Appeal 2007-0582
Application 09/832,069
(Answer 5.) The Examiner also states that the “specification has no working
examples of measuring the amount of mtDNA damage in tissue using
mitochondrial mRNA production,” etc. (id. at 6).
Appellants disagree with the “Examiner’s position that there is no
exemplary support in the specification” (Br. 8). Appellants point to
Examples 5-7 in the Specification, which they characterize as showing that
oxidative damage causes changes in mitochondrial mRNA production,
protein production, oxidative phosphorylation, ATP production, and redox
state (id.). Appellants argue that the Examiner’s reasoning in support of the
rejection is based on the effects of single mutations, while the claimed
method measures the cumulative effect of mutations in a population of
mitochondria (id. at 9).
We agree with Appellants that the Examiner has not provided an
adequate basis for concluding that the measurements recited in claims 16-20
would not be reasonably predictive of the amount of mitochondrial DNA
damage.
The Specification provides several relevant working examples,
describing experiments in which human umbilical vein endothelial cells
(HUVEC) and human aortic smooth muscle cells (HASMC) were treated in
vitro with the reactive oxygen species hydrogen peroxide (H2O2) and
peroxynitrite (ONOO–) (Specification 27-39).
The Specification reports that “[h]ydrogen peroxide treatment resulted
in increased mitochondrial DNA damage in both cell lines” (id. at 41: 6-7),
and “[p]eroxynitrite treatment resulted in preferential damage to the
mitochondrial DNA [compared to nuclear DNA] in HUVEC and HASMC”
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