A distinct negative leader propagation mode.

The common phenomenon of lightning still harbors many secrets such as what are the conditions for lightning initiation and what is driving the discharge to propagate over several tens of kilometers through the atmosphere forming conducting ionized channels called leaders. Since lightning is an electric discharge phenomenon, there are positively and negatively charged leaders. In this work we report on measurements made with the LOFAR radio telescope, an instrument primarily build for radio-astronomy observations. It is observed that a negative leader rather suddenly changes, for a few milliseconds, into a mode where it radiates 100 times more VHF power than typical negative leaders after which it spawns a large number of more typical negative leaders. This mode occurs during the initial stage, soon after initiation, of all lightning flashes we have mapped (about 25). For some flashes this mode occurs also well after initiation and we show one case where it is triggered twice, some 100 ms apart. We postulate that this is indicative of a small (order of 5 km[Formula: see text]) high charge pocket. Lightning thus appears to be initiated exclusively in the vicinity of such a small but dense charge pocket.

Specific sequestering agents for the actinides. 21. Synthesis and initial biological testing of octadentate mixed catecholate-hydroxypyridinonate ligands.

The linear octadentate ligand 3,4,3-LIHOPO, which contains four 1-hydroxy-2(1H)-pyridinone (1,2-HOPO) groups, is the most effective agent for in vivo chelation of Pu(IV) yet prepared. However, its clinical potential is limited by acute toxicity of the free ligand (but not Fe3+ complex) at high dosage. The high acidity of HOPO ligands and the much lower acidity of catechol (CAM) ligands suggested that mixed octadentate (CAM-HOPO) ligands containing one or two 1,2-HOPO and three (or two) catechol (CAM) groups might be as effective for Pu removal [fully eight-coordinated Pu(IV) complexes formed at pH > or = 6] and less toxic than 3,4,3-LIHOPO. Treatment of spermine with 3-(2,3-dimethoxybenzoyl)thiazol-idine-2-thione (1) (molar ratio 2:1) gave 1,14-bis(2,3-dimethoxybenzoyl)-1,5,10,14-tetraazatetradecane (2, DiCAM-spermine) in 80% yield. Addition of 2 to a 2-fold excess of the reaction product of 1-hydroxy-2-pyridone-6-carboxylic acid (HOPO-C) and 1,1'-carbonyldiimidazole (CDI) in N,N-dimethylformamide (DMF) and deprotection with BBr3 gave 1,14-bis(2,3-dihydroxybenzoyl)-5,10-bis(1-hydroxy-2-pyridon-6-oyl) -1,5,10,14-tetraaza-tetradecane [3, 3,4,3-LI(diCAM-diHOPO)] in 5% yield. Addition of 2 to an equimolar amount of the reaction product of HOPO-C and CDI in N,N-dimethylacetamide (DMAA), purification of the hexadentate intermediate, subsequent treatment with an equimolar amount of 2,3-dimethoxybenzoyl chloride (DMB), and deprotection with BBr3 gave 1,5,14-tris(2,3-dihydroxybenzoyl)-10-(1-hydroxy-2-pyridon-6-oyl)-1 ,5,10,14- tetraazatetradecane [4, 3,4,3-LI(triCAM-HOPO)] in 5% yield. Ligands were administered to mice [30 mumol kg-1 ip at 1 h or orally at 3 min after iv injection of plutonium(IV)-238 citrate, kill at 24 h]. Plutonium excretion after injection of either CAM-HOPO ligand was 700% of that for 24-h Pu-injected controls, 140% of that for mice given the tetracatecholate analogue 3,4,3-LICAM (significantly more, p < 0.01), but only 80% of that promoted by 3,4,3-LIHOPO (significantly less). Orally administered 3,4,3-LI-(diCAM-diHOPO) promoted significantly more Pu excretion than an equimolar amount of CaNa3DTPA. Potency of the CAM-HOPO ligands for in vivo chelation of Pu(IV) resembled that of structurally hexadentate tris-(hydroxypyridinonate) and tris(sulfocatecholate) ligands and functionally hexadentate tetrakis-(sulfocatecholate) and tetrakis(carboxycatecholate) ligands. The Pu complexes of the CAM-HOPO ligands are to some degree unstable at pH < 7.4, as judged by Pu residues in kidneys in excess of 24-h Pu-injected controls. Synthetic yields were insufficient for chemical investigations or evaluation of acute toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)

Chelation of 238Pu(IV) in vivo by 3,4,3-LICAM(C): effects of ligand methylation and pH.

The linear tetracarboxycatecholate ligand, 3,4,3-LICAM(C) (N1,N5,N10,N14-tetrakis(2,3-dihydroxy-4-carboxybenzoyl-tetraaza tet radecane, tetra sodium salt) injected within 1 h after injection of Pu(IV) citrate, removes about the same fraction of Pu from animals as CaNa3-DTPA (diethylenetriaminepentaacetate, calcium, sodium salt) but removes less inhaled Pu than CaNa3-DTPA and leaves a Pu residue in the renal cortex. However, the formation constant of the expected Pu-3,4,3-LICAM(C) complexes are orders of magnitude greater than that of Pu-DTPA, and 3,4,3-LICAM(C) is 100 times more efficient than CaNa3-DTPA for removing Pu from transferrin in vitro. Because the formation constants of their actinide complexes are central to in vivo actinide chelation, ligand design strategies are dominated by the search for ligands with large Pu complex stabilities, and it was necessary to explain the failure of 3,4,3-LICAM(C) to achieve its thermodynamic potential in vivo. All the batches of 3,4,3-LICAM(C) prepared at Berkeley or in France [Euro-LICAM(C)] were found by high-pressure liquid chromatography to be mixtures of the pure ligand [55% in Berkeley preparations, 8.5% in Euro-LICAM(C)] and its four methylesters. A revised synthesis for 3,4,3-LICAM(C) is appended to this report. All of the incompletely hydrolyzed 3,4,3-LICAM(C) preparations and the pure ligand were tested for removal of Pu from mice [238Pu(IV) citrate intravenous, 30 mumol kg-1 of ligand at 1 h, kill at 24 h, radioanalyze tissues and separated excretal]. The presence of methylesters did not significantly impair the ability of the ligands to remove Pu from mice, and it did not alter the fraction of injected Pu deposited in kidneys. Temporary elevation (reduction) of plasma and urine pH of mice by 0.5 mL of 0.1 M NaHCO3 (NH4Cl) injected before or simultaneously with pure 3,4,3-LICAM(C) somewhat improved (significantly reduced) Pu excretion but had little influence on Pu deposition in kidneys. Review of the investigations of Pu removal from animals by 3,4,3-LICAM(C) revealed that the fractional renal Pu deposit was characteristic of the species and that it could be reduced by vigorous alkalinization which indicated the need to examine the details of the pH dependence of Pu complexation by 3,4,3-LICAM(C).(ABSTRACT TRUNCATED AT 400 WORDS)