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  1 / 247261 MEDLINE  
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[PMID]:29444082
[Au] Autor:Khan MI; Su YK; Zou J; Yang LW; Chou RH; Yu C
[Ad] Endereço:National Tsing Hua University, Chemistry Department, Hsinchu, Taiwan.
[Ti] Título:S100B as an antagonist to block the interaction between S100A1 and the RAGE V domain.
[So] Source:PLoS One;13(2):e0190545, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ca2+-binding human S100A1 protein is a type of S100 protein. S100A1 is a significant mediator during inflammation when Ca2+ binds to its EF-hand motifs. Receptors for advanced glycation end products (RAGE) correspond to 5 domains: the cytoplasmic, transmembrane, C2, C1, and V domains. The V domain of RAGE is one of the most important target proteins for S100A1. It binds to the hydrophobic surface and triggers signaling transduction cascades that induce cell growth, cell proliferation, and tumorigenesis. We used nuclear magnetic resonance (NMR) spectroscopy to characterize the interaction between S100A1 and the RAGE V domain. We found that S100B could interact with S100A1 via NMR 1H-15N HSQC titrations. We used the HADDOCK program to generate the following two binary complexes based on the NMR titration results: S100A1-RAGE V domain and S100A1-S100B. After overlapping these two complex structures, we found that S100B plays a crucial role in blocking the interaction site between RAGE V domain and S100A1. A cell proliferation assay WST-1 also supported our results. This report could potentially be useful for new protein development for cancer treatment.
[Mh] Termos MeSH primário: Antígenos de Neoplasias/metabolismo
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Subunidade beta da Proteína Ligante de Cálcio S100/fisiologia
Proteínas S100/metabolismo
[Mh] Termos MeSH secundário: Cálcio/metabolismo
Seres Humanos
Interações Hidrofóbicas e Hidrofílicas
Ressonância Magnética Nuclear Biomolecular
Ligação Proteica
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (S100 Calcium Binding Protein beta Subunit); 0 (S100 Proteins); 0 (S100A1 protein); 0 (S100B protein, human); EC 2.7.11.22 (MOK protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190545


  2 / 247261 MEDLINE  
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[PMID]:29320819
[Au] Autor:Chaibangyang W; Geadkaew-Krenc A; Vichasri-Grams S; Tesana S; Grams R
[Ad] Endereço:Graduate Program in Biomedical Sciences, Faculty of Allied Health Sciences, Thammasat University, Pathumthani 12121, Thailand.
[Ti] Título:Molecular and Biochemical Characterization of Opisthorchis viverrini Calreticulin.
[So] Source:Korean J Parasitol;55(6):643-652, 2017 Dec.
[Is] ISSN:1738-0006
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:Calreticulin (CALR), a multifunctional protein thoroughly researched in mammals, comprises N-, P-, and C-domain and has roles in calcium homeostasis, chaperoning, clearance of apoptotic cells, cell adhesion, and also angiogenesis. In this study, the spatial and temporal expression patterns of the Opisthorchis viverrini CALR gene were analyzed, and calcium-binding and chaperoning properties of recombinant O. viverrini CALR (OvCALR) investigated. OvCALR mRNA was detected from the newly excysted juvenile to the mature parasite by RT-PCR while specific antibodies showed a wide distribution of the protein. OvCALR was localized in tegumental cell bodies, testes, ovary, eggs, Mehlis' gland, prostate gland, and vitelline cells of the mature parasite. Recombinant OvCALR showed an in vitro suppressive effect on the thermal aggregation of citrate synthase. The recombinant OvCALR C-domain showed a mobility shift in native gel electrophoresis in the presence of calcium. The results imply that OvCALR has comparable function to the mammalian homolog as a calcium-binding molecular chaperone. Inferred from the observed strong immunostaining of the reproductive tissues, OvCALR should be important for reproduction and might be an interesting target to disrupt parasite fecundity. Transacetylase activity of OvCALR as reported for calreticulin of Haemonchus contortus could not be observed.
[Mh] Termos MeSH primário: Calreticulina/genética
Calreticulina/metabolismo
Expressão Gênica
Opisthorchis/genética
Opisthorchis/metabolismo
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Calreticulina/fisiologia
Citrato (si)-Sintase/metabolismo
Fertilidade/genética
Técnicas In Vitro
Chaperonas Moleculares
Opisthorchis/fisiologia
Proteínas Recombinantes
Reprodução/genética
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calreticulin); 0 (Molecular Chaperones); 0 (Recombinant Proteins); EC 2.3.3.1 (Citrate (si)-Synthase); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3347/kjp.2017.55.6.643


  3 / 247261 MEDLINE  
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[PMID]:29238189
[Au] Autor:Zhang CY; Sun XY; Ouyang JM; Gui BS
[Ad] Endereço:Institute of Biomineralization and Lithiasis Research, Jinan University, Guangzhou.
[Ti] Título:Diethyl citrate and sodium citrate reduce the cytotoxic effects of nanosized hydroxyapatite crystals on mouse vascular smooth muscle cells.
[So] Source:Int J Nanomedicine;12:8511-8525, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Objective: This study aimed to investigate the damage mechanism of nanosized hydroxyapatite (nano-HAp) on mouse aortic smooth muscle cells (MOVASs) and the injury-inhibiting effects of diethyl citrate (Et Cit) and sodium citrate (Na Cit) to develop new drugs that can simultaneously induce anticoagulation and inhibit vascular calcification. Methods: The change in cell viability was evaluated using a cell proliferation assay kit, and the amount of lactate dehydrogenase (LDH) released was measured using an LDH kit. Intracellular reactive oxygen species (ROS) and mitochondrial damage were detected by DCFH-DA staining and JC-1 staining. Cell apoptosis and necrosis were detected by Annexin V staining. Intracellular calcium concentration and lysosomal integrity were measured using Fluo-4/AM and acridine orange, respectively. Results: Nano-HAp decreased cell viability and damaged the cell membrane, resulting in the release of a large amount of LDH. Nano-HAp entered the cells and damaged the mitochondria, and then induced cell apoptosis by producing a large amount of ROS. In addition, nano-HAp increased the intracellular Ca concentration, leading to lysosomal rupture and cell necrosis. On addition of the anticoagulant Et Cit or Na Cit, cell viability and mitochondrial membrane potential increased, whereas the amount of LDH released, ROS, and apoptosis rate decreased. Et Cit and Na Cit could also chelate with Ca to inhibit the intracellular Ca elevations induced by nano-HAp, prevent lysosomal rupture, and reduce cell necrosis. High concentrations of Et Cit and Na Cit exhibited strong inhibitory effects. The inhibitory capacity of Na Cit was stronger than that of Et Cit at similar concentrations. Conclusion: Both Et Cit and Na Cit significantly reduced the cytotoxicity of nano-HAp on MOVASs and inhibited the apoptosis and necrosis induced by nano-HAp crystals. The chelating function of citrate resulted in both anticoagulation and binding to HAp. Et Cit and Na Cit may play a role as anticoagulants in reducing injury to the vascular wall caused by nano-HAp.
[Mh] Termos MeSH primário: Citratos/farmacologia
Durapatita/efeitos adversos
Músculo Liso Vascular/citologia
Nanopartículas/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Anticoagulantes/farmacologia
Apoptose/efeitos dos fármacos
Calcinose/prevenção & controle
Cálcio/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Durapatita/química
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/metabolismo
Nanopartículas/química
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticoagulants); 0 (Citrates); 0 (Reactive Oxygen Species); 0 (diethyl citrate); 1Q73Q2JULR (sodium citrate); 91D9GV0Z28 (Durapatite); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S145386


  4 / 247261 MEDLINE  
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[PMID]:28934710
[Au] Autor:Kovácik J; Dresler S
[Ad] Endereço:Department of Biology, University of Trnava, Priemyselná 4, 918 43 Trnava, Slovak Republic. Electronic address: jozkovacik@yahoo.com.
[Ti] Título:Calcium availability but not its content modulates metal toxicity in Scenedesmus quadricauda.
[So] Source:Ecotoxicol Environ Saf;147:664-669, 2018 Jan.
[Is] ISSN:1090-2414
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Impact of calcium nutrition (pre-culture on solid medium with standard or elevated Ca dose, i. e. 0.17 and 4.40mM marked as low and high Ca) on acute metal toxicity (Cd, Mn and Pb, 24h of exposure to 10µM) in freshwater green alga Scenedesmus quadricauda was studied. Surprisingly, Ca content differed only slightly between low and high Ca samples and applied metals rather suppressed its amount. Na content was higher in metal-exposed high Ca samples, indicating that Ca/Na ratio may affect accumulation of metals. Content of heavy metals increased in order Cd < Mn < Pb and high Ca samples contained less metal than low Ca samples at least in absorbed fraction. Accumulation of ascorbic acid and thiols (GSH - glutathione and PC2 - phytochelatin 2) was affected mainly by Cd, GSH also by Mn and PC2 by Pb with often significant differences between low Ca and high Ca samples. Calcium nutrition also affected responses of algae to metals at the level of antioxidative enzyme activities (SOD, APX, and CAT) and elevated values were typically found in high Ca samples while ROS (hydrogen peroxide and superoxide radical) were mainly depleted in Mn treatment. These data confirm that Ca nutrition affects accumulation of metals in algae and metabolic parameters as observed in vascular plants but, unlike them, rather Ca/Na ratio than absolute Ca content seems to regulate the uptake of metals.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Monitoramento Ambiental/métodos
Metais Pesados/toxicidade
Scenedesmus/efeitos dos fármacos
Poluentes Químicos da Água/toxicidade
[Mh] Termos MeSH secundário: Antioxidantes/metabolismo
Disponibilidade Biológica
Metais Pesados/metabolismo
Modelos Teóricos
Espécies Reativas de Oxigênio/metabolismo
Scenedesmus/metabolismo
Poluentes Químicos da Água/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Metals, Heavy); 0 (Reactive Oxygen Species); 0 (Water Pollutants, Chemical); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE


  5 / 247261 MEDLINE  
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[PMID]:29441917
[Ti] Título:Analysis of the necessity of serum electrolyte monitoring for up to eight weeks after the completion of anti-epidermal growth factor receptor antibody administration.
[So] Source:Pharmazie;71(7):402-407, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Electrolyte disturbances are a known side effect of cetuximab (cmab) and panitumumab (pmab) administration and monitoring is recommended during and for at least 8 weeks after pmab administration. However, the recommended duration of electrolyte monitoring is not stated on the cmab package insert in the EU or Japan and no previous studies have investigated the appropriate monitoring period for cmab and pmab. We retrospectively investigated electrolyte levels in 16 cmab-treated patients and 7 pmab-treated patients between 1 June 2009 and 31 December 2014. The mean minimum levels of serum magnesium, potassium, and calcium were analyzed in these patients before administration (baseline) and in period A (during administration), period B (time of the last administration), period C (from the completion of administration to 4 weeks after), and period D (from 4-8 weeks after administration). Hypokalemia persisted until period D in 1 cmab-treated patient. Hypomagnesemia persisted until period D in two pmab-treated patients and hypokalemia persisted until period D in 1 pmab-treated patient. In addition, the serum magnesium levels in periods A, B, and C in the cmab-treated patients were significantly lower than the baseline level (P < 0.05). In pmabtreated patients, the serum magnesium levels in periods A, C, and D, and the serum calcium levels in periods A, B, and C were lower than the baseline levels (P < 0.05). These findings indicate that it is necessary to monitor electrolyte levels for at least 8 weeks after the completion of administration of cmab or pmab.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/efeitos adversos
Cetuximab/efeitos adversos
Eletrólitos/sangue
Receptor do Fator de Crescimento Epidérmico/antagonistas & inibidores
Desequilíbrio Hidroeletrolítico/induzido quimicamente
[Mh] Termos MeSH secundário: Adulto
Idoso
Anticorpos Monoclonais/uso terapêutico
Anticorpos Monoclonais Humanizados/efeitos adversos
Anticorpos Monoclonais Humanizados/uso terapêutico
Cálcio/sangue
Cetuximab/uso terapêutico
Feminino
Seres Humanos
Hipopotassemia/sangue
Hipopotassemia/induzido quimicamente
Deficiência de Magnésio/sangue
Deficiência de Magnésio/induzido quimicamente
Masculino
Meia-Idade
Monitorização Fisiológica
Estudos Retrospectivos
Desequilíbrio Hidroeletrolítico/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Monoclonal, Humanized); 0 (Electrolytes); 6A901E312A (panitumumab); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); PQX0D8J21J (Cetuximab); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6537


  6 / 247261 MEDLINE  
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[PMID]:29277915
[Au] Autor:Zhang X; Ping HY; Li JH; Duan SX; Jiang XW
[Ad] Endereço:Department of Pediatric Surgery, The Affiliated Maternal and Child Health Hospital of Shenzhen University Medical College, Shenzhen, China.
[Ti] Título:Diethylstilbestrol regulates mouse gubernaculum testis cell proliferation via PLC-Ca -CREB pathway.
[So] Source:Cell Biochem Funct;36(1):13-17, 2018 Jan.
[Is] ISSN:1099-0844
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recent evidence suggested a positive correlation between environmental estrogens (EEs) and high incidence of abnormalities in male urogenital system, but the mechanism remains unclear. Diethylstilbestrol (DES) is a nonsteroidal synthetic estrogen that disrupts the morphology and proliferation of gubernaculum testis cells, but the underlying mechanism is unclear. In this study, mouse gubernaculum testis cells were pretreated with phospholipase C (PLC) inhibitor U-73122 and then treated with DES. The results demonstrated that U-73122 impaired DES-evoked intracellular Ca2+ mobilization in gubernaculum testis cells and inhibited DES-induced proliferation of gubernaculum testis cells. Mechanistically, we found that U-73122 inhibited DES-induced activation of cAMP-response element binding protein (CREB) in gubernaculum testis cells. In conclusion, these data suggest that the effects of DES on mouse gubernaculum testis cells are mediated by PLC-Ca -CREB pathway. SIGNIFICANCE OF THE STUDY: Environmental estrogens remain a serious threat to male reproductive health, and it is important to understand the mechanism by which EEs affect the male productive system. Here we explore potential mechanisms how the proliferation and contractility of gubernaculum testis cells are regulated by diethylstilbestrol. Our findings provide the first evidence that PLC-Ca -CREB signalling pathway mediates the nongenomic effects of diethylstilbestrol on gubernaculum testis cells. These findings provide new insight into the role of diethylstilbestrol in the aetiology of male reproductive dysfunction and will help develop better approaches for the prevention and therapy of male reproductive malformation.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Dietilestilbestrol/farmacologia
Gubernáculo/efeitos dos fármacos
Testículo/efeitos dos fármacos
Fosfolipases Tipo C/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Estrenos/farmacologia
Gubernáculo/citologia
Gubernáculo/metabolismo
Masculino
Camundongos
Pirrolidinonas/farmacologia
Testículo/citologia
Testículo/metabolismo
Fosfolipases Tipo C/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic AMP Response Element-Binding Protein); 0 (Estrenes); 0 (Pyrrolidinones); 112648-68-7 (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione); 731DCA35BT (Diethylstilbestrol); EC 3.1.4.- (Type C Phospholipases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE
[do] DOI:10.1002/cbf.3312


  7 / 247261 MEDLINE  
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[PMID]:28464481
[Au] Autor:Hack CC; Stoll MJ; Jud SM; Heusinger K; Adler W; Haeberle L; Ganslandt T; Heindl F; Schulz-Wendtland R; Cavallaro A; Uder M; Beckmann MW; Fasching PA; Bayer CM
[Ad] Endereço:Department of Gynecology and Obstetrics, Erlangen University Hospital, Comprehensive Cancer Center Erlangen/European Metropolitan Area Nuremberg (CCC ER-EMN), Erlangen, Germany.
[Ti] Título:Correlation of mammographic density and serum calcium levels in patients with primary breast cancer.
[So] Source:Cancer Med;6(6):1473-1481, 2017 Jun.
[Is] ISSN:2045-7634
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Percentage mammographic breast density (PMD) is one of the most important risk factors for breast cancer (BC). Calcium, vitamin D, bisphosphonates, and denosumab have been considered and partly confirmed as factors potentially influencing the risk of BC. This retrospective observational study investigated the association between serum calcium level and PMD. A total of 982 BC patients identified in the research database at the University Breast Center for Franconia with unilateral BC, calcium and albumin values, and mammogram at the time of first diagnosis were included. PMD was assessed, using a semiautomated method by two readers. Linear regression analyses were conducted to investigate the impact on PMD of the parameters of serum calcium level adjusted for albumin level, and well-known clinical predictors such as age, body mass index (BMI), menopausal status and confounder for serum calcium like season in which the BC was diagnosed. Increased calcium levels were associated with reduced PMD (P = 0.024). Furthermore, PMD was inversely associated with BMI (P < 0.001) and age (P < 0.001). There was also an association between PMD and menopausal status (P < 0.001). The goodness-of-fit of the regression model was moderate. This is the first study assessing the association between serum calcium level and PMD. An inverse association with adjusted serum calcium levels was observed. These findings add to previously published data relating to vitamin D, bisphosphonates, denosumab, and the RANK/RANKL signaling pathway in breast cancer risk and prevention.
[Mh] Termos MeSH primário: Densidade da Mama
Neoplasias da Mama/sangue
Neoplasias da Mama/diagnóstico por imagem
Cálcio/sangue
[Mh] Termos MeSH secundário: Idoso
Feminino
Seres Humanos
Mamografia
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/cam4.1066


  8 / 247261 MEDLINE  
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[PMID]:29442032
[Au] Autor:Jiang JF; Zhai J; Liu ZR; Chao L; Zhao YF; Wu YJ; Cui MX
[Ti] Título:Ampelopsin sodium induces mitochondrial-mediated apoptosis in human lung adenocarcinoma SPC-A-1 cell line.
[So] Source:Pharmazie;71(8):455-459, 2016 08 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Ampelopsin is a well-known flavonoid which has variety of biological and pharmacological actions including anticancer effects and induction of apoptosis on the several cancer cell lines. The present study aimed to evaluate the role of ampelopsin sodium (Amp-Na) in the mitochondrial-mediated apoptosis of human lung adenocarcionma SPC-A-1 cells. The analysis of cell proliferation and ultrastructure were performed. Furthermore, to clarify its action mechanism by determining the mitochondrial membrane potential (Δψm), intracellular calcium (Ca2+) concentration, mitochondrial nitric oxide (NO) level and total ATPase activity. The results showed that Amp-Na markedly inhibited the SPC-A-1 cell proliferation and caused ultrastructural apoptosis feature in SPC-A-1 cells in a dose-dependent manner. Amp-Na led to a rapid and sustained Ca2+ elevation and Δψm reduction, and induced the mitochondrial NO production and decreased the total ATPase activity in SPC-A-1 cells. The results enhance the potential of Amp-Na as a therapeutic drug for treating lung cancer, and provide new information for mechanism of Amp-Na which induces mitochondrial-mediated apoptosis in tumor cells.
[Mh] Termos MeSH primário: Adenocarcinoma/tratamento farmacológico
Antineoplásicos Fitogênicos/farmacologia
Apoptose/efeitos dos fármacos
Flavonoides/farmacologia
Neoplasias Pulmonares/tratamento farmacológico
Mitocôndrias/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenocarcinoma/patologia
Adenocarcinoma/ultraestrutura
Adenosina Trifosfatases/metabolismo
Cálcio/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Relação Dose-Resposta a Droga
Seres Humanos
Neoplasias Pulmonares/patologia
Neoplasias Pulmonares/ultraestrutura
Potencial da Membrana Mitocondrial/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents, Phytogenic); 0 (Flavonoids); 27200-12-0 (ampelopsin); EC 3.6.1.- (Adenosine Triphosphatases); SY7Q814VUP (Calcium)
[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:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6571


  9 / 247261 MEDLINE  
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[PMID]:29362376
[Au] Autor:Ullman JC; Yang J; Sullivan M; Bendor J; Levy J; Pham E; Silm K; Seifikar H; Sohal VS; Nicoll RA; Edwards RH
[Ad] Endereço:Departments of Neurology and Physiology, UCSF School of Medicine, San Francisco, CA, 94143, USA.
[Ti] Título:A mouse model of autism implicates endosome pH in the regulation of presynaptic calcium entry.
[So] Source:Nat Commun;9(1):330, 2018 01 23.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Psychoactive compounds such as chloroquine and amphetamine act by dissipating the pH gradient across intracellular membranes, but the physiological mechanisms that normally regulate organelle pH remain poorly understood. Interestingly, recent human genetic studies have implicated the endosomal Na /H exchanger NHE9 in both autism spectrum disorders (ASD) and attention deficit hyperactivity disorder (ADHD). Plasma membrane NHEs regulate cytosolic pH, but the role of intracellular isoforms has remained unclear. We now find that inactivation of NHE9 in mice reproduces behavioral features of ASD including impaired social interaction, repetitive behaviors, and altered sensory processing. Physiological characterization reveals hyperacidic endosomes, a cell-autonomous defect in glutamate receptor expression and impaired neurotransmitter release due to a defect in presynaptic Ca entry. Acute inhibition of synaptic vesicle acidification rescues release but without affecting the primary defect due to loss of NHE9.
[Mh] Termos MeSH primário: Transtorno do Deficit de Atenção com Hiperatividade/metabolismo
Transtorno do Espectro Autista/metabolismo
Cálcio/metabolismo
Endossomos/metabolismo
Neurônios/metabolismo
Trocadores de Sódio-Hidrogênio/genética
[Mh] Termos MeSH secundário: Animais
Transtorno do Deficit de Atenção com Hiperatividade/genética
Transtorno do Deficit de Atenção com Hiperatividade/fisiopatologia
Transtorno do Espectro Autista/genética
Transtorno do Espectro Autista/fisiopatologia
Comportamento Animal
Modelos Animais de Doenças
Eletroencefalografia
Endossomos/patologia
Feminino
Expressão Gênica
Ácido Glutâmico/metabolismo
Hipocampo/metabolismo
Hipocampo/fisiopatologia
Seres Humanos
Concentração de Íons de Hidrogênio
Masculino
Camundongos
Camundongos Knockout
Neurônios/patologia
Terminações Pré-Sinápticas/metabolismo
Terminações Pré-Sinápticas/patologia
Cultura Primária de Células
Trocadores de Sódio-Hidrogênio/deficiência
Transmissão Sináptica/fisiologia
Vesículas Sinápticas/metabolismo
Vesículas Sinápticas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (NHE9 protein, mouse); 0 (Sodium-Hydrogen Exchangers); 3KX376GY7L (Glutamic Acid); SY7Q814VUP (Calcium)
[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:180125
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02716-5


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[PMID]:29348575
[Au] Autor:Neef J; Urban NT; Ohn TL; Frank T; Jean P; Hell SW; Willig KI; Moser T
[Ad] Endereço:Institute for Auditory Neuroscience and InnerEarLab, University Medical Center Göttingen, 37099, Göttingen, Germany.
[Ti] Título:Quantitative optical nanophysiology of Ca signaling at inner hair cell active zones.
[So] Source:Nat Commun;9(1):290, 2018 01 18.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ca influx triggers the release of synaptic vesicles at the presynaptic active zone (AZ). A quantitative characterization of presynaptic Ca signaling is critical for understanding synaptic transmission. However, this has remained challenging to establish at the required resolution. Here, we employ confocal and stimulated emission depletion (STED) microscopy to quantify the number (20-330) and arrangement (mostly linear 70 nm × 100-600 nm clusters) of Ca channels at AZs of mouse cochlear inner hair cells (IHCs). Establishing STED Ca imaging, we analyze presynaptic Ca signals at the nanometer scale and find confined elongated Ca domains at normal IHC AZs, whereas Ca domains are spatially spread out at the AZs of bassoon-deficient IHCs. Performing 2D-STED fluorescence lifetime analysis, we arrive at estimates of the Ca concentrations at stimulated IHC AZs of on average 25 µM. We propose that IHCs form bassoon-dependent presynaptic Ca -channel clusters of similar density but scalable length, thereby varying the number of Ca channels amongst individual AZs.
[Mh] Termos MeSH primário: Sinalização do Cálcio/fisiologia
Células Ciliadas Auditivas Internas/fisiologia
Microscopia/métodos
Nanotecnologia/métodos
[Mh] Termos MeSH secundário: Algoritmos
Animais
Cálcio/metabolismo
Canais de Cálcio Tipo L/fisiologia
Células Ciliadas Auditivas Internas/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Microscopia Confocal
Modelos Neurológicos
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/fisiologia
Sinapses/metabolismo
Sinapses/fisiologia
Transmissão Sináptica/genética
Transmissão Sináptica/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bsn protein, mouse); 0 (Calcium Channels, L-Type); 0 (Nerve Tissue Proteins); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02612-y



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