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[PMID]:27773752
[Au] Autor:O'Neill HS; Herron CC; Hastings CL; Deckers R; Lopez Noriega A; Kelly HM; Hennink WE; McDonnell CO; O'Brien FJ; Ruiz-Hernández E; Duffy GP
[Ad] Endereço:Tissue Engineering Research Group, Dept. of Anatomy, Royal College of Surgeons in Ireland (RCSI), Dublin, Ireland; Trinity Centre for Bioengineering, Trinity College Dublin (TCD), Dublin, Ireland; Advanced Materials and Bioengineering Research (AMBER) Centre, RCSI & TCD, Dublin, Ireland; School
[Ti] Título:A stimuli responsive liposome loaded hydrogel provides flexible on-demand release of therapeutic agents.
[So] Source:Acta Biomater;48:110-119, 2017 01 15.
[Is] ISSN:1878-7568
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Lysolipid-based thermosensitive liposomes (LTSL) embedded in a chitosan-based thermoresponsive hydrogel matrix (denoted Lipogel) represents a novel approach for the spatiotemporal release of therapeutic agents. The entrapment of drug-loaded liposomes in an injectable hydrogel permits local liposome retention, thus providing a prolonged release in target tissues. Moreover, release can be controlled through the use of a minimally invasive external hyperthermic stimulus. Temporal control of release is particularly important for complex multi-step physiological processes, such as angiogenesis, in which different signals are required at different times in order to produce a robust vasculature. In the present work, we demonstrate the ability of Lipogel to provide a flexible, easily modifiable release platform. It is possible to tune the release kinetics of different drugs providing a passive release of one therapeutic agent loaded within the gel and activating the release of a second LTSL encapsulated agent via a hyperthermic stimulus. In addition, it was possible to modify the drug dosage within Lipogel by varying the duration of hyperthermia. This can allow for adaption of drug dosing in real time. As an in vitro proof of concept with this system, we investigated Lipogels ability to recruit stem cells and then elevate their production of vascular endothelial growth factor (VEGF) by controlling the release of a pro-angiogenic drug, desferroxamine (DFO) with an external hyperthermic stimulus. Initial cell recruitment was accomplished by the passive release of hepatocyte growth factor (HGF) from the hydrogel, inducing a migratory response in cells, followed by the delayed release of DFO from thermosensitive liposomes, resulting in a significant increase in VEGF expression. This delayed release could be controlled up to 14days. Moreover, by changing the duration of the hyperthermic pulse, a fine control over the amount of DFO released was achieved. The ability to trigger the release of therapeutic agents at a specific timepoint and control dosing level through changes in duration of hyperthermia enables sequential multi-dose profiles. STATEMENT OF SIGNIFICANCE: This paper details the development of a heat responsive liposome loaded hydrogel for the controlled release of pro-angiogenic therapeutics. Lysolipid-based thermosensitive liposomes (LTSLs) embedded in a chitosan-based thermoresponsive hydrogel matrix represents a novel approach for the spatiotemporal release of therapeutic agents. This hydrogel platform demonstrates remarkable flexibility in terms of drug scheduling and sequencing, enabling the release of multiple agents and the ability to control drug dosing in a minimally invasive fashion. The possibility to tune the release kinetics of different drugs independently represents an innovative platform to utilise for a variety of treatments. This approach allows a significant degree of flexibility in achieving a desired release profile via a minimally invasive stimulus, enabling treatments to be tuned in response to changing symptoms and complications.
[Mh] Termos MeSH primário: Desferroxamina/farmacologia
Liberação Controlada de Fármacos
Hidrogel de Polietilenoglicol-Dimetacrilato/química
[Mh] Termos MeSH secundário: Materiais Biocompatíveis/farmacologia
Movimento Celular/efeitos dos fármacos
Quitosana/química
Glicerofosfatos/química
Fator de Crescimento de Hepatócito/farmacologia
Seres Humanos
Hipertermia Induzida
Lipossomos
Células Mesenquimais Estromais/citologia
Células Mesenquimais Estromais/efeitos dos fármacos
Células Mesenquimais Estromais/metabolismo
Fator A de Crescimento do Endotélio Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Glycerophosphates); 0 (Liposomes); 0 (Vascular Endothelial Growth Factor A); 25852-47-5 (Hydrogel, Polyethylene Glycol Dimethacrylate); 67256-21-7 (Hepatocyte Growth Factor); 9012-76-4 (Chitosan); J06Y7MXW4D (Deferoxamine); WWH06G87W6 (beta-glycerophosphoric acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


  2 / 4058 MEDLINE  
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[PMID]:28851247
[Au] Autor:Dai J; Long W; Liang Z; Wen L; Yang F; Chen G
[Ad] Endereço:a School of Pharmacy , Guangdong Pharmaceutical University , Guangzhou , China.
[Ti] Título:A novel vehicle for local protein delivery to the inner ear: injectable and biodegradable thermosensitive hydrogel loaded with PLGA nanoparticles.
[So] Source:Drug Dev Ind Pharm;44(1):89-98, 2018 Jan.
[Is] ISSN:1520-5762
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Delivery of biomacromolecular drugs into the inner ear is challenging, mainly because of their inherent instability as well as physiological and anatomical barriers. Therefore, protein-friendly, hydrogel-based delivery systems following local administration are being developed for inner ear therapy. Herein, biodegradable poly(lactic-co-glycolic acid) (PLGA) nanoparticles (NPs) containing interferon α-2 b (IFN α-2 b) were loaded in chitosan/glycerophosphate (CS/GP)-based thermosensitive hydrogel for IFN delivery by intratympanic injection. The injectable hydrogel possessed a physiological pH and formed semi-solid gel at 37 °C, with good swelling and deswelling properties. The CS/GP hydrogel could slowly degrade as visualized by scanning electron microscopy (SEM). The presence of NPs in CS/GP gel largely influenced in vitro drug release. In the guinea pig cochlea, a 1.5- to 3-fold increase in the drug exposure time of NPs-CS/GP was found than those of the solution, NPs and IFN-loaded hydrogel. Most importantly, a prolonged residence time was attained without obvious histological changes in the inner ear. This biodegradable, injectable, and thermosensitive NPs-CS/GP system may allow longer delivery of protein drugs to the inner ear, thus may be a potential novel vehicle for inner ear therapy.
[Mh] Termos MeSH primário: Quitosana/química
Orelha Interna/fisiologia
Excipientes/química
Glicerofosfatos/química
Hidrogel de Polietilenoglicol-Dimetacrilato/química
Interferon-alfa/química
Ácido Láctico/química
Nanopartículas/química
Ácido Poliglicólico/química
[Mh] Termos MeSH secundário: Animais
Sistemas de Liberação de Medicamentos
Cobaias
Proteínas Recombinantes/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excipients); 0 (Glycerophosphates); 0 (Interferon-alpha); 0 (Recombinant Proteins); 0 (polylactic acid-polyglycolic acid copolymer); 25852-47-5 (Hydrogel, Polyethylene Glycol Dimethacrylate); 26009-03-0 (Polyglycolic Acid); 33X04XA5AT (Lactic Acid); 43K1W2T1M6 (interferon alfa-2b); 9012-76-4 (Chitosan)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170831
[St] Status:MEDLINE
[do] DOI:10.1080/03639045.2017.1373803


  3 / 4058 MEDLINE  
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[PMID]:29208463
[Au] Autor:Hao W; Yang R; Yang Y; Jin S; Li Y; Yuan F; Guo Q; Xiao L; Wang X; Wang F; Wu Y; Teng X
[Ad] Endereço:Department of Anesthesiology, Hebei Provincial Hospital of traditional Chinese Medicine, Shijiazhuang 050011, China.
[Ti] Título:Stellate ganglion block ameliorates vascular calcification by inhibiting endoplasmic reticulum stress.
[So] Source:Life Sci;193:1-8, 2018 Jan 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Vascular calcification (VC) underlies substantial cardiovascular morbidity and mortality. No clinically therapies have emerged presently. Stellate ganglion block (SGB) is one of the most often used sympathetic blockade procedure, and regulates vascular dilation. However, the effect of SGB on VC is still unknown. Therefore, we aimed to identify the ameliorative effect of SGB on VC. KEY FINDING: In vivo VC was induced in rats by administering vitamin D3 plus nicotine (VDN), and in vitro calcification of rat aortic vascular smooth muscle cells (VSMC) was induced by ß-glycerophosphate. In VDN rats, alkaline phosphatase (ALP) activity and Calcium contents were higher than that in control rats. The transformation of VSMC from contractile to osteoblast-like phenotype was observed in calcified aorta. SGB ameliorated the increase of ALP activity and Calcium content, and the transformation of VSMC in calcified aorta. The stimulation of endoplasmic reticulum stress (ERS) in calcified aorta was also attenuated by SGB treatment. The inducer of ERS, tunicamycin could block the beneficial effect of SGB on VC, and the ERS inhibitor, 4-PBA could mimic the amelioration of SGB. Furthermore, SGB attenuated the increased plasma levels of norepinephrine in VDN rats. In vitro experiments, norepinephrine exaggerated VSMC calcification, phenotype transformation and ERS. SIGNIFICANCE: These results demonstrate that SGB could inhibit sympathetic nervous activity, and then prevent the activation of ERS followed by ameliorating VC. Sympathetic over-activation might play critical role in the pathogenesis of VC, which provides new strategy and target for therapy and prevention of VC.
[Mh] Termos MeSH primário: Estresse do Retículo Endoplasmático/efeitos dos fármacos
Gânglio Estrelado/fisiologia
Calcificação Vascular/terapia
[Mh] Termos MeSH secundário: Animais
Aorta/patologia
Bloqueio Nervoso Autônomo/métodos
Cálcio/farmacologia
Colecalciferol/farmacologia
Modelos Animais de Doenças
Retículo Endoplasmático/metabolismo
Estresse do Retículo Endoplasmático/fisiologia
Glicerofosfatos
Masculino
Músculo Liso Vascular/efeitos dos fármacos
Miócitos de Músculo Liso/patologia
Nicotina/farmacologia
Nordefrin
Ratos
Ratos Sprague-Dawley
Transdução de Sinais
Gânglio Estrelado/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycerophosphates); 1C6V77QF41 (Cholecalciferol); 6M3C89ZY6R (Nicotine); R81X549E70 (Nordefrin); SY7Q814VUP (Calcium); WWH06G87W6 (beta-glycerophosphoric acid)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


  4 / 4058 MEDLINE  
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[PMID]:28659287
[Au] Autor:Dragos SM; Bergeron KF; Desmarais F; Suitor K; Wright DC; Mounier C; Mutch DM
[Ad] Endereço:Department of Human Health & Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada; and.
[Ti] Título:Reduced SCD1 activity alters markers of fatty acid reesterification, glyceroneogenesis, and lipolysis in murine white adipose tissue and 3T3-L1 adipocytes.
[So] Source:Am J Physiol Cell Physiol;313(3):C295-C304, 2017 Sep 01.
[Is] ISSN:1522-1563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:White adipose tissue (WAT) has a critical role in lipid handling. Previous work demonstrated that SCD1 is an important regulator of WAT fatty acid (FA) composition; however, its influence on the various interconnected pathways influencing WAT lipid handling remains unclear. Our objective was to investigate the role of SCD1 on WAT lipid handling using knockout (KO) mice and SCD1-inhibited 3T3-L1 adipocytes by measuring gene, protein, and metabolite markers related to FA reesterification, glyceroneogenesis, and lipolysis. Triacylglycerol (TAG) content was higher in inguinal WAT (iWAT) from KO mice compared with wild-type, but significantly lower in epididymal WAT (eWAT). The SCD1 desaturation index was decreased in both WAT depots in KO mice. FA reesterification, as measured with a NEFA:glycerol ratio, was reduced in both WAT depots in KO mice, as well as SCD1-inhibited 3T3-L1 adipocytes. , , and gene expression was reduced in both WAT depots of KO mice, while and gene expression showed depot-specific regulation. , , and gene expression was reduced, and phosphoenolpyruvate carboxykinase protein content was ablated, in SCD1-inhibited adipocytes. Our data provide evidence that SCD1 has a broad impact on WAT lipid handling by altering TAG composition in a depot-specific manner, reducing FA reesterification, and regulating markers of lipolysis and glyceroneogenesis.
[Mh] Termos MeSH primário: Tecido Adiposo Branco/fisiologia
Ácidos Graxos/metabolismo
Glicerofosfatos/biossíntese
Metabolismo dos Lipídeos/fisiologia
Lipólise/fisiologia
Estearoil-CoA Dessaturase/metabolismo
[Mh] Termos MeSH secundário: Células 3T3-L1
Animais
Biomarcadores/metabolismo
Ativação Enzimática
Esterificação/fisiologia
Regulação Enzimológica da Expressão Gênica/fisiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Estearoil-CoA Dessaturase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Fatty Acids); 0 (Glycerophosphates); 9NTI6P3O4X (alpha-glycerophosphoric acid); EC 1.14.19.1 (Scd1 protein, mouse); EC 1.14.19.1 (Stearoyl-CoA Desaturase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170630
[St] Status:MEDLINE
[do] DOI:10.1152/ajpcell.00097.2017


  5 / 4058 MEDLINE  
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[PMID]:28648030
[Au] Autor:Bai YL; Xu JS; Tian T; Zhang JX; Cui LW; Zhang HR; Zhang SL
[Ad] Endereço:Department of Nephrology, Forth Hospital of Hebei Medical University, Shijiazhuang 050011, China.
[Ti] Título:[Effect and mechanism of intermittent alkaline stimulation on high phosphorus induced calcification in vascular smooth muscle cells of rats].
[So] Source:Zhonghua Xin Xue Guan Bing Za Zhi;45(6):519-525, 2017 Jun 24.
[Is] ISSN:0253-3758
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To explore the effect and possible mechanisms of intermittent alkaline on rat vascular smooth muscle cells (VSMCs) calcification induced by high phosphorus. VSMCs were isolated from rat thoracic aorta and cultured in vitro. The fourth generation VSMCs were randomly divided into control group, high phosphorus+ pH7.4, high phosphorus+ pH7.5, high phosphorus+ pH7.6 and high phosphorus+ pH7.7 group with random number table. The control group was cultured in DMEM with 10% fetal bovine serum. Other groups were cultured in DMEM with 10 mmol/L ß-glycerophosphate and alkalized by 7.4% NaHCO(3) to adjust the pH respectively. After the intervention of 4 hours, the control group was replaced with the normal medium containing 10% fetal bovine serum, the other 4 groups were replaced with high phosphorus based on the pH value of the culture medium, and then replaced the culture medium every other day. After 4 days intervention, the mRNA and protein expression of L type calcium channel ß(3) subunit(LTCC ß(3)) and Runt related transcription factor 2 (Runx2) were detected by RT-PCR and Western blot. After 4 days intervention, the level of VSMC calcium ion was detected by Fluo-3/AM. After 14 days intervention, alkaline phosphatase (ALP) activity was measured by enzyme linked immunosorbent assay (ELISA) and the calcification was observed by measuring calcium content. (1) Compared with control group, the gene and protein expressions of LTCC ß(3) were higher in high phosphorus+ pH7.4 group (0.49±0.03 vs. 0.23±0.02 and 0.45±0.03 vs. 0.26±0.02 respectively, all <0.05). Compared with high phosphorus+ pH7.4 group, the mRNA(0.86±0.05) and protein(0.62±0.04) expressions of LTCC ß(3) were higher in high phosphorus+ pH7.5 group ( <0.05). Compared with high phosphorus+ pH7.5 group, the mRNA(0.99±0.05) and protein(0.80±0.03) expressions of LTCC ß(3) were higher in high phosphorus+ pH7.5 group (all <0.05). Compared with high phosphorus+ pH7.6 group, the mRNA(1.16±0.05) and protein(0.93±0.03) expressions of LTCC ß(3) were higher in high phosphorus+ pH7.7 group (all <0.05). (2) Compared with control group, calcium ion influx were higher in high phosphorus+ pH7.4 group (124.61±6.06 vs. 75.68±7.82, <0.05). Compared with high phosphorus+ pH7.4 group, calcium ion influx was higher in high phosphorus+ pH7.5 group(210.85±9.75, <0.05). Compared with high phosphorus+ pH7.5 group, calcium ion influx was higher in high phosphorus+ pH7.6 group(298.44±11.42, <0.05). Compared with high phosphorus+ pH7.6 group, calcium ion influx was higher in high phosphorus+ pH7.7 group(401.13±11.41, <0.05). (3) Compared with control group, the mRNA and protein expressions of Runx2 and ALP were higher in high phosphorus+ pH7.4 group (0.60±0.04 vs. 0.34±0.03, 0.42±0.04 vs. 0.21±0.02, 67.2±4.3 vs. 23.2±2.3 respectively, all <0.05). Compared with high phosphorus+ pH7.4 group, the mRNA(0.76±0.05) and protein(0.68±0.03) expressions of Runx2 and ALP(102.1±5.4) were higher in high phosphorus+ pH7.5 group (all <0.05). Compared with high phosphorus+ pH7.5 group, the mRNA(0.90±0.05) and protein(0.90±0.05) expressions of Runx2 and ALP(139.3±4.9) were higher in high phosphorus+ pH7.6 group (all <0.05). Compared with high phosphorus+ pH7.6 group, the mRNA(1.11±0.05) and protein(1.08±0.06) expressions of Runx2 and ALP(197.0±6.7) were higher in high phosphorus+ pH7.7 group (all <0.05). (4) Compared with control group, the calcium content were higher in high phosphorus+ pH7.4 group ((75.4±4.3)mg/g pro vs.(25.2±2.1)mg/g pro, <0.05). Compared with high phosphorus+ pH7.4 group, the calcium content were higher in high phosphorus+ pH7.5 group ((100.8±5.7) mg/g pro, <0.05). Compared with high phosphorus+ pH7.5 group, the calcium content were higher in high phosphorus+ pH7.6 group ((143.5±6.1) mg/g pro, <0.05). Compared with high phosphorus+ pH7.6 group, the calcium content were higher in high phosphorus+ pH7.7 group ((205.1±8.2) mg/g pro, <0.05). Intermittent alkaline stimulation can promote high phosphorus induced rat VSMCs calcification possibly through upregulating LTCC ß(3) subunit gene and protein expression, increasing calcium ion influx and enhancing VSMCs phenotypic transformation.
[Mh] Termos MeSH primário: Glicerofosfatos
Músculo Liso Vascular
Fósforo
Calcificação Vascular
[Mh] Termos MeSH secundário: Compostos de Anilina
Animais
Aorta Torácica
Calcinose
Cálcio
Células Cultivadas
Subunidade alfa 1 de Fator de Ligação ao Core
Miócitos de Músculo Liso
Ratos
Regulação para Cima
Xantenos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Core Binding Factor Alpha 1 Subunit); 0 (Glycerophosphates); 0 (Xanthenes); 23D4W0B50Y (Fluo-3); 27YLU75U4W (Phosphorus); SY7Q814VUP (Calcium); WWH06G87W6 (beta-glycerophosphoric acid)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170627
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0253-3758.2017.06.015


  6 / 4058 MEDLINE  
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[PMID]:28644853
[Au] Autor:Alexander PM; Caudell DL; Kucera GL; Pladna KM; Pardee TS
[Ad] Endereço:Internal Medicine, Section on Hematology and Oncology, Wake Forest Baptist Health, Winston-Salem, North Carolina, United States of America.
[Ti] Título:The novel phospholipid mimetic KPC34 is highly active against preclinical models of Philadelphia chromosome positive acute lymphoblastic leukemia.
[So] Source:PLoS One;12(6):e0179798, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Philadelphia chromosome positive B cell acute lymphoblastic leukemia (Ph+ ALL) is an aggressive cancer of the bone marrow. The addition of tyrosine kinase inhibitors (TKIs) has improved outcomes but many patients still suffer relapse and novel therapeutic agents are needed. KPC34 is an orally available, novel phospholipid conjugate of gemcitabine, rationally designed to overcome multiple mechanisms of resistance, inhibit the classical and novel isoforms of protein kinase C, is able to cross the blood brain barrier and is orally bioavailable. KPC34 had an IC50 in the nanomolar range against multiple ALL cell lines tested but was lowest for Ph+ lines. In mice bearing either naïve or resistant Ph+ ALL, KPC34 treatment resulted in significantly improved survival compared to cytarabine and gemcitabine. Treatment with KPC34 and doxorubicin was more effective than doxorubicin and cytarabine. Mice with recurrence of their ALL after initial treatment with cytarabine and doxorubicin saw dramatic improvements in hind limb paralysis after treatment with KPC34 demonstrating activity against established CNS disease. Consistent with this KPC34 was better than gemcitabine at reducing CNS leukemic burden. These promising pre-clinical results justify the continued development of KPC34 for the treatment of Ph+ALL.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Desoxicitidina/análogos & derivados
Glicerofosfatos/farmacologia
Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/toxicidade
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/toxicidade
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Citarabina/farmacologia
Dano ao DNA/efeitos dos fármacos
Desoxicitidina/farmacologia
Desoxicitidina/toxicidade
Relação Dose-Resposta a Droga
Doxorrubicina/farmacologia
Resistência a Medicamentos Antineoplásicos
Ensaios de Seleção de Medicamentos Antitumorais
Glicerofosfatos/toxicidade
Seres Humanos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Transplante de Neoplasias
Cromossomo Filadélfia
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/metabolismo
Proteína Quinase C/antagonistas & inibidores
Proteína Quinase C/metabolismo
Distribuição Aleatória
Carga Tumoral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Glycerophosphates); 0 (KPC34 compound); 04079A1RDZ (Cytarabine); 0W860991D6 (Deoxycytidine); 80168379AG (Doxorubicin); B76N6SBZ8R (gemcitabine); EC 2.7.11.13 (Protein Kinase C)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179798


  7 / 4058 MEDLINE  
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[PMID]:28435144
[Au] Autor:Cozer AG; Trapp M; Martins TL; De Fraga LS; Vieira Marques C; Model JFA; Schein V; Kucharski LC; Da Silva RSM
[Ad] Endereço:Post-Graduate Program in Biological Science: Physiology, Department of Physiology, Institute of Health Basic Sciences, Universidade Federal do Rio Grande do Sul, Sarmento Leite, 500, 90050-170 Porto Alegre, RS, Brazil. Electronic address: alinecozer15@gmail.com.
[Ti] Título:Effects of Stanniocalcin-1 on glucose flux in rat brown adipose tissue.
[So] Source:Biochimie;138:50-55, 2017 Jul.
[Is] ISSN:1638-6183
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The present work assesses in vitro the role of human Stanniocalcin 1 (hSTC-1) in C-glucose metabolism in brown adipose tissue (BAT) from fed rat. In the fed state, hSTC-1 decreases the incorporation of C from glucose into lipids in the rat BAT. The data support the hypothesis that the capacity of the glycerol-3-phosphate (G3P)-generating pathway (glycolysis) from glucose is regulated by hSTC-1, decreasing the adequate supply of G3P needed for fatty acid esterification and triacylglycerol (TG) storage in BAT. The results also suggest the effect of hSTC-1 on de novo fatty acid synthesis from pyruvate generated by C-glucose in the glycolysis pathway. In addition, by decreasing lipogenesis, hSTC-1 increased ATP levels and these two factors may decrease BAT thermogenic function. The presence of hSTC-1 in the incubation medium did not alter C-glucose and C-1-palmitic acid oxidation. The uncoupling protein 1 (UCP-1) expression was not altered by hSTC-1 either. In conclusion, hSTC-1 is one of the hormonal factors that control glucose metabolism in BAT in the fed state. The decrease of TG capacity synthesis from C-glucose by hSTC-1 compromises the BAT thermogenic capacity. Furthermore, the increase in ATP levels would inhibit a futile cycle via UCP-1, which dissipates oxidative energy as heat.
[Mh] Termos MeSH primário: Tecido Adiposo Marrom/metabolismo
Glucose/metabolismo
Glicerofosfatos/metabolismo
Glicólise
Glicoproteínas/fisiologia
[Mh] Termos MeSH secundário: Animais
Lipogênese
Masculino
Ratos
Ratos Wistar
Proteína Desacopladora 1
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycerophosphates); 0 (Glycoproteins); 0 (Uncoupling Protein 1); 76687-96-2 (teleocalcin); 9NTI6P3O4X (alpha-glycerophosphoric acid); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE


  8 / 4058 MEDLINE  
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[PMID]:28411543
[Au] Autor:Ji J; Zhu P; Cui F; Pi F; Zhang Y; Sun X
[Ad] Endereço:School of Food Science, State Key Laboratory of Food Science and Technology, National Engineering Research Center for Functional Foods, Jiangnan University, Wuxi, Jiangsu, 214122, China; Synergetic Innovation Center for Food Safety and Nutrition, Jiangnan University, Wuxi, 214122, China.
[Ti] Título:The disorder metabolic profiling in kidney and spleen of mice induced by mycotoxins deoxynivalenol through gas chromatography mass spectrometry.
[So] Source:Chemosphere;180:267-274, 2017 Aug.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Gas chromatography mass spectrometry (GC-MS) based metabolomics strategy was implemented for the metabolites detection in kidney and spleen samples of mice, which were treated with 2 mg kg deoxynivalenol (DON), through intragastric administration for three weeks, for studying the toxicity of DON on the metabolic profiling in kidney and spleen. The spectrum was deconvoluted, aligned and identified with MS DIAL, equipped with Fiehn library. And the data matrix was processed with univariate analysis and multivariate analysis for selection of metabolites with VIP >1, t-test p value < 0.05. The metabolic pathway analysis was analyzed with MetaMapp and drew by CytoScape. Result shows that DON could induce an increased protein synthesis to repair the damaged membrane protein structure, in both kidney and spleen, with decrease of valine, leucine and phenylalanine, et al. essential precursors for protein synthesis and energy production; the energy metabolism in kidney disordered by DON, with the decreasing of ribitol, glycerol 1-phosphate, et al. Furthermore, DON could lead to the disorder in immunity function and nucleotide metabolism in spleen, with decreasing trend of cytidine and alanine.
[Mh] Termos MeSH primário: Rim/metabolismo
Metaboloma/fisiologia
Micotoxinas/toxicidade
Baço/metabolismo
Tricotecenos/toxicidade
[Mh] Termos MeSH secundário: Animais
Cromatografia Gasosa-Espectrometria de Massas/métodos
Glicerofosfatos
Espectrometria de Massas
Redes e Vias Metabólicas/efeitos dos fármacos
Metabolômica/métodos
Camundongos
Análise Multivariada
Micotoxinas/análise
Baço/química
Testes de Toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycerophosphates); 0 (Mycotoxins); 0 (Trichothecenes); 9NTI6P3O4X (alpha-glycerophosphoric acid); JT37HYP23V (deoxynivalenol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170416
[St] Status:MEDLINE


  9 / 4058 MEDLINE  
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[PMID]:28359787
[Au] Autor:Hassaninasab A; Han GS; Carman GM
[Ad] Endereço:Department of Food Science and the Rutgers Center for Lipid Research, New Jersey Institute for Food, Nutrition, and Health, Rutgers University, New Brunswick, NJ 08901, United States.
[Ti] Título:Tips on the analysis of phosphatidic acid by the fluorometric coupled enzyme assay.
[So] Source:Anal Biochem;526:69-70, 2017 Jun 01.
[Is] ISSN:1096-0309
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The fluorometric coupled enzyme assay to measure phosphatidic acid (PA) involves the solubilization of extracted lipids in Triton X-100, deacylation, and the oxidation of PA-derived glycerol-3-phosphate to produce hydrogen peroxide for conversion of Amplex Red to resorufin. The enzyme assay is sensitive, but plagued by high background fluorescence from the peroxide-containing detergent and incomplete heat inactivation of lipoprotein lipase. These problems affecting the assay reproducibility were obviated by the use of highly pure Triton X-100 and by sufficient heat inactivation of the lipase enzyme. The enzyme assay could accurately measure the PA content from the subcellular fractions of yeast cells.
[Mh] Termos MeSH primário: Ensaios Enzimáticos/métodos
Fluorometria/métodos
Lipase Lipoproteica/metabolismo
Octoxinol/metabolismo
Ácidos Fosfatídicos/análise
Saccharomyces cerevisiae/metabolismo
[Mh] Termos MeSH secundário: Glicerolfosfato Desidrogenase/metabolismo
Glicerofosfatos/metabolismo
Peróxido de Hidrogênio/metabolismo
Mutação/genética
Oxazinas/metabolismo
Oxirredução
Saccharomyces cerevisiae/genética
Espectrometria de Fluorescência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycerophosphates); 0 (Oxazines); 0 (Phosphatidic Acids); 635-78-9 (resorufin); 9002-93-1 (Octoxynol); BBX060AN9V (Hydrogen Peroxide); EC 1.1.- (Glycerolphosphate Dehydrogenase); EC 1.1.3.21 (glycerol-3-phosphate oxidase); EC 3.1.1.34 (Lipoprotein Lipase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170512
[Lr] Data última revisão:
170512
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170401
[St] Status:MEDLINE


  10 / 4058 MEDLINE  
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[PMID]:28280244
[Au] Autor:Mugabo Y; Zhao S; Lamontagne J; Al-Mass A; Peyot ML; Corkey BE; Joly E; Madiraju SRM; Prentki M
[Ad] Endereço:From the Montreal Diabetes Research Center and Centre de Recherche du Centre Hospitalier de l'Université de Montréal, Montréal, Québec H2X 0A9, Canada.
[Ti] Título:Metabolic fate of glucose and candidate signaling and excess-fuel detoxification pathways in pancreatic ß-cells.
[So] Source:J Biol Chem;292(18):7407-7422, 2017 May 05.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glucose metabolism promotes insulin secretion in ß-cells via metabolic coupling factors that are incompletely defined. Moreover, chronically elevated glucose causes ß-cell dysfunction, but little is known about how cells handle excess fuels to avoid toxicity. Here we sought to determine which among the candidate pathways and coupling factors best correlates with glucose-stimulated insulin secretion (GSIS), define the fate of glucose in the ß-cell, and identify pathways possibly involved in excess-fuel detoxification. We exposed isolated rat islets for 1 h to increasing glucose concentrations and measured various pathways and metabolites. Glucose oxidation, oxygen consumption, and ATP production correlated well with GSIS and saturated at 16 mm glucose. However, glucose utilization, glycerol release, triglyceride and glycogen contents, free fatty acid (FFA) content and release, and cholesterol and cholesterol esters increased linearly up to 25 mm glucose. Besides being oxidized, glucose was mainly metabolized via glycerol production and release and lipid synthesis (particularly FFA, triglycerides, and cholesterol), whereas glycogen production was comparatively low. Using targeted metabolomics in INS-1(832/13) cells, we found that several metabolites correlated well with GSIS, in particular some Krebs cycle intermediates, malonyl-CoA, and lower ADP levels. Glucose dose-dependently increased the dihydroxyacetone phosphate/glycerol 3-phosphate ratio in INS-1(832/13) cells, indicating a more oxidized state of NAD in the cytosol upon glucose stimulation. Overall, the data support a role for accelerated oxidative mitochondrial metabolism, anaplerosis, and malonyl-CoA/lipid signaling in ß-cell metabolic signaling and suggest that a decrease in ADP levels is important in GSIS. The results also suggest that excess-fuel detoxification pathways in ß-cells possibly comprise glycerol and FFA formation and release extracellularly and the diversion of glucose carbons to triglycerides and cholesterol esters.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Ácidos Graxos/metabolismo
Glucose/farmacologia
Células Secretoras de Insulina/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Ésteres do Colesterol/metabolismo
Fosfato de Di-Hidroxiacetona/metabolismo
Relação Dose-Resposta a Droga
Glucose/metabolismo
Glicerofosfatos/metabolismo
Glicogênio/metabolismo
Masculino
Malonil Coenzima A/metabolismo
Ratos
Ratos Wistar
Triglicerídeos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholesterol Esters); 0 (Fatty Acids); 0 (Glycerophosphates); 0 (Triglycerides); 524-14-1 (Malonyl Coenzyme A); 57-04-5 (Dihydroxyacetone Phosphate); 8L70Q75FXE (Adenosine Triphosphate); 9005-79-2 (Glycogen); 9NTI6P3O4X (alpha-glycerophosphoric acid); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170607
[Lr] Data última revisão:
170607
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170311
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.763060



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