Determination of micromolar bromate concentrations by adsorptive-catalytic stripping votammetry of the molybdenum-3-methoxy-4-hydroxymandelic acid complex.

Adsorptive-catalytic stripping voltammetry is commonly used for monitoring trace metals. This study reverses the scheme by developing a sensitive procedure for measuring the catalyst. The catalytic action of bromate upon the cathodic response of the adsorbed molybdenum-3-methoxy-4-hydroxymandelic acid (VMA) complex has been exploited for measuring bromate down to the micromolar concentration level. Experimental variables affecting the response, including the metal and ligand concentrations or the accumulation time and potential, were characterized and optimized to yield a highly linear response (up to at least 1x10(-4) mol l(-1)) and good precision (RSD of 3.5%; n=10; 2x10(-6) mol l(-1) bromate). Analogous adsorptive-catalytic stripping protocols may be utilized for the voltammetric detection of other catalysts.

Lab-on-a-Cable for electrochemical monitoring of phenolic contaminants.

The "Lab-on-a-Cable" concept, based on scaling down an electrochemical flow system to a cable platform, is described. The system integrates the analyte collection and the sample handling, with the electrochemical detection of the reaction product in a sealed cylindrical unit, connected to a long shielded cable. An enzymatic assay, involving collection of a phenolic substrate, its mixing with an internally delivered tyrosinase solution, and amperometric detection of the liberated quinone product, is used for illustrating the operation of the flow probe and demonstrating its advantages over remote phenol sensors. The internal buffer solution ensures independence of sample conditions such as pH, ionic strength, or natural conditions, that commonly influences the performance of remote sensors. The "built-in" flow pulsation of the integrated micropump is exploited for a sensitive hydrodynamic-modulation voltammetric detection of hydrazine and peroxide pollutants.

The vascular microanatomy of skin territory of posterior forearm and its clinical application.

We have undertaken a microanatomical study of a new donor site--the posterior forearm territory--on 43 cadaver arms. Two axial arteries were found, and both the fasciocutaneous flap and the fascial flap could be elevated with the two arteries on the posterior forearm. The posterior forearm flap was transferred to the hand to repair deformities of the wrist, the first web space, the dorsal hand, and the metacarpophalangeal joints in eight cases. The result was very satisfactory. The posterior forearm flap is near the hand, easy to perform, and reliable. It is a one-stage operation and does not sacrifice a main artery. In this article we demonstrate our own ideas about flap extension, which is valuable for clinical application.

Calcium-transport in quiescent and 1,25-dihydroxycholecalciferol-stimulated human osteosarcoma cells. Role in 24 hydroxylase enhancement.

The present study evaluates in osteosarcoma cells, the effects of a calcium channel inhibitor nicardipine in 24-hydroxylase activity and 45Ca desaturation curve in presence of 1,25-dihydroxycholecalciferol (1,25(OH)2D3). This sterol induced an increase in 24-OHase activity and 45Ca fluxes. Nicardipine reversed the effect of 1,25(OH)2D3 on 45Ca fluxes but reinforced the enhancement of the 24-OHase activity. The fact that the effects of 1,25(OH)2D3 were reduced by cycloheximide support the hypothesis of a de novo protein synthesis. Our study has allowed us to dissociate the effects of 1,25(OH)2D3 on 24-OHase enhancement from those on Ca2+ transport.

Comparative effects of the ionophore A23187 and vitamin D metabolites on 45Ca desaturation curves derived from bone cells: interaction of a calcium channel channel inhibitor diltiazem.

The effects of diltiazem, a calcium channel inhibitor, on the cellular transport of calcium were studied in isolated heterogenous rat bone cells. Efflux was measured after equilibrating the cells with 45Ca and adding the vitamin D metabolite (1,25dihydroxycholecalciferol-1,25(OH)2D3 or 24,25dihydrocholecalciferol-24,25(OH)2D3), the ionophore A23187 and/or diltiazem. Results were analysed by fitting the desaturation curve to a model of two exponential terms. Kinetic analyses of curve indicated the presence of 2 exchangeable pools with different rate constants of exchange between the medium and cells (expressed by K.). After incubation of bone cells with diltiazem (20 nmol/10(6) cells) the following changes were recorded: a marked decrease in the rate constant of efflux from the fast turnover calcium pool (K12) and a reduction of the calcium pool sizes. Incubation of 10(6) cells with 0.5 ng 1,25(OH)2D3 plus diltiazem significantly reduced K12 compared to incubation with 1,25(OH)2D3 alone. In presence of 24,25(OH)2D3, diltiazem did not significantly alter K12 which was raised by incubation with the metabolite alone. Ionophore A23187 (0.5 micrograms/10(6) cells) increased the value of slow turnover constants of efflux whose values were affected by diltiazem. The possible involvement of Ca movements in bone resorption does not seem confirmed in the present experiment since in vitro effects of diltiazem in organ culture (observed in an initial previous experiment) were not reflected in the calcium 45 desaturation kinetics in heterogenous bone cells.

Effects of the calcium antagonist, diltiazem on in vitro and in vivo/in vitro bone resorption.

The effect of the calcium antagonist diltiazem on bone resorption in organ culture has been investigated. It was found that diltiazem was ineffective alone but that in concentrations above 5 mumol/l it reduced mineral and organic resorption induced in vitro by 1.25 dihydroxycholecalciferol (1.25 (OH)2D3). No additivity with calcitonin effects was observed. Diltiazem did not significantly affect bone resorbing activity stimulated by 24,25(OH)2D3. Bone resorption was measured by an in vivo/in vitro technique using 45Ca prelabelled mice. Compared with 1.25(OH)2D3 alone treated group (0.480 pmol/g), it was found that diltiazem (100 nmol/g) reduced bone resorption without effect on calcium and phosphorus plasmatic concentrations at death. These data suggest that such a calcium antagonist is able to inhibit 1.25-(OH)2D3-increased-bone resorption either in vitro or in vivo/in vitro.

[Effects of 1,25-dihydroxyvitamin D3 on bone resorption and 45Ca2+ efflux in bone cells]. / Effets de la 1.25-dihydroxyvitamine D3 sur la résorption osseuse et l'efflux du 45Ca2+ dans les cellules osseuses.

1,25-dihydroxyvitamin D3[1,25(OH)2D3] effects on bone resorption in organ culture and on 45Ca2+ efflux rates in bone cells were measured in presence of a calcium channel inhibitor, diltiazem. Though, diltiazem reduced the 45Ca release from mice calvaria it did not act at the same Ca compartment as 1,25(OH)2D3 to alter Ca2+ flux parameters. It therefore seems difficult to hypothesize a simple relationship between bone resorption and Ca2+ movements in bone cells.