Appeal 2007-0582
Application 09/832,069
oxidative stress.” The claim language makes clear that oxidative stress is
determined based on the amount of mitochondrial DNA damage, not the
mere presence of damage.
4. ENABLEMENT
Claims 6 and 16-20 stand rejected under 35 U.S.C. § 112, first
paragraph, on the basis that the specification,
while being enabling for a method for measuring the amount of
oxidative stress in an individual by detecting the amount of
DNA damage per length of DNA using QPCR, does not
reasonably provide enablement for detecting mtDNA damage
by measuring mitochondrial mRNA production, mitochondrial
protein production, mitochondrial oxidative phosphorylation,
mitochondrial ATP production or mitochondrial redox state.
(Answer 3.)
Thus, the Examiner does not dispute that atherosclerotic heart disease
can be predicted by measuring mitochondrial DNA (mtDNA) damage; the
issue is whether mtDNA damage can be measured indirectly. Appellants
identify this as the real issue in the case (Br. 5-6) and the Examiner agrees
(Answer 11: “‘whether the assay is reasonably predictive of mtDNA
damage’ . . . [is] the true question of enablement in the instant application”).
The Examiner argues that the
specification provides no evidence teachings regarding the
relationship between mtDNA damage and mitochondrial
mRNA production, mitochondrial protein production,
mitochondrial oxidative phosphorylation, mitochondrial ATP
production or mitochondrial redox state. The specification does
not teach how these measurements are associated.
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