Poloidal E x B drift used as an effective rotational transform to achieve long confinement times in a toroidal electron plasma.

Electron plasmas with mean densities of 5.0 x 10(6) cm(-3) have been confined for as long as 18 ms in a partially toroidal trap with a purely toroidal magnetic field (B(0)=196 G, R(o)=43 cm, a=5 cm). Confinement is limited to 2.0 ms unless feedback is employed to suppress the growth of a toroidal version of the m=1 diocotron mode. The confinement time is much longer than all characteristic single-particle drift time scales and therefore confirms the existence of an equilibrium in which the space-charge-generated E x B drift acts as an effective rotational transform.

1,25 Dihydroxyvitamin D increases hepatocyte cytosolic calcium levels. A potential regulator of vitamin D-25-hydroxylase.

1,25 dihydroxyvitamin D (1,25(OH)2D) has been demonstrated to inhibit hepatic 25 hydroxyvitamin D (25 OHD) production. Changes in cytosolic calcium have been shown to regulate cellular processes. Using the fluorescent dye Quin 2, we have investigated the effects of 1,25(OH)2D and 24,25(OH)2D on cytosolic calcium levels in hepatocytes. 1,25(OH)2D exposure for 5 min increases cytosolic calcium levels by 24% at a concentration of 100 pg/ml, 39% at a concentration of 1 ng/ml, and 50% at a concentration of 2 ng/ml. The latter increment occurs in both the presence and absence of extracellular calcium, indicating that 1,25(OH)2D is mobilizing intracellular calcium pools. 24,25(OH)2D, 10 ng/ml, does not increase cytosolic calcium levels while the calcium ionophore A23187, 3 microM, increases levels by 52%. Calcium inhibits hepatic 25 OHD synthesis in liver homogenates in a dose-dependent fashion, which can be prevented by chelation of calcium with EGTA. 1,25(OH)2D and A23187 decrease hepatocyte 25 OHD synthesis. The inhibitory effect of A23187 can be prevented by chelation of extracellular calcium. The data demonstrate that 1,25(OH)2D increases hepatocyte cytosolic calcium, and that these increments in cytosolic calcium may regulate some of the hepatic actions of the vitamin D metabolite.

End product inhibition of hepatic 25-hydroxyvitamin D production in the rat: specificity and kinetics.

The role of vitamin D metabolites in the regulation of hepatic 25-hydroxyvitamin D production was investigated by examining the effects of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and 24,25-dihydroxyvitamin D on the synthesis of [25-3H]hydroxyvitamin D by rachitic rat liver homogenates. Production of [25-3H]hydroxyvitamin D was inhibited by 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, but not by 24,25-dihydroxyvitamin D. 25-Hydroxyvitamin D increased the Km of the vitamin D-25-hydroxylase enzyme(s), while 1,25-dihydroxyvitamin D decreased the Vmax with a Ki of 88.7 ng/ml. Inhibition of hepatic 25-hydroxyvitamin D production by 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D may be another control mechanism to regulate circulating vitamin D levels.

Acute metabolic acidosis stimulates 3H-25 hydroxyvitamin D production by the rachitic rat liver.

Acute metabolic acidosis alters 1,25 dihydroxyvitamin D metabolism in experimental animals. We have used the NH4Cl-treated rachitic rat as a model to investigate the effect of acidosis on hepatic 25 hydroxyvitamin D (25 OHD) production. NH4Cl ingestion for 4 days was associated with a significant decrease in blood pH (7.44 +/- 0.03 vs 7.17 +/- 0.03, P less than 0.001) and bicarbonate (22.2 +/- 0.9 vs 10.5 +/- 1.6 mEq/liter, P less than 0.001). Acute metabolic acidosis stimulated 3H-25 hydroxyvitamin D production in liver homogenates. Acidosis resulted in a 52% decrease in Km (50.9 nM vs 24.5 nM) and an 11% decrease in the Vmax (554 picomoles/g liver protein/3 h vs 491 picomoles/g liver protein/3 h). The data collectively suggest that an acid load in vivo increases hepatic 25 OHD production and apparently enhances enzyme affinity for substrate.

1,25 dihydroxyvitamin D-induced inhibition of 3H-25 hydroxyvitamin D production by the rachitic rat liver in vitro.

The effect of the vitamin D metabolites 1,25 dihydroxyvitamin D (100 pg/ml) and 25-hydroxyvitamin D (30 ng/ml) on hepatic production of 3H-25 hydroxyvitamin D was investigated using rachitic liver perfusions and homogenates. 1,25 dihydroxyvitamin D inhibited hepatic 3H-25 hydroxyvitamin D production in the liver perfusion (3.6 +/- 0.4 vs 2.0 +/- 0.5 pmol/liver, P less than 0.05) and in liver homogenates (11.9 +/- 0.6 vs 10.1 +/- 0.4 pmol/g liver protein/3 h, P less than 0.02). Inhibition was time and dose dependent. 25-hydroxyvitamin D inhibited production in liver homogenates (11.9 +/- 0.6 vs 9.2 +/- 0.1 pmol/g liver protein/3 h, P less than 0.05) but not in the intact liver (3.6 +/- 0.4 vs 3.4 +/- 0.5 pmol/liver). The data indicate that 1,25 dihydroxyvitamin D is able to feedback regulate the production of its precursor, 25-hydroxyvitamin D. Although 25-hydroxyvitamin D also inhibits its own production in liver homogenates, it failed to alter total production in the intact liver, suggesting that this metabolite may require immediate access to the vitamin D 25-hydroxylase, located on the microsomes and mitochondria, to induce inhibition.

Vitamin B and copper supplementation in beef calves.

Bodyweight responses to subcutaneous injections of vitamin B12 and copper were investigated using Hereford calves in the southeast of South Australia, an area known to produce cobalt and copper deficient sheep. Calves were allocated to one of four groups: control; copper; vitamin B12; copper plus vitamin B12. Responses in bodyweight gain to vitamin B12, and to copper were obtained during the trial of one year. The results of biochemical analysis of blood, hair and faeces from calves and of dam's milk are reported. It is concluded that calves raised on cobalt-deficient pastures will require cobalt or vitamin B12 supplementation prior to weaning.

Copper administration to young calves: oral dosing with copper oxide compared with subcutaneous copper glycinate injection.

Calves were dosed with 50 g of copper oxide granules orally or given 120 mg copper glycinate subcutaneously. There was no significant difference between the weights of calves given either treatment during the trial. However, the copper oxide treatment resulted in sustained higher concentration of plasma copper and higher liver reserves than the glycinate treatment.