58 results about "Hormone release" patented technology

A method and apparatus for delivering corrective therapy through hormone regulation is provided. Inhibition of sympathetic fibers by spinal cord stimulation is used to regulate the levels of hormones such as catecholamines, renin, and calcitonin gene-related peptide. The invention utilizes a closed or open loop feedback system in which physiological parameters such as the concentrations of hormones and sympathetic indicators such as heart rate and urine production are monitored and used to determine the appropriate level of neurostimulation. The site of electrical stimulation includes, but is not limited to, the spinal cord at levels T7–L2 and the associated neural fibers within a region of the T7–L2 dermatomes

A method and apparatus for delivering corrective therapy through hormone regulation is provided. Inhibition of sympathetic fibers by spinal cord stimulation is used to regulate the levels of hormones such as catecholamines, renin, and calcitonin gene-related peptide. The invention utilizes a closed or open loop feedback system in which physiological parameters such as the concentrations of hormones and sympathetic indicators such as heart rate and urine production are monitored and used to determine the appropriate level of neurostimulation. The site of electrical stimulation includes, but is not limited to, the spinal cord at levels T7-L2 and the associated neural fibers within a region of the T7-L2 dermatomes

The present invention provides, among other things, a site specific way to enhance a natural hormonal response to nutrients entering the small intestine after gastric emptying, thereby providing therapeutic value for obesity or diabetic patients. In one aspect, the present invention provides methods of stimulating the release of satiety hormone in a subject comprising applying a first electrical stimulus to a tissue in the lumen of the gastrointestinal system of the subject contemporaneously with the contacting of L-cells of the tissue with a nutrient stimulus. In another aspect, the present invention provides methods for predicting patient response to a weight loss surgery comprising applying a first electrical stimulus to a tissue of the gastrointestinal system of said patient contemporaneously with the contacting of L-cells of the tissue with a nutrient stimulus, assessing the effect of the electrical stimulus in said patient, and, correlating said effect to said patient's response to a weight loss surgery.

A complex is provided for the treatment of neurogenic conditions having the formula:where R1 isM is a metal ion Ca(II), Mg(II), Cu(II) or Ni(II); n is an integer 1 or 2; R is BBB peptide, transferrin, membrane transporter peptide, TAT peptide, bradykinin, beta-endorphin, bombesin, calcitonin, cholecystokinin, an enkephalin, dynorphin, insulin, gastrin, substance P, neurotensin, glucagon, secretin, somatostatin, motilin, vasopressin, oxytocin, prolactin, thyrotropin, an angiotensin, galanin, neuropeptide Y, thyrotropin-releasing hormone, gonadotropnin-releasing hormone, growth hormone-releasing hormone, luteinizing hormone, vasoactive intestinal peptidegluconate, L-lactate, L-leucine, L-tryptophan, and L-glutamate; and R is coupled to M through a carboxylate moiety. Magnesium(II) represents the preferred metal ion as magnesium is known to have neuroprotective effects. The metal ion is in part chelated by a non-steroidal anti-inflammatory drug that does not inhibit platelet activity and includes salicylate and ibuprofenate. The complex also includes a ligand operative in transport across the blood brain barrier. A process for making an inventive complex includes the stoichiometric addition of ligands containing carboxylate groups to a solution of the metal ion. In instances where the metal ion is magnesium(II), a stoichiometric ratio of 1:1:1 is found between the non-steroidal anti-inflammatory ligand:magnesium(II):transporter ligand.

A compound of the formulawhere R1 is H, C1–C4 alkyl and OH; R2 in is H, C1–C4 alkyl and OH; R3 is H and C1–C4 alkyl; R4 is H and C1–C4 alkyl; n is an integer between 0 and 2 inclusive; R5 is a nullity, NHR7C(O)—, C6H4—, C6H4—O—; R7 is C2–C6 alkyl; and R6 is a moiety capable of crossing the blood brain barrier and is as a free compound serotonin, dopamine, blood brain barrier (BBB) peptide, membrane translocating peptide, TAT peptides, bradykinin, beta-endorphin, bombesin, calcitonin, cholecystokinin, an enkephalin, dynorphin, insulin, gastrin, substance P, neurotensin, glucagon, secretin, somatostatin, motilin, vasopressin, oxytocin, prolactin, thyrotropin, an angiotensin, galanin, neuropeptide Y, thyrotropin-releasing hormone, gonadotropnin-releasing hormone, growth hormone-releasing hormone, luteinizing hormone, vasoactive intestinal peptidegluconate, transferrin, glucosylamine, amino saccharin, saccharin ester, lactylamine, leucine, tryptophan, amino glutamate and amino cholines.

The present invention relates to compositions comprising two sustained-release formulations, the first capable of releasing the gonadotropin-releasing hormone component and the second capable of releasing the estrogenic component. Compositions of the present invention can be used for improved androgen ablation therapy of prostate cancer to minimize loss of bone mineral density and frequency and severity of hot flashes by maintaining low adequate estrogen levels during treatment .

A system for delivering a growth hormone releasing peptide including a peptide, or a pharmaceutically acceptable salt form thereof, alternatively conjugated to a polymer via a biodegradable bond and dissolved in a liquid medium. Because extra-cellular fluids in vivo provide the appropriate environment to efficiently degrade peptides, the growth hormone releasing peptide will maintain chemical integrity and remain substantially coupled to the polymer while circulating through the body. The therapeutic agent is, therefore, protected from degradation and clearance.

The present invention provides a site specific way to enhance a natural hormonal response to nutrients entering the small intestine after gastric emptying, thereby providing therapeutic value for obesity or diabetic patients. In one aspect, the present invention provides methods of stimulating the release of satiety hormone in a subject comprising applying a first electrical stimulus to a tissue in the lumen of the gastrointestinal system of the subject contemporaneously with the contacting of L-cells of the tissue with a nutrient stimulus. The present invention also provides methods for predicting patient response to a weight loss surgery comprising applying a first electrical stimulus to a tissue of the gastrointestinal system of said patient contemporaneously with the contacting of L-cells of the tissue with a nutrient stimulus, assessing the effect of the electrical stimulus in said patient, and, correlating said effect to said patient's response to a weight loss surgery.

This invention relates to growth hormone releasing factor (GRF) derivatives. In particular, this invention relates to GRF peptide derivatives having an extended in vivo half-life, for promoting the endogenous production or release of growth hormone in humans and animals.

The invention discloses a novel growth hormone releasing hormone analogue peptide dimer and an application thereof. The amino acid sequence of the novel growth hormone releasing hormone analogue peptide dimer is as follows: (NH2)X1-ADAIFTNSYR-X12-VLGQLSAR-X21-LLQDIMS--C32-C32-theta-SMIDQLL-X21-RASLQGLV-X12-RYSNTFIADA-X1(NH2), wherein formula is R, RG or RGG; theta is GGR or GR and R or (NH2)X1-ADAIFTNSYR-X12-VLGQLSAR-X21-LLQDIMSRQQGESNQERGARAR--C46-C46-omega-RARAGREQNSEGQQRSMIDQLL-X21-RASLQGLV-X12-RYSNTFIADA-X1(NH2), wherein formula is L, LG or LGG and omega is GGL or GL and L. The growth hormone releasing hormone analogue peptide dimer can improve in vivo or in vitro growth hormone releasing activity and has a longer half life, so that the dimer has wide pharmacological activity, for example, promoting wound healing, promoting cardiac muscle cell reconstruction, improving sleeping quality, promoting proliferation and differentiation of generative cells so as to treat infertility, adjust immunity, reduce weight and treat diabetes.

Disclosed herein are methods demonstrating that growth-hormone releasing hormone (GHRH) directly activates cellular reparative mechanisms within the injured heart, in a GH / IGF-I independent fashion. Following experimental myocardial infarction (MI), rats were randomly assigned to receive, during a 4 week period, either placebo (n=14), rat recombinant GH (rrGH, n=8) or JI-38 (n=8; 50 μg / Kg / day), a potent GHRH-agonist. JI-38 did not elevate serum levels of GH or IGF-I, but markedly attenuated the degree of cardiac functional decline and remodeling after injury. In contrast, GH administration markedly elevated body weight, heart weight, circulating GH and IGF-I, but did not offset the decline in cardiac structure and function. Whereas, both JI-38 and GH augmented levels of cardiac precursor cell proliferation, only JI-38 increased anti-apoptotic gene expression. Collectively, these findings demonstrate that within the heart, GHRH-agonists can activate cardiac repair following MI.

A method of modulating glandular secretions by administering acoustic shock waves to a gland, includes the steps of activating acoustic shock waves of an acoustic shock wave generator to emit acoustic shock waves and subjecting the gland to acoustic shock waves stimulating the gland to have a modulated response. The modulated response is one of an adjustment in hormonal release which increases low level output, decreases high level output or stabilizes erratic output. The emitted acoustic shock waves are focused or unfocused low energy acoustic shock waves. The gland underlies the patient's skin. The shock wave generator is acoustically coupled to the patient's skin using a coupling gel or liquid. The gland is one of a testicle, ovary, pituitary gland, adrenal gland, thyroid gland, thymus, pineal gland, parathyroid, or hypothalamus. The method can be repeated one or more times.