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R D Cohen

Publications and source records attributed to R D Cohen.

At least 163 records · Page 9Linked to original sources
PubMed1978

Mechanism of the effect of varying PCO2 on gluconeogenesis from lactate in the perfused rat liver.

1. The effects of varying PCO2 on glucose output and the intracellular concentrations of lactate, pyruvate, phosphoenolpyruvate, 2-phosphoglycerate and 3-phosphoglycerate were studied in the isolated rat liver perfused with differing concentrations of lactate. 2. When the perfusate lactate concentration is above 1.5 mmol/l respiratory acidosis (simulated by high perfusate PCO2) inhibits gluconeogenesis from lactate, whereas respiratory alkalosis stimulates gluconeogenesis. 3. In general there were significant positive correlations between intracellular pH (pHi) and hepatocyte phosphoenolpyruvate, 2-phosphoglycerate and 3-phosphoglycerate concentrations, and negative correlations between pHi and lactate and pyruvate concentrations; there were usually significant correlations in the opposite sense between these metabolites and log PCO2. 4. The results suggest that CO2 exerts an inhibitory effect on gluconeogenesis at a step between pyruvate and phosphoenolypruvate; however, this is not the only effect of CO2 on the gluconeogenic sequence. CO2 probably acts by changing pHi, but direct effects of CO2 and HCO-3 cannot be excluded. 5. Except at low lactate concentrations, nonionic diffusion probably does not play a major role in the entry of lactate into the hepatocyte.

Animals↗
PubMed1978

Intestinal cholecalciferol absorption in the elderly and in younger adults.

1. A method for assessing cholecalciferol absorption in man is described. 2. The intestinal absorption of [3H]cholecalciferol was studied in 20 female geriatric patients, most of whom were vitamin D-depleted. 3. The plasma [3H]cholecalciferol response after oral ingestion was significantly lower than that of a group of younger female subjects. 4. The plasma response of labelled polar metabolites of cholecalciferol was also lower in the geriatric than in the younger group, suggesting that increased removal of label by conversion into more polar metabolites could not account for the reduced plasma [3H]cholecalciferol response. 5. There was no evidence that alteration in gastrointestinal motility could account for the different rate of appearance of the labelled vitamin in the plasma in the two groups. 6. It is suggested that there is a defect in intestinal absorption of cholecalciferol in the elderly.

Adult↗
PubMed1977

Vitamin-D metabolism in nephrotic syndrome.

Plasma concentrations of 25-hydroxy-cholecalciferol (25-OHD3) and vitamin-D-binding globulin (V.D.B.G.) were significantly reduced in ten nephrotic subjects. V.D.B.G., which is undetectable in normal urine, was present in substantial amounts in the urine of each nephrotic subject. Administration of 3H-labelled cholecalciferol to three subjects resulted in the rapid appearance of the labelled vitamin in the urine, mainly as the 25-hydroxylated metabolite bound to V.D.B.G. in amounts which could largely account for the low plasma-25-OHD3. The plasma half-life of 25-OHD3 was substantially reduced in the nephrotic syndrome.

Adult↗
PubMed1977

The mechanism of inhibition by acidosis of gluconeogenesis from lactate in rat liver.

1. Gluconeogenesis from lactate or pyruvate was studied in perfused livers from starved rats at perfusate pH7.4 or under conditions simulating uncompensated metabolic acidosis (perfusate pH6.7-6.8). 2. In 'acidotic' perfusions gluconeogenesis and uptake of lactate or pyruvate were decreased. 3. Measurement of hepatic intermediate metabolites suggested that the effect of acidosis was exerted at a stage preceding phosphoenolpyruvate. 4. Total intracellular oxaloacetate concentration was significantly decreased in the acidotic livers perfused with lactate. 5. It is suggested that decreased gluconeogenesis in acidosis is due to substrate limitation of phosphoenolypyruvate carboxykinase. 6. The possible reasons for the fall in oxaloacetate concentration in acidotic livers are discussed; two of the more likely mechanisms are inhibition of the pyruvate carboxylase system and a change in the [malate]/[oxaloacetate] ratio due to the fall in intracellular pH.

Animals↗
PubMed1977

Large branchiogenic cyst in a neonate producing upper airway obstruction.

We report on a large branchiogenic cyst in a neonate. The etiology of these cysts is assumed to be of branchial origin because of their communication with the pharynx and their intimate association with the thyroid and thymus glands. This report documents an additional occurrence of this rare lesion. Physicians are alerted to the fact that, should massive enlargements and compromise of the respiration be present, external decompression of these cysts is feasible.

Airway Obstruction↗
PubMed1976

Rapid diagnosis of thyroid disease using carbonic-anhydrase immunoassay.

Erythrocyte carbonic-anhydrase-I (C.A.I.) concentration was measured by radial immunodiffusion in 30 thyrotoxic patients and 15 myxoedemic patients, the results being compared with those found in a control group of 90 euthyroid individuals. In thyrotoxicosis the erythrocyte-C.A.I. concentration was found to be below 10-29 mg/g haemoglobin, whereas the normal range varied from 11-1 to 22-5 mg C.A.I./g Hb. Low values were found in 4 patients with triiodothyronine(T3)-toxicosis. In myxoedema, the mean erythrocyte-C.A.I. concentration, though elevated at 20-37 mg/g Hb, fell within the normal range. In pregnancy, the erythrocyte-C.A.I. concentration rose with time, the mean value at tern being 20-6 +/-S.D. 3-3 mg/g Hb. In a group of women taking oral contraceptives, a low erythrocyte-C.A.I. concentration was noted--an effect which was most obvious among those taking low-oestrogen contraceptives. It is suggested that erythrocyte-C.A.I. estimation provdes a rapid screening test for thyrotoxicosis.

Adolescent↗
PubMed1976

The haemodynamic effects of metabolic acidosis in the rat.

1. The effect of metabolic acidosis of 4-6 h duration on cardiac output, blood pressure, heart rate, and hepatic and renal blood flow has been studied in the rat. 2. In anaesthetized rats, blood pressure and heart rate fell linearly with blood pH in both sham-operated and nephrectomized rats. There was no significant difference between the two groups in the effect of acidosis on either variable. 3. Cardiac output showed a significant fall with increasing acidosis in the conscious rat. 4. Estimated hepatic blood flow in conscious rats showed a significant positive correlation with blood pH in both sham-operated and nephrectomized animals. There was no significant difference in estimated hepatic blood flow between the two groups of animals at any blood pH. 5. In conscious rats, increasing acidosis caused a progressive decrease in estimated renal blood flow. 6. It is concluded that the increase in the previously described apparent renal contribution to lactate removal in the acidotic rat cannot be explained by any circulatory effect mediated by the kidney. The possible relevance of the findings to lactate homeostasis is discussed.

Acidosis↗
PubMed1976

The effect of acidosis on lactate removal by the perfused rat kidney.

1. The isolated perfused kidneys of fed rats in normal acid-base status showed a constant rate of lactate removal from the perfusate between 5 and 90 min of perfusion at a perfusate pH of 7-4-7-5. 2. Lactate removal by kidneys of rats in normal acid-base status was stimulated within 30 min by a reduction in perfusate pH to 7-1-7-2, but depressed when perfusate pH was reduced further. 3. Kidneys taken from rats previously made acidotic and perfused with media of various pH values showed a progressive fall in the rate of lactate removal during the perfusion. 4. Glucose output by the kidneys of rats in normal acid-base status perfused with lactate as substrate was not affected by an alteration in perfusate pH. The kidneys of acidotic rats generally showed an increased rate of glucose output compared with those of control rats.

Acid-Base Imbalance↗
PubMed1976

Some problems of confidentiality in medical computing.

Patients have a right to consider that any information about themselves will be regarded as confidential, but inadvertently, and, very occasionally deliberately, that confidence may be broken. Therefore the principles on which the computer system at The London Hospital is based rest on maintaining confidentiality but at the same time using the facilities unique to the computer to the fullest extent for the benefit of patients. The system is described in outline, and a note is added of occasions when it would be desirable to suppress information on a patient and the reasons for so doing.

Computers↗
PubMed1975

The contribution of the kidney to the removal of a lactic acid load under normal and acidotic conditions in the conscious rat.

1. The rate of removal from the circulation of an intravenous lactic acid load has been studied in conscious rats, previously subjected either to bilateral nephrectomy or to a sham operation. 2. In rats with normal blood pH, the apparent contribution of the kidneys to removal of the lactic acid load is 30%; less than 12% of the renal contribution is attributable to urinary excretion. 3. In bilaterally nephrectomized rats made acidotic by administration of ammonium chloride, the rate of removal of a half-neutralized lacrtic acid load is progressively decreased with increasing severity of acidosis. No such effect is seen in sham-operated animals. 4. An increase in the ability of the kidney to remove lactate during acidosis compensates for approximately half of the simultaneous fall in the capacity of the remainder of the body for lactate assimilation. 5. Basal blood lactate concentrations fall in the presence of metabolic acidosis.

Acidosis↗
PubMed1975

Plasma free fatty acid turnover in total lipodystrophy.

Basal free fatty acid (FFA) turnover was found to be elevated or at the upper limit of normal in a patient with total lipodystrophy. The decrease in plasma FFA concentration which occurred after intravenous administration of insulin was shown to be primarily due to a fall in the inflow of FFA into the circulation. These results provide support for the suggestion that adipocytes in total lipodystrophy are able to synthesize triglycercide, but that they are unable to store it because of rapid lipolysis.

Adult↗
PubMed1975

Acid-base and metabolic disturbances in fulminant hepatic failure.

In 28 patients with fulminant hepatic failure alkalaemia was present in 49 of a total of 65 observations. Alkalaemia was due primarlily to a low Pa, C02 in 30 instances and to raised plasma bicarbonate in 16 instances. Blood lactate, pyruvate, and acetoacetate were significantly raised, and in individual cases, blood citrate, succinate, and fumarate were elevated. Blood citrate rose progressively as the clinical condition worsened. Metabolic acidosis was only present in four patients. In three of these patients, all of whom had taken an overdose of paracetamol, the acidosis was severe, present before the onset of clinical heparic failure, and associated with hypoglycaemiaand mild hypotension. In two of these patients the acidosis was shown to be due to accumulation of lactic acid. Plasma free fatty acid concentrations were elevated out of proportion to the degree of ketosis.

Acetoacetates↗
PubMed1975

Effect of phenformin on gluconeogenesis from lactate and intracellular pH in the isolated perfused guinea pig liver.

Gluconeogenesis from lactate and hepatic cell pH (pHi) were measured in the isolated perfused livers of starved guinea pigs in the presence and absence of phenformin (phenethylbiguanide). The observed decrease in lactate consumption and glucose output in the presence of phenformin was associated with a fall in pHi. The fall in glucose output observed was considerably greater than accountable for by the decrease in lactate consumption. A possible mechanism for the pathogenesis of clinical lactic acidosis due to phenformin therapy is suggested.

Acidosis↗