Abstract: Disclosed herein are methods of preventing or treating ALS by use of a modified EKLF polypeptide, a modified nucleic acid encoding the modified EKLF polypeptide, or modified bone marrow cells comprising the modified nucleic acid. According to embodiments of the present disclosure, the modified EKLF polypeptide comprises an amino acid modification that confers reduced sumoylation in a wild-type EKLF polypeptide.

Abstract: Provided herein are compounds of Formula (I). The compounds described herein are useful in treating a disease associated with the expression of endogenous embryonic/fetal globin (e.g., ? globin) in erythrocytes (e.g., treating ?-thalassemia and/or sickle cell disease through at least the induction of the globin gene expression in erythrocytes), and/or anemia (?-thalassemia and/or sickle cell anemia). The compounds described herein are useful in treating, delaying, and/or preventing the adverse effects of ?-thalassemia and/or sickle cell disease, inducing ? globin production, and/or inducing the expression of embryonic/fetal globin genes in a subject, cell, tissue, or biological sample. Also provided in the present disclosure are pharmaceutical compositions, kits, and methods of using the compounds for inducing ? globin production described herein and for treating any of the target diseases described herein.

Abstract: The invention relates to a genetically modified mouse comprising a heterozygous mutation of Tardbp (TDP-43) gene in that the Asn at amino acid 390 in TDP-43 is substituted with an amino acid that is different from Asn, wherein the genetically modified mouse exhibits Amyotrophic lateral sclerosis (ALS)-like phenotypes, TDP-43 proteinopathies and/or motor neuron degeneration. The invention also so relates to an isolated spinal cord motor neuron differentiated from an embryonic stem cell (ESC) that is obtained from an offspring of a genetically modified mouse according to the invention. Methods for identifying an agent alleviating and/or suppressing ALS-TDP pathogenesis are also disclosed.

Abstract: Provided herein are compounds of Formula (I). The compounds described herein are useful in treating a disease associated with the expression of endogenous embryonic/fetal globin (e.g., ? globin) in erythrocytes (e.g., treating ?-thalassemia and/or sickle cell disease through at least the induction of the globin gene expression in erythrocytes), and/or anemia (?-thalassemia and/or sickle cell anemia). The compounds described herein are useful in treating, delaying, and/or preventing the adverse effects of ?-thalassemia and/or sickle cell disease, inducing ? globin production, and/or inducing the expression of embryonic/fetal globin genes in a subject, cell, tissue, or biological sample. Also provided in the present disclosure are pharmaceutical compositions, kits, and methods of using the compounds for inducing ? globin production described herein and for treating any of the target diseases described herein.

Abstract: The invention found that first, the feasibility of transfer of tumor resistance and other healthy longevity characters through transplantation of bone marrow mononuclear cells (BMMNC) or hematopoietic stem cells (HSC)/hematopoietic stem and progenitor cells (HSPC) consisting of genetically engineered EKLF gene encoding the hematopoietic transcription factor EKLF. Secondly, the present invention demonstrates expression of EKLF in the long-term hematopoietic stem cells (LT-HSC), and thus EKLF as a target of regulation of hematopoiesis.

Abstract: The invention found that first, the feasibility of transfer of tumor resistance and other healthy longevity characters through transplantation of bone marrow mononuclear cells (BMMNC) or hematopoietic stem cells (HSC)/hematopoietic stem and progenitor cells (HSPC) consisting of genetically engineered EKLF gene encoding the hematopoietic transcription factor EKLF. Secondly, the present invention demonstrates expression of EKLF in the long-term hematopoietic stem cells (LT-HSC), and thus EKLF as a target of regulation of hematopoiesis.

Abstract: A genetically-modified non-human animal model of longevity and increased health span, which is associated with reduced tumorigenesis and tumor metastasis, as well as related methods for increasing longevity and health span, reducing tumorigenesis and tumor metastasis, and identifying active agents that confer increased longevity or health span, or reduced tumorigenesis or tumor metastasis.

Abstract: A genetically-modified non-human animal model of longevity and increased health span, which is associated with reduced tumorigenesis and tumor metastasis, as well as related methods for increasing longevity and health span, reducing tumorigenesis and tumor metastasis, and identifying active agents that confer increased longevity or health span, or reduced tumorigenesis or tumor metastasis.

Abstract: The invention relates to a genetically modified mouse comprising a heterozygous mutation of Tardbp (TDP-43) gene in that the Asn at amino acid 390 in TDP-43 is substituted with an amino acid that is different from Asn, wherein the genetically modified mouse exhibits Amyotrophic lateral sclerosis (ALS)-like phenotypes, TDP-43 proteinopathies and/or motor neuron degeneration. The invention also so relates to an isolated spinal cord motor neuron differentiated from an embryonic stem cell (ESC) that is obtained from an offspring of a genetically modified mouse according to the invention. Methods for identifying an agent alleviating and/or suppressing ALS-TDP pathogenesis are also disclosed.

Abstract: The invention found that first, the feasibility of transfer of tumor resistance and other healthy longevity characters through transplantation of bone marrow mononuclear cells (BMMNC) or hematopoietic stem cells (HSC)/hematopoietic stem and progenitor cells (HSPC) consisting of genetically engineered EKLF gene encoding the hematopoietic transcription factor EKLF. Secondly, the present invention demonstrates expression of EKLF in the long-term hematopoietic stem cells (LT-HSC), and thus EKLF as a target of regulation of hematopoiesis.

Abstract: The present invention includes a genetically-modified non-human animal model of longevity and increased health span, which is associated with reduced tumorigenesis and tumor metastasis, as well as related methods for increasing longevity and health span, reducing tumorigenesis and tumor metastasis, and identifying active agents that confer increased longevity or health span, or reduced tumorigenesis or tumor metastasis.

Abstract: Compounds, pharmaceutical compositions, and methods for treating anemia ?-thalassemia anemia or sickle cell anemia.

Abstract: The present invention includes a genetically-modified non-human animal model of longevity and increased health span, which is associated with reduced tumorigenesis and tumor metastasis, as well as related methods for increasing longevity and health span, reducing tumorigenesis and tumor metastasis, and identifying active agents that confer increased longevity or health span, or reduced tumorigenesis or tumor metastasis.

Abstract: A method for treating a progressive neurodegenerative disorder with bone marrow stem cells and a G-CSF receptor agonist.

Abstract: This invention discloses a method for identifying, tracking persons and objects of interest (POI) across multiple monitored areas through means of electromagnetic radiation, sounds and any other sensory inputs in conjunction of location data of electronic devices in the monitored areas. The methodology includes collecting anthropometric data, metrological measurements and any other data relating to persons and objects of interest and location data of electronic devices in the monitored areas. Applying multiple pattern recognition algorithms and statistical analysis of location data to the persons and objects of interests, the system can deduce and focus on the persons and objects of interest's location, movements across monitor areas of the system.

Abstract: Methods for identifying a test agent as a modulator of the active DNA demethylation activity of a DNA methyltransferase are disclosed. The method comprises: a) providing a methylated DNA; b) providing the DNA methyltransferase; c) allowing the methylated DNA to react with the DNA methyltransferase for a sufficient time to perform a demethylation reaction and generate a demethylated DNA product in the presence or absence of a test agent; d) analyzing the extent of demethylation; and d) comparing the extents of the demethylation in the presence and absence of the test agent, and thereby identify the test agent as a modulator of the DNA demethylation activity of the DNA methyltransferase.

Abstract: Compounds, pharmaceutical compositions, and methods for treating anemia (?-thalassemia anemia or sickle cell anemia.

Abstract: Techniques are disclosed for determining a preferred hashing algorithm for load balancing physical interface utilization in a network device, such as a switch, configured with a port-channel architecture. While a current hashing algorithm is being applied to network traffic flows, a forwarding engine of the network device retrieves snapshot data of each flow and evaluates the flows against other hashing algorithms. The forwarding engine, for each hashing algorithm result, calculates statistical measures, such as mean, variance, and coefficient of variation. These measures are used to determine the preferred hashing algorithm to subsequently be applied. Once determined, the networking device may notify a user (e.g., a system administrator) of the algorithm.

Abstract: Methods and systems to control an output frequency relative to a reference frequency. A frequency control system includes a dual-input bias generator to separately receive management and operational controls. The bias generator includes a first bias generator circuit to generate a bias control based on a difference between the management control and a bias feedback reference during a first mode of operation, a second bias generator circuit to generate the bias control based on a difference between the operational control and the bias feedback reference during a second mode of operation, and a bias feedback reference circuit to generate the bias feedback reference based on the bias control. The first mode may include a characterization and/or a start-up mode. The second mode may include an operational mode, such as a feedback-controlled mode.