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[PMID]:28463109
[Au] Autor:Tang X; Roessingh S; Hayley SE; Chu ML; Tanaka NK; Wolfgang W; Song S; Stanewsky R; Hamada FN
[Ad] Endereço:Visual Systems Group, Abrahamson Pediatric Eye Institute, Division of Pediatric Ophthalmology, Cincinnati Children's Hospital Medical Center, Cincinnati, United States.
[Ti] Título:The role of PDF neurons in setting the preferred temperature before dawn in .
[So] Source:Elife;6, 2017 05 02.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Animals have sophisticated homeostatic controls. While mammalian body temperature fluctuates throughout the day, small ectotherms, such as achieve a body temperature rhythm (BTR) through their preference of environmental temperature. Here, we demonstrate that pigment dispersing factor (PDF) neurons play an important role in setting preferred temperature before dawn. We show that small lateral ventral neurons (sLNvs), a subset of PDF neurons, activate the dorsal neurons 2 (DN2s), the main circadian clock cells that regulate temperature preference rhythm (TPR). The number of temporal contacts between sLNvs and DN2s peak before dawn. Our data suggest that the thermosensory anterior cells (ACs) likely contact sLNvs via serotonin signaling. Together, the ACs-sLNs-DN2s neural circuit regulates the proper setting of temperature preference before dawn. Given that sLNvs are important for sleep and that BTR and sleep have a close temporal relationship, our data highlight a possible neuronal interaction between body temperature and sleep regulation.
[Mh] Termos MeSH primário: Temperatura Corporal
Drosophila/fisiologia
Rede Nervosa/fisiologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Animais
Relógios Circadianos
Drosophila/efeitos da radiação
Proteínas de Drosophila/metabolismo
Homeostase
Neurônios/química
Neuropeptídeos/metabolismo
Serotonina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Drosophila Proteins); 0 (Neuropeptides); 0 (pdf protein, Drosophila); 333DO1RDJY (Serotonin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:29329072
[Au] Autor:De Prins A; Martin C; Van Wanseele Y; Skov LJ; Tömböly C; Tourwé D; Caveliers V; Van Eeckhaut A; Holst B; Rosenkilde MM; Smolders I; Ballet S
[Ad] Endereço:Research Group of Organic Chemistry, Departments of Chemistry and Bioengineering Sciences, Vrije Universiteit Brussel, Pleinlaan 2, 1050, Brussels, Belgium; Department of Pharmaceutical Chemistry, Drug Analysis and Drug Information, Center for Neurosciences (C4N), Vrije Universiteit Brussel, Laarbee
[Ti] Título:Development of potent and proteolytically stable human neuromedin U receptor agonists.
[So] Source:Eur J Med Chem;144:887-897, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Neuromedin U (NMU) is a highly conserved endogenous peptide that is involved in a wide range of physiological processes such as regulation of feeding behavior, the stress response and nociception. The major limitation to use NMU as a therapeutic is its short half-life. Here, we describe the development of a set of novel NMU-analogs based on NMU-8, by introducing unnatural amino acids into the native sequence. This approach shows that it is possible to generate molecules with increased potency and improved plasma stability without major changes of the peptidic nature or the introduction of large conjugates. When compared to the native NMU-8 peptide, compounds 16, 18 and 20 have potent agonist activity and affinity for both NMU receptors. Selectivity towards NMUR1 was observed when the Phe residue in position 4 was modified, whereas higher potencies at NMUR2 were found when substitutions of the Pro residue in position 6 were executed. To study the effect of the modifications on the proteolytic stability of the molecules, an in vitro stability assay in human plasma at 37 °C was performed. All analyzed analogs possessed an increased resistance against enzymatic degradation in human plasma resulting in half-lifes from 4 min for NMU-8, up to more than 23 h for compound 42.
[Mh] Termos MeSH primário: Neuropeptídeos/farmacologia
Proteólise/efeitos dos fármacos
Receptores de Neurotransmissores/agonistas
[Mh] Termos MeSH secundário: Relação Dose-Resposta a Droga
Seres Humanos
Estrutura Molecular
Neuropeptídeos/síntese química
Neuropeptídeos/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neuropeptides); 0 (Receptors, Neurotransmitter); 0 (neuromedin U receptor); 98530-27-9 (neuromedin U 8)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status: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


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[PMID]:29297993
[Au] Autor:Sharkova VA; Kovalev IA; Shivanova AY
[Ti] Título:Autoantibodies to Neuropeptides in the Different States of Opium Addiction.
[So] Source:Vestn Ross Akad Med Nauk;71(5):385-91, 2016.
[Is] ISSN:0869-6047
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:Background: During the last years the addiction rate remains stable high. While the neurochemical drug effect remains unclear. Aims: To analyze the changes of the idiotypic (аАТ1) and anti-idiotypic (аАТ2) autoantibodies to the neuroproteins S100, MBP, GFAP, NGF on the different stages of opium addiction and to indicate prognosis criteria of their effect. Materials and Methods: 70 patients (only men, aged 22−38) with diagnosis opium addiction underwent examination. According to the results of testing, we detected the intoxication in 24 patients, withdrawal ­ in 24, and 22 patients were at remission stage of 21−28 days. The control group included only healthy people (n=18). The survey was focused on the rate detection of the idiotypic and anti-idiotypic IgG class antibodies in relation to the rate of neural proteins (S100, MBP, GFAP, NGF) in the serum with the IEA. Results: In patients with opium intoxication, we revealed statistical assurance in the rate of autoantibodies amount and their counterweights to the neural proteins rate between control and experimental groups. Only the rate of the аАТ2 protein significantly decreased relatively to the MBP. In patients with abstinence, the rate of аАТ1 to the MBP, GFAP (р≤0,05) increased. The rate of аАТ2 in relation to the GFAP and MBP also increased (р≤0,05), at the same time it decreased in relation to the S100 and NGF (р≤0,05). The autoantibodies amount at the remission stage corresponded to the amount at the intoxication stage. The comparative analysis of the patient groups with the different stages of opium addiction detected the identity criteria both in the intoxication and remission. We revealed statistical assurance in the rates of аАТ1 to MBP and аАТ2 to NGF in patients with intoxication and abstinence, and in the rates of аАТ1 to GFAP, MBP, and аАТ2 to GFAP (decreased in the remission) and to S100, MBP (increased in the remission) in patients with abstinence and at remission. Conclusion: Levels of idiotypic and anti-idiotypic antibodies to the neural proteins S100, MBP, GFAP, NGF (especially аАТ2 to MPB) could be used as diagnostic factor and for accessing different states of opium addiction.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Neuropeptídeos/imunologia
Dependência de Ópio
Síndrome de Abstinência a Substâncias/imunologia
[Mh] Termos MeSH secundário: Adulto
Seres Humanos
Masculino
Neuropeptídeos/classificação
Dependência de Ópio/diagnóstico
Dependência de Ópio/imunologia
Gravidade do Paciente
Escalas de Graduação Psiquiátrica
Estatística como Assunto
Síndrome de Abstinência a Substâncias/diagnóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Neuropeptides)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.15690/vramn669


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[PMID]:29293515
[Au] Autor:Buntschuh I; Raps DA; Joseph I; Reid C; Chait A; Totanes R; Sawh M; Li C
[Ad] Endereço:Department of Biology, City College of New York, City University of New York, New York, NY, United States of America.
[Ti] Título:FLP-1 neuropeptides modulate sensory and motor circuits in the nematode Caenorhabditis elegans.
[So] Source:PLoS One;13(1):e0189320, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Parasitic nematodes infect over one quarter of the population worldwide, causing morbidity in over one billion people. Current anthelmintic drugs are beginning to lose effectiveness due to the presence of resistant strains. We are interested in the role of neuropeptides, which regulate behaviors in all organisms, as another possible target for anthelmintic drugs. FMRFamide-related peptides (FaRPs) are a family of neuropeptides that are conserved throughout the animal kingdom. In particular, nematodes contain the largest family of FaRPs identified thus far and many of these FaRPs are identical among different nematode species; FaRPs in nematodes are collectively referred to as FLPs (FMRFamide-like peptides). However, little is known about the function of these FLPs. We are using the non-parasitic nematode Caenorhabditis elegans as a model for examining FLPs in nematodes. C. elegans contains at least 31 flp genes that encode 72 potential FLPs. Among the flp genes, flp-1 is one of the few that is universally found in nematodes. FLP-1 neuropeptides were previously reported to be involved in sensory and motor functions. However, previous alleles of flp-1 also disrupted a neighboring gene, daf-10. To understand the phenotypes of flp-1, new alleles that specifically disrupt flp-1 were characterized. The previously reported locomotory and egg-laying defects were found to be due to loss of flp-1, while the osmolarity defect is due to loss of daf-10. In addition, loss of flp-1 and daf-10 both cause several phenotypes that increase in severity in the double mutants by disrupting different neurons in the neural circuits.
[Mh] Termos MeSH primário: Proteínas de Caenorhabditis elegans/fisiologia
Caenorhabditis elegans/fisiologia
Neuropeptídeos/fisiologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Caenorhabditis elegans/metabolismo
Proteínas de Caenorhabditis elegans/química
Locomoção
Neuropeptídeos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (Flp-1 protein, C elegans); 0 (Neuropeptides)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189320


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[PMID]:29269293
[Au] Autor:Tajima K; Akanuma S; Matsumoto-Akanuma A; Yamanaka D; Ishibashi KI; Adachi Y; Ohno N
[Ad] Endereço:Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.
[Ti] Título:Activation of macrophages by a laccase-polymerized polyphenol is dependent on phosphorylation of Rac1.
[So] Source:Biochem Biophys Res Commun;495(3):2209-2213, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Various physiologically active effects of polymerized polyphenols have been reported. In this study, we synthesized a polymerized polyphenol (mL2a-pCA) by polymerizing caffeic acid using mutant Agaricus brasiliensis laccase and analyzed its physiological activity and mechanism of action. We found that mL2a-pCA induced morphological changes and the production of cytokines and chemokines in C3H/HeN mouse-derived resident peritoneal macrophages in vitro. The mechanisms of action of polymerized polyphenols on in vitro mouse resident peritoneal cells have not been characterized in detail previously. Herein, we report that the mL2a-pCA-induced production of interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1) in C3H/HeN mouse-derived resident peritoneal cells was inhibited by treatment with the Rac1 inhibitor NSC23766 trihydrochloride. In addition, we found that mL2a-pCA activated the phosphorylation Rac1. Taken together, the results show that mL2a-pCA induced macrophage activation via Rac1 phosphorylation-dependent pathways.
[Mh] Termos MeSH primário: Lacase/química
Ativação de Macrófagos/imunologia
Macrófagos/imunologia
Macrófagos/patologia
Neuropeptídeos/imunologia
Polifenóis/administração & dosagem
Polifenóis/química
Proteínas rac1 de Ligação ao GTP/imunologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Relação Dose-Resposta a Droga
Ativação Enzimática
Ativação de Macrófagos/efeitos dos fármacos
Macrófagos/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C3H
Fosforilação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuropeptides); 0 (Polyphenols); 0 (Rac1 protein, mouse); EC 1.10.3.2 (Laccase); EC 3.6.5.2 (rac1 GTP-Binding Protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE


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[PMID]:29225168
[Au] Autor:Chai H; Tao Z; Chen W; Xu Y; Huang F; Su C; Chen X
[Ad] Endereço:The Department of Thoracic and Cardiovascular Surgery, Nanjing First Hospital, Nanjing Medical University, Changle Road 68, Nanjing 210006, Jiangsu, People's Republic of China.
[Ti] Título:Cortistatin attenuates angiotensin II-induced abdominal aortic aneurysm through inactivation of the ERK1/2 signaling pathways.
[So] Source:Biochem Biophys Res Commun;495(2):1801-1806, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Abdominal aortic aneurysm (AAA) is a fatal disease that is associated with chronic inflammation in the vessel wall. Cortistatin is implicated in inflammation, vascular smooth muscle cell migration and other cardiovascular pathologies. But, the hypothetical effect of cortistatin on AAA remains uncertain. We investigated the effect of cortistatin administration to angiotensin (Ang) II-induced AAA formation in apolipoprotein E deficient (Apoe ) mice. We showed that cortistatin administration significantly suppresses incidence and severity of AAA in Apoe mice. A significant increase in macrophage infiltration, excretion of inflammatory cytokines, activities and expression levels of MMP2 and MMP9, reactive oxygen species levels and cell apoptosis in aneurysmal aortic wall of Apoe mice infused with Ang-II, and these events were significantly alleviated by co-treatment with cortistatin. Mechanistic studies showed that the protective effects of cortistatin were related to the blocking of ERK1/2 signaling pathways, while does not was not actually affect JNK, P38 phosphorylation. In conclusion, cortistatin appears to play an essential role in the formation of AAA and indicate cortistatin may as novel therapeutic option for AAA.
[Mh] Termos MeSH primário: Aneurisma da Aorta Abdominal/prevenção & controle
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Neuropeptídeos/administração & dosagem
[Mh] Termos MeSH secundário: Angiotensina II/administração & dosagem
Animais
Aorta Abdominal/efeitos dos fármacos
Aorta Abdominal/metabolismo
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/etiologia
Aneurisma da Aorta Abdominal/metabolismo
Apoptose/efeitos dos fármacos
Linhagem Celular
Modelos Animais de Doenças
Elastina/metabolismo
Masculino
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Camundongos
Camundongos Knockout para ApoE
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/patologia
Proteólise/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuropeptides); 0 (Reactive Oxygen Species); 0 (cortistatin); 11128-99-7 (Angiotensin II); 9007-58-3 (Elastin); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, mouse); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


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[PMID]:27776345
[Au] Autor:Mateos-Hernández L; Villar M; Doncel-Pérez E; Trevisan-Herraz M; García-Forcada Á; Ganuza FR; Vázquez J; de la Fuente J
[Ad] Endereço:SaBio. Instituto de Investigación en Recursos Cinegéticos IREC-CSIC-UCLM-JCCM, Ronda de Toledo s/n, 13005 Ciudad Real, Spain.
[Ti] Título:Quantitative proteomics reveals Piccolo as a candidate serological correlate of recovery from Guillain-Barré syndrome.
[So] Source:Oncotarget;7(46):74582-74591, 2016 11 15.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Guillain-Barré syndrome (GBS) is an autoimmune-mediated peripheral neuropathy of unknown cause. However, about a quarter of GBS patients have suffered a recent bacterial or viral infection, and axonal forms of the disease are especially common in these patients. Proteomics is a good methodological approach for the discovery of disease biomarkers. Until recently, most proteomics studies of GBS and other neurodegenerative diseases have focused on the analysis of the cerebrospinal fluid (CSF). However, serum represents an attractive alternative to CSF because it is easier to sample and has potential for biomarker discovery. The goal of this research was the identification of serum biomarkers associated with recovery from GBS. To address this objective, a quantitative proteomics approach was used to characterize differences in the serum proteome between a GBS patient and her healthy identical twin in order to lessen variations due to differences in genetic background, and with additional serum samples collected from unrelated GBS (N = 3) and Spinal Cord Injury (SCI) (N = 3) patients with similar medications. Proteomics results were then validated by ELISA using sera from additional GBS patients (N = 5) and healthy individuals (N = 3). All GBS and SCI patients were recovering from the acute phase of the disease. The results showed that Piccolo, a protein that is essential in the maintenance of active zone structure, constitutes a potential serological correlate of recovery from GBS. These results provided the first evidence for the Piccolo´s putative role in GBS, suggesting a candidate target for developing a serological marker of disease recovery.
[Mh] Termos MeSH primário: Biomarcadores
Proteínas do Citoesqueleto/sangue
Síndrome de Guillain-Barré/metabolismo
Síndrome de Guillain-Barré/reabilitação
Neuropeptídeos/sangue
Proteômica
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Proteínas Sanguíneas
Estudos de Casos e Controles
Feminino
Seres Humanos
Masculino
Meia-Idade
Modelos Biológicos
Proteoma
Proteômica/métodos
Recuperação de Função Fisiológica
Reprodutibilidade dos Testes
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Blood Proteins); 0 (Cytoskeletal Proteins); 0 (Neuropeptides); 0 (PCLO protein, human); 0 (Proteome)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.12789


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[PMID]:28470106
[Au] Autor:Spellmann I; Riedel M; Städtler J; Zill P; Obermeier M; Cerovecki A; Dehning S; Schennach R; Epple M; Opgen-Rhein M; Müller N; Bondy B; Möller HJ; Musil R
[Ad] Endereço:a Department of Psychiatry and Psychotherapy , Ludwig-Maximilians-University Munich , Munich , Germany.
[Ti] Título:Associations of NEUROD2 polymorphisms and change of cognitive dysfunctions in schizophrenia and schizoaffective disorder after eight weeks of antipsychotic treatment.
[So] Source:Cogn Neuropsychiatry;22(4):280-297, 2017 Jul.
[Is] ISSN:1464-0619
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: NEUROD2 is a neurospecific helix-loop-helix transcription factor which has an impact on the regulation of glutamatergic and GABAergic genes. We investigated an association of NEUROD2 with neurocognitive dysfunctions in schizophrenia and schizoaffective disorder patients before and during treatment with different second-generation antipsychotics. METHODS: Patients were genotyped for four different polymorphisms of the NEUROD2 gene ((rs9889354(A/G), rs1877032(C/T), rs12453682(C/T) and rs11078918(C/G)). Cognitive function was assessed at baseline and week 8. Results of individual neuropsychological tests were assigned to six cognitive domains (reaction time and quality; executive function; working, verbal and visual memory) and a general cognitive index. RESULTS: 167 patients were included in the study. The NEUROD2 exonic polymorphism rs11078918 showed significant associations with verbal memory and executive functions, whereas the NEUROD2 polymorphism rs12453682 was significantly associated with working and verbal memory, executive functions and with a cognitive index. Significant associations were found at baseline and after eight weeks. Moreover, significant associations between the change in neuropsychological test results during antipsychotic treatment and the NEUROD2 polymorphisms rs11078918 and rs12453682 were observed. CONCLUSIONS: Our findings suggest that the NEUROD2 gene could play a role in the pathophysiology of neurocognitive dysfunctions as well as in the change of cognitive symptoms under antipsychotic treatment in schizophrenia and schizoaffective disorder.
[Mh] Termos MeSH primário: Antipsicóticos/uso terapêutico
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Transtornos Cognitivos/genética
Neuropeptídeos/genética
Polimorfismo Genético
Transtornos Psicóticos
Esquizofrenia
Psicologia do Esquizofrênico
[Mh] Termos MeSH secundário: Adulto
Cognição/fisiologia
Transtornos Cognitivos/fisiopatologia
Função Executiva/fisiologia
Feminino
Genótipo
Seres Humanos
Masculino
Memória/fisiologia
Meia-Idade
Testes Neuropsicológicos
Transtornos Psicóticos/tratamento farmacológico
Transtornos Psicóticos/genética
Transtornos Psicóticos/fisiopatologia
Transtornos Psicóticos/psicologia
Tempo de Reação
Esquizofrenia/tratamento farmacológico
Esquizofrenia/genética
Esquizofrenia/fisiopatologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (NEUROD2 protein, human); 0 (Neuropeptides)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1080/13546805.2017.1322502


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[PMID]:28452955
[Au] Autor:Grässel S; Muschter D
[Ad] Endereço:Department of Orthopedic Surgery, Exp. Orthopedics, ZMB/Biopark 1, University of Regensburg, 93053 Regensburg, Germany. susanne.graessel@ukr.de.
[Ti] Título:Peripheral Nerve Fibers and Their Neurotransmitters in Osteoarthritis Pathology.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 28.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The importance of the nociceptive nervous system for maintaining tissue homeostasis has been known for some time, and it has also been suggested that organogenesis and tissue repair are under neuronal control. Changes in peripheral joint innervation are supposed to be partly responsible for degenerative alterations in joint tissues which contribute to development of osteoarthritis. Various resident cell types of the musculoskeletal system express receptors for sensory and sympathetic neurotransmitters, allowing response to peripheral neuronal stimuli. Among them are mesenchymal stem cells, synovial fibroblasts, bone cells and chondrocytes of different origin, which express distinct subtypes of adrenoceptors (AR), receptors for vasoactive intestinal peptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP). Some of these cell types synthesize and secrete neuropeptides such as SP, and they are positive for tyrosine-hydroxylase (TH), the rate limiting enzyme for biosynthesis of catecholamines. Sensory and sympathetic neurotransmitters are involved in the pathology of inflammatory diseases such as rheumatoid arthritis (RA) which manifests mainly in the joints. In addition, they seem to play a role in pathogenesis of priori degenerative joint disorders such as osteoarthritis (OA). Altogether it is evident that sensory and sympathetic neurotransmitters have crucial trophic effects which are critical for joint tissue and bone homeostasis. They modulate articular cartilage, subchondral bone and synovial tissue properties in physiological and pathophysiological conditions, in addition to their classical neurological features.
[Mh] Termos MeSH primário: Neurotransmissores/metabolismo
Osteoartrite/patologia
Nervos Periféricos/metabolismo
[Mh] Termos MeSH secundário: Peptídeo Relacionado com Gene de Calcitonina/metabolismo
Condrócitos/citologia
Condrócitos/metabolismo
Seres Humanos
Neuropeptídeos/metabolismo
Osteoartrite/metabolismo
Receptores Adrenérgicos/metabolismo
Substância P/metabolismo
Peptídeo Intestinal Vasoativo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Neuropeptides); 0 (Neurotransmitter Agents); 0 (Receptors, Adrenergic); 33507-63-0 (Substance P); 37221-79-7 (Vasoactive Intestinal Peptide); 83652-28-2 (Calcitonin Gene-Related Peptide)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE



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