PubMed Health⌕ Search

Biomedical subjects

A Aronoff

Publications and source records attributed to A Aronoff.

17 recordsLinked to original sources
PubMed1985

Red cell choline in Korsakoff psychosis.

Red blood cell (RBC) choline was measured in 48 male patients with Korsakoff psychosis secondary to alcoholism and in 19 age-matched male controls using gas chromatography-mass spectrometry. The variance in RBC choline was significantly different between Korsakoff patients and controls (p less than 0.002). RBC choline was significantly higher in Korsakoff patients compared with controls (p less than 0.02). There was no significant correlation between age and RBC choline. Higher RBC choline levels suggest differences in membrane transport properties. Differences in membrane properties may indicate a neuronal membrane vulnerability to the toxic effect of alcohol or to thiamine deficiency which lead to the degenerative changes associated with Korsakoff psychosis.

Aged↗
PubMed1982

Hypothalamic-pituitary dopaminergic function in hepatic failure in man.

The growth hormone (GH) response to apomorphine HCl (Apo) (0.75 mg sc), a dopamine (DA) receptor agonist, was assessed in healthy chronic alcoholics without cirrhosis (N = 20) and in patients with alcoholic cirrhosis both with (N = 5) and without (N = 14) hepatic encephalopathy (HE). A significant number of cirrhotic patients with (P less than 0.004) and without (P less than 0.002) HE had an impaired GH response (peak increment less than 5 ng/ml) compared with non-cirrhotic individuals. An impaired GH response was independent of the presence of HE. The magnitude of the GH response was unrelated to plasma oestrone, oestradiol, or progesterone concentrations but was significantly correlated with plasma testosterone levels (P less than 0.01). None of the patients with an abnormally low testosterone concentration showed a normal GH response. None of the subjects with HE showed an arousal response to Apo. These results suggest that DA receptor sensitivity is decreased in liver cirrhosis and that this decrease is related to inadequate circulating levels of testosterone. The occurrence of HE is independent of impaired DA function. The present study only evaluates DA function in the hypothalamic-pituitary axis and therefore may not reflect changes in other regions of brain.

Alcoholism↗
PubMed1978

Definition of a conjugation of dysfunction in Gilbert's syndrome: studies of the handling of bilirubin loads and of the pattern of bilirubin conjugates secreted in bile.

1. Intravenous doses of bilirubin (3.4 mumol/kg) were given to normal subjects and patients with Gilbert's syndrome. Both groups displayed an identical initial disappearance of a substantial proportion of the bilirubin but, late in time, the Gilbert's patients exhibited reduced clearance with a sustained elevation of the plasma bilirubin and no reflux into the plasma space of conjugated bilirubin. Increasing the dose in normal subjects (by factors of 3 and 6) failed to reproduce the response found in the Gilbert's patients. 2. In the the bile-containing duodenal aspirates of Gilbert's patients the average proportion of bilirubin found as bilirubin diglucuronide was 68% (normal 88%) and of bilirubin monoglucuronide, 23% (normal 7%). Both differences were significant at the P less than 0.001 level. In the Gilbert's patients restriction of caloric intake to 1569 kJ/day for 2 days characteristically raised the serum bilirbuin with no modification of the biliary pigment pattern; phenobarbital (180 mg/day for 2 weeks) decreased the plasma bilirubin to the normal range with, concomitantly, a reversion of the biliary pigment pattern towards normal. 3. We conclude that there is no hepatic uptake defect in Gilbert's syndrome but that there is decreased activity in the conjugation process underlying the addition of the second glucuronic acid moiety to bilirubin, to form bilirubin diglucuronide.

Adolescent↗
PubMed1976

Studies on cyclic AMP in different compartments of cerebrospinal fluid.

Adenosine 3', 5'-monophosphate (cAMP) was measured in the CSF of 42 patients undergoing radiological investigation, neurosurgical procedures, or investigation of hepatic coma. The concentration of cAMP was significantly higher in ventricular CSF than in lumbar CSF. Premedication with pentobarbitone plus promethazine increased cAMP in lumbar CSF. There was no difference in cAMP concentration in lumbar CSF obtained before or after injection of air or after the administration of diazepam during lumbar pneumoencephalography. Lumbar CSF cAMP concentration was significantly increased in patients in hepatic coma. The concentration of cAMP in the lateral ventricle was not affected by general anaesthesia or by the presence of a complete block of the aqueduct of Sylvius. There was no decrease in lumbar CSF cAMP in patients with a complete stenosis of the aqueduct of Sylvius, partial blocks of CSF flow at the cervical level, or a complete block at the lower thoracic level. The concentration of cisternal CSF cAMP was similar to that of lumbar CSF. These results suggest that (1) there is a ventriculolumbar gradient in the concentration of cAMP but of insufficient magnitude to be detected by mixing of lumbar and ventricular CSF during pneumoencephalography, (2) lumbar CSF cAMP concentration is not dependent on brain as a source of this nucleotide; the source of this nucleotide may be largely derived from the spinal cord, (3) premedication may affect the concentration of cAMP in lumbar CSF cAMP, (4) the formation of cAMP is unimpaired in hepatic coma.

Adult↗
PubMed1975

Relationships between tryptophan in serum and CSF, and 5-hydroxyindoleacetic acid in CSF of man: effect of cirrhosis of liver and probenecid administration.

Tryptophan was measured in the lumbar CSF and serum of patients undergoing neurological investigation (controls) and in patients with hepatic cirrhosis. Samples were taken from the fasting patients at 8:00 a.m. Under these conditions, in the controls the mean CSF, free )mpm-albumin-bound) and total serum tryptophan were in the approximate ratio 1:4:24. In this cross-sectional study, for the controls, CSF tryptophan was correlated significantly and positively with the total serum but not with the free serum tryptophan. In patients with advanced hepatic cirrhosis the mean CSF tryptophan concentration was greatly elevated. However, the mean total serum tryptophan was unchanged and the free serum tryptophan only slightly elevated. Administration of probenecid, which displaces tryptophan from binding sites on serum albumin, and thereby increases the proportion of serum tryptophan in the free form, did not affect CSF tryptophan.

Adult↗
PubMed1973

Hepatitis with Australia antigenemia following renal transplantation.

Over a seven-year period 18 of 125 patients who underwent renal transplantation developed hepatitis. Acute hepatic necrosis occurred in two, chronic aggressive hepatitis progressing to posthepatitic cirrhosis in eight, chronic persistent hepatitis in five, acute hepatitis with recovery in two and cholestatic hepatitis in one. Hepatic failure was the cause of death in four and a major contributing factor in three. Fifteen of the 18 were of blood Group A. After renal transplantation Australia antigen (Au) was present in the blood of 12 of the 15 patients with hepatitis who were tested and in one of 38 patients without clinical evidence of liver disease. Once present, Au persisted in all patients but one. Particles measuring 210 to 250 A, characteristic of Au, were seen in liver cells by electronmicroscopy in nine of the 10 patients examined who had hepatitis with Australia antigenemia, but they were not seen in the two patients studied with Au-negative hepatitis.

Acute Disease↗
PubMed1972

Virus-like particles in Australia antigen-associated hepatitis. An immunoelectron microscopic study of human liver.

IN A PREVIOUS REPORT (HUANG SN: Hepatitis-associated antigen hepatitis: an electron microscopic study. Am J Pathol 64:483-500, 1971) liver biopsies of renal transplant patients who developed chronic progressive viral hepatitis associated with persistence of Australia antigenemia [Au(1)] while under immunosuppressive therapy were studied. Predominantly intranuclear 210-250 A spherical, virus-like particles were revealed in 12 of 13 biopsies examined by electron microscope. No such particles were found in biopsies from Australia antigen negative patients. To investigate the relationship of these virus-like particles to Australia antigen, 2 of the Au(1) hepatitis renal transplant patients were restudied 6 to 8 months later. Liver biopsy material was prepared for light microscopy, immunofluorescent microscopy, electron microscopy and immunoelectron microscopy. The specificity of the anti-Au(1) serum used in this study was ascertained by immunodiffusion and immunoelectrophoresis, and by immunoelectron microscopic studies of the antigen-antibody complex prepared in vitro by mixing the ferritin-conjugated anti-Au(1) reagent with the purified Au(1) particles. Electron microscopy of biopsies from liver not treated with antibody showed that virus-like particles persisted in liver cells. Immunofluorescent microscopy of teased liver biopsy suspensions showed nuclear and some cytoplasmic fluorescence, indicating the cellular localization of Au(1). The immunoelectron microscopic preparations showed agglutination of the virus-like particles and the presence of antibody coupled ferritin in the intranuclear and cytoplasmic particle agglutinates. No virus-like particles were seen in the biopsy from a control patient without Au(1) antigenemia, and results of the immunoelectron microscopic procedure were negative. Our observations that massive amounts of Au(1)-associated particles are located in liver cell nuclei of individuals with chronic active hepatitis strengthen the hypothesis of Blumberg et al that Au(1) is an infectious agent and/or the antigenic determinant of a hepatitis virus.

Antigen-Antibody Complex↗
PubMed1971

Regional lung function in patients with hepatic cirrhosis.

The lung volume at which the dependent lung zones begin to trap gas as a result of airway closure (i.e., the "closing volume") was measured with (133)Xe in 10 seated patients with hepatic cirrhosis. In all of them the closing volume was increased above normal, and in eight it was greater than the functional residual capacity, indicating the presence of airway closure and gas trapping during resting tidal volume breathing. Direct measurements made with (133)Xe in five cirrhotic patients (a) confirmed the presence of increased gas trapping in the lower lung zones both at residual volume and at functional residual capacity, and (b) indicated that in liver cirrhosis the ventilation-perfusion ratio of the dependent lung zones may be very low, primarily as a result of decreased ventilation due to airway closure. It is concluded that in hepatic cirrhosis, gas trapping in the dependent lung zones may be an important cause of impaired gas exchange within the lungs. It is suggested that the premature airway closure observed in this disease may be due to mechanical compression of small airways by dilated blood vessels and/or interstitial pulmonary edema.

Adolescent↗
PubMed1965

Adrenocortical hyperfunction associated with bronchogenic carcinoma: report of five cases.

Five patients with bronchogenic carcinoma associated with adrenocortical hyperfunction are described. The clinical features, laboratory studies and autopsy findings are discussed and compared with previously reported cases. Four patients presented most of the typical features of this disorder as previously described, whereas the fifth was atypical in some respects. Typical features included: acute onset of adrenocortical hyperfunction in a middle-aged male, rapid downhill course, slight or absent physical signs of Cushing's syndrome, frequently impaired glucose tolerance, markedly elevated plasma and urinary 17-hydroxycorticosteroids not suppressed by exogenous steroids, absent diurnal variation of plasma corticoids, hypokalemic alkalosis with normal aldosterone excretion, and tumour histology of the oat cell variety. The adrenal glands of two patients were of normal or slightly increased weight, and mean 17-ketosteroid excretion values were normal in three; this contrasts with the marked increase in adrenal weight and 17-ketosteroid excretion in most reported cases.

17-Ketosteroids↗