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 .
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 5/6/2026 has been entered.
Claims status
Claims 1-3, 6-9, 11, 12, 17-19, 33, 41, 43-60 is/are currently pending with claims 1-3, 6-9, 11, 12, 17-19, 45, 46 is/are withdrawn. Claims 33, 41, 43, 44, 47-60 is/are under examination.
Withdrawn Objections
The objections presented herein represent the full set of objections currently pending in this application. Any objections not specifically reiterated are hereby withdrawn.
Claim Objections
Claim 41 is objected to under 37 CFR 1.75 as being a substantial duplicate of claim 33.
Claims 58, 59, 60, 53, 54, 5, 56 and 57, that depend from claim 41, are objected to under 37 CFR 1.75 as being a substantial duplicate of claims 43, 44, 47, 48, 49, 50, 51 and 52 respectively, that depend from claim 33.
Claim 33 and 41 recite identical method steps. The preamble in claim 33 recites that it is a method intended for screening candidate drugs for treating pulmonary fibrosis while claim 41 recites that it is a method for evaluating therapeutic effects of a candidate drug for pulmonary fibrosis. A method that screens a candidate drug for treatment of a disease implicitly evaluates the therapeutic effect of the candidate drugs. Thus, claims 33 and 41 are directed to methods that have patentably indistinct intended purpose and have identical step.
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 § 112(b)
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 33, 41, 43, 44, 47-60 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 33 is directed to method for screening candidate drugs from treating pulmonary fibrosis by applying the candidate drugs to a mouse model which is constructed by “knocking-out Cdc42 genes in the AT2 cells and subsequently increasing mechanical tension”. This limitation remains unclear because it remains unclear if the method requires the application of mechanical tension to the Cdc42 knockout mouse during the screening method or if it is sufficient that mechanical tension is applied to the Cdc42 knockout mouse prior to its use in the instant screening method. In other words, it is unclear if the candidate drugs are applied to Cdc42 gene knockout mouse that is already exposed to increased mechanical tension by aging or PNX or if the drugs are applied to the Cdc42 gene knockout mouse and then the mouse is exposed to aging or PNX.
Claim 33 is amended to recite a single step wherein the candidate drugs are applied to a mouse model however the claim does not set forth any active step that would produce the intended method that screens these candidate drugs. Further, it appears that a plurality of drugs are applied simultaneously. It is unclear how these plurality of drugs are being screened.
Claim 41 is directed to method for evaluation of therapeutic effects of a candidate drug for pulmonary fibrosis by applying the candidate drug to a mouse model which is constructed by “knocking-out Cdc42 genes in the AT2 cells and subsequently increasing mechanical tension”. This limitation remains unclear for the same reasons as noted above for claim 33.
Claim 41 is amended to recite a single step wherein the candidate drug is applied to a mouse model however the claim does not set forth any active step that would produce the intended method that evaluates these candidate drugs. It is unclear how the drugs are being evaluated.
Claim 49 recites an additional step of performing PNX to the mouse model. The claim requires this step to be performed before increasing mechanical tension on the alveolar epithelium. This claim is wholly unclear. Claim 49 depends from claim 33 that already includes performing PNX for the purposes of increasing mechanical tension on the alveolar epithelium. For the purpose of compact prosecution, the claim(s) 49 is/are interpreted as “wherein mechanical tension is increased by PNX.”
Claim 53 continues to recite “wherein the step of knocking-out Cdc42 gene in AT2 cells in a PNX-treated animal comprises knocking out Cdc42 specifically in lung AT2 cells by using a Spc-CreER allele”. There is insufficient antecedent basis for a “step of knocking-out Cdc42 gene in AT2 cells in a PNX-treated animal”. No such step is recited in claim 41. Although the method of claim 41 uses an animal constructed by knocking out Cdc42 gene in AT2 cells, this is not an active step in claim 41. Furthermore, claim 41 has no recitation of “PNX-treated animal. For the purpose of compact prosecution, the claim(s) 53 is/are interpreted as “wherein the mouse model of pulmonary fibrosis constructed by knocking out Cdc42 gene in AT2 cells and mechanical tension is increased by PNX.”
Claim 54 recites an additional step of performing PNX to the mouse model. Claim 54 depends from claim 41 that already includes performing PNX. For the purpose of compact prosecution, the claim(s) 54 is/are interpreted as “wherein mechanical tension is increased by PNX.”
Claims 43, 44, 47-52 is/are rejected due their dependence on claim 33 because they do not clarify the 112b issue noted with claim 33.
Claims 53-60 is/are rejected due their dependence on claim 41 because they do not clarify the 112b issue noted with claim 41.
Claim 50 is/are rejected due their dependence on claim 49 because they do not clarify the 112b issue noted with claim 49.
Claim 55 is/are rejected due their dependence on claim 54 because they do not clarify the 112b issue noted with claim 54.
Claim Rejections - 35 USC § 112(a)
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
New Matter
Rejection of Claims 33, 41, 43, 44, 47-60 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement due to introduction of new matter is withdrawn because of deletion of new matter from the claims.
Written Description
Rejection of Claims 33, 41, 47, 43, 44, 48-60 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement is withdrawn in light of amendments to claims 33 and 41 that recite specific means of increasing mechanical tension supported by the specification.
Scope of Enablement
Rejection of Claims 33, 41, 47, 43, 44, 48-60 under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the scope of enablement requirement is withdrawn in light of amendments to claims 33 and 41 that recite specific means of increasing mechanical tension enabled by the specification.
Claim Interpretation
Claim 33 is directed to a method for screening candidate drugs and claim 41 is directed to a method of evaluating the therapeutic effects of a candidate drug. In both these claims, the candidate drug is applied to a mouse model of pulmonary fibrosis. The claims recite product-by-process limitations regarding the mouse model of pulmonary fibrosis (see use of phrase “constructed by”). According to MPEP 2113, “Product-by-process claims are not limited to the manipulations of the recited steps, only the structure implied by the steps.” The process steps of “constructed by knocking-out Cdc42 genes in AT2 cells” impart the following structure to the claimed mouse model of pulmonary fibrosis: the mouse comprises a Cdc42 knockout at least in the AT2 cells. In view of 112b issue noted above, the claimed methods are interpreted to apply the drugs either before or after mechanical tension.
Claim 43, 44 and claims 58, 59, recite means for detecting Cdc42 knockout in the mouse model. These claims do not recite an active method step or provide additional meaning, purpose or structure to the active steps of claims 33, 41 (See MPEP 2111.04(I)). A means for detecting Cdc42 knockout, such as by using primers, does not limit the mouse model recited in the active steps of claims 33 or 41. Therefore, prior art(s) that anticipates and/or renders obvious a mouse model comprising Cdc42 knockout at least in AT2 cells meets the claim limitations of claims 43, 44, 58, 59.
Claim 50 recites “wherein the mouse model shows progressive lung fibrosis phenotype after” PNX. This is not an active method step or provide any additional structure to the mouse model of claim 49 which already comprises a Cdc42 gene knockout with PNX. The feature recited in claim 50 is inherent to a Cdc42 gene knockout mouse especially when combined with PNX. Therefore, prior art(s) that anticipates and/or renders obvious a mouse model comprising Cdc42 knockout at least in AT2 cells, especially along with PNX, meets the claim limitations of claims 50.
Similar interpretation is applicable to claim 55, that depends from independent claim 41.
Claim 51 recites “wherein the mouse model without undergoing PNX shows progressive lung fibrosis phenotype in middle age and old age”. Claim 52 recites “wherein the mouse model without undergoing PNX shows progressive lung fibrosis phenotype in middle age and old age”. Similar to claim 50, these claims do not recite an active method step or provide any additional structure to the mouse model of claim 33 which already comprises a Cdc42 gene knockout. The feature recited in claims 51 and 52 are inherent to a Cdc42 gene knockout mouse. Therefore, prior art(s) that anticipates and/or renders obvious a mouse model comprising Cdc42 knockout at least in AT2 cells meets the claim limitations of claims 51 and 52.
Similar interpretation is applicable to claims 56, 57, that depend from independent claim 41.
Claim Rejections - 35 USC § 103
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.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim(s) 33, 41, 43, 44, 47-60 is/are rejected under 35 U.S.C. 103 as being unpatentable over Lv et al (PLoS ONE 8(7): e68631. doi:10.1371/journal.pone.0068631) and Liu et al (Cell Reports 16, 1810–1819, August 16, 2016; ref of record) in view of Sisson et al (Am J Respir Crit Care Med Vol 181. pp 254–263, 2010; ref of record).
Regarding claims 33 and 41, Lv teaches method for screening candidate drug and evaluating its therapeutic efficacy by applying the candidate drug to a mouse model of pulmonary fibrosis (Materials and Methods: Generation of pulmonary fibrosis and therapeutic protocol, Morphological evaluation of lung sections; Figure 1, 2, S1A, S2A).
Lv uses bleomycin and silica induced pulmonary fibrosis.
Lv does not use a mouse model of pulmonary fibrosis wherein the mouse comprises a Cdc42 knockout in AT2 cells followed by increase in mechanical tension on alveolar epithelium either before or after drug application.
Liu teaches a mouse model comprising Cdc42 knockout in AT2 cells followed by increase in mechanical tension on alveolar epithelium by PNX treatment (Figure 4C; as required by claim 49 and 54). Liu generates the AT2 cell specific Cdc42 knockout by Spc-Cre, which is a AT2 cell specific promoter driving Cre expression (Figure 4C; as required by claim 48 and 53). Liu teaches that their mouse model has reduced AT2 proliferation (Figure 4G). Liu also discloses that the knockout of downstream effector of Cdc42 (i.e. Yap) results in reduction in AT1 cells and reduction in differentiation of AT2 cells into AT1 cells (Figure 1H-K).
Regarding claims 43, 44, 58 and 59, based on the claim interpretation above, since Liu teaches the mouse model with the structure of the mouse model of claim 33 and 41, Liu’s model can be inherently detected on the basis of SEQ ID NO: 4 using primers SQ ID NO: 1 and 2.
Regarding claims 50, 55, based on the claim interpretation above, since Liu teaches the mouse model with the structure of the mouse model of claim 49 and 54, Liu mouse model inherently shows progressive lung fibrosis after PNX.
Regarding claims 51, 52, 56 and 57, based on the claim interpretation above, since Liu teaches the mouse model with the structure of the mouse model of claim 33 and 41, Liu mouse model inherently shows age-dependent lung fibrosis in middle and old age, including 12 months of age, without PNX.
Therefore, it would be obvious to a person of ordinary skill in the art before the effective filing date of the claimed invention to substitute the mouse model of Lv with mouse model of Liu to in Lv’s method for screening candidate drug for pulmonary fibrosis. Furthermore, an ordinary artisan using the mouse model of Liu would apply the drug before or after the additional mechanical tension to establish the best time frame for therapeutic treatment. An ordinary artisan is motivated to make such a substitution because an ordinary artisan is motivated to test candidate drugs in more than one model for a disease. An ordinary artisan would reasonably expect to substitute the mouse model of Lv with mouse model of Liu in a method for screening candidate drug for pulmonary fibrosis because Liu teaches that their mouse model that comprises AT2-specific Cdc42 knockout and PNX induced mechanical tension which results in reduction in AT2 proliferation and knockout of downstream effector of Cdc42 (i.e. Yap) results in reduction in AT1 cells and reduction in differentiation of AT2 cells into AT1 cells. This is because an ordinary artisan was aware of the role of AT2, reduction in AT2 proliferation and resultant reduction in AT1 in pulmonary fibrosis, including idiopathic pulmonary fibrosis. For example, Sisson teaches that idiopathic pulmonary fibrosis results from “type II alveolar epithelial cells fail to repair the damaged epithelium as a result of ineffectual proliferation, migration, and/or differentiation, and this leads to interstitial scarring (1).” (page 254, col. 1, para 2). Sisson also developed a mouse model for idiopathic pulmonary fibrosis by specifically targeting AT2 in vivo using diphtheria toxin that results in AT2 cell death (Generation of Transgenic Mice; Figure 8). Sisson conclude that “Our findings provide direct evidence specifically linking the targeting of type II cells for injury to the development of lung fibrosis” (Discussion, last para). Since Liu’s mouse model shows reduced AT2 proliferation and suggest reduction in AT2 differentiation into AT1, both of which are known mechanisms for pulmonary fibrosis, an ordinary artisan reasonably expects Liu’s mouse model to recapitulate some aspect of pulmonary fibrosis, including idiopathic pulmonary fibrosis and thus have utility in methods for screening drug candidates for pulmonary fibrosis, including idiopathic pulmonary fibrosis (as required by claims 47, 60).
Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in
the art at the effective time of filing of the invention, especially in the absence of evidence to the
contrary.
Response to Arguments
Applicant's arguments filed 05/06/2026 regarding the U.S.C. 112b rejection of the claims have been fully considered and persuasive in part due to claim amendments. However, arguments regarding claims 33, 41 and 53 were unpersuasive.
Regarding claims 33 and 41, Applicant argue that the claims 33 and 41 as amended “require increasing mechanical tension on alveolar epithelium of the mouse model by aging and/or PNX as a necessary condition for developing pulmonary fibrosis.” (page 10, para 1).
In response, as noted in the previous 112b rejection and further elaborated in the instant action, claims do not clarify the relationship between when conditions, such as aging or PNX now recited in the claim, that cause mechanical tension are applied in relation to the application of the drug. As written, it is interpreted that the drug application could occur before or after mechanical tension. It appears that the Applicant is suggesting that the mouse model of pulmonary fibrosis is not limited to the Cdc42 knockout but requires both Cdc42 knockout with a means for increasing mechanical tension. If so, then the claim could be amended as follows:
A method for […]] pulmonary fibrosis, comprising applying the candidate drugs for treating pulmonary fibrosis to a mouse model of pulmonary fibrosis; wherein the mouse model is constructed by knocking-out Cdc42 gene in AT2 cells of the mouse and subsequently increasing mechanical tension on alveolar epithelium of the mouse
Regarding claim 53, Applicant argue that “the recitation of "the step of knocking-out Cdc42 gene in AT2 cells in a PNX-treated animal" has proper antecedent basis because claim 53 depends from claim 41, which recites increasing mechanical tension "by aging and/or pneumonectomy (PNX)." Claim 53 simply narrows the mouse model to one wherein PNX is employed,” (page 10, para 2)
In response, as noted in the rejection, claim 41 does not recite a step of knocking out Cdc42, let alone knocking out Cdc42 in an animal that is already PNX treated. Claim 41 explicitly states that PNX is subsequent to knockout. If the purpose of dependent claim 53 is to further limit the means of increasing mechanical stimulation to PNX, then this already accomplished by claims 54 and 55. The additional limitation in claim 53 is regarding the AT2 cell specific promoter. Claim 48 which had essentially the same clarity issue as claim 53 was amended in accordance with the interpretation presented in the OA dated 2/5/2026 but no amendment to claim 53 is provided.
Applicant’s arguments with respect to the U.S.C. 103 rejection of claim(s) 33, 41, 43, 44, 47-60 in view of Lv, Liu and Sisson have been considered but are unpersuasive.
Applicant argue that “Lv does not use a model of pulmonary fibrosis wherein the mouse comprises a Cdc42 knockout in AT2 cells followed by increase in mechanical tension on alveolar epithelium" (emphasis in original). Office Action at 19. Neither Liu or Liu and Sisson cure the deficiencies of Lv to arrive at the instant claims.” (page 13, para 3). In support, Applicant allege that Liu and Sisson “do NOT disclose a mouse model of pulmonary fibrosis can be constructed by knocking-out Cdc42 gene in AT2 cells and subsequently increasing mechanical tension on alveolar epithelium of the mouse model by aging and/or pneumonectomy (PNX).” (page 13-14, bridging para). Applicant point to figure 9A and 9B in Sisson that shows that in their diptheria toxin-induced AT2 cell death model for pulmonary fibrosis “NO difference in the total number of SPC-positive AT2 cells between control and the mice treated with DT (Figure 9A), with more SPC-BrdU double positive cells in the SPC-DTR mice treated with DT (Figure 9B), indicating active proliferation of AT2 cells after injury. That is, AT2 injury-induced lung fibrosis occurred in the absence of a detected decrease in type II cell number and active cell proliferation. “ (page 14, para 1). Applicant then point to Figure 4G in Liu that shows that in their AT2-Cdc-42 knockout with PNX mouse model, “the proliferation of AT2 cells were strongly suppressed following PNX (Figure 4G).” (page 15, para 1).Applicant allege that these results “are totally different” such that “a skilled artisan is unable to envision the Cdc42 AT2 null mice of Liu could develop pulmonary fibrosis.” (page 15, para 2). Applicant point to a para in Barkausas wherein they compare their diptheria toxin-induced AT2 cell death model with Sissons and find different results (page 15, para 2). Thus, Applicant allege that “link between AT2 injury with lung fibrosis” is unclear (page 15, para 2). Applicant then point to post-filing art of Ghosh and Lin wherein AT2 cells and Cdc42 in AT2 are implicated in other pulmonary diseases (page 15, 16) thus concluding that these post-filing art support that “inducing AT2 defects via Cdc42 knockout in mice had not been expected to and would not be directly equated to causing pulmonary fibrosis alone, as the outcome may involve concurrent or alternative lesions such as emphysema.” (emphasis added; page 16, last para).
In response, regarding the post-filing art, these cannot be used to establish the knowledge in the field at the time of filing. Furthermore, these art do not teach that Cdc42 knockout, especially with PNX, would not lead to pulmonary fibrosis (i.e. these are not teaching away). Exclusivity is not a requirement for animal models for disease, especially when the disease system maybe concurrent, as noted but the Applicant, and especially for diseases like idiopathic pulmonary fibrosis with no clear cause.
Regarding Figure 9 in Sisson, this data shows the expected outcome of AT2 injury which is induction of AT2 proliferation (Figure 9B) and thus no reduction in total AT2 cell number is also expected (Figure 9A). This is supported by Barkauskas as well, noting “Our recent genetic lineage-tracing studies in the mouse clearly established that SFTPC+ AEC2s, as a population, proliferate in vivo and give rise to AEC1s (13). These data also showed that these processes, which are normally quite slow, are stimulated after injury with bleomycin, a chemotherapeutic agent that damages multiple cell types in the alveoli and induces transient inflammation and fibrosis (14).” (emphasis added; Introduction, para 3). Sisson also notes similarly that “alveolar progenitor cells can rapidly divide in response to cell injury, thus minimizing the consequences from a single dose of DT. Our data showing increased type II cell proliferation at Day 7 of DT exposure are consistent with this possibility.” (Discussion, para 2). Barkauskas also provides support for this using a mouse model in which diptheria toxin is expressed in AT2 cells after Cre-recombination which is induced by tamoxifen (Methods: Mice). Using a single “low dose” of tamoxifen that triggers cell death in “some” AEC, at least transiently, Barkauskas show that diptheria toxin-induced injury to AT2 leads to their proliferation “not unexpectedly” (Figure 4; See characterization of dose as low in Barkauskas on pg. 3028, col. 2, para 1; See characterization of observed proliferation as expected on pg. 3029, col. 1, last para).
Of note, the para cited by the Applicant from Barkauskas does not establish that “link between AT2 injury with lung fibrosis” is unclear. Barkauskas acknowledges the known link between AT2 cell injury and fibrosis in the prior art (pg. 3025, col. 2, para 1; pg. 3025, col.2, last para; ). Although in Barkauskas model fibrosis was not observed, this does not lend to lack of clarity. As noted above, Barkauskas uses a low dose of tamoxifen that triggers cell death in some AEC transiently at day 2 but proliferation and repair process start rapidly already at day 2, already mostly done by day 7 and is over by day 21 (Figure 4C). Even in the repeat dose, Barkauskas maintained low dose given every 2 weeks which would not be sufficient to maintain AT2 injury to level where their rapid proliferation would not overcome it. Sisson also acknowledges this ability of AT2 to rapidly proliferate during post-injury repair and thus use a daily toxin regimen. Sisson state “Our dosing approach differs from many of these prior studies (e.g., hepatocytes, cardiomyocytes, podocytes, and osteocytes), in that more than one administration of DT was used to achieve the fibrotic phenotype. […] There are several possible explanations for why repeated doses of DT were required for a phenotype in our model. One potential explanation is that alveolar progenitor cells can rapidly divide in response to cell injury, thus minimizing the consequences from a single dose of DT.” (page 260, col. 1, last para). This rapid proliferation is in fact supported by Barkauskas. Thus, expectedly in Barkauskas model where only low dose toxin was used to target few cells at really long intervals fibrosis was not achieved (longer than the proliferation rate of AT2 shown by Barkauskas).
Finally, data in Sisson and Liu are not “totally different”. Sisson provides “direct evidence specifically linking the targeting of type II cells for injury to the development of lung fibrosis” (Discussion, last para). Sisson also teaches that idiopathic pulmonary fibrosis results from “type II alveolar epithelial cells fail to repair the damaged epithelium as a result of ineffectual proliferation, migration, and/or differentiation, and this leads to interstitial scarring (1).” (emphasis added, page 254, col. 1, para 2). Barkauskas also provide support for need for AT2 cell proliferation after injury for the repair process (Figure 4; pg 3025, col. 2, last para). Liu’s data shows that their mouse model reduces AT2 cell proliferation, thus teaching that this model would be either unable to have reduced reparative capacity and can be used to identify targets that can enhance repair.
Conclusion
No claim is allowed.
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/MATASHA DHAR/Examiner, Art Unit 1632
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