DETAILED ACTION Notice of Pre-AIA or AIA Status The present application is being examined under the pre-AIA first to invent provisions. 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. Priority The present application is filed as a Divisional of application No. 16/209/100, filed 12/04/2018 (Patent US 11,768,202). Application No. 16/209,100 is a continuation of 15/157,949, filed 05/18/2016 (abandoned), which is a continuation of 13/718,288, filed 12/18/2012 (abandoned). Application 13/718,288 claims benefit under 35 U.S.C. 119(e) to provisional application No. 61/579,546 , filed 12/22/2011 . Information Disclosure Statement The information disclosure statement filed 09/25/2023 fails to comply with 37 CFR 1.98(a)(2), which requires a legible copy of each cited foreign patent document; each non-patent literature publication or that portion which caused it to be listed; and all other information or that portion which caused it to be listed. It has been placed in the application file, but the information referred to therein has not been considered. Citation A4 is lined through because there is no copy. It appear as though it could be a duplicate of A6 (the copy of A6 is present). Applicant should clarify in their response. Citations A7 are also lined through because there does not appear to be a copy (in the present, or prior filed applications ; see also A7 appears to be a duplicate citation for A8, however Black et al. appears to be accurately cited at A8 because the date on the publication that correlates with that issue number and page number is 1998 not 1988 ). A typographical error has been corrected by the Examiner at citation A35 (“ Nayeux et al.” should be “Mayeux et al.”. Claim Objections Claims 1, 3, 4 and 5 are objected to because of the following informalities: Claims 1, 3, 4, and 5 recite abbreviations in the claims, see specifically each of “PANDAS”, “GABHS”, “ELAVL2”, “ELAVL3”, “ELAVL4”, “Nova-1”, “Nova-2”, “Cdr1”, “Cdr2”, and “Cdr3”. At the first instance an abbreviation is recited at the claims, it should be accompanied by the full meaning/term for clarity. Claim 1 is objected to for a typographical error, it appears that “ Syndenham’s chorea” should be spelled as “Sydenham’s chorea”. Appropriate correction is required. Claim Rejections - 35 USC § 112 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 appl icant regards as his invention. Claim s 1-8 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 1, step (b) (ii) recites “not having one of said diseases caused by the Streptococcal infection”. There is insufficient antecedent basis for this limitation in the claim , for example, while step (b) ( i ) does recite “having a disease selected from the group consisting of PANDAS, post-GABHS glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea” in those subject’s with previous Streptococcal infection upon detection of the one more autoantibodies, these disease are not recited as “diseases caused by Streptococcal infection” and as such “said diseases caused by Streptococcal infection” does not have antecedent basis in the claims. Additionally, from the recited language, “not having one of said diseases caused by the Streptococcal infection”, it is unclear if this language does or does not encompass a subject still having one of the diseases PANDAS, post-GABHS, glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea, just not as a result of PANDAS, post-GABHS, glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea caused by Streptococcal infection (i.e., rather does have the disease, just by a different cause). In the interest of compact prosecution, rejections are made under both 35 U.S.C. 112(a), regarding scope of enablement (to address the method comprising diagnosing disease as claimed based on the presence or absence of autoantibodies as claimed) and under 35 U.S.C. 103 (to address for example, diagnosing a subject with PANDAS but not as a result of Streptococcal infection, the subject not having autoantibodies as claimed). 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. Claim s 1-8 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA), first paragraph, because the specification, while being enabling for performing an assay to detect autoantibodies to ELAVL2, ELAVL3, ELAVL4, Nova-1, Nova-2, Cdr1, Cdr2 and Cdr3 antigens in a subject having had a previous Streptococcal infection, does not reasonably provide enablement for a method for diagnosing a disease based on the presence o r absence of autoantibodies to the claimed antigens (not enabled for diagnosing a subject with PANDAS, post-GABHS, glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea , when the presence of one or more of the autoantibodies is detected, and diagnosed as not having PANDAS, post-GABHS, glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea caused by the Streptococcal infection when each of said autoantibodies is present). The factors considered when determining if the disclosure satisfies the enablement requirement and whether any necessary experimentation is "undue" include, but are not limited to: 1) nature of the invention, 2) state of the prior art, 3) relative skill of those in the art, 4) level of predictability in the art, 5) existence of working examples, 6) breadth of claims, 7) amount of direction or guidance by the inventor, and 8) quantity of experimentation needed to make or use the invention. In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988). Regarding the nature of the invention , the method is a diagnostic method for indicating a subject having had a previous Streptococcal infection either has PANDAS, post-GABHS, glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea based on the detected presence of the claimed antibodies, or does not have PANDAS, post-GABHS, glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea as a result of Streptococcal infection, based on the absence of the claimed antibodies (see the issue raised further above under 35 U.S.C. 112(b), as it is not clear if step (b)(ii) is that the subject is not diagnosed with one of the claimed diseases, or rather is merely not diagnosed as having one of said diseases caused by Streptococcal infection). Regardless of the claim interpretation under 35 U.S.C. 112(b), the nature of the invention is a diagnostic assay case based on the presence or absence of an autoantibody that is recognized in the prior art as having an unpredictable presence in relation to the claimed diseases (the claimed autoantibodies being occasionally present and occasionally not present in those having previous Streptococcal infection (see as discussed further in detail later below), particularly in those diagnosed with the claimed diseases, PANDAS, post-GABHS, glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea ). The breadth of the claim encompasses (relevant to the independent claim) determining the presence or absence of the claimed autoantibodies in any biological sample obtained from a subject with a previous Streptococcal infection. Considering that the claimed autoantibodies, and antineuronal antibodies in general, are not consistently found in all or a majority of subjects having the claimed diseases, and given the extreme spectrum of disorders covered by some of the claimed species of disease (e.g., autism , see Hodges et al. cited below ), there is a natural unpredictability in achieving a diagnos i s based on the presence or absence of the autoantibodies as claimed. For example, regarding the state of the prior art and the level of predictability in the art , specific to PANDAS , Peters et al. ( Peters et al., Abstract 84: Abstracts of the 106 th Annual Meeting of the German Society for Pediatrics and Adolescent Medicine (DGKJ), (2010) (Machine English Translation obtained via Google Scholar, 2 pages) ) abstract teach that there are 5 criteria for diagnosing PANDAS, 1. Onset after the age of 3, but before puberty; 2. Presence of obsessive-compulsive symptoms and/or tics; 3. Sudden onset and/or episodic course; 4. Temporal association between GABHS infection and symptom worsening; 5. Choreiform movements during symptom worsening. Peters et al. describe a patient (11 year old boy) who is diagnosed as having PANDAS, but who did not have anti-Hu or anti-Ma (antineuronal type) antibodies. Peters teaches that a lthough their patient did not present with anti-Hu or anti-ma antibodies, Peters does acknowledge that cross-reactive antibodies have been bound, and there is evidence of structural changes in MRI reflecting the inflammatory process as well as in vitro models suggesting a direct pathogenic effect of the antineuronal antibodies. Therefore, although their patient did not present with such antibodies, these anti-neuronal antibodies were recognized in the prior art as occurrin g, and Peters is evidence that not all subjects with PANDAS have the claimed autoantibodies. Kurlan et al. ( Kurlan et al., The Pediatric Autoimmune Neuropsychiatric Disorders associated with Streptococcal infection (PANDAS) Etiology for Tics and Obsessive-Compulsive symptoms: Hypothesis or Entity? Practical Considerations for the Clinician, Pedatirics , 113(4), (2004), p. 883-886 (attached 6 pages, IDS entered 09/25/2023)) teach until more definitive scientific proof is forthcoming, there seems to be insufficient evidence to support 1) routine microbiologic or serologic testing for group A streptococcus in children who present with neuropsychiatric symptoms or 2) the clinical use of antibiotic or immune-modifying therapies in such patients (see at the abstract). Kurlan , similar to Peters, disclose a similar 5 point criteria for evaluating PANDAS (see at Table 1). Kurlan does teach (page 883) that it additionally was suggested (in the art) that, by process of molecular mimicry, somatic epitopes of the Group A beta-hemolytic streptococcus (GABHS) evoke antibodies that are capable of cross reacting with specific areas of the human brain to produce neuropsychiatric and behavioral symptoms. Kurlan et al. report that two research laboratory tests, measurement for circulating anti-neuronal antibodies and an assay for presence of an alleged rheumati c fever associated T lymphocyte alloantigen, have not been able to correlate reliably and consistently with suspected PANDAS. As a result, Kurlan further support the unpredictability in relying on antineuronal antibodies diagnostically (not reliable or consistent) . Walker et al. (Walker et al., Differential Diagnosis of Chorea, Curr. Neurol> Neurosci . Rep., 11, (2011), p. 385-395, IDS entered 09/25/202 3) teach (regarding chorea, i.e., movement disorders, which include Syndeham’s chorea a claimed) that correct diagnosis is essential for appropriate genetic counselling and for future therapies (page 385, col. 1, para 1). See at Table 2, Walker present laboratory evaluation for a patient presenting with chorea, the evaluation including tests such as ASO (for the possible diagnosis of Sydenham’s chorea), and tests for antineuronal antibodies (e.g., anti-Hu, anti- Yo , for possible diagnosis of paraneoplastic syndromes). In the case of antineuronal antibodies, anti-Hu and anti- Yo , Walker suggest the presence of these antibodies as indicating a possible diagnosis of Paraneoplastic syndromes and in their table, do not indicate presence of such antibodies as indicative of Syndeham’s chorea. Given that these autoantibodies are known to correlate with paraneoplastic syndromes, one having ordinary skill would not expect to be able to rely on them for diagnoses as presently claimed. Regarding, for example, just the species of autoantibody that is anti-Hu autoantibodies, anti-Hu autoantibodies are not post-streptococcal infection specific, see for example Sumaruth et al. ( Sumaruth et al., Complexities in the Diagnosis and Management of Anti-Hu Antibody-Associated Paraneoplastic Syndrome, Cureus , 16(9), (2024), (5 pages) ) , this species of autoantibody is recognized as the most commonly associated antibody in paraneoplastic syndrome- mainly secondary to small cell lung cancer, breast cancer, thymoma, and lymphoma (see at abstract, and page 1, last paragraph, of Sumaruth et al.). Bagnall-Moreau et al. (Bagnall-Moreau et al., Maternal brain reactive antibodies profile in autism spectrum disorder: an updated, Springer Nature, 13(37), (2023) (10 pages)) teach that t he relevance of anti-Ri and anti- Yo antibodies in ASD (autism spectrum disorder) remains to be determined , the reference teaching that it is interesting to note that these antibodies are associated with paraneoplastic cerebellar degeneration, often secondary to various types of cancer including carcinoma of the breast or fallopian tube, adenocarcinoma in an axillary lymph node, and others. Bagnall-Moreau teach that t he cerebellum has been implicated in social behavior, and changes in cerebellar function have been observed in both rodent models and humans with ASD , that u ptake of anti-Ri and anti- Yo antibodies has been observed in Purkinje cells in cerebellar slice cultures, which might explain how these antibodies targeting intracellular antigens can trigger a pathologic process leading to ASD, although the mechanism of their internalization is not understood. This reference therefore further supports there is an inherent unpredictability in relying on the claimed autoantibodies (at least those that are anti-Ri and anti- Yo ) for diagnoses such as autism. Even further, regarding the species of disease “autism” alone, autism itself is recognized as a broad spectrum disorder, not defined by any one particular etiology (see for example Hodges et al., Autism spectrum disorder: definition, epidemiology, causes and clinical evaluation, Transl. Pediatr ., 9(Suppl. 1), (2020), S55-s65). Regarding ASD causes, Hodges teach (page s59, col. 1, para 1 of Causes Section) there is no single unifying cause that has been elucidated, that genetic factors play a role in susceptibility (para 2), that while genetics play a role in etiology, phenotypic expression of genetic susceptibility remains extremely variable within ASD. Hodges et al. teach (s59, col. 2, para 4) that ultimately, research continues to reveal factors that correlate with ASD risk, but no casual determinations have been made. Based on the teachings of Hodges, it further appears that autism in general (ASD) is inherently unpredictable in terms of being diagnosable based on a single causative agent such as a biomarker, this reference further supporting unpredictability surrounding a diagnosis relying on the autoantibodies as claimed, particularly considering there is not a singular recognized etiology for this particular diagnosis. Further, Applicant’s own originally filed specification (see at para [0005]) acknowledges that because the molecular mechanisms underlying the disease (referring to the claimed diseases) are largely unknown, there is no clear diagnostic test for these diseases. See the originally filed specification at para [0024], Applicant acknowledges difficulty in achieving diagnosis due to the lack of consistent biological markers found in subjects with these diseases. It is not disputed that the prior art supports presence and detection of the claimed anti-neuronal antibodies in some subjects post Streptococcal infection who have a diagnosis of one or more of PANDAS, post-GABHS glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea (for example, as noted Peters, referenced previously above, reference such detection, however noted no such detection was achieved in their patient) . However, the prior art does not appear to support a reliable nexus between a diagnosis of PANDAS, post-GABHS glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea based on autoantibody detection (autoantibodies to the claimed antigens, namely antineuronal antibodies, such as anti-Ri, Hu and Yo ) . The relative level of skill of those in the prior art is deemed to be high , as the invention is related to clinical diagnostics/diagnostic biomarker assay detection (e.g., PhD/MD ); however, even one skilled in the relevant art could not predictably achieve a diagnosis based on the presence/absence of the claimed autoantibodies based on what is known in the prior art cited above. Since the prior art establishes unpredictability , and little is known regarding the use of the claimed autoantibodies to predictably diagnose any one of PANDAS, post-GABHS glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea , it is necessary to rely on Applicant’s originally filed specification to provide more detail as to how to make and use the invention in order to be enabling. MPEP 2164.03, “the amount of guidance or direction needed to enable the invention is inversely related to the amount of knowledge in the state of the art as well as the predictability of the art” In re Fisher , 427 F.2d 833, 839, 166 USPQ 18, 24 (CCPA 1970). The amount of guidance or direction refers to that information in the application, as originally filed, that teaches exactly how to make or use the invention. The more that is known in the prior art about the nature of the invention, how to make, and how to use the invention, and the more predictable the art is, the less information needs to be explicitly stated in the specification. In contrast, if little is known in the prior art about the nature of the invention and the art is unpredictable, the specification would need more detail as to who to make and use the invention in order to be enabling.” Regarding Applicant’s working examples and actual reduction to practice, the originally filed specification reports a single example, Example 1, titled Hu, Ri, Yo Antibody Immunofluorescence Assay (see starting at para [0048]). Applicant reports biological samples obtained and tested first for ASO (anti-streptolysin O antibodies), reporting 80 ASO positive serum samples, 30 ASO negative samples, and 10 normal serum samples (relying on 200IU/ml to determine positive or negative). Applicant reports diluted sera and controls applied to reaction wells on slides with monkey cerebellar tissues (para [0049]), controls consisted of samples with antibodies known to have reactivity to one or all of Hu, Yo and Ri antigens. Among the samples, twelve are reported with fluorescence using immunofluorescence assay, those samples then tested in Euroimmune anti-neuronal antigens Westernblot IgG assay, along with four samples that were negative, the results shown in the table at page 17-18 of the originally filed specification. However, the example provided in the originally filed specification is not commensurate in scope with the diagnostic assay claims presently recited , and there is insufficient direction or guidance as to how to make or use the claimed invention, in order to achieve diagnosis of a disease as claimed . The example appears only to be relevant in support of the ability to sometimes detect some antineuronal anti-Hu, Yo and Ri autoantibodies in some serum samples known to be positive for ASO. The example does not appear to be relevant to the diagnosis of any particular ASO related or unrelated diseases, for example the singular example provided makes no nexus between the presence of autoantibodies (to the claimed antigens) as claimed and any one diagnosis of PANDAS, post-GABHS glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea . Even am ong those samples considered to be ASO positive (referring to Applicant’s data) , the data presented in the table shows an in consistent pattern amo ng the three species of autoantibodies claimed . For example, of the 12 positive samples, only 1 is positive for anti-Hu, only 4 were positive for anti-Ri, and only 2 had positive results for anti- Yo . Additionally, regarding the level of the skill in the art and the level of predictability , o ne skilled in the art would also recognize that in order to be employed in a method for diagnostic evaluation, a biomarker must be specific to the disease to be evaluated. See for example Mayeux et al., Biomarkers: Potential Uses and Limitations, NeuroRx , 1, (2004), p. 182-188 (IDS entered 09/25/2023) , which teaches that biomarkers are validated by a number of criteria, including the extent to which the biomarker correlates with the specific disease under study (see e.g. page 186, col. 1, first full paragraph). As noted in detail previously above, the claimed autoantibodies are not particularly recognized as diagnostic for any of those disease as claimed (while the art recognizes they can be present, the art supports there is uncertainty in relying on them diagnostically, and the art supports they are not consistently detectable in relation to the claimed diseases) , and to the contrary , are well accepted as detectable in relation to diseases distinct from those claimed, for example paraneoplastic diseases (referring to above, Walker et al. and Sumaruth et al.). Also, a s discussed above (referring to rejection under 35 U.S.C. 112(b)) , claim 1 is indefinite as to what exactly is encompassed by claim 1 step (b)(ii), however even if the claim is interpreted as indicating a subject does not have one of PANDAS, post-GABHS glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea upon absence (i.e., negative for any of the diseases upon absence of detection) of the claimed autoantibodies, the results of Peter et al. contradicts the claim (a patient having PANDAS but not the autoantibodies) , and as discussed above, Applicant’s examples in the originally filed specification provide no supportive evidence that the claimed absence as claimed, indicates that a subject having previous streptococcal infection has no disease selected from PANDAS, post-GABHS, glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea (the working example does not support the claim) . The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make or use the invention commensurate in scope with these claims , without undue experimentation . Claim Rejections - 35 USC § 101 35 U.S.C. 101 reads as follows: Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title. Claims 1-8 are rejected under 35 U.S.C. 101 because the claimed invention is directed to laws of nature/natural phenomenon without significantly more. The U.S. Patent and Trademark Office recently revised the MPEP with regard to § 101 (see the MPEP at 2106). Regarding the MPEP at 2106, in determining what concept the claim is “directed to,” we first look to whether the claim recites: (1) any judicial exceptions, including certain groupings of abstract ideas ( i.e. , mathematical concepts, certain methods of organizing human activity such as a fundamental economic practice, or mental processes); and (2) additional elements that integrate the judicial exception into a practical application (see MPEP § 2106.05(a)-(c), (e)-(h)). Only if a claim (1) recites a judicial exception and (2) does not integrate that exception into a practical application, do we then look to whether the claim contains an “‘inventive concept’ sufficient to ‘transform’” the claimed judicial exception into a patent-eligible application of the judicial exception. Alice , 573 U.S. at 221 (quoting Mayo , 566 U.S. at 82). In so doing, we thus consider whether the claim: (3) adds a specific limitation beyond the judicial exception that is not “well-understood, routine, conventional” in the field (see MPEP § 2106.05(d)); or (4) simply appends well-understood, routine, conventional activities previously known to the industry, specified at a high level of generality, to the judicial exception. See MPEP 2106. ELIGIBILITY STEP 2A: WHETHER A CLAIM IS DIRECTED TO A JUDICIAL EXCEPTION Step 2A, Prong 1 Claim 1 recite s : “ identifying the subject as (1) having disease selected from the group consisting of PANDAS, post-GABHS, glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea, when the presence of one or more antibodies is detected or, (ii) not having one of said diseases caused by the Streptococcal infection when each of said antibodies is absent ”. The claims are directed to a naturally occurring correlation, namely the correlation between a marker that is autoantibodies to any one of ELAVL2, ELAV3, ELAVL4, Nova-1, Nova-2, Cdr1, Cdr2, and Cdr3, and PANDAS, post-GABHS, glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea . The natural relationship to which the claims are directed (i.e., the relation between the marker (autoantibodies) and PANDAS, post-GABHS, glomerulonephritis, rheumatic fever, autism and Syndenham’s chorea ) is a law of nature. Similar concepts have been held by the courts to constitute law of nature/ natural phenomena, as in the identification of a correlation between the presence of in a bodily sample (such as blood or plasma) and cardiovascular disease risk in Cleveland Clinic Foundation v. True Health Diagnostics , LLC, 859 F.3d 1352, 1361, 123 USPQ2d 1081, 1087 (Fed. Cir. 2017). In Mayo, the Supreme Court found that a claim was directed to a natural law, where the claim required administering a drug and determining the levels of a metabolite following administration, where the level of metabolite was indicative of a need to increase or decrease the dosage of the drug. See Mayo Collaborative Services v. Prometheus Labs., Inc ., 566 U.S. 66, 74 (2012). The instant claims are similar to those in Mayo as they involve a "relation itself [which] exists in principle apart from any human action" (id. at 77), namely the relationship between the naturally occurring autoantibodies and the presence of disease . The correlation is a judicial exception as it exists in principle apart from any human action; the correlation itself therefore cannot form the basis for eligibility. Step 2A, Prong 2 The above discussed limitations are themselves insufficient to integrate the judicial exceptions into a practical application because they represent the judicial exceptions themselves and not a practical application thereof. In addition to the judicial exception itself, the claim also recites “determining the presence or absence of one or more autoantibodies in a biological sample form the subject with previous Streptococcal infection, wherein the one or more autoantibodies recognized an antigen from a protein selected from the group consisting of LAVL2, ELAVL3, ELAVL4, Nova-1, Nova-2, Cdrl , Cdr2, and Cdr3 ” , such steps are directed to insignificant pre-solution activity (see is also data gathering) . The “determining” step is extremely generic, and is not, for example, limited to any particular assay or method of determining. T here is no additional limitation or element recited at independent claim 1 which relie s on, applies or uses the judicial exception in such a way that amount s to an integration of the judicial exception into a practical application of the judicial exception. There are no other additional recited steps or elements recited at the dependent claims such to further apply, rely on or use the judicial exception in a manner that imposes meaningful limit on the judicial exception (not additional limitations that amount to a practical application of the judicial exceptions). Rather, see the additionally recited limitations (claims 2-8) merely further narrow or limit the judicial exception itself (for example, the disease/autoantibody target antigen) or the subject and/or sample. ELIGIBILITY STEP 2B: WHETHER THE ADDITIONAL ELEMENTS CONTRIBUTE AN "INVENTIVE CONCEPT" Regarding the additionally claimed steps or elements considered under step 2B, other than the judicial exception, the claim merely recites determining the one or more autoantibodies in a biological sample from the subject with a previous Streptococcal infection . Specifically, it was well-known in the art at the time to perform evaluation of a subject testing for at least a marker for streptococcal infection in addition to testing for autoantibodies as claimed. See for example, Walker et al., Differential Diagnosis of Chorea, Curr. Neurol. Neurosci . Rep, 11, (2011), p. 385-395 (IDS entered 09/25/2023) , teaching laboratory evaluation inclusive of both marker of streptococcal infection (ASO titer), as well as antineuronal antibodies (anti-Hu and anti- Yo ) (see Table 2 at page 386). As further example see Kiryluk et al., Acute chorea and bilateral basal ganglia lesions in a hemodialysis patient, Kidney International, 73, (2008), p. 1087-1091 (IDS entered 09/25/2023) , page 1089, Table is another example of a different ial diagnosis, testing a patient for both ASO and anti-hu autoantibodies. Based on the evidence as cited above, the combination of testing for a streptococcal marker in addition to anti-neuronal autoantibodies was routinely performed in the assay art when providing differential diagnosis. Also see Applicant’s own originally filed disclosure which supports such immunoassay techniques for the characterization of such autoantibody targets as those claimed were well known and routine in the assay art (see page 11, “ Autoantibodies and/or antibodies can be detected in a sample by a variety of known methods. As described previously, these methods include, for example, Enzyme-linked Immunosorbent Assay (ELISA), ELISPOT-Assay, Western-Blot or Immunoassays. Such methods may comprise optical, radioactive, chromatographic methods, fluorescence detection methods, radioactivity detection methods, Coomassie-Blue staining, Silver staining or other protein staining methods, electron microscopy methods, methods for staining tissue sections by immunohistochemistry or by direct or indirect immunofluorescence, etc. ”). T here is no additionally recited meaningful limitation, such as a particular or unconventional machine or a transformation of a particular article, in the active step s of “ determining ” that distinguish the claimed determining step from well-understood, routine, and conventional data gathering activity engaged in by scientists prior to applicant’s invention, and at the time the application was filed, e.g., the routine and conventional techniques of detecting marker for Streptococcal infection and autoantibodies to the claimed protein biomarker(s) . See also MPEP 2106.05(g). There is also evidence of record to indicate that the additional elements, alone or in combination, do not go beyond well-understood, routine and conventional activity in that others had previously measured the targets of the two recited steps as claimed. For all of these reasons, the additional steps/ elements in the claim, when considered alone or in combination, are insufficient to add significantly more. Regarding the limitations specific to the subject from which the biological sample is from, i.e., “from the subject with a previous Streptococcal infection ” (claim 1), “subject is a human” (claim 6), “subject is a pediatric subject” (claim 7) , such limitations also fail to add significantly more than the recited judicial exceptions because limitations specific to the subject fail to constitute a technical advancement or improvement to the method or the art. In particular, it is not the case that the active assay steps of the method would be performed any differently dependent on the subject from which the sample is obtained. For all of these reasons, the claims fail to include additional elements that are sufficient to either integrate the judicial exception(s) into practical application(s) thereof, or amount to significantly more than the judicial exception(s). Claim Rejections - 35 USC § 102 The following is a quotation of the appropriate paragraphs of pre-AIA 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) the invention was known or used by others in this country, or patented or described in a printed publication in this or a foreign country, before the invention thereof by the applicant for a patent. (b) the invention was patented or described in a printed publication in this or a foreign country or in public use or on sale in this country, more than one year prior to the date of application for patent in the United States. Claim(s) 1-3 and 5-7 are rejected under pre-AIA 35 U.S.C. 102 (a)/102(b) as being anticipated by Peters et al., Abstract 84: Abstracts of the 106 th Annual Meeting of the German Society for Pediatrics and Adolescent Medicine (DGKJ), (2010) (Machine English Translation obtained via Google Scholar, 2 pages) . Peters et al. abstract teach there are 5 criteria for diagnosing PANDAS, 1. Onset after the age of 3, but before puberty; 2. Presence of obsessive-compulsive symptoms and/or tics; 3. Sudden onset and/or episodic course; 4. Temporal association between GABHS infection and symptom worsening; 5. Choreiform movements during symptom worsening. Peters et al. describe a patient (11 year old boy) who is diagnosed as having PANDAS, but who did not have anti-Hu or anti-Ma (antineuronal type) antibodies. Although their patient did not present with anti-Hu or anti-ma antibodies, Peters does teach that cross-reactive antibodies have been bound, and there is evidence of structural changes in MRI reflecting the inflammatory process as well as in vitro models suggesting a direct pathogenic effect of the antineuronal antibodies . Therefore, although their patient did not present with such antibodies, these anti-neuronal antibodies were recognized in the prior art as occurring. Peters et al. is teaching diagnosis of the disease PANDAS based on the 5 criteria, Peters is determining the presence or absence of one or more autoantibodies (in the case of Peters, is teaching absence of anti-Hu and anti-Ma) in a biological sample from the subject, the subject having previously had a Streptococcal infection. Anti-Hu antibodies are antibodies recognizing at least ELAVL family antigens (see consistent with Applicant, for example claim 2, the present application refers to these autoantibodies as anti-Hu). The claimed invention recite at step (b) “identifying the subject as ( i ) having a disease selected from the group consisting of PANDAS, post-GABHS, glomerulonephritis, rheumatic fever, autism, Syndenham’s chorea, when the presence of one or more autoantibodies is detected” or “(ii) not having one of said diseases caused by the Streptococcal infection when each of said antibodies is absent”. Step (b)(ii) as literally recited does not exclude a subject from having one of said diseases, instead it limits to the subject not having one of said diseases as “caused by the Streptococcal infection” (i.e., the claim language encompasses a scenario wherein the subject has the disease as a result of a different causative factor. In the present case, Peters et al. is considered to anticipate the claim. Based on Peters et al., a subject having previous Streptococcal infection can have PANDAS with or without antineuronal antibodies. Regarding claim 2, see as cited above, Peters is in reference to autoantibodies that are anti-Hu. Regarding claim 5-7, Peters is teaching a subject that is a human pediatric subject that is diagnosed with a disease that is PANDAS. Claim Rejections - 35 USC § 103 The following is a quotation of pre-AIA 35 U.S.C. 103(a) which forms the basis for all obviousness rejections set forth in this Office action: (a) A patent may not be obtained though the invention is not identically disclosed or described as set forth in section 102, if the differences between the subject matter sought to be patented and the prior art are such that the subject matter as a whole would have been obvious at the time the invention was made to a person having ordinary skill in the art to which said subject matter pertains. Patentability shall not be negated by the manner in which the invention was made. Claim 8 is rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Peters et al. in view of Black et al., Serologic survey of adult patients with obsessive-compulsive disorder for neuron-specific and other autoantibodies, Psychiatry Research, 81, (1998) (IDS entered 09/25/2023) . Peters et al. fails to teach sample comprising blood serum or plasms (Peters is silent as to the sample) . Black et al. teach serum immunoassay to detect a panel of autoantibodies, specifically looking to detect neuron-specific autoantibodies, as well as other organ and non-organ specific autoantibodies (see abstract). Considering it was known in the art (Black at al.) that serum is a suitable sample type of the detection of neuron specific autoantibodies (antineuronal antibodies), it would have been prima facie obvious to one of ordinary skill in the art that Peters et al. perform their detection in a sample that is a serum sample (try to detect the autoantibodies in a serum sample) . In particular, Peters is silent as to sample type, and the prior art taught assay to detect autoantibodies as referenced in Peters (anti-neuronal autoantibodies) in sample that is serum. It would have been obvious to have tried, namely by relying a sample recognized in the art for such detection, because since serum is an art recognized suitable sample, one would have a reasonable and predictable expectation of success. Correspondence Any inquiry concerning this communication or earlier communications from the examiner should be directed to FILLIN "Examiner name" \* MERGEFORMAT ELLEN J MARCSISIN whose telephone number is FILLIN "Phone number" \* MERGEFORMAT (571)272-6001 . The examiner can normally be reached FILLIN "Work Schedule?" \* MERGEFORMAT M-F 8:00am-4:30pm . Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice. 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If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. /ELLEN J MARCSISIN/ Primary Examiner, Art Unit 1677