The degradation of 2-chloro-4-ethylamino-6isopropylamino-s-triazine (atrazine) and 2chloro-4-(l-cyano-l-methylethylamino)-6-ethylamino-s-triazine (cyanazine) was investigated in a Perth clay loam soil. Atrazine and cyanazine were applied at rates of 1, 2, and 3 lb/A of active ingredients as pre-and postemergence treatments. Soil was sampled from plots after 0, 2, 3.5, 5, and 12 months at 0-2.5, 2.5-5, and 5-10 in. depths. Atrazine, cyanazine, and their phytotoxic metabolites were extracted with a 65% acetonitrile-water mixture and quantitated on a Coulson conductivity detection system. Presented data indicate that atrazine is converted into deethylated atrazine (2-chloro-4-amino-6isopropylamino-s-triazine) as a major and deisopropylated atrazine (2-chloro-4-amino-6-ethylamino-s-triazine) as a minor phytotoxic metabolite and that cyanazine is changed to deisopropylated atrazine as a major phytotoxic metabolite.Cyanazine amide[2-chloro-4-(l-carbamoyl-lmethylethylamino)-6-ethylamino-s-triazine] was found. It is proposed that the hydrolysis precedes the microbiological degradation to the deisopropylated atrazine.Atrazine and cyanazine are selective herbicides used for the control of annual broadleaf and grassy weeds in corn and sorghum. Both herbicides may be applied at the rates of 1-4 lb/A active Cyanazine, developed at the Woodstock Agricultural Research Centre in England, is marketed by the Shell Chemical Co. under the trade name Bladex. It is claimed by the manufacturer to be less persistent in soil than atrazine and therefore less detrimental on the subsequent crops. The unstable nature of the cyanazine molecule also allows it to be used as a herbicide in potatoes, peas, barley, and wheat (Beynon et al., 1970).

The quantitative structure-activity relationships (QSARs) for polychlorinated biphenyl (PCB) congeners have been determined by comparing the EC50 values for three in vitro test systems, namely, aryl hydrocarbon hydroxylase (AHH) and ethoxyresorufin O-deethylase (EROD) induction in rat hepatoma H-4-II-E cells and competitive binding avidities to the rat cytosolic receptor protein (using 2,3,7,8-tetrachlorodibenzo-p-dioxin as a radioligand). For several PCB congeners that are in vivo inducers of rat hepatic microsomal AHH, there was a linear correlation between the -log EC50 values for receptor and the -log EC50 values for AHH (or EROD) induction; moreover, a comparable linear relationship was observed between the -log EC50 values for AHH and EROD induction. Previous in vivo studies have shown that the most active PCB congeners 3,3',4,4'-tetra-, 3,4,4',5-tetra-, 3,3',4,4',5-penta-, and 3,3',4,4',5,5'-hexachlorobiphenyl, cause many of the biologic and toxic effects reported for the highly toxic halogenated aryl hydrocarbon, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Moreover, the monoortho-substituted homologs of the four coplanar PCBs also elicit comparable in vivo biologic and toxic responses. It was evident from the QSARs for PCBs that there was an excellent correspondence between the in vivo and in vitro potencies of the individual PCB congeners. The effects of substituents on both receptor binding and AHH/EROD induction was determined for a series of 4'-substituted (X)-2,3,4,5-tetrachlorobiphenyls (where X = H, Cl, Br, I, OH, OCH3, NO2, COCH3, F, CF3, CH3, C2H5, i-C3H7, n-C4H9 and t-C4H9). Not unexpectedly, there was a linear relationship between the -log EC50 values for AHH and EROD induction, and these results confirm that both enzymatic oxidations are catalyzed by the same cytochrome P-450 isozyme(s). The effects of substituent structure on receptor binding for 12 substituents was subjected to multiple regression analysis which correlates the relative binding affinities of the compounds with the physical chemical characteristics of the substituents. The analysis gave the following equation: log (1/EC50) = 1.53 sigma + 1.47 pi + 1.09 HB + 4.08 for n = 12, s = 0.18, r = 0.978; where n is the number of substituents, s is the standard deviation, r is the correlation coefficient, and sigma = electronegativity, pi = hydrophobicity (log P) and HB = hydrogen bonding capacity for the substituent groups.(ABSTRACT TRUNCATED AT 400 WORDS)

This study examined the Personality Assessment Inventory (PAI) in 95 individuals who had suffered a traumatic brain injury (TBI). Participants were recruited from a rehabilitation hospital (n=60) and a military hospital (n=35); despite differences in demographics and injury characteristics groups did not differ on any of the clinical scales and were thus combined. In the combined group, the highest mean clinical scale elevations were on Somatic Complaints, Depression, and Borderline Features and the most common configural profiles, based on cluster analysis, were Cluster 1 (no prominent elevations), Cluster 6 (social isolation and confused thinking), and Cluster 2 (depression and withdrawal). Factor analysis indicated a robust three-factor solution that accounted for 74.86 percent of the variance and was similar to findings from the psychiatric and non-psychiatric populations in the standardization sample. The above findings are compared with the previous literature on psychopathology in TBI, particularly in regards to the Minnesota Multiphasic Personality Inventory-2 (MMPI-2), as well as previous psychometric research on the PAI.

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