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The manufacturing experience for the cables of the Large Hadron Collider's (LHC) Inner Triplet Quadrupole magnet is reported.

Calcium-activated potassium channels and nitric oxide coregulate estrogen-induced vasodilation. Am J Physiol Heart Circ Physiol 279: H319-H328, 2000.--Nitric oxide synthase (NOS) contributes to estradiol 17[Beta] ([E.sub.2][Beta])-induced uterine vasodilation, but additional mechanisms are involved, and the cellular pathways remain unclear. We determined if 1) uterine artery myocytes express potassium channels, 2) [E.sub.2][Beta] activates these channels, and 3) channel blockade plus NOS inhibition alters [E.sub.2][Beta]-induced uterine vasodilation. Studies of cell-attached patches identified a 107 [+ or -] 7 pS calcium-dependent potassium channel ([BK.sub.Ca]) in uterine artery myocytes that rapidly increased single-channel open probability 70-fold (P [is less than] 0.05) after exposure to 100 nM [E.sub.2][Beta] through an apparent cGMP-dependent mechanism. In ovariectomized nonpregnant ewes (n = 11) with uterine artery flow probes and catheters, local [BK.sub.Ca] blockade with tetra-ethylammonium (TEA; 0.05-0.6 mM) dose dependently inhibited [E.sub.2][Beta]-induced uterine vasodilation (n = 37, R = 0.77, P [is less than] 0.0001), with maximum inhibition averaging 67 [+ or -] 11%. Mean arterial pressure (MAP) and [E.sub.2][Beta]-induced increases (P [is less than or equal to] 0.001) in heart rate (13%) and contralateral uterine blood flow (UBF, ~5-fold) were unaffected. Local NOS inhibition plus [BK.sub.Ca] blockade, using submaximal doses of nitro-L-arginine methyl ester (5 mg/ml) and TEA (0.3 mM), did not alter basal UBF but completely inhibited ipsilateral [E.sub.2][Beta]-induced uterine vasodilation without affecting MAP and [E.sub.2][Beta]-induced increases in contralateral UBF and heart rate. Acute [E.sub.2][Beta]-mediated uterine vasodilation involves rapid activation of uterine artery [BK.sub.Ca] and NOS, and the pathway for their interaction appears to include activation of guanylyl cyclase. uterine blood flow; estradiol-17[Beta]; nonpregnant sheep

Coal tar is a complex mixture that exhibits high carcinogenic potency in lungs of animals when administered in the diet. Studies have noted that lung tumor induction does not correlate with the benzo[a]pyrene content of coal tar, suggesting that other hydrocarbons may be involved in the observed tumorigenicity. Our previous studies have demonstrated that a major `unknown' chemical–DNA adduct is formed in the lung of mice exposed to coal tar. We have used an in vitro rat microsomal activation system to generate the `unknown' adduct with neat coal tar and fractions of coal tar obtained by chemical fractionation and HPLC. Chemical–DNA adduct formation was evaluated by 32P-postlabeling using both multi-dimensional TLC and HPLC. GC–MS analysis of the coal tar fractions obtained from HPLC, which produced the `unknown' adduct in vitro, demonstrated that the adducting hydrocarbon had a mass of 216. A careful evaluation of candidate hydrocarbons led to the conclusion that a benzofluorene derivative may be responsible for forming the `unknown' chemical–DNA adduct. Comparative in vitro and in vivo studies on the adducting properties of all three isomers of benzofluorene indicated that 7H-benzo[c]fluorene is responsible for producing the `unknown' adduct observed in the lung of mice ingesting coal tar. Animal feeding studies also demonstrated that 7H-benzo[c]fluorene formed considerably more lung DNA adducts than 11H-benzo[a]fluorene and 11H-benzo[b]fluorene. These data indicate that the four-ring polycyclic aromatic hydrocarbon 7H-benzo[c]fluorene, a hydrocarbon not previously shown to form DNA adducts in lung, is in fact a potent lung DNA adductor and is a candidate PAH for causing lung tumors in animals treated with coal tar. [ABSTRACT FROM PUBLISHER]