Relevant bibliographies by topics / BETA3

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Academic literature on the topic 'BETA3'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "BETA3"

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Brechet, S., P. Plaisancie, V. Dumoulin, JA Chayvialle, JC Cuber, and J. Claustre. "Involvement of beta1- and beta2- but not beta3-adrenoceptor activation in adrenergic PYY secretion from the isolated colon." Journal of Endocrinology 168, no. 1 (January 1, 2001): 177–83. http://dx.doi.org/10.1677/joe.0.1680177.

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The secretion of PYY by endocrine L cells of the terminal gut is under the control of nutrients, the autonomic nervous system and hormones. Catecholamines, and the non-specific beta-adrenergic agonist isoproterenol induce PYY secretion from rat isolated colon or ileum. Because beta3-adrenergic receptors now appear to mediate many of the effects of catecholamines in the gastrointestinal tract, we investigated the involvement of beta1-, beta2-, and beta3-adrenoceptor stimulation in PYY secretion from the isolated, vascularly perfused rat colon. Infusion of 10(-6) M isoproterenol induced a transient increase in PYY secretion (from 36+/-4 to 87+/-20 fmol/2 min; n=7, P<0.05), that was abolished by a previous infusion of the beta1- and beta2-adrenergic blocker (and partial beta3-agonist) alprenolol (10(-6) M). The beta1-adrenergic agonist dobutamine and the beta-2 agonist terbutaline also (both at 10(-5) M) significantly stimulated PYY secretion, from 29+/-1 to 79+/-12 fmol/2 min and from 19+/-1 to 73+/-13 fmol/2 min respectively (n=7, P<0.05). Neither of the beta3-adrenergic agonists tested (BRL 37 344 (10(-5), 10(-6) M) and SR 58 611A (10(-6) M)) significantly stimulated PYY secretion, thus confirming the exclusive involvement of beta1- and beta2-receptors in beta-adrenergic agonist induced hormone secretion.
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Taya, Y., S. O'Kane, and M. W. Ferguson. "Pathogenesis of cleft palate in TGF-beta3 knockout mice." Development 126, no. 17 (September 1, 1999): 3869–79. http://dx.doi.org/10.1242/dev.126.17.3869.

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We previously reported that mutation of the transforming growth factor-beta3 (TGF-beta3) gene caused cleft palate in homozygous null (−/−) mice. TGF-beta3 is normally expressed in the medial edge epithelial (MEE) cells of the palatal shelf. In the present study, we investigated the mechanisms by which TGF-beta3 deletions caused cleft palate in 129 × CF-1 mice. For organ culture, palatal shelves were dissected from embryonic day 13.5 (E13.5) mouse embryos. Palatal shelves were placed singly or in pairs on Millipore filters and cultured in DMEM/F12 medium. Shelves were placed in homologous (+/+ vs +/+, −/− vs −/−, +/− vs +/−) or heterologous (+/+ vs −/−, +/− vs −/−, +/+ vs +/−) paired combinations and examined by macroscopy and histology. Pairs of −/− and −/− shelves failed to fuse over 72 hours of culture whereas pairs of +/+ (wild-type) and +/+ or +/− (heterozygote) and +/−, as well as +/+ and −/− shelves, fused within the first 48 hour period. Histological examination of the fused +/+ and +/+ shelves showed complete disappearance of the midline epithelial seam whereas −/− and +/+ shelves still had some seam remnants. In order to investigate the ability of TGF-beta family members to rescue the fusion between −/− and −/− palatal shelves in vitro, either recombinant human (rh) TGF-beta1, porcine (p) TGF-beta2, rh TGF-beta3, rh activin, or p inhibin was added to the medium in different concentrations at specific times and for various periods during the culture. In untreated organ culture −/− palate pairs completely failed to fuse, treatment with TGF-beta3 induced complete palatal fusion, TGF-beta1 or TGF-beta2 near normal fusion, but activin and inhibin had no effect. We investigated ultrastructural features of the surface of the MEE cells using SEM to compare TGF-beta3-null embryos (E 12. 5-E 16.5) with +/+ and +/− embryos in vivo and in vitro. Up to E13.5 and after E15.5, structures resembling short rods were observed in both +/+ and −/− embryos. Just before fusion, at E14.5, a lot of filopodia-like structures appeared on the surface of the MEE cells in +/+ embryos, however, none were observed in −/− embryos, either in vivo or in vitro. With TEM these filopodia are coated with material resembling proteoglycan. Interestingly, addition of TGF-beta3 to the culture medium which caused fusion between the −/− palatal shelves also induced the appearance of these filopodia on their MEE surfaces. TGF-beta1 and TGF-beta2 also induced filopodia on the −/− MEE but to a lesser extent than TGF-beta3 and additionally induced lamellipodia on their cell surfaces. These results suggest that TGF-beta3 may regulate palatal fusion by inducing filopodia on the outer cell membrane of the palatal medial edge epithelia prior to shelf contact. Exogenous recombinant TGF-beta3 can rescue fusion in −/− palatal shelves by inducing such filopodia, illustrating that the effects of TGF-beta3 are transduced by cell surface receptors which raises interesting potential therapeutic strategies to prevent and treat embryonic cleft palate.
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Amour, Julien, Xavier Loyer, Morgan Le Guen, Nejma Mabrouk, Jean-Stéphane David, Emmanuel Camors, Nunzia Carusio, et al. "Altered Contractile Response due to Increased β3-Adrenoceptor Stimulation in Diabetic Cardiomyopathy." Anesthesiology 107, no. 3 (September 1, 2007): 452–60. http://dx.doi.org/10.1097/01.anes.0000278909.40408.24.

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Background In the diabetic heart, the positive inotropic response to beta-adrenoceptor stimulation is altered and beta1 and beta2 adrenoceptors are down-regulated, whereas beta3 adrenoceptor is up-regulated. In heart failure, beta3-adrenoceptor stimulation induces a negative inotropic effect that results from endothelial nitric oxide synthase (NOS3)-derived nitric oxide production. The objective of our study was to investigate the role of beta3-adrenoceptor in diabetic cardiomyopathy. Methods beta-Adrenergic responses were investigated in vivo (dobutamine echocardiography) and in vitro (left ventricular papillary muscle) in healthy and streptozotocin-induced diabetic rats. The effect of beta3-adrenoceptor inhibition on the inotropic response was studied in vitro. Immunoblots and NOS activities were performed in heart homogenates (electron paramagnetic resonance) and isolated cardiomyocytes. Data are mean percentage of baseline +/- SD. Results The impaired positive inotropic effect was confirmed in diabetes both in vivo (121 +/- 15% vs. 160 +/- 16%; P &lt; 0.05) and in vitro (112 +/- 5% vs. 179 +/- 15%; P &lt; 0.05). In healthy rat, the positive inotropic effect was not significantly modified in presence of beta3-adrenoceptor antagonist (174 +/- 20%), nonselective NOS inhibitor (N -nitro-l-arginine methylester [l-NAME]; 183 +/- 19%), or selective NOS1 inhibitor (vinyl-l-N-5-(1-imino-3-butenyl)-l-ornithine [l-VNIO]; 172 +/- 13%). In diabetes, in parallel with the increase in beta3-adrenoceptor protein expression, the positive inotropic effect was partially restored by beta3-adrenoceptor antagonist (137 +/- 8%; P &lt; 0.05), l-NAME (133 +/- 11%; P &lt; 0.05), or l-VNIO (130 +/- 13%; P &lt; 0.05). Nitric oxide was exclusively produced by NOS1 within diabetic cardiomyocytes. NOS2 and NOS3 proteins were undetectable. Conclusions beta3-Adrenoceptor is involved in altered positive inotropic response to beta-adrenoceptor stimulation in diabetic cardiomyopathy. This effect is mediated by NOS1-derived nitric oxide in diabetic cardiomyocyte.
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Peyton, M., C. M. Stellrecht, F. J. Naya, H. P. Huang, P. J. Samora, and M. J. Tsai. "BETA3, a novel helix-loop-helix protein, can act as a negative regulator of BETA2 and MyoD-responsive genes." Molecular and Cellular Biology 16, no. 2 (February 1996): 626–33. http://dx.doi.org/10.1128/mcb.16.2.626.

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Using degenerate PCR cloning we have identified a novel basic helix-loop-helix (bHLH) transcription factor, BETA3, from a hamster insulin tumor (HIT) cell cDNA library. Sequence analysis revealed that this factor belongs to the class B bHLH family and has the highest degree of homology with another bHLH transcription factor recently isolated in our laboratory, BETA2 (neuroD) (J. E. Lee, S. M. Hollenberg, L. Snider, D. L. Turner, N. Lipnick, and H. Weintraub, Science 268:836-844, 1995; F. J. Naya, C. M. M. Stellrecht, and M.-J. Tsai, Genes Dev. 8:1009-1019, 1995). BETA2 is a brain- and pancreatic-islet-specific bHLH transcription factor and is largely responsible for the tissue-specific expression of the insulin gene. BETA3 was found to be tissue restricted, with the highest levels of expression in HIT, lung, kidney, and brain cells. Surprisingly, despite the homology between BETA2 and BETA3 and its intact basic region, BETA3 is unable to bind the insulin E box in bandshift analysis as a homodimer or as a heterodimer with the class A bHLH factors E12, E47, or BETA1. Instead, BETA3 inhibited both the E47 homodimer and the E47/BETA2 heterodimer binding to the insulin E box. In addition, BETA3 greatly repressed the BETA2/E47 induction of the insulin enhancer in HIT cells as well as the MyoD/E47 induction of a muscle-specific E box in the myoblast cell line C2C12. In contrast, expression of BETA3 had no significant effect on the GAL4-VP16 transcriptional activity. Immunoprecipitation analysis demonstrates that the mechanism of repression is via direct protein-protein interaction, presumably by heterodimerization between BETA3 and class A bHLH factors.
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Birenbaum, Aurélie, Angela Tesse, Xavier Loyer, Pierre Michelet, Ramaroson Andriantsitohaina, Christophe Heymes, Bruno Riou, and Julien Amour. "Involvement of β3-Adrenoceptor in Altered β-Adrenergic Response in Senescent Heart." Anesthesiology 109, no. 6 (December 1, 2008): 1045–53. http://dx.doi.org/10.1097/aln.0b013e31818d7e5a.

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Background In senescent heart, beta-adrenergic response is altered in parallel with beta1- and beta2-adrenoceptor down-regulation. A negative inotropic effect of beta3-adrenoceptor could be involved. In this study, the authors tested the hypothesis that beta3-adrenoceptor plays a role in beta-adrenergic dysfunction in senescent heart. Methods beta-Adrenergic responses were investigated in vivo (echocardiography-dobutamine, electron paramagnetic resonance) and in vitro (isolated left ventricular papillary muscle, electron paramagnetic resonance) in young adult (3-month-old) and senescent (24-month-old) rats. Nitric oxide synthase (NOS) immunolabeling (confocal microscopy), nitric oxide production (electron paramagnetic resonance) and beta-adrenoceptor Western blots were performed in vitro. Data are mean percentages of baseline +/- SD. Results An impaired positive inotropic effect (isoproterenol) was confirmed in senescent hearts in vivo (117 +/- 23 vs. 162 +/- 16%; P &lt; 0.05) and in vitro (127 +/- 10 vs. 179 +/- 15%; P &lt; 0.05). In the young adult group, the positive inotropic effect was not significantly modified by the nonselective NOS inhibitor N-nitro-L-arginine methylester (L-NAME; 183 +/- 19%), the selective NOS1 inhibitor vinyl-L-N-5(1-imino-3-butenyl)-L-ornithine (L-VNIO; 172 +/- 13%), or the selective NOS2 inhibitor 1400W (183 +/- 19%). In the senescent group, in parallel with beta3-adrenoceptor up-regulation and increased nitric oxide production, the positive inotropic effect was partially restored by L-NAME (151 +/- 8%; P &lt; 0.05) and L-VNIO (149 +/- 7%; P &lt; 0.05) but not by 1400W (132 +/- 11%; not significant). The positive inotropic effect induced by dibutyryl-cyclic adenosine monophosphate was decreased in the senescent group with the specific beta3-adrenoceptor agonist BRL 37344 (167 +/- 10 vs. 142 +/- 10%; P &lt; 0.05). NOS1 and NOS2 were significantly up-regulated in the senescent rat. Conclusions In senescent cardiomyopathy, beta3-adrenoceptor overexpression plays an important role in the altered beta-adrenergic response via induction of NOS1-nitric oxide.
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Dare, E., O. Kifor, EM Brown, and G. Weber. "Characterization of the phosphatidylinositol-specific phospholipase C isozymes present in the bovine parathyroid and in human kidney HEK293 cells stably transfected with the human parathyroid Ca2+-sensing receptor." Journal of Molecular Endocrinology 21, no. 1 (August 1, 1998): 7–17. http://dx.doi.org/10.1677/jme.0.0210007.

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The regulation of parathyroid hormone secretion by the chief cells of the parathyroid is mediated by a 7-transmembrane (7-TM) Ca2+-sensing receptor (CaR), which signals via activation of pertussis toxin-insensitive G proteins, causing stimulation of phosphatidylinositol-specific phospholipase C (PI-PLC). We have identified the PI-PLC isoforms expressed in two model systems utilized for studying CaR signal transduction, i.e. dispersed bovine parathyroid cells and a human embryonic kidney cell line (HEK 293) stably transfected with the human parathyroid CaR-cDNA. All of the eight PI-PLC isozymes examined in this study were found to be expressed to varying extents in the bovine parathyroid gland and in the CaR-transfected HEK cells as assessed by immunoblotting. We localized the expression of the more abundant isozymes (beta1, beta2, beta3, gamma1, gamma2, delta2) to the chief cells of the bovine parathyroid by immunocytochemistry, while the two less abundant isozymes (delta1, beta4) were not detectable in parathyroid sections. G proteins activated by 7-TM receptors are known to activate mainly PI-PLC of the beta class. Therefore, beta1, beta2, beta3 and beta4, all expressed in the bovine parathyroid, are candidate isozymes for coupling to the CaR. A comparison of the levels of expression of PI-PLC isozymes between CaR-transfected HEK cells and non-transfected HEK cells suggested that the expression of the CaR in this human cell line does not cause a significant up-regulation of any of the PLCbeta and PLCgamma isozymes. PLCdelta2, showing predominantly nuclear localization in the parathyroid, was the sole PI-PLC isozyme with higher levels of expression in CaR-transfected HEK cells.
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Zhao, Jin, Barbara Cannon, and Jan Nedergaard. "Carteolol is a weak partial agonist on β3-adrenergic receptors in brown adipocytes." Canadian Journal of Physiology and Pharmacology 76, no. 4 (April 1, 1998): 428–33. http://dx.doi.org/10.1139/y98-058.

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The ability of the Beta1/Beta2 partial agonist carteolol to act as an agonist on Beta3-adrenergic receptors was investigated by studying its ability to stimulatethermogenesis (oxygen consumption) in brown fat cells isolated from hamsters. Carteolol wasable to induce thermogenesis, with an EC50 of 5 µM, but it was only a partial(40%) agonist. D,L-Propranolol had a pKB of 5.1 as anantagonist against carteolol in this system, indicating that the carteolol effect was probablymediated via Beta3-receptors. Also in mouse and rat cells, carteolol was a partial agonist withEC50 values around 1 µM. Being a partial agonist, carteolol acted as an antagonistagainst norepinephrine-, BRL-37344-, or CGP-12177-stimulated thermogenesis with apKB of approximately5. The partial agonist effects of carteolol are discussed in relation to the absence of agonisteffect of this compound on guinea-pig taenia cecum Beta3-receptors and in relation to the possible plurality of Beta3-receptors.Key words: carteolol, Beta3-adrenergic receptor, brown fat cells, nonshivering thermogenesis.
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Desai, Rooma, Dirk Ruesch, and Stuart A. Forman. "γ-Amino Butyric Acid Type A Receptor Mutations at β2N265 Alter Etomidate Efficacy While Preserving Basal and Agonist-dependent Activity." Anesthesiology 111, no. 4 (October 1, 2009): 774–84. http://dx.doi.org/10.1097/aln.0b013e3181b55fae.

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Background Etomidate acts at gamma-Aminobutyric acid type A (GABAA) receptors containing beta2 or beta3, but not beta1 subunits. Mutations at beta residue 265 (Ser in beta1; Asn in beta2 or beta3) profoundly affect etomidate sensitivity. Whether these mutations alter etomidate binding remains uncertain. Methods Heterologously expressed alpha1beta2gamma2L GABAA receptors and receptors with beta2(N265S) or beta2(N265M) mutations were studied electrophysiologically in both Xenopus oocytes and HEK293 cells. Experiments quantified the impact of beta2N265 mutations or substituting beta1 for beta2 on basal channel activation, GABA EC50, maximal GABA efficacy, etomidate-induced leftward shift in GABA responses, etomidate direct activation, and rapid macrocurrent kinetics. Results were analyzed in the context of an established allosteric co-agonist mechanism. Results Mutations produced only small changes in basal channel activity, GABA EC50, maximal GABA efficacy, and macrocurrent kinetics. Relative to wild-type, beta2(N265S) reduced etomidate enhancement of apparent GABA affinity six-fold, and it reduced etomidate direct activation efficacy 14-fold. beta2(N265M) totally eliminated both etomidate modulation of GABA responses and direct channel activation. Mechanism-based analysis showed that the function of both mutants remains consistent with the allosteric co-agonist model and that beta2(N265S) reduced etomidate allosteric efficacy five-fold, whereas etomidate-binding affinity dropped threefold. Experiments swapping beta2 subunits for beta1 indicated that etomidate efficacy is reduced 34-fold, whereas binding affinity drops less than two-fold. Conclusions Mutations at beta2N265 profoundly alter etomidate sensitivity with only small changes in basal and GABA-dependent channel activity. Mutations at the beta2N265 residue or replacement of beta2 with beta1 influence etomidate efficacy much more than binding to inactive receptors.
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Kum, Winnie WS, Kevin B. Laupland, and Anthony W. Chow. "Defining a novel domain of staphylococcal toxic shock syndrome toxin-1 critical for major histocompatibility complex class II binding, superantigenic activity, and lethality." Canadian Journal of Microbiology 46, no. 2 (February 1, 2000): 171–79. http://dx.doi.org/10.1139/w99-121.

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Staphylococcal toxic shock syndrome toxin-1 (TSST-1) is implicated in the pathogenesis of superantigen-mediated shock. We previously identified TSST-1 residues G31/S32 to be important for major histocompatibility complex (MHC) class II binding, as well as superantigenic and lethal activities. However, the site-directed TSST-1 mutant toxin, G31R, could still induce mitogenesis and low-level TNFalpha secretion, suggesting that additional MHC class II binding sites other than G31/S32 may exist. In the current study, a TSST-1-neutralizing monoclonal antibody, MAb5, was found to inhibit TSST-1 binding to human peripheral blood mononuclear cells, neutralize TSST-1-induced mitogenesis and cytokine secretion, and protect against TSST-1-induced lethality in vivo. Epitope mapping revealed that MAb5 bound to TSST-1 residues 51-56 (T(51-56);51YYSPAF56). Peptide T(51-56) was synthesized and found to also inhibit TSST-1 binding to human monocytes as well as TSST-1-induced mitogenesis, cytokine secretion, and lethality in vivo. This T(51-56) epitope, located within the beta3/beta4 loop, and the previously identified G31/S32 epitope, within the beta1/beta2 loop of TSST-1, are separated within the primary sequence, but spatially juxtaposed to each other. Collectively, these findings suggest that a discontinuous epitope comprising of regions within both the beta1/beta2 and beta3/beta4 loops, are critical for MHC class II binding, and the consequent superantigenic and lethal activities of TSST-1.
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Gawaz, M., F. Besta, J. Ylanne, T. Knorr, H. Dierks, T. Bohm, and W. Kolanus. "The NITY motif of the beta-chain cytoplasmic domain is involved in stimulated internalization of the beta3 integrin A isoform." Journal of Cell Science 114, no. 6 (March 15, 2001): 1101–13. http://dx.doi.org/10.1242/jcs.114.6.1101.

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Beta3 integrin adhesion molecules play important roles in wound repair and the regulation of vascular development and three beta3 integrin isoforms (beta3-A, -B, -C) have been described so far. Surface expression of beta3 integrins is dynamically regulated through internalization of beta3 integrins, however, the molecular mechanisms are understood incompletely. To evaluate the role of the cytoplasmic domain of beta3 integrins for internalization, we have generated single chain chimeras with variant and mutated forms of beta3 cytoplasmic domains. Upon transient transfection into chinese hamster ovary cells, it was found that the beta3-A chimera had strongly reduced cell surface expression compared with the corresponding beta3-B, or beta3-C fusion proteins, or the tail-less constructs, whereas steady state levels of all chimeras were near identical. Studies employing cytoplasmic domain mutants showed that the NITY motif at beta3-A 756–759 is critical for plasma membrane expression of beta3-A. Furthermore, delivery of beta3-A to the cell surface was specifically modulated by the cytoplasmic protein beta3-endonexin, a previously described intracellular protein. Coexpression of the native, long form of beta3-endonexin, which does not interact with the beta3 tail, acted as a dominant negative inhibitor of beta3-A-internalization and enhanced steady-state surface expression of the beta3-A-chimera. Furthermore, anti-beta3 antibody-induced internalization of the native beta3 integrin (alpha(IIb)beta3 was dramatically reduced for the Tyr(759)-Ala substitution mutant (alpha(IIb)beta3) (Y759A) and expression of the long isoform of beta3-endonexin substantially decreased the internalization of wild-type alpha(IIb)beta3. Thus, the NITY motif of the beta-chain cytoplasmic domain is involved in stimulated internalization of the beta3 integrin A isoform and beta3-endonexin appears to couple the beta3-A isoform to a specific receptor-recycling pathway.
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Dissertations / Theses on the topic "BETA3"

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Kiesow, Claudia. "Pathogenese der equinen Endometrose: Bedeutung der Wachstumsfaktoren Transforming growth factor-alpha, -beta1, -beta2 und -beta3 sowie der Matrixmetalloproteinase-2." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-65079.

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Ziel der vorliegenden Arbeit war die immunhistologische Charakterisierung der Expression der profibrotischen Wachstumsfaktoren Transforming growth factor-beta-1, -beta2 und -beta3 und des Enzyms Matrixmetalloproteinase-2 (MMP-2) im equinen Endometrium während des Zyklus sowie innerhalb der verschiedenen Erscheinungsformen der equinen Endometrose. Zudem wurde der potentielle Einfluss einer gleichzeitig auftretenden Endometritis auf die glanduläre und stromale Wachstumsfaktor- und Enzym-Expression untersucht. Die Ergebnisse dieser Studie sollten klären, ob und inwieweit den untersuchten Wachstumsfaktoren unter Beteiligung von MMP-2 in der Pathogenese der equinen Endometrose eine mit anderen Organfibrosen vergleichbare Schlüsselrolle zukommt. Zu diesem Zweck standen an definierten Tagen entnommene Endometriumbioptate (n=21) von drei zyklisch aktiven, klinisch und gynäkologisch gesunden Maidenstuten sowie Endometriumbioptate von 60 Stuten mit graduell variabler Endometrose unterschiedlichen Charakters und Endometriumbioptate von 22 Stuten mit mittelgradiger Endometrose und gleichzeitiger mittelgradiger eitriger (n=16) bzw. nichteitriger (n=6) Endometritis aus dem Routineeinsendungsmaterial des Institutes für Veterinär-Pathologie der Universität Leipzig zur Verfügung. Die Wachstumsfaktoren TGF-beta1, -beta2 und -beta3 sowie das Enzym MMP-2 zeigen im Zyklus ein typisches, zellspezifisches Reaktionsmuster, das unterschiedlichen Regulations-mechanismen zu unterliegen scheint. Ein Maximum der TGF-beta1-Expression in den luminalen Epithelzellen, Stroma- und Drüsenzellen kann in der endometrialen Sekretionsphase mit Anstieg bzw. einem Maximum der Serumprogesteron-Konzentration beobachtet werden. Im Gegensatz dazu tritt eine Expression von MMP-2 in den Stromazellen in der Sekretionsphase mit Abfall der Progesteronkonzentration im Serum auf. Das luminale Epithel und die Stromazellen zeigen eine maximale Expression von TGF-beta2 beim Vorliegen hoher Progesteronspiegel im Serum bzw. mit Abfall der Serumprogesteron-Konzentration in der Sekretionsphase. TGF-beta3 weist im luminalen Epithel ein ähnliches Expressionsmuster auf, eine deutliche Abhängigkeit zu den Serumhormon-Konzentrationen lässt sich jedoch nicht feststellen. Die stromale Expression von TGF-alpha unterliegt im equinen Endometrium keinen zyklusabhängigen Variationen. Die Stromazellen innerhalb der verschiedenen Endometroseherde zeigen, im Vergleich zum unveränderten Endometrium, vor allem eine verminderte Expression von TGF-alpha. Das Expressionsmuster der TGF-beta-Wachstumsfaktoren ist grundsätzlich variabel, es fällt jedoch auf, dass die Stromazellen insbesondere in inaktiven Endometrosen eine geringere Expression der TGF-beta-Isoformen aufweisen. Ursache ist möglicherweise eine gestörte hormonelle Stimulation bzw. eine stromale Synthesestörung in Folge veränderter epithelial/stromaler Wechselwirkungen. Das Enzym MMP-2 wird dagegen in den Stromazellen aller Endometroseherde, unabhängig von deren Differenzierung und dem Auftreten glandulärer Alterationen, deutlich vermehrt nachgewiesen. Dies ist sehr wahrscheinlich Folge der Extra-zellularmatrix-Akkumulation innerhalb der Endometroseherde und für die fortschreitende Zerstörung der glandulären Basalmembranen verantwortlich. Die glanduläre Expression innerhalb der Endometroseherde gleicht weitgehend der der unveränderten Drüsenzellen, lediglich in destruierenden Endometrosen werden TGF-alpha, TGF-beta2 und MMP-2 in den involvierten Drüsenzellen vermehrt nachgewiesen. Mögliche Ursachen wären eine Diffusion durch die geschädigte glanduläre Basalmembran bzw. eine Anregung der Synthese im Rahmen der epithelialen Wundheilung. Eine Anregung der glandulären und stromalen Expression der untersuchten Wachstumsfaktoren und des Enzyms MMP-2 im Rahmen der Endometrose durch die Anwesenheit von Entzündungszellen konnte nicht nachgewiesen werden. Eine der Leber- und Lungenfibrose ähnelnde, überschießende Wundheilungsreaktion durch eine primär epithelial bedingte, vermehrte TGF-Wachstumsfaktorproduktion sowie direkte Zusammenhänge zwischen der MMP-2- und TGF-beta-Wachstumsfaktor-Expression waren in der equinen Endometrose nicht festzustellen. Da vor allem die Stromazellen in der Endometrose eine veränderte Expression der Wachstumsfaktoren aufwiesen, ist möglicherweise eine primäre stromale Fehldifferenzierung der Ausgangspunkt für die Entstehung der Endometrose. Eine mit der Leber- und Lungenfibrose vergleichbare Schlüsselrolle der TGF-Wachstumsfaktoren in der Pathogenese der equinen Endometrose konnte nicht eindeutig belegt werden.
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Bouaouina, Mohamed. "Etude de la voie de signalisation activatrice des intégrines beta2 et beta3 dans les neutrophiles et les plaquettes." Paris 6, 2004. http://www.theses.fr/2004PA066013.

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Alsalhin, Aisha Khlani Hassan. "The role of the beta3-adrenergic receptor (β3-AR) in cardioprotection." Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/97812.

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Thesis (MScMedSc)--Stellenbosch University, 2015.
ENGLISH ABSTRACT: It is well-established that transient activation of the β-adrenergic signalling pathway with ligands such as isoproterenol, formoterol and dobutamine, elicits cardioprotection against subsequent long periods of ischaemia. Initially the focus was on the β1- and β2-adrenergic receptors (β1-AR, β2-AR), but recently the β3-AR also emerged as a potential target in the treatment of heart disease. In heart failure, β1- and β2-AR are typically known to be down-regulated while β3-ARs, on the other hand, are up-regulated (Moniotte et al., 2001). Thus, it has become important to examine the significance of the β3-AR and its downstream signalling under similar states of stress. It has been shown that β3-AR stimulation is resistant to short term agonist-promoted desensitization in vitro and in vivo (Liggett et al., 1993) and after being activated, this receptor is able to convey continual intracellular signals (Lafontan et al., 1994). Thus, it could be an ideal target for therapeutic intervention, also in ischaemic heart disease. We hypothesized that selective β3-AR stimulation during ischaemia / reperfusion may be cardioprotective, whereas selective inhibition of this receptor may prove useful in the end stages of sustained ischaemia and early reperfusion. Methods: The isolated working rat heart, subjected to 35 min of regional ischaemia (RI) and 60 min reperfusion was used as model. The β3-AR agonist (BRL37344) (1 μM) or antagonist (SR59230A) (0.1 μM) were applied as follows: (i) before 35 min RI (PT), (ii) during the last 10 min of RI (PerT) and /or (iii) at the onset of reperfusion (PostT) and (iv) administration of BRL37344 during the last 10 min of RI BRL37344 (PerT) was followed by SR59230A during first 10 min of reperfusion SR59230A (Post). The contribution of nitric oxide synthase (NOS) in β3-AR was assessed, using the non-specific NOS inhibitor, L-NAME (50 μM). Endpoints were functional recovery and infarct size. In another set of experiments BRL37344 and SR59230A were applied according to the same protocols, but the left ventricle was dissected from the heart and freeze clamped at 10 min reperfusion for Western blot analysis of extracellular signal-regulated kinase (ERK p44/p42), protein kinase B (PKB/Akt), glycogen synthase kinase-3β (GSK-3β), and endothelial nitric oxide synthase (eNOS). Data were analyzed with one or two-way analysis of variance (ANOVA). Results: Administration of the selective β3-AR agonist (BRL37344) (1μM) before 35 min RI (BRL37344 (PT), significantly reduced infarct size when compared to the non-pretreatment group (NPT) (21.43±2.52 vs 43.17±1.20, p < 0.001). BRL37344 had similar effects on infarct size when applied during the last 10 min of regional ischaemia BRL37344 (PerT) (14.94±2.34, vs NPT, p < 0.001) or at the onset of reperfusion BRL37344 (PostT) (19.06±1.81, vs NPT, p < 0.001). When BRL37344 was applied as a (PerT+PostT) strategy, infarct size was once again significantly reduced (20.55±2.01 vs 43.17±1.20, p <0.001). In contrast, administration of the β3-antagonist SR59230A according to the same protocol did not reduce infarct size and values similar to those of untreated hearts (NPT) were obtained. Surprisingly, when BRL37344 was applied during the last 10 min of regional ischaemia followed by the administration of the β3-AR antagonist (SR59230A) at the onset of reperfusion, [BRL37344 (PerT) & SR59230A (PostT)], infarct size was significantly reduced to 20.78±3.02 (p <0.001 vs NPT and SR59230A (PerT + PostT). Involvement of nitric oxide (NO) was shown since the reduction in infarct size elicited by BRL37344 was totally abolished by, L-NAME, when administered in combination with BRL37344 for 10 minutes prior to RI or at the onset of reperfusion for 10 minutes (% infarct size: 41.48±3.18 and 35.75±3.54, p <0.001 vs BRL37344 (PT) and BRL37344 (PostT), respectively. Western blot results show that PKB/Akt is activated by BRL37344 regardless of the time of administration. The intervention BRL37344 (PerT+PostT), exhibited the most significant phosphorylation of PKB/Akt (fold increase: 14.2±3.71, p<0.01 vs NPT and p<0.05 vs BRL37344 (PostT). In addition, BRL37344 (PT), (PerT), (PostT) and [BRL37344 (PerT) +SR59230A (PostT)] showed significant activation of this kinase (2.92±0.22, 5.54±0.43, 4.73±0.47, and 6.60±0.78, respectively). ERKp44/p42 however, was not significantly activated by any of the treatments. Phosphorylation of eNOS and GSK-3β was significant only in the BRL37344 (PerT+PostT) and [BRL37344 (PerT) + SR59230A (PostT)] groups. The activation of eNOS-S-1177 in the BRL37344 (PerT+PostT) group was (2.82±0.46, p<0.01 and 0.05 vs NPT and BRL37344 (PostT), respectively) and in the [BRL37344 (PerT) + SR59230A (PostT)] group was (2.26±0.48, p<0.05 vs NPT). A very significant increased phosphorylation of GSK-3β was seen in the same two groups (68.8±7.73, p<0.001 vs NPT and 25.5±5.42 vs NPT, p<0.05, respectively). Conclusion: β3-AR has potent cardioprotective effects when administered either before, during and after ischaemia during early reperfusion as indicated by the reduction in infarct size as well as activation of PKB, GSK-3β and eNOS. These beneficial effects can be linked to NO production through activation of eNOS.
AFRIKAANSE OPSOMMING: Dit is bekend dat verbygaande aktivering van die β-adrenerge seinpad, met ligande soos isoproterenol, formoterol en dobutamien, die hart teen daaropvolgende lang periodes van iskemie beskerm. Aanvanklik was die fokus op die β1- en β2-adrenerge reseptore (β1-AR, β2-AR); maar onlangs is ook die β3-AR as 'n potensiële teiken in die behandeling van hartsiektes ge-eien. In hartversaking, is dit bekend dat β1- en β2-AR afreguleer word, terwyl β3-ARs, aan die ander kant, opreguleer word (Moniotte et al., 2001). Dit het dus belangrik geword om die belang van die β3-AR en sy stroomaf seinpad onder soortgelyke strestoestande te ondersoek. Dit is bewys dat β3-AR stimulasie teen korttermyn agonis geïnduseerde desensitisering in vitro en in vivo bestand is (Liggett et al., 1993) en wanneer geaktiveer, is hierdie reseptor in staat om intrasellulêre seine voortdurend oor te dra (Granneman, 1995). Dit kan dus ‘n ideale teiken vir terapeutiese intervensie wees, ook in iskemiese hartsiekte. Ons hipotetiseer dat selektiewe β3-AR stimulasie tydens iskemie / reperfusie kardiobeskermende mag wees, terwyl selektiewe inhibisie van hierdie reseptor effektief kan wees in die eindstadia van volgehoue iskemie en vroeë herperfusie. Metodes: Die geïsoleerde werkende rothart, onderwerp aan 35 min van streeksiskemie (SI) en 60 min herperfusie, is as model gebruik. Die β3-AR agonis (BRL37344) (1μM) of antagonis (SR59230A) (0.1 μM), is as volg toegedien: (i) voor 35 min SI (PT), (ii) gedurende die laaste 10 min van SI (PerT) en / of (iii) tydens die aanvang van herperfusie (PostT) en (iv) gedurende die laaste 10 min van SI is BRL toediening BRL37344 (PerT) gevolg deur SR59230A tydens die eerste 10 min van herperfusie SR59230A (Post). Die rol van stikstofoksiedsintase (NOS) in β3-AR is met behulp van die nie-spesifieke NOS inhibitor, L-NAME (50 μM) ondersoek. Eindpunte was funksionele herstel tydens herperfusie en infarktgrootte. In 'n ander reeks eksperimente is BRL37344 en SR59230A volgens dieselfde protokolle toegedien, maar die linker ventrikel is uit die hart gedissekteer na 10 min herperfusie en gevriesklamp vir Western klad analise van ekstrasellulêre-sein gereguleerde kinase (ERK p44/p42), proteïen kinase B (PKB/Akt), glikogeen sintase kinase-3β (GSK-3β), en endoteel stikstofoksied- sintase (eNOS). Data is met een of twee-rigting variansie analise (ANOVA) ontleed. Resultate: Administrasie van die selektiewe β3-AR agonis (BRL37344) (1μM) voor 35 min SI BRL37344 (PT), het die infarktgrootte beduidend verminder vergeleke met die nie-behandelde groep (NPT) (21.43±2.52 vs 43.17±1.20, p<0.001). BRL37344 het ‘n soortgelyke effek op infarktgrootte wanneer dit gedurende die laaste 10 min van streeksiskemie BRL37344 (PerT) (14.94±2.34, vs NPT, p<0.001) of by die aanvang van herperfusie (BRL37344 (PostT) (19.06±1.81, vs NPT, p<0.001) toegedien word. Wanneer BRL37344 as 'n (PerT+PostT) strategie toegedien is, was infarktgrootte weereens beduidend verlaag (20.55±2.01 vs 43.17±1.20, p<0.001). In teenstelling hiermee, het administrasie van die β3-antagonis SR59230A volgens dieselfde protokol, nie infarktgrootte verminder nie en waardes soortgelyk aan dié van onbehandelde harte (NPT) is verkry. Interessant, wanneer BRL37344 gedurende die laaste 10 min van streeksiskemie toegedien is, gevolg deur die administrasie van die β3-AR antagonis (SR59230A) by die aanvang van herperfusie, [BRL37344(PerT) & SR59230A(PostT)], was infarktgrootte aansienlik verminder tot 20.78±3.02 (p<0.001 vs NPT en SR59230A (PerT+PostT). Die betrokkenheid van stikstofoksied (NO) is waargeneem deurdat die vermindering in infarktgrootte ontlok deur BRL37344, heeltemal deur L-NAME opgehef is, wanneer dit in kombinasie met BRL37344 vir 10 minute voor SI of by die aanvang van herperfusie vir 10 minute toegedien is (% infarktgrootte: 41.48±3.18 en 35.75±3.54, p<0.001 vs BRL37344 (PT) en BRL37344 (PostT) onderskeidelik). Western kladresultate toon dat PKB/Akt deur BRL37344 geaktiveer word ongeag die tyd van die administrasie. Die intervensie BRL37344 (PerT+PostT), toon die mees beduidende fosforilering van PKB/Akt (voudige toename: 14.2±3.71, p<0.01 vs NPT en p<0.05 vs BRL37344 (PostT). Daarbenewens het BRL37344 (PT), (PerT), (PostT) en [BRL37344 (PerT) + SR59230A (PostT)] ook beduidende aktivering van hierdie kinase tot gevolg gehad (2.92±0.22, 5.54±0.43, 4.73±0.47 en 6.60±0.78, onderskeidelik). ERKp44/p42 is egter nie deur enige van die behandelings geaktiveer nie. Fosforilering van eNOS en GSK-3β was net beduidend in die BRL37344 (PerT+PostT) en [BRL37344 (PerT) + SR59230A (PostT)] groepe. Die aktivering van eNOS-S-1177 was beduidend in die BRL37344 (PerT+PostT) en [BRL37344 (PerT) + SR59230A (PostT)] groepe. 'n Baie beduidende toename in fosforilering van GSK-3β is in dieselfde twee groepe (68.8±7.73, p<0.001 en 25.5±5.42, p<0.05 vs NPT onderskeidelik) waargeneem. Gevolgtrekking: β3-AR het kragtige kardiobeskermende effekte wanneer dit, hetsy voor, tydens en na iskemie gedurende vroeë herperfusie toegedien word, soos deur die vermindering in infarktgrootte sowel as die aktivering van PKB, GSK-3β en eNOS aangedui is. Hierdie voordelige effekte kan aan NO produksie deur aktivering van eNOS gekoppel word.
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Pancewicz, Elena. "The role of the uncoupling protein-1 (UCP-1) and the beta3-adrenoreceptor ([Beta]3AR) genes in weight loss /." Title page and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09SB/09sbp188.pdf.

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Chabadel, Anne. "Structures, stabilité et fonctions du cytosquelette d’actine dans les ostéoclastes mâtures." Lyon, École normale supérieure (sciences), 2007. http://www.theses.fr/2007ENSL0413.

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L'ostéoclaste est une cellule spécialisée dans la résorption de la matrice osseuse. Elle présente une organisation différente de l'actine selon les substrats sur lesquels elle est ensemencée. Sur verre ou plastique, l'actine est sous forme de "podosomes", alors que sur un substrat résorbable, elle se ré-organise en une ceinture conttinue, la zone de scellement (SZ). L'étude de cellules déficientes en WIP nous a permis de démontrer qu'un ostéoclaste sur verre forme 2 domaines d'actine distincts: les coeurs de podosomes et le nuage. Ces 2 domaines sont induits par différents récepteurs, CD44 et Beta3, polymérisés par des voies distinctes, et ont pour fonction l'adhérence et la contraction. Ils se ré-organisent en une unique structure, la SZ, quand l'ostéoclaste est transféré sur un substrat résorbable. Nous avons également démontré que le maintien de la ceinture de podosomes dépend d'un réseau de microtubules intact
Osteoclasts are hematopoietic cells specialized in bone resorption. Actin cytoskeleton organisation depends on substrates: podosomes are observed on glass or plastic slides, whereas an homogenous actin belt, the sealing zone (SZ) is organized on resorption substrates. Study of WIP deficient cells allows us to demontrate existence of 2 actin domains: podosomes cores surrounded by actin cloud. These 2 domains are induced by different receptors, CD44 and Beta3, polymerized by 2 distinct pathways, and are implicated in adhesion and contraction os osteoclast. Podosomes cores and actin cloud reorganized into an unique structure, the SZ, when osteoclast is seeded on apatite or dentin slides. We have also demonstrated that stability of podosomes belt depends on microtubules
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BLIN, NATHALIE. "Le recepteur beta3-adrenergique : caracterisation pharmacologique et etude des relations structure-activite." Paris 11, 1993. http://www.theses.fr/1993PA112402.

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La caracterisation moleculaire et pharmacologique des recepteurs beta3-adrenergiques humain et murin a permis de reveler que ces recepteurs presentaient de grandes similarites entre eux et avec les recepteurs beta-atypiques caracterises dans le tissu adipeux et l'appareil digestif des rongeurs. Une analyse quantitative des relations structure-activite assistee par ordinateur a demontre des capacites de prediction de l'activite pharmacologique de nouvelles structures, constituant de fait un outil de choix pour developper et rationaliser la synthese de nouvelles molecules beta3-specifiques, a visee therapeutique dans le traitement de l'obesite et des dysfonctions de l'appareil digestif. L'analyse des structures chimiques des ligands, de leurs conformations tridimensionnelles et des modeles des recepteurs beta2 et beta3, a conduit a proposer un modele d'activation receptoriel selon lequel les molecules beta3-specifiques, longues et encombrantes, adopteraient une conformation repliee par gene sterique dans le site beta2, tandis qu'une conformation plus etendue permise dans le site beta3 leur permettrait d'atteindre une region transmembranaire du recepteur qui serait critique pour la transduction du signal et rendrait compte des effets agonistes beta3-specifiques de ces ligands
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Ghorbani, Masoud. "The role of beta3-adrenergic receptors in control of brown and white adipose tissues and of energy balance: Reversal of obesity by CL 316,243, a new beta3-adrenergic agonist." Thesis, University of Ottawa (Canada), 1998. http://hdl.handle.net/10393/4102.

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Obesity is a prevalent health hazard that is associated with other metabolic disorders, in particular with insulin resistance and non-insulin-dependent diabetes mellitus. Treatment of obesity requires an increase in energy expenditure or a decrease in energy intake or both of these. One target for raising energy expenditure in the treatment of obesity with drugs is the $\beta$3-adrenergic receptor in brown and white adipose tissues. Selective $\beta$3-adrenergic receptor agonists have been developed that will stimulate both the mobilization of fat from white adipose tissue, the site of triacylglycerol storage in the body, and the oxidation of this fat in brown adipose tissue, a site of thermogenesis. The principal objectives of the work described in this thesis were to find out whether a selective $\beta$3-adrenergic receptor agonist could reverse obesity and insulin-resistance in rats and to elucidate the mechanisms involved. Two models of obesity were studied: young Sprague-Dawley rats which became obese because they were eating a high-fat diet and continued to eat this diet during the treatment (diet-induced obesity) and old Zucker fa/fa rats (genetic obesity). Rats were treated by continuous subcutaneous infusion of the selective $\beta$3-adrenergic receptor agonist, CL 316,243; control rats received infusion of saline. Lean rats of the same age and strain were similarly treated. Rats with diet-induced obesity had a hypertrophic obesity (enlarged white adipocytes but no increase in number of adipocytes) while rats with genetic obesity had a hyperplastic obesity (increase in number of white adipocytes). Treatment with CL 316,243 reversed obesity in both animal models. Reduction in fat stores was associated with shrinking of enlarged animal models. Reduction in fat white adipocytes but no reduction in their number, even when this was elevated as in the genetically obese fa/fa rats. Reversal of obesity was associated with a large increase in energy expenditure. This was associated not only with growth of the presumed site of this increase in energy expenditure, brown adipose tissue, but also with appearance of abundant brown adipocytes in white adipose tissues, a site in which they do not normally occur. Reversal of obesity was not associated with any reduction in energy intake, except in the genetically obese rats in which the hyperphagia was reversed. Treatment reduced the concentration of leptin in serum when this was elevated, as in the rats with diet-induced obesity and in the moderately obese old control Zucker rats. Treatment did not, however, reduce the elevated level of leptin in the blood of fa/fa rats. There was thus no correlation of drug-induced changes in leptin concentration with changes in food intake. Studied only in fa/fa rats, treatment improved insulin resistance, decreasing both hyperglycaemia and hyperinsulinaemia. This improvement was correlated with a reduction of expression of a suggested mediator of insulin resistance, tumour necrosis factor $\alpha$, in white adipose tissues. Results show that CL 316,243, a selective agonist for rodent $\beta$3-adrenergic receptors, is an effective anti-obesity agent in rat models of obesity. Future development of similar compounds that are selective for human $\beta$3-adrenergic receptors will be needed before this approach to treatment of obesity and insulin resistance can be useful in humans.
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Schneck, Alexander Christian. "Einfluss des [beta]3-adrenergen [Beta3-adrenergen] Rezeptors auf die langsame Komponente des Delayed-rectifier-Kaliumstroms in ventrikulären Kardiomyozyten des Meerschweinchens." [S.l. : s.n.], 2003. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB10733058.

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Kanzler, Sandro Aparecido. "Participação dos receptores Beta3 adrenérgicos no controle da ingestão de alimentos em ratos." reponame:Repositório Institucional da UFSC, 2012. http://repositorio.ufsc.br/xmlui/handle/123456789/95601.

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Dissertação (mestrado) - Universidade Federal de Santa Catarina, Centro de Ciências Biológicas, Programa de Pós-Graduação em Neurociências, Florianópolis, 2011
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Neste estudo investigamos os efeitos da injeção intracerebroventricular (icv) de BRL37344 (agonista seletivo de receptores ß3-adrenérgicos, nas doses de 2 e 20 nmol), e SR59230 A (antagonista seletivo de receptores ß3-adrenérgicos, nas doses de 10 e 50 nmol) sobre a ingestão de alimento em ratos submetidos ao jejum de 24 horas. Os animais também foram previamente tratados por via ICV com o veículo ou o antagonista do receptor ß3-adrenérgicos (SR59230A na dose de 50 nmol), administrados 10 min antes da injeção ICV do agonista ß3-adrenérgicos (BRL37344 na dose de 20 nmol) ou veículo, com o objetivo de determinar a seletividade dos efeitos provocados pelo BRL37344 e SR59230A sobre ingestão de alimentos e avaliação de risco. Após as injeções, cada animal foi colocado na caixa de registro para avaliar os comportamentos ingestivos e não-ingestivos, como a avaliação de risco. Os resultados mostraram que a injeção ICV de BRL37344 na dose de 20 nmol provoca redução no consumo de alimento 1h após o tratamento. O tratamento ICV com ambas as doses de SR59230A diminuiu a freqüência de avaliação de risco. A injeção prévia via ICV de SR59230A aboliu a resposta hipofágica induzida pelo BRL37344. A presença do agonista do receptor ß3-adrenérgico suprimiu a redução na frequência de avaliação de risco, um comportamento relacionado à ansiedade, que neste estudo foi provocada pelo antagonista SR59230A de receptores ß3-adrenérgicos . A duração, a freqüência e latência para iniciar a alimentação, bem como a duracão e a frequência dos outros comportamentos não ingestivos não foram afetados pelos diferentes tratamentos. Esses resultados, demonstram que a resposta hipofágica provocada pelo BRL3744 é seletivamente mediada por receptores ß3-adrenérgicos encontrados no sistema nervoso central e além disso, sugerem a participação desses receptores adrenérgicos nos circuitos neurais centrais que controlam o comportamento de ansiedade.
Involvement of â3- adrenergic receptors in the control of food intake in rats (dissertation). Florianopolis; Masters in Neurosciences, Universidade Federal de Santa Catarina, 2011. This study examined the alteration in food intake evoked by intracerebroventricular (icv) injection of BRL37344 (a selective agonist of â3-adrenergic receptors) in 24 h-fasted rats at the doses of 2 nmol and 20 nmol. The effects on food intake of icv injection of SR59230A (a selective antagonist of â3-adrenergic receptors) at the doses of 10 nmol and 50 nmol was also investigated. The icv injection of saline (vehicle) was used as control. The animals were also treated with the VEH or with the antagonist of â3-adrenergic receptor (SR59230A at a dose of 50 nmol) administered icv 10 min before the injection of the â3- adrenergic agonist (BRL37344 at the dose of 20 nmol) or the VEH, in order to determine the selectivity of the effects evoked by the adrenergic agonist on food intake or the selectivity of the effects evoked by the antagonist on risk assessment behavior. The results showed that the icv injection of BRL37344 at the dose of 20 nmol evoked a reduction in food intake 1 h after the treatment .While the icv injetion with both doses of SR59230A failed to affect food intake, this treatment reduced the frequency (number/30 min) of risk assessment , an ethological parameter related to anxiety. Pretreatment with SR59230A abolished the hypophagic response induced by BRL37344. On the other hand, the â3-adrenergic receptor agonist suppressed in the reduction in frequency of risk assessment caused by the antagonist of these receptors. Feeding duration, frequency and latency to start feeding were not affected by the different treatments. These results show that the hypophagic response caused by BRL3744 is selectively mediated by â3 adrenergic receptors found in the central nervous system. Moreover, they suggest the involvement of these receptors in the central circuits that control anxiety.
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Pettersson, Ulrika. "Blood Flow Regulation and Inflammatory Response in Experimental Models of Diabetes." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-161807.

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Type 2 diabetes is caused by defect pancreatic islet β-cells together with peripheral insulin resistance. The disease is often accompanied by obesity with associated low-grade visceral adipose tissue inflammation, which contributes to insulin resistance. As a consequence of, and a possible compensation for the increased insulin demand, blood flow to the pancreatic islets is increased in animal models of diabetes. This increased blood perfusion might with time affect the vascular network as well as β-cells within the islets. This thesis investigates the role of changes of blood perfusion in pancreatic islets and adipose tissues, as well as the recruitment to and composition of leukocyte subpopulations in insulin-sensitive tissues in experimental models of diabetes. Blood flow measurements in islets and adipose tissues of rats and mice were performed using the microsphere technique, while leukocyte recruitment was studied in the mouse cremaster muscle using intravital microscopy. Increased islet blood flow was observed in the GK rat model of type 2 diabetes, which was decreased by acute as well as continuous 2-week inhibition of β3-adrenoceptors without affecting plasma insulin concentrations. Increased inflammatory leukocyte recruitment was observed in both alloxan-induced and high-fat diet-induced diabetes. However, an impaired bacterial clearance was observed in diabetic mice, which was due to impaired phagocytosis. A gender difference was detected in mice fed a high-fat diet, since obese female mice did not show increased levels of pro-inflammatory circulatory markers or inflammatory leukocytes in the adipose tissue. The main effector cell in the adipose tissue inflammation in high-fat-fed male mice seemed to be the pro-inflammatory macrophage. The Treg population in adipose tissue was increased in female mice, but remained unchanged in male mice on high-fat diet. In conclusion, increased islet blood flow in type 2 diabetes could be reversed by β3-adrenoceptor inhibition, which may maintain islet function. The diabetes-associated hyperglycemia activated leukocytes but impaired their phagocytic ability. High-fat-fed female mice showed less peripheral inflammation due to a smaller number of recruited inflammatory macrophages and a high-fat diet-induced Treg population in intra-abdominal adipose tissues.
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Books on the topic "BETA3"

1

Campbell, John Y. Bad beta, good beta. Cambridge, Mass: National Bureau of Economic Research, 2003.

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Grosdanoff, P., F. Kaindl, and O. Kraupp, eds. Beta-Rezeptoren und Beta-Rezeptorenblocker. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110856293.

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Santos, Tano. Conditional betas. Cambridge, MA: National Bureau of Economic Research, 2004.

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Dr Betam. London: Collins Educational, 1995.

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Rezayî, Yûnis. Şîntirîn betał. Taran [Iran]: Întişaratî ʻAbîd, 2001.

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ʻAmiḳam, Ron. Ani ohev otakh Betar: Toldot Betar Yerushalayim. Yerushalayim: Medyah 41, 2007.

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Alpha Beta. New York: John Wiley & Sons, Ltd., 2002.

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Katie, Cook, Cates Donny, and Chu Amy, eds. Deviations: Beta. San Diego, CA: Idea & Design Works, LLC, 2017.

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Frère, Jean-Marie. Beta-lactamases. Hauppauge, N.Y: Nova Science Publishers, 2011.

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V, Melʹchakova N., and Rudenko N. P, eds. [Beta]-Diketony. Moskva: "Nauka", 1986.

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Book chapters on the topic "BETA3"

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Neubert, D. "Tierschutz - Menschenschutz, eine Herausforderung in der heutigen Zeit." In Beta-Rezeptoren und Beta-Rezeptorenblocker, edited by P. Grosdanoff, F. Kaindl, and O. Kraupp, 3–14. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110856293-001.

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Alexander, M. "Die Verantwortung des klinischen Prüfers bei der Entwicklung von Arzneimitteln." In Beta-Rezeptoren und Beta-Rezeptorenblocker, edited by P. Grosdanoff, F. Kaindl, and O. Kraupp, 15–20. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110856293-002.

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Frölich, J. C. "Ethik der Humanuntersuchung - ein Problem unserer Zeit." In Beta-Rezeptoren und Beta-Rezeptorenblocker, edited by P. Grosdanoff, F. Kaindl, and O. Kraupp, 21–28. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110856293-003.

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Schnieders, B. "Einführung." In Beta-Rezeptoren und Beta-Rezeptorenblocker, edited by P. Grosdanoff, F. Kaindl, and O. Kraupp, 29–32. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110856293-004.

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Göthert, M. "Neue physiologische und pathophysiologische Aspekte der Beta-Adrenozeptoren des Kreislaufsystems: Rolle des vaskulären Renin-Angiotensin-Systems." In Beta-Rezeptoren und Beta-Rezeptorenblocker, edited by P. Grosdanoff, F. Kaindl, and O. Kraupp, 35–46. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110856293-005.

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Schütz, W., M. Freissmuth, V. Hausleithner, and S. Nees. "Verteilung von Betai1 und Beta2-Adrenozeptoren im Herzen." In Beta-Rezeptoren und Beta-Rezeptorenblocker, edited by P. Grosdanoff, F. Kaindl, and O. Kraupp, 47–54. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110856293-006.

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Strasser, R. H. "Neue Wege zur Regulation beta-adrenerger Rezeptoren: Modulation der neu entdeckten beta-adrenergen Rezeptorkinase als möglicher therapeutischer Ansatzpunkt." In Beta-Rezeptoren und Beta-Rezeptorenblocker, edited by P. Grosdanoff, F. Kaindl, and O. Kraupp, 55–72. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110856293-007.

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Spieckermann, P. G. "Herzstoffwechsel und seine Beeinflussung durch Beta-Rezeptorenblocker." In Beta-Rezeptoren und Beta-Rezeptorenblocker, edited by P. Grosdanoff, F. Kaindl, and O. Kraupp, 73–76. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110856293-008.

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Haeusler, G. "Pharmakologische Aspekte und Theorien zur antihypertensiven Wirkung von Beta-Blockern." In Beta-Rezeptoren und Beta-Rezeptorenblocker, edited by P. Grosdanoff, F. Kaindl, and O. Kraupp, 79–92. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110856293-009.

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Raberger, G. "Möglichkeiten zur Charakterisierung von Beta-Rezeptorenblockern: Wirkung von Beta-Rezeptorenblockern in Ruhe und während Belastung am wachen Hund." In Beta-Rezeptoren und Beta-Rezeptorenblocker, edited by P. Grosdanoff, F. Kaindl, and O. Kraupp, 93–110. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110856293-010.

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Conference papers on the topic "BETA3"

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Janus-Bell, E., N. Receveur, C. Mouriaux, B. Hechler, J. Reiser, C. Gachet, B. Ho-Tin-Noé, and P. Mangin. "Cooperation of platelet beta1 and beta3 integrins in the arrest of inflammatory bleeding in mice." In 65th Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1728163.

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Caggia, Silvia, Saverio Candido, Massimo Libra, and Venera Cardile. "Abstract 4074: Transcription factors involved in the genesis and progression of cancer differently modulated by transforming growth factor-beta3 (TGF-Beta3) in prostate cell lines." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4074.

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Terabe, Masaki, Faith Robertson, Shingo Kato, Emma De Ravin, Katharine Clark, Amer M. Mizra, and Jay A. Berzofsky. "Abstract LB-233: Blockade of TGF-beta1 and 2 without TGF-beta3 blockade is sufficient to facilitate tumor vaccine efficacy." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-lb-233.

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Kovacheva, Marineta, Michael Zepp, and Martin R. Berger. "Abstract 6086: Integrin beta3 is a target for treating breast cancer skeletal metastasis." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-6086.

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Sekine, Ayumi, Nobuhiro Tanabe, Satoru Kitazono, Miyako Kitazono, Rintaro Nishimura, Yoriko Takada, Takayuki Jujo, et al. "G Protein Beta3 Subunit GNB3 C825T Polymorphism Affects The Efficacy Of Sildenafil On Pulmonary Hypertension." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2421.

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Shah, Parag P., and Sham S. Kakar. "Abstract 3431: Regulation of integrins AlphaV Beta3 and focal adhesion kinase signaling by PTTG in induction of EMT." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3431.

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Curnis, Flavio, Angelina Sacchi, Renato Longhi, Barbara Colombo, Anna Gasparri, and Angelo Corti. "Abstract 5617: A new alphaV/beta3 integrin selective carrier for nanodrug delivery to tumors based on isoDGR-tagged albumin." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5617.

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Bu, Xiao-Bo, and Jie Song. "Notice of Retraction: Polymorphism Analysis G Protein beta3 Subunit in Population of Essential Hypertension in the Mudanjiang Region of China." In 2011 5th International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2011. http://dx.doi.org/10.1109/icbbe.2011.5780690.

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Zheng, Yanbin, Patricia Chu, and Stephen X. Skapek. "Abstract 1140: C/ebp beta repressesArfinduction by tgf-beta2." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1140.

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Novella, Pau. "NEXT: results from NEXT-White and roadmap toward the $\beta\beta0\nu$ search." In European Physical Society Conference on High Energy Physics. Trieste, Italy: Sissa Medialab, 2020. http://dx.doi.org/10.22323/1.364.0403.

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Reports on the topic "BETA3"

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Languino, Lucia R. Beta1 and Beta3 Integrins in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada414864.

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Huang, Shuang. Vitronectin and Integrin alpha(v)Beta3 in Ovarian Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, July 2003. http://dx.doi.org/10.21236/ada420884.

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Munger, John S. The Role of Alpha(v)Beta6-Mediated Latent TGF(Beta)1 Activation in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada414426.

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Campbell, John, and Tuomo Vuolteenaho. Bad Beta, Good Beta. Cambridge, MA: National Bureau of Economic Research, February 2003. http://dx.doi.org/10.3386/w9509.

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Santos, Tano, and Pietro Veronesi. Conditional Betas. Cambridge, MA: National Bureau of Economic Research, April 2004. http://dx.doi.org/10.3386/w10413.

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Hong, Harrison, and David Sraer. Speculative Betas. Cambridge, MA: National Bureau of Economic Research, November 2012. http://dx.doi.org/10.3386/w18548.

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Pritychenko, B. Imperfect World of beta beta-decay Nuclear Data Sets. Office of Scientific and Technical Information (OSTI), January 2015. http://dx.doi.org/10.2172/1169034.

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Welch, Ivo. Simpler Better Market Betas. Cambridge, MA: National Bureau of Economic Research, July 2019. http://dx.doi.org/10.3386/w26105.

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Rabiti, Cristian, Andrea Alfonsi, Joshua Joseph Cogliati, Diego Mandelli, Robert Arthur Kinoshita, Congjian Wang, Daniel Patrick Maljovec, and Paul William Talbot. RAVEN Beta Release. Office of Scientific and Technical Information (OSTI), February 2016. http://dx.doi.org/10.2172/1245532.

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Frazzini, Andrea, and Lasse Pedersen. Betting Against Beta. Cambridge, MA: National Bureau of Economic Research, December 2010. http://dx.doi.org/10.3386/w16601.

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