Interference No. 104,021 Paper No. 112
Griffin v. Bertina Page 5
exon 10 or as nucleotide 1691 (nt 1691) of the complementary DNA (cDNA) (Paper No. 94 at 15
n.2). This mutation results in a substitution of glutamine (Q) for arginine (R) at amino acid 506
(hence, the nomenclature "R506Q" in Paper No. 70).
F6. Drs. Griffin and Greengard testified that in the summer of 1993 they were seeking
mutations in Factor V protein as a cause or contributing cause of APC resistance (G019-20 &
G028-29).
F7. In July 1993, Drs. Griffin and Greengard were billed for the production of the
following eight twenty-base oligonucleotides (G038; Exh. 1029):
FV1 made 07-27-93
FV2 made 07-27-93
FV3 made 07-27-93
FV4 made 07-27-93
FV5 made 07-27-93
FV6 made 07-27-93
FV7 made 07-27-93
FV8A made 07-27-93
F8. The only use of such primers apparent from the record is the amplification of the
DNA of Factor V cleavage sites (e.g., G028; Exh. 1001).
F9. As of 28 July 1993, Dr. Greengard intended to use the primers to examine
Factor V from APC-resistant patients (Exh. 1001).
F10. By 4 August 1993, Xiao Xu, a colleague of Drs. Griffin and Greengard, had
identified "best" conditions for amplifying the primers (G032; Exh. 1020).
F11. On 23 August 1993, the Centers for Disease Control and Prevention shipped to
Dr. Griffin stabilized blood samples from the "S" family (G042).
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