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[PMID]:28450830
[Au] Autor:Elliott KL; Kersigo J; Pan N; Jahan I; Fritzsch B
[Ad] Endereço:Department of Biology, University of IowaIowa City, IA, USA.
[Ti] Título:Spiral Ganglion Neuron Projection Development to the Hindbrain in Mice Lacking Peripheral and/or Central Target Differentiation.
[So] Source:Front Neural Circuits;11:25, 2017.
[Is] ISSN:1662-5110
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:We investigate the importance of the degree of peripheral or central target differentiation for mouse auditory afferent navigation to the organ of Corti and auditory nuclei in three different mouse models: first, a mouse in which the differentiation of hair cells, but not central auditory nuclei neurons is compromised ( ); second, a mouse in which hair cell defects are combined with a delayed defect in central auditory nuclei neurons ( ), and third, a mouse in which both hair cells and central auditory nuclei are absent ( ). Our results show that neither differentiated peripheral nor the central target cells of inner ear afferents are needed (hair cells, cochlear nucleus neurons) for segregation of vestibular and cochlear afferents within the hindbrain and some degree of base to apex segregation of cochlear afferents. These data suggest that inner ear spiral ganglion neuron processes may predominantly rely on temporally and spatially distinct molecular cues in the region of the targets rather than interaction with differentiated target cells for a crude topological organization. These developmental data imply that auditory neuron navigation properties may have evolved before auditory nuclei.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/deficiência
Diferenciação Celular/genética
Células Ciliadas Auditivas/fisiologia
Malformações do Sistema Nervoso/patologia
Fator de Transcrição PAX2/deficiência
Rombencéfalo/patologia
Gânglio Espiral da Cóclea
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Vias Auditivas/embriologia
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Núcleo Coclear/citologia
Núcleo Coclear/embriologia
Núcleo Coclear/crescimento & desenvolvimento
Embrião de Mamíferos
Camundongos
Camundongos Knockout
Malformações do Sistema Nervoso/genética
Fator de Transcrição PAX2/genética
Gânglio Espiral da Cóclea/embriologia
Gânglio Espiral da Cóclea/crescimento & desenvolvimento
Gânglio Espiral da Cóclea/patologia
beta-Galactosidase/genética
beta-Galactosidase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Atoh1 protein, mouse); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (PAX2 Transcription Factor); 0 (Pax2 protein, mouse); EC 3.2.1.23 (beta-Galactosidase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.3389/fncir.2017.00025


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[PMID]:29254304
[Au] Autor:Li JK; Wang C; Gong HD; Li HZ
[Ad] Endereço:Department of Neurosurgery, Affiliated HongQi Hospital of Mu Dan Jiang Medical University, Mudanjiang City, China.
[Ti] Título:Coagulation in hindbrain membrane meningioma patients treated with different injections using acute hypervolemic hemodilution.
[So] Source:J Biol Regul Homeost Agents;31(4):991-996, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to analyze the changes in coagulation in meningioma patients treated with different injections using the method of acute hypervolemic hemodilution (AHH). One hundred fifty hindbrain membrane meningioma patients were randomly divided into 5 groups, 30 per group. The first group were injected 40ml/time with Danhong after anesthesia induction; the second group were injected with 40ml~60ml/time Kangai and combined with interventional chemotherapy and embolization procedure; the third group of AHH were injected with polygeline 15ml/kg; the fourth group were injected with hydroxyethyl starch (130/0.4) sodium chloride in doses of 15ml/kg; the control group underwent basic treatment for lowering blood pressure and lowering blood fat. The changes of coagulation index were recorded before and after surgery and before and after the injection of different medications. Compared to the control group, for the first group of AHH, after being treated for 10 days and 30 days, the concentrations of bone specific alkaline phosphatase (BALP), bone Gla protein (BGP) and pro-collagen carboxy-terminal propeptide (PICP) were higher than that of the control group, the levels of endotoxin (ET) and C-reactive protein (CRP) were decreased compared to the control group (p less than 0.05); for the second group of AHH, after being treated for 10 days, the index of prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen (Fg) were not significantly changed, but the related level of vascular endothelial growth factor (VEGF) significantly decreased (p less than 0.05). Comparing the coagulation function index after surgery in the third and fourth groups, there were no significant changes in mean arterial pressure (MAP) level, heart rate (HR) value presented a low decrease, central venous pressure (CVP) level increased and the level of interleukin IL-6 showed a steady state after increasing. Analyzing the levels of interleukin IL-8 and tumor necrosis factor-α (TNF-α) after surgery, it was seen that in the third group they increased and in the fourth group they decreased (p less than 0.05). Danhong injection improved the coagulation function and microcirculation of patients, Kangai injection and interventional chemotherapy and embolization restrained the appearance of tumor angiogenesis, AHH operation with polygeline injection and hydroxyethyl starch (130/0.4) sodium chloride kept blood flow in normal parameters.
[Mh] Termos MeSH primário: Coagulação Sanguínea/efeitos dos fármacos
Cardiotônicos/uso terapêutico
Medicamentos de Ervas Chinesas/uso terapêutico
Hemodiluição/métodos
Neoplasias Meníngeas/tratamento farmacológico
Meningioma/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Fosfatase Alcalina/genética
Fosfatase Alcalina/metabolismo
Pressão Arterial/efeitos dos fármacos
Pressão Arterial/fisiologia
Biomarcadores/metabolismo
Viscosidade Sanguínea/efeitos dos fármacos
Proteína C-Reativa/genética
Proteína C-Reativa/metabolismo
Embolização Terapêutica/métodos
Endotoxinas/metabolismo
Feminino
Fibrinogênio/genética
Fibrinogênio/metabolismo
Expressão Gênica
Frequência Cardíaca/efeitos dos fármacos
Frequência Cardíaca/fisiologia
Seres Humanos
Derivados de Hidroxietil Amido/administração & dosagem
Masculino
Neoplasias Meníngeas/sangue
Neoplasias Meníngeas/patologia
Neoplasias Meníngeas/cirurgia
Meningioma/sangue
Meningioma/patologia
Meningioma/cirurgia
Meia-Idade
Osteocalcina/genética
Osteocalcina/metabolismo
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Substitutos do Plasma/administração & dosagem
Poligelina/administração & dosagem
Pró-Colágeno/genética
Pró-Colágeno/metabolismo
Rombencéfalo/efeitos dos fármacos
Rombencéfalo/metabolismo
Rombencéfalo/patologia
Rombencéfalo/cirurgia
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cardiotonic Agents); 0 (Drugs, Chinese Herbal); 0 (Endotoxins); 0 (Hydroxyethyl Starch Derivatives); 0 (Peptide Fragments); 0 (Plasma Substitutes); 0 (Procollagen); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (danhong); 0 (procollagen type I carboxy terminal peptide); 104982-03-8 (Osteocalcin); 9001-32-5 (Fibrinogen); 9007-41-4 (C-Reactive Protein); 9015-56-9 (Polygeline); EC 3.1.3.1 (Alkaline Phosphatase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


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[PMID]:28747407
[Au] Autor:Roberts ZS; Wolden-Hanson T; Matsen ME; Ryu V; Vaughan CH; Graham JL; Havel PJ; Chukri DW; Schwartz MW; Morton GJ; Blevins JE
[Ad] Endereço:Veterans Affairs Puget Sound Health Care System, Office of Research and Development, Medical Research Service, Department of Veterans Affairs Medical Center, Seattle, Washington.
[Ti] Título:Chronic hindbrain administration of oxytocin is sufficient to elicit weight loss in diet-induced obese rats.
[So] Source:Am J Physiol Regul Integr Comp Physiol;313(4):R357-R371, 2017 Oct 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxytocin (OT) administration elicits weight loss in diet-induced obese (DIO) rodents, nonhuman primates, and humans by reducing energy intake and increasing energy expenditure. Although the neurocircuitry underlying these effects remains uncertain, OT neurons in the paraventricular nucleus are positioned to control both energy intake and sympathetic nervous system outflow to interscapular brown adipose tissue (BAT) through projections to the hindbrain nucleus of the solitary tract and spinal cord. The current work was undertaken to examine whether central OT increases BAT thermogenesis, whether this effect involves hindbrain OT receptors (OTRs), and whether such effects are associated with sustained weight loss following chronic administration. To assess OT-elicited changes in BAT thermogenesis, we measured the effects of intracerebroventricular administration of OT on interscapular BAT temperature in rats and mice. Because fourth ventricular (4V) infusion targets hindbrain OTRs, whereas third ventricular (3V) administration targets both forebrain and hindbrain OTRs, we compared responses to OT following chronic 3V infusion in DIO rats and mice and chronic 4V infusion in DIO rats. We report that chronic 4V infusion of OT into two distinct rat models recapitulates the effects of 3V OT to ameliorate DIO by reducing fat mass. While reduced food intake contributes to this effect, our finding that 4V OT also increases BAT thermogenesis suggests that increased energy expenditure may contribute as well. Collectively, these findings support the hypothesis that, in DIO rats, OT action in the hindbrain evokes sustained weight loss by reducing energy intake and increasing BAT thermogenesis.
[Mh] Termos MeSH primário: Tecido Adiposo Marrom/fisiopatologia
Obesidade/tratamento farmacológico
Obesidade/fisiopatologia
Ocitocina/farmacologia
Rombencéfalo/fisiopatologia
Termogênese/efeitos dos fármacos
Perda de Peso/efeitos dos fármacos
[Mh] Termos MeSH secundário: Tecido Adiposo Marrom/efeitos dos fármacos
Animais
Depressores do Apetite/farmacologia
Dieta Hiperlipídica/efeitos adversos
Relação Dose-Resposta a Droga
Infusões Intraventriculares
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Obesidade/etiologia
Ratos
Ratos Long-Evans
Ratos Sprague-Dawley
Rombencéfalo/efeitos dos fármacos
Especificidade da Espécie
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Appetite Depressants); 50-56-6 (Oxytocin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00169.2017


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[PMID]:28749941
[Au] Autor:Thierion E; Le Men J; Collombet S; Hernandez C; Coulpier F; Torbey P; Thomas-Chollier M; Noordermeer D; Charnay P; Gilardi-Hebenstreit P
[Ad] Endereço:Ecole normale supérieure, PSL Research University, CNRS, Inserm, Institut de Biologie de l'Ecole normale supérieure (IBENS), Paris, France.
[Ti] Título:Krox20 hindbrain regulation incorporates multiple modes of cooperation between cis-acting elements.
[So] Source:PLoS Genet;13(7):e1006903, 2017 Jul.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Developmental genes can harbour multiple transcriptional enhancers that act simultaneously or in succession to achieve robust and precise spatiotemporal expression. However, the mechanisms underlying cooperation between cis-acting elements are poorly documented, notably in vertebrates. The mouse gene Krox20 encodes a transcription factor required for the specification of two segments (rhombomeres) of the developing hindbrain. In rhombomere 3, Krox20 is subject to direct positive feedback governed by an autoregulatory enhancer, element A. In contrast, a second enhancer, element C, distant by 70 kb, is active from the initiation of transcription independent of the presence of the KROX20 protein. Here, using both enhancer knock-outs and investigations of chromatin organisation, we show that element C possesses a dual activity: besides its classical enhancer function, it is also permanently required in cis to potentiate the autoregulatory activity of element A, by increasing its chromatin accessibility. This work uncovers a novel, asymmetrical, long-range mode of cooperation between cis-acting elements that might be essential to avoid promiscuous activation of positive autoregulatory elements.
[Mh] Termos MeSH primário: Proteína 1 de Resposta de Crescimento Precoce/genética
Elementos Facilitadores Genéticos
Elementos Reguladores de Transcrição/genética
Rombencéfalo/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Animais
Padronização Corporal/genética
Cromatina/genética
Proteína 1 de Resposta de Crescimento Precoce/biossíntese
Regulação da Expressão Gênica no Desenvolvimento
Camundongos Knockout
Mutação
Rombencéfalo/metabolismo
Homologia de Sequência do Ácido Nucleico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromatin); 0 (Early Growth Response Protein 1); 0 (Egr1 protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006903


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[PMID]:28407732
[Au] Autor:Lumb R; Buckberry S; Secker G; Lawrence D; Schwarz Q
[Ad] Endereço:Centre for Cancer Biology, University of South Australia and SA Pathology, Frome Road, Adelaide, SA, 5000, Australia.
[Ti] Título:Transcriptome profiling reveals expression signatures of cranial neural crest cells arising from different axial levels.
[So] Source:BMC Dev Biol;17(1):5, 2017 Apr 13.
[Is] ISSN:1471-213X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cranial neural crest cells (NCCs) are a unique embryonic cell type which give rise to a diverse array of derivatives extending from neurons and glia through to bone and cartilage. Depending on their point of origin along the antero-posterior axis cranial NCCs are rapidly sorted into distinct migratory streams that give rise to axial specific structures. These migratory streams mirror the underlying segmentation of the brain with NCCs exiting the diencephalon and midbrain following distinct paths compared to those exiting the hindbrain rhombomeres (r). The genetic landscape of cranial NCCs arising at different axial levels remains unknown. RESULTS: Here we have used RNA sequencing to uncover the transcriptional profiles of mouse cranial NCCs arising at different axial levels. Whole transcriptome analysis identified over 120 transcripts differentially expressed between NCCs arising anterior to r3 (referred to as r1-r2 migratory stream for simplicity) and the r4 migratory stream. Eight of the genes differentially expressed between these populations were validated by RT-PCR with 2 being further validated by in situ hybridisation. We also explored the expression of the Neuropilins (Nrp1 and Nrp2) and their co-receptors and show that the A-type Plexins are differentially expressed in different cranial NCC streams. CONCLUSIONS: Our analyses identify a large number of genes differentially regulated between cranial NCCs arising at different axial levels. This data provides a comprehensive description of the genetic landscape driving diversity of distinct cranial NCC streams and provides novel insight into the regulatory networks controlling the formation of specific skeletal elements and the mechanisms promoting migration along different paths.
[Mh] Termos MeSH primário: Perfilação da Expressão Gênica/métodos
Redes Reguladoras de Genes
Crista Neural/citologia
Crista Neural/crescimento & desenvolvimento
Análise de Sequência de RNA/métodos
[Mh] Termos MeSH secundário: Animais
Movimento Celular
Diencéfalo/citologia
Diencéfalo/crescimento & desenvolvimento
Regulação da Expressão Gênica no Desenvolvimento
Mesencéfalo/citologia
Mesencéfalo/crescimento & desenvolvimento
Camundongos
Proteínas do Tecido Nervoso/genética
Neuropilina-1/genética
Neuropilina-2/genética
Rombencéfalo/citologia
Rombencéfalo/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nerve Tissue Proteins); 0 (Neuropilin-2); 144713-63-3 (Neuropilin-1)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170421
[Lr] Data última revisão:
170421
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.1186/s12861-017-0147-z


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[PMID]:28379214
[Au] Autor:Tamrakar P; Briski KP
[Ad] Endereço:Department of Basic Pharmaceutical Sciences, School of Pharmacy, The University of Louisiana at Monroe, Monroe, USA.
[Ti] Título:Impact of recurrent hypoglycemic stress on hindbrain A2 nerve cell energy metabolism and catecholamine biosynthesis: modulation by estradiol.
[So] Source:Acta Neurobiol Exp (Wars);77(1):31-44, 2017.
[Is] ISSN:1689-0035
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:It is unclear if habituation of hindbrain A2 metabolo­sensory neurons to recurrent insulin-induced hypoglycemia (RIIH) correlates with estradiol-dependent adjustments in energy metabolism that favor positive energy balance. Laser-microdissected A2 cells from estradiolor oil-implanted ovariectomized female rats were analyzed by Western blot to assess effects of three prior daily insulin injections on basal and hypoglycemic patterns of catecholamine biosynthetic enzyme dopamine-beta-hydroxylase (DßH) and rate-limiting energy pathway enzyme protein expression. Precedent hypoglycemia respectively decreased or increased baseline DßH expression in estradiol- (E) vs. oil (O)-treated rats; this protein profile was further suppressed or augmented in those animals at 2 hr after re-induction of hypoglycemia. These data suggest that estradiol may curtail A2 noradrenergic­controlled functions both in the midst of and between hypoglycemic bouts. Results also show that prior hypoglycemia exposure upregulated A2 neuron glycolytic enzyme protein levels when E was present, and exerted differential effects on basal and hypoglycemia-associated respiratory chain and fatty acid synthetic pathway enzyme expression. E may thus accordingly amplify glycolysis-derived metabolites/energy, coupled with reduced reliance on oxidative phosphorylation, and activate the fatty acid synthetic pathway during RIIH. E may also be of benefit by preventing maladaptive reductions in A2 neuron Krebs cycle/electron transport enzyme expression during re-exposure to hypoglycemia. Augmentation of negative energy balance during this recurring metabolic stress in the absence of E is a likely impetus for augmented vs. decreased A2 signaling of energy imbalance by DßH in O vs. E rats during RIIH.
[Mh] Termos MeSH primário: Catecolaminas/metabolismo
Metabolismo Energético/efeitos dos fármacos
Estradiol/farmacologia
Estrogênios/farmacologia
Hipoglicemia/patologia
Neurônios/efeitos dos fármacos
Rombencéfalo/patologia
[Mh] Termos MeSH secundário: Animais
Glicemia/efeitos dos fármacos
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Hipoglicemia/induzido quimicamente
Hipoglicemia/fisiopatologia
Hipoglicemiantes/toxicidade
Insulina/toxicidade
Complexos Multienzimáticos/metabolismo
Neurônios/metabolismo
Ovariectomia
Biossíntese de Proteínas/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Catecholamines); 0 (Estrogens); 0 (Hypoglycemic Agents); 0 (Insulin); 0 (Multienzyme Complexes); 4TI98Z838E (Estradiol)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170414
[Lr] Data última revisão:
170414
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE


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[PMID]:28371402
[Au] Autor:Dempsey JC; Phelps IG; Bachmann-Gagescu R; Glass IA; Tully HM; Doherty D
[Ad] Endereço:Department of Pediatrics, University of Washington, Seattle, Washington.
[Ti] Título:Mortality in Joubert syndrome.
[So] Source:Am J Med Genet A;173(5):1237-1242, 2017 May.
[Is] ISSN:1552-4833
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Joubert syndrome (JS) is a rare, recessively inherited neurodevelopmental disorder characterized by a distinctive mid-hindbrain malformation. Little is known about mortality in affected individuals. Identifying the timing and causes of death will allow for development of healthcare guidelines for families and providers and, thus, help to prolong and improve the lives of patients with JS. We evaluated information on 40 deceased individuals with JS to characterize age and cause of death. We compared this population with 525 living individuals with JS to estimate associations between risk of death and extra-neurological features. Genetic causes were examined in both groups. Mean age of death in this cohort was 7.2 years, and the most prevalent causes of death were respiratory failure (35%), particularly in individuals younger than 6 years, and kidney failure (37.5%), which was more common in older individuals. We identified possible associations between risk of death and kidney disease, liver fibrosis, polydactyly, occipital encephalocele, and genetic cause. This work highlights factors (genetic cause, extra-neurological organ involvement, and other malformations) likely to be associated with higher risk of mortality in JS, which should prompt increased monitoring for respiratory issues, kidney disease, and liver fibrosis.
[Mh] Termos MeSH primário: Anormalidades Múltiplas/mortalidade
Cerebelo/anormalidades
Anormalidades do Olho/mortalidade
Doenças Renais Císticas/mortalidade
Insuficiência Renal/mortalidade
Retina/anormalidades
[Mh] Termos MeSH secundário: Anormalidades Múltiplas/genética
Anormalidades Múltiplas/fisiopatologia
Adolescente
Cerebelo/fisiopatologia
Criança
Pré-Escolar
Anormalidades do Olho/complicações
Anormalidades do Olho/genética
Anormalidades do Olho/fisiopatologia
Feminino
Seres Humanos
Doenças Renais Císticas/complicações
Doenças Renais Císticas/genética
Doenças Renais Císticas/fisiopatologia
Masculino
Insuficiência Renal/complicações
Insuficiência Renal/genética
Insuficiência Renal/patologia
Retina/fisiopatologia
Rombencéfalo/anormalidades
Rombencéfalo/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170508
[Lr] Data última revisão:
170508
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE
[do] DOI:10.1002/ajmg.a.38158


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[PMID]:28285134
[Au] Autor:Wang H; Luo L; Yang D
[Ad] Endereço:Key Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Beibei, 400715 Chongqing, China.
[Ti] Título:Loss of Gspt1l disturbs the patterning of the brain central arteries in zebrafish.
[So] Source:Biochem Biophys Res Commun;486(1):156-162, 2017 Apr 22.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cranial vasculature is crucial for the survival and development of the central nervous system and is closely related to brain pathologies. Characterizations of the underlying mechanisms by which cranial vessels acquire their stereotypic patterning remain to be the key interest in the cerebrovascular research. In this report, we show an interesting zebrafish cq37 mutant displaying aberrant patterning of the central arteries. Genetic mapping results indicate that the gene responsible for cq37 encodes G1 to S phase transition 1, like (Gspt1l) with a nonsense mutation. Complementation studies with a CRISPR-generated allele, as well as mRNA rescues, together strongly demonstrate that gspt1l is the cq37 gene. Zebrafish gspt1l is broadly expressed in the brain with enhanced expression in hindbrain during central artery sprouting. Further studies reveal that vascular endothelial growth factor (VEGF) signaling and unfolded protein response (UPR) pathway are activated in gspt1l mutants. In addition, expression analysis shows that vegfa and activating transcription factor-4 (atf4) are strongly upregulated in regions of gspt1l expression. Our results suggest that loss of Gspt1l activates the UPR pathway, which in turn induces ectopic expression of vegfa via Atf4, thus disturbing the patterning of the central arteries.
[Mh] Termos MeSH primário: Artérias/metabolismo
Padronização Corporal/genética
Encéfalo/irrigação sanguínea
Proteínas de Ciclo Celular/genética
Mutação
Proteínas de Peixe-Zebra/genética
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Fator 4 Ativador da Transcrição/genética
Fator 4 Ativador da Transcrição/metabolismo
Animais
Apoptose/genética
Artérias/embriologia
Sequência de Bases
Proteínas de Ciclo Celular/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Hibridização In Situ
Hibridização in Situ Fluorescente
Neovascularização Fisiológica/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Rombencéfalo/irrigação sanguínea
Resposta a Proteínas não Dobradas/genética
Fator A de Crescimento do Endotélio Vascular/genética
Fator A de Crescimento do Endotélio Vascular/metabolismo
Peixe-Zebra/embriologia
Peixe-Zebra/metabolismo
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Gspt1l protein, zebrafish); 0 (Vascular Endothelial Growth Factor A); 0 (Zebrafish Proteins); 145891-90-3 (Activating Transcription Factor 4)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170313
[St] Status:MEDLINE


  9 / 2629 MEDLINE  
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[PMID]:28249783
[Au] Autor:Sen T; Cawthon CR; Ihde BT; Hajnal A; DiLorenzo PM; de La Serre CB; Czaja K
[Ad] Endereço:Department of Veterinary Biosciences & Diagnostic Imaging, College of Veterinary Medicine, The University of Georgia, Athens, GA 30602, United States.
[Ti] Título:Diet-driven microbiota dysbiosis is associated with vagal remodeling and obesity.
[So] Source:Physiol Behav;173:305-317, 2017 May 01.
[Is] ISSN:1873-507X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obesity is one of the major health issues in the United States. Consumption of diets rich in energy, notably from fats and sugars (high-fat/high-sugar diet: HF/HSD) is linked to the development of obesity and a popular dietary approach for weight loss is to reduce fat intake. Obesity research traditionally uses low and high fat diets and there has been limited investigation of the potential detrimental effects of a low-fat/high-sugar diet (LF/HSD) on body fat accumulation and health. Therefore, in the present study, we investigated the effects of HF/HSD and LF/HSD on microbiota composition, gut inflammation, gut-brain vagal communication and body fat accumulation. Specifically, we tested the hypothesis that LF/HSD changes the gut microbiota, induces gut inflammation and alters vagal gut-brain communication, associated with increased body fat accumulation. Sprague-Dawley rats were fed an HF/HSD, LF/HSD or control low-fat/low-sugar diet (LF/LSD) for 4weeks. Body weight, caloric intake, and body composition were monitored daily and fecal samples were collected at baseline, 1, 6 and 27days after the dietary switch. After four weeks, blood and tissues (gut, brain, liver and nodose ganglia) were sampled. Both HF/HSD and LF/HSD-fed rats displayed significant increases in body weight and body fat compared to LF/LSD-fed rats. 16S rRNA sequencing showed that both HF/HSD and LF/HSD-fed animals exhibited gut microbiota dysbiosis characterized by an overall decrease in bacterial diversity and an increase in Firmicutes/Bacteriodetes ratio. Dysbiosis was typified by a bloom in Clostridia and Bacilli and a marked decrease in Lactobacillus spp. LF/HSD-fed animals showed a specific increase in Sutterella and Bilophila, both Proteobacteria, abundances of which have been associated with liver damage. Expression of pro-inflammatory cytokines, such as IL-6, IL-1ß and TNFα, was upregulated in the cecum while levels of tight junction protein occludin were downregulated in both HF/HSD and LF/HSD fed rats. HF/HSD and LF/HSD-fed rats also exhibited an increase in cecum and serum levels of lipopolysaccharide (LPS), a pro-inflammatory bacterial product. Immunofluorescence revealed the withdrawal of vagal afferents from the gut and at their site of termination the nucleus of the solitary tract (NTS) in both the HF/HSD and LF/HSD rats. Moreover, there was significant microglia activation in the nodose ganglia, which contain the vagal afferent neuron cell bodies, of HF/HSD and LF/HSD rats. Taken together, these data indicate that, similar to HF/HSD, consumption of an LF/HSD induces dysbiosis of gut microbiota, increases gut inflammation and alters vagal gut-brain communication. These changes are associated with an increase in body fat accumulation.
[Mh] Termos MeSH primário: Disbiose/induzido quimicamente
Microbiota/efeitos dos fármacos
Obesidade/metabolismo
Obesidade/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Composição Corporal
Peso Corporal
Proteínas de Ligação ao Cálcio/metabolismo
Citocinas/metabolismo
Dieta Hiperlipídica
Modelos Animais de Doenças
Ingestão de Alimentos
Ingestão de Energia/fisiologia
Glicoproteínas/metabolismo
Lectinas/metabolismo
Lipopolissacarídeos/farmacologia
Masculino
Proteínas dos Microfilamentos/metabolismo
RNA Ribossômico 16S/metabolismo
Ratos
Ratos Sprague-Dawley
Rombencéfalo/metabolismo
Estatísticas não Paramétricas
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Calcium-Binding Proteins); 0 (Cytokines); 0 (Glycoproteins); 0 (Lectins); 0 (Lipopolysaccharides); 0 (Microfilament Proteins); 0 (RNA, Ribosomal, 16S); 0 (isolectin B4-binding glycoprotein, rat)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE


  10 / 2629 MEDLINE  
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[PMID]:28218622
[Au] Autor:Gaykema RP; Newmyer BA; Ottolini M; Raje V; Warthen DM; Lambeth PS; Niccum M; Yao T; Huang Y; Schulman IG; Harris TE; Patel MK; Williams KW; Scott MM
[Ti] Título:Activation of murine pre-proglucagon-producing neurons reduces food intake and body weight.
[So] Source:J Clin Invest;127(3):1031-1045, 2017 Mar 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peptides derived from pre-proglucagon (GCG peptides) act in both the periphery and the CNS to change food intake, glucose homeostasis, and metabolic rate while playing a role in anxiety behaviors and physiological responses to stress. Although the actions of GCG peptides produced in the gut and pancreas are well described, the role of glutamatergic GGC peptide-secreting hindbrain neurons in regulating metabolic homeostasis has not been investigated. Here, we have shown that chemogenetic stimulation of GCG-producing neurons reduces metabolic rate and food intake in fed and fasted states and suppresses glucose production without an effect on glucose uptake. Stimulation of GCG neurons had no effect on corticosterone secretion, body weight, or conditioned taste aversion. In the diet-induced obese state, the effects of GCG neuronal stimulation on gluconeogenesis were lost, while the food intake-lowering effects remained, resulting in reductions in body weight and adiposity. Our work suggests that GCG peptide-expressing neurons can alter feeding, metabolic rate, and glucose production independent of their effects on hypothalamic pituitary-adrenal (HPA) axis activation, aversive conditioning, or insulin secretion. We conclude that GCG neurons likely stimulate separate populations of downstream cells to produce a change in food intake and glucose homeostasis and that these effects depend on the metabolic state of the animal.
[Mh] Termos MeSH primário: Peso Corporal/fisiologia
Ingestão de Alimentos/fisiologia
Sistema Hipotálamo-Hipofisário/metabolismo
Neurônios/metabolismo
Sistema Hipófise-Suprarrenal/metabolismo
Proglucagon/metabolismo
[Mh] Termos MeSH secundário: Animais
Gluconeogênese/genética
Camundongos
Camundongos Transgênicos
Proglucagon/genética
Rombencéfalo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
55963-74-1 (Proglucagon)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170221
[St] Status:MEDLINE



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