Abstract: The disclosure provides compounds of Formula I, which may be useful as aldehyde dehydrogenase inhibitors and the pharmaceutically acceptable salts thereof. The variables, J, R4, G, Q, and ring A are defined herein. Aldehyde dehydrogenase inhibitors of Formula I are useful for treating a variety of conditions including cancer and inflammation. The disclosure includes methods for using compounds and salts of Formula I to treat colon cancer, pancreatic cancer, nasopharyngeal carcinoma, thyroid cancer, prostate cancer, ovarian cancer, head and neck squamous cell carcinoma, lung cancer, hepatocellular carcinoma, leukemia, brain tumors breast cancer, atherosclerosis, ischaemic heart disease, acne vulgaris, asthma, autoimmune diseases, autoinflammatory diseases, chronic prostatitis, glomerulonephritis, inflammatory bowel disease, pelvic inflammatory disease, reperfusion injury, rheumatoid arthritis, sarcoidosis, transplant rejection, vasculitis, and interstitial cystitis.

Abstract: Disclosed herein are compositions for fixing tissue for cytologic, histomorphologic, and/or molecular analysis (e.g., DNA, RNA, and/or protein analysis). In some embodiments, the fixatives are aldehyde-free fixatives, for example, formaldehyde- or formalin-free fixatives. Particular disclosed compositions include buffered ethanol. The buffer is a phosphate buffer or phosphate buffered saline (PBS) in some examples. In further embodiments, the fixative includes additional components, such as glycerol and/or acetic acid.

Abstract: The present invention provides variant VEGF polypeptides which have been altered in their C-terminal heparin binding region to lower their heparin binding affinity. These variants have been found to act as receptor antagonists for VEGF receptors and antagonize angiogenesis. These variants are useful to treat diseases characterized by pathological angiogenesis.

Abstract: An embodiment of the invention provides a chimeric antigen receptor (CAR) comprising an antigen binding domain specific for FLT3, a transmembrane domain, and an intracellular T cell signaling domain. Nucleic acids, recombinant expression vectors, host cells, populations of cells, antibodies, or antigen binding portions thereof, and pharmaceutical compositions relating to the CARs are disclosed. Methods of detecting the presence of a proliferative disorder, e.g., cancer, in a mammal and methods of treating or preventing a proliferative disorder, e.g., cancer, in a mammal are also disclosed.

Abstract: Disclosed herein are method of producing NK cells that include one or more heterologous nucleic acids. The methods include culturing a population of isolated NK cells in the presence of one or more cytokines to produce a population of activated NK cells. The population of activated NK cells are transduced with a viral vector comprising the one or more heterologous nucleic acids, for example by contacting the activated NK cells with viral particles including the viral vector. The resulting transduced NK cells are then cultured in the presence of one or more cytokines, and optionally in the presence of irradiated feeder cells, to produce a population of expanded transduced NK cells. Also disclosed are methods of treating a subject with a disorder (such as a tumor or hyperproliferative disorder) by administering to the subject NK cells produced by the methods described herein.

Abstract: Described herein are RSV polynucleotide sequences that make use of multiple codons that are containing silent nucleotide substitutions engineered in multiple locations in the genome, wherein the substitutions introduce a numerous synonymous codons into the genome. Due to the large number of defects involved, the attenuated viruses disclosed herein provide a means of producing attenuated, live vaccines against RSV.

Abstract: Disclosed herein are methods of reducing cytotoxicity of a chemotherapeutic agent to non-cancer cells by administering to a subject with cancer an effective amount of an agent that inhibits CD47 signaling and a chemotherapeutic agent. Example disclosed methods reduce cardiotoxicity of a chemotherapeutic agent. Also disclosed are methods of increasing cytotoxicity of a chemotherapeutic agent in cancer cells by administering to a subject with a tumor an effective amount of an agent that inhibits CD47 signaling and a chemotherapeutic agent. In some embodiments, the inhibitor of CD47 signaling is administered to the subject before, during, or after the administration of the chemotherapeutic agent.

Abstract: Described herein is the design and construction of a class of lipoprotein targeting protease inhibitors. Small peptides with protease inhibitor activity are conjugated to hydrophobic, lipoprotein targeting molecules using, for instance, amine reactive chemistry. Methods of use of the resultant lipoprotein targeting protease inhibitor (antiprotease) molecules are also described. Also described is the production and use of protease inhibitor enriched HDL particles, as well as A1AT-peptide-enriched HDL particles, and their use in various therapeutic contexts.

Abstract: Probe sets capable of detecting pathogen nucleic acids in a sample are described. The probe set can be provided on a solid support, such as a microarray. Methods of detecting pathogen nucleic acids in a sample using the probe set are also provided. In some examples, the probes and methods are capable of detecting one or more RNA viruses, one or more DNA viruses, one or more bacterial nucleic acids, and/or one or more protozoan nucleic acids in a sample.

Abstract: Disclosed herein are methods for detecting presence of a target nucleic acid (such as an influenza virus nucleic acid) in a sample. In some embodiments, the methods include contacting the sample with a first probe capable of hybridizing to the target nucleic acid and a second probe capable of hybridizing to the target nucleic acid, contacting the resulting complex with one or more gap filling reagents, thereby producing a gap-filled target nucleic acid, isolating and amplifying the gap-filled target nucleic acid. The amplified gap-filled target nucleic acid covalently linked to the substrate is then detected, for example with a detectably labeled probe. Also disclosed herein are probes capable of hybridizing to influenza virus nucleic acids. The disclosure also includes kits for detecting and/or discriminating influenza virus nucleic acids in a sample. In some examples, the kits include two or more of the disclosed probes.

Abstract: Some embodiments of the invention include inventive compounds (e.g., compounds of Formula (I)). Other embodiments include compositions (e.g., pharmaceutical compositions) comprising the inventive compound. Still other embodiments of the invention include compositions (e.g., pharmaceutical compositions) for treating, for example, certain diseases using the inventive compounds. Some embodiments include methods of using the inventive compound (e.g., in compositions or in pharmaceutical compositions) for administering and treating (e.g., diseases such as cancer or blood disorders). Further embodiments include methods for making the inventive compounds. Additional embodiments of the invention are also discussed herein.

Abstract: Chimeric polypeptides including (a) an extracellular targeting domain; (b) a transmembrane domain; (c) an intracellular linker for activation of T cells (LAT) domain or SLP-76 domain; and (d) an intracellular ZAP70 domain, wherein (a)-(d) are in N-terminal to C-terminal order are provided. Chimeric polypeptides including (a) an extracellular targeting domain; (b) a transmembrane domain; and (c) a ZAP70 domain, wherein (a)-(c) are in N-terminal to C-terminal order are also provided. In some embodiments, the chimeric polypeptide further includes a hinge domain, a signal sequence domain, and/or an intracellular signaling domain. Nucleic acid molecules encoding the chimeric polypeptides and expression vectors including the nucleic acids are also provided. Isolated cells (such as T cells or natural killer cells) expressing the chimeric polypeptides and methods of treating a subject with cancer with the isolated cells are provided.

Abstract: Kits and methods to distinguish between false and true labor are provided. The kits and methods can utilize differences in abundance and/or differences in the rate of change in abundance of B7-H2, SORC2, TF, C1-Esterase Inhibitor, Ran, IMD-H1 and/or PGAM1, as markers of true labor.

Abstract: The disclosure provides apolipoprotein C-II (apoC-II) mimetic peptides and methods for treating hypertriglyceridemia in a patient with an effective amount of an apoC-II mimetic peptide.

Abstract: Some embodiments of the invention include polypeptides comprising a myomerger polypeptide or an extracellular myomerger polypeptide. Other embodiments of the invention include nucleic acid molecules encoding polypeptides comprising a myomerger polypeptide or an extracellular myomerger polypeptide. Other embodiments of the invention include vectors comprising the nucleic acid molecule. Yet other embodiments of the invention include methods of using a myomerger polypeptide or an extracellular myomerger polypeptide. Additional embodiments of the invention are also discussed herein.

Abstract: Embodiments of a recombinant human Parainfluenza Virus (hPIV) F ectodomain trimer stabilized in a prefusion conformation are provided. Also disclosed are nucleic acids encoding the hPIV F ectodomain trimer and methods of producing the hPIV F ectodomain trimer. Methods for inducing an immune response in a subject are also disclosed. In some embodiments, the method can be a method for treating or inhibiting a hPIV infection in a subject by administering a effective amount of the recombinant hPIV F ectodomain trimer to the subject.

Abstract: Disclosed herein are codon-optimized nucleic acids encoding a reduced-size ATP7A protein. Also disclosed are vectors and recombinant viruses (such as recombinant adeno-associated viruses) including the codon-optimized nucleic acids encoding the reduced-size ATP7A protein and compositions including the disclosed vectors and viruses. Further disclosed herein are methods of treating copper transport disorders, for example by administering a disclosed nucleic acid, vector, or recombinant virus to a subject with a copper transport disorder, such as Menkes disease, occipital horn syndrome, or ATP7A-related distal motor neuropathy.

Abstract: A system for planning and performing a repeat interventional procedure includes a registration device (116) and an image generation device (120) which map current targets in a reference image (104) for a first interventional procedure to at least one guidance image (112) acquired from a different imaging modality. Biopsy locations are recorded to the guidance images during the first interventional procedure and the biopsy locations are mapped to the reference image to provide a planning image for use in a subsequent interventional procedure on the patient. In a subsequent interventional procedure, the prior planning image (124) may be registered to a current reference image (126) and the prior biopsy locations and prior and current targets are mapped to a guidance image acquired from a different imaging modality. Biopsy locations are then mapped to the guidance image (115) and mapped back to the current reference image.

Abstract: The present Disclosure is directed to methods for inhibiting or suppressing metastasis of a tumor in a mammalian subject using a cysteamine product, e.g., cysteamine or cystamine or a derivative thereof. Also described herein is a method for treating pancreatic cancer in a mammalian subject by administering a cysteamine product described herein.

Abstract: The disclosure provides methods of tolerizing or treating a subject suffering from an autoimmune or autoinflammatory disease or disorder to an antigen associated with the autoimmune disease or disorder. The disclosure also features kits for carrying out the methods.