Ex Parte Runge et al - Page 2

               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.                                    


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