Abstract: A powertrain apparatus for an electric vehicle, includes a planetary gear set including three rotation elements, a first motor connected to a first rotation element of the planetary gear set, a differential engaged to a second rotation element of the planetary gear set, a second motor connected to a third rotation element of the planetary gear set, and a synchronizer configured to selectively connect or disconnect between a driveshaft coupled to one side of the differential and the second motor and to selectively connect or disconnect between the second rotation element of the planetary gear set and the third rotation element of the planetary gear set.

Abstract: A frame structure for a purpose built vehicle (PBV) includes: two main side members extending while gradually rising toward a front of the PBV and extending in a front/rear direction to be disposed on either side of the PBV; two auxiliary side members respectively extending in a front/rear direction to be disposed on a lower side of the two main side members; a front cross member connecting the two auxiliary side members in a lateral direction of the PBV; and a plurality of vertical members respectively connecting the main side members and the auxiliary side members in a vertical direction.

Abstract: The present invention relates to a fusion protein comprising a SARS-CoV-2-derived receptor-binding domain and a nucleocapsid protein, and the use thereof. The fusion protein comprising a coronavirus-derived receptor-binding domain and a nucleocapsid protein is highly applicable to a multivalent vaccine composition having greatly improved in-vivo half-life and remarkably superior efficacy compared to an immunogenic composition comprising only a receptor-binding domain. In particular, the fusion protein can greatly improve the titer of the coronavirus-specific antibody formation and T-cell immune response, and is thus useful for the prevention and treatment of coronaviruses comprising SARS-CoV-2.

Abstract: The invention provides anti-SIRPA antibodies, methods of generating such antibodies, and therapeutic uses and methods employing the antibodies.

Abstract: Provided is a peptide composition for preventing or treating Alzheimer's dementia. A peptide or a salt substituent thereof according to the presently claimed subject matter exhibits effects such as suppression of LPS-mediated cytokine production, suppression of LPS-induced neuroinflammation, amelioration of cognitive impairment, suppression of beta amyloid or tau protein aggregation, and suppression of neuronal loss. The polypeptide or the salt substituent thereof can permeate the blood-brain barrier, and thus, is expected to be usefully used for preventing or treating Alzheimer's dementia.

Abstract: A frame for a purpose-built vehicle (PBV) includes: a front part frame positioned at a front side of a vehicle; a rear part frame positioned at a rear side of the vehicle; and a center part frame. The center part frame has a rectangular planar shape and is coupled between the front part frame and the rear part frame.

Abstract: The present disclosure is generally directed to compositions that include antibodies, e.g., monoclonal, chimeric, humanized antibodies, antibody fragments, etc., that specifically bind on or more epitopes within a Siglec-9 protein, e.g., human Siglec-9 or a mammalian Siglec-9, and use of such compositions in preventing, reducing risk, or treating an individual in need thereof.

Abstract: The present disclosure is generally directed to compositions that include antibodies, e.g., monoclonal, antibodies, antibody fragments, etc., that specifically bind a MerTK polypeptide, e.g., a mammalian MerTK or human MerTK, and use of such compositions in treating an individual in need thereof.

Abstract: The invention provides anti-SIRPA antibodies, methods of generating such antibodies, and therapeutic uses and methods employing the antibodies.

Abstract: The present disclosure is generally directed to compositions that include antibodies, e.g., monoclonal, antibodies, antibody fragments, etc., that specifically bind a TREM2 protein, e.g., a mammalian TREM2 or human TREM2, and use of such compositions in preventing, reducing risk, or treating an individual in need thereof.

Abstract: The present disclosure is generally directed to compositions that include antibodies, e.g., monoclonal, chimeric, humanized antibodies, antibody fragments, etc., that specifically bind a TREM2 protein, e.g., a mammalian TREM2 or human TREM2, and use of such compositions in preventing, reducing risk, or treating an individual in need thereof.

Abstract: The present invention features compositions and methods for editing deleterious mutations associated with hemoglobinopathies, such as sickle cell disease (SCD). In particular embodiments, the invention provides methods for correcting mutations in a beta globin polynucleotide using modified adenosine base editors termed “ABE8” having unprecedented levels (e.g., >60-70%) of efficiency.

Abstract: Disclosed are novel PH20 variants or fragments thereof with improved thermal stability and enzymatic activity of human hyaluronidase, which is an enzyme that hydrolyzes hyaluronic acid, and more particularly novel PH20 variants or fragments thereof including one or more amino acid residue substitutions in the variant having the amino acid sequence of SEQ ID NO: 3, wherein one or more amino acid residues at the N-terminus and/or the C-terminus are optionally further deleted.

Abstract: An organic hole transport material according to an embodiment of the present disclosure is an organic hole transport material doped with an acid-base adduct, in which the acid-base adduct is formed by an acid-base reaction involving an acid and a base, and the acid contains hydrogen ions (H+) and has the formula H+X?, where H+ corresponds to a hydrogen ion, and X? corresponds to an anion and corresponds to TFSI?.

Abstract: The present disclosure is generally directed to compositions that include antibodies, e.g., monoclonal, chimeric, humanized antibodies, antibody fragments, etc., that specifically bind one or more epitopes within a Siglec-9 protein, e.g., human Siglec-9 or a mammalian Siglec-9, and use of such compositions in preventing, reducing risk, or treating an individual in need thereof.

Abstract: The invention provides compositions comprising novel programmable adenosine base editor systems (e.g., ABE8) that provide methods of treating a disease or disorder, (e.g., Parkinson's disease, Hurler syndrome, Rett syndrome, or Stargardt disease) in a subject by administering to the subject a programmable adenosine base editor system (e.g., ABE8) that have increased efficiency and methods of using these adenosine deaminase variants for editing a disease-associated gene.

Abstract: The present invention features compositions and methods for editing deleterious mutations associated with hemoglobinopathies, such as sickle cell disease (SCD). In particular embodiments, the invention provides methods for correcting mutations in a beta globin polynucleotide using modified adenosine base editors termed “ABE8” having unprecedented levels (e.g., >60-70%) of efficiency.

Abstract: The present disclosure is generally directed to compositions that include antibodies, e.g., monoclonal, antibodies, antibody fragments, etc., that specifically bind a TREM2 protein, e.g., a mammalian TREM2 or human TREM2, and use of such compositions in preventing, reducing risk, or treating an individual in need thereof.

Abstract: The present disclosure is generally directed to compositions that include antibodies, e.g., monoclonal, chimeric, humanized antibodies, antibody fragments, etc., that specifically bind a TREM1 protein, e.g., a mammalian TREM1 or human TREM1, and use of such compositions in preventing, reducing risk, or treating an individual in need thereof.

Abstract: The present invention features compositions and methods for editing deleterious mutations associated with alpha-1 anti-trypsin (A1AT) deficiency. In particular embodiments, the invention provides methods for correcting mutations in an A1AT polynucleotide using an adenosine deaminase base editor, ABE8, having unprecedented levels of efficiency.