Abstract: The present disclosure provides methods and compositions for the treatment of diseases and genetic disorders linked to CSTB loss and/or misfunction. The methods and compositions of the present disclosure include rAAV vectors and rAAV viral vectors comprising transgene nucleic acid molecules encoding CSTB polypeptides.

Abstract: Embodiments may provide techniques that protect voice-controllable devices and systems such that the microphone can be shielded from attacking modulated laser beams. Embodiments may provide a physical device that may include two or more layers of integrated material that sits on top of the microphones of the voice-controllable devices and/or systems. The device may act as a physical barrier against the injected malicious laser beams while allowing sound waves reach the microphone for normal operation. For example, in an embodiment, an apparatus may comprise a first layer including at least one opening and a second layer including at least one opening, wherein the at least one opening in the first layer and the at least one opening in the second layer are arranged so as to block the passage of light, but to allow the passage of sound.

Abstract: Immunogenic compositions comprising viral vectors and surfactants are provided. Methods for administration and preparation of such compositions are also provided.

Abstract: Aspects of the present disclosure are directed to methods for treating a subject having cancer. Certain aspects relate to treatment with an anthracene derivative after treatment with one or more pyrimidine analog antimetabolites. Further aspects relate to methods for improving the efficacy of one or more pyrimidine analog antimetabolites by administering to a subject a therapeutically effective amount of an anthracene derivative after administration of the one or more pyrimidine analog antimetabolites.

Abstract: Methods and compositions used to identify and characterize novel rhodopsin domains, which are kalium (potassium)-conducting channelrhodopsins. The rhodopsin domain of these kalium (potassium)-conducting channelrhodopsins have been cloned, optimized and expressed in mammalian systems and thus may be used in, among others, optogenetic applications and as therapeutic agents for electrically active cell mediated disorders.

Abstract: A magnetic tunnel junction is provided. The magnetic tunnel junction comprises an insulating tunnel barrier and a fixed ferromagnet layer adjacent the tunnel barrier. The fixed ferromagnet comprises a fixed magnetization along an easy axis approximately normal to an interface between the fixed ferromagnet and the tunnel barrier. A free ferromagnet layer is adjacent the tunnel barrier on the side opposite the fixed ferromagnet. The free ferromagnet layer comprises a bistable magnetization along the easy axis that can switch between a parallel state and an anti-parallel state with the fixed ferromagnet. A heavy metal layer is adjacent the free ferromagnet on the side opposite the tunnel barrier. A unidirectional electric current pulse through the heavy metal layer switches the bistable magnetization of the free ferromagnet, thereby switching an electrical resistance state of the magnetic tunnel junction.

Abstract: Orthosis device and related methods for controlling the device to counteract a gravitational force exerted on the person without directing the orthosis device in a pre-determined pattern of motion.

Abstract: Disclosed herein are ACE2 recombinant proteins and methods of using such for therapeutic and/or diagnostic purposes. Also provided herein are methods for producing such recombinant proteins.

Abstract: The present invention includes compositions and methods for treating an autoimmune disorder or a cancer in a subject in need thereof, the method comprising: administering an effective amount of a composition comprising an oligonucleotide that specifically binds a complementary sequence of the Interleukin-7 receptor (IL7R) pre-mRNA that influences splicing of exon 6, wherein the SM-ASO increases or decreases inclusion of exon 6 in IL7R pre-mRNAs and respectively decreases or increases expression of the soluble isoform of IL7R (sIL7R). In certain embodiments, the oligonucleotide is an antisense oligonucleotide (ASO), or a splice-modulating antisense oligonucleotide (SM-ASO).

Abstract: Aspects of the present disclosure relate to systems and methods for analyzing a tumor, and more specifically, analyzing a tumor to identify a biological aggressiveness of the tumor. One example method for tumor analysis includes: receiving one or more input features associated with a geometric shape of a tumor, the one or more input features including at least a value indicating a circularity of the tumor; determining, via a machine learning component, a characteristic of the tumor based on the one or more input features, the characteristic being indicative of patient survivability; and outputting an indication of the characteristic.

Abstract: Methods and compositions related to the use of a protein with kynureninase activity are described. For example, in certain aspects there may be disclosed a modified kynureninase capable of degrading kynurenine. Furthermore, certain aspects of the invention provide compositions and methods for the treatment of cancer with kynurenine depletion using the disclosed proteins or nucleic acids.

Abstract: An apparatus for a heart of a patient having a cardiac assist device adapted to be implanted into the patient to assist the heart with pumping blood. The apparatus has a sensor adapted to be implanted into the patient. The sensor in communication with the cardiac assist device and the heart which measures native volume of the heart. Alternatively, the sensor monitors the heart based on admittance while the cardiac assist device. Alternatively, the sensor monitors the heart based on impedance.

Abstract: The present disclosure provides ?2?-1 C-terminal domain mimetics for the treatment of pain, epilepsy or other disorders in a subject. Further provided is an ?2?-1 C-terminal domain peptide which blocks binding of ?2?-1 to the glutamate receptors NMDAR and AMPAR.

Abstract: The present disclosure concerns methods and compositions related to adoptive cell therapy and its efficacy related to the gut microbiome. In specific cases, it may be determined for an individual whether or not a chimeric antigen receptor (CAR) T-cell therapy will be effective for an individual based on their gut microbiome. An individual may be provided a composition comprising one or more particular microbe compositions based on analysis of the gut microbiome of the individual and prior to administration of CAR T-cell therapy, in specific embodiments.

Abstract: Modular dendrimers with cationic groups and lipophilic groups are provided herein. In some aspects, the dendrimers provided herein may be formulated in compositions which contain a nucleic acid and one or more helper excipients. In some aspects, these compositions may also be used to treat diseases or disorders with a therapeutic nucleic acid.

Abstract: The current disclosure describes effective therapeutic treatments and diagnostic/prognostic methods for colorectal cancer based on the expression or activity level of biomarkers. Aspects of the disclosure relate to a method for treating a subject for colorectal cancer, the method comprising treating the subject for colorectal cancer after the expression level of one or more biomarker genes from Table 1, Table 2, Table 3, Table 4, Table 5, Table S2, Table S3, Table S4, Table S5, FIG. 4A, and/or FIG. 4B has been determined in a sample from the subject.

Abstract: Chronic tobacco smoke exposure (TSE)-induced lung injury includes increased alveolar and airway inflammation, type II alveolar epithelial cells (A2Cs) senescence and apoptosis, and mucus hypersecretion by airway epithelial cells (AECs) that can be treated by the caveolin-1 peptide CSP7 (SEQ ID NO:1). Caveolin-1 and p53 mediated induction of plasminogen activator inhibitor-1 (PAI-1) expression by interleukin 17A, TSE, pollution and other causes leads to lung injury, which can be abrogated by CSP7 treatment, which abolishes A2Cs senescence and apoptosis and AEC mucus hypersecretion. CSP7 treatment of lung tissue of patients with TSE-induced lung injury decreases A2C apoptosis and AEC mucus hypersecretion. Lung injury with A2Cs senescence and apoptosis and AEC mucus hypersecretion caused by TSE-induced PAI-1 expression in lung tissue of patients is abolished by CSP7.

Abstract: Methods for diagnosis and treatment of cancers by use of exosomes comprising miRNAs and precursors thereof. For example, in some aspects, a cancer may be diagnosed or evaluated by determining the miRNA content of exosomes in a sample from a subject or by detecting miRNA processing in exosomes.

Abstract: Compounds and methods of using the same to inhibit glycolysis and treat cancer and other diseases are disclosed.

Abstract: The present disclosure provides a method of preventing, treating, or inhibiting migraine in a subject, by administering to the subject an amount of first therapeutic selected from cercosporamide, eFT508, or 4EGI-1 sufficient to prevent, treat, or inhibit said migraine. The present disclosure further provides a composition including at least two of cercosporamide. eFT508, or 4EGI-1, both in an amount sufficient to prevent, treat, or inhibit migraine in a subject and a pharmaceutically acceptable carrier. The present disclosure further provides a composition including at least one of cercosporamide, eFT508, or 4EGI-1 and at least one additional migraine therapeutic, both in an amount sufficient to prevent, treat, or inhibit migraine in a subject, and a pharmaceutically acceptable carrier.