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Pesquisa : D27.505.519.914.500 [Categoria DeCS]
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  1 / 20037 MEDLINE  
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PMID:29231025
Autor:Shen X; Li M; Wang YL; Chen YL; Lin Y; Zhao ZM; Que TZ
Endereço:Department of Forensic Medicine, Medical College of Soochow University, Suzhou 215123, China.
Título:[Comparison of MPure-12 Automatic Nucleic Acid Purification and Chelex-100 Method].
Fonte:Fa Yi Xue Za Zhi; 33(2):168-170, 2017 Apr.
ISSN:1004-5619
País de publicação:China
Idioma:chi
Resumo:OBJECTIVES: To explore the forensic application value of MPure-12 automatic nucleic acid purification (MPure-12 Method) for DNA extraction by extracting and typing DNA from bloodstains and various kinds of biological samples with different DNA contents. METHODS: Nine types of biological samples, such as bloodstains, semen stains, and saliva were collected. DNA were extracted using MPure-12 method and Chelex-100 method, followed by PCR amplification and electrophoresis for obtaining STR-profiles. RESULTS: The samples such as hair root, chutty, butt, muscular tissue, saliva stain, bloodstain and semen stain were typed successfully by MPure-12 method. Partial alleles were lacked in the samples of saliva, and the genotyping of contact swabs was unsatisfactory. Additional, all of the bloodstains (20 µL, 15 µL, 10 µL, 5 µL, 1 µL) showed good typing results using Chelex-100 method. But the loss of alleles occurred in 1 µL blood volume by MPure-12 method. CONCLUSIONS: MPure-12 method is suitable for DNA extraction of a certain concentration blood samples.Chelex-100 method may be better for the extraction of trace blood samples.This instrument used in nucleic acid extraction has the advantages of simplicity of operator, rapidity, high extraction efficiency, high rate of reportable STR-profiles and lower man-made pollution.
Tipo de publicação: COMPARATIVE STUDY; JOURNAL ARTICLE
Nome de substância:0 (Chelating Agents); 0 (Polystyrenes); 0 (Polyvinyls); 0 (Resins, Synthetic); 11139-85-8 (Chelex 100); 80208-96-4 (chelex); 9007-49-2 (DNA)


  2 / 20037 MEDLINE  
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PMID:29334633
Autor:Kiyokawa E; Hayama T; Yoshida H; Yamaguchi M; Nohta H
Endereço:Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Johnan, Fukuoka 814-0180, Japan.
Título:Fluorous-assisted metal chelate affinity extraction for nucleotides followed by HILIC-MS/MS analysis.
Fonte:J Chromatogr B Analyt Technol Biomed Life Sci; 1074-1075:86-90, 2018 Feb 01.
ISSN:1873-376X
País de publicação:Netherlands
Idioma:eng
Resumo:We herein developed a selective method for the determination of nucleotides by fluorous-assisted metal chelate affinity extraction followed by hydrophilic interaction liquid chromatography (HILIC) combined with tandem mass spectrometric (MS/MS) analysis. In this study, the nucleotides were selectively chelated by Fe(III)-immobilized perfluoroalkyliminodiacetic acid, and the resulting chelates were subsequently extracted into a fluorous solvent. The nucleotides present in the fluorous solvent were then back-extracted into a non-fluorous solution, such as a solution of ammonia in aqueous acetonitrile. The resulting non-fluorous solution containing the nucleotides was then directly injected into an amide-type HILIC column using a mixture of acetonitrile and aqueous ammonium bicarbonate as the mobile phase for gradient elution, and the nucleotides were detected using the negative electrospray ionization MS/MS mode. In this method, the extraction recoveries of the nucleotides ranged from 43.2 to 94.7% within a relative standard deviation of 17%. This method enabled the determination of intracellular concentrations of nucleotides.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Chelating Agents); 0 (Nucleotides); Q80VPU408O (Fluorides)


  3 / 20037 MEDLINE  
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PMID:28464802
Autor:Neradova A; Schumacher SP; Hubeek I; Lux P; Schurgers LJ; Vervloet MG
Endereço:Department of Nephrology, VU University Medical Center, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands. a.neradova@vumc.nl.
Título:Phosphate binders affect vitamin K concentration by undesired binding, an in vitro study.
Fonte:BMC Nephrol; 18(1):149, 2017 May 02.
ISSN:1471-2369
País de publicação:England
Idioma:eng
Resumo:BACKGROUND: Vascular calcification is a major contributing factor to mortality in end stage renal disease (ESRD). Despite the efficacy of phosphate binders to improve hyperphosphatemia, data on vascular calcification are less clear. There seems to be a difference in attenuation or delay in progression between different binders. In this in vitro experiment we tested whether phosphate binders could limit bioavailability of vitamin K2 by undesired binding. Vitamin K-deficiency limits activation of the vascular tissue mineralization inhibitor matrix γ-carboxyglutamate (Gla) protein (MGP) thereby exacerbating vascular calcification. METHODS: In this experiment vitamin K2 (menaquinone-7; MK-7) binding was assessed by adding 1 mg of vitamin K2 to a medium with pH 6 containing 67 mg phosphate binder with either 7 mg of phosphate or no phosphate. Five different phosphate binders were tested. After five and a half hours vitamin K was analyzed by HPLC. All experiments were performed in triplicate. RESULTS: Sucroferric-oxyhydroxide and sevelamer carbonate did not significantly bind vitamin K2, both in solution only containing vitamin K2 or in combination with phosphate. Calcium acetate/magnesium carbonate binds vitamin K2 strongly both in absence (p = 0.001) and presence of phosphate (p = 0.003). Lanthanum carbonate significantly binds vitamin K2 in solution containing only vitamin K2 (p = 0.005) whereas no significant binding of vitamin K2 was observed in the solution containing vitamin K2 and phosphate (p = 0.462). Calcium carbonate binds vitamin K2 significantly in a solution with vitamin K2 and phosphate (p = 0.009) whereas without phosphate no significant binding of vitamin K2 was observed (p = 0.123). CONCLUSIONS: Sucroferric-oxyhydroxide and sevelamer carbonate were the only binders of the five binders studied that did not bind vitamin K2 in vitro. The presence or absence of phosphate significantly interferes with vitamin K2 binding so phosphate binders could potentially limit bioavailability vitamin K2.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Chelating Agents); 0 (Phosphates); 12001-79-5 (Vitamin K)


  4 / 20037 MEDLINE  
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PMID:29311459
Autor:Mitsuboshi S; Yamada H; Nagai K; Okajima H
Endereço:Department of Pharmacy, Kaetsu Hospital.
Título:[Low Continuity Rate of Sucroferric Oxyhydroxide among Japanese Hemodialysis Patients with High Phosphate Binder Pill Burden].
Fonte:Yakugaku Zasshi; 138(1):135-139, 2018.
ISSN:1347-5231
País de publicação:Japan
Idioma:jpn
Resumo:This prospective observational study was conducted to evaluate the continuity, efficacy, and tolerability of sucroferric oxyhydroxide (SO) among hemodialysis (HD) patients who switched to SO from sevelamer hydrochloride (SH) or bixalomer (BX). Participants were 9 HD patients in Kaetsu Hospital who had been receiving more than 9 tablets/d of SH or BX and were switched to SO 750 mg/d. All the participants were men. Over a 6-month observational period, 6 of the 9 patients (67%) discontinued SO because of adverse events, including diarrhea, atheroma, and polycythemia. Although the diarrhea and atheroma were mild, the affected patients did not wish to restart SO. On the other hand, 3 of the 9 patients (33%) continued taking SO throughout the observation period. These patients tended to have increased levels of serum calcium, hematocrit, and serum ferritin; a decreased number of phosphate binder tablets (from 21 tablets/d to 8 tablets/d); and a decreased dosage of erythropoiesis-stimulating agents. Serum phosphate levels tended to decrease in continuers, but tended to increase in discontinuers. It may be preferable to increase the SO dosage gradually rather than switching from SH or BX all at once, and patients who switch to SO should be carefully monitored.
Tipo de publicação: JOURNAL ARTICLE; OBSERVATIONAL STUDY
Nome de substância:0 (Chelating Agents); 0 (Drug Combinations); 0 (Ferric Compounds); 0 (Phosphates); 0 (Polyamines); 0 (Tablets); 0 (sucroferric oxyhydroxide); 3160WY51LV (bixalomer); 57-50-1 (Sucrose); 9YCX42I8IU (Sevelamer)


  5 / 20037 MEDLINE  
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PMID:29287249
Autor:Pati ML; Niso M; Spitzer D; Berardi F; Contino M; Riganti C; Hawkins WG; Abate C
Endereço:Dipartimento di Farmacia-Scienze del Farmaco, Università degli Studi di Bari ALDO MORO, Via Orabona 4, I-70125 Bari, Italy; Department of Surgery, Division of Hepatobiliary, Pancreatic, and Gastrointestinal Surgery, Washington University School of Medicine, St. Louis, MO, USA.
Título:Multifunctional thiosemicarbazones and deconstructed analogues as a strategy to study the involvement of metal chelation, Sigma-2 (σ ) receptor and P-gp protein in the cytotoxic action: In vitro and in vivo activity in pancreatic tumors.
Fonte:Eur J Med Chem; 144:359-371, 2018 Jan 20.
ISSN:1768-3254
País de publicação:France
Idioma:eng
Resumo:The aggressiveness of pancreatic cancer urgently requires more efficient treatment options. Because the sigma-2 (σ ) receptor was recently proposed as a promising target for pancreatic cancer therapy, we explored our previously developed multifunctional thiosemicarbazones, designed to synergistically impair cell energy levels, by targeting σ and P-gp proteins and chelating Iron. A deconstruction approach was herein applied by removing one function at a time from the potent multifunctional thiosemicarbazones 1 and 2, to investigate the contribution to cytotoxicity of each target involved. The results from in vitro (panel of pancreatic tumor cells) and in vivo experiments (C57BL/6 bearing KP02 tumor), suggest that while the multifunctional activity was not required for the antitumor activity of these thiosemicarbazones, σ -targeting appeared to allow alternative tumor cell death mechanisms, leading to potent and less toxic off-targets toxicities compared to other thiosemicarbazones devoid of σ -targeting.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Antineoplastic Agents); 0 (Chelating Agents); 0 (Receptors, sigma); 0 (Thiosemicarbazones); 0 (sigma-2 receptor)


  6 / 20037 MEDLINE  
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PMID:29309810
Autor:Zhuang C; She Y; Zhang H; Song M; Han Y; Li Y; Zhu Y
Endereço:Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Título:Cytoprotective effect of deferiprone against aluminum chloride-induced oxidative stress and apoptosis in lymphocytes.
Fonte:Toxicol Lett; 285:132-138, 2018 Mar 15.
ISSN:1879-3169
País de publicação:Netherlands
Idioma:eng
Resumo:Aluminum (Al) is a toxic metal, and excessive Al accumulation causes immunosuppression. Deferiprone (DFP) is a well-known chelator and used in dialysis patients for removing Al from tissues. The present study aimed to investigate whether DFP treatment can attenuate immunotoxicity induced by aluminum chloride (AlCl ) in cultured lymphocytes. Lymphocytes were treated with 0 and 0.6 mmol/L AlCl ∙6H O (pH 7.2) and/or 1.8 mmol/L DFP, respectively. Immune function of lymphocytes was assessed by T and B lymphocytes proliferation rates, T lymphocyte subpopulations and IL-2, IL-6 and TNF-α contents. In addition, lymphocyte damage was assessed by LDH activity, NO and MDA contents, NOS, SOD and GSH-Px activities, lymphocyte apoptosis index. These results showed that AlCl exposure reduced T and B lymphocyte proliferation rates, CD3 and CD4 T lymphocyte subpopulations, CD4 /CD8 ratio, IL-2, IL-6 and TNF-α contents, SOD and GSH-Px activities, early and later lymphocyte apoptosis indexes while enhanced CD8 T lymphocyte subpopulation, NO and MDA contents, LDH activity. DFP treatment attenuated the immunotoxicity of lymphocytes and reduced oxidative stress and lymphocyte apoptosis induced by AlCl , indicating that DFP could protect lymphocytes against immunosuppression induced by AlCl through attenuating oxidative stress and apoptosis.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Aluminum Compounds); 0 (Chelating Agents); 0 (Chlorides); 0 (Cytokines); 0 (Pyridones); 2BTY8KH53L (deferiprone); 3CYT62D3GA (aluminum chloride)


  7 / 20037 MEDLINE  
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PMID:29233652
Autor:Wang S; Gai Y; Zhang S; Ke L; Ma X; Xiang G
Endereço:School of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China.
Título:Synthesis and evaluation of a class of 1,4,7-triazacyclononane derivatives as iron depletion antitumor agents.
Fonte:Bioorg Med Chem Lett; 28(2):117-121, 2018 01 15.
ISSN:1464-3405
País de publicação:England
Idioma:eng
Resumo:Iron depletion has been confirmed as an efficient strategy for cancer treatment. In the current study, a series of 1,4,7-triazacyclononane derivatives HE-NO2A, HP-NO2A and NE2P2A, as well as the bifunctional chelators p-NO -PhPr-NE3TA and p-NH -PhPr-NE3TA were synthesized and evaluated as iron-depleting agents for the potential anti-cancer therapy against human hepatocellular carcinoma. The cytotoxicity of these chelators was measured using hepatocellular cancer cells and compared with the clinically available iron depletion agent DFO and the universal metal chelator DTPA. All these 1,4,7-triazacyclononane-based chelators exhibited much stronger antiproliferative activity than DFO and DTPA. Among them, chelators with phenylpropyl side chains, represented by p-NO -PhPr-NE3TA and p-NH -PhPr-NE3TA, displayed the highest antiproliferative activity against HepG2 cells. Hence, these compounds are attractive candidates for the advanced study as iron depletion agents for the potential anti-cancer therapy, and could be further in conjugation with a targeting moiety for the future development in targeted iron depletion therapy.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Antineoplastic Agents); 0 (Chelating Agents); 0 (Heterocyclic Compounds); 4730-54-5 (1,4,7-triazacyclononane); E1UOL152H7 (Iron)


  8 / 20037 MEDLINE  
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PMID:28458351
Autor:Yamaguchi M; Saito SY; Nishiyama R; Nakamura M; Todoroki K; Toyo'oka T; Ishikawa T
Endereço:Department of Pharmacology, School of Pharmaceutical Sciences, University of Shizuoka.
Título:Caffeine Suppresses the Activation of Hepatic Stellate Cells cAMP-Independently by Antagonizing Adenosine Receptors.
Fonte:Biol Pharm Bull; 40(5):658-664, 2017.
ISSN:1347-5215
País de publicação:Japan
Idioma:eng
Resumo:During liver injury, hepatic stellate cells (HSCs) are activated by various cytokines and transdifferentiated into myofibroblast-like activated HSCs, which produce collagen, a major source of liver fibrosis. Therefore, the suppression of HSC activation is regarded as a therapeutic target for liver fibrosis. Several epidemiological reports have revealed that caffeine intake decreases the risk of liver disease. In this study, therefore, we investigated the effect of caffeine on the activation of primary HSCs isolated from mice. Caffeine suppressed the activation of HSC in a concentration-dependent manner. BAPTA-AM, an intracellular Ca chelator, had no effect on the caffeine-induced suppression of HSC activation. None of the isoform-selective inhibitors of phosphodiesterase1 to 5 affected changes in the morphology of HSC during activation, whereas CGS-15943, an adenosine receptor antagonist, inhibited them. Caffeine had no effect on intracellular cAMP level or on the phosphorylation of extracellular signal-regulated kinase (ERK)1/2. In contrast, caffeine significantly decreased the phosphorylation of Akt1. These results suggest that caffeine inhibits HSC activation by antagonizing adenosine receptors, leading to Akt1 signaling activation.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Chelating Agents); 0 (Phosphodiesterase Inhibitors); 0 (Quinazolines); 0 (Receptors, Purinergic P1); 0 (Triazoles); 104615-18-1 (9-chloro-2-(2-furyl)-(1,2,4)triazolo(1,5-c)quinazolin-5-imine); 139890-68-9 (1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester); 3G6A5W338E (Caffeine); 526U7A2651 (Egtazic Acid); E0399OZS9N (Cyclic AMP)


  9 / 20037 MEDLINE  
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PMID:27770270
Autor:Nagy G; Baksa V; Kiss A; Turani M; Banfalvi G
Endereço:Department of Biotechnology and Microbiology, University of Debrecen, 1 Egyetem Square, Debrecen, 4010, Hungary. bigdegu@gmail.com.
Título:Gadolinium induced effects on mammalian cell motility, adherence and chromatin structure.
Fonte:Apoptosis; 22(2):188-199, 2017 Feb.
ISSN:1573-675X
País de publicação:Netherlands
Idioma:eng
Resumo:The toxicity of gadolinium is reduced by chelating agents that render this heavy metal into contrast complexes used for medical magnetic resonance imaging. However, the dissociation of gadolinium chelates is known to generate Gd ions, the cellular toxicity of which has not been tested in details. The cytotoxic effects of Gd(III) ions were evaluated by monitoring the proliferation, measuring the cellular motility and following chromatin changes in various cell lines upon Gd treatment. Measurements applied long-term scanning microscopy and a perfusion platform that replaced the medium with test solutions, bypassed physical contact with the cell culture during experiments, and provided uninterrupted high time-resolution time-lapse photomicrography for an extended period of time. Genotoxicity specific chromatin changes characteristic to Gd(III) were distinguished in human skin keratinocytes (HaCaT), human limbal stem cells (HuLi), colorectal adenocarcinoma (CaCO ), murine squamous carcinoma (SCC) and Indian muntjac (IM) cell lines. Characteristic features of Gd(III) toxicity were: loss of cellular motility, irreversible attachment of cells to the growth surface and cell death. Injury-specific chromatin changes manifested at micromolar Gd concentrations as premature chromatin condensation and highly condensed sticky chromatin patches. Gd(III) concentration- and cell type-dependent reduction of normal adherence, as well as premature chromatin condensation confirmed apoptosis. The risk related to the release of toxic Gd ions from gadolinium complexes and their effects on mono- and multi-layer cellular barriers have to be reconsidered when these chelated complexes are used as contrasting agents especially in relation to possible blood-brain barrier damages.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Chelating Agents); 0 (Chromatin); 0 (Contrast Media); 0 (Metals, Heavy); AU0V1LM3JT (Gadolinium)


  10 / 20037 MEDLINE  
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PMID:29369876
Autor:Aschenbrenner DS
Endereço:Diane S. Aschenbrenner is an assistant professor at Notre Dame of Maryland University in Baltimore. She also coordinates Drug Watch: daschenbrenner@ndm.edu.
Título:Potential Drug Interactions with Sodium Polystyrene Sulfonate.
Fonte:Am J Nurs; 118(2):47, 2018 Feb.
ISSN:1538-7488
País de publicação:United States
Idioma:eng
Tipo de publicação: NEWS
Nome de substância:0 (Chelating Agents); 0 (Polystyrenes); 70KO0R01RY (polystyrene sulfonic acid)



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