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. Priority Acknowledgement is made that the instant application is a National Stage of International application No. PCT/IB2022/000338 (filed 06/17/2022), which claims the benefits of US Provisional Application No. 63/211,946 (filed 06/17/2021). Claim Objections Claim 15 is objected to because of the following informalities: Claim 15 appears to be missing the word “than” in the phrase “less 1 week”. 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 applicant regards as his invention. Claim FILLIN "Enter claim indentification information" \* MERGEFORMAT 20 is 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. The term “ FILLIN "Enter the relative term that renders the claim indefinite." \* MERGEFORMAT limited amount ” in claim FILLIN "Identify the claim." \* MERGEFORMAT 20 is a relative term which renders the claim indefinite. The term “limited amount” is not defined by the claim, the specification does not provide a standard for ascertaining the requisite degree, and one of ordinary skill in the art would not be reasonably apprised of the scope of the invention. FILLIN "Explain which parameter or quantity or other limitation in the claim has been rendered indefinite by the use of the term appearing in bracket 1." \* MERGEFORMAT It is unclear how many cells are considered a "limited amount". Thus, the claim can be interpreted as allowing any number of cells to cross a blood-brain barrier. . 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. (a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention. Claims FILLIN "Insert the claim numbers which are under rejection." \d "[ 1 ]" 1- 3 , 10, 11, and 18 are rejected under 35 U.S.C. 102 FILLIN "Insert either \“(a)(1)\” or \“(a)(2)\” or both. If paragraph (a)(2) of 35 U.S.C. 102 is applicable, use form paragraph 7.15.01.aia, 7.15.02.aia or 7.15.03.aia where applicable." \d "[ 2 ]" (a)(1) as being FILLIN "Insert either—clearly anticipated—or—anticipated—with an explanation at the end of the paragraph." \d "[ 3 ]" anticipated by FILLIN "Insert the prior art relied upon." \d "[ 4 ]" Laskowitz et al (Stem Cells Translational Medicine, 2018) as evidenced by Merriam Webster Dictionary ( definition for intravascular ) and Hu et al (Theranostics, 2018) . Laskowitz discloses a method of treating ischemic stroke comprising intravenous infusion of allogeneic umbilical cord blood (UCB) to patients with ischemic stroke (See abstract and study design and overview). The patients were infused with 0.84 -2.92 x 10 9 total nucleated cells (See Table 1). Laskowitz further teaches the UCB units were tested for viable CD34+ cells. The treatment resulted in improvement of at least one grade in the mRS scale and at least 4 points in NIHSS scale (See abstract). Improvements in mRS, NIHSS, and BI scales were quantified at 3 months post infusion (See Table 2). Regarding claims 1- 2 : Laskowitz discloses a method of treating ischemic stroke (reads on a neurological dysfunction) comprising administering UCB to the patients. The treatment method resulted in improvement of at least one grade in the mRS scale and at least 4 points in the NIHSS scale which reads on whereby treatment of a neurological dysfunction results. Regarding claim 3: Following the discussion of claim 1 above, Las k owitz discloses administering the UBC intravenously. Given that veins are blood vessels and intravascular is defined as administered into a blood vessel (See Merriam Webster Dictionary) , the intravenous administration of Laskowitz reads on intravascular. Regarding claim 10: Following the discussion of claim 1 above, Laskowitz discloses treating ischemic stroke with human UCB which comprises viable CD34+ cells (reads on progenitor cells expressing cell surface antigen CD34). Hu teaches exosomes are present in human UCB and can be isolated by centrifugation (See Sec. isolation from human UCB plasma). Given that Laskowitz does not disclose removing exosomes from UCB, the UCB of Laskowitz inherently comprises exosomes. Regarding claim 11: Following the discussion of claim 1 above, Laskowitz discloses measuring improvements in mRS, NIHSS, and BI scales at three months post UCB infusion which reads on neurological dysfunction is treated within about 10 minutes to about 1 year after administration of UCB. Regarding claim 18: Following the discussion of claim 1 above, Laskowitz discloses administering 0.84 -2.92 x 10 9 total nucleated cells to the patients. 0.84 x 10 9 reads on 1 x10 3 to about 1 x 10 9 . Claims FILLIN "Insert the claim numbers which are under rejection." \d "[ 1 ]" 1-3, 5, 6, 11, 12, 18, and 20 are rejected under 35 U.S.C. 102 FILLIN "Insert either \“(a)(1)\” or \“(a)(2)\” or both. If paragraph (a)(2) of 35 U.S.C. 102 is applicable, use form paragraph 7.15.01.aia, 7.15.02.aia or 7.15.03.aia where applicable." \d "[ 2 ]" (a)(1) and 102(a)(2) as being FILLIN "Insert either—clearly anticipated—or—anticipated—with an explanation at the end of the paragraph." \d "[ 3 ]" anticipated by FILLIN "Insert the prior art relied upon." \d "[ 4 ]" Wang (WO2021034996A2) . Wang discloses a method of treating or ameliorating a cardiovascular disease or brain injury comprising administering an effective amount of umbilical cord blood (See claim 1). In exemplary embodiments, the UCB of Wang is plasma-depleted UCB (PD-UCB) (See pg. 29 Example 1). Wang further teaches the UCB comprises CD34+ cells (See pg. 20, lns 1-2). The disease can comprise an ischemic stroke (See pg. 3, lns 31-33 ). The treatment method comprises injecting U CB containing 2-5 x 10 8 monocytes intravenously (See pg. 36, step 5). Alternatively, the UCB cells can be grafted into a patient’s brain or spinal cord or administered intraarterially (See pg. 12, lns 31-33). Patients showed improved motor function 7-14 days after UCB infusion (See pg. 39, lns 24-30). Additionally , the treatment method results in improvement, lessening of the severity of, or slowing of the progression of altered smell, taste, hearing, or vision loss (See pg. 13 , ln 33 – pg. 14, ln 16). The UCB cells can be administered with a blood-brain-barrier permeabilizer , allowing the UCBs to cross the blood-brain-barrier resulting in synaptogenesis, proliferation of immature neurons, and migration of neuronal cells (See pg. 2, lns 23-25 and pg. 40, lns 15-18 ). Regarding claims 1 and 2: Wang discloses a method of treating a neurological disease such as an ischemic stroke by administering UCBs to a patient which reads on a method of treating a neurological dysfunction in a subject comprising administering an effective amount of UCB whereby treatment of a neurological dysfunction results. Regarding claims 3 and 5: Following the discussion of claim 1 above, Wang discloses the UCB can be administered intravenously (reads on intravascular), intra-arterially, or grafted into a patient’s brain or spinal cord (reads on intracerebral and intraspinal and the UCB are administered in brain tissue). Regarding claim 6: Following the discussion of claim 1 above, Wang et al discloses the UBCs can be administered with a blood-brain-barrier permeabilizer resulting in synaptogenesis, proliferation of immature neurons, and migration of neuronal cells which reads on stimulates neurogenesis and incorporation of neurons into neuronal circuitry of the brain. Regarding claim 11: Following the discussion of claim 1 above, Wang discloses the treatment results in improvement 7-14 days after UCB administration which reads on the neurological dysfunction is treated within about 10 minutes to about 1 year after administration of UCB. Regarding claim 12: Following the discussion of claim 1 above, Wang discloses the treatment method results in improvement, lessening of the severity of, or slowing of the progression of altered smell, taste, hearing, or vision loss which reads on enhances visual and auditory function, and smell and taste function. Regarding claim 18: Following the discussion of claim 1 above, Wang discloses an exemplary embodiment wherein the treatment method comprises injecting UCB containing 2-5 x 10 8 monocytes intravenously which reads on 1 x10 3 to about 1 x 10 9 cells. Regarding claim 20: Following the discussion of claim 1 above, Wang discloses administering a blood-brain-barrier permeabilizer which allows UCBs to cross the blood-brain-barrier which reads on a limited amount of the administered cells of UCB cross a blood-brain barrier of the subject (See claim interpretation above). Claims FILLIN "Insert the claim numbers which are under rejection." \d "[ 1 ]" 1 -3, 6, 8, 9, 11, and 12 - 18 are rejected under 35 U.S.C. 102 FILLIN "Insert either \“(a)(1)\” or \“(a)(2)\” or both. If paragraph (a)(2) of 35 U.S.C. 102 is applicable, use form paragraph 7.15.01.aia, 7.15.02.aia or 7.15.03.aia where applicable." \d "[ 2 ]" (a)(1) as being FILLIN "Insert either—clearly anticipated—or—anticipated—with an explanation at the end of the paragraph." \d "[ 3 ]" anticipated by FILLIN "Insert the prior art relied upon." \d "[ 4 ]" Nakano-Doi et al (Stem Cells, 2010) as evidenced by Proteintech (Proliferating cells: BrdU and Ki-67 cellular markers, 2026) and Merriam Webster Dictionary ( definition for intravascular ) . Nakano-Doi discloses using bone marrow mononuclear cells (BMMCs) to treat ischemic stroke in mice (See abstract). Focal cerebral ischemia was produced in mice by ligation and disconnection of the distal portion of the left middle cerebral artery (See Sec. Induction of Focal Cerebral Ischemia). On post stroke day 2, 1 x 10 6 BMMCs were injected intravenously via the tail vein (See Sec. BMMCs Transplantation in Poststroke Mice). Seven days after stroke induction BMMC treated mice had significantly increased CD31/BrdU double positive endothelial cells in ischemic core and peri-stroke regions compared to controls indicating endothelial cell proliferation in the cortex (See Sec. BMMCs Increase ECs in and Around the Poststroke Cortex and Fig. 4). Seven days after stroke induction BMMC treated mice further had an increase in Nestin/ BrdU double positive cells in the ischemic core (See Sec. BMMCs Promotes the Proliferation of Ischemia-Induced NSPs and Accelerates Neurogenesis with Functional Recovery). On post-stroke day 30, BMMC treated mice had a larger number of NeuN/BrdU double positive cells compared to controls (See Sec. BMMCs Promotes the Proliferation of Ischemia-Induced NSPs and Accelerates Neurogenesis with Functional Recovery). Functional recovery of mice subjected to stroke and then treated with BMMCs was investigated by behavioral testing measuring locomotion during a light phase 30 days post stroke. Mice treated with BMMCs had significantly improved cortical function (i.e. reduction of locomotion) during the light phase (See Sec. BMMCs Promotes the Proliferation of Ischemia-Induced NSPs and Accelerates Neurogenesis with Functional Recovery, last paragraph). Regarding claims 1 and 2: Nakano-Doi discloses using bone marrow mononuclear cells to treat ischemic stroke in mice which reads on a method of treating a neurological dysfunction in a subject comprising administering an effective amount of mononuclear cells to a subject, whereby treatment of neurological dysfunction results. Regarding claim 3: Following the discussion of claim 1 above, Nakano-Doi discloses administering the BMMCs intravenously. Given that veins are blood vessels and intravascular is defined as administered into a blood vessel (See Merriam Webster Dictionary) , the intravenous administration of Nakano-Doi reads on intravascular. Regarding claim 6: Following the discussion of claim 1 above, Nakano-Doi teaches administration of BMMCs to ischemic mice results in proliferation of neurons in in the ischemic core which reads on administration of MNC stimulates neurogenesis and incorporation of new neurons into neuronal circuitry of brain. Regarding claims 8 and 9: Following the discussion of claim 1 above, Nakano-Doi teaches administration of BMMC to ischemic mice results in proliferation of endothelial cells in the ischemic core and peri-stroke regions which reads on stimulates vasculogenesis an incorporation of new vascular cells to repair vascular damage to at least one organ or tissue wherein the organ or tissue is brain. Regarding claim 11: Following the discussion of claim 1 above, Nakano-Doi performs measurements at 7 and 30 days post stroke induction and finds increased proliferation of endothelial cells and neurons and improved cortical function which reads on the neurological dysfunction is treated within about 10 minutes to about 1 year after administration of MNCs. Regarding claim 12: Following the discussion of claim 1 above, Nakano-Doi teaches BMMC treated mice showed improved cortical function during exposure to light phase which reads on administration of MNCs enhances sensory perception. Regarding claim 13: Following the discussion of claim 1 above, Nakano-Doi teaches BMMC treatments in mice results in proliferation of neurons in the cortex. Nakano-Doi further teaches BMMC treated mice demonstrated improved cortical function in sensory response tests . Thus, Nakano-Doi teaches administration of UCB replaces neurons and restores function in the sensory cortex. Regarding claims 14 and 15: Following the discussion of claims 1 and 6 above, Nakano-Doi teaches treating mice with BMMCs 2 days post stroke then measuring an increase in Nestin/ BrdU double positive neurons 7 days post stroke (reads on 5 days after administration of BMMCs which reads on less than 1 week ). Nakano-Doi does not specifically state the Nestin/ BrdU double positive neurons express Ki67. Proteintech teaches BrdU labels cells during the S phase of cel l proliferation while Ki67 labels cells in the G1, S, G2, and M phases (Proteintech, See BrdU & Ki67 FAQs). Given that BrdU and Ki67 both label cells in the S phase of cell proliferation, the Nestin/ BrdU double positive cells of Nakano-Doi inherently express Ki67. Regarding claims 16 and 17: Following the discussion of claims 1 and 6 above, Nakano-Doi teaches treating mice with BMMCs 2 days post stroke then measuring an increase in NeuN/ BrdU double positive neurons 30 days post stroke (reads on about 1 month). Nakano-Doi does not specifically state the NeuN/ BrdU double positive neurons express Ki67. Proteintech teaches BrdU labels cells during the S phase of cell proliferation while Ki67 labels cells in the G1, S, G2, and M phases (Proteintech, See BrdU & Ki67 FAQs). Given that BrdU and Ki67 both label cells in the S phase of cell proliferation, the NeuN/ BrdU double positive cells of Nakano-Doi inherently express Ki67. Regarding claim 18: Following the discussion of claim 1 above, Nakano-Doi discloses administering 1 x 10 6 BMMCs which reads on 1 x10 3 to about 1 x 10 9 MNCs. Claims FILLIN "Insert the claim numbers which are under rejection." \d "[ 1 ]" 1, 2, 10-12 , 18, 20, and 21 are rejected under 35 U.S.C. 102 FILLIN "Insert either \“(a)(1)\” or \“(a)(2)\” or both. If paragraph (a)(2) of 35 U.S.C. 102 is applicable, use form paragraph 7.15.01.aia, 7.15.02.aia or 7.15.03.aia where applicable." \d "[ 2 ]" (a)(1) as being FILLIN "Insert either—clearly anticipated—or—anticipated—with an explanation at the end of the paragraph." \d "[ 3 ]" anticipated by FILLIN "Insert the prior art relied upon." \d "[ 4 ]" Nakanishi et al (Scientific Reports, 2017) as evidenced by Sahoo (Circ Res, 2012) . Nakanishi discloses a method of treating rats with hypoxic-ischemic (HI) brain injury by administering stem-cell-enriched umbilical cord blood cells (SCE-U C BCs) derived by culturing MNCs from UCB (See abstract and Sec. Expansion of rat mononuclear cells derived from UCBCs). The SCE-UCBCs of Nakanishi are comprise CD133 and CD34 positive cells (See Sec. Expansion of rat mononuclear cells derived from UCBCs). The method of Nakanishi comprises inducing HI in rats on postnatal day 7 then administering 2 × 10 6 SCE-UBCs intraperitoneally 3 days after HI (See Sec. Intraperitoneal injection of SCE-UCBCs reduced the infarct volume after HI). Cylinder tests were performed 21 days after insult to access motor function in SCE-UCBCs treated rats. Rats that received SCE-UCBCs had increased use of intact forelimb compared to control rats. Additionally, ro t arod tests which measure motor coordination demonstrated improve d endurance times in SCE-UCBCs treated rats compared to control rats (See Sec. Intraperitoneal injection of SCE-UCBCs ameliorated motor function in HI-injured rats). Nakanishi further discloses the population of SCE-UBCs which migrate to the CNS was low with only 43.8 ± 15.7 cells being detected in the brain 4 days after administration. Regarding claims 1 and 2: Nakanishi discloses a method of treating rats with HI by administering SCE-UCBCs derived by culturing MNCs obtained from UCB which reads on a method of treating a neurological dysfunction in a subject comprising administering an effective amount of MNCs to the subject whereby treatment of the neurological dysfunction results and wherein the neurological dysfunction is hypoxic ischemic encephalopathy. Regarding claim 10: Following the discussion of claim 1 above, Nakanishi discloses treating rats with HI by administering SCE-UCBCs comprising CD133 and CD34 positive cells which reads on UCB comprises progenitor cells expressing surface antigens CD34 and CD133. Sahoo teaches CD34+ cells release exosomes. Given that Nakanishi does not discloses depleting exosomes released by SCE-UCBCs prior to administration, the SCE-UCBCs administered in the method of Nakanishi inherently comprise exosomes. Regarding claim 11: Following the discussion of claim 1 above, Nakanishi discloses improvement in motor function 21 days after insult in SCE-UCBC treated rats which reads on the neurological dysfunction is treated within about 10 minutes to about 1 year after administration of MNCs. Regarding claim 12: Following the discussion of claim 1 above, Nakanishi discloses improvement in motor function, as measured by cylinder tests and rotarod tests which reads on administration of the MNC enhances locomotor function and motor coordination. Regarding claim 18: Following the discussion of claim 1 above, Nakanishi discloses administering 2 × 10 6 SCE-UBCs which reads on the quantity of cells from UCB/MNC administered to the subject is about 1 x10 3 to about 1 x 10 9 . Regarding claims 20 and 21: Following the discussion of claim 1 above, Nakanishi discloses the population of SCE-UBCs which migrate to the CNS was low with only 43.8 ± 15.7 cells being detected in the brain which reads on a limited amount of cells cross a blood-brain barrier. Additionally, while Nakanishi does not disclose the weight of the brain at the time of measurement, since only 43.8 ± 15.7 cells were detected per individual, the number of cells is inherently less than about 50 cells per 25 mg of brain tissue . Claims FILLIN "Insert the claim numbers which are under rejection." \d "[ 1 ]" 1 - 3, 11, 12, 18, and 19 are rejected under 35 U.S.C. 102 FILLIN "Insert either \“(a)(1)\” or \“(a)(2)\” or both. If paragraph (a)(2) of 35 U.S.C. 102 is applicable, use form paragraph 7.15.01.aia, 7.15.02.aia or 7.15.03.aia where applicable." \d "[ 2 ]" (a)(1) as being FILLIN "Insert either—clearly anticipated—or—anticipated—with an explanation at the end of the paragraph." \d "[ 3 ]" anticipated by FILLIN "Insert the prior art relied upon." \d "[ 4 ]" Borlongan et al (Stroke, 2004) as evidenced by Merriam Webster Dictionary ( definition for intravascular ) . Borlongan discloses treating rats subjected to right middle cerebral artery occlusion with intravenous injection of human umbilical cord blood (HUCB) (See abstract). Rats were treated with 200,000 HUCB cells along with the blood-brain barrier permeabilizer, mannitol, or with vehicle (See abstract). Borlongan discloses intravenous administration of low dose HUCB cells were not detected in brains of animals at 3 days after stroke even when cells were co - infused with mannitol (See abstract). Although HUCB cells did not cross the blood-brain barrier, behavioral tests measuring motor and cognitive function including memory , 3 days after stroke, demonstrated improvement in rats receiving HUCB plus mannitol (See Sec. HUCB “Grafts Improve Motor and Cognitive Performance). Regarding claims 1 and 2: Borlongan discloses a method of treating rats subjected to right middle cerebral artery occlusion (reads on a stroke model) by administering HUCB to the rats which reads on a method of treating a neurological dysfunction in a subject comprising administering an effective amount of UCB to the subject whereby treatment of a neurological dysfunction results. Regarding claim 3: Following the discussion of claim 1 above, Borlongan discloses administering the HU CB s intravenously. Given that veins are blood vessels and intravascular is defined as administered into a blood vessel (See Merriam Webster Dictionary) , the intravenous administration of Borlongan reads on intravascular. Regarding claim 11: Following the discussion of claim 1 above, Borlongan discloses improvement in motor and cognitive tests 3 days after stroke which reads on the neurological dysfunction is treated within about 10 minutes to about 1 year after administration of UCB. Regarding claim 12: Following the discussion of claim 1 above, Borlongan discloses improvement in motor and cognitive tests, including tests measuring memory of a task, in HUCB +mannitol treated rats which reads on administration of UCB enhances locomotor function, cognition, and memory. Regarding claim 18: Following the discussion of claim 1 above, Borlongan discloses administering 200,000 HUCB cells which reads on about 1 x10 3 to about 1 x 10 9 cells. Regarding claim 19: Following the discussion of claim 1 above, Borlongan discloses the HUCB cells do not cross the blood-brain barrier even when co-administered with mannitol which reads on the administered cells of UCB do not cross a blood-brain barrier of the subject. Claims 1 - 3, 7, 11, 12, and 18 are rejected under 35 U.S.C. 102 FILLIN "Insert either \“(a)(1)\” or \“(a)(2)\” or both. If paragraph (a)(2) of 35 U.S.C. 102 is applicable, use form paragraph 7.15.01.aia, 7.15.02.aia or 7.15.03.aia where applicable." \d "[ 2 ]" (a)(1) as being FILLIN "Insert either—clearly anticipated—or—anticipated—with an explanation at the end of the paragraph." \d "[ 3 ]" anticipated by FILLIN "Insert the prior art relied upon." \d "[ 4 ]" Nan et al (Ann. N.Y. Acad. Sci, 2005) as evidenced by Merriam Webster Dictionary ( definition for intravascular ) . Nan teaches a method of treating intracerebral hemorrhage (ICH) in rats by administering human umbilical cord blood (HUCB) intravenously (See abstract). Twenty four hours after the induction of ICH rats received intravenous infusions of 2.4 × 10 6 to 3.2 to 10 6 cells (See abstract). Rats receiving HUCB had improvements in step tests by the seventh day after ICH and body-s w ing tests by 14 days after ICH (See Figs. 1 and 2). Limb placement tests which measure combined sensorimotor deficits also showed improvement at days 7 and 16 in mice treated with HUCB (See Fig. 3). HUCB cells were stained with human nuclei marker MAB1281 . Cells were further stained for astrocyte marker GFAP and MAB1281 GFAP double positive cells were found in the wall of cavity formed by hemorrhage (See claim 4). Regarding claims 1 and 2: Nan teaches a treatment method for rats with intracerebral hemorrhage (reads on neurological dysfunction and stroke). The treatment method comprises administering HUCB which reads on administering an effective amount of umbilical cord blood whereby treatment of neurological dysfunction results. Regarding claim 3: Following the discussion of claim 1 above, Nan discloses administering the HUCBs intravenously. Given that veins are blood vessels and intravascular is defined as administered into a blood vessel (See Merriam Webster Dictionary) , the intravenous administration of Nan reads on intravascular. Regarding claim 7: Following the discussion of claim 1 above, Nan teaches cells double positive for human nuclei marker MAB1281 and astrocyte marker GFAP were found in the wall of cavity formed by hemorrhage indicating HUCB cells differentiate to astrocytes which reads on UCB stimulates gliogenesis and incorporation of new astrocytes. “ [T]o repair a blood brain barrier” is an inherent function performed by astrocytes thus the MAB1281, GFAP double positive cells repair the blood brain barrier in the ICH rats of Nan. Regarding claim 11: Following the discussion of claim 1 above, Nan discloses improvement in sensorimotor deficit 7 days after ICH (i.e. 6 days after HUCB administration) which reads on within 10 minutes to about 1 year after administration of UCB. Regarding claim 12: Following the discussion of claim 1 above, Nan discloses improvement in sensorimotor deficit tests, step tests, and body-swing tests which reads on enhances locomotor function and motor coordination. Regarding claim 18: Following the discussion of claim 1 above, Nan discloses administering 2.4 × 10 6 to 3.2 to 10 6 cells which reads on about 1 x10 3 to about 1 x 10 9 cells. Conclusion Any inquiry concerning this communication or earlier communications from the examiner should be directed to FILLIN "Examiner name" \* MERGEFORMAT MARISOL A O'NEILL whose telephone number is FILLIN "Phone number" \* MERGEFORMAT (571)272-2490 . The examiner can normally be reached FILLIN "Work Schedule?" \* MERGEFORMAT Monday - Friday 7:30 - 5:00 EST . 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. If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, FILLIN "SPE Name?" \* MERGEFORMAT Christopher Babic can be reached at FILLIN "SPE Phone?" \* MERGEFORMAT (571) 272-8507 . The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300. Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000. /MARISOL ANN O'NEILL/ Examiner, Art Unit 1633 /ALLISON M FOX/ Primary Examiner, Art Unit 1633