Recombination Line vs. Forbidden Line Abundances in Planetary Nebulae

Recombination lines (RLs) of C II, N II, and O II in planetary nebulae (PNs) have been found to give abundances that are much larger in some cases than abundances from collisionally-excited forbidden lines (CELs). The origins of this abundance discrepancy are highly debated. We present new spectroscopic observations of O II and C II recombination lines for six planetary nebulae. With these data we compare the abundances derived from the optical recombination lines with those determined from collisionally-excited lines. Combining our new data with published results on RLs in other PNs, we examine the discrepancy in abundances derived from RLs and CELs. We find that there is a wide range in the measured abundance discrepancy Delta(O+2) = log O+2(RL) - log O+2(CEL), ranging from approximately 0.1 dex up to 1.4 dex. Most RLs yield similar abundances, with the notable exception of O II multiplet V15, known to arise primarily from dielectronic recombination, which gives abundances averaging 0.6 dex higher than other O II RLs. We compare Delta(O+2) against a variety of physical properties of the PNs to look for clues as to the mechanism responsible for the abundance discrepancy. The strongest correlations are found with the nebula diameter and the Balmer surface brightness. An inverse correlation of Delta(O+2) with nebular density is also seen. Similar results are found for carbon in comparing C II RL abundances with ultraviolet measurements of C III].Comment: 48 pages, 14 figures, accepted for publication in the Astrophysical Journal Supplemen

The pathogenesis of trimethyltin chloride-induced nephrotoxicity

In exploratory studies aimed at elucidating CNS effects due to heavy metal toxicity, signs of compromised renal function were seen in rats. The studies reported here describe the sequential steps of the development of nephrotoxicity by trimethyltin chloride (TMT) in rats. Single doses of 12.25 mg/kg TMT administered orally to 150- to 175-g Long-Evans rats elicited overt signs of toxicity including behavioral abnormalities and marked weight loss. Concurrent with the development of these signs, nephrotoxicity was manifested as functional kidney compromise and associated histopathologic evidence of tubular damage. Pathological changes in the kidneys from treated rats were hyaline droplet inclusions, attenuated brush border, basolateral vacuolization, and eosinophilic granular casts in the proximal tubule cells. These lesions were detected as early as 2 days post-treatment and progressed with time in an orderly and sequential fashion. Renal lesions between 5 and 8 days were mild to severe cortical tubular dilatation, hydropic degeneration, and diffuse hyaline droplet deposition in the lower nephron tubules. Medullary edema and exfoliation of degenerated tubular epithelial cells with cast formation followed from 8 to 11 days. The morphological changes were accompanied by marked elevation of blood urea nitrogen, parallel with polyuria at Day 2 and oliguria by Day 14. Behavioral abnormalities as well as weight loss correlated well with the time course and severity of renal dysfunction and progression of morphological changes. A second experiment compared the effects of TMT in rats of different weights. Heavier rats were more sensitive than lighter rats to the nephrotoxic effects of TMT. These effects were independent of recognizable neurotoxic effects of TMT in the hippocampus.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26824/1/0000383.pd

Electrophysiologic changes following treatment with organophosphorus-induced delayed neuropathy-producing agents in the adult hen

Although clinical, pathological, and biochemical effects of organophosphorus-induced delayed neuropathy (OPIDN) have been intensively investigated in the adult hen, detailed electrophysiological studies are lacking. Adult white leghorn hens were treated with a single oral dose of either 30 mg/kg tri-2-cresyl phosphate (TOCP), 750 mg/kg TOCP, 4 mg/kg di-n-butyl-2,2-dichlorovinyl phosphate (DBCV), or 30 mg/kg di-n-butyl-2,2-dichlorovinyl phosphinate (DBCV-P). The 750 mg/kg TOCP and DBCV, but not the 30 mg/kg TOCP and DBCV-P, treatments resulted in clinical signs of OPIDN and mild to marked damage of the tibial nerve 21 days after dose. Twenty-four hr lymphocyte neurotoxic esterase (NTE) inhibition was used as an index of brain NTE inhibition for the various organophosphorus compound (OP) treatment. Twenty-four hr lymphocyte NTE inhibition for 30 mg/kg TOCP, 750 mg/kg TOCP, DBCV, and DBCV-P was 54.1, 87.1, 84.8, and 68.3%, respectively. Twenty-one days after dose, the TOCP-treated hens exhibited some abnormalities in conduction velocity and action potential duration in the tibial or sciatic nerves. No abnormalities were observed in action potential parameters of either the DBCV or DBCV-P treatments. Neurotoxic OP (TOCP and DBCV) treatment resulted in decreased refractoriness in the tibial nerve, increased refractoriness in the sciatic nerve, and elevated strength duration threshold for both nerves. These changes were not present in nerves from DBCV-P (a non-neurotoxic NTE inhibitor)-treated hens. These results suggest that refractory period and strength duration abnormalities in peripheral nerve correlated well with the production of OPIDN and are evident without coincident clinical signs or histopathology.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26771/1/0000323.pd