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Pesquisa : Lamina and Tipo and A [Palavras]
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  1 / 9334 MEDLINE  
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[PMID]:29390291
[Au] Autor:Al Kaissi A; Kuranova M; Pleskach N; Kenis V; Nassib NM; Grill F; Ganger R; Gerit Kircher S
[Ad] Endereço:Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK and AUVA Trauma Centre Meidling, First Medical Department, Hanusch Hospital.
[Ti] Título:Are parents of children with Cockayne syndrome manifesting features of the disorder?: Case reports.
[So] Source:Medicine (Baltimore);96(50):e8970, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Postnatal growth failure and progressive neurologic dysfunction and increasing multiorgan involvement are the main clinical features of Cockayne syndrome (CS). CS is a rare autosomal recessive disorder of the group of DNA repair diseases. Usually, genetic carriers, such as parents of patients, are not at risk for developing the disease. PATIENT CONCERNS: A series of 14 family subjects (6 children with age range from 6 months to 4 years with CS) and 9 parents (aged from 23 to 34 years) from consanguineous families is reported. DIAGNOSES: Ultraviolet irradiation studies were performed on these children and were indicative of CS. INTERVENTIONS: Cells of skin fibroblast from these children with the disease showed a symmetrical accumulation of chromosomal aberrations and the nuclear lamina aberrations. Our results showed a significant and simultaneous increase of percent of blebbs and invaginations of the nuclear lamina in all cases CS. The pronounced changes in 12.6 times at atypical form (girl); in 8.5 times at severe form (boy) and in 5.6 times at light form (boy). Percentage of metaphases with chromosomal aberration is significantly higher in CS cells: in 4 times at atypical form, in 3 times at hard form, and in 2 times at light form. The parents of these families (consanguineous families) were intellectually variable between normal/borderline intelligence, though most manifested a constellation of skeletal and extraskeletal abnormalities and notably, the characteristic cachectic facial appearance. The parents were considered as manifesting the mild type of CS, because they showed no abnormalities of DNA repair. OUTCOMES: Clinical manifestations in heterozygote carriers of an autosomal recessive disorders is a rare phenomenon as carriers are usually healthy. LESSONS: The interesting finding of the families studied is that there appeared to be a multitude of carriers manifesting with normal to borderline intelligence but with a wide spectrum of skeletal and extraskeletal abnormalities.
[Mh] Termos MeSH primário: Síndrome de Cockayne/genética
Pais
[Mh] Termos MeSH secundário: Adulto
Pré-Escolar
Consanguinidade
Feminino
Predisposição Genética para Doença
Heterozigoto
Seres Humanos
Lactente
Inteligência
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008970


  2 / 9334 MEDLINE  
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[PMID]:29197877
[Au] Autor:Gerbino A; Bottillo I; Milano S; Lipari M; Zio R; Morlino S; Mola MG; Procino G; Re F; Zachara E; Grammatico P; Svelto M; Carmosino M
[Ad] Endereço:Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, Bari, Italy.
[Ti] Título:Functional Characterization of a Novel Truncating Mutation in Lamin A/C Gene in a Family with a Severe Cardiomyopathy with Conduction Defects.
[So] Source:Cell Physiol Biochem;44(4):1559-1577, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Truncating LMNA gene mutations occur in many inherited cardiomyopathy cases, but the molecular mechanisms involved in the disease they cause have not yet been systematically investigated. Here, we studied a novel frameshift LMNA variant (p.D243Gfs*4) identified in three members of an Italian family co-segregating with a severe form of cardiomyopathy with conduction defects. METHODS: HEK293 cells and HL-1 cardiomyocytes were transiently transfected with either Lamin A or D243Gfs*4 tagged with GFP (or mCherry). D243Gfs*4 expression, cellular localization and its effects on diverse cellular mechanisms were evaluated with western blotting, laser-scanning confocal microscopy and video-imaging analysis in single cells. RESULTS: When expressed in HEK293 cells, GFP- (or mCherry)-tagged LMNA D243Gfs*4 colocalized with calnexin within the ER. ER mislocalization of LMNA D243Gfs*4 did not significantly induce ER stress response, abnormal Ca2+ handling and apoptosis when compared with HEK293 cells expressing another truncated mutant of LMNA (R321X) which similarly accumulates within the ER. Of note, HEK293-LMNA D243Gfs*4 cells showed a significant reduction of connexin 43 (CX43) expression level, which was completely rescued by activation of the WNT/ß-catenin signaling pathway. When expressed in HL-1 cardiomyocytes, D243Gfs*4 significantly impaired the spontaneous Ca2+ oscillations recorded in these cells as result of propagation of the depolarizing waves through the gap junctions between non-transfected cells surrounding a cell harboring the mutation. Furthermore, mCh-D243Gfs*4 HL-1 cardiomyocytes showed reduced CX43-dependent Lucifer Yellow (LY) loading and propagation. Of note, activation of ß-catenin rescued both LY loading and LMNA D243Gfs*4 -HL-1 cells spontaneous activity propagation. CONCLUSION: Overall, the present results clearly indicate the involvement of the aberrant CX43 expression/activity as a pathogenic mechanism for the conduction defects associated to this LMNA truncating alteration.
[Mh] Termos MeSH primário: Doença do Sistema de Condução Cardíaco/genética
Cardiomiopatias/genética
Lamina Tipo A/genética
[Mh] Termos MeSH secundário: Apoptose
Sequência de Bases
Cálcio/metabolismo
Calnexina/metabolismo
Doença do Sistema de Condução Cardíaco/complicações
Doença do Sistema de Condução Cardíaco/patologia
Cardiomiopatias/complicações
Cardiomiopatias/patologia
Linhagem Celular
Conexina 43
Retículo Endoplasmático/metabolismo
Feminino
Junções Comunicantes/metabolismo
Células HEK293
Seres Humanos
Lamina Tipo A/metabolismo
Repetições de Microssatélites/genética
Microscopia Confocal
Meia-Idade
Mutagênese Sítio-Dirigida
Miócitos Cardíacos/citologia
Miócitos Cardíacos/metabolismo
Linhagem
Polimorfismo de Nucleotídeo Único
Imagem com Lapso de Tempo
Via de Sinalização Wnt
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (LMNA protein, human); 0 (Lamin Type A); 139873-08-8 (Calnexin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE
[do] DOI:10.1159/000485651


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[PMID]:29310440
[Au] Autor:Kodama H; Kumai Y; Nishimoto K; Toya Y; Miyamaru S; Furushima S; Yumoto E
[Ad] Endereço:1 Department of Otolaryngology Head and Neck Surgery, Kumamoto University Graduate School of Medicine, Kumamoto, Japan.
[Ti] Título:The Ferret as a Surgical Model for Vocal Fold Scar Creation and Treatment.
[So] Source:Ann Otol Rhinol Laryngol;127(3):146-154, 2018 Mar.
[Is] ISSN:1943-572X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To develop a vocal fold (VF) scarring procedure in the ferret, characterize the scars histologically, and test the injectability of the lamina propria (LP). Secondarily, to compare laryngeal anatomy of the ferret with rat and rabbit. MATERIALS AND METHODS: The larynges of 18 male ferrets were prepared by unilateral scarring, and normal larynges from 6 female Wistar rats and 5 male albino rabbits were used for comparative purposes. For scarring, the right VF were electrocauterized, ablating the entire LP. Prior to harvesting the larynges at 4 and 16 weeks, each ferret was re-anesthetized, and in 3 animals, India ink was injected into the LPs of both normal and scarred VFs. RESULTS: Laryngoscopic methods and instrumentation for precise visualization, scarring, and injection were developed. The scarred VFs had reduced hyaluronic acid and increased collagen type I, III, and fibronectin compared with normal VFs. The 2 timepoints (4 and 16 weeks) differed significantly only in collagen type III level (levels were higher at 4 weeks). Injected ink migrated from scarred LP to muscle layer just beneath the scarred tissue 3 hours after injection. CONCLUSION: The ferret is a promising species for creation and experimental treatment of vocal fold scar.
[Mh] Termos MeSH primário: Cicatriz
Eletrocoagulação/métodos
Laringoscopia
Membrana Mucosa
Prega Vocal/cirurgia
[Mh] Termos MeSH secundário: Animais
Cicatriz/etiologia
Cicatriz/metabolismo
Cicatriz/patologia
Colágeno Tipo I/análise
Colágeno Tipo III/análise
Feminino
Furões
Fibronectinas/análise
Laringoscopia/instrumentação
Laringoscopia/métodos
Modelos Anatômicos
Membrana Mucosa/patologia
Membrana Mucosa/cirurgia
Coelhos
Ratos
Prega Vocal/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Collagen Type III); 0 (Fibronectins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1177/0003489417750165


  4 / 9334 MEDLINE  
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[PMID]:29381917
[Au] Autor:Zhou L; Fan J; Cheng L; Jiang T; Yun B; Tang G; Yin J; Fang J; Yin G
[Ad] Endereço:Department of Orthopedics, the First Affiliated Hospital of Nanjing Medical University.
[Ti] Título:Changes of cervical sagittal alignments during motions in patients with cervical kyphosis.
[So] Source:Medicine (Baltimore);96(47):e8410, 2017 Nov.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Changes of cervical sagittal alignment during motion in cervical kyphosis patients have never been published before. This study was to investigate the changes and provide a better reference for orthopedic treatment.Randomized double-blind repeat trial was carried out on 60 patients with cervical kyphosis. On standard position, hyper flexion, and hyper extension sagittal radiographs, the following measurements were made: the C2-7 vertebral body spatial alignment angle (∠A), C2-7 vertebral lower terminal lamina tilt angle (∠B), C2/3 to C6/7 segmental intervertebral space angle (∠C), the distance from the posterior edge of odontoid to C7 vertebral body (D value), and the difference of angle A, B, and C between cervical flexion and extension movement. Another 60 healthy volunteers were enrolled, of whom the cervical curve apex was determined using Borden's method to compare change and distribution characteristics to patients with cervical kyphosis and C value.In standard lateral position, ∠A was positive and increased from C2 to C7. In hyper extension position, ∠A decreased with reducing amplitude from C2 to C7 compared with the standard position, whereas in hyper flexion position, the average value of ∠A increased with decreasing amplitude from C2 to C7. ∠B followed similar change regularities as ∠A with a larger mean value. In cervical flexion and extension movement, ∠A change of upper vertebral body (∠D) was almost equal to ∠A change of lower vertebral body and ∠C change between the adjacent 2 vertebral bodies (∠E). The curve apex distribution was almost between C4 and C5 in cervical kyphosis patients. A significant difference was observed between cervical kyphosis patients and normal people in C value and D value.The correction of the cervical kyphosis can be carried out from the apex of the cervical spine that provides a solid theoretical foundation for the correction of the cervical kyphosis.
[Mh] Termos MeSH primário: Vértebras Cervicais
Cabeça/fisiologia
Cifose/fisiopatologia
Amplitude de Movimento Articular/fisiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Fenômenos Biomecânicos
Método Duplo-Cego
Feminino
Seres Humanos
Masculino
Meia-Idade
Movimento (Física)
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008410


  5 / 9334 MEDLINE  
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[PMID]:29320541
[Au] Autor:Ozturk MC; Xu Q; Cinar A
[Ad] Endereço:Department of Chemical and Biological Engineering, Illinois Institute of Technology, Chicago, IL, United States of America.
[Ti] Título:Agent-based modeling of the interaction between CD8+ T cells and Beta cells in type 1 diabetes.
[So] Source:PLoS One;13(1):e0190349, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We propose an agent-based model for the simulation of the autoimmune response in T1D. The model incorporates cell behavior from various rules derived from the current literature and is implemented on a high-performance computing system, which enables the simulation of a significant portion of the islets in the mouse pancreas. Simulation results indicate that the model is able to capture the trends that emerge during the progression of the autoimmunity. The multi-scale nature of the model enables definition of rules or equations that govern cellular or sub-cellular level phenomena and observation of the outcomes at the tissue scale. It is expected that such a model would facilitate in vivo clinical studies through rapid testing of hypotheses and planning of future experiments by providing insight into disease progression at different scales, some of which may not be obtained easily in clinical studies. Furthermore, the modular structure of the model simplifies tasks such as the addition of new cell types, and the definition or modification of different behaviors of the environment and the cells with ease.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Diabetes Mellitus Tipo 1/imunologia
Ilhotas Pancreáticas/imunologia
Modelos Biológicos
[Mh] Termos MeSH secundário: Animais
Membrana Basal/imunologia
Ilhotas Pancreáticas/fisiopatologia
Camundongos
Regeneração
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190349


  6 / 9334 MEDLINE  
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[PMID]:29293568
[Au] Autor:Do K; Laing BT; Landry T; Bunner W; Mersaud N; Matsubara T; Li P; Yuan Y; Lu Q; Huang H
[Ad] Endereço:Department of Kinesiology, East Carolina University, Greenville, North Carolina, United States of America.
[Ti] Título:The effects of exercise on hypothalamic neurodegeneration of Alzheimer's disease mouse model.
[So] Source:PLoS One;13(1):e0190205, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alzheimer's disease is a neurodegenerative disorder that affects the central nervous system. In this study, we characterized and examined the early metabolic changes in the triple transgenic mouse AD model (3xtg-AD), and their relationship with the hypothalamus, a key regulator of metabolism in the central nervous system. We observed that the 3xtg-AD model exhibited significantly higher oxygen consumption as well as food intake before reported amyloid plaque formation, indicating that metabolic abnormalities occurred at early onset in the 3xtg-AD model compared with their counterparts. Analysis of gene expression in the hypothalamus indicated increased mRNA expression of inflammation- and apoptosis-related genes, as well as decreased gene expression of Agouti-related protein (AgRP) and Melanocortin 4 receptor (MC4R) at 12 weeks of age. Immunofluorescence analysis revealed that pro-opiomelanocortin (POMC) and NPY-expressing neurons decreased at 24 weeks in the 3xtg-AD model. Four weeks of voluntary exercise were sufficient to reverse the gene expression of inflammation and apoptotic markers in the hypothalamus, six weeks of exercise improved glucose metabolism, moreover, 8 weeks of voluntary exercise training attenuated apoptosis and augmented POMC and NPY-expressing neuronal populations in the hypothalamus compared to the control group. Our results indicated that early onset of metabolic abnormalities may contribute to the pathology of AD, which is associated with increased inflammation as well as decreased neuronal population and key neuropeptides in the hypothalamus. Furthermore, early intervention by voluntary exercise normalized hypothalamic inflammation and neurodegeneration as well as glucose metabolism in the 3xtg-AD model. The data, taken as a whole, suggests a hypothalamic-mediated mechanism where exercise prevents the progression of dementia and of Alzheimer's disease.
[Mh] Termos MeSH primário: Doença de Alzheimer/patologia
Modelos Animais de Doenças
Hipotálamo/patologia
Condicionamento Físico Animal
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Regulação da Expressão Gênica
Glucose/metabolismo
Hipotálamo/metabolismo
Marcação In Situ das Extremidades Cortadas
Camundongos
Camundongos Transgênicos
Mitocôndrias/metabolismo
Pró-Opiomelanocortina/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 66796-54-1 (Pro-Opiomelanocortin); IY9XDZ35W2 (Glucose)
[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:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190205


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[PMID]:28745620
[Au] Autor:Iturri L; Saenz Coronilla J; Lallemand Y; Gomez Perdiguero E
[Ad] Endereço:Department of Developmental and Stem Cell Biology, CNRS UMR3738, Department of Immunology, Institut Pasteur; Cellule Pasteur UPMC, University Pierre et Marie Curie.
[Ti] Título:Identification Of Erythromyeloid Progenitors And Their Progeny In The Mouse Embryo By Flow Cytometry.
[So] Source:J Vis Exp;(125), 2017 Jul 17.
[Is] ISSN:1940-087X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Macrophages are professional phagocytes from the innate arm of the immune system. In steady-state, sessile macrophages are found in adult tissues where they act as front line sentinels of infection and tissue damage. While other immune cells are continuously renewed from hematopoietic stem and progenitor cells (HSPC) located in the bone marrow, a lineage of macrophages, known as resident macrophages, have been shown to be self-maintained in tissues without input from bone marrow HSPCs. This lineage is exemplified by microglia in the brain, Kupffer cells in the liver and Langerhans cells in the epidermis among others. The intestinal and colon lamina propria are the only adult tissues devoid of HSPC-independent resident macrophages. Recent investigations have identified that resident macrophages originate from the extra-embryonic yolk sac hematopoiesis from progenitor(s) distinct from fetal hematopoietic stem cells (HSC). Among yolk sac definitive hematopoiesis, erythromyeloid progenitors (EMP) give rise both to erythroid and myeloid cells, in particular resident macrophages. EMP are only generated within the yolk sac between E8.5 and E10.5 days of development and they migrate to the fetal liver as early as circulation is connected, where they expand and differentiate until at least E16.5. Their progeny includes erythrocytes, macrophages, neutrophils and mast cells but only EMP-derived macrophages persist until adulthood in tissues. The transient nature of EMP emergence and the temporal overlap with HSC generation renders the analysis of these progenitors difficult. We have established a tamoxifen-inducible fate mapping protocol based on expression of the macrophage cytokine receptor Csf1r promoter to characterize EMP and EMP-derived cells in vivo by flow cytometry.
[Mh] Termos MeSH primário: Embrião de Mamíferos/citologia
Citometria de Fluxo/métodos
Células-Tronco/citologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Células Cultivadas
Desenvolvimento Embrionário/efeitos dos fármacos
Feminino
Antígenos Comuns de Leucócito/metabolismo
Macrófagos/citologia
Macrófagos/metabolismo
Camundongos
Proteínas Proto-Oncogênicas c-kit/metabolismo
Receptores de Fator Estimulador das Colônias de Granulócitos e Macrófagos/genética
Receptores de Fator Estimulador das Colônias de Granulócitos e Macrófagos/metabolismo
Células-Tronco/metabolismo
Tamoxifeno/farmacologia
Gravação em Vídeo
Saco Vitelino/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Csf1r protein, mouse); 0 (Receptors, Granulocyte-Macrophage Colony-Stimulating Factor); 094ZI81Y45 (Tamoxifen); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 3.1.3.48 (Leukocyte Common Antigens)
[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:170727
[St] Status:MEDLINE
[do] DOI:10.3791/55305


  8 / 9334 MEDLINE  
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[PMID]:29191657
[Au] Autor:Shiozawa K; Shuting J; Yoshioka Y; Ochiya T; Kondo T
[Ad] Endereço:Division of Rare Cancer Research, National Cancer Center Research Institute, Tokyo, Japan, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan. Electronic address: kshiozaw@ncc.go.jp.
[Ti] Título:Extracellular vesicle-encapsulated microRNA-761 enhances pazopanib resistance in synovial sarcoma.
[So] Source:Biochem Biophys Res Commun;495(1):1322-1327, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The development of drug resistance in tumor cells leads to relapse and distant metastasis. Secreted microRNAs (miRNAs) enclosed in extracellular vesicles (EVs) can act as intercellular messengers. The objective of our study was to elucidate the role of secreted miRNAs to better understand the regulatory network underlying pazopanib-resistance in synovial sarcoma cells. We performed a comprehensive analysis of secreted miRNA abundance in pazopanib treated/untreated synovial sarcoma cells from four different cell lines (SYO-1, HS-SYII, 1273/99, and YaFuSS) using microarray technology, and discovered miR-761 in EVs as a potential biomarker of pazopanib-resistance in synovial sarcoma. Furthermore, we showed that miR-761 putatively targeted three proteins, thyroid hormone receptor interactor 6 (TRIP6), lamin A/C (LMNA), and NAD-dependent protein deacetylase sirtuin-3 (SIRT3). Knockdown of any of these proteins was shown in previous studies to confer increased resistance to chemotherapeutic agents. Our findings provide new insight into the potential role of miR-761, an EV-secreted miRNA from synovial sarcoma cells, making it a potential candidate for use in sarcoma therapy in the future.
[Mh] Termos MeSH primário: Resistência a Medicamentos Antineoplásicos
Vesículas Extracelulares/metabolismo
MicroRNAs/metabolismo
Pirimidinas/administração & dosagem
Sarcoma Sinovial/tratamento farmacológico
Sarcoma Sinovial/metabolismo
Sulfonamidas/administração & dosagem
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Antineoplásicos/administração & dosagem
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Seres Humanos
Proteínas com Domínio LIM/metabolismo
Lamina Tipo A/metabolismo
Sarcoma Sinovial/patologia
Sirtuína 3/metabolismo
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Antineoplastic Agents); 0 (LIM Domain Proteins); 0 (LMNA protein, human); 0 (Lamin Type A); 0 (MicroRNAs); 0 (Pyrimidines); 0 (Sulfonamides); 0 (TRIP6 protein, human); 0 (Transcription Factors); 0 (microRNA761 microRNA, human); 7RN5DR86CK (pazopanib); EC 3.5.1.- (SIRT3 protein, human); EC 3.5.1.- (Sirtuin 3)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


  9 / 9334 MEDLINE  
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[PMID]:29190650
[Au] Autor:Stalvey MS; Havasi V; Tuggle KL; Wang D; Birket S; Rowe SM; Sorscher EJ
[Ad] Endereço:Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, United States of America.
[Ti] Título:Reduced bone length, growth plate thickness, bone content, and IGF-I as a model for poor growth in the CFTR-deficient rat.
[So] Source:PLoS One;12(11):e0188497, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Reduced growth and osteopenia are common in individuals with cystic fibrosis (CF). Additionally, improved weight and height are associated with better lung function and overall health in the disease. Mechanisms for this reduction in growth are not understood. We utilized a new CFTR knockout rat to evaluate growth in young CF animals, via femur length, microarchitecture of bone and growth plate, as well as serum IGF-I concentrations. METHODS: Femur length was measured in wild-type (WT) and SD-CFTRtm1sage (Cftr-/-) rats, as a surrogate marker for growth. Quantitative bone parameters in Cftr-/- and WT rats were measured by micro computed tomography (micro-CT). Bone histomorphometry and cartilaginous growth plates were analyzed. Serum IGF-I concentrations were also compared. RESULTS: Femur length was reduced in both Cftr-/- male and female rats compared to WT. Multiple parameters of bone microarchitecture (of both trabecular and cortical bone) were adversely affected in Cftr-/- rats. There was a reduction in overall growth plate thichkness in both male and female Cftr-/- rats, as well as hypertrophic zone thickness and mean hypertrophic cell volume in male rats, indicating abnormal growth characteristics at the plate. Serum IGF-I concentrations were severely reduced in Cftr-/- rats compared to WT littermates. CONCLUSIONS: Despite absence of overt lung or pancreatic disease, reduced growth and bone content were readily detected in young Cftr-/- rats. Reduced size of the growth plate and decreased IGF-I concentrations suggest the mechanistic basis for this phenotype. These findings appear to be intrinsic to the CFTR deficient state and independent of significant clinical confounders, providing substantive evidence for the importance of CFTR on maintinaing normal bone growth.
[Mh] Termos MeSH primário: Desenvolvimento Ósseo
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Fibrose Cística/patologia
Lâmina de Crescimento/patologia
Fator de Crescimento Insulin-Like I/metabolismo
[Mh] Termos MeSH secundário: Animais
Fibrose Cística/metabolismo
Modelos Animais de Doenças
Feminino
Técnicas de Silenciamento de Genes
Lâmina de Crescimento/metabolismo
Masculino
Ratos
Ratos Sprague-Dawley
Microtomografia por Raio-X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CFTR protein, rat); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 67763-96-6 (Insulin-Like Growth Factor I)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188497


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[PMID]:29182640
[Au] Autor:Kim HJ; Kim N; Kim YS; Nam RH; Lee SM; Park JH; Choi D; Hwang YJ; Lee J; Lee HS; Kim MS; Lee MY; Lee DH
[Ad] Endereço:Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, S. Korea.
[Ti] Título:Changes in the interstitial cells of Cajal and neuronal nitric oxide synthase positive neuronal cells with aging in the esophagus of F344 rats.
[So] Source:PLoS One;12(11):e0186322, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aging-associated cellular and molecular changes in esophagus have not been established, yet. Thus we evaluated histological structure, interstitial cells of Cajal (ICCs), neuronal nitric oxide synthase (nNOS)-positive cells, and contractility in the esophagus of Fischer 344 rat at different ages (6-, 31-, 74-weeks, and 2-years). The lamina propria thickness and endomysial area were calculated. The immunoreactivity of c-Kit, nNOS and protein gene product (PGP) 9.5 was counted after immunohistochemistry. Expression of c-Kit, stem cell factor (SCF), nNOS and PGP 9.5 mRNA was measured by real-time PCR, and expression of c-Kit and nNOS protein was detected by Western blot. Isovolumetric contractile force measurement and electrical field stimulation (EFS) were conducted. The lamina propria thickness increased (6 week vs 2 year, P = 0.005) and the endomysial area of longitudinal muscle decreased with aging (6 week vs 2 year, P<0.001), while endomysial area of circular muscle did not significantly decrease. The proportions of NOS-immunoreactive cells and c-Kit-immunoreactive areas declined with aging (6 week vs 2 year; P<0.001 and P = 0.004, respectively), but there was no significant change of PGP 9.5-immunopositiviy. The expressions of nNOS, c-Kit and SCF mRNA also reduced with aging (6 week vs 2 year; P = 0.006, P = 0.001 and P = 0.006, respectively), while the change of PGP 9.5 mRNA expression was not significant. Western blot showed the significant decreases of nNOS and c-Kit protein expression with aging (6 week vs 2 year; P = 0.008 and P = 0.012, respectively). The EFS-induced esophageal contractions significantly decreased in 2-yr-old rat compared with 6-wk-old rats, however, L-NG-Nitroarginine methylester did not significantly increase the spontaneous and EFS-induced contractions in the 6-wk- and 2-yr-old rat esophagus. In conclusion, an increase of lamina propria thickness, a decrease of endomysial area, c-Kit, SCF and NOS expression with preserved total enteric neurons, and contractility in aged rat esophagus may explain the aging-associated esophageal dysmotility.
[Mh] Termos MeSH primário: Envelhecimento
Esôfago/citologia
Células Intersticiais de Cajal/citologia
Neurônios/enzimologia
Óxido Nítrico Sintase Tipo I/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Esôfago/metabolismo
Células Intersticiais de Cajal/metabolismo
Masculino
Proteínas Proto-Oncogênicas c-kit/metabolismo
Ratos
Ratos Endogâmicos F344
Reação em Cadeia da Polimerase em Tempo Real
Fator de Células-Tronco/genética
Fator de Células-Tronco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Stem Cell Factor); EC 1.14.13.39 (Nitric Oxide Synthase Type I); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186322



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