Abstract: The present invention relates to apparatuses for use in electrophoretic separation of macromolecules and/or cells, and in which circulating buffer streams are not required for the electrophoretic separation of macromolecules and/or cells. In certain embodiments, the electrophoretic apparatus disclosed herein comprise a sample chamber and a harvest chamber separated by a size-exclusion membrane; non-circulating buffer chambers flanking each respective sample chamber and harvest chamber, wherein each buffer chamber is separated from each respective sample chamber and harvest chamber by an ion-permeable membrane (restriction membrane), and wherein the buffer chambers are sealed and contain a buffer solution; and an electrode positioned in each buffer chamber. Also disclosed are related methods of using the electrophoretic apparatus disclosed herein.

Abstract: In one aspect, the invention provides a peptide comprising a chaperone-mediated autophagy (CMA)-targeting signal domain; a protein-binding domain that selectively binds to a target cytosolic protein; and a cell membrane penetrating domain (CMPD). In another aspect, the invention provides methods for reducing the intracellular expression level of an endogenous target protein in vitro and in an animal, wherein the method involves administration of the peptide. Methods are also provided for treating a pathological condition in an animal, the methods comprising administering the peptide to the animal. In one embodiment, the pathological condition is a neurodegenerative disease. In another embodiment of the invention, the target cytosolic protein is death associated protein kinase I and the CMPD is protein transduction domain of the HIV-1 Tat protein.

Abstract: The present invention relates to a composition comprising a hydrophilic drug and an amphiphilic carbohydrate compound for use in therapy wherein the composition is intranasally administered to the human or animal body. The composition can be used to treat a variety of disorders, including schizophrenia, obesity, pain and sleep disorders, psychiatric diseases, neurodegenerative conditions, brain cancers and infective diseases.

Abstract: The invention described herein pertains to compositions and methods for treating PTSD and related diseases. In particular, the invention described herein pertains to compositions and methods for treating PTSD and related diseases by administering modulators of NMDA NR2-PSD95-nNOS signaling.

Abstract: The invention provides animal models and clinical trials for assessing agents for potential use in treating and effecting prophylaxis stroke and other neurological diseases, particularly those mediated at least in part by excitoxitity. The invention also provides preferred dosage and infusion regimes and pharmaceutical compositions for clinical application of such agents.

Abstract: The present invention provides a method for ameliorating inflammatory and/or neuropathic pain in a subject by modifying the activity of N-methyl-D-aspartate (NMDA) receptors in cells of the subject by inhibition of the interaction of the unique domain of the tyrosine kinase Src enzyme and the NMDA receptor complex.

Abstract: The disclosure relates, at least in part, to methods of treating neuropathic pain in a patient in need thereof by administering an effective amount of a disclosed compound, e.g. a peptide NMDA receptor partial agonist.

Abstract: The present invention provides lyophilized formulations of active agents, particularly of TAT-NR2B9c. TAT-NR2B9c has shown promise for treating stroke, aneurysm, subarachnoid hemorrhage and other neurological or neurotraumatic conditions. Such formulations are stable at room temperature thus facilitating maintenance of supplies of such a formulation in ambulances for administration at the scene of illness or accident or in transit to a hospital.

Abstract: The invention provides agents useful for treating pain. An exemplary agent comprises or consists of the a portion of a retroviral Tat protein. One such agent is the peptide Tat-NR2B9c. This peptide has previously been described as an agent for inhibiting damaging effects of stroke and similar conditions via inhibition of PSD95 interactions with NMDA receptors and/or NOS. The present application provides data showing that the Tat-NR2B9c peptides is effective in alleviation of pain. The alleviation of pain can be obtained at a dose of the peptide below the dose required to inhibit PSD-95 interactions with NMDAR or NOS.

Abstract: The invention provides methods of treating stroke and related conditions exacerbated by fever and/or hyperglycemia by administering peptides or peptidomimetics that inhibit binding of NMDAR 2B to PSD-95 to a patient.

Abstract: A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron the method comprising administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor neuronal protein. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARs) to pathways mediating excitotoxicity and ischemic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95/NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults and dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia.

Abstract: The present invention is directed to the use of compounds of the formula: for treating pain, in particular neuropathic pain, bipolar disease and migraine headaches.

Abstract: The present invention relates to novel compounds suitable for or already radiolabeled with 18F, methods of making such compounds and use of such compounds for diagnostic imaging. Such labeled compounds are characterized by Formula II, wherein the substituents G, Q, L, Y and U have the meaning as defined in the specification and claims.

Abstract: The invention is based on the discovery that GM-CSF antagonists can be used for the treatment of a patient that has Alzheimer's disease or vascular dementia, or is at risk for developing Alzheimer's disease. Accordingly, the invention provides methods of administering a GM-CSF antagonist, e.g., a GM-CSF antibody and pharmaceutical compositions comprising such antagonists.

Abstract: The invention provides agents useful for treating pain. An exemplary agent comprises or consists of the a portion of a retroviral Tat protein. One such agent is the peptide Tat-NR2B9c. This peptide has previously been described as an agent for inhibiting damaging effects of stroke and similar conditions via inhibition of PSD95 interactions with NMDA receptors and/or NOS. The present application provides data showing that the Tat-NR2B9c peptides is effective in alleviation of pain. The alleviation of pain can be obtained at a dose of the peptide below the dose required to inhibit PSD-95 interactions with NMDAR or NOS.

Abstract: The present invention provides a synthetic regulator of protein function, which regulator is a light-sensitive regulator. The present invention further provides a light-regulated polypeptide that includes a subject synthetic regulator. Also provided are cells and membranes comprising a subject light-regulated polypeptide. The present invention further provides methods of modulating protein function, involving use of light. The present invention further provides methods of identifying agents that modulate protein function.

Abstract: The disclosure relates, at least in part, to methods of treating neuropathic pain in a patient in need thereof by administering an effective amount of a disclosed compound, e.g. a peptide NMDA receptor partial agonist.

Abstract: The present invention provides a synthetic regulator of glutamate receptor function, which regulator is a light-sensitive (photoreactive) regulator. The present invention further provides a light-regulated glutamate receptor that includes a subject synthetic regulator non-covalently associated with the glutamate receptor. Also provided are cells and membranes comprising a subject light-regulated glutamate receptor. The present invention further provides methods of modulating glutamate receptor function, involving use of light. The present invention further provides methods of identifying agents that modulate glutamate receptor function.

Abstract: The present invention provides a method for ameliorating inflammatory and/or neuropathic pain in a subject by modifying the activity of N-methyl-D-aspartate (NMDA) receptors in cells of the subject by inhibition of the interaction of the unique domain of the tyrosine kinase Src enzyme and the NMDA receptor complex.

Abstract: The present invention provides a synthetic regulator of protein function, which regulator is a light-sensitive regulator. The present invention further provides a light-regulated polypeptide that includes a subject synthetic regulator. Also provided are cells and membranes comprising a subject light-regulated polypeptide. The present invention further provides methods of modulating protein function, involving use of light. The present invention further provides methods of identifying agents that modulate protein function.

Abstract: Provided are methods for detecting various subunits and isoforms of NMDA receptors to help diagnose and differentiate (1) the anatomical location of NMDA receptor over-expression. (2) ischemic conditions in the central and peripheral nervous systems, and (3) the type and cause of chronic pain.