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Biomedical subjects

I Diamond

Publications and source records attributed to I Diamond.

At least 91 records · Page 5Linked to original sources
PubMed1986

Ethanol regulates calcium channels in clonal neural cells.

The acute and long-term effects of ethanol on voltage-dependent Ca channel function were studied in PC12, a clonal cell line of neural crest origin. Acute exposure to ethanol produced a concentration-dependent decrease in depolarization-evoked 45Ca2+ uptake, while prolonged (2-10 days) exposure led to a reciprocal increase in 45Ca2+ uptake and in the number of Ca-channel binding sites labeled by the dihydropyridine Ca-channel antagonist [3H]nitrendipine. Uptake was restored to control levels following withdrawal of ethanol from cultures. These findings indicate that cellular adaptation to ethanol may involve enhanced expression of dihydropyridine-sensitive, voltage-dependent Ca channels.

Animals↗
PubMed1986

Ethanol regulation of adenosine receptor-stimulated cAMP levels in a clonal neural cell line: an in vitro model of cellular tolerance to ethanol.

The acute and chronic neurologic effects of ethanol appear to be due to its interaction with neural cell membranes. Chronic exposure to ethanol induces changes in the membrane that lead to tolerance to the effects of ethanol. However, the actual membrane changes that account for tolerance to ethanol are not understood. We have developed a model cell culture system, using NG108-15 neuroblastoma-glioma hybrid cells, to study cellular tolerance to ethanol. We have found that adenosine receptor-stimulated cAMP levels increased markedly upon acute exposure to ethanol. However, the cells became tolerant to ethanol, since chronically treated cells required ethanol to maintain normal adenosine-stimulated cAMP levels. Moreover, the cells appeared to be dependent on ethanol, as evidenced by reduced adenosine-stimulated cAMP levels in the absence of ethanol. Recovery occurred after ethanol was withdrawn. These cellular changes appear to parallel the clinical events of acute ethanol intoxication, tolerance, and dependence.

Animals↗
PubMed1985

Criteria for the clinical laboratory director.

The Board of Governors of the College of American Pathologists approved in 1984 a set of criteria for the directorship of a hospital clinical laboratory. This article is a commentary on those criteria. The opinions expressed are the author's and do not necessarily reflect the position of the College.

Administrative Personnel↗
PubMed1985

The hospital laboratory 50 years ago.

Few things remain the same, and the laboratory is no exception. As technology evolved and scientific knowledge advanced, the hospital laboratory changed in ways never dreamed of. In this article Dr. Diamond recalls--for our amusement and enlightenment--long-forgotten practices. The reminiscences of other pathologists will be published periodically in "Looking Back."

History, 20th Century↗
PubMed1984

Interaction of ethanol with neural cells in culture: a model of intoxication, tolerance and withdrawal.

The interaction of ethanol with the nervous system produces acute intoxication, tolerance and withdrawal phenomena. Additionally, there are several alcohol-related neurological disorders which develop in alcoholic patients. Current evidence suggests that ethanol produces some of these changes by altering the structure and function of neural membranes. Therefore, neurotransmitter receptors and receptor-dependent molecular events in the nervous system may be highly sensitive to ethanol. The murine neuroblastoma X glioma hybrid cell line NG108-15 was used to study the acute and chronic interactions of ethanol with intact cells. Ethanol acutely inhibited opiate receptor binding, but after chronic exposure the cells exhibited an apparent adaptive increase in the number of opiate binding sites; this was reversible when ethanol was withdrawn. High levels of ethanol (200 mM) increased opiate binding after 18-24 hours; lower concentrations (25-50 mM) produced similar changes after two weeks. This model system has great potential for exploring the cellular and molecular mechanisms which underlie ethanol intoxication, tolerance and withdrawal.

Adaptation, Physiological↗
PubMed1984

Chromatographic separation of the C(1), C(1a), and C(2) components of gentamicin and the assessment of their individual binding to serum proteins.

[3H]gentamicin and [14C]gentamicin samples were purified by Sephadex column chromatography and separated by an HPLC technique into the three major, medicinally active gentamicin components. These separated components were used in equilibrium dialysis studies to determine their percent binding to serum proteins. The bindings of the components were inversely related to concentrations of ionized calcium and magnesium. When dialyzed against a buffer containing physiological concentrations of the divalent cations, the binding of the C(1) component was 2.2 +/- 1.0%, the binding of the C(1a) component was 1.2 +/- 1.9%, and the binding of the C(2) component was 5.0 +/- 2.0%. The percent bindings are not identical and, due to their low values, probably have negligible clinical significance. The radioactive composition and purity of the 3H- and 14C-labeled gentamicin samples differed and these may be important factors in the variance of reported gentamicin bindings.

Blood Proteins↗
PubMed1984

Irreversible inhibition of phospholipid methylation and protein carboxymethylation does not alter acetylcholine receptor function in muscle cells.

The role of methyltransferase (MT) reactions in acetylcholine (ACh)-evoked depolarization and contraction in primary chick myotubes was determined by using a mixture of erythro-9-(2-hydroxy-3-nonyl) adenine, homocysteine thiolactone, and adenosine which together inhibit the activity of MT. Carboxy-MT and lipid-MT activities were inhibited irreversibly by 91 and 100%, respectively. ACh-induced muscle contraction was also inhibited within 10 min after application of the inhibitor mixture. However, in contrast to permanent inhibition of MT activities, inhibition of acetylcholine receptor (AChR)-dependent muscle contraction was reversible. Moreover, physiological studies showed that the inhibitor mixture had no effect on resting membrane potential or ACh-induced depolarization or desensitization. These results suggest that AChR function is not altered by methylation inhibitors and that changes in AChR-mediated contraction are not due to inhibition of MT activities.

Acetylcholine↗
PubMed1984

Ethanol and the gamma-aminobutyric acid-benzodiazepine receptor complex.

Ethanol appears to enhance gamma-aminobutyric acid (GABA)-mediated synaptic transmission. Using radioligand binding techniques, we investigated the possibility that the GABA-benzodiazepine receptor complex is the site responsible for this effect. Ethanol at concentrations up to 100 mM failed to alter binding of [3H]flunitrazepam (FNZ), [3H]Ro 15-1788, or [3H]methyl-beta-carboline-3-carboxylate (MBCC) to benzodiazepine receptors, or of [3H]muscimol to GABA receptors in rat brain membranes. Scatchard analyses of the binding of these radioligands at 4 degrees C and 37 degrees C revealed no significant effects of 100 mM ethanol on receptor affinity or number. A variety of drugs as well as chloride ion increased binding of [3H]FNZ and/or [3H]muscimol, but these influences were not modified by ethanol. These findings indicate that ethanol probably potentiates GABAergic neurotransmission at a signal transduction site beyond the GABA-benzodiazepine receptor complex.

Animals↗
PubMed1984

Quality circles in the clinical laboratory.

The success of the quality circles in Japanese industry has led many American firms to institute the circles into their operations. A few hospitals have also done this, but little has been published about quality circles in the clinical laboratory. This paper describes briefly the structure and function of the quality circles and discusses their possible role in the laboratory.

Group Processes↗
PubMed1984

Curious neurologic sequelae in galactosemia.

Two siblings with classic transferase deficiency galactosemia that was detected at birth have been treated with lactose restriction since the neonatal period. Both patients developed a unique and progressive neurologic syndrome of mental retardation, tremor, and ataxia. Careful review of the family history and medical records, the absence of metabolic disturbances other than those related to galactosemia, and the aggregate physical findings and neurodiagnostic studies ruled out other neurologic disorders in these siblings. It is therefore proposed that these patients represent a subgroup of transferase-deficient galactosemic patients, who develop characteristic neurologic sequelae with conventional dietary management. The existence of this subgroup should be considered in evaluations of therapeutic responses in cohorts of patients with galactosemia. Further, galactosemia should be included in the differential diagnosis of tremor and ataxia in the setting of mental retardation.

Adolescent↗
PubMed1983

Ethanol modulation of opiate receptors in cultured neural cells.

The mouse neuroblastoma-rat glioma hybrid cell line NG108-15 was used to study the acute and chronic interaction of ethanol with intact neural cells. In the short term, ethanol inhibited opiate receptor binding, but after long-term exposure the cells exhibited an apparent adaptive increase in the number of opiate binding sites; this was reversible when ethanol was withdrawn. High concentrations of ethanol (200 mM) increased opiate binding after 18 to 24 hours, whereas lower concentrations (25 to 50 mM) produced similar changes after 2 weeks. This model system has potential for exploring the cellular and molecular mechanisms underlying ethanol intoxication, tolerance, and withdrawal.

Animals↗
PubMed1983

Phospholipid methylation in myogenic cells.

The biosynthesis of phosphatidylcholine from successive N-methylation of phosphatidylethanolamine has been implicated as a major mechanism for the transduction of several receptor-mediated signals including beta-adrenergic coupling to adenylate cyclase. In this report we demonstrate L-isoproterenol stimulation of adenylate cyclase activity in two myogenic cell lines, L8 and BC3H-1. Using a sensitive high performance liquid chromatography method for qualitative and quantitative determination of phospholipids we found an active membrane phospholipid methylation pathway in these cells. Despite beta-adrenergic simulation of adenylate cyclase no alteration in the transmethylation pathway could be demonstrated.

Adenylyl Cyclases↗
PubMed1983

Activation of acetylcholine receptors causes the partition of hydrophobic cations into postsynaptic membrane vesicles.

In the continued presence of cholinergic ligands, the acetylcholine receptor-channel complex (AChR) in postsynaptic membranes undergoes a sequence of conformational changes. On addition of the ligand, the receptor rapidly changes from a closed channel to an open channel conformation, then slowly changes to a nonconducting state termed desensitization. The lifetime of the open channel conformation and the rate of desensitization are both dependent on the magnitude of the membrane potential, suggesting that the ligand-induced conformational changes in AChR may involve the movement of electrical charges within the membrane. Measurements of charge redistribution in AChR-containing membranes following ligand binding have not been reported. Recently, measurements of changes in the membrane partition coefficient of hydrophobic ions have been used to detect electrostatic changes in both biological and model membranes. We report here that cholinergic ligands induce changes in the partition coefficient of the hydrophobic cation tetraphenylphosphonium (TPP) into AChR-enriched membranes. The extent and time course of these changes in TPP partition coefficient are accounted for in a kinetic model. We conclude that TPP movement is a monitor of a molecular event which may be associated with the slow component of AChR desensitization.

Animals↗
PubMed1983

Identification of a molecular weight 43,000 protein kinase in acetylcholine receptor-enriched membranes.

A photoaffinity ATP ligand is used to identify the protein kinase present in acetylcholine receptor-enriched membranes from Torpedo californica. Incubation of these membranes with 8-azido-[alpha-32P]ATP and subsequent irradiation with UV light resulted in covalent labeling of a major band of Mr 43,000. Alkali-stripped membranes that show a selective reduction in the Mr 43,000 polypeptide also show a corresponding reduction in incorporation of photoaffinity label. In addition, the neutralized alkaline extract also showed one band at Mr 43,000 when labeled with the photoaffinity ligand. After alkali extraction, endogenous protein kinase activity decreased in the membranes in proportion to the loss of Mr 43,000 peptide. Moreover, the alkaline extract was able to phosphorylate casein in an exogenous assay system. These results suggest that a Mr 43,000 polypeptide in acetylcholine receptor-enriched membranes is the acetylcholine receptor kinase.

Animals↗
PubMed1983

Nosocomial patient-related laboratory abuse.

Improper and excessive use of laboratory procedures constitute a significant waste of money. This article describes a number of common forms of laboratory abuse and attempts to alleviate the headaches with a dash of humor.

Health Services↗