Biomedical subjects
Publications and source records attributed to M Adler.
This note studies the relationship between the complete integrability of geodesic flow on SO(4) with a left-invariant metric and the geometry of the intersection of four quadrics in P(6).
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Synapses between neuroblastoma-hybrid cells and myotubes exhibit a high degree of plasticity. Increase of cyclic adenosine monophosphate (AMP) levels of the hybrid cells for several days results in the appearance of functional voltage-sensitive Ca2+ channels, which are required for evoked secretion of acetylcholine. The results show that cyclic AMP regulates synaptogenesis by regulating the expression of voltage-sensitive Ca2+ channels, and suggest that cyclic AMP affects posttranslational modifications of some glycoproteins and cellular levels of certain proteins.
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The electrophysiological properties of the mouse anterior pituitary cell line AtT-20/D16-16 were investigated with intracellular and patch-clamp techniques. Clonal AtT-20/D16-16 cells were found to be electrically excitable, with most cells exhibiting spontaneous bursting action potentials. The mean burst rates varied from 1.4 Hz at -55mV to 8.2 Hz at -25mV, showing an approximately linear frequency-current relationship in the low current range. The bursts consisted of one to several fast Na+ spikes superimposed on a slow pacemaker potential, followed by a Ca2+ spike and a Ca2+-sensitive afterhyperpolarization. Removal of either Na+ or Ca2+ from the bathing medium led to cessation of spontaneous activity and the appearance of arrhythmic firing patterns. Single channel recordings revealed the presence of Ca2+-dependent K+ channels with unitary conductances of approximately equal to 130 pS in physiological medium. These channels were activated by both intracellular Ca2+ and membrane depolarization. Addition of norepinephrine (10 microM) led to increases in burst frequency and beta-endorphin secretion mediated by activation of beta-adrenergic receptors. Our results, in conjunction with previous work, suggest that the Ca2+ that enters the cell during the burst may be involved in hormone secretion.
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Prolonged immobilization may result in hypercalcemia, hypercalciuria, and osteoporosis. Although bone resorption is central to this syndrome, the mechanism of resorption is uncertain. In particular, the role of systemic calcium-regulating hormones remains unclear. In 14 immobilized subjects we measured fasting calcium excretion, 24-hour urinary calcium excretion during restricted calcium intake, the renal phosphorus threshold, plasma 1,25-dihydroxyvitamin D, nephrogenous cyclic AMP, and immunoreactive parathyroid hormone. Mean serum calcium levels were normal, but fasting and 24-hour calcium excretion were markedly elevated (0.28 mg per deciliter of glomerular filtrate and 314 mg per 24 hours, respectively). The mean levels of serum phosphorus (4.8 mg per deciliter) and the renal phosphorus threshold (4.3 mg per deciliter) were elevated. Mean plasma 1,25-dihydroxyvitamin D was strikingly reduced (9.9 pg per milliliter), as were nephrogenous cyclic (0.64 nmol per deciliter of glomerular filtrate) and immunoreactive parathyroid hormone in both assays. These findings indicate that the parathyroid--1,25-dihydroxyvitamin D axis is suppressed in patients with immobilization-induced hypercalciuria, as would be predicted by a model of resorptive hypercalciuria.
A software package for the hardcopy graphic display of two-dimensional data had been developed. It is written in BASIC and is compatible with a microcomputer interfaced to an intelligent digital plotter. The core of the package is a plotting program. It features a command menu that displays 15 user-controllable parameters. Most of these parameters are automatically tabulated and can be changed in an interactive manner. The data which is plotted is either entered by hand or read from pre-existing data files. The package has several other important features. One subroutine within the plotting program determines and draws the best fit of a curve through a set of points. Using another program, the user can edit and manipulate the information contained in data files. All the program commands are written in simple and precise language, therefore the user needs no previous experience with computers. Furthermore the programs can be easily modified to suit personalized needs.
Single Ca2+-dependent K+-channel currents were recorded in intact and excised inside-out membrane patches of the anterior pituitary clone AtT-20/D16-16. The frequency of channel openings and lifetimes depends both on membrane potential and on the Ca2+ concentrations at the inner membrane surface. The curve of the open-state probability of the channel as a function of membrane potential appears to translate along the voltage axis with changes in internal Ca2+ concentration. For Ca2+ concentrations between 10(-7) and 10(-6) M, the shift is consistent with the hypothesis that three Ca2+ ions are required to open a Ca2+-dependent K+ channel. Single channel conductances are estimated to be 124 pS in patches with normal external K+ (5.4 mM) and 208 pS in excised patches with symmetrical K+ (145 mM) across the membrane. Tetraethylammonium (20 mM) added to the cytoplasmic surface reversibly blocks the Ca2+-dependent K+ channel.
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The effects of various organic Ca2+ channel inhibitors were investigated on the binding of the alpha 1-antagonist 3H-labeled 2-[(2',6'-dimethoxyphenoxyethyl)aminomethyl]-1,4-benzodioxane ([3H]WB-4101) to membranes from rat brain and neuroblastoma-glioma hybrid cells (NG108-15). As found by monitoring binding of [3H]WB-41-1, the Ca2+ channel inhibitors methoxyverapamil (D600), verapamil, and the nifedipine analogue YC-93 bind to two different sites in rat brain: a high-affinity site (dissociation constant Kd = 2.9 nM and binding capacity B = 360 fmol/mg of protein) and a low-affinity site (Kd = 260 nM and B = 2700 fmol/mg of protein). In NG108-15 cells, where no alpha 1 receptors were detected with [3H]WB-4101, the Ca2+ antagonists were found to bind to nonadrenergic sites in the membrane with a capacity B = 976 fmol/mg of protein. The binding of Ca2+ antagonists to [3H]WB-41-1 sites led to the investigation of WB-4101 as a Ca2+ inhibitor by electrophysiological techniques. WB-4101 depressed the amplitude and reduced the rate of rise of the CA2+ spike with an affinity slightly greater than that observed for D600. The concentration for 50% inhibition of the Ca2+ spike amplitude was 48 microM for WB-4101 and 80 microM for D600. The WB-4101-induced blockade of the Ca2+ spike was antagonized by high Ca2+ concentrations, indicating a common site for Ca2+ and the alpha-antagonist. D600 and WB-4101 also inhibited voltage-dependent Na+ and K+ conductances. The results suggest that Ca2+ channels can account for a fraction of the sites labeled with [3H]WB-4101 in membrane preparations from brain and NG108-15 cells.
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