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Endocrine Technology

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Hobbs T.R.,Oregon National Primate Research Center | Blue S.W.,Endocrine Technology | Park B.S.,Oregon Health And Science University | Greisel J.J.,Oregon National Primate Research Center | And 2 more authors.
Journal of the American Association for Laboratory Animal Science | Year: 2015

Most biomedical facilities that use rhesus macaques (Macaca mulatta) limit the amount of blood that may be collected for experimental purposes. These limits typically are expressed as a percentage of blood volume (BV), estimated by using a fixed ratio of blood (mL) per body weight (kg). BV estimation ratios vary widely among facilities and typically do not factor in variables known to influence BV in humans: sex, age, and body condition. We used indicator dilution methodology to determine the BV of 20 adult rhesus macaques (10 male, 10 female) that varied widely in body condition. We measured body composition by using dual-energy X-ray absorptiometry, weight, crown-to-rump length, and body condition score. Two indicators, FITC-labeled hydroxyethyl starch (FITC-HES) and radioiodinated rhesus serum albumin (125I-RhSA), were injected simultaneously, followed by serial blood collection. Plasma volume at time 0 was determined by linear regression. BV was calculated from the plasma volume and Hct. We found that BV calculated by using FITC-HES was consistently lower than BV calculated by using 125I-RhSA. Sex and age did not significantly affect BV. Percentage body fat was significantly associated with BV. Subjects categorized as having 'optimal' body condition score had 18% body fat and 62.1 mL/kg BV (by FITC-HES; 74.5 mL/kg by 125I-RhSA). Each 1% increase in body fat corresponded to approximately 1 mL/kg decrease in BV. Body condition score correlated with the body fat percentage (R2 = 0.7469). We provide an equation for calculating BV from weight and body condition score.


PubMed | Oregon Health And Science University, Texas Tech University Health Sciences Center, Endocrine Technology and Oregon National Primate Research Center
Type: Journal Article | Journal: Journal of the American Association for Laboratory Animal Science : JAALAS | Year: 2015

Most biomedical facilities that use rhesus macaques (Macaca mulatta) limit the amount of blood that may be collected for experimental purposes. These limits typically are expressed as a percentage of blood volume (BV), estimated by using a fixed ratio of blood (mL) per body weight (kg). BV estimation ratios vary widely among facilities and typically do not factor in variables known to influence BV in humans: sex, age, and body condition. We used indicator dilution methodology to determine the BV of 20 adult rhesus macaques (10 male, 10 female) that varied widely in body condition. We measured body composition by using dual-energy X-ray absorptiometry, weight, crown-to-rump length, and body condition score. Two indicators, FITC-labeled hydroxyethyl starch (FITC-HES) and radioiodinated rhesus serum albumin ((125)I-RhSA), were injected simultaneously, followed by serial blood collection. Plasma volume at time 0 was determined by linear regression. BV was calculated from the plasma volume and Hct. We found that BV calculated by using FITC-HES was consistently lower than BV calculated by using (125)I-RhSA. Sex and age did not significantly affect BV. Percentage body fat was significantly associated with BV. Subjects categorized as having optimal body condition score had 18% body fat and 62.1 mL/kg BV (by FITC-HES; 74.5 mL/kg by (125)I-RhSA). Each 1% increase in body fat corresponded to approximately 1 mL/kg decrease in BV. Body condition score correlated with the body fat percentage (R(2) = 0.7469). We provide an equation for calculating BV from weight and body condition score.


Glucagon-like peptide-1 (GLP-1), a metabolic signal molecule, regulates reproduction, although, the involved molecular mechanisms have not been elucidated, yet. Therefore, responsiveness of gonadotropin-releasing hormone (GnRH) neurons to the GLP-1 analog Exendin-4 and elucidation of molecular pathways acting downstream to the GLP-1 receptor (GLP-1R) have been challenged. Loose patch-clamp recordings revealed that Exendin-4 (100 nM-5 M) elevated firing rate in hypothalamic GnRH-GFP neurons of male mice via activation of GLP-1R. Whole-cell patch-clamp measurements demonstrated increased excitatory GABAergic miniature postsynaptic currents (mPSCs) frequency after Exendin-4 administration, which was eliminated by the GLP-1R antagonist Exendin-3(9-39) (1 M). Intracellular application of the G-protein inhibitor GDP--S (2 mM) impeded action of Exendin-4 on mPSCs, suggesting direct excitatory action of GLP-1 on GnRH neurons. Blockade of nitric-oxide (NO) synthesis by N-Nitro-L-arginine methyl ester hydrochloride (L-NAME; 100 M) or N(5)-[Imino(propylamino)methyl]-L-ornithine hydrochloride (NPLA; 1 M) or intracellular scavenging of NO by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (CPTIO; 1 mM) partially attenuated the excitatory effect of Exendin-4. Similar partial inhibition was achieved by hindering endocannabinoid pathway using cannabinoid receptor type-1 (CB1) inverse-agonist 1-(2,4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-(1-piperidyl) pyrazole-3-carboxamide (AM251; 1 M). Simultaneous blockade of NO and endocannabinoid signaling mechanisms eliminated action of Exendin-4 suggesting involvement of both retrograde machineries. Intracellular application of the transient receptor potential vanilloid 1 (TRPV1)-antagonist 2E-N-(2, 3-Dihydro-1,4-benzodioxin-6-yl)-3-[4-(1, 1-dimethylethyl)phenyl]-2-Propenamide (AMG9810; 10 M) or the fatty acid amide hydrolase (FAAH)-inhibitor PF3845 (5 M) impeded the GLP-1-triggered endocannabinoid pathway indicating an anandamide-TRPV1-sensitive control of 2-arachidonoylglycerol (2-AG) production. Furthermore, GLP-1 immunoreactive (IR) axons innervated GnRH neurons in the hypothalamus suggesting that GLP-1 of both peripheral and neuronal sources can modulate GnRH neurons. RT-qPCR study confirmed the expression of GLP-1R and neuronal NO synthase (nNOS) mRNAs in GnRH-GFP neurons. Immuno-electron microscopic analysis revealed the presence of nNOS protein in GnRH neurons. These results indicate that GLP-1 exerts direct facilitatory actions via GLP-1R on GnRH neurons and modulates NO and 2-AG retrograde signaling mechanisms that control the presynaptic excitatory GABAergic inputs to GnRH neurons.


News Article | September 16, 2014
Site: businesswireindia.com

Endocrine Technology, L.L.C. is a New York-based biotechnology company detailed at www.etbondusa.com. Kumar Shah, M.D., President of the company, brings the most advanced technology to solve the ebola crisis. There is an enormous humanitarian and scientific need for the masses to get united to fight the ebola crisis. There is a growing scientific consensus that: a. An expedient solution to the crisis must be found in an available drug. b. Evidence-based scientific data should be unearthed that is deeply buried in medical literature. c. The potential solution must be in keeping with cutting edge advances in genomics and fundamentals of immunology. “It is expected that meeting the above criteria will give confidence and galvanize global cooperation to advance such technology to save lives expediently. The mortality rate may surge to 1.2 million in the coming year,” Dr. Kumar Shah stated. Endocrine Technology, LLC and its dedicated “ETBOND Team members” have advanced such a technology. www.etbondusa.com provides links to patent application, references, interim drug draft label and slide presentations. The patent application details a novel immune modulation drug. During therapy it down regulates inflammatory and bleeding responses seen in ebola infected patients by inhibiting serine proteases. During the recovery phase the drug stimulates host immune responses to kill ebola. The later strategy can be extended to asymptomatic patients to cure ebola infection. The modeling of three-dimensional interaction of ebola with host and its immune system suggest that ebola is a highly charged particle that activates proteases and can be effectively neutralized by ET 007, a drug that is a nano formulated version of a globally available drug. It is safe and effective to initiate global efforts to treat and eradicate the ebola crisis. Kumar Shah, M.D. is the USA trained Board Certified Physician, President and Patent developer. He has 20 plus years of medical and biotechnology industry experience. He is in charge of global Medical and Technology Consulting services for ebola. He is assisted by a dedicated ETBOND Team.


PubMed | Endocrine Technology
Type: Journal Article | Journal: Journal of clinical lipidology | Year: 2011

Familial hypobetalipoproteinemia (FHBL) is a co-dominant disorder associated with low circulating levels of low-density lipoprotein (LDL) cholesterol and apolipoprotein B100 (ApoB). A proband was identified in whom the condition was due to an E110X mutation of APOB, creating a particularly early truncation of ApoB in the region of the molecule necessary for very-low-density lipoprotein (VLDL) assembly. The mutation was also associated with nonalcoholic fatty liver disease.To assess the effect of the mutation on metabolism and the formation of VLDL and LDL subfractions.Both the proband and his son, who had the same mutation, had low LDL cholesterol and decreased ApoB, but an increased small-dense LDL level. Lipoprotein profiles were normal in the probands sister and grandson, in whom the mutation was absent. In the proband. there was a profoundly diminished rate of production of VLDL-2. VLDL-1 production, however, was relatively preserved and, because of its decreased catabolism, its pool size was increased. Direct formation of intermediate-density lipoprotein (IDL) and LDL was undetectable. Intermediate-density lipoprotein catabolism was greatly increased and its conversion to LDL was increased. The LDL produced was entirely small-dense LDL. High-density lipoprotein cholesterol levels were low, perhaps also related to the relative increase in VLDL-1, which is an avid acceptor of cholesteryl ester.This novel mutation provides evidence to support the hypothesis that hepatic production of large VLDL-1 leads to the creation of small-dense LDL.

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