DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Election/Restrictions
Applicant’s election without traverse of Group I previously recited in claims 105-125 in the reply filed on 10/21/2025 is acknowledged.
Priority
Acknowledgement is made of Applicants’ claim for benefit to prior filed US Provisional Application 63/013,342, filed on 04/21/2020.
This application claims the benefit of priority to Patent Application PCT/US21/28489.
Acknowledgement is made of Applicants’ claim for benefit to prior filed to Patent Application
Number PCT/US21/28489, filed on 04/21/2021.
Information Disclosure Statement
The Information Disclosure Statements filed 10/21/2022, 02/06/2023, and 12/19/2024 have been considered by the Examiner.
Status of Claims
Claims 153-200 are under examination.
Claim 1-152 are cancelled.
Claim Objections
Claims 159 and 171-174 are objected to as being dependent upon a rejected base claim, but would be allowable if rewritten in independent form including all of the limitations of the base claim and any intervening claims.
Claim 177 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 153. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 178 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 154. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 179 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 155. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 180 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 156. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 181 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 157. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 182 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 158. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 183 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 159. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 184 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 160. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 185 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 161. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 186 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 162. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 187 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 163. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 188 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 164. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 189 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 165. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 190 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 166. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 191 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 167. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 192 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 168. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 193 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 169. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 194 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 170. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 195 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 171. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 196 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 172. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 197 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 173. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 198 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 174. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 199 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 175. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim 200 objected to under 37 CFR 1.75 as being a substantial duplicate of claim 176. When two claims in an application are duplicates or else are so close in content that they both cover the same thing, despite a slight difference in wording, it is proper after allowing one claim to object to the other as being a substantial duplicate of the allowed claim. See MPEP § 608.01(m).
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 153-156, 175-180, 199-200 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Lee et al. (US 9,920,317 B2).
Regarding claims 153-154 and 177-178, Lee et al. teach nucleic acid sequences on vectors, viruses, or hybrids which are genetically engineered and amplified. Lee et al. teach nucleic acid sequences that can be inserted into delivery vectors and expressed from transcription units within the vectors (column 56, lines 10-19). Expressed from transcription units reads on the artificial expression comprising a promoter and a coding sequence. Lee et al. teach a method of increasing expression of a tumor suppressor in a mammal (column 88, lines 8-14). Lee et al. teach a stem cell that is contacted with the inhibitory nucleic acid, PRC2-binding lncRNA, or fragment thereof. Lee et al. teach as a result of the contacting the cell may enhance pluripotency, enhance differentiation, or induce the stem cell to differentiation to a nerve, neuron, or dopaminergic neuron (column 10, lines 42-48). Lee et al. teach the enhancer can be Seq ID NO: 8565 which is the same as SEQ ID NO: 5 of the present application, SEQ ID NO: 7338 which is the same as SEQ ID NO:12 of the present application, SEQ ID NO: 19202 which is the same as SEQ ID NO: 21 of the present application, SEQ ID NO: 7338 which is the same as SEQ ID NO:10 of the present application, 45033 which is the same as SEQ ID NO: 8, SEQ ID NO: 10805 which is the same as SEQ ID NO: 23 of the present application, SEQ ID NO: 10799 which is the same as SEQ ID NO: 16 of the present application, SEQ ID NO: 1633 which is the same as SEQ ID NO: 9 of the present applications, SEQ ID NO: 8565 which is the same as SEQ ID NO: 6 of the present application.
Regarding claims 155-156 and 179-180, Lee et al. teach the nucleic acid sequences are expressed from transcription units (column 56, lines 10-19). Lee et al. teach a stem cell is contacted with the inhibitory nucleic acid, PRC2-binding lncRNA, or fragment thereof, ex vivo, in order to enhance pluripotency, enhance differentiation, or induce the stem cell to differentiation to a nerve cell, neuron, or dopaminergic neuron (column 10, lines 42-48). Therefore, the coding sequence encodes an effector element that modulates gene expression to enhance pluripotency, enhance differentiation, or induce the stem cell to differentiation.
Regarding claims 175 and 199, Lee et al. teach an artificial expression construct. Lee et al. further teach the inhibitory nucleic acid may be formulated as a sterile composition for administration (column 4, lines 40-43).
Regarding claims 176 and 200, Lee et al. teach mixing the synthesized nucleic acid with a carrier (column 6, lines 46-48).
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 157-158, 161-162, 165-170, 181-182, and 185-186, and 189-194 are rejected under 35 U.S.C. 103 as being unpatentable over Lee et al. (US 9,920,317 B2) as applied to claims 153, 155-156, 175, and 177-178 above, and further in view of Chen et al. (US 2017/0239373).
Lee et al. teach nucleic acid sequences can be inserted into delivery vectors and expressed from transcription units within the vectors (column 56, lines 10-19). Lee et al. teach the enhancer can be one of various sequences of the present application including SEQ ID NOs: 5-6, 8-10, 12, 16, 21 and 23.
Regarding claims 157 and 181, Lee et al. teach an artificial expression construct, previously presented in regard to claim 156.
Lee et al. do not teach a reporter protein or the reporter protein comprises a fluorescent protein.
Chen et al. teach methods and materials for generating GABAergic neurons in brains (cover page, abstract). Chen et al. teach a polycistronic retroviral vector expressing NeuroDl and Dlx2 together under the control of NG2 promoter (page 10, paragraph 0069). Chen et al. further teach the vector can include the fluorescent protein GFP or mCherry (page 8, paragraph 0056).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have combined the teachings of Lee et al. for an artificial expression construct with the teachings of Chen et al. for a fluorescent reporter protein. Chen et al. provide motivation by teaching that successful infection of the cells could be demonstrated with retrovirus expressing GFP under the control of human NG2 promoter (page 9, paragraph 0067). One of skill in the art would have had a reasonable expectation of success at combining Lee et al. and Chen et al. because both teach nucleic acids delivered for differentiating neurons.
Regarding claims 158 and 182, Lee et al. teach an artificial expression construct, previously presented in regard to claim 156.
Lee et al. do not teach the functional molecule comprises a functional ion transporter, enzyme, transcription factor, receptor, membrane protein, cellular trafficking protein, signaling molecule, neurotransmitter, calcium reporter, channelrhodopsin, CRISPR/Cas molecule, editase, guide RNA molecule, homologous recombination donor cassette, designer receptor exclusively activated by designer drug (DREADD), growth factor, or pro-survival gene.
Chen et al. teach methods and materials for generating GABAergic neurons in brains (cover page, abstract). Chen et al. teach a polycistronic retroviral vector expressing NeuroDl and Dlx2 together under the control of NG2 promoter (page 10, paragraph 0069). Chen et al. teach delivery of the transcription factors NeuroD1 and Dlx2 (page 9, paragraphs 0066 and 0068). Chen et al. teach the genome editing technique can be a CRISPR/Cas9-mediated gene editing (page 5, paragraph 0037).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have combined the teachings of Lee et al. for an artificial expression construct with the teachings of Chen et al. for a delivery of transcription factors and the CRISPR/Cas9- mediated editing technique. Chen et al. provide motivation by teaching that the CRISPR/Cas9- mediated editing allows for co-expression of NeuroDl and Dlx2 which increases the conversion efficiency (page 9, paragraph 0068). One of skill in the art would have had a reasonable expectation of success at combining Lee et al. and Chen et al. because both teach nucleic acids delivered for differentiating neurons.
Regarding claims 161-162 and 185-186, Lee et al. teach an artificial expression construct, previously presented in regard to claim 156.
Lee et al. do not teach the expressible element comprises a non-functional molecule.
Chen et al. teach methods and materials for generating GABAergic neurons in brains (cover page, abstract). Chen et al. teach a polycistronic retroviral vector expressing NeuroDl and Dlx2 together under the control of NG2 promoter (page 10, paragraph 0069). Chen et al. teach delivery of the transcription factors NeuroD1 and Dlx2 (page 9, paragraphs 0066 and 0068). Chen et al. teach to specifically target NG2 cells and achieve stable transgene insertion, a Cre-FLEx (flip-excision) system. Chen et al. teach the Cre-FLEx includes a vector expressing Cre recombinase under the control of human NG2 promoter (NG2::Cre) and a vector with Cre-mediated FLEx switch of the inverted coding sequence of NeuroD1-P2A-mCherry or Dlx2-P2AmCherry (page 10, paragraph 0071). Therefore, only when Cre recombinase is expressed the transcription factors NeuroD1 and Dlx2 will be switched from an inverted (nonfunctional) orientation to the correct orientation (functional).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have combined the teachings of Lee et al. for an artificial expression construct with the teachings of Chen et al. for addition of a Cre-FLEx (flip-excision) system. Chen et al. provide motivation by teaching that a Cre-FLEx (flip-excision) system allows targeting of NG2 cells and achieves stable transgene insertion in those cells. One of skill in the art would have had a reasonable expectation of success at combining Lee et al. and Chen et al. because both teach nucleic acids delivered for differentiating neurons.
Regarding claims 165-167 and 189-191, Lee et al. teach an artificial expression construct. Lee et al. do not teach wherein the artificial expression construct comprises or encodes a skipping element.
Chen et al. teach methods and materials for generating GABAergic neurons in brains (cover page, abstract). Chen et al. teach a polycistronic retroviral vector expressing NeuroDl and Dlx2 together under the control of NG2 promoter (page 10, paragraph 0069). Chen et al. teach the vector may include a 2A skipping element, which could be E2A or P2A (page 7, paragraphs 0054-0056).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have combined the teachings of Lee et al. for an artificial expression construct with the teachings of Chen et al. for a polycistronic retroviral vector expressing NeuroDl and Dlx2 together with a 2A peptide skipping element between. Chen et al. provide motivation by teaching that co-expression of NeuroDl and Dlx2 increases the conversion efficiency (page 9, paragraph 0068). One of skill in the art would have had a reasonable expectation of success at combining Lee et al. and Chen et al. because both teach nucleic acids delivered for differentiating neurons.
Regarding claims 168 and 192, Chen et al. teach the skipping element comprises an internal ribosome entry site (IRES) (page 7, paragraph 0054).
Regarding claims 169 and 193, Lee et al. teach an artificial construct with a promoter, but Lee does not teach a specific promoter.
Chen et al. teach methods and materials for generating GABAergic neurons in brains (cover page, abstract). Chen et al. teach a polycistronic retroviral vector expressing NeuroDl and Dlx2 together under the control of NG2 promoter (page 10, paragraph 0069). Chen et al. further teach the promoter is a CMV promoter (page 14, claim 18).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have combined the teachings of Lee et al. for an artificial expression construct with the teachings of Chen et al. for a CMV promoter. Chen et al. provide motivation by teaching that CMV is a tissue-specific promoter that can be used to drive expression in glial cells (page 9, paragraph 0068). One of skill in the art would have had a reasonable expectation of success at combining Lee et al. and Chen et al. because both teach nucleic acids delivered for differentiating neurons.
Regarding claims 170 and 194, Lee et al. teach an artificial expression construct.
Lee et al. do not teach wherein the artificial expression construct includes a CMV promoter, Cre recombinase, and a fluorescent protein.
Chen et al. teach methods and materials for generating GABAergic neurons in brains (cover page, abstract). Chen et al. teach a polycistronic retroviral vector expressing NeuroDl and Dlx2 together under the control of NG2 promoter (page 10, paragraph 0069). Chen et al. further teach the promoter is a CMV promoter (page 14, claim 18). Chen et al. teach the capsid comprises AAV9 (page 3, paragraph 0029). Chen et al. teach a Cre-FLEx (flip-excision) system, which includes a vector expressing Cre recombinase under the control of human NG2 promoter (page 10, paragraph 0071). Chen et al. further teach the vector can include the fluorescent protein GFP or mCherry (page 8, paragraph 0056).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have combined the teachings of Lee et al. for an artificial expression construct with the teachings of Chen et al. for an AAV vector, CMV promoter, Cre recombinase, and a fluorescent protein. Chen et al. provide motivation by teaching that a Cre-FLEx (flip-excision) system allows targeting of NG2 cells and achieves stable transgene insertion in those cells. Chen et al. further provide motivation by teaching that CMV is a tissue-specific promoter that can be used to drive expression in glial cells include, without limitation (page 9, paragraph 0068). Chen et al. further provide motivation by teaching that successful infection of the cells could be demonstrated with retrovirus expressing GFP under the control of human NG2 promoter (page 9, paragraph 0067). One of skill in the art would have had a reasonable expectation of success at combining Lee et al. and Chen et al. because both teach nucleic acids delivered for differentiating neurons.
Claims 163-164 and 187-188 rejected under 35 U.S.C. 103 as being unpatentable over Lee et al. (US 9,920,317 B2) as applied to claim 153 above, and further in view of Chen et al. (US 2017/0239373) and as evidenced by Ellsworth et al. (PlosOne, 2019).
Lee et al. teach nucleic acid sequences can be inserted into delivery vectors and expressed from transcription units within the vectors (column 56, lines 10-19). Lee et al. teach the enhancer can be one of various sequences of the present application including SEQ ID NOs: 5-6, 8-10, 12, 16, 21 and 23.
Regarding claims 163 and 187, Lee et al. teach an artificial expression construct.
Lee et al. do not teach the artificial expression construct is associated with a capsid that crosses a blood brain barrier.
Chen et al. teach methods and materials for generating GABAergic neurons in brains (cover page, abstract). Chen et al. teach a polycistronic retroviral vector expressing NeuroDl and Dlx2 together under the control of NG2 promoter (page 10, paragraph 0069). Chen et al. teach the capsid comprises AAV9 (page 3, paragraph 0029). Chen et al. do not specifically teach the clade F virus, AAV9, crosses the blood brain barrier, however AAV9 does cross the blood brain barrier as evidenced by Ellsworth et al. (Discussion, page 24).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have combined the teachings of Lee et al. for an artificial expression construct with the teachings of Chen et al. for an AAV9 capsid. Chen et al. provide motivation by teaching that NeuroDl and Dlx2 expressed using AAV9 viral vectors mediate glia-to-neuron conversion (page 3, paragraph 0028). One of skill in the art would have had a reasonable expectation of success at combining Lee et al. and Chen et al. because both teach nucleic acids delivered via viral vector for differentiating neurons.
Regarding claims 164 and 188, Chen et al. teach the capsid comprises AAV9 (page 3, paragraph 0029).
Claims 160 and 184 are rejected under 35 U.S.C. 103 as being unpatentable over Lee et al. (US 9,920,317 B2) as applied to claims 153, 155, 156, 177, 179, and 180, and further in view of Ji et al. (Neuroscience Research, 2013).
Lee et al. teach nucleic acid sequences can be inserted into delivery vectors and expressed from transcription units within the vectors (column 56, lines 10-19). Lee et al. teach the enhancer can be one of various sequences of the present application including SEQ ID NOs: 5-6, 8-10, 12, 16, 21 and 23.
Regarding claims 160 and 184, Lee et al. teach the artificial expression construct which includes an effector element comprises a functional molecule.
Lee et al. do not teach the functional molecule comprises a functional ion transporter.
Ji et al. teach ChRs are light-activated cation channels which mediate the light-dependent behavior (page 7, Molecular biology of ChRs). Ji et al. teach ChR-based gene therapies for neurological diseases (page 7, Introduction).
It would have been obvious to one of ordinary skill in the art at the time the invention was made to have combined the teachings of Lee et al. for artificial expression construct which includes an effector element with the teachings of Ji et al. utilizing ChR ion channels as a functional element for a method of gene therapy treating neurological diseases. Ji et al. provide motivation by teaching that gene therapy with ChR can overcome previous limitations in therapies because ChR can be used to manipulate complex neural activities. One of skill in the art would have had a reasonable expectation of success at combining Lee et al. and Ji et al. because both teach gene therapy for the treatment of neurological diseases.
Conclusion
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/C.L.M./Examiner, Art Unit 1638
/Anna Skibinsky/
Primary Examiner, AU 1635