摘要:
Methods for the treatment, inhibition, prevention, etc. of metabolic syndrome (MetSyn) and/or Type-2 diabetes (T2D) using a T cell activating antibody that stimulates activation and immunomodulation of T-cells to affect the immune environment of adipose tissue and improve insulin sensitivity. Also methods for the treatment, inhibition, prevention, amelioration, reversal, etc., of metabolic syndrome (MetSyn) and/or Type-2 diabetes (T2D) using leukemia inhibitory factor (LIF), or a functional portion thereof. Compositions administered to individuals having or at risk of developing MetSyn and/or T2D may include pharmaceutical compositions. Methods may also provide tolerogenic vaccines based on the administration of identified auto-antigens from individuals having or at risk of developing MetSyn and/or T2D.
摘要:
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-β-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.
摘要:
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-β-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.
摘要:
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.
摘要:
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-β-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.
摘要:
An optical resonator can include an optical feedback structure disposed on a substrate, and a composite including a matrix including a chromophore. The composite disposed on the substrate and in optical communication with the optical feedback structure. The chromophore can be a semiconductor nanocrystal. The resonator can provide laser emission when excited.