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  1 / 40495 MEDLINE  
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[PMID]:29373588
[Au] Autor:Muszynski S; Tomaszewska E; Kwiecien M; Dobrowolski P; Tomczyk-Warunek A
[Ad] Endereço:Department of Physics, Faculty of Production Engineering, University of Life Sciences in Lublin, Lublin, Poland.
[Ti] Título:Subsequent somatic axis and bone tissue metabolism responses to a low-zinc diet with or without phytase inclusion in broiler chickens.
[So] Source:PLoS One;13(1):e0191964, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Zinc is required for normal bone development and cartilage formation. The purpose of this study was to assess the effect of with adding organic Zn (alone or phytase inclusion) at the reduced dose to growing male Ross 308 chickens on somatic axis and bone tissue metabolism. 200 one-day old broilers were divided into the negative control group fed diet without Zn or phytase inclusion, positive control group receiving Zn in the 100% of daily recommended dose from ZnO, and two experimental groups fed diet introduced Zn in 25% of daily recommendation as a glycine chelate (Zn-Gly) with or without phytase inclusion (500 FTU·kg-1). Supplemental organic Zn increased bone Zn and Mg content, serum IGF-1, growth hormone and leptin concentration. Additional phytase inclusion increased body weight gain, blood plasma Ca, Fe, Zn and osteocalcin concentration and tibia ash percentage when compared to the Zn-deprived control. Bone geometry, yield and ultimate strengths were enhanced in both organic Zn supplemented groups, and the overall mechanical strength parameters of bone were better in these groups than in the positive control group supplemented with standard dose of inorganic Zn. Also marked improvements in the thickness of articular and the growth plate cartilages as well as real bone volume and thickness of metaphyseal trabeculae were achieved in all broilers fed Zn-supplemented diet irrespective of phytase inclusion, however, the highest cancellous bone mass and the best trabecular structure were noted after ZnO supplementation. In concludion, although dietary organic Zn given to growing broilers in 25% of daily recommended dose improved general bone properties and mechanical strength, the obtained results do not allow to unambiguously state that organic Zn supplementation at this level, even after phytase inclusion, is sufficient for proper bone development.
[Mh] Termos MeSH primário: 6-Fitase/metabolismo
Osso e Ossos/metabolismo
Zinco/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Galinhas
Hormônio do Crescimento/metabolismo
Fator de Crescimento Insulin-Like I/metabolismo
Leptina/metabolismo
Magnésio/metabolismo
Masculino
Zinco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Leptin); 67763-96-6 (Insulin-Like Growth Factor I); 9002-72-6 (Growth Hormone); EC 3.1.3.26 (6-Phytase); I38ZP9992A (Magnesium); J41CSQ7QDS (Zinc)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191964


  2 / 40495 MEDLINE  
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[PMID]:29424977
[Au] Autor:Santibáñez-Morales A; Durán-Boullosa E; Colín-Licea EO
[Ti] Título:[Use of growth hormone for in vitro fertilization].
[Ti] Título:Indicación de hormona de crecimiento en ciclos de fertilización in vitro..
[So] Source:Ginecol Obstet Mex;84(9):567-72, 2016 Sep.
[Is] ISSN:0300-9041
[Cp] País de publicação:Mexico
[La] Idioma:spa
[Ab] Resumo:Background: Ovarian stimulation is the cornerstone in fertility treatments, it produces multifolicular development and in consequence, a greater pregnancy rate. Poor responder patients have bad outcomes in IVF, several medical approaches have been proposed in managing these patients, including Growth Hormone. Objetive: To report our results with the use of growth hormone and review published data. Material and method: Case series conducted from January 2013 to May 2015 in patients to Centro de Reproducción PROCREA, Mexico City, poor responders according to the criteria of consensus Bologna cycles in fresh stimulation protocol Flare up, application of growth hormone as adjuvant, complete cycles of stimulation (stimulation, oocyte capture, and embryo transfer pregnancy test) and complete records. For statistical analysis, averages and percentages were used. Results: 40 cases were analyzed. Age and BMI were 39.1 ± 2.1 years and 24.6 ± 2.8 kg/m2, respectively. Total gonadotrophin dose was 2128.6 ± 1078.9 UI, retrieved oocytes and fertilized eggs were 7.1 ± 4.0 y 5.4 ± 2.8 respectively. Fertilization rate was 76.3% and pregnancy rate was 59.5%. Conclusion: There is insufficient evidence for prescribing GH in all patients requiring IVF, nevertheless, in poor responder patients, there seems to be an improvement in egg quality leading to better fertilization and pregnancy rate, with no adverse effects.
[Mh] Termos MeSH primário: Fertilização In Vitro/métodos
Hormônio do Crescimento/administração & dosagem
Indução da Ovulação/métodos
[Mh] Termos MeSH secundário: Adulto
Feminino
Gonadotropinas/administração & dosagem
Seres Humanos
México
Gravidez
Taxa de Gravidez
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gonadotropins); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180210
[St] Status:MEDLINE


  3 / 40495 MEDLINE  
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[PMID]:28464910
[Au] Autor:Han X; He Y; Zeng G; Wang Y; Sun W; Liu J; Sun Y; Yu J
[Ad] Endereço:Department of Integrative Medicine, Children's Hospital of Fudan University, No.399, Wan Yuan Road, Min Hang District, Shanghai, China.
[Ti] Título:Intracerebroventricular injection of RFRP-3 delays puberty onset and stimulates growth hormone secretion in female rats.
[So] Source:Reprod Biol Endocrinol;15(1):35, 2017 May 02.
[Is] ISSN:1477-7827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Puberty onset is a complex, organized biological process with multilevel regulation, and its physiopathological mechanisms are yet to be elucidated. RFRP-3, the mammalian ortholog to gonadotropin-inhibitory hormone, is implicated in inhibiting the synthesis and release of gonadotropin in mammals. However, it is unclear whether RFRP-3 participates in regulating pubertal development. METHODS: This study investigated the functional significance and regulatory mechanism of hypothalamic RFRP-3 neuropeptide in the onset of puberty in young female rats. On postnatal day 22, we implanted cannulas into the lateral ventricles of female rat pups. From postnatal day 28 to postnatal day 36, the intracerebroventricular injection of RFRP-3, or vehicle, was conducted twice a day. To investigate whether puberty onset was affected, we examined the body weight, age of vaginal opening, serum hormone levels, uterus and ovary development, and hypothalamic Kiss-1 mRNA expression. RESULTS: Intracerebroventricular injection of RFRP-3 significantly decreased the serum concentrations of luteinizing hormone and estradiol, delayed uterine maturation, and postponed the time of vaginal opening. This study suggests that RFRP-3 can delay the onset of puberty in young female rats; the expression of Kiss-1 mRNA is potently inhibited in the RFRP-3 group. Moreover, our data show that RFRP-3 elevates serum growth hormone levels. CONCLUSIONS: These data suggest that intracerebroventricular injection of RFRP-3 significantly delays the onset of puberty in female rats. Additionally, RFRP-3 may be associated with prepubertal rise in the secretion of growth hormone.
[Mh] Termos MeSH primário: Hormônio do Crescimento/secreção
Neuropeptídeos/administração & dosagem
Maturidade Sexual/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Feminino
Hipotálamo/efeitos dos fármacos
Hipotálamo/metabolismo
Injeções Intraventriculares
Neuropeptídeos/farmacologia
Ratos
Ratos Sprague-Dawley
Via Secretória/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuropeptides); 0 (RFamide peptide); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12958-017-0254-5


  4 / 40495 MEDLINE  
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[PMID]:29443755
[Au] Autor:Cai X; Yu D; Xie Y; Zhou H
[Ad] Endereço:Department of Pediatrics, West China Second University Hospital.
[Ti] Título:Argininemia as a cause of severe chronic stunting and partial growth hormone deficiency (PGHD): A case report.
[So] Source:Medicine (Baltimore);97(7):e9880, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Argininemia is an autosomal recessive inherited disorder of the urea cycle. Because of its atypical symptoms in early age, diagnosis can be delayed until the typical chronic manifestations - including spastic diplegia, deterioration in cognitive function, and epilepsy - appear in later childhood. PATIENT CONCERNS: A Chinese boy initially presented with severe stunting and partial growth hormone deficiency (PGHD) at 3 years old and was initially treated with growth hormone replacement therapy. Seven years later (at 10 years old), he presented with spastic diplegia, cognitive function lesions, epilepsy, and peripheral neuropathy. DIAGNOSES: Ultimately, the patient was diagnosed with argininemia with homozygous mutation (c.32T>C) of the ARG1 gene at 10 years old. Blood tests showed mildly elevated blood ammonia and creatine kinase, and persistently elevated bilirubin. INTERVENTIONS: Protein intake was limited to 0.8 g/kg/day, citrulline (150-200 mg [kg d]) was prescribed. OUTCOMES: The patient's mental state and vomiting had improved after 3 months treatment. At 10 years and 9 month old, his height and weight had reached 121cm and 22kg, respectively, but his spastic diplegia symptoms had not improved. LESSONS: This case demonstrates that stunting and PGHD that does not respond to growth hormone replacement therapy might hint at inborn errors of metabolism (IEM). IEM should also be considered in patients with persistently elevated bilirubin with or without abnormal liver transaminase, as well as elevated blood ammonia and creatine kinase, in the absence of hepatic disease.
[Mh] Termos MeSH primário: Transtornos do Crescimento
Hiperargininemia
[Mh] Termos MeSH secundário: Arginase/genética
Bilirrubina/análise
Criança
Pré-Escolar
Diagnóstico Diferencial
Transtornos do Crescimento/diagnóstico
Transtornos do Crescimento/etiologia
Hormônio do Crescimento/análise
Hormônio do Crescimento/deficiência
Hormônio do Crescimento/uso terapêutico
Terapia de Reposição Hormonal/efeitos adversos
Terapia de Reposição Hormonal/métodos
Seres Humanos
Hiperargininemia/diagnóstico
Hiperargininemia/genética
Hiperargininemia/fisiopatologia
Hiperargininemia/terapia
Masculino
Mutação
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
9002-72-6 (Growth Hormone); EC 3.5.3.1 (Arginase); RFM9X3LJ49 (Bilirubin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009880


  5 / 40495 MEDLINE  
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[PMID]:29372967
[Au] Autor:Pankova MV; Kukhlevsky AD; Brykov VA
[Ti] Título:[Fish growth hormone genes: Divergence of coding sequences in salmonid fishes].
[So] Source:Genetika;53(2):201-13, 2017 Feb.
[Is] ISSN:0016-6758
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Comparison of coding nucleotide sequences of the paralogous GH1 and GH2 genes, as well as of the growth hormone amino acid sequences, in the species of closely related salmonid genera Salvelinus, Oncorhynchus, and Salmo was performed. It was demonstrated that, in different groups of salmonids, the amino acid substitution rates were considerably different. In some cases, an obvious discrepancy between the divergence of growth hormone genes and phylogenetic schemes based on other methods and approaches was revealed. These findings suggest that the reason may be multidirectional selection at duplicated genes at different stages of evolution.
[Mh] Termos MeSH primário: Evolução Molecular
Proteínas de Peixes/genética
Hormônio do Crescimento/genética
Filogenia
Salmonidae/genética
[Mh] Termos MeSH secundário: Animais
Especificidade da Espécie
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fish Proteins); 9002-72-6 (Growth 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:180127
[St] Status:MEDLINE


  6 / 40495 MEDLINE  
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[PMID]:29238946
[Au] Autor:Banaszak-Ziemska M; Niedziela M
[Ti] Título:PAPP-A2 a new key regulator of growth.
[So] Source:Endokrynol Pol;68(6):682-691, 2017.
[Is] ISSN:2299-8306
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Short stature is the main problem that paediatric endocrinologists have to grapple with. Endocrine disorders account for only 5% of patients with short stature, but this is still one of the most common causes of reports to the endocrine clinic and hospitalisation in the endocrine department. A properly functioning growth hormone/insulin-like growth factor (GH/IGF) axis is one of the most important factors in proper growth. A lot of genetic defects in this axis lead to syndromes marked by impaired growth, like Laron syndrome, muta-tions in the STAT5B, insulin-like growth factor 1 (IGF1), and insulin-like growth factor 1 receptor (IGF1R) and mutations in the acid labile subunit (ALS). Two proteases important for the proper functioning of the GH/IGF axis: pregnancy-associated plasma protein-A (PAPP-A) and pregnancy-associated plasma protein-A2 (PAPP-A2), have been described. The first description of the new syndrome of growth failure associated with mutation in the PAPP-A2 gene was given by Andrew Dauber et al. This review evaluates the current data concerning PAPP-A2 function, and particularly the effect of PAPP-A2 mutation on growth.
[Mh] Termos MeSH primário: Crescimento/genética
Mutação
Proteína Plasmática A Associada à Gravidez/fisiologia
[Mh] Termos MeSH secundário: Animais
Feminino
Hormônio do Crescimento
Seres Humanos
Fator de Crescimento Insulin-Like I
Masculino
Camundongos
Proteína Plasmática A Associada à Gravidez/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
67763-96-6 (Insulin-Like Growth Factor I); 9002-72-6 (Growth Hormone); EC 3.4.- (PAPPA2 protein, human); EC 3.4.24.- (PAPPA2 protein, mouse); EC 3.4.24.- (Pregnancy-Associated Plasma Protein-A)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180130
[Lr] Data última revisão:
180130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.5603/EP.a2017.0060


  7 / 40495 MEDLINE  
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[PMID]:29176323
[Au] Autor:He W; Huang L; Li M; Yang Y; Chen Z; Shen X
[Ti] Título:MiR-148b, MiR-152/ALCAM Axis Regulates the Proliferation and Invasion of Pituitary Adenomas Cells.
[So] Source:Cell Physiol Biochem;44(2):792-803, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Aberrant expression of miRNA has been found in many tumor tissues to regulate the tumorigenesis by binding to the 3`- untranslated region (3`-UTR) of the target genes. The aim of this study is to investigate the role of miR-148b, miR-152/ALCAM axis in human pituitary adenomas (PAs). METHODS: First, we detected the expression level of miR-148b-3p and miR-152 in human PAs samples by using qRT-PCR. Then we studied the role of miR-148b-3p, miR-152 on human PAs cell proliferation, invasion and apoptosis by using MTS assay, Transwell invasion assay and Annexin V/PI Staining Test. To study the relationship between miR-148b-3p, miR-152 and activated leukocyte antigen molecule (ALCAM), we overexpressed miR-148-3p or miR-152 by transfecting specific mimics. Lucifearase reporter assay was then performed to confirm the target. Next, we studied the biological functions of ALCAM in human PAs cells. Finally, the role of miR-148b-3p, miR-152/ALCAM axis in PAs cells was studied. RESULTS: The expression level of miR-148-3p and miR-152 in invasive PAs samples was lower than those in noninvasive samples. Overexpression of miR-148b-3p, miR-152 could repress proliferation and invasion, and promote apoptosis. Moreover, miR-148b-3p and miR-152 could repress activated leukocyte antigen molecule (ALCAM) expression. Knockdown of ALCAM could repress proliferation and invasion and promote apoptosis. By contrary, overexpression of ALCAM promoted proliferation and invasion. Further, the rescue experiments indicated that overexpression of ALCAM significantly restored the proliferation, apoptosis, and invasion influenced by miR-148b-3p and miR-152. CONCLUSIONS: Our study suggests that miR-148b-3p, miR-152 may serve as suppressors in PAs through downregulating ALCAM expression. miR-148b, miR-152/ ALCAM axis may be a new therapeutic target in the future.
[Mh] Termos MeSH primário: Molécula de Adesão de Leucócito Ativado/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Molécula de Adesão de Leucócito Ativado/química
Molécula de Adesão de Leucócito Ativado/genética
Animais
Antagomirs/metabolismo
Sequência de Bases
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Ensaio de Imunoadsorção Enzimática
Hormônio do Crescimento/análise
MicroRNAs/antagonistas & inibidores
MicroRNAs/genética
Neoplasias Hipofisárias/metabolismo
Neoplasias Hipofisárias/patologia
Prolactina/análise
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Ratos
Alinhamento de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Activated-Leukocyte Cell Adhesion Molecule); 0 (Antagomirs); 0 (MicroRNAs); 0 (RNA, Small Interfering); 9002-62-4 (Prolactin); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485342


  8 / 40495 MEDLINE  
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[PMID]:27770281
[Au] Autor:Indini A; Schiavello E; Biassoni V; Bergamaschi L; Magni MC; Puma N; Chiaravalli S; Pallotti F; Seregni E; Diletto B; Pecori E; Gandola L; Poggi G; Massimino M
[Ad] Endereço:Pediatric Oncology Unit, Fondazione IRCCS, Istituto Nazionale dei Tumori, Via Venezian 1, 20133, Milan, Italy. alice.indini@istitutotumori.mi.it.
[Ti] Título:Long-term safety of growth hormone replacement therapy after childhood medulloblastoma and PNET: it is time to set aside old concerns.
[So] Source:J Neurooncol;131(2):349-357, 2017 01.
[Is] ISSN:1573-7373
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To assess the long-term safety of administering growth hormone (GH) in patients with GH deficiency due to treatment for childhood medulloblastoma and primitive neuroectodermal tumor (PNET). Data were retrospectively retrieved on children receiving GH supplementation, assessing their disease-free and overall survival outcomes and risk of secondary malignancies using Kaplan-Meier and Cox models. Overall 65 children were consecutively collected from May 1981 to April 2013. All patients had undergone craniospinal irradiation (total dose 18-39 Gy), and subsequently received GH for a median (interquartile range, IQR) of 81 (50.6-114.9) months. At a median (IQR) of 122.4 months (74.4-149.5) after the end of their adjuvant cancer treatment, two patients (3 %) experienced recurrent disease and 8 (12.3 %) developed secondary malignancies, all but one of them (an osteosarcoma) related to radiation exposure and occurring within the radiation fields. There was no apparent correlation between the administration of GH replacement therapy (or its duration) and primary tumor relapse or the onset of secondary malignancies [HR: 1.01 (95 % CI: 0.98, 1.03) for every additional 12 months of GH supplementation; p = 0.36). At univariate analysis, the large cell or anaplastic medulloblastoma subtype, metastases and myeloablative chemotherapy correlated with a higher risk of secondary malignancies (p < 0.1), but multivariate analysis failed to identify any factors independently associated with this risk. Our data supports once more the safety of long-term GH replacement therapy in children treated for medulloblastoma/PNET, previously reported in larger data sets. The neurooncology community now need to warrant large-scale meta-analyses or international prospective trials in order to consolidate our knowledge of factors other than GH, such as genetic predisposition, high-grade/metastatic disease, high-dose chemotherapy and era of treatment, in promoting the occurrence of secondary malignancies.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/tratamento farmacológico
Hormônio do Crescimento/efeitos adversos
Terapia de Reposição Hormonal/efeitos adversos
Meduloblastoma/tratamento farmacológico
Tumores Neuroectodérmicos Primitivos/tratamento farmacológico
[Mh] Termos MeSH secundário: Criança
Feminino
Hormônio do Crescimento/uso terapêutico
Seres Humanos
Estimativa de Kaplan-Meier
Masculino
Estudos Retrospectivos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180119
[Lr] Data última revisão:
180119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1007/s11060-016-2306-7


  9 / 40495 MEDLINE  
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[PMID]:29283520
[Au] Autor:Tishevskaya NV; Gevorkyan NM; Kozlova NI
[Ti] Título:Sensitivity of T-Lymphocytes to Hormones of the Anterior Pituitary Gland.
[So] Source:Usp Fiziol Nauk;48(1):80-90, 2017 Jan-Mar.
[Is] ISSN:0301-1798
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The review provides information about the features of the sensitivity of thymocytes, lymphoid organs' cells and T-lymphocytes of peripheral blood to the hormones secreted by anterior pituitary gland's cells: growth hormone, thyrotropin, adrenocorticotropic hormone, prolactin and ß-endorphin. Some aspects of the T-lymphocytes's response to humoral signals from the hypophysis are shown in the article. Also the pituitary hormones' role in the regulation of proliferation, differentiation, and cytokine production of T-lymphocytes in normal and pathological conditions of the organism being discussed.
[Mh] Termos MeSH primário: Hormônio Adrenocorticotrópico/farmacologia
Hormônio do Crescimento/farmacologia
Adeno-Hipófise/secreção
Prolactina/farmacologia
Timócitos/efeitos dos fármacos
Tireotropina/farmacologia
beta-Endorfina/farmacologia
[Mh] Termos MeSH secundário: Hormônio Adrenocorticotrópico/genética
Hormônio Adrenocorticotrópico/imunologia
Animais
Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Regulação da Expressão Gênica
Hormônio do Crescimento/genética
Hormônio do Crescimento/imunologia
Seres Humanos
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/efeitos dos fármacos
Leucócitos Mononucleares/imunologia
Cultura Primária de Células
Prolactina/genética
Prolactina/imunologia
Transdução de Sinais
Timócitos/citologia
Timócitos/imunologia
Tireotropina/genética
Tireotropina/imunologia
beta-Endorfina/genética
beta-Endorfina/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
60617-12-1 (beta-Endorphin); 9002-60-2 (Adrenocorticotropic Hormone); 9002-62-4 (Prolactin); 9002-71-5 (Thyrotropin); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171229
[St] Status:MEDLINE


  10 / 40495 MEDLINE  
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[PMID]:29175438
[Au] Autor:Ahmed RG; El-Gareib AW; Shaker HM
[Ad] Endereço:Division of Anatomy and Embryology, Zoology Department, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt. Electronic address: r_g_a_ahmed@science.bsu.edu.eg.
[Ti] Título:Gestational 3,3',4,4',5-pentachlorobiphenyl (PCB 126) exposure disrupts fetoplacental unit: Fetal thyroid-cytokines dysfunction.
[So] Source:Life Sci;192:213-220, 2018 Jan 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Exposure to polychlorinated biphenyls (PCBs) is related to several endocrine disorders. This study examined the effect of maternal exposure of 3,3',4,4',5-pentachlorobiphenyl (PCB 126) on the fetoplacental unit and fetal thyroid-cytokine axis during the pregnancy. Pregnant albino rats received PCB 126 (20 or 40µg/kgb.wt.) by oral gavage from gestation day (GD) 1 to 20. Potential effects of PCB 126 were evaluated by following the histopathological changes in the placenta by Haematoxylin and Eosin (H&E) stain and measuring the maternofetal thyroid axis (ELIZA), maternofetal body weight, and fetal growth markers (ELIZA), and cytokines (ELIZA) at embryonic day (ED) 20. Placental tissues of both treated groups showed hyperemia, hemorrhage, degeneration and apoptosis in labyrinth layer and spiral artery at GD 20. Both administrations of PCB 126 elevated serum thyrotropin (TSH) concentration, and decreased free thyroxine (FT4) and free triiodothyronine (FT3) concentrations, resulting in a maternofetal hypothyroidism. The presence of hypothyroidism increased fetal serum concentration of transforming growth factor-ß (TGF-ß), leptin (LEP), tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and decreased the fetal serum insulin growth factor-I (IGF-I), IGF-II, insulin, adiponectin (ADP), and growth hormone (GH) in both treated groups at ED 20. However, the increase in resistin (RETN) and interferon-γ (IFN-γ) was non-significant in low-dose group and highly significant in high-dose group. Simultaneously, the reduction in body weight of the dams and fetuses was observed in both PCB 126 groups of examined day with respect to the control group. The maternal PCB 126 distorted the fetoplacental unit might disrupt the fetal thyroid-cytokines axis and prenatal development.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Poluentes Ambientais/toxicidade
Feto/efeitos dos fármacos
Placenta/efeitos dos fármacos
Bifenilos Policlorados/toxicidade
Doenças da Glândula Tireoide/induzido quimicamente
[Mh] Termos MeSH secundário: Adiponectina/biossíntese
Animais
Peso Corporal/efeitos dos fármacos
Feminino
Peso Fetal/efeitos dos fármacos
Feto/metabolismo
Hormônio do Crescimento/biossíntese
Fator de Crescimento Insulin-Like I/biossíntese
Fator de Crescimento Insulin-Like II/biossíntese
Placenta/metabolismo
Placenta/patologia
Gravidez
Ratos
Ratos Wistar
Tireotropina/sangue
Tiroxina/sangue
Tri-Iodotironina/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adiponectin); 0 (Cytokines); 0 (Environmental Pollutants); 0 (insulin-like growth factor II, rat); 0 (insulin-like growth factor-1, rat); 06LU7C9H1V (Triiodothyronine); 67763-96-6 (Insulin-Like Growth Factor I); 67763-97-7 (Insulin-Like Growth Factor II); 9002-71-5 (Thyrotropin); 9002-72-6 (Growth Hormone); DFC2HB4I0K (Polychlorinated Biphenyls); Q51BO43MG4 (Thyroxine); TSH69IA9XF (3,4,5,3',4'-pentachlorobiphenyl)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE



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