FCEP was measured on twenty normal subjects at four different segments of the leg. The average differences between auscultatory brachial mean blood pressure and FCEP were: thigh 12.0 mmHg (SD 7.6); calf 10.4 mmHg (SD 7.4); ankle 12.9 mmHG (SD 10.1); foot 20.2 mmHg (SD 12.1). The SD of the difference between measurements on two different days, performed in forty-four patients with different degrees of occlusive arterial disease, varied between 5.6 and 8.3 mmHg at the different levels. The present data indicate that the skin perfusion pressure on the legs in normal subjects lies approximately 10 mmHg lower than the systemic mean arterial blood pressure.

Arterial Occlusive Diseases↗
PubMed1975

Rapid separation of isolated hepatocytes or similar tissue fragments for analysis of cell constituents.

A simple device is described for the rapid centrifugal separation of isolated hepatocytes or similar tissue fragments from the suspending medium. Rapid separation is essential if meaningful information on the concentrations of cell constituents and their distribution between cell and suspension medium is to be obtained. The usefulness of the technique is illustrated by measurements of hepatocyte constituents (glutamate, aspartate, alanine, K+) which show large concentration gradients against the extracellular medium.

Alanine↗
PubMed1975

Effect of adenosine on the adenine nucleotide content and metabolism of hepatocytes.

ADENOSINE (0.5 MM) added to hepatocyte suspensions increased the intracellular concentration of ATP and total adenine nucleotides within 60 min up to three-fold. 2. Adenosine at 0.5 mM inhibited gluconeogenesis from lactate by about 50%. At higher adenosine concentrations the inhibition was less. There was no strict parallelism between the time-course of the increase of the adenine nucleotide content and the time-course of the inhibition of gluconeogenesis from lactate. 3. Adenosine abolished the accelerating effects of oleate and dibutyryl cyclic AMP on gluconeogenesis from lactate. 4. Gluconeogenesis was no significant effect of adenosine with fructose, dihydroxyacetone or glycerol. With asparagine, adenosine caused anacceleration of glucose formation. 5. Adenosine incorporation into adenine nucleotides accounted for about 20% of the adenosine removal. 6. Inosine, hypoxanthine or adenine compared with adenosine gave relatively slight increases of adenine nucleotides. 7. Urea synthesis from NH4Cl under optimum conditions i.e. in the presence of ornithine, lactate and oleate, was also inhibited by adenosine. The inhibition increased with the adenosine concentration and was 65% at 4 mM-adenosine. Again there was no correlation between the degree of inhibition of urea synthesis and the increase in the adenine nucleotide content. 8. The basal O2 consumption, the increased O2 consumption on the addition of oleate and the rate of formation of ketone bodies were not affected by the addition of adenosine. The [beta-hydroxybutyrate]/[acetoacetate] ratio was increased by adenosine, provided that lactate was present. 9. The increase of the adenine nucleotide content of the hepatocytes on the addition of adenosine may be explained on the assumption that adenosine kinase is not regulated by feedback but by substrate supply.

Adenosine↗
PubMed1975

Investigation of NZB mice born to BALB/c immunized against NZB allotype.

Allotype suppression is held to be an example of T-cell suppressor function. Failure of generalized suppressor T-cell function is considered to be responsible for the chronic and progressive disease of the NZB. The possible association of allotype suppression and autoimmune disease has been investigated here in a group of NZB mice, transplanted and born from BALB/c recipients whilst producing anti-NZB allotype. In this situation it was anticipated that if allotype suppression should fail this would coincide with the development of autoimmune disease; both processes reflecting failure of T-cell suppressor function. However, in spite of the fact that allotype suppression was not achieved, certain observations seem important. The fact that NZB born the BALB/c were in no way different from normally derived NZB confirms that the cause of the NZB disease is established prior to the stage of implantation. Maternal influence at or beyond this stage appears of little consequence in terms of effecting the development or progression of the NZB disease. The failure to induce allotype suppression in the NZB is important. In this context this strain appears to be no different from the majority of other strains that have been tested as homozygotes. The suppression obtained with (BALB/c X SJL/J)F1 hybrids in which chronic suppression has been achieved therefore seems to represent an exceptional situation and this suggests that it is perhaps unwise to base general assumptions as to the universal adaptability of T-cell control mechanisms upon unusual findings. It must be remembered that only homozygotes were examined here. Earlier attempts to induce allotype suppression in homozygotes also failed, even in the SJL/J. Since allotype suppression has only been demonstrated in heterozygote mice there is a distinct possibility that this phenomenon never occurs in the homozygote situation. The significance of this possibility is discussed.

Age Factors↗
PubMed1974

The effect of lysine on gluconeogenesis from lactate in rat hepatocytes.

1. In freshly prepared isolated rat liver cells there is a lag in gluconeogenesis from lactate. The magnitude of the lag increases with increasing lactate concentration. 2. The lag is virtually abolished by lysine. 3. A few other amino acids (tyrosine, arginine, asparagine, ornithine) and NH(4)Cl had effects similar to, but less pronounced than, lysine during the early stage of incubation. Lysine was unique in accelerating gluconeogenesis beyond the lag period. 4. The effects of the accelerators are not additive. 5. Glycine, serine, threonine, cysteine, tryptophan and histidine at 2mm markedly inhibit (>20%) gluconeogenesis from lactate. 6. Oleate, which promotes gluconeogenesis from lactate by supplying acetyl-CoA required for the pyruvate carboxylase reaction, had no effect on the lag, yet oleate oxidation showed no lag. 7. Preincubation of cells decreased the lag and decreased the magnitude of the lysine effect. 8. Pyruvate (added at 1mm to give an initial [lactate]/[pyruvate] ratio of 10) also abolished the lag and decreased the lysine effect by about 50%. 9. Lysine reversed the inhibition by ethanol of gluconeogenesis from lactate. 10. All accelerators increased the rate of re-oxidation of cytosolic NADH as shown by a rapid re-adjustment of the [lactate]/[pyruvate] ratio on addition of 10mm-lactate. 11. The accelerated rates of gluconeogenesis are associated with an increased formation of aspartate and glutamate and especially alanine. 12. The existence of the lag period can be explained on the basis of the fact that the accumulation of pyruvate during the lag diverts oxaloacetate from gluconeogenesis to malate formation, i.e. that the re-oxidation of cytosolic NADH takes precedence over gluconeogenesis. This means that much oxaloacetate formed by the pyruvate carboxylase reaction has to be transferred twice from the mitochondria to the cytosol by the aspartate shuttle. Under these conditions the operation of the shuttle limits the rate of gluconeogenesis from lactate. Lysine and other accelerators may increase the effectiveness of the shuttle by providing components of the aspartate aminotransferases involved. The question of why lysine specifically accelerates gluconeogenesis beyond the lag period is discussed.

Alanine↗
PubMed1973

Acceleration of gluconeogenesis from lactate by lysine (Short Communication).

l-Lysine (2mm) causes an increase (mean 60%) in the rate of gluconeogenesis from lactate in isolated liver cells. The effect is of a catalytic nature. No other amino acid has the same effect, though ornithine is slightly active. The effect is additional to the stimulatory effects of oleate and of dibutyryl cyclic AMP.

Journal Article↗
PubMed1973

Accumulation of amino acids by the perfused rat liver in the presence of ethanol.

1. The rate of gluconeogenesis from alanine in the perfused rat liver is affected by the presence of other metabolizable substances, especially fatty acids, ornithine and ethanol. Gluconeogenesis is accelerated by oleate and by ornithine. When both oleate and ornithine were present the acceleration was greater than expected on the basis of mere additive effects. 2. Much NH(3) and some urea were formed from alanine when no ornithine was added. With ornithine almost all the nitrogen released from alanine appeared as urea. 3. Lactate was a major product of alanine metabolism. Addition of oleate, and especially of oleate plus ornithine, decreased lactate formation. 4. Ethanol had no major effect on gluconeogenesis from alanine when this was the sole added precursor. Gluconeogenesis was strongly inhibited (87%) when oleate was also added, but ethanol greatly accelerated gluconeogenesis when ornithine was added together with alanine. 5. In the absence of ethanol the alanine carbon and alanine nitrogen removed were essentially recovered in the form of glucose, lactate, pyruvate, NH(3) and urea. 6. In the presence of ethanol the balance of both alanine carbon and alanine nitrogen showed substantial deficits. These deficits were largely accounted for by the formation of aspartate and glutamine, the formation of which was increased two- to three-fold. 7. When alanine was replaced by lactate plus NH(4)Cl, ethanol also caused a major accumulation of amino acids, especially of aspartate and alanine. 8. Earlier apparently discrepant results on the effects of ethanol on gluconeogenesis from alanine are explained by the fact that under well defined conditions ethanol can inhibit, or accelerate, or be without major effect on the rate of gluconeogenesis. 9. It is pointed out that in the synthesis of urea through the ornithine cycle half of the nitrogen must be supplied in the form of asparate and half in the form of carbamoyl phosphate. The accumulation of aspartate and other amino acids suggests that ethanol interferes with the control mechanisms which regulate the stoicheiometric formation of aspartate and carbamoyl phosphate.

Alanine↗
PubMed1973

Synthesis of essential amino acids from their alpha-keto analogues by perfused rat liver and muscle.

Most essential amino acids can be replaced by their alpha-keto-analogues in the diet. These ketoacids have therefore been proposed as substitutes for dietary protein. In order to determine their fate in tissues of normal animals, isolated rat liver and hindquarter (muscle) preparations were perfused with keto-analogues of valine, leucine, isoleucine, methionine, or phenylalanine. When perfused at 1.5-2.0 mM, all five compounds were utilized rapidly by the liver of 48-h starved rats, at rates varying from 49 to 155 mumol/h per 200g rat. The corresponding amino acids appeared in the medium in significantly increased concentrations. Perfusion with phenylpyruvate also led to the appearance of tyrosine. Urea release was unaltered. Measurement of metabolite concentrations in freeze-clamped liver revealed two abnormalities, particularly at ketoacid concentrations of 5 mM or above: a large increase in alpha-ketoglutarate, and a moderate to marked decrease in tissue glutamine. This decrease was quantitatively sufficient to account for nitrogen appearing in newly synthesized amino acids. Isolated hindquarters of fed rats were perfused with the same ketoacids at concentrations of 1.3-8.0 mM. All were utilized at rates varying from 1.4 to 7.0 mumol/h per g muscle perfused. The corresponding amino acids were released at greatly increased rates. Alanine and glutamate levels fell in some perfusions, but the principal nitrogen donor in muscle was not identified; the content of glutamine in tissue, and its rate of release into the perfusate remained constant.

Acetoacetates↗
PubMed1972

The effects of halothane (2-bromo-2-chloro-1,1,1-trifluoroethane) on glycolysis and biosynthetic processes of the isolated perfused rat liver.

1. With reference to the post-operative dysfunction of the liver observed after halothane anaesthesia, the effects of the anaesthetic on some metabolic functions were studied in the isolated perfused rat liver. Oxygen uptake, glycolysis, gluconeogenesis and urea synthesis were affected by halothane at a concentration (2.5% of the gas phase) within the range used in clinical anaesthesia. 2. At this concentration of halothane uptake of oxygen was inhibited in livers from both fed and starved rats. 3. In livers from fed rats there was a 16-fold increase in lactate production. This was accompanied by a fivefold decrease in the tissue content of 2-oxoglutarate and a more than twofold decrease in citrate. The calculated [free NAD(+)]/[free NADH] ratio in both cytoplasm and mitochondria was lower in the halothane-exposed livers than in controls. 4. In livers of starved rats the rate of gluconeogenesis from lactate was decreased by halothane to 30% of the control rate. 5. Halothane inhibited gluconeogenesis from alanine and propionate to the same extent as from lactate, whereas glucose formation from dihydroxyacetone, glycerol, fructose and sorbitol was relatively unaffected. 6. During gluconeogenesis from 10mm-lactate the tissue content of ATP was decreased by 50%, glutamate by 50% and 2-oxoglutarate was decreased eightfold in the halothane-exposed livers. 7. Halothane decreased urea synthesis in the presence of 10mm-NH(4)Cl and 2mm-ornithine to 15% of the control rate. 8. The inhibitions of gluconeogenesis and urea synthesis were completely abolished within 15min of withdrawal of the anaesthetic. 9. The stimulation of uptake of oxygen brought about by the addition of lactate or precursors of urea was abolished by halothane. 10. Effects on gluconeogenesis similar to those of halothane occurred in livers exposed to the anaesthetic methoxyflurane, although normal rates were not restored on withdrawal of the drug. Other anaesthetic agents tested (ketamine-HCl and trichloroethylene) decreased gluconeogenesis to 66% of the control rate. 11. The inhibitory effects of halothane are consistent with an interference at the stage of the NADH dehydrogenase of the electron-transport chain.

Acetone↗