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The idea of direct plasma injection scheme (DPIS) was proposed in 2000. This new technique has been studied and proven to accelerate intense ion beams. To provide medium mass ions with highly charged states, small tabletop solid lasers were used for plasma production. Based on the measured plasma properties, aluminum and carbon ions were accelerated with more than 60 mA of current. The next experiments will use an radio frequency quadrupole designed for q/m=1/6 and explore beam productions using targets up to silver, and future work will explore production up to uranium. The DPIS has been established and is ready to be used with various accelerators which require pulsed high current, high charge state ion beams.

Acceleration of a 17 mA, 100 keV/ u C 6+ ion beam has been successfully achieved with an radio frequency quadrupole ͑RFQ͒ linac by means of "direct injection scheme." The C 6+ beam produced by a laser ion source with a Nd:YAG laser was injected to the high current RFQ linac. It has been experimentally proved that the fully stripped carbon ion beam with a current more than 10 mA was accelerated by the RFQ linac.

We performed a molecular analysis of a subject whose platelets and monocytes did not express any cell surface CD36 (designated as a type I CD36 deficiency). Amplification of the 5′ half of platelet and monocyte CD36cDNA (corresponding to nucleotide [nt] 191–1009 of the published CD36 cDNA sequence [Oquendo et al, Cell, 58:95, 1989]) showed that two different-sized CD36 cDNAs existed. One cDNA was of predicted normal size, whereas the other was about 150 bp smaller than that predicted for normal CD36 cDNA. Amplification of the 3′ region of CD36 cDNA (nt 962–1714) in this subject showed only normal-sized CD36 cDNA. Cloning and nt sequence analysis of the cDNAs showed that the smaller sized CD36 cDNA had 161-bp deletion (from nt 331 to 491), and a dinucleotide deletion starting at nt position 539. The same dinucleotide deletion was also detected in the normal sized CD36 cDNA. Both deletions caused a frameshift leading to the appearance of a translation stop codon. RNA blot analysis and quantitative assay using the reverse transcription- polymerase chain reaction (RT-PCR) showed that the CD36 transcripts in both platelets and monocytes were greatly reduced. Comparison of the determined cDNA sequences with the genomic DNA sequence for the human CD36 gene showed that the dinucleotide deletion was located in exon 5, and that the 161-bp deletion corresponded to a loss of exon 4. PCR- based analysis using genomic DNA showed that this subject was homozygous for the dinucleotide deletion in exon 5. Except for the dinucleotide deletion, we could not find any abnormalities around exon 3, 4, and 5 including the splice junctions. These results suggested that the deletions in CD36 mRNA were likely to be responsible for instability of the transcripts, and the dinucleotide deletion in exon 5 might affect the splicing of exon 4.