Relevant bibliographies by topics / Receptor de calcitonina

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Receptor de calcitonina'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Receptor de calcitonina.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Receptor de calcitonina"

1

Maciel, Rui M. B. "O Laboratório no Diagnóstico e Seguimento de Doenças Auto-Imunes e Neoplásicas de Tiróide." Arquivos Brasileiros de Endocrinologia & Metabologia 46, no. 1 (February 2002): 65–71. http://dx.doi.org/10.1590/s0004-27302002000100009.

Full text
Abstract:
O laboratório é fundamental no diagnóstico das doenças auto-imunes e neoplásicas da tiróide. O teste mais importante para o diagnóstico etiológico da tiroidite de Hashimoto, doença de alta prevalência, é a determinação do anticorpo anti-tiroperoxidase (A-TPO), dosagem que pode também ser útil no diagnóstico de doença de Graves, do risco de hipotiroidismo em pacientes com hipotiroidismo sub-clínico e do risco de gestantes apresentarem tiroidite pós-parto. Outro teste útil nas doenças autoimunes é a determinação dos anticorpos anti-receptor de TSH (TRAb) naqueles casos de doença de Graves pouco sintomáticos ou quando a mesma ocorre em pacientes com bócio multi-nodular. Nas doenças neoplásicas da tiróide, a tiroglobulina (Tg) é fundamental e de alta sensibilidade no seguimento dos pacientes com câncer diferenciado da tiróide (papilífero e folicular), enquanto que a dosagem de calcitonina é obrigatória para o diagnóstico e seguimento do câncer medular da tiróide.
APA, Harvard, Vancouver, ISO, and other styles
2

Blakely, P., D. A. Vaughn, and D. D. Fanestil. "Amylin, calcitonin gene-related peptide, and adrenomedullin: effects on thiazide receptor and calcium." American Journal of Physiology-Renal Physiology 272, no. 3 (March 1, 1997): F410—F415. http://dx.doi.org/10.1152/ajprenal.1997.272.3.f410.

Full text
Abstract:
We previously reported that salmon calcitonin, but not rat calcitonin, increased renal thiazide receptor (TZR) density and decreased renal calcium [urinary calcium excretion (U(Caex))] in the rat. Since calcitonins, islet amyloid polypeptide (amylin), calcitonin-gene related peptide (CGRP), and adrenomedullin interact with a family of calcitonin-related receptors, we examined the effects of these peptides on 1) TZR density, as quantitated by binding of [3H]metolazone to renal membranes; 2) plasma ionic composition; and 3) urinary electrolyte excretion. Subcutaneous amylin both increased TZR density nearly twofold and decreased U(Caex), with maximal effects by 24 h. The decreased U(Caex) occurred with plasma amylin levels in the physiological range, whereas the increased TZR did not reach maximum even with plasma amylin >100 times above normal. Similar doses of adrenomedullin increased TZR density modestly but without effect on U(Caex), whereas CGRP did not alter TZR density and tended to increase U(Caex). We propose that U(Caex) and TZR density in the rat kidney are regulated by rat amylin but not by rat calcitonin.
APA, Harvard, Vancouver, ISO, and other styles
3

Hendrikse, Erica R., Rebekah L. Bower, Debbie L. Hay, and Christopher S. Walker. "Molecular studies of CGRP and the CGRP family of peptides in the central nervous system." Cephalalgia 39, no. 3 (March 22, 2018): 403–19. http://dx.doi.org/10.1177/0333102418765787.

Full text
Abstract:
Background Calcitonin gene-related peptide is an important target for migraine and other painful neurovascular conditions. Understanding the normal biological functions of calcitonin gene-related peptide is critical to understand the mechanisms of calcitonin gene-related peptide-blocking therapies as well as engineering improvements to these medications. Calcitonin gene-related peptide is closely related to other peptides in the calcitonin gene-related peptide family of peptides, including amylin. Relatedness in peptide sequence and in receptor biology makes it difficult to tease apart the contributions that each peptide and receptor makes to physiological processes and to disorders. Summary The focus of this review is the expression of calcitonin gene-related peptide, related peptides and their receptors in the central nervous system. Calcitonin gene-related peptide is expressed throughout the nervous system, whereas amylin and adrenomedullin have only limited expression at discrete sites in the brain. The components of two receptors that respond to calcitonin gene-related peptide, the calcitonin gene-related peptide receptor (calcitonin receptor-like receptor with receptor activity-modifying protein 1) and the AMY1 receptor (calcitonin receptor with receptor activity-modifying protein 1), are expressed throughout the nervous system. Understanding expression of the peptides and their receptors lays the foundation for more deeply understanding their physiology, pathophysiology and therapeutic use.
APA, Harvard, Vancouver, ISO, and other styles
4

Zaidi, M., S. D. Brain, J. R. Tippins, V. Di Marzo, B. S. Moonga, T. J. Chambers, H. R. Morris, and I. MacIntyre. "Structure-activity relationship of human calcitonin-gene-related peptide." Biochemical Journal 269, no. 3 (August 1, 1990): 775–80. http://dx.doi.org/10.1042/bj2690775.

Full text
Abstract:
The calcitonin-calcitonin-gene-related peptide (CGRP) gene complex encodes a small family of peptides: calcitonin, CGRP and katacalcin. Calcitonin is a circulating hormone that prevents skeletal breakdown by inhibiting the resorption of bone by osteoclasts. CGRP, a potent vasodilator, is involved in normal regulation of blood flow. The calcitonins structurally resemble the CGRP peptides, and both are known to cross-react at each others' receptors. The present study was undertaken to examine the structural prerequisites for biological activity of the intact CGRP molecule. We therefore prepared eight chymotryptic and tryptic fragments of CGRP and synthesized its acetylated and S-carboxyamidomethylcysteinyl analogues. The analogues were purified by h.p.l.c. and their structures were confirmed by fast-atom bombardment mass spectrometry. We have examined the effects of structurally modified analogues and fragments of human CGRP in a calcitonin-receptor-mediated assay, the osteoclast bone resorption assay, and in one or two CGRP-receptor-mediated assays, the rabbit skin blood flow assay and the oedema formation assay. The results showed that (1) in the osteoclast bone resorption assay, both CGRP peptides, alpha and beta, were equipotent, and were both at least 1000-fold were both approx. 1000-fold more potent than salmon calcitonin; human calcitonin had no effect; (3) the bis- and N-acetylated CGRP analogues retained reduced levels of biological activity in all assays, whereas S-carboxyamidomethylcysteinyl-human CGRP was without activity; and (4) all tryptic and chymotryptic fragments of CGRP were without biological activity, with the exception of hCGRP-(Ala1-Lys35): this fragment had much reduced activity compared with the intact peptide in inhibiting osteoclastic bone resorption and increasing blood flow in the rabbit skin. The results suggest that: (1) calcitonin and CGRP act at distinct receptors to mediate different physiological effects; (2) minor amino acid substitutions, as between the alpha and beta forms of CGRP (these two forms have 94% structural similarity) do not result in differences in biological activity; (3) the intact peptide is required for full biological activity of the CGRP molecule, and even the loss of two amino acids at the C-terminus of the molecule results in a marked decrease in activity; (4) the disulphide bridge appears to play an important role in the interaction of the intact CGRP molecule with its receptor; and (5) the C-terminal region is probably necessary for the peptide to assume the right conformation in the interaction with the receptor.
APA, Harvard, Vancouver, ISO, and other styles
5

Magalhães, Patrícia K. R., Margaret de Castro, Lucila L. K. Elias, and Léa M. Z. Maciel. "Carcinoma medular de tireóide: da definição às bases moleculares." Arquivos Brasileiros de Endocrinologia & Metabologia 47, no. 5 (October 2003): 515–28. http://dx.doi.org/10.1590/s0004-27302003000500004.

Full text
Abstract:
O carcinoma medular de tireóide (CMT) é um tumor maligno raro com origem nas células parafoliculares da tireóide, tendo como principal produto secretório a calcitonina. Representa 3 a 10% de todos os tumores tireoidianos e é responsável por um grande número de mortes em portadores de câncer de tireóide. Em 75-90% dos pacientes, o CMT ocorre de forma esporádica e, nos demais casos, é uma doença hereditária autossômica dominante com alto grau de penetrância e variabilidade de expressão, podendo fazer parte de 3 síndromes distintas: neoplasia endócrina múltipla (NEM) 2A, NEM 2B ou CMT familiar. As diferentes formas clínicas do CMT, principalmente as hereditárias, estão relacionadas com mutações no proto-oncogene RET, as quais resultam em ativação constitutiva do receptor de membrana tirosina-quinase RET. A distinção entre estas formas é de extrema relevância clínica por causa das diferenças apresentadas entre elas em termos de prognóstico e pela necessidade de um rastreamento familiar, aconselhamento genético e seguimento das formas hereditárias. A eficiência do rastreamento genético, pela pesquisa de mutações no proto-oncogene RET, está bem estabelecida no diagnóstico e na identificação de portadores assintomáticos das formas hereditárias de CMT, permitindo uma intervenção cirúrgica precoce e efetiva, reduzindo a morbidade e a mortalidade associadas a esta doença.
APA, Harvard, Vancouver, ISO, and other styles
6

Smith, D. M., H. A. Coppock, D. J. Withers, A. A. Owji, D. L. Hay, T. P. Choksi, P. Chakravarty, S. Legon, and D. R. Poyne. "Adrenomedullin: receptor and signal transduction." Biochemical Society Transactions 30, no. 4 (August 1, 2002): 432–37. http://dx.doi.org/10.1042/bst0300432.

Full text
Abstract:
Adrenomedullin is a vascular tissue peptide and a member of the calcitonin family of peptides, which includes calcitonin, calcitonin-gene-related peptide (CGRP) and amylin. Its many biological actions are mediated via CGRP type 1 (CGRP1) receptors and by specific adrenomedullin receptors. Although the pharmacology of these receptors is distinct, they are both represented in molecular terms by the type II family G-protein-coupled receptor, calcitonin-receptor-like receptor (CRLR). The specificity here is defined by co-expression of receptor-activity-modifying proteins (RAMPs). CGRP1 receptors are represented by CRLR and RAMP1, and specific adrenomedullin receptors by CRLR and RAMP2 or 3. Here we discuss how CRLR/RAMP2 relates to adrenomedullin binding, pharmacology and pathophysiology, and how chemical cross-linking of receptor-ligand complexes in tissue relates to that in CRLR/RAMP2-expressing cells. CRLR, like other type II family G-protein-coupled receptors, signals via Gs and adenylate cyclase activation. We demonstrated that adrenomedullin signalling in cell lines expressing specific adrenomedullin receptors followed this expected pattern.
APA, Harvard, Vancouver, ISO, and other styles
7

Oliver, K. R. "CGRP Receptor Family and Accessory Protein Localization: Implications for Predicted Function." Scientific World JOURNAL 1 (2001): 10. http://dx.doi.org/10.1100/tsw.2001.431.

Full text
Abstract:
Calcitonin gene-related peptide (CGRP), adrenomedullin, amylin, and calcitonin are functionally related neuropeptides. Certain of these peptides mediate their action through receptors which have common components, such as the receptor activity modifying proteins (RAMPs) and CGRP-receptor component protein, as well as possibly through other distinct receptors. Specifically, the molecular pharmacology of CGRP and adrenomedullin is determined by coexpression of one of three receptor activity-modifying proteins (RAMPs) with calcitonin receptor-like receptor (CRLR). Additionally, through formation of another hetero-oligomer, RAMPs also govern the pharmacology of the calcitonin receptor, which in association with RAMP1 or RAMP3, binds amylin with high affinity. We have used multiple approaches to discern the regional and cellular expression of these various receptor components and binding sites for the above neuropeptides in multiple species and in different tissues. Techniques applied include in situ hybridization, immunohistochemistry and radioligand autoradiography. These data allow further understanding of both the complexity of receptor-receptor component and receptor-ligand interactions in vivo. Interestingly, these localization data suggest that RAMPs may interact with receptors additional to those already identified for the CGRP family and may be involved in binding innate neuropeptides or other neurotransmitters which are not members of the calcitonin gene-related peptide fam
APA, Harvard, Vancouver, ISO, and other styles
8

Razzaque, Z., D. Shaw, M. Bock, L. Maskell, J. Pickard, D. Sirinathsinghji, and J. Longmore. "Study of Cgrp-Receptors in Human Isolated Middle Meningeal Arteries Using Bibn4096Bs, Compound 1, and HαCgrp(8-37)." Scientific World JOURNAL 1 (2001): 17. http://dx.doi.org/10.1100/tsw.2001.437.

Full text
Abstract:
Calcitonin, CGRP, adrenomedullin, and amylin require both CRLR (calcitonin-gene receptor like receptor) and receptor activity modifying proteins (RAMP1, RAMP2, and RAMP3) in different combinations for expression of selective, functional receptors[1]. We investigated whether the antagonists BIBN4096BS[2], Compound 1 (WO98/11128, [3]), and CGRP(8-37) are functionally selective for CGRP receptors in human middle meningeal arteries (HMMA).
APA, Harvard, Vancouver, ISO, and other styles
9

Warfvinge, Karin, and Lars Edvinsson. "Distribution of CGRP and CGRP receptor components in the rat brain." Cephalalgia 39, no. 3 (August 31, 2017): 342–53. http://dx.doi.org/10.1177/0333102417728873.

Full text
Abstract:
Background Calcitonin gene-related peptide and its receptor, consisting of receptor activity-modifying protein 1 and calcitonin receptor-like receptor, are of considerable interest because of the role they play in migraine and recently developed migraine therapies. Methods To better understand the function of this neuropeptide, we used immunohistochemistry to determine a detailed distribution of calcitonin gene-related peptide, receptor activity-modifying protein 1 and calcitonin receptor-like receptor in the rat brain in a region of 0.5–1.5 mm lateral to the midline. We found calcitonin gene-related peptide immunoreactivity in most of the neurons of the cerebral cortex, hippocampus, cerebellum, thalamic nuclei, hypothalamic nuclei and brainstem nuclei. In contrast, receptor activity-modifying protein 1 and calcitonin receptor-like receptor immunoreactivity were found almost exclusively in the neuronal processes in the investigated regions. Conclusion Overall, the degree of expression of calcitonin gene-related peptide and calcitonin gene-related peptide receptor components in the central nervous system is astonishingly complex and suggestive of many different brain functions, including a possible role in migraine. However, currently, the presence of calcitonin gene-related peptide and the nature of its receptors throughout the brain is an enigma yet to be solved.
APA, Harvard, Vancouver, ISO, and other styles
10

Faria, Sara Socorro, and Pedro Leme Silva Pedro Leme Silva Pedro Leme Silva. "Revisão Sistemática sobre Tratamento Medicamentoso para Dor no Membro Fantasma." Revista Neurociências 22, no. 2 (June 30, 2014): 177–88. http://dx.doi.org/10.34024/rnc.2014.v22.8091.

Full text
Abstract:
Objetivo. Realizar revisão sistemática da literatura sobre as possíveis condutas farmacológicas utilizadas para tratamento da dor do mem­bro fantasma. Método. A estratégia de busca foi realizada nas bases de dados eletrônicas Cochrane, Pubmed e Lilacs através da consulta de descritores específicos. A busca consistiu de artigos apresentados na íntegra, escritos em inglês ou espanhol, adultos humanos de ambos os sexos, publicados no período de 1990 a 2012. Resultados. Após a aplicação dos critérios de exclusão, foram selecionados 20 artigos. Através da análise, verificou-se que existem possibilidades terapêuticas positivas a curto prazo a serem utilizadas, dentre elas destacam-se os opióides, gabapentina e a quetamina. A morfina (oral e intravenosa) foi eficaz na diminuição da intensidade da dor a curto-prazo. Com ex­ceção da memantina, os antagonistas do receptor NMDA, morfina e a quetamina apresentaram efeitos analgésicos. Entretanto, os resultados obtidos com a gabapentina em termos de alívio da dor não foram sig­nificativos. O direcionamento da eficácia da calcitonina e dextrome­torfano necessitam maiores esclarecimentos. Conclusão. A morfina e a quetamina demonstraram ser eficazes como analgésicos de curta duração. Maiores estudos tornam-se necessários para esclarecer os re­ais benefícios da amitriptilina, o cloridrato de tramadol, memantina e a toxina botulínica. Intervenções em pesquisas com maior número de participantes são importantes, a fim de estabelecer recomendações na prática terapêutica.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Receptor de calcitonina"

1

Martins, Allisson Filipe Lopes. "Expressão de osteocalcina e de receptores da calcitonina e glicocorticoide em lesão central de células gigantes do complexo maxilo-mandibular." Universidade Federal de Goiás, 2015. http://repositorio.bc.ufg.br/tede/handle/tede/5042.

Full text
Abstract:
Submitted by Luciana Ferreira (lucgeral@gmail.com) on 2015-12-10T09:47:46Z No. of bitstreams: 2 Dissertação - Allison Filipe Lopes Martins - 2015.pdf: 3205167 bytes, checksum: 5c24397e18241a8a809af753bb233428 (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5)
Approved for entry into archive by Luciana Ferreira (lucgeral@gmail.com) on 2015-12-10T10:03:57Z (GMT) No. of bitstreams: 2 Dissertação - Allison Filipe Lopes Martins - 2015.pdf: 3205167 bytes, checksum: 5c24397e18241a8a809af753bb233428 (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5)
Made available in DSpace on 2015-12-10T10:03:57Z (GMT). No. of bitstreams: 2 Dissertação - Allison Filipe Lopes Martins - 2015.pdf: 3205167 bytes, checksum: 5c24397e18241a8a809af753bb233428 (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) Previous issue date: 2015-03-27
Conselho Nacional de Pesquisa e Desenvolvimento Científico e Tecnológico - CNPq
The Central Giant Cell Lesion (CGCL) is an intraosseous lesion that can be classified into non aggressive and aggressive. Due to the aesthetic and functional defects of surgical treatment of CGCL, therapies with drugs have been reported, such as glucocorticoid injections and calcitonin. The studies reported in the literature support the use of these drugs through the investigation of the presence of glucocorticoid receptors (RGC) and calcitonin (RCT) in CGCL; however there is no consensus if all lesions express these receptors and if there is any difference between non aggressive and aggressive lesion. In addition, there are no studies that evaluated the bone formation potential through the investigation of Osteocalcin (OC) in aggressive and non-aggressive lesions. The aim of this study was to compare, using immunohistochemistry, the GR and CTR and osteocalcin protein (OC) expression in non aggressive (n = 20) and aggressive (n = 11) CGCL, and the correlation between the OC expression and these receptors determined in both groups of lesions. The number of mononuclear cells in mitosis (MOC), and the number of multinucleated giant cells (MGC) were also investigated using immunohistochemical techniques (hematoxylin and eosin). Our results show that all the cases express the GR and CTR and that there is no difference in the expression of these receptors or the number of mitosis between non aggressive and aggressive lesions. The OC expression was rare and higher in non aggressive lesions, however, not statistically significant (p> 0.05). There was a correlation between the CTR expression in MOC and MGC (r = 0.45; p <0.01). Considering the different variants of CGCL, there was a correlation between CTR expression in MOC and MGC in non aggressive lesions (r = 0.66; p <0.01) and between the CTR and OC expression in MGC (r = 0.718; p = 0.01). There was a higher number of MGC in aggressive lesions (p = 0.01). The results indicate that all cases express GR and CTR and that there are no differences between non aggressive and aggressive CGCL lesions of these receptors expression, these results strengthens CGCL treatment with glucocorticoids and calcitonin. Aggressive lesions have a higher number of MGC. The CGCL express glucocorticoid and calcitonin receptors and this finding give biological basis to the CGCL treatment with intralesional glucocorticoid and calcitonin either in non aggressive and aggressive cases. It was also identified osteocalcin positive cells, that may be related to bone repair, it is believed that these cells may also serve as a therapeutic target.
A Lesão Central de Células Gigantes (LCCG) é uma lesão intraóssea que pode ser classificada em não agressiva e agressiva. Devido aos defeitos estéticos e funcionais do tratamento cirúrgico da LCCG, terapias medicamentosas tem sido relatadas, como injeções de glicocorticoide e calcitonina. Há na literatura estudos que suportam o uso desses medicamentos através da investigação da presença de receptores de glicocorticoides (RGC) e de calcitonina (RCT) em LCCG. No entanto não existe consenso se todas as LCCG expressam esses receptores e se existe alguma diferença entre lesões agressivas e não agressivas. Além disso, não existem estudos sobre a avaliação do potencial de formação óssea através da Osteocalcina (OC) em lesões agressivas e não agressivas. O propósito deste estudo foi avaliar comparativamente, por meio de imunohistoquímica, a expressão de RGC e RCT e da OC em LCCG não agressivas (n= 20) e agressivas (n= 11) e a correlação entre a expressão da OC e desses receptores nos dois grupos de lesões estudados. O número de mitoses nas células mononucleares e o número de células gigantes multinucleadas também foram investigados, utilizando técnica histoquímica (hematoxilina e eosina). Nossos resultados mostram que todos os casos analisados expressam o RGC e RCT e que não existe diferença na expressão do RGC, RCT ou do número de mitoses entre lesões não agressivas e agressivas. A expressão de OC em células mononucleares foi rara e maior em lesões não agressivas, no entanto, sem diferenças estatisticamente significantes (p>0,05). Houve correlação entre a expressão do RCT em células mononucleares e células gigantes multinucleadas (r=0,45; p<0,01). Considerando as diferentes variantes foi verificada correlação do RCT entre o componente mononuclear e as células gigantes multinucleadas nas lesões não agressivas (r=0,66; p<0,01) e entre a expressão de OC e RCT em células gigantes multinucleadas (r= 0,718; p=0,01). Houve maior número de células gigantes em lesões agressivas (p= 0,01). Os resultados indicam que todos os casos expressam RGC e RCT e que não há diferenças entre lesões agressivas e não agressivas de LCCG quanto à expressão desses receptores, fortalecendo a recomendação o tratamento da LCCG com o uso de glicocorticoide e calcitonina. Lesões agressivas apresentam maior número de CGM. As células da LCCG expressam o RGC e RCT e esse achado pode fornecer bases biológicas para o tratamento com injeções intralesionais de glicocorticoides e o uso de calcitonina, seja em lesões não agressivas ou agressivas. Adicionalmente, foram identificadas células expressando OC, que podem estar relacionadas ao reparo ósseo, acredita-se que essa linhagem celular também pode se tornar um alvo terapêutico.
APA, Harvard, Vancouver, ISO, and other styles
2

Nogueira, Renato Luiz Maia. "AvaliaÃÃo clÃnica da corticoterapia intralesional em lesÃo cen-tral de cÃlulas gigantes dos maxilares : relevÃncia da expressÃo dos receptores de corticÃide e calcitonina, Cox-2, p16 e amplificaÃÃo da ciclina D1." Universidade Federal do CearÃ, 2010. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=4974.

Full text
Abstract:
CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
FundaÃÃo de Amparo à Pesquisa do Estado do CearÃ
Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico
A LesÃo Central de CÃlulas Gigantes dos maxilares (LCCG) à intra-Ãssea, nÃo tem predileÃÃo por sexo, classifica-se em agressivas e nÃo-agressivas, histologicamente consistem tecido fi-broso e celularizado fusiforme associado a cÃlulas gigantes multinucleadas (CGM), focos de hemorragia e neovascularizaÃÃo, tendo na cirurgia seu habitual tratamento. Novas abordagens terapÃuticas foram propostas, sendo a principal delas o uso de corticÃides intralesionais. Este trabalho analisa retrospectivamente 21 pacientes portadores de LCCG que foram tratados por hexacetonido de triancinolona intralesional, atravÃs do seguinte protocolo: injeÃÃo de hexace-tonido de triancinolona 20mg/ml diluÃdo na soluÃÃo anestÃsica de lidocaÃna 2%/epinefrina 1:200.000 numa proporÃÃo de 1:1; infiltrando 1ml de soluÃÃo para cada 1cm3 de lesÃo, totali-zando 06 aplicaÃÃes em intervalos quinzenais. Estabeleceu-se 04 critÃrios clÃnicos para classi-ficar a resposta ao tratamento: 1- estabilizaÃÃo ou regressÃo clÃnica da lesÃo 2- ausÃncia de sintomas 3- aumento da densidade nos controles radiogrÃficos 4- aumento da resistÃncia a infiltraÃÃo intralesional da droga, bem como, fez-se uma anÃlise imunohistoquÃmica quanto à expressÃo dos Receptores de corticÃides (GCR) e Calcitonina (CTR), Cox-2, proteÃna p16 e amplificaÃÃo gÃnica da Ciclina D1 por CISH, comparando quanto a agressividade e a resposta terapÃutica a corticoterapia intralesional. Dos 21 pacientes incluÃdos neste estudo, 11 eram homens e 10 mulheres, 09 tinham lesÃo em maxila, 12 em mandÃbula. Dez eram lesÃes agres-sivas e 11 nÃo-agressivas, 15 (71,4%) apresentaram uma boa resposta ao tratamento, 04(19%) moderada e 02(9,1%) negativa. Das 11 nÃo agressivas, 10(90,9%) apresentaram boa resposta e 01 (9,1%) resposta moderada, das 10 agressivas 05(50%), 03(30%) e 02(20%) apresentaram boa, moderada e negativa resposta respectivamente, nenhuma apresentou recidiva apÃs o tra-tamento, com preservaÃÃo que variou entre 04 a 08 anos. Os achados histopatolÃgicos mos-traram uma reduÃÃo da densidade e do tamanho das CG, e um estroma fibro-colagenoso das lesÃes. Dentre os marcadores pesquisados, apenas GCR em CG antes do tratamento mostrou significÃncia estatÃstica (p<0,004) com relaÃÃo a uma boa resposta terapÃutica. O CTR ex-pressou-se em cÃlulas gigantes e mononucleares de forma variada. A p16 apresentou-se ex-pressa em 30% da amostra, COX2 nÃo apresentou expressÃo na lesÃo e 33% da amostra apre-sentou amplificaÃÃo gÃnica da ciclina D1. NÃo mostraram significÃncia estatÃstica nem quanto à agressividade, nem quanto resposta ao tratamento, nenhum dos marcadores, exceto o GCR. O estudo mostrou que a corticoterapia intralesional à efetiva e segura para o tratamento das LCCG, com tendÃncia a melhor resposta nas lesÃes nÃo-agressivas do que nas agressivas. Mostrou ainda que a marcaÃÃo para GCR em CG demonstrou ser um parÃmetro confiÃvel para prever a resposta à terapÃutica com a corticoterapia intralesional e que 33% das LCCG tÃm comportamento neoplÃsico pela amplificaÃÃo gÃnica da ciclina D1.
Central Giant Cells Lesion (CGCL) of the jaws is an intra-bone lesion with no predilection for sex and clinically divided into aggressive and non-aggressive subtypes. Histological, it shows as fibrous tissue with fusiform cells, as well as multinucleated giant cells (GC) clusters, he-morrhagic foci and neovascularization. Surgery is the regular treatment option. As new the-rapeutic approaches have been proposed, intralesional glucocorticoid injection is the main option. This paper assesses retrospectively 21 patients presenting CGCL, treated with intrale-sional triamcinolone hexacetonide by using the following protocol: intralesional injection of triamcinolone hexacetonide 20mg/mL, diluted in a solution of lidocain 2% plus epinephrine 1:200000, at a 1:1 proportion; 1mL of this final solution for each 1cm3 of lesion volume was the injected, with a total of 06 injections, one in every 15 days. Four clinical criteria were sta-bilished to evaluate treatment outcome: 1- Clinical regression or stabilization of the lesion; 2- Absence of symptoms; 3- Raising in density on radiographic controls; 4-Increased resistence when injecting the drug intralesionally. It was also performed immunohistochemical assess-ment for glucocorticoid receptor (GCR) expression, calcitonin receptor (CTR) expression, COX-2 expression, p16 expression and Ciclin D1 gene amplification by CISH, making com-parisons related to aggressivity and to therapeutic outcome. Eleven out of 21 patients of this study were women, and 10 were men. Nine of the patients had lesion located in the maxilla, 12 in the mandible. Ten patients showed aggressive lesions and 11 non-aggressive lesions. Fifteen patients showed good treatment outcome, four patients showed moderate outcome, and two patients showed negative answer to the treatment. Among the 11 patients with non-aggressive lesions, ten showed good outcome and the other, moderate outcome. Among the ten aggressive lesions, five patients showed good outcome, three patients showed moderate outcome and the remaining two patients showed negative answer to the treatment. None of them showed reicidive in a four to eight years follow-up period. Morphologic analysis found positive correlation between volume density of GC/mm2 and lesion aggressiveness, as well as significant reduction in number of GC/mm2 after treatment. Among the markers, only GCR in GC showed statistical relevance associated to the treatment. CTR was espresse in GC and in mononuclear cells in a varying way; p16 was expressed in 30% of the sample; COX-2 was not expressed at all in lesion samples and 33% of the sample showed gene amplification in Ciclin D1. None of the markers showed any statistical significant difference related to aggres-siveness nor to treatment outcome, except for GCR. The study showed the feasibility of the adopted treatment, with tendency to better outcomes in non-aggressive lesion, if compared to the aggressive ones. It also showed evidence pointing to GCR expression in GC as a reliable parameter to predict therapeutic responsiveness to glucocorticoids; and it showed that 33% of CGCL have neoplastic behaviour by Ciclin D1 gene amplification.
APA, Harvard, Vancouver, ISO, and other styles
3

Kappus, Christoph [Verfasser], and Ludwig [Akademischer Betreuer] Benes. "Die Expression des Calcitonin receptor-like receptors in humanen Gliomen / Christoph Kappus. Betreuer: Ludwig Benes." Marburg : Philipps-Universität Marburg, 2014. http://d-nb.info/106409743X/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Hay, Deborah Lucy. "Investigation of the calcitonin receptor-like receptor and activity-modifying proteins." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396319.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Han, Ziqun. "Molecular cloning and characterisation of an orphan receptor from the calcitonin receptor family." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267579.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Winfield, Ian J. "Quantifying biased agonism of adenosine and calcitonin-like receptors." Thesis, University of Warwick, 2017. http://wrap.warwick.ac.uk/100406/.

Full text
Abstract:
G protein-coupled receptors (GPCRs) elicit an ability to activate multiple downstream signalling pathways. It is becoming evident that for many GPCRs, agonists are able to activate several of these pathways, each to differing extents; a phenomenon termed pathway bias, or biased agonism. Here, work is presented quantifying biased agonism for the: adenosine A1 and A2A receptors, as well as the calcitonin-like receptor (CLR). For the adenosine receptors, novel selective, and non-selective, agonists are identified and characterised. Further, the extent of biased agonism is determined for A1R agonists with respect to their abilities to positively and negatively regulate cAMP production, mobilise intracellular Ca2+ and activate ERK1/2. The activity of triazoloquinazoline compounds against the A2AR is validated, identifying 3 to be selective. Further investigations into the ability of triazoloquinazolines to mediate cAMP production and ERK1/2 activation uncovers each tested agonist to be biased towards activating ERK1/2, at the A2AR. A characterisation of the effects of receptor activity modifying proteins (RAMPs) upon signalling from the CLR is presented: quantifying the extent of biased agonism, with respect to the ability of RAMP-CLR heterodimers to: mediate cAMP production and inhibition, as well as mobilise intracellular Ca2+, uncovering this to be a Gαq/11-mediated process. Further, through applying a saturation mutagenesis approach to the CLR, a potential interaction is identified between intracellular loop 1 (ICL1) and helix 8, which is broken upon receptor activation, further identifying ICL1 to be a region of the CLR responsible for influencing G protein specificity. Ultimately, these findings relating to both adenosine and CLR-based receptors uncovers further evidence of biased agonism at GPCRs, which may have potential implications upon improving the efficacy and safety profiles of novel pharmaceutics targeting these clinically relevant GPCRs.
APA, Harvard, Vancouver, ISO, and other styles
7

Raggatt, Liza. "Cellular and molecular mechanisms by which the insert negative isoform of the human calcitonin receptor regulates cell growth /." Title page, contents and abstract only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phr142.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Tomlinson, Ann E. "Characterisation of calcitonin gene-related peptide (CGRP) and amylin receptors." Thesis, Aston University, 1995. http://publications.aston.ac.uk/14312/.

Full text
Abstract:
The aims of this study were to examine the binding characteristics of the rat CGRP receptor and to further the classification of CGRP and amylin receptors in guinea-pig tissue preparations. Binding characteristics of CGRP were investigated on rat splenic, cerebellar and liver membrane preparations. Human-a-CGRP, rat-a-CGRP and the CGRP receptor analogues TyrO -CGRPC28-37) and [Cys (ACMh,7 ]-human CGRP and the CGRP receptor antagonist CGRPC8-37) were utilised in competitive radioligand binding experiments to identify possible CGRP receptor subtypes in these tissues. There appeared to be no significant differences between the rat CGRP receptors examined. A panel of monoclonal antibodies (Mabs) raised against CGRP were employed to investigate the structure-activity relationships of CGRP and its receptor. No differences between the tissue receptors were observed using this panel of Mabs. The effects of human-a, human-~, rat.ca-CGRP, human and rat amylin and adrenomedullil1{13-52) were examined on the spontaneously beating right atria and on electrically evoked twitch contractions of isolated guinea-pig ileum, vas deferens and left atria. All of the peptides caused concentration-dependent inhibition of twitch amplitude in the ileum and vas deferens. CGRP produced positive inotropic effects in the right and left atria and positive chronotropic effects in the right atria. A variety of CGRP receptor antagonists and putative amylin receptor antagonists were used to antagonise these effects. CGRPC8-37) is currently used as a basis for CGRP receptor classification (Dennis, et al., 1989). Based upon results obtained using CGRPC8-37) it has been shown that the guinea-pig ileum contains mainly CGRP 1 receptors and the vas deferens contain CGRP2 receptors. Amylin was shown to act at receptors distinct from those for CGRP and it is postulated that amylin has its own receptors in these preparations. Experiments using CGRP (19-37) and TyrO -CGRPC28-37) indicate that human and rat CGRP act at distinct receptors in guinea-pig ileum and vas deferens. The amylin receptor antagonist amylinC8-37) and the putative antagonist AC 187 provide evidence to suggest human and rat amylin also act at receptors able to distinguish between the two types of amylin.
APA, Harvard, Vancouver, ISO, and other styles
9

Huang, Xiaofang. "Functional study of amylin and regulation of amylin receptor." Diss., Temple University Libraries, 2010. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/114036.

Full text
Abstract:
Pharmacology
Ph.D.
Amylin, a 37 amino acid peptide secreted from pancreatic beta cells upon stimulation by meal/glucose, belongs to the family of the calcitonin or calcitonin gene-related peptide (CGRP) and shares up to 50% homology with CGRP, which is a well-documented pain-related peptide. The amylin receptor is composed of a calcitonin receptor (CTR) and receptor activity modifying proteins (RAMPs). Numerous studies have shown that amylin plays an important role in glucose homeostasis and food intake. Few studies have been conducted with respect to the effect of amylin in the central or peripheral neuraxis. In this thesis, immunohistochemical study revealed a dense network of amylin-immunoreactive (irAMY) cell processes in the superficial dorsal horn of the mice. Numerous dorsal root ganglion and trigeminal ganglion cells expressed moderate to strong irAMY. Reverse transcriptase-polymerase chain reaction (RT-PCR) revealed amylin receptor mRNA in the mouse spinal cord, brain stem, cortex, hypothalamus and hippocampus. The nociceptive or antinociceptive effects of amylin were evaluated in the tail flick and acetic acid-induced writhing test. Amylin (1-10 µg, i.t.) reduced the number of writhing in a dose-dependent manner. Pretreatment of the mice with the amylin receptor antagonist salmon calcitonin (8-32) [sCT(8-32)]or AC187 by i.t. antagonized the effect of amylin on acetic acid-induced writhing test. Locomotor activity was not significantly modified by amylin injected either i.p. (0.01-1 mg/kg) or i.t. (1-10 µg). Measurement of c-fos mRNA by RT-PCR or proteins by Western blot showed that the levels were up-regulated in the spinal cord of mice in acetic acid-induced visceral pain model and the increase was attenuated by pretreatment with amylin. Pretreatment of sCT[8-32] or AC187 significantly reversed the effect of amylin on c-fos expression in the spinal cord. As the neuronal response to amylin is closely dependent on the molecular property of amylin receptor, the localization, internalization and regulation of the calcitonin and amylin receptor were examined in the second part of the thesis. Immunofluorescence microscopy demonstrated the surface expression of CTRa, and intracellular distribution of RAMP1. Moreover, co-expression of CTRa translocated the RAMP1 to the cell surface and generated the amylin receptor phenotype. Both immunocytochemistry and on cell western analysis showed the internalization of CTRa and amylin receptor (CTRa/RAMP1) stimulated by different agonists, which was partially ß-arrestin dependent. Moreover, RAMP1 did not change the surface expression pattern of CTRa, but co-localized with the receptor with and without agonist treatment. sCT and amylin activated the ERK1/2 in HEK293 cells stably expressing amylin receptors, indicating the involvement of MAPK in amylin receptor signaling cascade. Collectively, these results led us to conclude that 1) irAMY is expressed in dorsal root ganglion neurons with their cell processes projecting to the superficial layers of the dorsal horn, and that the peptide by interacting with amylin receptors in the spinal cord may be antinociceptive; 2) RAMP1 does not change the pattern of CTR cell-surface localization and internalization, but receptor phenotype, presumably through a direct or indirect effect on the ligand-binding site; 3) amylin internalizes the amylin receptor (CTRa/RAMP1 complex); which is partially ß-arrestin dependent. Our studies extend the current knowledge of amylin on the spinal cord and new insight on the cellular and molecular mechanism underlying the antinociceptive effect of amylin. Also we demonstrate for the first time agonist induced-internalization of CTR/RAMP complex and its possible regulation pathway.
Temple University--Theses
APA, Harvard, Vancouver, ISO, and other styles
10

Granholm, Susanne. "The calcitonin gene family of peptides : receptor expression and effects on bone cells." Doctoral thesis, Umeå : Univ, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1571.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Receptor de calcitonina"

1

Tomlinson, Ann Elaine. Characterisation of calcitonin generelated peptide(CGRP) and amylin receptors. Birmingham: Aston University. Department of Civil Engineering, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Eleftheriadis, Theodoros. Vitamin D receptor agonists and kidney diseases. Hauppauge, N.Y: Nova Science Publishers, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Trepiccione, Francesco, and Giovambattista Capasso. Calcium homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0026.

Full text
Abstract:
Ca2+ homeostasis is achieved through a fine balance among three main organs: the intestine, the kidney, and bone. Blood levels of Ca2+ are accurately tuned through the Ca2+ sensing receptors and regulated by several hormones, including parathyroid hormone (PTH), active vitamin D, and calcitonin. The most recent findings in Ca2+ handling are described. The role of the Ca2+ sensing receptor, as well as Klotho, a new player participating in Ca2+ homeostasis, are described. Finally, the effects of diuretics, calcineurin inhibitors, and the link between hypertension and Ca2+ metabolism are reviewed.
APA, Harvard, Vancouver, ISO, and other styles
4

(Editor), David Poyner, Ian Marshall (Editor), and Susan D. Brain (Editor), eds. The CGRP Family: Calcitonin Gene-Related Peptide (CGRP), Amylin, and Adrenomedullin (Molecular Biology Intelligence Unit). Landes Bioscience, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Houillier, Pascal. Magnesium homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0027.

Full text
Abstract:
Magnesium is critically important in the process of energy release. Although most magnesium is stored outside the extracellular fluid compartment, the regulated concentration appears in blood. Urinary magnesium excretion can decrease rapidly to low values when magnesium entry rate into the extracellular fluid volume is low, which has several important implications: cell and bone magnesium do not play a major role in the defence of blood magnesium concentration; while a major role is played by the kidney and especially the renal tubule, which adapts to match the urinary magnesium excretion and net entry of magnesium into extracellular fluid. In the kidney, magnesium is reabsorbed in the proximal tubule, the thick ascending limb of the loop of Henle (TALH), and the distal convoluted tubule (DCT). Magnesium absorption is mainly paracellular in the proximal tubule and TALH, whereas it is transcellular in the DCT. The hormone(s) regulating renal magnesium transport and blood magnesium concentration are not fully understood. Renal tubular magnesium transport is altered by a number of hormones, mainly in the TALH and DCT. Parathyroid hormone, calcitonin, arginine vasopressin, ß-adrenergic agonists, and epidermal growth factor, all increase renal tubular magnesium reabsorption; in contrast, prostaglandin E2 decreases magnesium reabsorption. Non-hormonal factors also influence magnesium reabsorption: it is decreased by high blood concentrations of calcium and magnesium, probably via the action of divalent cations on the calcium-sensing receptor; metabolic acidosis decreases, and metabolic alkalosis increases, renal magnesium reabsorption.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Receptor de calcitonina"

1

Lee, Sang-Min, and Augen A. Pioszak. "Calcitonin Receptor." In Encyclopedia of Signaling Molecules, 648–55. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101586.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Lee, Sang-Min, and Augen A. Pioszak. "Calcitonin Receptor." In Encyclopedia of Signaling Molecules, 1–7. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101586-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Downs Jr., Robert W. "The Calcitonin Receptors." In Peptide Hormone Receptors, edited by M. Y. Kalimi and J. R. Hubbard, 639–62. Berlin, Boston: De Gruyter, 1987. http://dx.doi.org/10.1515/9783110850246-014.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Garelja, Michael L., and Debbie L. Hay. "Calcitonin Family Receptors." In Encyclopedia of Molecular Pharmacology, 1–6. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21573-6_10055-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Hay, Debbie L. "CGRP Receptor Biology: Is There More Than One Receptor?" In Calcitonin Gene-Related Peptide (CGRP) Mechanisms, 13–22. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_131.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Cottrell, Graeme S. "CGRP Receptor Signalling Pathways." In Calcitonin Gene-Related Peptide (CGRP) Mechanisms, 37–64. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/164_2018_130.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Just, Rasmus, John Simms, Sebastian G. B. Furness, Arthur Christopoulos, and Patrick M. Sexton. "Understanding Amylin Receptors." In The calcitonin gene-related peptide family, 41–57. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2909-6_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Goltzman, David. "Characteristics of Brain Calcitonin Receptors." In Neuropeptides and Stress, 199–209. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3514-9_16.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Salvatore, Christopher A., and Stefanie A. Kane. "CGRP Receptor Antagonists for Migraine: Challenges and Promises." In The calcitonin gene-related peptide family, 185–97. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2909-6_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Barwell, James, John Simms, Alex Conner, Debbie Hay, Mark Wheatley, and David Poyner. "Ligand Binding and Activation of the CGRP Receptor." In The calcitonin gene-related peptide family, 23–40. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2909-6_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Receptor de calcitonina"

1

Aldahish, Afaf, Arvind Thakkar, and Girish V. Shah. "Abstract 1890: Calcitonin receptor is required for T-antigen-induced prostate carcinogenesis." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1890.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Aldahish, Afaf, Arvind Thakkar, and Girish V. Shah. "Abstract 1890: Calcitonin receptor is required for T-antigen-induced prostate carcinogenesis." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1890.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Shah, Girish V., Pratistha Tamrakar, Shibu Thomas, Vijaybasker Lakshmikanthan, Parash Parajuli, Seetharama Sathyanarayanajois, Suleiman Bahouth, Alan Fanning, and James Anderson. "Abstract LB-13: Calcitonin receptor-zonnula occludens-1 interaction is critical for calcitonin-induced destabilization of tight junctions and s prostate cancer metastasis." 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-lb-13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Aljameeli, Ahmed, Arvind Thakkar, Shibu Thomas, and Girish V. Shah. "Abstract 3308: A-kinase anchoring protein 2 is required for calcitonin receptor-stimulated invasion of prostate cancer cells." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3308.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Shah, Girish V., Shibu Thomas, Arvind Thakkar, and Alan Fanning. "Abstract 4218: Calcitonin receptor increases invasion of prostate cancer cells by activating cAMP-dependent protein kinase (PKA) and promoting phosphorylation of tight junction proteins." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4218.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Receptor de calcitonina"

1

Halker Singh, Rashmi B., Juliana H. VanderPluym, Allison S. Morrow, Meritxell Urtecho, Tarek Nayfeh, Victor D. Torres Roldan, Magdoleen H. Farah, et al. Acute Treatments for Episodic Migraine. Agency for Healthcare Research and Quality (AHRQ), December 2020. http://dx.doi.org/10.23970/ahrqepccer239.

Full text
Abstract:
Objectives. To evaluate the effectiveness and comparative effectiveness of pharmacologic and nonpharmacologic therapies for the acute treatment of episodic migraine in adults. Data sources. MEDLINE®, Embase®, Cochrane Central Registrar of Controlled Trials, Cochrane Database of Systematic Reviews, PsycINFO®, Scopus, and various grey literature sources from database inception to July 24, 2020. Comparative effectiveness evidence about triptans and nonsteroidal anti-inflammatory drugs (NSAIDs) was extracted from existing systematic reviews. Review methods. We included randomized controlled trials (RCTs) and comparative observational studies that enrolled adults who received an intervention to acutely treat episodic migraine. Pairs of independent reviewers selected and appraised studies. Results. Data on triptans were derived from 186 RCTs summarized in nine systematic reviews (101,276 patients; most studied was sumatriptan, followed by zolmitriptan, eletriptan, naratriptan, almotriptan, rizatriptan, and frovatriptan). Compared with placebo, triptans resolved pain at 2 hours and 1 day, and increased the risk of mild and transient adverse events (high strength of the body of evidence [SOE]). Data on NSAIDs were derived from five systematic reviews (13,214 patients; most studied was ibuprofen, followed by diclofenac and ketorolac). Compared with placebo, NSAIDs probably resolved pain at 2 hours and 1 day, and increased the risk of mild and transient adverse events (moderate SOE). For other interventions, we included 135 RCTs and 6 comparative observational studies (37,653 patients). Compared with placebo, antiemetics (low SOE), dihydroergotamine (moderate to high SOE), ergotamine plus caffeine (moderate SOE), and acetaminophen (moderate SOE) reduced acute pain. Opioids were evaluated in 15 studies (2,208 patients).Butorphanol, meperidine, morphine, hydromorphone, and tramadol in combination with acetaminophen may reduce pain at 2 hours and 1 day, compared with placebo (low SOE). Some opioids may be less effective than some antiemetics or dexamethasone (low SOE). No studies evaluated instruments for predicting risk of opioid misuse, opioid use disorder, or overdose, or evaluated risk mitigation strategies to be used when prescribing opioids for the acute treatment of episodic migraine. Calcitonin gene-related peptide (CGRP) receptor antagonists improved headache relief at 2 hours and increased the likelihood of being headache-free at 2 hours, at 1 day, and at 1 week (low to high SOE). Lasmiditan (the first approved 5-HT1F receptor agonist) restored function at 2 hours and resolved pain at 2 hours, 1 day, and 1 week (moderate to high SOE). Sparse and low SOE suggested possible effectiveness of dexamethasone, dipyrone, magnesium sulfate, and octreotide. Compared with placebo, several nonpharmacologic treatments may improve various measures of pain, including remote electrical neuromodulation (moderate SOE), magnetic stimulation (low SOE), acupuncture (low SOE), chamomile oil (low SOE), external trigeminal nerve stimulation (low SOE), and eye movement desensitization re-processing (low SOE). However, these interventions, including the noninvasive neuromodulation devices, have been evaluated only by single or very few trials. Conclusions. A number of acute treatments for episodic migraine exist with varying degrees of evidence for effectiveness and harms. Use of triptans, NSAIDs, antiemetics, dihydroergotamine, CGRP antagonists, and lasmiditan is associated with improved pain and function. The evidence base for many other interventions for acute treatment, including opioids, remains limited.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Receptor de calcitonina' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography