Abstract: Methods and products for the attenuation or treatment of pain and the reduction of nociception are described. The methods and products are based on the modulation of neuroglia-derived BDNF expression or activity. Also described herein are commercial packages and uses based on such modulation. Related methods for identifying or characterizing compounds for the treatment of pain and the reduction of nociception are also described.

Abstract: The present invention provides a method of altering the function of TRPV1+ sensory afferent neurons in the pancreas as a way of treating, managing, alleviating, etc., the symptoms and/or underlying causes of diabetes or abnormal glucose metabolism by increasing the release of neuropeptides, such as substance P (sP) or other tachykinin peptide, in the pancreas. This may be achieved by injecting a TRPV1 agonist, such as a capsaicinoid compound or capsaicin analog, or a neuropeptide, such as sP or other tachykinin peptide, directly into the pancreas, or alternatively, by stimulating one or more intercostal and/or subcostal nerves of spinal nerves derived from one or more thoracic segments T8 through T12 by chemical, electrical, surgical, mechanical, etc., methods.

Abstract: Methods and products for the attenuation or treatment of pain and the reduction of nociception are described. The methods an products are based on the modulation of neuroglia-derived BDNF expression or activity. Also described herein are commercial packages and uses based on such modulation. Related methods for identifying or characterizing compounds for the treatment of pain and the reduction of nociception are also described.

Abstract: A process is disclosed for controlling inflammatory tissue access through release of neuropeptides, such as substance P (sP), to insulin-responsive sensory neurons, whereby simultaneous control of insulin sensitivity/resistance is manifested. In models of Type 1 and Type 2 diabetes, sensory afferents, in particular TRPV1, have fundamental roles in insulin/glucose homeostasis, islet physiology and autoimmune tissue inflammation. By manipulation of the TRPV1 neuro-?-cell circuit or enhancement of pancreatic sP levels, normalization of insulin resistance, clearance of inflammation and prevention of both Type 1 and Type 2 diabetes is realized.

Abstract: A process is disclosed for controlling inflammatory tissue access through release of neuropeptides, such as substance P (sP), to insulin-responsive sensory neurons, whereby simultaneous control of insulin sensitivity/resistance is manifested. In models of Type 1 and Type 2 diabetes, sensory afferents, in particular TRPV1, have fundamental roles in insulin/glucose homeostasis, islet physiology and autoimmune tissue inflammation. By manipulation of the TRPV1 neuro-?-cell circuit or enhancement of pancreatic sP levels, normalization of insulin resistance, clearance of inflammation and prevention of both Type 1 and Type 2 diabetes is realized.

Abstract: A process is disclosed for controlling inflammatory tissue access through release of neuropeptides, such as substance P (sP), to insulin-responsive sensory neurons, whereby simultaneous control of insulin sensitivity/resistance is manifested. In models of Type 1 and Type 2 diabetes, sensory afferents, in particular TRPV1, have fundamental roles in insulin/glucose homeostasis, islet physiology and autoimmune tissue inflammation. By manipulation of the TRPV1 neuro-?-cell circuit or enhancement of pancreatic sP levels, normalization of insulin resistance, clearance of inflammation and prevention of both Type 1 and Type 2 diabetes is realized.

Abstract: A movable support surface supported arms may be moved when a driving mechanism including a motor that drives the arms. Guides guide the arms such that the movable support surface moves between extended and retracted positions. A movable barrier is pivotally attached to a flexible rack using a clip assembly. A motor drives the flexible rack such that the movable barrier moves between open and closed positions. When disposed in a display case, the movable support moves between storage and display positions such that the movable barrier moves between a closed position to protect items in storage and an open position to display items on the movable support. The movable support surface and movable barrier are controlled by a control mechanism that may include limit switches to facilitate automatic control. The control mechanism may be responsive to various outside signals, and a plurality of display cases may be simultaneously controlled.

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 method for modifying the activity of NMDA (N-methyl-D-aspartate)receptors in cells by inhibition of the interaction of the unique domain of the tyrosine kinase Src enzyme and the NMDA receptor complex.