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Journal articles on the topic 'CEHC'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

Galli, Piroddi, Iannone, Pagliarani, Tomasi, and Floridi. "A comparison between the antioxidant and peroxynitrite-scavenging functions of the vitamin E metabolites alpha- and gamma-carboxyethyl-6-hydroxychromans." International Journal for Vitamin and Nutrition Research 74, no. 5 (September 1, 2004): 362–73. http://dx.doi.org/10.1024/0300-9831.74.5.362.

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Carboxyethyl-6-hydroxychromans (CEHC) are vitamin E metabolites with proposed in vitro antioxidant function. In this study we compared the antioxidant potency of the two main CEHC metabolites found in biological fluids (i.e., alpha-CEHC and gamma-CEHC) using two different experimental models of lipid oxidation: 1) plasma diluted 1/50 vol/vol in phosphate buffered saline (PBS) exposed to 50 muM Cu2+ ions, and 2) LDL (100 mug of proteins) exposed to different pro-oxidants as 2.5 muM Cu2+, 1 mM of the water soluble peroxyl radical generator 2,2'-Azobis(2-amidinopropane) hydrochloride (AAPH) and human macrophages (4 x 105 cells). Moreover, the two CEHC homologues were assessed for the inhibitory effect on the peroxynitrite (ONOO–)-induced nitration of tyrosine (Tyr). The results showed that in the concentration range 0.015–5 muM the CEHC metabolites and the hydrosoluble analogue Trolox exert similar concentration-dependent inhibition of the Cu2+-induced lipid oxidation of plasma. After in vitro exposure to tert-butyl hydroperoxide/Fe2+, CEHC formed chromanoxyl radicals with electron spin resonance spectra matching exactly those of their parent tocopherols. The LDL oxidation induced by AAPH or Cu2+ was significantly and similarly inhibited by 1 muM of both the CEHC homologues and Trolox. gamma-CEHC showed a slight but significantly higher inhibition of the macrophage-induced low-density lipoprotein (LDL) oxidation than alpha-CEHC. Both the CEHC homologues inhibit Tyr nitration induced by ONOO–. However, gamma-CEHC produced a slightly greater inhibitory effect than alpha-CEHC through the formation of the nitrated congener 5-nitro-gamma-CEHC. In all the systems under investigation, low nanomolar concentrations of CEHC (i.e., the concentration range in the blood of subjects with normal dietary intake of vitamin E) produced feeble antioxidant effects. In conclusion, gamma-CEHC and alpha-CEHC show similar concentration-dependent inhibition of plasma and LDL lipid oxidation. gamma-CEHC has a fairly higher potency than alpha-CEHC as ONOO– scavenger through the formation of 5-nitro-gamma-CEHC. CEHC metabolites show the same in vitro antioxidant chemistry of their parent tocopherols, but the characteristic hydrophilicity of these metabolites could result in different biopotency and roles. Further studies are needed to clarify whether CEHC could contribute to the antioxidant network in biological fluids and tissues.

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2

Li, Youyou, Leena P. Bharath, Ying Qian, Ting Ruan, Pon Velayutham Anandh Babu, Richard S. Bruno, J. David Symons, and Thunder Jalili. "γ−Carboxyethyl hydroxychroman, a metabolite of γ−tocopherol, preserves nitric oxide bioavailability in endothelial cells challenged with high glucose." Experimental Biology and Medicine 241, no. 18 (July 28, 2016): 2056–62. http://dx.doi.org/10.1177/1535370216661780.

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Endothelial dysfunction occurs when there are imbalances between factors that regulate the synthesis and degradation of nitric oxide (NO•), and has been reported in patients with hyperglycemia and insulin resistance. We reported that supplementation with γ-tocopherol (γ-T) in humans limits impairments in endothelial function otherwise induced by postprandial hyperglycemia. Given the rapid metabolism of γ-T into γ-carboxyethyl hydroxychroman (γ-CEHC), we hypothesized that the vasoprotective activities of γ-T could be attributed to its metabolite γ-CEHC. To test this, human aortic endothelial cells (HAECs) treated with 0 (vehicle control) or 3 µM γ-CEHC for 24 h prior to incubation with normal (5 mM) or high (25 mM) glucose for 48 h. High-glucose increased levels of uncoupled endothelial nitric oxide synthase (eNOS) as evidenced by reduced ( p < 0.05) eNOS dimer:monomer. High glucose also prevented insulin-stimulated increases in p-AktSer473: total Akt, p-eNOSSer1177: total eNOS, and NO• production. These adverse changes were accompanied by increased ( p < 0.05) reactive oxygen species and mRNA expression of inflammatory mediators (VCAM-1, E-selectin, IL-8). However, each deleterious response evoked by high glucose was prevented when HAECs were incubated with γ-CEHC prior to the high glucose challenge. Taken together, our data support the hypothesis that vascular protection provided by γ-T in vivo may be elicited through the bioactivity of its metabolite, γ-CEHC. Furthermore, it is possible that the antioxidant and anti-inflammatory activities of γ-CEHC may mediate this protective activity.

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3

Lewin, Allison, Allister Crow, Christopher T. C. Hodson, Lars Hederstedt, and Nick E. Le Brun. "Effects of substitutions in the CXXC active-site motif of the extracytoplasmic thioredoxin ResA." Biochemical Journal 414, no. 1 (July 29, 2008): 81–91. http://dx.doi.org/10.1042/bj20080356.

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The thiol–disulfide oxidoreductase ResA from Bacillus subtilis fulfils a reductive role in cytochrome c maturation. The pKa values for the CEPC (one-letter code) active-site cysteine residues of ResA are unusual for thioredoxin-like proteins in that they are both high (>8) and within 0.5 unit of each other. To determine the contribution of the inter-cysteine dipeptide of ResA to its redox and acid–base properties, three variants (CPPC, CEHC and CPHC) were generated representing a stepwise conversion into the active-site sequence of the high-potential DsbA protein from Escherichia coli. The substitutions resulted in large decreases in the pKa values of both the active-site cysteine residues: in CPHC (DsbA-type) ResA, ΔpKa values of −2.5 were measured for both cysteine residues. Increases in midpoint reduction potentials were also observed, although these were comparatively small: CPHC (DsbA-type) ResA exhibited an increase of +40 mV compared with the wild-type protein. Unfolding studies revealed that, despite the observed differences in the properties of the reduced proteins, changes in stability were largely confined to the oxidized state. High-resolution structures of two of the variants (CEHC and CPHC ResA) in their reduced states were determined and are discussed in terms of the observed changes in properties. Finally, the in vivo functional properties of CEHC ResA are shown to be significantly affected compared with those of the wild-type protein.

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4

Martens, Leon G., Jiao Luo, Fleur L. Meulmeester, Nadia Ashrafi, Esther Winters van Eekelen, Renée de Mutsert, Dennis O. Mook-Kanamori, et al. "Associations between Lifestyle Factors and Vitamin E Metabolites in the General Population." Antioxidants 9, no. 12 (December 15, 2020): 1280. http://dx.doi.org/10.3390/antiox9121280.

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The antioxidant vitamin E (α-tocopherol, α-TOH) protects lipids from oxidation by reactive oxygen species. We hypothesized that lifestyle factors associate with vitamin E metabolism marked by urinary α-tocopheronolactone hydroquinone (α-TLHQ) and α-carboxymethyl-hydroxychroman (α-CEHC levels), as potential reflection of lipid oxidation. We conducted a cross-sectional study in the Netherlands Epidemiology of Obesity Study. Serum α-TOH, and urinary α-TLHQ and α-CEHC were quantified by liquid chromatography coupled with tandem mass spectrometry. Information on the lifestyle factors (sleep, physical activity (PA), smoking and alcohol) were collected through questionnaires. Multivariable linear regression analyses were performed to assess the associations between the lifestyle factors and α-TOH measures. A total of 530 participants (46% men) were included with mean (SD) age of 56 (6) years. Of the examined lifestyle factors, only poor sleep was associated with a higher serum α-TOH (mean difference: 4% (95% CI: 1, 7%)). Current smoking was associated with higher urinary α-CEHC (32%: (14%, 53%)), with evidence of a dose–response relationship with smoking intensity (low pack years, 24% (2, 52%); high pack years, 55% (25, 93%)). Moderate physical activity was associated with a lower α-TLHQ relative to α-CEHC (−17%: (−26, −6%), compared with low PA). Only specific lifestyle factors associate with vitamin E metabolism. Examining serum α-TOH does not provide complete insight in vitamin E antioxidant capacity.

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5

Traber, Maret G., Scott W. Leonard, Ifechukwude Ebenuwa, Pierre-Christian Violet, Mahtab Niyyati, Sebastian Padayatty, Sheila Smith, Gerd Bobe, and Mark Levine. "Vitamin E catabolism in women, as modulated by food and by fat, studied using 2 deuterium-labeled α-tocopherols in a 3-phase, nonrandomized crossover study." American Journal of Clinical Nutrition 113, no. 1 (November 12, 2020): 92–103. http://dx.doi.org/10.1093/ajcn/nqaa298.

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ABSTRACT Background Human vitamin E (α-tocopherol) catabolism is a mechanism for regulating whole-body α-tocopherol. Objectives To determine the roles of the intestine and liver on α-tocopherol catabolism as affected by fat or fasting, 2 deuterium-labeled (intravenous d6- and oral d3-) forms of α-tocopherol were used. Methods Healthy women received intravenous d6-α-tocopherol and consumed d3-α-tocopherol with a 600-kcal defined liquid meal (DLM; 40% or 0% fat, n = 10) followed by controlled meals; or the 0% fat DLM (n = 7) followed by a 12-h fast (0% fat-fast), then controlled meals ≤72 h. The order of the 3-phase crossover design was not randomized and there was no blinding. Samples were analyzed by LC/MS to determine the α-tocopherol catabolites and α-carboxyethyl hydroxychromanol (α-CEHC) in urine, feces, and plasma that were catabolized from administered oral d3- and intravenous d6-α-tocopherols. Results Urinary and plasma d3- and d6-α-CEHC concentrations varied differently with the interventions. Mean ± SEM cumulative urinary d6-α-CEHC derived from the intravenous dose excreted over 72 h during the 40% fat (2.50 ± 0.37 μmol/g creatinine) and 0% fat (2.37 ± 0.37 μmol/g creatinine) interventions were similar, but a ∼50% decrease was observed during the 0% fat-fast (1.05 ± 0.39 μmol/g creatinine) intervention (compared with 0% fat, P = 0.0005). Cumulative urinary d3-α-CEHC excretion was not significantly changed by any intervention. Total urinary and fecal excretion of catabolites accounted for <5% of each of the administered doses. Conclusions Differential catabolism of the intravenous d6-α-tocopherol and oral d3-α-tocopherol doses shows both liver and intestine have roles in α-tocopherol catabolism. During the 40% fat intervention, >90% of urinary d3-α-CEHC excretion was estimated to be liver-derived, whereas during fasting <50% was from the liver with the remainder from the intestine, suggesting that there was increased intestinal α-tocopherol catabolism while d3-α-tocopherol was retained in the intestine in the absence of adequate fat/food for α-tocopherol absorption. This trial was registered at clinicaltrials.gov as NCT00862433.

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6

Li, Yi-Jen, Sheng-Ching Luo, Yi-Jing Lee, Fu-Jung Lin, Chi-Cheng Cheng, Yung-Shung Wein, Yueh-Hsiung Kuo, and Ching-jang Huang. "Isolation and Identification of α-CEHC Sulfate in Rat Urine and an Improved Method for the Determination of Conjugated α-CEHC." Journal of Agricultural and Food Chemistry 56, no. 23 (December 10, 2008): 11105–13. http://dx.doi.org/10.1021/jf802459d.

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7

Fais, Antonella, Enrico Cacace, Luigi Atzori, Benedetta Era, and Valeria Ruggiero. "Plasma phospholipase, γ-CEHC and antioxidant capacity in fibromyalgia." International Journal of Rheumatic Diseases 20, no. 5 (November 20, 2015): 550–54. http://dx.doi.org/10.1111/1756-185x.12787.

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8

Flisiak, Robert. "Meeting of Initiative Group for Central European Hepatologic Collaboration (CEHC)." Clinical and Experimental Hepatology 1 (2016): 1. http://dx.doi.org/10.5114/ceh.2016.58848.

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9

Mazzini, Francesco, Francesco Galli, and Piero Salvadori. "Vitamin E Metabolites: Synthesis of [D2]- and [D3]-γ-CEHC." European Journal of Organic Chemistry 2006, no. 24 (December 2006): 5588–93. http://dx.doi.org/10.1002/ejoc.200600652.

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10

Otter, Don, Mingshu Cao, Hui-Ming Lin, Karl Fraser, Shelley Edmunds, Geoff Lane, and Daryl Rowan. "Identification of Urinary Biomarkers of Colon Inflammation in IL10-/-Mice Using Short-Column LCMS Metabolomics." Journal of Biomedicine and Biotechnology 2011 (2011): 1–12. http://dx.doi.org/10.1155/2011/974701.

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The interleukin-10-deficient (IL10-/-) mouse develops colon inflammation in response to normal intestinal microflora and has been used as a model of Crohn's disease. Short-Column LCMS metabolite profiling of urine from IL10-/-and wild-type (WT) mice was used, in two independent experiments, to identify mass spectral ions differing in intensity between these two genotypes. Three differential metabolites were identified as xanthurenic acid and as the glucuronides of xanthurenic acid and of α-CEHC (2,5,7,8-tetramethyl-2-(2′-carboxyethyl)-6-hydroxychroman). The significance of several differential metabolites as potential biomarkers of colon inflammation was evaluated in an experiment which compared metabolite concentrations in IL10-/-and WT mice housed, either under conventional conditions and dosed with intestinal microflora, or maintained under specific pathogen-free (SPF) conditions. Concentrations of xanthurenic acid, α-CEHC glucuronide, and an unidentified metabolitem/z495-/497+were associated with the degree of inflammation in IL10-/-mice and may prove useful as biomarkers of colon inflammation.

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11

Burke, Matthew, Pratik Pal, Peiyi Zhang, Xuan Zhang, and Guangrong Zheng. "Concise Synthesis of (S)-δ-CEHC, a Metabolite of Vitamin E." ACS Omega 6, no. 6 (February 2, 2021): 4355–61. http://dx.doi.org/10.1021/acsomega.0c05658.

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12

Mondul, Alison M., Steven C. Moore, Stephanie J. Weinstein, Anne M. Evans, Edward D. Karoly, Satu Männistö, Joshua N. Sampson, and Demetrius Albanes. "Serum Metabolomic Response to Long-Term Supplementation withall-rac-α-Tocopheryl Acetate in a Randomized Controlled Trial." Journal of Nutrition and Metabolism 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/6158436.

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Background. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, a randomized controlled cancer prevention trial, showed a 32% reduction in prostate cancer incidence in response to vitamin E supplementation. Two other trials were not confirmatory, however.Objective. We compared the change in serum metabolome of the ATBC Study participants randomized to receive vitamin E to those who were not by randomly selecting 50 men from each of the intervention groups (50 mg/day all-rac-α-tocopheryl acetate (ATA), 20 mg/dayβ-carotene, both, placebo).Methods. Metabolomic profiling was conducted on baseline and follow-up fasting serum (Metabolon, Inc.).Results. After correction for multiple comparisons, five metabolites were statistically significantly altered (βis the change in metabolite level expressed as number of standard deviations on the log scale):α-CEHC sulfate (β=1.51,p=1.45×10-38),α-CEHC glucuronide (β=1.41,p=1.02×10-31),α-tocopherol (β=0.97,p=2.22×10-13),γ-tocopherol (β=-0.90,p=1.76×10-11), andβ-tocopherol (β=-0.73,p=9.40×10-8). Glutarylcarnitine, beta-alanine, ornithine, and N6-acetyllysine were also decreased by ATA supplementation (βrange 0.40 to −0.36), but not statistically significantly.Conclusions. Comparison of the observed metabolite alterations resulting from ATA supplementation to those in other vitamin E trials of different populations, dosages, or formulations may shed light on the apparently discordant vitamin E-prostate cancer risk findings.

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13

Pope, Simon A. S., Guillaume E. Burtin, Peter T. Clayton, David J. Madge, and David P. R. Muller. "Synthesis and analysis of conjugates of the major vitamin E metabolite, α-CEHC." Free Radical Biology and Medicine 33, no. 6 (September 2002): 807–17. http://dx.doi.org/10.1016/s0891-5849(02)00974-7.

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14

LEONARD, SCOTT W., RICHARD S. BRUNO, RAJASEKHAR RAMAKRISHNAN, TAMMY BRAY, and MARET G. TRABER. "Cigarette Smoking Increases Human Vitamin E Requirements as Estimated by Plasma Deuterium-Labeled CEHC." Annals of the New York Academy of Sciences 1031, no. 1 (December 2004): 357–60. http://dx.doi.org/10.1196/annals.1331.044.

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15

Leonard, Scott W., Gerd Bobe, and Maret G. Traber. "Stability of antioxidant vitamins in whole human blood during overnight storage at 4°C and frozen storage up to 6 months." International Journal for Vitamin and Nutrition Research 88, no. 3-4 (June 1, 2018): 151–57. http://dx.doi.org/10.1024/0300-9831/a000485.

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Abstract. To determine optimal conditions for blood collection during clinical trials, where sample handling logistics might preclude prompt separation of erythrocytes from plasma, healthy subjects (n=8, 6 M/2F) were recruited and non-fasting blood samples were collected into tubes containing different anticoagulants (ethylenediaminetetra-acetic acid (EDTA), Li-heparin or Na-heparin). We hypothesized that heparin, but not EDTA, would effectively protect plasma tocopherols, ascorbic acid, and vitamin E catabolites (α- and γ-CEHC) from oxidative damage. To test this hypothesis, one set of tubes was processed immediately and plasma samples were stored at −80°C, while the other set was stored at 4°C and processed the following morning (~30 hours) and analyzed, or the samples were analyzed after 6 months of storage. Plasma ascorbic acid, as measured using HPLC with electrochemical detection (LC-ECD) decreased by 75% with overnight storage using EDTA as an anticoagulant, but was unchanged when heparin was used. Neither time prior to processing, nor anticoagulant, had any significant effects upon plasma α- or γ-tocopherols or α- or γ-CEHC concentrations. α- and γ-tocopherol concentrations remained unchanged after 6 months of storage at −80°C, when measured using either LC-ECD or LC/mass spectrometry. Thus, refrigeration of whole blood at 4°C overnight does not change plasma α- or γ-tocopherol concentrations or their catabolites. Ascorbic acid is unstable in whole blood when EDTA is used as an anticoagulant, but when whole blood is collected with heparin, it can be stored overnight and subsequently processed.

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16

Lecea, Mercedes, Gloria Hernández-Torres, Antonio Urbano, M. Carmen Carreño, and Françoise Colobert. "Enantioselective Total Synthesis of the Natural γ-Tocopherol Metabolite (S)-γ-CEHC [(S)-LLU-α]." Organic Letters 12, no. 3 (February 5, 2010): 580–83. http://dx.doi.org/10.1021/ol9027804.

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17

Mazzini, Francesco, Thomas Netscher, and Piero Salvadori. "First Synthesis ofrac-(5-2H3)-α-CEHC, a Labeled Analogue of a Major Vitamin E Metabolite." Journal of Organic Chemistry 69, no. 26 (December 2004): 9303–6. http://dx.doi.org/10.1021/jo048514u.

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18

Liu, Kilia Y., and Qing Jiang. "Tocopherols and Tocotrienols Are Bioavailable in Rats and Primarily Excreted in Feces as the Intact Forms and 13′-Carboxychromanol Metabolites." Journal of Nutrition 150, no. 2 (September 9, 2019): 222–30. http://dx.doi.org/10.1093/jn/nxz217.

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ABSTRACT Background Vitamin E α-, γ-, or δ-tocopherol (αT, γT, δT) and γ- or δ-tocotrienol (γTE, δTE) are metabolized to hydroxychromanols and carboxychromanols including 13′-carboxychromanol (13′-COOH), 11′-COOH, and carboxyethyl hydroxychroman (CEHC), some of which have unique bioactivities compared with the vitamers. However, the bioavailability of these metabolites has not been well characterized. Objective We investigated the pharmacokinetics (PK) of vitamin E forms and metabolites in rats. Methods Six-week-old male Wistar rats received 1-time gavage of γT-rich tocopherols (50 mg/kg) containing γT/δT/αT (57.7%, 21.9%, and 10.9%, respectively) or δTE-rich tocotrienols (35 mg/kg) containing δTE/γTE (8:1). We quantified the time course of vitamin E forms and metabolites in the plasma and their 24-h excretion to the urine and feces. The general linear model repeated measure was used for analyses of the PK data. Results In the rats’ plasma, Cmax of γT or δTE was 25.6 ± 9.1 μM (Tmax = 4 h) or 16.0 ± 2.3 μM (Tmax = 2 h), respectively, and sulfated CEHCs and sulfated 11′-COOHs were the predominant metabolites with Cmax of 0.4–0.5 μM (Tmax ∼5–7 h) or ∼0.3 μM (Tmax at 4.7 h), respectively. In 24-h urine, 2.7% of γT and 0.7% of δTE were excreted as conjugated CEHCs. In the feces, 17–45% of supplemented vitamers were excreted as unmetabolized forms and 4.9–9.2% as unconjugated carboxychromanols, among which 13′-COOHs constituted ∼50% of total metabolites and the amount of δTE-derived 13′-COOHs was double that of 13′-COOH derived from γT. Conclusions PK data of vitamin E forms in rats reveal that γT, δT, γTE, and δTE are bioavailable in the plasma and are mainly excreted as unmetabolized forms and long-chain metabolites including 13′-COOHs in feces, with more metabolites from tocotrienols than from tocopherols.

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19

Radosavac, Dragan, Peter Graf, M. Cristina Polidori, Helmut Sies, and Wilhelm Stahl. "Tocopherol metabolites 2, 5, 7, 8-tetramethyl-2-(2'-carboxyethyl)-6-hydroxychroman (α-CEHC) and 2, 7, 8-trimethyl-2-(2'-carboxyethyl)-6-hydroxychroman (γ-CEHC) in human serum after a single dose of natural vitamin E." European Journal of Nutrition 41, no. 3 (June 2002): 119–24. http://dx.doi.org/10.1007/s00394-002-0365-3.

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20

Michels, Alexander J., Scott W. Leonard, Sandra L. Uesugi, Gerd Bobe, Balz Frei, and Maret G. Traber. "Daily Consumption of Oregon Hazelnuts Affects α-Tocopherol Status in Healthy Older Adults: A Pre-Post Intervention Study." Journal of Nutrition 148, no. 12 (December 1, 2018): 1924–30. http://dx.doi.org/10.1093/jn/nxy210.

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ABSTRACT Background Inadequate vitamin E and magnesium intakes are of concern for older adults owing to the associated incidence of age-related diseases. Objective This study was designed to determine the extent to which a 16-wk intervention with hazelnuts alters vitamin E and magnesium status in a group of older men and women, and used a pre-post intervention design without a control group to adjust for temporal changes. Methods Participants (n = 32 including 22 women; mean ± SD age: 63 ± 6 y) consumed hazelnuts (∼57 g/d) for 16 wk. Blood and urine samples and anthropomorphic measures were taken at the start and end of the intervention to determine plasma concentrations of α-tocopherol and serum concentrations of magnesium, lipids, glucose, insulin, and high-sensitivity C-reactive protein along with urinary vitamin E metabolites; several other micronutrients were measured by a lymphocyte proliferation assay. There were 3 primary endpoints, calculated as the mean changes in measurements between baseline and the end of the 16-wk intervention for 1) plasma α-tocopherol, 2) urinary α-carboxyethyl hydroxychromanol (α-CEHC; an α-tocopherol metabolite), and 3) serum magnesium. Results Hazelnut consumption increased concentrations of the urinary α-tocopherol metabolite α-CEHC (mean ± SD: 0.84 ± 0.45 to 1.14 ± 0.50 µmol/g creatinine; P = 0.0006). In addition, hazelnut consumption increased serum concentrations of magnesium (+2.1%, P = 0.05), decreased concentrations of fasting glucose (−3.4%, P = 0.03) and LDL cholesterol (−6.0%, P = 0.02), and decreased total:HDL cholesterol ratios (−4.5%, P = 0.009). No significant changes were observed in blood pressure, lymphocyte proliferation assays, and serum concentrations of insulin, high-sensitivity C-reactive protein, triglyceride, α-tocopherol, or HDL cholesterol. Conclusions Consuming hazelnuts improves a biomarker of vitamin E status in older adults. Vitamin E is a shortfall micronutrient, as identified by the Dietary Guidelines for Americans 2015–2020, which frequently is consumed at levels less than the Estimated Average Requirement of 12 mg/d; thus, hazelnuts should be considered as part of a healthy dietary pattern. This trial was registered at clinicaltrials.gov as NCT03485989.

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Betancor-Fernandez, Alejandro, Helmut Sies, Wilhelm Stahl, and M. Cristina Polidori. "In Vitro Antioxidant Activity of 2,5,7,8-tetramethyl-2-(2′-carboxyethyl)-6-hydroxychroman (α-CEHC), a Vitamin E Metabolite." Free Radical Research 36, no. 8 (January 2002): 915–21. http://dx.doi.org/10.1080/1071576021000005357.

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22

Li, Yi-Jen, and Huey-Mei Shaw. "Pregnenolone and dexamethasone, modulators of cytochrome P450-3A, not increase but reduce urinary α-CEHC excretion in rats." BioFactors 31, no. 1 (2007): 67–76. http://dx.doi.org/10.1002/biof.5520310107.

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23

Takata, Jiro, Ryoji Hidaka, Akihiko Yamasaki, Akihiro Hattori, Takeshi Fukushima, Maiko Tanabe, Kazuhisa Matsunaga, Yoshiharu Karube, and Kazuhiro Imai. "Noveld-γ-tocopherol derivative as a prodrug ford-γ-tocopherol and a two-step prodrug forS-γ-CEHC." Journal of Lipid Research 43, no. 12 (September 16, 2002): 2196–204. http://dx.doi.org/10.1194/jlr.d200027-jlr200.

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24

Boroch, E., and E. Kaldist. "Phase transitions in the CeH2CeH3 system." Inorganica Chimica Acta 140 (December 1987): 89–91. http://dx.doi.org/10.1016/s0020-1693(00)81056-7.

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25

Freiser, Helene, and Qing Jiang. "Optimization of the enzymatic hydrolysis and analysis of plasma conjugated γ-CEHC and sulfated long-chain carboxychromanols, metabolites of vitamin E." Analytical Biochemistry 388, no. 2 (May 2009): 260–65. http://dx.doi.org/10.1016/j.ab.2009.02.027.

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Kuchan, Matthew J., Katherine M. Ranard, Priyankar Dey, Sookyoung Jeon, Geoff Y. Sasaki, Karen J. Schimpf, Richard S. Bruno, Martha Neuringer, and John W. Erdman. "Infant Rhesus Macaque Brain α-Tocopherol Stereoisomer Profile Is Differentially Impacted by the Source of α-Tocopherol in Infant Formula." Journal of Nutrition 150, no. 9 (July 2, 2020): 2305–13. http://dx.doi.org/10.1093/jn/nxaa174.

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ABSTRACT Background α-Tocopherol (αT) in its natural form [2′R, 4′R, 8′R αT (RRR-αT)] is more bioactive than synthetic α-tocopherol (all rac-αT). All rac-αT is widely used in infant formulas, but its accretion in formula-fed infant brain is unknown. Objective We sought to compare αT and stereoisomer status in infant rhesus macaques (Macaca mulatta) fed infant formula (RRR-αT or all rac-αT) with a reference group fed a mixed diet of breast milk and maternal diet. Methods From 1 d after birth until 6 mo of age, infants (n = 23) were either nursery reared and exclusively fed 1 of 2 formulas by staff personnel or were community housed with their mothers and consumed a mixed reference diet of breast milk (69 mL/d at 6 mo) transitioning to monkey diet at ∼2 mo (MF; n = 8). Formulas contained either 21 μmol RRR-αT/L (NAT-F; n = 8) or 30 μmol all rac-αT/L (SYN-F; n = 7). Total αT and αT stereoisomers were analyzed in breast milk at 2, 4, and 6 mo and in monkey plasma and liver and 6 brain regions at 6 mo of age. α-Tocopherol transfer protein (α-TTP), lipoprotein αT, and urinary α-carboxyethyl-hydroxychroman (α-CEHC) were measured. One-way ANOVA with Tukey's post-hoc test was used for analysis. Results At study termination, plasma, liver, lipoprotein, and brain total αT did not differ between groups. However, the NAT-F–fed group had higher RRR-αT than the SYN-F–fed group (P < 0.01) and the MF group (P < 0.0001) in plasma (1.7- and 2.7-fold) and brain (1.5- and 2.5-fold). Synthetic αT 2R stereoisomers (SYNTH-2R) were generally 3- and 7-fold lower in brain regions of the NAT-F group compared with those of the SYN-F and MF groups (P < 0.05). SYNTH-2R stereoisomers were 2-fold higher in MF than SYN-F (P < 0.0001). The plasma percentage of SYNTH-2R was negatively correlated with the brain percentage of RRR-αT (r = −0.99, P < 0.0001). Brain αT profiles were not explained by α-TTP mRNA or protein expression. Urine α-CEHC was 3 times higher in the NAT-F than in the MF group (P < 0.01). Conclusions Consumption of infant formulas with natural (NAT-F) compared with synthetic (SYN-F) αT differentially impacted brain αT stereoisomer profiles in infant rhesus macaques. Future studies should assess the functional implications of αT stereoisomer profiles on brain health.

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Traber, Maret G., Angelika Elsner, and Regina Brigelius-Flohé. "Synthetic as compared with natural vitamin E is preferentially excreted as α-CEHC in human urine: studies using deuterated α-tocopheryl acetates." FEBS Letters 437, no. 1-2 (October 16, 1998): 145–48. http://dx.doi.org/10.1016/s0014-5793(98)01210-1.

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Traber, Maret G., Lisbeth K. Siddens, Scott W. Leonard, Bettina Schock, Kishorchandra Gohil, Sharon K. Krueger, Carroll E. Cross, and David E. Williams. "α-Tocopherol modulates Cyp3a expression, increases γ-CEHC production, and limits tissue γ-tocopherol accumulation in mice fed high γ-tocopherol diets." Free Radical Biology and Medicine 38, no. 6 (March 2005): 773–85. http://dx.doi.org/10.1016/j.freeradbiomed.2004.11.027.

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Wierzbowska, Agnieszka, Tadeusz Robak, Anna Krawczynska, Agnieszka Pluta, Agata Wrzesien-Kus, Barbara Cebula, and Piotr Smolewski. "Kinetics and Apoptotic Profile of Circulating Endothelial Cells as an Indicator of Response to Treatment in Acute Myeloid Leukemia Patients." Blood 108, no. 11 (November 16, 2006): 4490. http://dx.doi.org/10.1182/blood.v108.11.4490.4490.

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Abstract The circulating endothelial cells (CEC) are proposed to be a noninvasive marker of angiogenesis. Previously we have found that the number of resting (rCEC), activated (aCEC) CEC and circulating endothelial progenitor cells (CEPC) in peripheral blood of patients (pts) with AML is significantly higher than in healthy controls and correlates with tumour burden. In the present study we analysed CEC count in 111 AML pts at the time of diagnosis and 32 healthy controls. Additionally, we evaluated the kinetics of both rCEC, aCEC, CEPC as well as apoptotic CEC count in 40 AML pts treated with standard induction chemotherapy (ChT). In that group of pts measurements were performed additionally 24 hours after the first (day +1) and last (day +7) dose of ChT as well as at the time of response evaluation. The levels of CEC and their apoptotic profile were correlated with response to treatment. CEC were evaluated by the four colour flow cytometry using a panel of previously described monoclonal antibodies. CEPC were identified as CD45−/ D34+/ CD31+ and CD133+. rCEC were defined as CD45−/CD133−/ CD31+/CD34+/CD146+ and CD105−/CD106− cells. CD105+ or CD106+ CEC were classified as aCEC. Apoptotic CEC were detected as CD146+/Annexin V+ cells (CECAnnV+) CEC level (22,9/μL) was 7-fold higher in untreated AML pts than in the controls (2,95/μL) p<0,0001. The median (Me) numbers of aCEC (12,7/μL), rCEC (12,3/μL) and CEPC (1,7/μL) were higher in AML pts at diagnosis compared to controls (aCEC 0,9/μL, rCEC 1,6/μL and 0,1/μL; p<0,0001). The CECAnnV+ count was 16-fold higher in AML (2,4/μL) than in controls (0,15/μL; p<0,0001). In our group of AML pts high counts of CEC were associated with worse outcome. The lower probability complete remission (CR) achieved after the first cours of induction ChT was observed in pts with a pretreatment number of CEC >30/μL; (p<0,01) and CEPC>10/μL (p<0,03) compared to the pts with CEC<30/μL and CEPC<10/μL respectively. There was also trend toward a higher probability of CR in pts with increased number of apoptotic CEC (CECAnnV+ >Me) (p=0,056) than in pts with CECAnnV+<Me. The numbers of aCEC, rCEC, CEPC and CECAnnV+ evaluated at the diagnosis were comparable in pts who achieved CR and in pts refractory to treatment (NR). In CR pts the counts of aCEC, rCEC, CEPC and CECAnnV+ determined at the time of response’s evaluation were significantly lower then those found at the time of diagnosis (p<0,001, p<0,01, p<0,05, p<0,05 respectively). Moreover, in those CR pts we observed a significant drop in the count of CEC 24 hours after the first as well as the last dose of the induction ChT (p<0,005 and p<0,003, respectively) and increase in the number of CECAnnV+ (p<0,0002, p<0,001 respectively). In pts resistant to treatment the aCEC, rCEC, CEPC and CECAnnV+ counts assessed before and after induction ChT did not differ significantly. In those NR pts a significant decrease in CEC count and increase of CECAnnV+ number was noted only at day +7 after the induction ChT regimen (p<0,03; p<0,05). In conclusion, the CEC and CECAnnV+ levels are significantly higher in AML pts than in healthy subjects and correlate with response to treatment. The high numbers of circulating CEC, both aCEC and rCEC, or CEPC can be a predictor of worse response to induction ChT in AML. Moreover, an early decrease in CEC and increase in CECAnnV+ counts may predict good sensitivity to the treatment. In contrast, the antiapoptotic pattern of CEC may contribute to ChT resistance in AML.

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Jeanes, Yvonne M., Wendy L. Hall, Anna R. Proteggente, and John K. Lodge. "Cigarette Smokers have Decreased Lymphocyte and Platelet α-tocopherol Levels and Increased Excretion of the γ-tocopherol Metabolite γ-carboxyethyl-hydroxychroman (γ-CEHC)." Free Radical Research 38, no. 8 (August 2004): 861–68. http://dx.doi.org/10.1080/10715760410001715149.

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Tanabe, Maiko, Takeshi Fukushima, Noriko Usui, Nozomi Aoyama, Makoto Tsunoda, and Kazuhiro Imai. "Intravenous administration of 2,7,8-trimethyl-2-(?-carboxyethyl)-6-hydroxy chroman (?-CEHC) to rats and determination of its plasma concentration and urinary sodium excretion." Biomedical Chromatography 18, no. 9 (2004): 727–34. http://dx.doi.org/10.1002/bmc.385.

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Kishi, Takayuki, Jonathan Chipman, Melvina Evereklian, Khanh Nghiem, Maryalice Stetler-Stevenson, Margaret E. Rick, Michael Centola, Frederick W. Miller, and Lisa G. Rider. "Endothelial Activation Markers as Disease Activity and Damage Measures in Juvenile Dermatomyositis." Journal of Rheumatology 47, no. 7 (August 1, 2019): 1011–18. http://dx.doi.org/10.3899/jrheum.181275.

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Objective.Circulating endothelial cells (CEC), von Willebrand factor (vWF) antigen, P-selectin, and thrombomodulin are released from damaged endothelium, while decreases in circulating endothelial progenitor cells (CEPC) have been associated with poor vascular outcomes. We examined these markers in the peripheral blood of patients with juvenile dermatomyositis (JDM) and their correlations with disease assessments.Methods.Peripheral blood endothelial cells and biomarkers were assessed in 20 patients with JDM and matched healthy controls. CEC and CEPC were measured by flow cytometry, while vWF antigen and activity, factor VIII, P-selectin, and thrombomodulin were measured in plate-based assays. Disease activity and damage, nailfold capillary density, and brachial artery flow dilation were assessed. Serum cytokines/chemokines were measured by Luminex.Results.CEC, vWF antigen, factor VIII, and thrombomodulin, but not vWF activity, CEPC, or P-selectin, were elevated in the peripheral blood of patients with JDM. CEC correlated with pulmonary activity (rs = 0.56). The vWF antigen correlated with Patient’s/Parent’s Global, cutaneous, and extramuscular activity (rs = 0.47–0.54). CEPC negatively correlated with muscle activity and physical function (rs = −0.52 to −0.53). CEPC correlated inversely with endocrine damage. The vWF antigen and activity correlated with interleukin 10 and interferon-gamma inducible protein-10 (rs = 0.64–0.82).Conclusion.Markers of endothelial injury are increased in patients with JDM and correlate with extramuscular activity. CEPC correlate inversely with muscle activity, suggesting a functional disturbance in repair mechanisms.

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Wierzbowska, Agnieszka, Tadeusz Robak, Anna Krawczynska, Agata Wrzesien-Kus, Agnieszka Pluta, Barbara Cebula, and Piotr Smolewski. "Circulating Endothelial Cells Are an Indicator of Response to Treatment in Acute Myeloid Leukemia Patients." Blood 106, no. 11 (November 16, 2005): 2776. http://dx.doi.org/10.1182/blood.v106.11.2776.2776.

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Abstract Introduction. The circulating endothelial cells (CEC) are proposed to be a noninvasive marker of angiogenesis. The number of CEC in peripheral blood of patients (pts) with acute myeloid leukemia (AML) has not been investigated so far. Patients and Methods. We evaluated the count of resting (rCEC) and activated (aCEC) CEC and circulating endothelial progenitor cells (CEPC) as well as apoptotic CEC (CECAnnV+) in 62 AML pts at the time of diagnosis and 30 healthy controls. Additionally in 26 pts measurements were performed at the time of response evaluation and in 15 pts also 24 h after the first and last dose of chemotherapy. The levels of CEC were correlated with known prognostic factors and response to treatment. CEC were evaluated by the four colour flow cytometry using a panel of previously described monoclonal antibodies and an appropriate analysis gate. CEPC were defined as negative for hematopoietic marker CD45 and positive for endothelial cells markers CD34, CD31 and the endothelial progenitor marker CD133. Resting CEC were defined as CD45−, CD133−, CD31+, CD34+, CD146+ and negative for activation markers (CD105, CD106). CD105 or CD106 positive mature endothelial cells were classified as activated CEC. Apoptotic CEC were CD146 and Annexin V positive. Results. In untreated AML pts we observed 10-fold higher CEC level (median 29,3/μL) than in the control group (2,95/μL) p<0,0001. The numbers of aCEC (12,7/μL), rCEC (12,3/μL) and CEPC (1,7/μL) were significantly higher in AML pts at diagnosis when compared to healthy controls (aCEC 0,9/μL, rCEC 1,6/μL and 0,1/μL; p<0,0001). CECAnnV+ count was also 10-fold higher in AML (1,5/μL) than in controls (0,15/μL; p<0,0001). Both CEC and CECAnnV+ counts did not correlate with WBC, hemoglobin and platelets count as well as percentage of blasts in bone marrow and absolute blast count. The positive correlations between CEC number and CEPC count (r=0,435; p<0,001), CECAnnV+ count (r=0,502; p<0,01) as well as LDH activity (r=0,328; p<0,02) were found. The significant decrease of aCEC and rCEC numbers 24 hours after the first dose of chemotherapy was noted in patients who achieved complete remission (CR)(p<0,04) but not in pts refractory to treatment. Moreover aCEC, rCEC, CEPC and CECAnnV+ counts determined at the time of response’s evaluation were significantly lower then at the time of diagnosis in pts who achieved CR (p<0,01) and did not differ in refractory AML. There was no difference between levels of both viable and apoptotic CEC in AML pts in CR and in the control group (p>0,05). Conclusions. The CEC and CECAnnV+ levels are significantly higher in AML patients than in healthy subjects and correlate with response to treatment. Further investigation should be undertaken to better determine their prognostic and therapeutic value.

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Habib, Hadi, Carrie J. Finno, Ingrid Gennity, Gianna Favro, Erin Hales, Birgit Puschner, and Benjamin C. Moeller. "Simultaneous quantification of vitamin E and vitamin E metabolites in equine plasma and serum using LC-MS/MS." Journal of Veterinary Diagnostic Investigation 33, no. 3 (April 13, 2021): 506–15. http://dx.doi.org/10.1177/10406387211005433.

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Vitamin E deficiencies can impact normal growth and development in humans and animals, and assessment of circulating levels of vitamin E and its metabolites may be an important endpoint for evaluation. Development of a sensitive method to detect and quantify low concentrations of vitamin E and metabolites in biological specimens allows for a proper diagnosis for patients and animals that are deficient. We developed a method to simultaneously extract, detect, and quantify the vitamin E compounds alpha-tocopherol (α-TP), gamma-tocopherol (γ-TP), alpha-tocotrienol (α-TT), and gamma-tocotrienol (γ-TT), and the corresponding metabolites formed after β-oxidation of α-TP and γ-TP, alpha-carboxymethylbutyl hydroxychroman (α-CMBHC) and alpha- or gamma-carboxyethyl hydroxychroman (α- or γ-CEHC), respectively, from equine plasma and serum. Quantification was achieved through liquid chromatography–tandem mass spectrometry. We applied a 96-well high-throughput format using a Phenomenex Phree plate to analyze plasma and serum. Compounds were separated by using a Waters ACQUITY UPLC BEH C18 column with a reverse-phase gradient. The limits of detection for the metabolites and vitamin E compounds were 8–330 pg/mL. To validate the method, intra-day and inter-day accuracy and precision were evaluated along with limits of detection and quantification. The method was then applied to determine concentrations of these analytes in plasma and serum of horses. Alpha-TP levels were 3–6 µg/mL of matrix; the metabolites were found at much lower levels, 0.2–1.0 ng/mL of matrix.

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Boroch, E., and E. Kaldis. "Progress in the T-X Phase Diagram of the Solid Solution CeH2— CeH3." Zeitschrift für Physikalische Chemie 163, Part_1 (January 1989): 117–24. http://dx.doi.org/10.1524/zpch.1989.163.part_1.0117.

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Conder, K., J. Schefer, E. Kaldis, and Cai Ru-Xiu. "Progress in the T-X Phase Diagram of the Solid Solution CeH2— CeH3." Zeitschrift für Physikalische Chemie 163, Part_1 (January 1989): 125–34. http://dx.doi.org/10.1524/zpch.1989.163.part_1.0125.

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Kaldis, E., E. Boroch, and M. Tellefsen. "Phase relationships and phase transitions in the homogeneity range of pure CeH2–CeH3." Journal of the Less Common Metals 129 (February 1987): 57–64. http://dx.doi.org/10.1016/0022-5088(87)90033-6.

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Goodin, Douglas S., Jorge R. Oksenberg, Venceslas Douillard, Pierre-Antoine Gourraud, and Nicolas Vince. "Genetic susceptibility to multiple sclerosis in African Americans." PLOS ONE 16, no. 8 (August 9, 2021): e0254945. http://dx.doi.org/10.1371/journal.pone.0254945.

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Objective To explore the nature of genetic-susceptibility to multiple sclerosis (MS) in African-Americans. Background Recently, the number of genetic-associations with MS has exploded although the MS-associations of specific haplotypes within the major histocompatibility complex (MHC) have been known for decades. For example, the haplotypes HLA-DRB1*15:01~HLA-DQB1*06:02, and HLA-DRB1*03:01~ HLA-DQB1*02:01 have odds ratios (ORs) for an MS-association orders of magnitude stronger than many of these newly-discovered associations. Nevertheless, all these haplotypes are part of much larger conserved extended haplotypes (CEHs), which span both the Class I and Class II MHC regions. African-Americans are at greater risk of developing MS compared to a native Africans but at lesser risk compared to Europeans. It is the purpose of this manuscript to explore the relationship between MS-susceptibility and the CEH make-up of our African-American cohort. Design/methods The African-American (AA) cohort consisted of 1,305 patients with MS and 1,155 controls, who self-identified as being African-American. For comparison, we used the 18,492 controls and 11,144 MS-cases from the predominantly European Wellcome Trust Case Control Consortium (WTCCC) and the 28,557 phased native Africans from the multinational “Be the Match” registry. The WTCCC and the African-Americans were phased at each of five HLA loci (HLA-A, HLA-C, HLA-B, HLA-DRB1 and HLA-DQB1) and the at 11 SNPs (10 of which were in non-coding regions) surrounding the Class II region of the DRB1 gene using previously-published probabilistic phasing algorithms. Results Of the 32 most frequent CEHs, 18 (56%) occurred either more frequently or exclusively in Africans) whereas 9 (28%) occurred more frequently or exclusively in Europeans. The remaining 5 CEHs occurred in neither control group although, likely, these were African in origin. Eight of these CEHs carried the DRB1*15:03~DQB1*06:02~a36 haplotype and three carried the DRB1*15:01~DQB1*06:02~a1 haplotype. In African Americans, a single-copy of the European CEH (03:01_07:02_07:02_15:01_06:02_a1) was associated with considerable MS-risk (OR = 3.30; p = 0.0001)–similar to that observed in the WTCCC (OR = 3.25; p<10−168). By contrast, the MS-risk for the European CEH (02:01_07:02_07:02_15:01_06:02_a1) was less (OR = 1.49; ns)–again, similar to the WTCCC (OR = 2.2; p<10−38). Moreover, four African haplotypes were “protective” relative to a neutral reference, to three European CEHs, and also to the five other African CEHs. Conclusions The common CEHs in African Americans are divisible into those that are either African or European in origin, which are derived without modification from their source population. European CEHs, linked to MS-risk, in general, had similar impacts in African-Americans as they did in Europeans. By contrast, African CEHs had mixed MS-risks. For a few, the MS-risk exceeded that in a neutral-reference group whereas, for many others, these CEHs were “protective”–perhaps providing a partial rationale for the lower MS-risk in African-Americans compared to European-Americans.

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Tellefsen, M., E. Kaldis, and E. Jilek. "The phase diagram of the Ce-H2 system and the CeH2-CeH3 solid solutions." Journal of the Less Common Metals 110, no. 1-2 (August 1985): 107–17. http://dx.doi.org/10.1016/0022-5088(85)90311-x.

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Szmigielska-Kaplon, Anna, Krawczynska Anna, Czemerska Magdalena, Agnieszka Pluta, Barbara Cebula-Obrzut, Anna Wolska, Olga Grzybowska-Izydorczyk, Piotr Smolewski, Tadeusz Robak, and Agnieszka Wierzbowska. "Kinetics and Apoptotic Profile of Circulating Endothelial Cells In Patients Undergoing Autologous Stem Cell Transplantation." Blood 118, no. 21 (November 18, 2011): 2961. http://dx.doi.org/10.1182/blood.v118.21.2961.2961.

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Abstract Abstract 2961 Objectives: Tumor growth and progression are influenced by endothelial cells proliferation and differentiation. In patients with hematological malignancies circulating endothelial cells (CEC) are elevated at the diagnosis and decrease after successful chemotherapy. The other spectrum of interest is evaluation of CEC in the context of their influence on regeneration of hematopoiesis from damage caused by high dose chemotherapy and stem cells transplantation. The aim of our study was to assess the kinetics of CEC and their subsets (mature, progenitor and apoptotic CEC) in patients undergoing autologous hematopoietic stem cells transplantation. Additionally we analyzed the relationship between the number of CEC subsets and clinical course in the post-transplant period and time to engraftment. Methods: CEC were measured in peripheral blood of 39 patients (18 males and 21females, median age 54; range 26–69) scheduled for high dose chemotherapy with autologous stem cell transplantation. The group consisted of 29 multiple myeloma patients and 10 lymphoma patients. All of the patients were in best response to previous treatment before transplantation, 20 in CR and 19 in PR. Conditioning treatment in patients with myeloma was Melphalan 200 mg/m2, while in lymphoma patients BEAM. Evaluation of CEC: Blood samples were collected at different time points: 1) at baseline - directly before conditioning; 2) a day after finishing of chemotherapy; 3) at the day “0” just before transplantation of CD34+ HSC and 4) four times after transplantation :1hour and 1 day after HSC transfusion, at the time of the nadir in peripheral blood and at the day of neutrophil engraftment). CEC were evaluated by 4 colour flow-cytometry according to the procedure described previously. Circulating progenitor cells (CEPC) were defined as negative for hematopoietic marker CD45 and positive for the endothelial cell markers CD 34, CD31 and the endothelial progenitor marker CD133. CD105 and CD106 positive CEC were classified as activated CEC (aCEC). Expression of CD36 characterized CEC originating from microvessels. Apoptotic CEC (apoCEC) were defined as CD146 positive and Annexin V positive. Results: The median (Me) CEC number at the baseline was 9, 5/μL and dropped significantly 24 h after chemotherapy (Me 8, 3/μL; p=0, 002). At day “0” before infusion of HSC, the count of CEC continued to decrease (Me 6, 6/ μL, p<0, 0001 when compared to baseline) and remained stable shortly after transplantation (1h and 1day after transplantation Me 6, 2/μL p=0, 0001 and 6, 8/μL, p=0, 0002 respectively). At nadir of WBC count, the nadir of CEC (Me 4, 6/μL) was also observed. CEC number increased at the engraftment period, but did not reach pretreatment values (Me 5, 3/μL, p0, 0001). The number of aCEC and CEPC followed CEC kinetics. In contrast, the count of apoptotic CEC 24h after conditioning (Me 4, 15/μL) was significantly enhanced in comparison to baseline values (Me 3, 1/μL; p=0, 0005) and drop down 1 day after transplantation to pretreatment values (Me 3, 6/μL; p=0, 4), and then continued to decrease (WBC nadir - Me 2, 1/μL, engraftment Me 1, 85 /μL).For the purpose of the study CEC and their subsets were evaluated as dichotomous variables using median value as cut-off to divide patients into low- or high- expressers groups. Patients with low (<Me) expression apoCEC at baseline had significantly shorter time for neutrophil engraftment (Me 13; range11–18 days) than high expressers: (Me15, 5; range 11–21days, p=0, 028). Additionally we observed significant correlation between the higher number of CEPC at 1 h after transplantation with shorter time to neutrophil engraftment (Spearman rank coefficient r= −0, 49, p=0, 008). Similar correlation between the increased count of endothelial cells originating from microvessels measured 1h after transplantation and shorter time to neutrophil engraftment was also observed (r= −0, 39, p=0, 04). Conclusions: Low count of apoptotic CEC at baseline correlates with shorter time to engraftment which may suggest that intact bone marrow microenviroment takes part in effective engraftment. Additionally, our results indicate that progenitor CEC and CEC derived from microvessels could support bone marrow regeneration after HSCT. The role of CEC and their subsets in the context of hematopoietic recovery after high dose chemotherapy and autoHSCT needs further evaluation. Disclosures: No relevant conflicts of interest to declare.

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Akaho, Nami, Jiro Takata, Takeshi Fukushima, Kazuhisa Matsunaga, Akihiro Hattori, Ryoji Hidaka, Kosuke Fukui, et al. "Preparation and In Vivo Evaluation of a Water-Soluble Prodrug for 2R-γ-Tocotrienol and as a Two-Step Prodrug for 2,7,8-Trimethyl-2S-(β-carboxyethyl)-6-hydroxychroman (S-γ-CEHC) in Rat." Drug Metabolism and Disposition 35, no. 9 (May 30, 2007): 1502–10. http://dx.doi.org/10.1124/dmd.106.014365.

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Bartolini, Desirée, Rita Marinelli, Danilo Giusepponi, Roberta Galarini, Carolina Barola, Anna Maria Stabile, Bartolomeo Sebastiani, et al. "Alpha-Tocopherol Metabolites (The Vitamin E Metabolome) and Their Interindividual Variability during Supplementation." Antioxidants 10, no. 2 (January 25, 2021): 173. http://dx.doi.org/10.3390/antiox10020173.

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The metabolism of α-tocopherol (α-TOH, vitamin E) shows marked interindividual variability, which may influence the response to nutritional and therapeutic interventions with this vitamin. Recently, new metabolomics protocols have fostered the possibility to explore such variability for the different metabolites of α-TOH so far identified in human blood, i.e., the “vitamin E metabolome”, some of which have been reported to promote important biological functions. Such advances prompt the definition of reference values and degree of interindividual variability for these metabolites at different levels of α-TOH intake. To this end, a one-week oral administration protocol with 800 U RRR-α-TOH/day was performed in 17 healthy volunteers, and α-TOH metabolites were measured in plasma before and at the end of the intervention utilizing a recently validated LC-MS/MS procedure; the expression of two target genes of α-TOH with possible a role in the metabolism and function of this vitamin, namely pregnane X receptor (PXR) and the isoform 4F2 of cytochrome P450 (CYP4F2) was assessed by immunoblot in peripheral blood leukocytes. The levels of enzymatic metabolites showed marked interindividual variability that characteristically increased upon supplementation. With the exception of α-CEHC (carboxy-ethyl-hydroxychroman) and the long-chain metabolites M1 and α-13′OH, such variability was found to interfere with the possibility to utilize them as sensitive indicators of α-TOH intake. On the contrary, the free radical-derived metabolite α-tocopheryl quinone significantly correlated with the post-supplementation levels of α-TOH. The supplementation stimulated PXR, but not CYP4F2, expression of leucocytes, and significant correlations were observed between the baseline levels of α-TOH and both the baseline and post-supplementation levels of PXR. These findings provide original analytical and molecular information regarding the human metabolism of α-TOH and its intrinsic variability, which is worth considering in future nutrigenomics and interventions studies.

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Huang, Jiaqi, Stephanie Weinstein, Wendy Mack, Howard Hodis, and Demetrius Albanes. "Serum Metabolomic Response to Low and High Dose Vitamin E Supplementation in Two Randomized Controlled Trials." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 1810. http://dx.doi.org/10.1093/cdn/nzaa067_037.

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Abstract Objectives Vitamin E is an essential micronutrient and critical human antioxidant that has been tested for cancer and cardiovascular preventative effects for decades with conflicting results. For example, prostate cancer incidence was reduced by a low-dose vitamin E supplement in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, but the findings were not replicated by high-dose vitamin E trials such as the Selenium and Vitamin E Cancer Prevention Trial (SELECT). The present investigation examined the serum metabolomic responses to low- and high-dose vitamin E supplementation in order to gain biological insight into the divergent trial outcomes. Methods We examined baseline and on-study serum samples for 154 men randomly assigned to receive 400 IU vitamin E (as alpha-tocopheryl acetate; ATA) or placebo daily in the Vitamin E Atherosclerosis Prevention Study (VEAPS), and 100 men administered 50 IU ATA or placebo daily in the ATBC Study. Over 970 known metabolites were identified using an ultrahigh-performance LC-MS/MS platform. Linear regression models estimated the change in serum metabolites of men supplemented with vitamin E to those assigned to placebo in VEAPS compared with ATBC. Results Serum alpha-carboxyethyl hydrochroman (CEHC) sulfate, alpha-tocopherol, and beta-/gamma-tocopherol were significantly altered by supplementation with ATA in both the VEAPS and ATBC trials (all P-values ≤ 5.1 × 10−5, the Bonferroni multiple-comparisons corrected statistical threshold). Serum C22 lactone sulfate was also significantly decreased in response to the high-dose vitamin E supplement in VEAPS (β = −0.70, P-value = 8.1 × 10−6), but not altered in the low-dose ATBC trial (β = −0.17, P-value = 0.4). Additionally, changes in several androgenic steroid metabolites were strongly related to the vitamin E supplement-associated change in C22 lactone sulfate only in the high-dose VEAPS trial. Conclusions We found evidence of a dose-dependent vitamin E supplementation effect on a novel C22 lactone sulfate compound as well as several androgenic steroids that may have relevance to previous controlled trial findings for prostate cancer. Funding Sources This research was supported by the Intramural Research Program of the National Cancer Institute, National Institutes of Health, U.S. Public Health Service, Department of Health and Human Services.

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Balius i Juli, Ramon. "Cesc." Apunts. Medicina de l'Esport 42, no. 153 (January 2007): 55–62. http://dx.doi.org/10.1016/s1886-6581(07)70037-3.

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45

Watts, Malcolm S. M. "Cehp." Möbius: A Journal for Continuing Education Professionals in Health Sciences 6, no. 2 (April 1986): 46–47. http://dx.doi.org/10.1002/chp.4760060208.

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46

ARNAUD, CELIA HENRY. "THOMAS CECH." Chemical & Engineering News 86, no. 16 (April 21, 2008): 52. http://dx.doi.org/10.1021/cen-v086n016.p052.

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47

Sousa, D. R., M. A. Silva, J. L. Sequeira, A. P. Madureira, and L. C. Nunes. "Caracterização do imunofenótipo das células envolvidas no processo fibrótico de fígados bovinos cronicamente infectados por Fasciola hepatica." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 69, no. 3 (June 2017): 570–78. http://dx.doi.org/10.1590/1678-4162-9249.

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Abstract:

RESUMO A fasciolose é uma doença parasitária causada por trematódeo do gênero Fasciola sp., que pode ocasionar fibrose hepática. Objetivou-se caracterizar o imunofenótipo das células que participam da fibrogênese de fígados bovinos frente à infecção por F. hepatica. Foram utilizados fragmentos dos lobos direito e esquerdo de 74 fígados bovinos com fasciolose. Os fragmentos foram submetidos a processamento histológico, coloração com tricrômico de Masson e imuno-histoquímica. Utilizaram-se análise estatística descritiva e teste de correlação de Spearmann com 5% de probabilidade. Na classificação do grau de fibrose, observou-se prevalência do grau 1, com associação positiva e significativa entre o grau de fibrose e o lobo hepático esquerdo (ρ=0,41; P<0,0001). Os imunofenótipos observados foram células estreladas hepáticas (CEHs) no parênquima e miofibroblastos (MFs) no espaço porta (EP). Não foram encontrados fibroblastos. Não houve correlação significativa entre o grau de fibrose e a quantidade de CEH nos lobos hepáticos, direito e esquerdo. Verificou-se aumento do número de estruturas portais, bem como do número de camadas circundando cada estrutura no EP, contudo não houve influência de qualquer estrutura sobre o grau de fibrose hepática (P>0,05). Concluiu-se que as células CEH e os MFs participam da fibrogênese de fígados bovinos com fasciolose crônica.

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Hernández, Bernat. "Crónica del CEAC." Nuevas de Indias. Anuario del CEAC 1 (December 22, 2016): 175. http://dx.doi.org/10.5565/rev/nueind.15.

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Bai, Yun-Feng. "Cech-complete maps." Glasnik Matematicki 43, no. 1 (May 25, 2008): 219–29. http://dx.doi.org/10.3336/gm.43.1.15.

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Devenish, Philip, and Odysseas G. Repousis. "CEAC v Montenegro1." ICSID Review - Foreign Investment Law Journal 33, no. 1 (2018): 81–87. http://dx.doi.org/10.1093/icsidreview/six035.

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