Base de dados : MEDLINE
Pesquisa : D06.472.699.327.740.880 [Categoria DeCS]
Referências encontradas : 12204 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 1221 ir para página                         

  1 / 12204 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29305326
[Au] Autor:Fernandez MO; Bourguignon NS; Arocena P; Rosa M; Libertun C; Lux-Lantos V
[Ad] Endereço:Consejo Nacional de Investigaciones Cientificas y Técnicas, Instituto de Biología y Medicina Experimental, Vuelta de Obligado 2490, CABA, Argentina. Electronic address: mfernandez@dna.uba.ar.
[Ti] Título:Neonatal exposure to bisphenol A alters the hypothalamic-pituitary-thyroid axis in female rats.
[So] Source:Toxicol Lett;285:81-86, 2018 Mar 15.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Bisphenol A (BPA) is a component of polycarbonate plastics, epoxy resins and polystyrene found in many common products. Several reports revealed potent in vivo and in vitro effects. In this study we analyzed the effects of the exposure to BPA in the hypothalamic-pituitary-thyroid axis in female rats, both in vivo and in vitro. Female Sprague-Dawley rats were injected sc from postnatal day 1 (PND1) to PND10 with BPA: 500 µg 50 µl oil (B500), or 50 µg 50 µl (B50), or 5 µg 50 µl (B5). Controls were injected with 50 µl vehicle during the same period. Neonatal exposure to BPA did not modify TSH levels in PND13 females, but it increased them in adults in estrus. Serum T4 was lower in B5 and B500 with regards to Control, whereas no difference was seen in T3. No significant differences were observed in TRH, TSHß and TRH receptor expression between groups. TSH release from PPC obtained from adults in estrus was also higher in B50 with regard to Control. In vitro 24 h pre-treatment with BPA or E increased basal TSH as well as prolactin release. On the other hand, both BPA and E lowered the response to TRH. The results presented here show that the neonatal exposure to BPA alters the hypothalamic pituitary-thyroid axis in adult rats in estrus, possibly with effects on the pituitary and thyroid. They also show that BPA alters TSH release from rat PPC through direct actions on the pituitary.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/toxicidade
Disruptores Endócrinos/toxicidade
Hipotálamo/efeitos dos fármacos
Fenóis/toxicidade
Hipófise/efeitos dos fármacos
Glândula Tireoide/efeitos dos fármacos
[Mh] Termos MeSH secundário: Envelhecimento/sangue
Envelhecimento/efeitos dos fármacos
Animais
Animais Recém-Nascidos
Células Cultivadas
Relação Dose-Resposta a Droga
Feminino
Hipotálamo/crescimento & desenvolvimento
Hipotálamo/metabolismo
Hipófise/crescimento & desenvolvimento
Hipófise/metabolismo
Ratos Sprague-Dawley
Receptores do Hormônio Liberador da Tireotropina/genética
Receptores do Hormônio Liberador da Tireotropina/metabolismo
Glândula Tireoide/crescimento & desenvolvimento
Glândula Tireoide/metabolismo
Tireotropina/sangue
Tireotropina/genética
Hormônio Liberador de Tireotropina/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Endocrine Disruptors); 0 (Phenols); 0 (Receptors, Thyrotropin-Releasing Hormone); 5Y5F15120W (Thyrotropin-Releasing Hormone); 9002-71-5 (Thyrotropin); MLT3645I99 (bisphenol A)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


  2 / 12204 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28974369
[Au] Autor:Ávila-Mendoza J; Pérez-Rueda E; Urban-Sosa V; Carranza M; Martínez-Moreno CG; Luna M; Arámburo C
[Ad] Endereço:Departamento de Neurobiología Celular y Molecular, Instituto de Neurobiología, Campus Juriquilla, Universidad Nacional Autónoma de México, Querétaro, Qro. 76230, Mexico.
[Ti] Título:Characterization and distribution of GHRH, PACAP, TRH, SST and IGF1 mRNAs in the green iguana.
[So] Source:Gen Comp Endocrinol;255:90-101, 2018 Jan 01.
[Is] ISSN:1095-6840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The somatotropic axis (SA) regulates numerous aspects of vertebrate physiology such as development, growth, and metabolism and has influence on several tissues including neural, immune, reproductive and gastric tract. Growth hormone (GH) is a key component of SA, it is synthesized and released mainly by pituitary somatotrophs, although now it is known that virtually all tissues can express GH, which, in addition to its well-described endocrine roles, also has autocrine/paracrine/intracrine actions. In the pituitary, GH expression is regulated by several hypothalamic neuropeptides including GHRH, PACAP, TRH and SST. GH, in turn, regulates IGF1 synthesis in several target tissues, adding complexity to the system since GH effects can be exerted either directly or mediated by IGF1. In reptiles, little is known about the SA components and their functional interactions. The aim of this work was to characterize the mRNAs of the principal SA components in the green iguana and to develop the tools that allow the study of the structural and functional evolution of this system in reptiles. By employing RT-PCR and RACE, the cDNAs encoding for GHRH, PACAP, TRH, SST and IGF1 were amplified and sequenced. Results showed that these cDNAs coded for the corresponding protein precursors of 154, 170, 243, 113, and 131 amino acids, respectively. Of these, GHRH, PACAP, SST and IGF1 precursors exhibited a high structural conservation with respect to its counterparts in other vertebrates. On the other hand, iguana's TRH precursor showed 7 functional copies of mature TRH (pyr-QHP-NH ), as compared to 4 and 6 copies of TRH in avian and mammalian proTRH sequences, respectively. It was found that in addition to its primary production site (brain for GHRH, PACAP, TRH and SST, and liver for IGF1), they were also expressed in other peripheral tissues, i.e. testes and ovaries expressed all the studied mRNAs, whereas TRH and IGF1 mRNAs were observed ubiquitously in all tissues considered. These results show that the main SA components in reptiles of the Squamata Order maintain a good structural conservation among vertebrate phylogeny, and suggest important physiological interactions (endocrine, autocrine and/or paracrine) between them due to their wide peripheral tissue expression.
[Mh] Termos MeSH primário: Hormônio Liberador de Hormônio do Crescimento/genética
Iguanas/genética
Fator de Crescimento Insulin-Like I/genética
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/genética
Somatostatina/genética
Hormônio Liberador de Tireotropina/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Hormônio Liberador de Hormônio do Crescimento/química
Hormônio Liberador de Hormônio do Crescimento/metabolismo
Fator de Crescimento Insulin-Like I/química
Fator de Crescimento Insulin-Like I/metabolismo
Filogenia
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/química
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Somatostatina/química
Somatostatina/metabolismo
Hormônio Liberador de Tireotropina/química
Hormônio Liberador de Tireotropina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (RNA, Messenger); 51110-01-1 (Somatostatin); 5Y5F15120W (Thyrotropin-Releasing Hormone); 67763-96-6 (Insulin-Like Growth Factor I); 9034-39-3 (Growth Hormone-Releasing Hormone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE


  3 / 12204 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28684460
[Au] Autor:Yuan PQ; Taché Y
[Ad] Endereço:CURE/Digestive Diseases Research Center, Center for Neurobiology of Stress and Resilience, Vatche and Tamar Manoukian Digestive Diseases Division, Department of Medicine and Brain Research Institute, University of California, Los Angeles, California; and pqyuan@mednet.ucla.edu.
[Ti] Título:Abdominal surgery induced gastric ileus and activation of M1-like macrophages in the gastric myenteric plexus: prevention by central vagal activation in rats.
[So] Source:Am J Physiol Gastrointest Liver Physiol;313(4):G320-G329, 2017 Oct 01.
[Is] ISSN:1522-1547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammation plays a role in abdominal surgery (AS)-induced intestinal ileus that is alleviated by electrical vagal stimulation. Intracisternal injection of RX-77368, the stable thyrotropin-releasing hormone agonist, activates dorsal motor nucleus neurons and gastric vagal efferent discharges. We investigated the gastric inflammation induced by AS and the modulation by intracisternal RX-77368 in rats. RX-77368 (50 ng/rat) or saline was injected followed, 1 h later, by laparotomy and small intestinal/cecal manipulation. The sham group had anesthesia alone. After 6 h, gastric emptying (GE) and the inflammation in gastric corpus were determined. AS inhibited GE by 72% vs. control and doubled the number of M1-like macrophage immunoreactive for major histocompatibility complex class II (MHCII; M1 marker) but not for cluster of differentiation 206 (CD206; M2 marker) (MHCII /CD206 ) while there was no change in M2-like macrophages (MHCII /CD206 ). AS increased mRNA levels of interleukin-1ß (IL-1ß) and tumor necrosis factor α (TNF-α) by 1.7- and 1.5-fold, respectively, in the gastric submucosa plus muscle layers and the infiltration of neutrophils labeled by myeloperoxidase by 9.5-fold in the muscularis externa. RX-77368 inhibited AS-related gastric changes while not altering these parameters in the sham group. There was a significant negative correlation between GE and IL-1ß ( = -0.46), TNF-α ( = -0.44), M1 macrophage ( = -0.82), and neutrophils ( = -0.91). The M2-like macrophages and IL-10 expression were unchanged by AS with intracisternal saline or RX-77368. These data indicate that AS activates gastric M1 macrophages and increases proinflammatory cytokines expression, which are prevented by central vagal activation and may contribute to the correlated dampening of postoperative gastric ileus. MHCII /CD206 (M1) and MHCII /CD206 (M2) constitute two distinct populations of macrophages that are in close apposition to the cholinergic neurons in the rat gastric myenteric plexus (MP). Abdominal surgery (6 h) activates M1 macrophage leading to inflammation in the gastric MP correlated with the delayed gastric emptying, which was abolished by central vagal stimulation via intracisternal injection of RX-77368. Vagal stimulation linked with the cephalic phase may have potential beneficial effects to curtail postoperative gastric ileus.
[Mh] Termos MeSH primário: Enterostomia/efeitos adversos
Motilidade Gastrointestinal/imunologia
Pseudo-Obstrução Intestinal/imunologia
Pseudo-Obstrução Intestinal/prevenção & controle
Ativação de Macrófagos/imunologia
Plexo Mientérico/fisiopatologia
Nervo Vago/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Motilidade Gastrointestinal/efeitos dos fármacos
Pseudo-Obstrução Intestinal/etiologia
Ativação de Macrófagos/efeitos dos fármacos
Masculino
Plexo Mientérico/efeitos dos fármacos
Complexo Mioelétrico Migratório/efeitos dos fármacos
Complexo Mioelétrico Migratório/imunologia
Ácido Pirrolidonocarboxílico/administração & dosagem
Ácido Pirrolidonocarboxílico/análogos & derivados
Ratos
Ratos Sprague-Dawley
Hormônio Liberador de Tireotropina/administração & dosagem
Hormônio Liberador de Tireotropina/análogos & derivados
Resultado do Tratamento
Nervo Vago/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
5Y5F15120W (Thyrotropin-Releasing Hormone); 76820-40-1 (L-pyroglutamyl-L-histidyl-3,3-dimethylprolinamide); SZB83O1W42 (Pyrrolidonecarboxylic Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1152/ajpgi.00121.2017


  4 / 12204 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28324000
[Au] Autor:Turgeon MO; Silander TL; Doycheva D; Liao XH; Rigden M; Ongaro L; Zhou X; Joustra SD; Wit JM; Wade MG; Heuer H; Refetoff S; Bernard DJ
[Ad] Endereço:Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec, Canada.
[Ti] Título:TRH Action Is Impaired in Pituitaries of Male IGSF1-Deficient Mice.
[So] Source:Endocrinology;158(4):815-830, 2017 04 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Loss-of-function mutations in the X-linked immunoglobulin superfamily, member 1 (IGSF1) gene cause central hypothyroidism. IGSF1 is a transmembrane glycoprotein of unknown function expressed in thyrotropin (TSH)-producing thyrotrope cells of the anterior pituitary gland. The protein is cotranslationally cleaved, with only its C-terminal domain (CTD) being trafficked to the plasma membrane. Most intragenic IGSF1 mutations in humans map to the CTD. In this study, we used CRISPR-Cas9 to introduce a loss-of-function mutation into the IGSF1-CTD in mice. The modified allele encodes a truncated protein that fails to traffic to the plasma membrane. Under standard laboratory conditions, Igsf1-deficient males exhibit normal serum TSH levels as well as normal numbers of TSH-expressing thyrotropes. However, pituitary expression of the TSH subunit genes and TSH protein content are reduced, as is expression of the receptor for thyrotropin-releasing hormone (TRH). When challenged with exogenous TRH, Igsf1-deficient males release TSH, but to a significantly lesser extent than do their wild-type littermates. The mice show similarly attenuated TSH secretion when rendered profoundly hypothyroid with a low iodine diet supplemented with propylthiouracil. Collectively, these results indicate that impairments in pituitary TRH receptor expression and/or downstream signaling underlie central hypothyroidism in IGSF1 deficiency syndrome.
[Mh] Termos MeSH primário: Imunoglobulinas/genética
Proteínas de Membrana/genética
Hipófise/metabolismo
Receptores do Hormônio Liberador da Tireotropina/metabolismo
Hormônio Liberador de Tireotropina/metabolismo
Tireotropina/metabolismo
[Mh] Termos MeSH secundário: Animais
Imunoglobulinas/metabolismo
Masculino
Proteínas de Membrana/metabolismo
Camundongos
Camundongos Knockout
Receptores do Hormônio Liberador da Tireotropina/genética
Transdução de Sinais/fisiologia
Tireotropina/genética
Hormônio Liberador de Tireotropina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulins); 0 (Membrane Proteins); 0 (Receptors, Thyrotropin-Releasing Hormone); 5Y5F15120W (Thyrotropin-Releasing Hormone); 9002-71-5 (Thyrotropin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1210/en.2016-1788


  5 / 12204 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28063130
[Au] Autor:Sotelo-Rivera I; Cote-Vélez A; Uribe RM; Charli JL; Joseph-Bravo P
[Ad] Endereço:Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), UNAM, A.P. 510-3, Cuernavaca, Morelos, 62271, Mexico.
[Ti] Título:Glucocorticoids curtail stimuli-induced CREB phosphorylation in TRH neurons through interaction of the glucocorticoid receptor with the catalytic subunit of protein kinase A.
[So] Source:Endocrine;55(3):861-871, 2017 Mar.
[Is] ISSN:1559-0100
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Corticosterone prevents cold-induced stimulation of thyrotropin-releasing hormone (Trh) expression in rats, and the stimulatory effect of dibutyryl cyclic-adenosine monophosphate (dB-cAMP) on Trh transcription in hypothalamic cultures. We searched for the mechanism of this interference. METHODS: Immunohistochemical analyses of phosphorylated cAMP-response element binding protein (pCREB) were performed in the paraventricular nucleus (PVN) of Wistar rats, and in cell cultures of 17-day old rat hypothalami, or neuroblastoma SH-SY5Y cells. Cultures were incubated 1h with dB-cAMP, dexamethasone and both drugs combined; their nuclear extracts were used for chromatin immunoprecipitation; cytosolic or nuclear extracts for coimmunoprecipitation analyses of catalytic subunit of protein kinase A (PKAc) and of glucocorticoid receptor (GR); their subcellular distribution was analyzed by immunocytochemistry. RESULTS: Cold exposure increased pCREB in TRH neurons of rats PVN, effect blunted by corticosterone previous injection. Dexamethasone interfered with forskolin increase in nuclear pCREB and its binding to Trh promoter; antibodies against histone deacetylase-3 precipitated chromatin from nuclear extracts of hypothalamic cells treated with tri-iodothyronine but not with dB-cAMP + dexamethasone, discarding chromatin compaction as responsible mechanism. Co-immunoprecipitation analyses of cytosolic or nuclear extracts showed protein:protein interactions between activated GR and PKAc. Immunocytochemical analyses of hypothalamic or SH-SY5Y cells revealed diminished nuclear translocation of PKAc and GR in cells incubated with forskolin + dexamethasone, compared to either forskolin or dexamethasone alone. CONCLUSIONS: Glucocorticoids and cAMP exert mutual inhibition of Trh transcription through interaction of activated glucocorticoid receptor with protein kinase A catalytic subunit, reducing their nuclear translocation, limiting cAMP-response element binding protein phosphorylation and its binding to Trh promoter.
[Mh] Termos MeSH primário: Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Dexametasona/farmacologia
Glucocorticoides/farmacologia
Neurônios/metabolismo
Receptores de Glucocorticoides/metabolismo
Hormônio Liberador de Tireotropina/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Células Cultivadas
Temperatura Baixa
Hipotálamo/efeitos dos fármacos
Hipotálamo/metabolismo
Neurônios/efeitos dos fármacos
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Núcleo Hipotalâmico Paraventricular/metabolismo
Fosforilação/efeitos dos fármacos
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic AMP Response Element-Binding Protein); 0 (Glucocorticoids); 0 (Receptors, Glucocorticoid); 5Y5F15120W (Thyrotropin-Releasing Hormone); 7S5I7G3JQL (Dexamethasone); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170108
[St] Status:MEDLINE
[do] DOI:10.1007/s12020-016-1223-z


  6 / 12204 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27434852
[Au] Autor:Pekary E; Sattin A
[Ad] Endereço:Research Service, VA Greater Los Angeles Healthcare System, Los Angeles, USA.
[Ti] Título:TRH and TRH-Like Peptide Levels Co-Vary with Reproductive and Metabolic Rhythms.
[So] Source:Horm Metab Res;49(2):86-94, 2017 Feb.
[Is] ISSN:1439-4286
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Photoperiod-synchronized rhythms in non-CSN tissues persist in total darkness. Clock genes involved in maintaining regular biorhythms within the suprachiasmatic nucleus (SCN) of the hypothalamus are expressed in extra-CNS tissues and continue periodic expression in vitro. Understanding the details of how the SCN clock is coupled with peripheral clocks is only incompletely understood and may involve a multiplicity of feedback systems. The present study is an extension of our previous work showing that brain levels of TRH (pGlu-His-Pro-NH ) and TRH-like peptides (X-TRH: pGlu-X-Pro-NH , where "X" can be any amino acid residue) fluctuate throughout the day-night cycle. Male rats were maintained in a stable environment, lights on 6-18 h. TRH and TRH-like peptides in liver, pancreas, testis, prostate, epididymis, and heart were measured at 3, 10, 16, and 22 h. The greatest change in peptide level was a 12-fold increase for TRH in prostate at 16 h relative to the corresponding value at 3 h. The TRH, Tyr-TRH and Phe-TRH levels in liver declined steadily to about 40% of the 3-h values by 22 h. Changes, in the order of decreasing number of significant increases (↑) and/or decreases (↓), were: testis (5↑, 1↓), liver (3↓), epididymis (2↑), prostate (1↑, 1↓) and heart (1↑). Peptide levels in liver and testis correlated with serum leptin and serum corticosterone, respectively, which are potent releasers of these peptides. Testosterone and glucose were also highly correlated. These tripeptides may participate in the regulation of metabolic and reproductive functions, which change during the day-night cycle.
[Mh] Termos MeSH primário: Ritmo Circadiano
Peptídeos/metabolismo
Reprodução
Hormônio Liberador de Tireotropina/metabolismo
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Cromatografia Líquida de Alta Pressão
Corticosterona/sangue
Hormônios/sangue
Leptina/sangue
Masculino
Fotoperíodo
Ratos Sprague-Dawley
Testosterona/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Hormones); 0 (Leptin); 0 (Peptides); 3XMK78S47O (Testosterone); 5Y5F15120W (Thyrotropin-Releasing Hormone); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170313
[Lr] Data última revisão:
170313
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160720
[St] Status:MEDLINE
[do] DOI:10.1055/s-0042-111012


  7 / 12204 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27810782
[Au] Autor:Rajput SK; Sharma AK; Meena CL; Pant AB; Jain R; Sharma SS
[Ad] Endereço:Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Sector-67, S.A.S. Nagar, Mohali, Punjab, 160062, India; Amity Institute of Pharmacy, Amity University, Noida, Uttar Pradesh, 201303, India. Electronic address: neuropharmacology2015@gmail.
[Ti] Título:Effect of L-pGlu-(1-benzyl)-l-His-l-Pro-NH against in-vitro and in-vivo models of cerebral ischemia and associated neurological disorders.
[So] Source:Biomed Pharmacother;84:1256-1265, 2016 Dec.
[Is] ISSN:1950-6007
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Central nervous system plays a vital role in regulation of most of biological functions which are abnormally affected in various disorders including cerebral ischemia, Alzheimer's and Parkinson's (AD and PD) worldwide. Cerebral stroke is an extremely fatal and one of the least comprehensible neurological disorders due to limited availability of prospective clinical approaches and therapeutics. Since, some endogenous peptides like thyrotropin-releasing hormone have shown substantial neuroprotective potential, hence present study evaluates the newer thyrotropin-releasing hormone (TRH) analogue L-pGlu-(1-benzyl)-l-His-l-Pro-NH for its neuroprotective effects against oxygen glucose deprivation (OGD), glutamate and H O induced injury in pheochromocytoma cell lines (PC-12 cells) and in-vivo ischemic injury in mice. Additionally, the treatment was further analyzed with respect to models of AD and PD in mice. Cerebral ischemia was induced by clamping both bilateral common carotid arteries for ten minutes. Treatment was administered to the mice five minute after restoration of blood supply to brain. Consequential changes in neurobehavioural, biochemical and histological parameters were assessed after a week. L-pGlu-(1-benzyl)-l-His-l-Pro-NH showed significant reduction in glutamate, H O and OGD -induced cell death in concentration and time dependent manner. Moreover, L-pGlu-(1-benzyl)-l-His-l-Pro-NH resulted in a substantial reduction in CA1 (Cornus Ammonis 1) hippocampal neuronal cell death, inflammatory cytokines, TNF-α, IL-6 and oxidative stress in hippocampus. In addition, L-pGlu-(1-benzyl)-l-His-l-Pro-NH was found to be protective in two acute models of AD and PD as well these findings demonstrate the neuroprotective potential of L-pGlu-(1-benzyl)-l-His-l-Pro-NH in cerebral ischemia and other diseases, which may be mediated through reduction of excitotoxicity, oxidative stress and inflammation.
[Mh] Termos MeSH primário: Isquemia Encefálica/complicações
Isquemia Encefálica/tratamento farmacológico
Hormônio Liberador de Tireotropina/análogos & derivados
[Mh] Termos MeSH secundário: 1-Metil-4-Fenil-1,2,3,6-Tetra-Hidropiridina
Animais
Isquemia Encefálica/patologia
Isquemia Encefálica/fisiopatologia
Catalepsia/complicações
Catalepsia/tratamento farmacológico
Catalepsia/patologia
Catalepsia/fisiopatologia
Morte Celular/efeitos dos fármacos
Modelos Animais de Doenças
Glucose/deficiência
Ácido Glutâmico/toxicidade
Haloperidol
Hipocampo/efeitos dos fármacos
Hipocampo/fisiopatologia
Mediadores da Inflamação/metabolismo
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Transtornos da Memória/complicações
Transtornos da Memória/tratamento farmacológico
Transtornos da Memória/patologia
Transtornos da Memória/fisiopatologia
Camundongos
Modelos Biológicos
Atividade Motora/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Neurônios/patologia
Oxigênio/toxicidade
Células PC12
Ratos
Hidrobrometo de Escopolamina
Hormônio Liberador de Tireotropina/química
Hormônio Liberador de Tireotropina/farmacologia
Hormônio Liberador de Tireotropina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inflammation Mediators); 0 (L-pGlu-(1-benzyl)-L-His-L-ProNH2); 3KX376GY7L (Glutamic Acid); 451IFR0GXB (Scopolamine Hydrobromide); 5Y5F15120W (Thyrotropin-Releasing Hormone); 9P21XSP91P (1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine); IY9XDZ35W2 (Glucose); J6292F8L3D (Haloperidol); S88TT14065 (Oxygen)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE


  8 / 12204 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27741548
[Au] Autor:Patel N; Kashanian JA
[Ad] Endereço:Department of Urology, Weill Cornell Medicine, New York, New York.
[Ti] Título:Thyroid Dysfunction and Male Reproductive Physiology.
[So] Source:Semin Reprod Med;34(6):356-360, 2016 Nov.
[Is] ISSN:1526-4564
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Normal thyroid physiology is paramount for the proper development and important for the maintenance of male reproduction. Both short- and long-term deviations in thyroid hormone levels have been shown to alter male reproductive function on a micro- and macroscopic level. Thyrotoxicosis and hypothyroidism are associated with changes in spermatogenesis, semen quality, levels of sexual hormones, and erectile function. However, the degree to which thyroid dysfunction is clinically responsible for male infertility has not been clearly elucidated.
[Mh] Termos MeSH primário: Infertilidade Masculina/fisiopatologia
Reprodução
Doenças da Glândula Tireoide/fisiopatologia
Glândula Tireoide/fisiologia
[Mh] Termos MeSH secundário: Seres Humanos
Hipotálamo
Infertilidade Masculina/complicações
Masculino
Análise do Sêmen
Espermatogênese
Doenças da Glândula Tireoide/complicações
Hormônio Liberador de Tireotropina/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
5Y5F15120W (Thyrotropin-Releasing Hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161015
[St] Status:MEDLINE


  9 / 12204 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27601155
[Au] Autor:Usui S; Hama S; Tominaga A; Kinoshita Y; Kurisu K
[Ad] Endereço:Department of Neurosurgery, Graduate School of Biomedical and Health Science, Hiroshima University, Minami-Ku, Hiroshima, Japan. Electronic address: usui@hiroshima-u.ac.jp.
[Ti] Título:Effect of Gonadotropin and Adrenocorticotropic Hormone Secretion on Invasiveness of Clinically Nonfunctioning Pituitary Adenomas: A Cell Culture Study.
[So] Source:World Neurosurg;96:578-584.e1, 2016 Dec.
[Is] ISSN:1878-8769
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The aim of this study was to clarify the correlation between clinical features (especially cyst formation and cavernous sinus invasion) and minor secretion of anterior pituitary hormones, especially adrenocorticotropic hormone (ACTH) and gonadotropin, by clinically nonfunctioning pituitary adenomas (CNFPAs) in cell culture. METHODS: We examined anterior pituitary hormones secreted by samples from 63 cases of CNFPAs grown in cell culture. Magnetic resonance imaging, including determination of the Knosp grade, cystic changes, and intraoperative cavernous sinus invasion, was performed. RESULTS: Detection of minor hormone secretion using cell culture showed that 61.9% (39/63) of CNFPAs secreted luteinizing hormone, follicle-stimulating hormone, and thyroid-stimulating hormone, 44.4% (28/63) secreted ACTH, 57.1% (36/63) secreted prolactin, and 28.6% (18/63) secreted growth hormone; only 1 case of the null-cell adenoma was observed (1.6%). Cystic changes, Knosp grade 4 status, and cavernous sinus invasion were predominantly observed in cases of ACTH-secreting adenomas. Gonadotropin-secreting adenomas showed opposite characteristics to ACTH-secreting adenomas. CONCLUSIONS: Minor secretion of ACTH and gonadotropin may be related to clinical features, especially cystic changes and invasiveness of CNFPAs, suggesting that our cell culture method could be helpful for elucidating the mechanisms of pituitary cyst formation and the invasiveness of CNFPAs.
[Mh] Termos MeSH primário: Adenoma/patologia
Hormônio Adrenocorticotrópico/secreção
Gonadotropinas/farmacologia
Neoplasias Hipofisárias/patologia
Células Tumorais Cultivadas/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenoma/diagnóstico por imagem
Adolescente
Hormônio Adrenocorticotrópico/farmacologia
Adulto
Idoso
Idoso de 80 Anos ou mais
Células Cultivadas
Feminino
Hormônio Foliculoestimulante/secreção
Seres Humanos
Hormônio Luteinizante/secreção
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Neoplasias Hipofisárias/diagnóstico por imagem
Prolactina/secreção
Estudos Prospectivos
Estatísticas não Paramétricas
Hormônio Liberador de Tireotropina/secreção
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gonadotropins); 5Y5F15120W (Thyrotropin-Releasing Hormone); 9002-60-2 (Adrenocorticotropic Hormone); 9002-62-4 (Prolactin); 9002-67-9 (Luteinizing Hormone); 9002-68-0 (Follicle Stimulating Hormone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160908
[St] Status:MEDLINE


  10 / 12204 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27515033
[Au] Autor:Joseph-Bravo P; Jaimes-Hoy L; Charli JL
[Ad] Endereço:Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Av. Universidad 2001, 62250, Cuernavaca MOR, Morelos, México. joseph@ibt.unam.mx.
[Ti] Título:Advances in TRH signaling.
[So] Source:Rev Endocr Metab Disord;17(4):545-558, 2016 Dec.
[Is] ISSN:1573-2606
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The activity of the hypothalamus-pituitary-thyroid axis (HPT) is coordinated by hypophysiotropic thyrotropin releasing hormone (TRH) neurons present in the paraventricular nucleus of the hypothalamus. Hypophysiotropic TRH neurons act as energy sensors. TRH controls the synthesis and release of thyrotropin, which activates the synthesis and secretion of thyroid hormones; in target tissues, transporters and deiodinases control their local availability. Thyroid hormones regulate many functions, including energy homeostasis. This review discusses recent evidence that covers several aspects of TRH role in HPT axis regulation. Knowledge about the mechanisms of TRH signaling has steadily increased. New transcription factors engaged in TRH gene expression have been identified, and advances made on how they interact with signaling pathways and define the dynamics of TRH neurons response to acute and/or long-term influences. Albeit yet incomplete, the relationship of TRH neurons activity with positive energy balance has emerged. The importance of tanycytes as a central relay for the feedback control of the axis, as well as for HPT responses to alterations in energy balance, and other stimuli has been reinforced. Finally, some studies have started to shed light on the interference of prenatal and postnatal stress and nutrition on HPT axis programing, which have confirmed the axis susceptibility to early insults.
[Mh] Termos MeSH primário: Glândula Tireoide/metabolismo
Glândula Tireoide/patologia
Hormônio Liberador de Tireotropina/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Ependimogliais/metabolismo
Células Ependimogliais/patologia
Seres Humanos
Hipotálamo/metabolismo
Hipotálamo/patologia
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
5Y5F15120W (Thyrotropin-Releasing Hormone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171121
[Lr] Data última revisão:
171121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160813
[St] Status:MEDLINE
[do] DOI:10.1007/s11154-016-9375-y



página 1 de 1221 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde