Journal articles: 'Secreció'

1

Chaine, B. "Secreción uretral masculina." EMC - Tratado de Medicina 25, no. 2 (June 2021): 1–5. http://dx.doi.org/10.1016/s1636-5410(21)45105-6.

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OHNAMI, SHUMPEI, CHIKASHI NAKAYAMA, TOMOKO TERADA, TAMAKI KURODA, and FUJIO ZEZE. "DEVELOPMENT OF A RADIOIMMUNOASSAY (RIA) FOR SECRETIN USING I-125-DESAMINOTYROSYL-β-ALANIN-SECRETIN (I-125-DATA-SECRETIN) AS A LABELLED ANTIGEN." Japanese Journal of Radiological Technology 41, no. 1 (1985): 22–28. http://dx.doi.org/10.6009/jjrt.kj00001371908.

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3

Chahud Isee, Alfredo, and Hernán Espejo Romero. "El débito ácido máximo con estímulo al Histalog Comparación del Débito Ácido Máximo empleando el Histalog y la insulina como estimulantes." Anales de la Facultad de Medicina 50, no. 2 (April 9, 2014): 279. http://dx.doi.org/10.15381/anales.v50i2.5300.

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Los autores estudian la secreción gástrica empleando el Histalog a la cuádruple dosis con dos objetos: primero, determinar el Débito Ácido Máximo o sea la máxima secreción gástrica y segundo, comparar el efecto estimulante del Histalog con el de la hipoglicemia insulínica para lo cual utilizan dos series de pacientes: la primera, compuesta de 170 personas (30 normales, 30 con úlcera gástrica, 71 con úlcera duodenal, 30 con gastritis atrófica y 9 con gastritis superficial), y en los cuales encuentra que la máxima secreción gástrica se determina en el período de los 30' - 90' de estimulación; la segunda serie compuesta de 80 personas (7 normales, 20 ulcerosos gástricos, 40 ulcerosos duodenales y 13 portadores de gastritis atrófica), en los que determinan que la secreción gástrica estimulada por el Histalog es superior a la estimulada por la hipoglicemia insulínica. Concluyen discutiendo el probable mecanismo de acción del Histalog y la acción de la hipoglicemia insulínica y de la misma insulina sobre la secreción gástrica como factor de inhibición de la secreción gástrica que explicaría la diferencia de valores que encuentran.

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Jaworski, Lech. "TAJEMNICA DZIENNIKARSKA I ZASADY ZWALNIANIA Z NIEJ." Studia Iuridica, no. 87 (October 12, 2021): 198–213. http://dx.doi.org/10.31338/2544-3135.si.2020-87.10.

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Journalistic secrecy is professional. In the light of Article 15 of the Press Law (Pr.L.) the journalist is obliged to keep secret the identity of his informants and the authors of the press material, the mail to the editorial office or other material of this nature, if they deserve the right to remain anonymmous. This obligation also applies to other persons employed in editorial offices, press publishing houses and other press organizational units. In addition, it covers any information, the disclosure of which could violate the legitimate interests of third parties. This corresponds to the content of Article 12 § 1 (2) Pr.L., according to which a journalist is obliged to protect the personal rights and interests of informants acting in good faith and other people who trust him or her. Breaking journalistic secrecy is a crime prosecuted ex officio. However, in certain situations journalistic secrecy is excluded (Article 16 Pr.L. and Article 180 of the Code of Criminal Procedure).

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5

&NA;. "Secretin." Reactions Weekly &NA;, no. 1405 (June 2012): 33–34. http://dx.doi.org/10.2165/00128415-201214050-00116.

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6

Chey, William Y., and Ta-Min Chang. "Secretin." Pancreas 43, no. 2 (March 2014): 162–82. http://dx.doi.org/10.1097/01.mpa.0000437325.29728.d6.

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7

Solomon, Travis E., Gabor Varga, Ning Zeng, S. Vincent Wu, John H. Walsh, and Joseph R. Reeve. "Different actions of secretin and Gly-extended secretin predict secretin receptor subtypes." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 1 (January 1, 2001): G88—G94. http://dx.doi.org/10.1152/ajpgi.2001.280.1.g88.

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Only one secretin receptor has been cloned and its properties characterized in native and transfected cells. To test the hypothesis that stimulatory and inhibitory effects of secretin are mediated by different secretin receptor subtypes, pancreatic and gastric secretory responses to secretin and secretin-Gly were determined in rats. Pancreatic fluid secretion was increased equipotently by secretin and secretin-Gly, but secretin was markedly more potent for inhibition of basal and gastrin-induced acid secretion. In Chinese hamster ovary cells stably transfected with the rat secretin receptor, secretin and secretin-Gly equipotently displaced125I-labeled secretin (IC50 values 5.3 ± 0.5 and 6.4 ± 0.6 nM, respectively). Secretin, but not secretin-Gly, caused release of somatostatin from rat gastric mucosal D cells. Thus the equipotent actions of secretin and secretin-Gly on pancreatic secretion appear to result from equal binding and activation of the pancreatic secretin receptor. Conversely, secretin more potently inhibited gastric acid secretion in vivo, and only secretin released somatostatin from D cells in vitro. These results support the existence of a secretin receptor subtype mediating inhibition of gastric acid secretion that is distinct from the previously characterized pancreatic secretin receptor.

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8

Maggs, Peter B., and Raymond Hutchings. "Soviet Secrecy and Non-Secrecy." Russian Review 50, no. 3 (July 1991): 379. http://dx.doi.org/10.2307/131103.

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9

Solomon, Travis E., John H. Walsh, Louis Bussjaeger, Yumei Zong, James W. Hamilton, F. J. Ho, Terry D. Lee, and Joseph R. Reeve. "COOH-terminally extended secretins are potent stimulants of pancreatic secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 4 (April 1, 1999): G808—G816. http://dx.doi.org/10.1152/ajpgi.1999.276.4.g808.

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Posttranslational processing of preprosecretin generates several COOH-terminally extended forms of secretin and α-carboxyl amidated secretin. We used synthetic canine secretin analogs with COOH-terminal -amide, -Gly, or -Gly-Lys-Arg to examine the effects of COOH-terminal extensions of secretin on bioactivity and detection in RIA. Synthetic products were purified by reverse-phase and ion-exchange HPLC and characterized by reverse-phase isocratic HPLC and amino acid, sequence, and mass spectral analyses. Secretin and secretin-Gly were noted to coelute during reverse-phase HPLC. In RIA using eight different antisera raised against amidated secretin, COOH-terminally extended secretins had little or no cross-reactivity. Bioactivity was assessed by measuring pancreatic responses in anesthetized rats. Amidated canine and porcine secretins were equipotent. Secretin-Gly and secretin-Gly-Lys-Arg had potencies of 81 ± 9% ( P > 0.05) and 176 ± 13% ( P < 0.01), respectively, compared with amidated secretin, and the response to secretin-Gly-Lys-Arg lasted significantly longer. These data demonstrate that 1) amidated secretin and secretin-Gly are not separable under some chromatographic conditions, 2) current RIA may not detect bioactive COOH-terminally extended forms of secretin in tissue extracts or blood, and 3) the secretin receptor mediating stimulation of pancreatic secretion recognizes both amidated and COOH-terminally extended secretins.

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10

Tam, Janice K. V., Leo T. O. Lee, Jun Jin, and Billy K. C. Chow. "MOLECULAR EVOLUTION OF GPCRS: Secretin/secretin receptors." Journal of Molecular Endocrinology 52, no. 3 (June 2014): T1—T14. http://dx.doi.org/10.1530/jme-13-0259.

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In mammals, secretin is a 27-amino acid peptide that was first studied in 1902 by Bayliss and Starling from the extracts of the jejunal mucosa for its ability to stimulate pancreatic secretion. To date, secretin has only been identified in tetrapods, with the earliest diverged secretin found in frogs. Despite being the first hormone discovered, secretin's evolutionary origin remains enigmatic, it shows moderate sequence identity in nonmammalian tetrapods but is highly conserved in mammals. Current hypotheses suggest that although secretin has already emerged before the divergence of osteichthyans, it was lost in fish and retained only in land vertebrates. Nevertheless, the cognate receptor of secretin has been identified in both actinopterygian fish (zebrafish) and sarcopterygian fish (lungfish). However, the zebrafish secretin receptor was shown to be nonbioactive. Based on the present information that the earliest diverged bioactive secretin receptor was found in lungfish, and its ability to interact with both vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide potently suggested that secretin receptor was descended from a VPAC-like receptor gene before the Actinopterygii–Sarcopterygii split in the vertebrate lineage. Hence, secretin and secretin receptor have gone through independent evolutionary trajectories despite their concurrent emergence post-2R. A functional secretin–secretin receptor axis has probably emerged in the amphibians. Although the pleiotropic actions of secretin are well documented in the literature, only limited information of its physiological functions in nonmammalian tetrapods have been reported. To decipher the structural and functional divergence of secretin and secretin receptor, functional characterization of the ligand–receptor pair in nonmammals would be the next perspective for investigation.

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11

Sans, Maria Dolors, Maria Eugenia Sabbatini, Stephen A. Ernst, Louis G. D'Alecy, Ichiko Nishijima, and John A. Williams. "Secretin is not necessary for exocrine pancreatic development and growth in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 5 (November 2011): G791—G798. http://dx.doi.org/10.1152/ajpgi.00245.2011.

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Adaptive exocrine pancreatic growth is mediated primarily by dietary protein and the gastrointestinal hormone cholecystokinin (CCK). Feeding trypsin inhibitors such as camostat (FOY-305) is known to induce CCK release and stimulate pancreatic growth. However, camostat has also been reported to stimulate secretin release and, because secretin often potentiates the action of CCK, it could participate in the growth response. Our aim was to test the role of secretin in pancreatic development and adaptive growth through the use of C57BL/6 mice with genetic deletion of secretin or secretin receptor. The lack of secretin in the intestine or the secretin receptor in the pancreas was confirmed by RT-PCR. Other related components, such as vasoactive intestinal polypeptide (VIP) receptors (VPAC1and VPAC2), were not affected. Secretin increased cAMP levels in acini from wild-type (WT) mice but had no effect on acini from secretin receptor-deleted mice, whereas VIP and forskolin still induced a normal response. Secretin in vivo failed to induce fluid secretion in receptor-deficient mice. The pancreas of secretin or secretin receptor-deficient mice was of normal size and histology, indicating that secretin is not necessary for normal pancreatic differentiation or maintenance. When WT mice were fed 0.1% camostat in powdered chow, the pancreas doubled in size in 1 wk, accompanied by parallel increases in protein and DNA. Camostat-fed littermate secretin and secretin receptor-deficient mice had similar pancreatic mass to WT mice. These results indicate that secretin is not required for normal pancreatic development or adaptive growth mediated by CCK.

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12

Guevara D., José, Juan Guevara G., Esther Valencia, Hércules Alcalá, and José Guevara G. "Enterococcus en la Rutina del Trabajo Microbiológico." Anales de la Facultad de Medicina 58, no. 4 (April 7, 2014): 245. http://dx.doi.org/10.15381/anales.v58i4.4655.

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Objetivo.- Enterococcus ha surgido en los últimos años como una bacteria causante de infecciones intrahospitalarias de difícil tratamiento debido a la resistencia que presenta a los antimicrobianos, por esta razón se ha realizado el presente trabajo. Metodología.- En la rutina del trabajo microbiológico se ha empleado medios selectivos para su aislamiento, métodos diferenciales para identificar la especie y su susceptibilidad a los antimicrobianos, empleando el método de disco-difusión estandarizado. Resultados.- Entre Marzo y Noviembre de 1996 se aislaron 113 cepas de Enterococcus, procediendo el 65,4% de secreción vaginal y el resto de otras muestras tales como semen, orina, secreción faríngea, líquido ascítico, esputo, lesiones dérmicas, secreción prostática y secreción uretral. El 88,5% fueron E. faecalis y el resto E. faeccium, E. pseudoavium, E. avium, E. durans y E. raffinosus. En el antibiograma se empleó 13 antimicrobianos y 2 combinaciones con inhibidores de betalactamasa y el 97,3% de los Enterococcus fueron sensibles a la ampicilina. Conclusión.- Los Enterococcus aislados son hasta el presente poco resistentes a la ampicilina.

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13

Fernández Merjildo, Diana, Coralith García Apac, Jaime Zegarra Piérola, and Luis Granados Bullon. "Susceptibilidad antimicrobiana en aislamientos de secreción endotraqueal en la unidad de cuidados intensivos de un hospital nacional de Lima, 2016." Revista Medica Herediana 28, no. 4 (December 21, 2017): 236. http://dx.doi.org/10.20453/rmh.v28i4.3223.

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Objetivos: Determinar la frecuencia de microorganismos y el patrón de susceptibilidad antimicrobiana en aislamientos de cultivos de secreción endotraqueal en la unidad de cuidados intensivos de un hospital nacional de Lima. Material y métodos: Estudio observacional, descriptivo. Se incluyeron 195 cultivos positivos de secreción endotraqueal de pacientes en ventilación mecánica durante el periodo enero a diciembre del 2016. Resultados: Acinetobacter sp. fue la bacteria más frecuentemente aislada (28%) seguido por Pseudomonas aeruginosa (22%) y Klebsiella pneumoniae (14%), Los aislamientos con Acinetobacter sp. presentaron una elevada resistencia a antibióticos carbapenémicos (meropenem 90% eimipenem 88%). Conclusiones: Se identificó una elevada frecuencia de Acinetobacter sp. En cultivos de secreción traqueal en la unidad de cuidados intensivos, con un patrón de multirresistencia.

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14

Wang, Xiaofang, Hong Ye, Christopher J. Ward, Jessica Y. S. Chu, Tatyana V. Masyuk, Nicholas F. LaRusso, Peter C. Harris, Billy K. C. Chow, and Vicente E. Torres. "Insignificant effect of secretin in rodent models of polycystic kidney and liver disease." American Journal of Physiology-Renal Physiology 303, no. 7 (October 1, 2012): F1089—F1098. http://dx.doi.org/10.1152/ajprenal.00242.2012.

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Polycystic kidney (PKD) and liver (PLD) diseases cause significant morbidity and mortality. A large body of evidence indicates that cyclic AMP plays an important role in their pathogenesis. Clinical trials of drugs that reduce cyclic AMP levels in target tissues are now in progress. Secretin may contribute to adenylyl cyclase-dependent urinary concentration and is a major agonist of adenylyl cyclase in cholangiocytes. To investigate the role of secretin in PKD and PLD, we have studied the expression of secretin and the secretin receptor in rodent models orthologous to autosomal recessive ( PCK rat) and dominant ( Pkd2 −/WS25 mouse) PKD; the effects of exogenous secretin administration to PCK rats, PCK rats lacking circulating vasopressin ( PCK di/di), and Pkd2 −/WS25 mice; and the impact of a nonfunctional secretin receptor on disease development in Pkd2 −/WS25 :SCTR −/− double mutants. Renal and hepatic secretin and secretin receptor mRNA and plasma secretin were increased in both models, and secretin receptor protein was increased in the kidneys and liver of Pkd2 −/WS25 mice. However, exogenous secretin administered subcutaneously via osmotic pumps had minimal or negligible effects and the absence of a functional secretin receptor had no influence on the severity of PKD or PLD. Therefore, it is unlikely that by itself secretin plays a significant role in the pathogenesis of PKD and/or PLD.

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15

Bawab, Wafa, Eric Chastre, and Christian Gespach. "Functional and structural characterization of the secretin receptors in rat gastric glands: Desensitization and glycoprotein nature." Bioscience Reports 11, no. 1 (February 1, 1991): 33–42. http://dx.doi.org/10.1007/bf01118603.

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We have documented and characterized the down-regulation of the125I-secretin binding sites and the associated desensitization of the secretin receptor-cAMP system in rat gastric glands. Secretin induced a rapid decrease of the high-affinity125I-secretin binding sites with t1/2=30 min at 37°C. Half-maximal down-regulation and desensitization occurred at 10−9 M secretin, a physiological concentration corresponding to the half-maximal activation of the secretin receptor. The Scatchard parameters of the low-affinity125I-secretin binding sites were unaffected by the pretreatment. This desensitization is heterologous in view of the loss of responsiveness to the truncated glucagon-like peptide 1 (TGLP-1), and pharmacologically selective since the sectetin-related analogue VIP (10−7 M) does not alter the secretin-induced cAMP generation in rat gastric glands. The glycoprotein nature of the secretin receptor has also been demonstrated using WGA-agarose affinity chromatography of the solubilized125I-secretin receptor complex.

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16

Lenzen, R., G. Alpini, and N. Tavoloni. "Secretin stimulates bile ductular secretory activity through the cAMP system." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 4 (October 1, 1992): G527—G532. http://dx.doi.org/10.1152/ajpgi.1992.263.4.g527.

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Although convincing evidence has been obtained to support a ductular origin of secretin choleresis, the precise mechanism of the choleretic effect of the hormone is poorly understood. The present studies were carried out to 1) further clarify the anatomic site at which secretin stimulates bile flow and 2) establish the signal transduction system underlying this effect. To this end, parenchymal and nonparenchymal liver cells, the latter enriched in bile duct cells, were isolated from rats with ductular cell hyperplasia, and the effect of secretin on intracellular formation of both adenosine 3',5'-cyclic monophosphate (cAMP) and inositol phosphates (IPs) was compared with that observed with glucagon and [Tyr10,13,Phe22,Trp25]secretin (SG-secretin). In the pancreas, secretin stimulates both messenger systems, while SG-secretin activates only the cAMP cascade. In isolated hepatocytes, both secretin and SG-secretin failed to increase formation of cAMP and IPs, which were instead activated by glucagon. In isolated bile duct cells, secretin induced formation of both cAMP and IPs, while SG-secretin stimulated solely the cAMP system, as in the pancreas. Glucagon did not stimulate either messenger system in this cell preparation. In vivo, both secretin and SG-secretin stimulated a bicarbonate-rich fluid in rats with bile ductular cell hyperplasia and in normal guinea pigs, which was demonstrated to originate at the distal biliary epithelium. These findings support the existing view that glucagon stimulates canalicular bile flow, while secretin increases secretory activity at the bile ductules and/or ducts. More importantly, they indicate that stimulation of ductular secretory activity by secretin is mediated by the cAMP system and does not involve the IP signal transduction pathway.

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17

Sastre, J., L. Sabater, and L. Aparisi. "Fisiología de la secreción pancreática." Gastroenterología y Hepatología 28 (February 2005): 3–9. http://dx.doi.org/10.1157/13071380.

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18

Claudine, Piérard-Franchimont, and Piérard Gérald E. "Fisiología de la secreción sebácea." EMC - Dermatología 36, no. 1 (2002): 1–7. http://dx.doi.org/10.1016/s1761-2896(02)70110-6.

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19

Chaine, B., and M. Janier. "Secreción uretral en el varón." EMC - Tratado de Medicina 12, no. 4 (January 2008): 1–4. http://dx.doi.org/10.1016/s1636-5410(08)70574-9.

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Chaine, B., and M. Janier. "Secreción uretral en el varón." EMC - Tratado de Medicina 19, no. 1 (March 2015): 1–4. http://dx.doi.org/10.1016/s1636-5410(15)69766-5.

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21

Adriá Micó, José Manuel, and Pilar Ibor Alós. "Varón con secreción nasal persistente." FMC - Formación Médica Continuada en Atención Primaria 15, no. 3 (March 2008): 144–46. http://dx.doi.org/10.1016/s1134-2072(08)70760-6.

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22

Chesterton, G. K. "Secrecy." Chesterton Review 15, no. 4 (1989): 439–40. http://dx.doi.org/10.5840/chesterton1989/199015/164/141.

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23

P., F. "Secrecy." Res: Anthropology and Aesthetics 25 (March 1994): 5–9. http://dx.doi.org/10.1086/resv25n1ms20166887.

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24

Jones, Graham M. "Secrecy." Annual Review of Anthropology 43, no. 1 (October 21, 2014): 53–69. http://dx.doi.org/10.1146/annurev-anthro-102313-030058.

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25

Young, Ruth C., and Joe D. Francis. "SECRECY." Focus on Geography 44, no. 1 (March 1994): 7–9. http://dx.doi.org/10.1111/j.1949-8535.1994.tb00067.x.

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26

Duarte Contreras, Alberto. "Valor semiológico de la secreción mucosa genital de la recién nacida." Revista Colombiana de Obstetricia y Ginecología 44, no. 2 (June 30, 1993): 153–57. http://dx.doi.org/10.18597/rcog.844.

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Toda recién nacida a término debe presentar en los primeros días de vida una secreción mucosa en el vestíbulo vaginal.Esta secreción fisiológica no se encuentra:1- En las recién nacidas prematuras.2- En las recién nacidas a término con malformaciones congénitas que obstruyen la luz del canal genital.3- En recién nacidas a término con atresia o con agenesia del cérvix uterino.Estas malformaciones se pueden diagnosticar o al menos sospechar durante el período neonatal a partir de un "síntoma negativo", la falta de secreción cérvico vaginal en el introito vaginal.Los métodos de diagnóstico son la clínica, la vaginoscopia y la ecografía.El tratamiento es quirúrgico: en algunos casos se debe practicar de urgencia y en otros se pospone para la adolescencia.

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Kim, C. D., P. Li, K. Y. Lee, D. H. Coy, and W. Y. Chey. "Effect of [(CH2NH)4,5]secretin on pancreatic exocrine secretion in guinea pigs and rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 5 (November 1, 1993): G805—G810. http://dx.doi.org/10.1152/ajpgi.1993.265.5.g805.

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[psi 4,5]Secretin was shown to be a secretin receptor antagonist that inhibits secretin-stimulated increase in adenosine 3',5'-cyclic monophosphate in isolated pancreatic acini of the guinea pig. To determine whether it inhibits pancreatic exocrine secretion in vivo, we have studied the effect of [psi 4,5]secretin on the pancreatic secretion stimulated by secretin in anesthetized guinea pigs and rats. In basal state, [psi 4,5]secretin given intravenously for 2 or 3 h in varying doses of 1.6-32.7 nmol.kg-1.h-1 dose dependently increased pancreatic secretion of both fluid and bicarbonate during the 1st h, but it returned gradually to basal level within 2 or 3 h. On the other hand, [psi 4,5]secretin significantly inhibited the pancreatic secretion stimulated by either exogenous or endogenous secretin in a dose-related manner. The inhibitory effect of [psi 4,5]secretin in guinea pigs was greater than that in rats. However, it did not completely block the secretin-stimulated pancreatic secretion, whereas a rabbit antisecretin serum suppressed it completely. We conclude that 1) in the unstimulated state, [psi 4,5]secretin is a partial agonist of pancreatic exocrine secretion of both fluid and bicarbonate; and 2) when pancreatic secretion is stimulated by secretin, unlike an antisecretin serum, it is a partial inhibitor in intact guinea pigs and rats.

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&NA;. "Secretin - Repligen." Drugs in R & D 3, no. 3 (2002): 217–19. http://dx.doi.org/10.2165/00126839-200203030-00018.

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Christ, Andreas, Baseli Werth, Pius Hildebrand, Klaus Gyr, Georg A. Stalder, and Christoph Beglinger. "Human secretin." Gastroenterology 94, no. 2 (February 1988): 311–16. http://dx.doi.org/10.1016/0016-5085(88)90417-9.

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30

Caligiuri, Alessandra, Shannon Glaser, Rebecca E. Rodgers, Jo Lynne Phinizy, Willie Robertson, Emanuela Papa, Massimo Pinzani, and Gianfranco Alpini. "Endothelin-1 inhibits secretin-stimulated ductal secretion by interacting with ETA receptors on large cholangiocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 4 (October 1, 1998): G835—G846. http://dx.doi.org/10.1152/ajpgi.1998.275.4.g835.

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We studied the expression of endothelin-1 (ET-1) receptors (ETA and ETB) and the effects of ET-1 on cholangiocyte secretion. The effects of ET-1 on cholangiocyte secretion were assessed in normal and bile duct-ligated (BDL) rats by measuring 1) basal and secretin-induced choleresis in vivo, 2) secretin receptor gene expression and cAMP levels in small and large cholangiocytes, and 3) luminal expansion in response to secretin in intrahepatic bile duct units (IBDU). ETA and ETB receptors were expressed by small and large cholangiocytes. ET-1 had no effect on basal bile flow or bicarbonate secretion in normal or BDL rats but decreased secretin-induced bicarbonate-rich choleresis in BDL rats. ET-1 decreased secretin receptor gene expression and secretin-stimulated cAMP synthesis in large cholangiocytes and secretin-induced luminal expansion in IBDU from normal or BDL rats. The inhibitory effects of ET-1 on secretin-induced cAMP synthesis and luminal duct expansion were blocked by specific inhibitors of the ETA (BQ-610) receptor. ET-1 inhibits secretin-induced ductal secretion by decreasing secretin receptor and cAMP synthesis, two important determinants of ductal secretion.

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Velmurugan, Sathya, Paula J. Brunton, Gareth Leng, and John A. Russell. "Circulating Secretin Activates Supraoptic Nucleus Oxytocin and Vasopressin Neurons via Noradrenergic Pathways in the Rat." Endocrinology 151, no. 6 (March 23, 2010): 2681–88. http://dx.doi.org/10.1210/en.2009-1440.

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Secretin is a 27-amino acid brain-gut peptide from duodenal S-cells. We tested the effects of systemic administration of secretin to simulate its postprandial release on neuroendocrine neurons of the supraoptic nucleus (SON) in urethane-anesthetized female rats. Secretin dose-dependently increased the firing rate of oxytocin neurons, more potently than cholecystokinin, and dose-dependently increased plasma oxytocin concentration. The effect of secretin on SON vasopressin neurons was also predominantly excitatory, in contrast to the inhibitory actions of cholecystokinin. To explore the involvement of noradrenergic inputs in secretin-induced excitation, benoxathian, an α1-adrenoceptor antagonist, was infused intracerebroventricularly. Benoxathian intracerebroventricular infusion blocked the excitation by secretin of both oxytocin and vasopressin neurons. To test the role of local noradrenaline release in the SON, benoxathian was microdialyzed onto the SON. The basal firing rate of oxytocin neurons was slightly reduced and the secretin-induced excitation was attenuated during benoxathian microdialysis. Hence, noradrenergic pathways mediate the excitation by systemic secretin of oxytocin neurons via α1-adrenoceptors in the SON. As both systemic secretin and oxytocin are involved in regulating gastrointestinal functions and natriuresis, systemically released secretin might act partly through oxytocin.

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Hernandez, Victor O. Fuentes. "La producción lechera, el stres y la fertilidad." Brazilian Journal of Animal and Environmental Research 5, no. 3 (July 30, 2022): 2948–55. http://dx.doi.org/10.34188/bjaerv5n3-028.

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Se discute la interacción de los opioides endógenos con la reproducción en bovinos y los experimentos previos para relacionar las endorfinas con la secreción de LH y FSH a nivel Hipotalámico. Se discute el uso de antagonistas opioides para estudiar la interacción de las endorfinas con la secreción de gonadotrofinas. Se discute el uso de antagonistas opioides en diferentes dosis. Se hace énfasis en la presencia de diferentes receptores opioides endógenos y su interacción con antagonistas opioides en función de la dosis administrada. Se discute el uso de pequeñas dosis de antagonistas opioides para de manera selectiva interferir con receptores endógenos micro, relacionados íntimamente con su función sobre la secreción de GnRH hipotalámica, efecto que permite contemplar el uso de antagonistas opioides para el tratamiento de quistes foliculares en vacas repetidoras.

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Fried, M., A. S. Fink, L. R. DeSouza, C. Beglinger, K. Gyr, and J. H. Meyer. "Release of secretin along the canine small intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 255, no. 1 (July 1, 1988): G7—G11. http://dx.doi.org/10.1152/ajpgi.1988.255.1.g7.

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The profile of secretin release along the entire canine small intestine was examined in this study. Four equal loops of the small gut, from the duodenal bulb to the ileocoecal valve, were isolated. In eight anesthetized dogs the four segments were perfused for 40 min each in random order with an acidified (pH 2.5) emulsion of 20 mM oleic acid. In four dogs control experiments were performed using 0.15 M saline. Secretin release in portal venous blood was measured by a sensitive radioimmunoassay. Although secretin was mainly released in the first quarter of the small intestine (310 pM X 40 min), large amounts of secretin, 33% of the total secretin release, were liberated in the second quarter of the small intestine (164 pM X 40 min). Minute amounts of secretin (23 pM X 40 min) were released in the third quarter, whereas perfusion of the last quarter of the small gut failed to release secretin. We conclude that the major portion of secretin is releasable in the first quarter of the small gut. High amounts of secretin can be liberated in the second quarter of intestine, an area that is probably never exposed to pH below 4.5 (the known threshold for secretin release by acid), but is still exposed to fatty acids (other releasers of secretin).

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Steiner, T. S., A. W. Mangel, D. C. McVey, and S. R. Vigna. "Secretin receptors mediating rat forestomach relaxation." American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no. 5 (May 1, 1993): G863—G867. http://dx.doi.org/10.1152/ajpgi.1993.264.5.g863.

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Frozen sections of the rat stomach were incubated with 125I-labeled porcine secretin, and then secretin binding sites were localized by autoradiography. Saturable binding was observed only in the muscularis externa (circular and longitudinal smooth muscle layers) of the proximal nonglandular forestomach. Saturable binding was quantitated by densitometry. 125I-porcine secretin bound to a single class of high-affinity binding sites with a dissociation constant of 0.6 nM. Porcine and rat secretins were nearly equipotent in inhibiting saturable 125I-porcine secretin binding, and vasoactive intestinal polypeptide, peptide histidine-isoleucine, and glucagon were much weaker. Carbachol (100 microM) stimulated a sustained increase in tension in forestomach muscle in vitro, and porcine secretin caused relaxation of this stimulated contraction. We conclude that rat forestomach smooth muscle expresses a high-affinity specific secretin binding site that mediates relaxation. This putative secretin receptor may mediate some of the actions of secretin on gastric motility.

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Chang, Cecilia H., William Y. Chey, Brian Erway, David H. Coy, and Ta-Min Chang. "Modulation of secretin release by neuropeptides in secretin-producing cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 2 (August 1, 1998): G192—G202. http://dx.doi.org/10.1152/ajpgi.1998.275.2.g192.

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Nerve fibers containing bombesin (BB)/gastrin-releasing polypeptide (GRP), pituitary adenylate cyclase-activating polypeptide (PACAP), vasoactive intestinal polypeptide (VIP), or galanin are known to innervate the mucosa of the upper small intestine. Both BB/GRP and PACAP have been shown to elicit secretin secretion in vivo. We studied whether the above-mentioned neuropeptides can act directly on secretin-producing cells, including the murine neuroendocrine cell line STC-1 and a secretin cell-enriched preparation isolated from rat upper small intestinal mucosa. Secretin release from both cell types was stimulated by various agents known to elicit secretin release and by the neuropeptides BB, GRP, and PACAP, suggesting a comparable response between the two cell preparations. The effects of neuropeptides were further studied in STC-1 cells. BB, GRP, and PACAP stimulated secretin release time and concentration dependently. VIP also stimulated secretin release concentration dependently. Stimulation by BB/GRP or PACAP was accompanied by elevation of inositol-1,4,5-trisphosphate (IP3) or cAMP, respectively. The stimulatory effect of PACAP on secretin release was synergistically enhanced by BB without any synergistic increase in IP3 or cAMP production, suggesting cross talk between different signal transduction pathways downstream of the production of these two second messengers. The L-type Ca2+ channel blocker diltiazem (10 μM) and the Ca2+ chelator EGTA (1 mM) significantly inhibited BB-stimulated secretin release by 64% and 59%, respectively, and inhibited PACAP-stimulated release by 75% and 55%, respectively. The protein kinase A-specific inhibitor Rp-cAMPS (100 μM) also inhibited both BB- and PACAP-stimulated secretin release by 30% and 62%, respectively. Galanin inhibited BB- and PACAP-stimulated secretin release and production of second messengers in a concentration-dependent and pertussis toxin-sensitive manner. These results suggested that the neuropeptides BB/GRP, PACAP, VIP, and galanin can modulate secretin release in secretin-producing cells and that STC-1 cells can serve as a useful model for studying the cellular mechanism of secretin secretion elicited by luminal secretagogues and neuropeptides.

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Trimble, E. R., R. Bruzzone, T. J. Biden, and R. V. Farese. "Secretin induces rapid increases in inositol trisphosphate, cytosolic Ca2+ and diacylglycerol as well as cyclic AMP in rat pancreatic acini." Biochemical Journal 239, no. 2 (October 15, 1986): 257–61. http://dx.doi.org/10.1042/bj2390257.

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Previous studies have shown that the dose-response relationship for secretin-stimulated cyclic AMP accumulation is different from that for secretin-stimulated enzyme secretion in the rat exocrine pancreas. Here we show that secretin concentrations of 10(-10) M and higher stimulated a rise in cyclic AMP levels, with maximum effect on cyclic AMP accumulation being achieved already with 10(-8) M-secretin. However, at this concentration of secretin, enzyme secretion rates were approximately half-maximal. Unexpectedly, at concentrations of secretin greater than 10(-8) M there was evidence suggestive of phosphatidylinositol bisphosphate hydrolysis with rapid increases in inositol trisphosphate, cytosolic free calcium and diacylglycerol content of rat pancreatic acini. Furthermore, there was a dose-response relationship among secretin concentration (in the range 10(-8) M-2 × 10(-6) M), increases in inositol trisphosphate and increases in cytosolic free calcium ([Ca2+]i). Contrary to what has been previously believed, these results clearly indicate that in rat pancreatic acini secretin not only stimulates cyclic AMP accumulation but also raises inositol trisphosphate, [Ca2+]i and diacylglycerol. Thus, two second messenger systems may play a role in the regulation of secretin-induced amylase release.

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Lam, Ian P. Y., Leo T. O. Lee, Hueng-Sik Choi, Gianfranco Alpini, and Billy K. C. Chow. "Bile acids inhibit duodenal secretin expression via orphan nuclear receptor small heterodimer partner (SHP)." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 1 (July 2009): G90—G97. http://dx.doi.org/10.1152/ajpgi.00094.2009.

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Small heterodimer partner (SHP) is an orphan nuclear receptor in which gene expression can be upregulated by bile acids. It regulates its target genes by repressing the transcriptional activities of other nuclear receptors including NeuroD, which has been shown to regulate secretin gene expression. Here, we evaluated the regulation on duodenal secretin gene expression by SHP and selected bile acids, cholic acid (CA) and chenodeoxycholic acid (CDCA). In vitro treatment of CDCA or fexaramine elevated the SHP transcript level and occupancy on secretin promoter. The increase in the SHP level, induced by bile acid treatment or overexpression, reduced secretin gene expression, whereas this gene inhibitory effect was reversed by silencing of endogenous SHP. In in vivo studies, double-immunofluorescence staining demonstrated the coexpression of secretin and SHP in mouse duodenum. Feeding mice with 1% CA-enriched rodent chow resulted in upregulation of SHP and a concomitant decrease in secretin transcript and protein levels in duodenum compared with the control group fed with normal chow. A diet enriched with 5% cholestyramine led to a decrease in SHP level and a corresponding increase in secretin expression. Overall, this study showed that bile acids via SHP inhibit duodenal secretin gene expression. Because secretin is a key hormone that stimulates bile flow in cholangiocytes, this pathway thus provides a novel means to modulate secretin-stimulated choleresis in response to intraduodenal bile acids.

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Jin, H. O., K. Y. Lee, T. M. Chang, W. Y. Chey, and A. Dubois. "Secretin: a physiological regulator of gastric emptying and acid output in dogs." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 4 (October 1, 1994): G702—G708. http://dx.doi.org/10.1152/ajpgi.1994.267.4.g702.

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Secretin has been known to inhibit gastric acid secretion in several species. However, the physiological role of secretin on the postprandial acid output and gastric emptying in an intact stomach remains controversial. In the present study, we reinvestigated the role of secretin in physiological dose range and endogenous secretin on gastric acid secretion and emptying in the stomach without influencing intragastric luminal pH in dogs. In seven conscious dogs with gastric cannulas, a 4% amino acid meal was administered intragastrically, and three different doses of secretin and an antisecretin serum were infused intravenously in each dog on separate days. Gastric emptying and net acid output were measured using a dye dilution technique, and plasma secretin and gastrin were determined by specific radioimmunoassays. After the meal, gastric emptying was exponential: acid output peaked at 25 min, and plasma concentrations of gastrin and secretin peaked at 15 and 60 min, respectively. Intravenous infusion of secretin at 1.25, 2.5, and 5.0 pmol.kg-1.h-1 dose dependently increased plasma levels of the peptide and suppressed postprandial plasma gastrin response and gastric acid output and emptying of the meal. Immunoneutralization of circulating secretin with a rabbit antisecretin serum abolished the postprandial rise of plasma secretin and significantly increased plasma gastrin, and augmented gastric emptying as well as acid output. It is concluded that, in dogs, secretin plays a physiological role in the regulation of gastric emptying and acid output after a liquid amino acid meal and that these effects may be mediated in part by suppression of the release of gastrin.

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Aguado, Paola Isaira Correa, Zimri Cortés Vidauri, Carlos Fernando Aréchiga Flores, Romana Melba Rincón Delgado, Claudia Elisa Valdez Miramontes, Marco Antonio López Carlos, and Ignacio Mejía Haro. "El ciclo reproductivo de la oveja." South Florida Journal of Development 3, no. 6 (December 8, 2022): 6903–29. http://dx.doi.org/10.46932/sfjdv3n6-040.

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La hormona melatonina regula el ciclo reproductivo de la oveja, para que los partos ocurran en primavera y verano, por ser la temporada del año más favorable para la supervivencia de los corderos recién nacidos. La melatonina se produce en la glándula pineal durante las horas de obscuridad del día y ejerce su acción sobre la pars tuberalis (PT) de la hipófisis. El fotoperiodo bajo del otoño e invierno (i.e., pocas horas luz por día) y una mayor secreción de melatonina estimulan al eje hipotalámico-hipofisiario-gonadal (H-H-G) para iniciar la actividad ovárica, comenzar la ciclicidad estral y garantizar la concepción en las ovejas. Generalmente, la gestación se logra durante el otoño e invierno y los partos se presentan durante la primavera. Es decir, las ovejas estarían lactando durante primavera y verano. El anestro de las ovejas se presenta durante los días con mayor número de horas luz por día (primavera-verano). La hormona prolactina (PRL), se secreta durante la lactancia y su producción se incrementa durante los días con mayor cantidad de horas luz por día. Por lo tanto, la secreción de prolactina se comporta de manera inversa a la producción de melatonina. En los días con mayor cantidad de horas luz se reduce la secreción de melatonina en la pars tuberalis (anestro), y se promueve la síntesis de la isoforma del factor de crecimiento vascular endotelial (VEGF) relacionado con la angiogénesis. Aunado a ello, se incrementa la sintesis de taquicininas, sustancia P y neuroquinina A en la pars tuberalis y se estimula la síntesis de prolactina en la pars distalis (PD) de la hipófisis. Al disminuir la melatonina, se incrementa la expresión del factor de transcripción Eya3, el cual a través de la secreción de tirotropina (TSH) reduce la liberación episódica de GnRH y probablemente se relacione con el establecimiento de la retroalimentación negativa del estradiol sobre el hipotálamo para reducir la secreción de GnRH, efecto estimulado por la dopamina. El VGFA también inhibe la expresión del gen FSH, con lo que se inactiva al eje H-H-G. La prolactina, junto con la dopamina, reducen el efecto de la GnRH sobre la secreción de ambas gonadotropinas: hormona folículo-estimulante (FSH) y hormona luteinizante (LH), por parte de la adenohipófisis.

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Lu, Y., and C. Owyang. "Secretin at physiological doses inhibits gastric motility via a vagal afferent pathway." American Journal of Physiology-Gastrointestinal and Liver Physiology 268, no. 6 (June 1, 1995): G1012—G1016. http://dx.doi.org/10.1152/ajpgi.1995.268.6.g1012.

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Secretin is an important modulator of gastric motility. In this study, we investigated the site(s) and mechanism(s) of action of secretin to inhibit gastric motility, using an in vivo rat model. Intragastric pressure response to graded doses of secretin was recorded in anesthetized rats by a balloon attached to a catheter passed through an incision in the duodenum into the body of the stomach. The intragastric pressure was set at 10 cmH2O with balloon distension. Intravenous infusion of secretin (1.4, 2.8, 5.6, 11.2, and 22.4 pmol.kg-1.h-1) decreased intragastric pressure in a dose-dependent manner. The threshold dose was 2.8 pmol.kg-1.h-1, and the effective dose at 50% (ED50) was 5.6 pmol.kg-1.h-1, which produced physiological levels of plasma secretin. Pretreatment with hexamethonium (10 mg/kg) markedly reduced gastric motor response to secretin (5.6 pmol.kg-1.h-1). Bilateral truncal vagotomy also significantly diminished gastric motor responses to secretin. In contrast, secretin (5.6 pmol.kg-1.h-1) had no effect on gastric contraction evoked by electrical vagal stimulation (1.25-5 Hz) or carbachol (10(-6) to 3 x 10(-5) M). These observations indicate that physiological concentrations of secretin act via stimulation of presynaptic cholinergic neurons in a vagally mediated pathway. In subsequent studies, we demonstrated that perivagal treatment 4 days before with the sensory neurotoxin, capsaicin, abolished gastric motor response to secretin but did not affect contraction evoked by electrical vagal stimulation. Similarly, we also showed that gastroduodenal application of capsaicin for 30 min also markedly reduced gastric response to secretin. These observations indicate that physiological doses of secretin act on vagal afferent pathways originating from the gastroduodenal mucosa to induce gastric relaxation.

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Voskamp, D., and H. C. Beyerman. "BIOLOGICAL POTENCY AND CHROMATOGRAPHIC PROPERTIES OF [ASPARTOYL3]-SECRETIN, [β-ASP3]-SECRETIN, AND SECRETIN (4-27):." International Journal of Peptide and Protein Research 18, no. 3 (January 12, 2009): 284–88. http://dx.doi.org/10.1111/j.1399-3011.1981.tb02982.x.

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Pérez, Carlos Ortega, Noé Rigoberto Rivera, Xochitl Sandoval López, and Carlos Enrique Hernández Ávila. "Muestra de saliva para diagnóstico de SARS-CoV-2 por RT-qPCR en población ambulatoria." Alerta, Revista científica del Instituto Nacional de Salud 4, no. 2 (May 20, 2021): 38–45. http://dx.doi.org/10.5377/alerta.v4i2.11476.

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Introducción. En El Salvador a la fecha, la técnica utilizada por el sistema nacional de salud para la obtención de la muestra para realizar PCR para SARS-CoV-2 es hisopado nasofaríngeo, diferentes investigadores han descrito la muestra de saliva como una muestra biológica útil para la detección de SARS-Cov-2, por esta razón se observa la oportunidad de aplicarla como una alternativa disponible para el diagnóstico de esta enfermedad. Objetivo. Evaluar la autotoma de muestra de saliva y secreción nasofaríngea por pacientes no hospitalizados como una alternativa de menor riesgo biológico y de menor costo que los hisopados nasofaríngeos convencionales. Metodología. Se procesaron las muestras de una mezcla de saliva y secreción faríngea obtenida por carraspeo autotomada por el paciente; la amplificación se realizó por RT-qPCR de los genes E y RdRp. Las muestras positivas se reevaluaron desde su extracción para confirmar la estabilidad de material genético de SARS-CoV-2 en la saliva y secreción nasofaríngea. Resultados. El promedio de resultados positivos por cada 100 pruebas fue de 7,05 por cada 100 pruebas COVID-19 realizadas con hisopado, este resultado es similar al 8 % de positividad durante el mismo período de estudio utilizando como muestra saliva y secreción faríngea autotomada por el paciente. Las ocho muestras positivas mantuvieron su reactividad para los genes E y RdRp al primer, tercer y quinto mes posdiagnóstico inicial para los dos protocolos utilizados. De igual forma, los eluidos de ARN positivos iniciales se mantuvieron positivos al primer, tercer y quinto mes. Conclusión. La muestra de saliva y secreción faríngea y su utilización para el diagnóstico de infección por SARS-CoV-2 podría ser una alternativa de bajo costo, no invasiva, al menos de igual utilidad que el hisopado nasofaríngeo para el estudio de población sintomática ambulatoria o con exposición a nivel comunitario.

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Kwon, Hyeok Y., Ta-Min Chang, Kae Y. Lee, and William Y. Chey. "Vagus nerve modulates secretin binding sites in the rat forestomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 4 (April 1, 1999): G1052—G1058. http://dx.doi.org/10.1152/ajpgi.1999.276.4.g1052.

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Secretin is well known for its inhibitory action on gastric motility. It has been reported that secretin in a physiological dose inhibits gastric motility through mediation by the vagal afferent pathway. Secretin also elicited relaxation of carbachol-stimulated rat forestomach muscle strips by binding to its receptors, suggesting a direct action on this peripheral tissue. We hypothesized that vagal input may affect the action of secretin by modulating the level of secretin receptor in the forestomach. Several treatments, including vagal ligation, vagotomy, perivagal application of capsaicin or colchicine, intravenous infusion of tetrodotoxin, and intraperitoneal injection of atropine, were performed to investigate their effects on secretin receptor binding to forestomach membranes. Specific binding of125I-labeled secretin to forestomach membranes was significantly decreased (45%) by vagal ligation, vagotomy (50%), or perivagal colchicine treatment (40%). On the contrary, specific binding of125I-secretin was not affected by perivagal capsaicin treatment, intravenous infusion of tetrodotoxin, or intraperitoneal injection of atropine. By Scatchard analysis of the binding data, the capacity of the high-affinity binding sites in forestomach membranes was found to decrease significantly after vagal ligation compared with membranes from the sham-operated group. However, the affinity at the high-affinity binding sites, the binding parameters of the low-affinity binding sites, and binding specificity were not changed. Vagal ligation but not perivagal capsaicin treatment reduced the inhibitory effect of secretin on bethanechol-stimulated contraction of isolated forestomach muscle strips, causing a right shift in the dose-response curve. These results suggest that vagal input through axonal transport plays a significant role on secretin action by modulating the capacity of secretin binding sites (but not affinity or specificity), at least in rat forestomach.

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García Lucero, Orlando, and Rolando Figueroa Barrios. "Estudio de la secreción gástrica en la cirrosis hepática." Anales de la Facultad de Medicina 50, no. 2 (April 9, 2014): 209. http://dx.doi.org/10.15381/anales.v50i2.5296.

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Se estudia la secreción gástrica con la máxima estimulación histamínica en un grupo de 31 pacientes con cirrosis hepática, comparando los resultados con los valores encontrados en un grupo de personas normales llamados controles y en otro grupo con úlcera duodenal. Los pacientes con cirrosis hepática secretan muy poco ácido clorhídrico, tanto en condiciones basales como después de la máxima estimulación histamínica, siendo el DAB 1.77 ± 1.66 mEq de HCl total, y el DAM 7.13 ± 5.35 mEq. Esta hiposecreción gástrica no depende del grado de descompensación hepática. Es posible que se deba a un reducido número de células parietales, por una gastritis crónica atrófica consecuente a la acción tóxica del alcohol, de la malnutrición o de algún otro factor. Sería interesante estudiar la secreción gástrica en alcohólicos sin cirrosis y en malnutridos sin cirrosis, para explicar Este hallazgo. En 24 cirróticos sometidos a estudio radio lógico digestivo alto se encontró 20% con úlcera duodena!, incidencia mayor que la existente para la población general (10). La secreción gástrica en los cirróticos con úlcera duodenal fue más alta que en los sin úlcera, y estadísticamente semejante a la secreción de los controles y ulcerosos duodenales. El DAB fue 9.51 ± 6.17 y el DAM: 29.23 ± 4.69 mEq de HCl total. Es necesario ampliar el estudio con mayor número de casos pera obtener conclusiones más definitivas.

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Simancas-Escorcia, Victor Hugo, Antonio Díaz-Caballero, and Adel Martinez-Martinez. "Localización inmunohistoquímica de receptores de potencial transitorio tipo vaniloide 5 en ameloblastos de ratones Swiss." Revista MVZ Córdoba 27, no. 3 (September 1, 2022): e2681. http://dx.doi.org/10.21897/rmvz.2681.

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Objetivo. Determinar la localización de los receptores de potencial transitorio de tipo vaniloide-5 (TRPV5) en los ameloblastos de ratones Swiss. Materiales y métodos. Estudio experimental In vitro donde fueron analizados cortes en parafina de 12 incisivos de crecimiento continuo de ratones machos Swiss salvajes de 7 días de nacidos. Las etapas del desarrollo de la formación del esmalte dental se identificaron por medio de la coloración hematoxilina-eosina. La inmunodetención de los receptores de potencial transitorio de tipo vaniloide-5 fue efectuada por medio del anticuerpo primario policlonal anti-TRPV5. Las observaciones se llevaron a cabo mediante un microscopio Leica DM 500. Resultados. Se identificaron las diferentes etapas implicadas en la formación del esmalte dental, entre ellas, la etapa de secreción y maduración. En ellas, se evidenció que los ameloblastos eran células alargadas con núcleos ovalados en posición proximal y con áreas manifiestamente desarrolladas de secreción medial y distal. Fue visualizado un inmunomarcaje de TRPV5 en la membrana plasmática y citoplasma de los ameloblastos de secreción y maduración de todos los ratones analizados. Los TRPV5 también fueron inmunolocalizado en los odontoblastos, endotelio vascular y células pulpares. Conclusiones. Los receptores de potencial transitorio de tipo vaniloide-5 se localizan en los ameloblastos de secreción y maduración de ratones Swiss. Particularmente, los TRPV5 son inmunodetectados en los odontoblastos, endotelio vascular y células de la pulpa dental.

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Padmanaban, Gowtham, M. K. Kayalvizhi, Kalyanasundaram Kasiviswanathan, Ruckmani Arunachalam, and Vishnu Kumar Urkavalan. "Neuroprotective effect of secretin in chronic hypoxia induced neurodegeneration in rats." International Journal of Basic & Clinical Pharmacology 6, no. 2 (January 28, 2017): 298. http://dx.doi.org/10.18203/2319-2003.ijbcp20170318.

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Background: Hypoxia is a condition in any stage in the delivery of oxygen to cells which include decreased partial pressures of oxygen, less diffusion of oxygen in the lungs, insufficient hemoglobin, inefficient blood flow to the end tissue, and breathing rhythm. Secretin is an amino acid which plays proper functioning of gastro intestinal system.Methods: The current study was conducted to evaluvate the effect of exogenously administrated secretin on chronic hypoxic damage of brain in rat model. Experimental design consists of control animals, Control animals + secretin hypoxia exposed animals; hypoxia exposed animals +secretin (20ng/kg.bw).Results: The results of this study point to a possible role of Secretin as neuroprotectant.Conclusions: Further research on secretin needs to be conducted in order to confirm the deductions made by this study.

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UCHIYAMA, MIKIO, TAKASHI SATO, HIROSHI YOSHINO, YUTAKA TSUCHIYA, TOSHIRO TSUDA, MASAYUKI KONISHI, MASAHIKO TSUJII, YOSHIHIKO HISATAKE, and ATSUSHI KOIWA. "Studies on secretin. I. Synthesis of completely protected secretin." CHEMICAL & PHARMACEUTICAL BULLETIN 33, no. 5 (1985): 1990–99. http://dx.doi.org/10.1248/cpb.33.1990.

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Gafvelin, Guro, Mats Carlquist, and Viktor Mutt. "A proform of secretin with high secretin-like bioactivity." FEBS Letters 184, no. 2 (May 20, 1985): 347–52. http://dx.doi.org/10.1016/0014-5793(85)80636-0.

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Gong, Peixian, J. R. Reeve, J. H. Walsh, Yumei Zong, F. J. Ho, and T. E. Solomon. "Comparison of secretin-NH2, secretin-gly, and secretin-OH on pancreatic and gastric secretion indicates the existence of a secretin receptor subtype." Gastroenterology 114 (April 1998): A1146. http://dx.doi.org/10.1016/s0016-5085(98)84663-5.

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Wheeler, M. B., J. Nishitani, A. M. Buchan, A. S. Kopin, W. Y. Chey, T. M. Chang, and A. B. Leiter. "Identification of a transcriptional enhancer important for enteroendocrine and pancreatic islet cell-specific expression of the secretin gene." Molecular and Cellular Biology 12, no. 8 (August 1992): 3531–39. http://dx.doi.org/10.1128/mcb.12.8.3531-3539.1992.

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It is well established that the gene encoding the hormone secretin is expressed in a specific enteroendocrine cell, the S cell. We now show that the secretin gene is transiently expressed in insulin-producing B cells of the developing pancreatic islets in addition to the intestine. Furthermore, secretin is produced by most established islet cell lines. In order to identify and characterize the regulatory elements within the secretin gene that control tissue-specific expression, we have introduced secretin reporter gene constructions into the secretin-producing HIT and STC-1 cell lines as well as the nonexpressing INR1-G9 glucagonoma line. Analysis of deletion mutants revealed that sequences between 174 and 53 bp upstream from the transcriptional start site are required for maximal expression in secretin-producing cells. This positive element functioned independently of position and orientation. Further deletions into the enhancer resulted in a stepwise loss of transcriptional activity, suggesting the presence of several discrete control elements. The sequence CAGCTG within the secretin enhancer closely resembles that of the core of the B-cell-specific enhancer in the insulin gene. Point mutations introduced into this putative element led to greater than 85% reduction in transcriptional activity. Gel mobility shift assays suggested that a factor in B cells closely related or identical to proteins that bind to the insulin enhancer interacts with the CAGCTG motif in the secretin gene.

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Journal articles on the topic 'Secreció'

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