Appeal 2007-0582
Application 09/832,069
species” (Specification 4: 1-2). “Numerous studies have implicated the
mitochondria as a vulnerable target for reactive oxygen species” (id. at 5: 1-
2).
The Specification states that because “mitochondrial DNA is more
susceptible to reactive oxygen species-mediated damage, and because
increased oxidative stress is believed to play a role in the early events of
atherogenesis, . . . the mitochondrial DNA in aortic tissues destined to
become atherosclerotic has increased damage” (id. at 7: 1-6). The
Specification discloses
methods of predicting coronary atherosclerotic heart disease . . .
based upon the extent of mitochondrial DNA damage or upon
related measurement of mitochondrial dysfunction that is the
result of mitochondrial DNA damage including changes in
mitochondrial protein production, changes in mitochondrial
oxidative phosphorylation or changes in mitochondrial ATP
production.
(Id. at 8: 20 to 9: 5.)
DISCUSSION
1. CLAIMS
Claims 6, 8, 9, and 14-23 are pending and on appeal. Claims 6 and 16
are representative and read as follows:
6. A method of measuring the amount of oxidative stress
in a human individual, comprising the steps of:
(a) collecting a blood sample from said individual;
(b) assessing the amount of mitochondrial DNA damage
in cells from said sample wherein such amount of damage is
indicative of oxidative stress in said individual.
2
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Last modified: September 9, 2013