Abstract: An inventory tracking system includes storage modules that hold one or more items. Each item is positionable at locations within the storage modules independent of physical characteristics of the item. Inventory monitoring modules are included to monitor storage modules for adding an item, retrieving an item, consuming of the item, returning an unused item, discarding at least a portion of a consumed item, or combinations thereof. Each act is used to determine information about items utilized in the act, including the location within the storage modules of the items. Each storage module updates a central inventory database about a location of the storage module, a revised inventory of the items stored within the storage modules, or both. The location of the storage modules, the revised inventory of the items stored within the storage modules, or both, is used to order a replenishment of the items held within the storage modules.

Abstract: The present disclosure related to methods of treating pruritus in a subject by topically administering detomidine, or a pharmaceutically acceptable salt thereof, to the subject.

Abstract: The present disclosure related to methods of treating pruritus in a subject by topically administering detomidine, or a pharmaceutically acceptable salt thereof, to the subject.

Abstract: A game play device includes a gesture detection system that utilizes a single inertial measurement unit (IMU) and associated gesture detection software executing on a processor of the game play device. Unique gesture movements as detected by the game play device may be construed as menu navigation and control commands used to select audible, visible and tactile features relating to the game play device as well as game play modes executed by the game play device. The game play device immerses the user into an authentic game play experience using aesthetic qualities and multi-dimensional capabilities that are imagined to be those consistent with authentic magic wands used by actual wizards.

Abstract: The present invention relates to variants of the general amyloid interaction motif (GAIM) of bacteriophage gene 3 protein (g3p) and fusion proteins thereof. The GAIM variants and fusion proteins of the invention are partially or fully deimmunized and demonstrate superior binding and specificity to a diverse array of amyloid proteins, and exhibit enhanced amyloid remodeling and inhibition of amyloid aggregation. The present invention further relates to nucleic acids, vectors, host cells, and methods of making the GAIM variants and fusion proteins thereof. The present invention also relates to pharmaceutical compositions and methods of increasing bacteriophage infectivity, methods of detecting amyloid aggregates, and methods of diagnosing and/or treating a disease associated with misfolded and/or aggregated amyloid protein.

Abstract: The invention is directed to fibrous structures finished with active pharmaceutical ingredients, as well as methods of their manufacturer and use.

Abstract: The invention relates to polypeptides that comprise a portion of filamentous bacteriophage gene 3 protein (g3p) sufficient to bind to and/or disaggregate amyloid, e.g., the N1-N2 portion of g3p and mutants and fragments thereof, wherein that g3p amino acid sequence has been modified through amino acid deletion, insertion or substitution to remove a putative glycosylation signal. The invention further relates to such polypeptides that are also modified through additional amino acid substitution to be substantially less immunogenic than the corresponding wild-type g3p amino acid sequence when used in vivo. The polypeptides of the invention retain their ability to bind and/or disaggregate amyloid. The invention further relates to the use of these g3p-modified polypeptides in the treatment and/or prevention of diseases associated with misfolding or aggregation of amyloid.

Abstract: The present invention relates to variants of the general amyloid interaction motif (GAIM) of bacteriophage gene 3 protein (g3p) and fusion proteins thereof. The GAIM variants and fusion proteins of the invention are partially or fully deimmunized and demonstrate superior binding and specificity to a diverse array of amyloid proteins, and exhibit enhanced amyloid remodeling and inhibition of amyloid aggregation. The present invention further relates to nucleic acids, vectors, host cells, and methods of making the GAIM variants and fusion proteins thereof. The present invention also relates to pharmaceutical compositions and methods of increasing bacteriophage infectivity, methods of detecting amyloid aggregates, and methods of diagnosing and/or treating a disease associated with misfolded and/or aggregated amyloid protein.

Abstract: The present invention provides a method of treating a disease or disorder caused by and/or associated with ABCD1 dysfunction in a human patient, the method comprising administering to the patient in need thereof an effective amount of a compound that increases the activity of triggering receptor expressed on myeloid cells 2 (TREM2). In some embodiments, compound that increases the activity of TREM2 is an agonist of TREM2. In some embodiments, the agonist of TREM2 is a small molecule agonist of TREM2 or an antibody agonist of TREM2.

Abstract: Provided are methods and compositions for treating nocturnal symptoms of Parkinson's disease, morning akinesia, or associated symptoms thereof in a human subject in need thereof, wherein circulating plasma levels of levodopa are provided for an extended period of time following a period of delay after administration.

Abstract: Provided are methods and compositions for treating nocturnal symptoms of Parkinson's disease, morning akinesia, or associated symptoms thereof in a human subject in need thereof, wherein circulating plasma levels of levodopa are provided for an extended period of time following a period of delay after administration.

Abstract: The present disclosure related to methods of treating pruritus in a subject by topically administering an alpha-2 adrenoreceptor agonist to a subject.

Abstract: The present invention provides a method of treating a disease or disorder caused by and/or associated with CSF1R dysfunction in a human patient, the method comprising administering to the patient in need thereof an effective amount of a compound that increases the activity of triggering receptor expressed on myeloid cells 2 (TREM2). In some embodiments, compound that increases the activity of TREM2 is an agonist of TREM2. In some embodiments, the agonist of TREM2 is a small molecule agonist of TREM2 or an antibody agonist of TREM2.

Abstract: The present disclosure related to methods of treating pruritus in a subject by topically administering detomidine, or a pharmaceutically acceptable salt thereof, to the subject.

Abstract: The present disclosure related to methods of treating pruritus in a subject by topically administering detomidine, or a pharmaceutically acceptable salt thereof, to the subject.

Abstract: The present invention relates to variants of the general amyloid interaction motif (GAIM) of bacteriophage gene 3 protein (g3p) and fusion proteins thereof. The GAIM variants and fusion proteins of the invention are partially or fully deimmunized and demonstrate superior binding and specificity to a diverse array of amyloid proteins, and exhibit enhanced amyloid remodeling and inhibition of amyloid aggregation. The present invention further relates to nucleic acids, vectors, host cells, and methods of making the GAIM variants and fusion proteins thereof. The present invention also relates to pharmaceutical compositions and methods of increasing bacteriophage infectivity, methods of detecting amyloid aggregates, and methods of diagnosing and/or treating a disease associated with misfolded and/or aggregated amyloid protein.

Abstract: Embodiments include apparatuses, methods, and systems for dynamically adjusting intelligent fraud rules based on payment transactions within a payment processing system. The embodiments receive a request to evaluate a transaction based on a false positive ratio (FPR) associated with a user's FPR threshold; and retrieve a first list of fraudulent transaction rules having fraud rules and FPRs; and remove fraudulent transaction rules from the first list of fraudulent transaction rules to create first fraudulent transaction rules aligned with the first FPR. The embodiments determine whether a set of parameters associated with the first fraudulent transaction rules are met based on the first FPR; transmit a decline response based on determination that the first fraudulent transaction rules are met; and generate a second list of fraudulent transaction rules dynamically adjusted based on the first list of fraudulent transaction rules and feedback data associated with the first fraudulent transaction rules.

Abstract: Dynamic adjustment of intelligent fraud rules includes receiving a request to evaluate a transaction based on a false positive ratio (FPR) threshold of a user. A list of fraudulent transaction rules is received comprising a plurality of fraud rules that have an associated FPR. The fraud rules are selected from the list of fraudulent transaction rules that are aligned with the FPR threshold of the user. It is determined whether a set of parameters associated with the one or more fraud rules are met based on the transaction and the FPR threshold of the user. A decline response to the request is transmitted to evaluate the transaction based on the determination that the one or more fraud rules are met. The list of fraudulent transaction rules is then dynamically adjusted based on feedback data associated with the plurality of fraud rules or the list of fraudulent transaction rules.

Abstract: The invention relates to polypeptides that comprise a portion of filamentous bacteriophage gene 3 protein (g3p) sufficient to bind to and/or disaggregate amyloid, e.g., the N1-N2 portion of g3p and mutants and fragments thereof, wherein that g3p amino acid sequence has been modified through amino acid deletion, insertion or substitution to remove a putative glycosylation signal. The invention further relates to such polypeptides that are also modified through additional amino acid substitution to be substantially less immunogenic than the corresponding wild-type g3p amino acid sequence when used in vivo. The polypeptides of the invention retain their ability to bind and/or disaggregate amyloid. The invention further relates to the use of these g3p-modified polypeptides in the treatment and/or prevention of diseases associated with misfolding or aggregation of amyloid.

Abstract: Provided are methods and compositions for treating nocturnal symptoms of Parkinson's disease, morning akinesia, or associated symptoms thereof in a human subject in need thereof, wherein circulating plasma levels of levodopa are provided for an extended period of time following a period of delay after administration.