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That the petitioner was not the leader in the offense but said that he did not gather from his conversations with him that the petitioner could be easily led. Trial counsel testified that he went over the guilty pleas with the petitioner three or four times, which included reading the guilty plea form aloud to him. In his opinion, the petitioner fully understood the nature and consequences of the pleas, and he had no concerns that the petitioner did not understand exactly what he was doing at the time he entered the pleas. Trial counsel acknowledged, however, that the petitioner initially expressed confusion to the trial court at the plea colloquy, informing the court that he had a "really bad mental problem." He said that the trial court took a break to allow him to go over the plea with the petitioner again and that the petitioner thereafter entered his pleas without incident. Trial counsel acknowledged the record in the case reflected the following: Previous trial counsel filed a motion on April 14, 2004, requesting a psychological evaluation; the petitioner was evaluated by Pathways Behavioral Health Services, which recommended that he be referred to Western Mental Health Institute for further inpatient evaluation; and Western Mental Health Institute determined that the petitioner was competent to stand trial and that a defense of insanity could not be supported. Trial counsel further agreed that the Western Mental Health Institute staff also recommended that the petitioner receive continued competency assessments and treatment while in jail awaiting trial. Following the petitioner's return to jail, the staff psychiatrist at Pathways Behavioral Health Services wrote a letter to the trial court stating that the petitioner had again been determined to be incompetent and recommending that he be referred back to Western Mental Health Institute to be reevaluated for competency to stand trial and for malingering. Trial counsel acknowledged that, as a result of that letter, he had filed a motion on October 26, 2004, requesting that the trial court declare the petitioner incompetent to stand trial. As a result, the petitioner was readmitted to Western Mental Health Institute for an inpatient evaluation of his competency to stand trial and for a determination of whether he was malingering. At the conclusion of that evaluation, the Western Mental Health Institute reported to the trial court that the petitioner had been determined to be competent to stand trial and that the malingering probability scale indicated a 99.9% probability that he was malingering. Trial counsel acknowledged that he did not request funds for an independent psychological examination but said he believed that it would have been unlikely to change the outcome of the case. On cross-examination, trial counsel testified that he met with the petitioner's previously appointed attorney to discuss the motions that attorney had filed in the case. He said he also discussed the petitioner's prior convictions and mental status with the public defender who had represented the petitioner in various cases in juvenile court. Trial counsel agreed that there was no guarantee that the trial court would have approved funds for independent psychological testing or that an independent psychologist or psychiatrist would have reached a different conclusion with respect to the petitioner's competency. He testified that the petitioner was always engaging and involved in his conversations with him, asking relevant questions and suggesting possible defenses, -3.

September 20-24, conference on psy chopharmacology, sponsored by the Association for the Advancement in Neurosciences, Rome, Italy. Con, for example, . MATERIALS AND METHODS Yeast strains and growth conditions. All strains were isogenic with W303 leu2-3, 112 his3-11, 15 ura3-1 ade2-1 trp1-1 can1-100 rad5-535 ; 32 ; . For the strains used in this study, the rad5-535 allele was replaced with the wild-type RAD5 gene by crossing and was tested by PCR as described elsewhere 6 ; . All genetic manipulations and transformations with plasmid DNA were performed as previously described 13 ; . The yeast strains RCY407-12d and RCY409-2a both wild type ; and RCY407-1d and RCY409-4b both dap1 : : LEU2 ; have been described previously 14 ; . The erg2 strain JRY7187 was a gift from Jasper Rine's laboratory. Plasmids. The plasmids used in this study are summarized in Table 1. The ERG11 gene was amplified using the primers ERG11-300F-Hind and ERG11 1650R-Bam. The sequences of all primers used in this study are available at the website www2 y Pharmacology rjc research . The PCR product was digested with HindIII and BamHI and ligated to the plasmid YEplac195 12 ; , which was digested with the same enzymes. The resulting plasmid called pRH4 ; contained the entire ERG11 open reading frame, along with 300 bp of its upstream sequence. The ERG1 gene was amplified by PCR using the primers ERG1-290F-Bam and ERG1 1524R-Hind, and the resulting PCR product was subcloned into the plasmid YEplac195, forming the plasmid pJM60. For epitope tagging the ERG11 open reading frame, the entire ERG11 gene was amplified using W303a genomic DNA as a template with the primers ERG11-300F-Hind and ERG11 1650-MYCR-Bam. The PCR product was digested with BamHI and HindIII and cloned into the corresponding sites of the single-copy plasmid pRS316. The resulting plasmid was called pRH7. For DAP1 mutagenesis, DAP1 was amplified by PCR using the primers DAP200F and DAP 470R and subcloned into the plasmid pCR3.1 Invitrogen ; , forming the plasmid pRC31. The Dap1p-D91G mutation was created with the ExCite mutagenesis kit Stratagene ; using the manufacturer's instructions and the primers DAP1-D91G-F and DAP1 265R with pRC31 as a template, forming the plasmid pRC34. After confirming the integrity of the D91G mutation, the DAP1-D91G mutant was subcloned into the XhoI and EcoRI sites of the plasmid pRS313, forming the plasmid pRC39. The wild-type gene was similarly cloned into pRS313, forming the plasmid pRC41. For production of a Dap1p fusion protein with glutathione S-transferase, the DAP1 open reading frame from bp 4 to 459 was amplified by PCR using the primers DAP1 4F-Bgl and DAP1 457R-Xho, with W303a genomic DNA as a template. The PCR product was then subcloned into the BamHI and XhoI sites of the plasmid pGEX-4T-1 Amersham ; , forming the plasmid pGC5. The DAP1D91G mutant was subcloned similarly. To construct the plasmid encoding the Dap1p protein containing the D91G mutation, the mutated DAP1 open reading frame was amplified using the same primers with pRC34 as a template and subcloned into the same sites of pGEX-4T-1. The resulting plasmid was called pGC4. The sequences of all cloned genes were confirmed by automated sequenc.
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1. Ottesen EA. The global programme to eliminate lymphatic filariasis. Trop Med Int Health 2000; 5: 591-4. Ottesen EA, Duke BOL, Karam M, Behbehani K. Strategies and tools for the control elimination of lymphatic filariasis. Bull World Health Organ 1997; 75: 491-503. Building partnerships for lymphatic filariasis -- strategic plan. Geneva: WHO; 1999. 4. Molyneux DH, Hotez PJ, Fenwick A. "Rapid-impact interventions": how a policy of integrated control for Africa's neglected tropical diseases could benefit the poor. PLoS Med 2005; 2: e336. 5. Neglected tropical diseases: hidden successes, emerging opportunities. Geneva: WHO; 2006. 6. Lymphatic filariasis: infection and disease. Control strategies. Report of a consultative meeting held at the Universiti Sains Malaysia, Penang. Geneva: WHO; 1994. 7. Lymphatic filariasis: the disease and its control. Fifth report of the WHO expert committee on filariasis. Geneva: WHO; 2002. 8. Esterre P, Plichart C, Sechan Y, Nguyen NL. The impact of 34 years of massive DEC chemotherapy on Wuchereria bancrofti infection and transmission: the Maupiti cohort. Trop Med Int Health 2001; 6: 190-5. Sunish IP, Rajendran R, Mani TR, Munirathinam A, Tewari SC, Hiriyan J et al. Resurgence in filarial transmission after withdrawal of mass drug administration and the relationship between antigenaemia and microfilaraemia - a longitudinal study. Trop Med Int Health 2002; 7: 59-69. Bandyopadhyay L. Lymphatic filariasis and the women of India. Soc Sci Med 1996; 42: 1401-10. Remme JHF, Raadt P, Godal T. The burden of tropical disease. Med J Aust 1993; 158: 465. Evans DB, Gelband H, Vlassoff C. Social and economic factors and the control of lymphatic filariasis: a review. Acta Trop 1993; 53: 1-26. Mujinja PGM, Gasarasi DB, Premji ZG, Nguma J. Social and economic impact of lymphatic filariasis in Rufiji district, Southeast Tanzania. In: Lymphatic filariasis research and control in Africa. Report on a workshop held in Tanga, Tanzania. Tanzania: Danish Bilharziasis Laboratory, Denmark & National Institute for Medical Research; 1997. 14. Rauyajin O, Kamthornwachara B, Yablo P. Socio-cultural and behavioural aspects of mosquito-borne lymphatic filariasis in Thailand: a qualitative analysis. Soc Sci Med 1995; 41: 1705-13. Dreyer G, Medeiros Z, Netto MJ, Leal NC, Gonzaga de Castro L, Piessens WF. Acute attacks in the extremities of persons living in an area endemic for Bancroftian filariasis: differentiation of two syndromes. Trans R Soc Trop Med Hyg 1999; 93: 413-7. Amazigo UO, Obikeze DS. Social consequences of onchocercal skin lesions on adolescent girls in rural Nigeria. WHO TDR Discussion Paper. Geneva: WHO; 1992. 17. Gender and tropical diseases. Geneva: WHO; 1995. 18. Muhondwa EPY. Community involvement in filariasis control: the Tanzania experiment. Geneva: WHO; 1983.

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