BioFactors

Cover image for Vol. 41 Issue 6

Edited By: Angelo Azzi

Impact Factor: 4.592

ISI Journal Citation Reports © Ranking: 2014: 26/128 (Endocrinology & Metabolism); 60/290 (Biochemistry & Molecular Biology)

Online ISSN: 1872-8081

Associated Title(s): Biochemistry and Molecular Biology Education, Biotechnology and Applied Biochemistry, IUBMB Life

Featured

  • Ampelopsin protects endothelial cells from hyperglycemia-induced oxidative damage by inducing autophagy via the AMPK signaling pathway

    Ampelopsin protects endothelial cells from hyperglycemia‐induced oxidative damage by inducing autophagy via the AMPK signaling pathway

    Hyperglycemia-induced autophagy impairment in HUVECs. (A) Endothelial cells were exposed to a series of glucose concentrations (5.5, 17, and 33 mM) for 24 h, and then total lysates of cells were immunoblotted with anti-LC3, anti-Beclin1, anti-Atg5, anti-P62, and anti-β-actin antibodies. The values, which (n = 3 for each group) were normalized against β-actin, are presented as fold increases compared with the basal level (control). (B) Cells were treated with or without 3-MA (5 mM) or rapamycin (10 μM) for 3 h and incubated under low glucose or hyperglycemic conditions for 24 h. Representative TEM images demonstrating the ultrastructure of cells; arrows indicate autophagosomes. (C) HUVECs were transfected with a plasmid expressing GFP-MAP1LC3B for 4 h, and then treated identical to (B), and visualized by confocal microscopy. The values are expressed as the mean ± SD (n = 3). The mean values were significantly different vs low-glucose group: *P < 0.05, ***P < 0.001; vs hyperglycemia-treated group: ###P < 0.001.

  • Endogenously elevated n-3 polyunsaturated fatty acids alleviate acute ethanol-induced liver steatosis

    Endogenously elevated n‐3 polyunsaturated fatty acids alleviate acute ethanol‐induced liver steatosis

    Increased hepatic n-3 PUFA alleviates alcoholic liver steatosis. Transgenic fat-1 mice and their littermate WT mice received oral gavage of ethanol (n = 8 for WT+ALC and Fat1+ALC) or isocaloric maltose dextrin solution as control (n = 6 for WT and Fat-1) every 12 H for three times; liver portions were either embedded in frozen tissue matrix or fixed in 10% formalin for histological analysis. A: Representative gross morphology of mouse livers. B: Liver weight. C: Liver/body weight ratios. D: Hepatic TG content. E: Representative Oil Red O-stained liver sections at 200× magnification. F: Representative H&E-stained liver sections at 200× magnification. G: Quantification of lipid droplet accumulation by Oil Red O staining. H: Quantification of hepatocyte ballooning by H&E staining. Data are presented as means ± SEM. *P < 0.05; aP < 0.01 compared with the WT+ALC group; bP < 0.01, compared with the Fat1+ALC group. WT: wild type; H&E: hematoxylin and eosin.

  • Piperine alleviates osteoclast formation through the p38/c-Fos/NFATc1 signaling axis

    Piperine alleviates osteoclast formation through the p38/c‐Fos/NFATc1 signaling axis

    Piperine attenuates osteoclastogenesis from the onset of the differentiation. (A) RAW 264.7 macrophages (5 × 103/well) were differentiated with RANKL (15 ng/mL) alone or in combination with piperine (100 µM) for 3, 4, or 5 days and stained for TRAP (scale bars: 50 µm). (B) Quantification of multinucleated osteoclasts (containing three or more nuclei) after treatment with RANKL alone or RANKL plus indicated concentrations of piperine for 3, 4, or 5 days. Values represent mean ±SD and are representative of three independent experiments performed in triplicate. (*P < 0.05, **P < 0.01, ***P < 0.001 vs. RANKL).

  • Less increase of copeptin and MR-proADM due to intervention with selenium and coenzyme Q10 combined: Results from a 4-year prospective randomized double-blind placebo-controlled trial among elderly Swedish citizens

    Less increase of copeptin and MR‐proADM due to intervention with selenium and coenzyme Q10 combined: Results from a 4‐year prospective randomized double‐blind placebo‐controlled trial among elderly Swedish citizens

    CONSORT diagram illustrating a flow chart of the study.

  • Curcumin inhibits B[a]PDE-induced procarcinogenic signals in lung cancer cells, and curbs B[a]P-induced mutagenesis and lung carcinogenesis

    Curcumin inhibits B[a]PDE‐induced procarcinogenic signals in lung cancer cells, and curbs B[a]P‐induced mutagenesis and lung carcinogenesis

    Curcumin inhibits B[a]P-induced lung carcinogenesis: (A) Schematic representation of animal experiment. (B) Morphology of the lungs of the representative mice administered with curcumin and B[a]P, alone and in combination and lung tissues of (C). Thirteen out of 15 animals survived in each treatment group at the termination of the experiments except in group III, where 14 out of 15 animals survived. Lung tissues of all the survived animals were analyzed for tumor incidence by histopathological staining and the percentage of tumor incidence was calculated. Percentage of tumor incidence and the average number of tumor nodules of mice from all four groups is given in the figure. (D) H and E stained lung tissue sections of representative samples of mice administered with curcumin and B[a]P, alone and in combination.

  • Metabolic responses to dietary leucine restriction involve remodeling of adipose tissue and enhanced hepatic insulin signaling

    Metabolic responses to dietary leucine restriction involve remodeling of adipose tissue and enhanced hepatic insulin signaling

    Time-dependent increase in energy expenditure and food intake by leucine restriction. Energy expenditure (A), activity (B), and food intake (C) were measured in a TSE PhenoMaster/LabMaster Home Cage System. Mice were acclimated to the control (CON) diet and TSE system for 3 days prior to half of the 16 mice being randomized to remain on CON diet or be switched to the leucine-restricted (LR) diet. Mouse boxes were changed out on day 4 as indicated in Fig. 1C, resulting in a loss of several hours of sampling, causing a blip on the EE and activity graphs and an appearance of less food intake on day 4. Shaded bars in (A) and (B) denote night (lights off) and intervening light areas denote lights on. Means annotated with asterisks in Fig. 1C differ from Con group at P < 0.05.

  • Ampelopsin protects endothelial cells from hyperglycemia‐induced oxidative damage by inducing autophagy via the AMPK signaling pathway
  • Endogenously elevated n‐3 polyunsaturated fatty acids alleviate acute ethanol‐induced liver steatosis
  • Piperine alleviates osteoclast formation through the p38/c‐Fos/NFATc1 signaling axis
  • Less increase of copeptin and MR‐proADM due to intervention with selenium and coenzyme Q10 combined: Results from a 4‐year prospective randomized double‐blind placebo‐controlled trial among elderly Swedish citizens
  • Curcumin inhibits B[a]PDE‐induced procarcinogenic signals in lung cancer cells, and curbs B[a]P‐induced mutagenesis and lung carcinogenesis
  • Metabolic responses to dietary leucine restriction involve remodeling of adipose tissue and enhanced hepatic insulin signaling

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IUBMB Joint Virtual Issue on Cancer Therapies

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We’re pleased to present a new Joint Virtual Issue on Cancer Therapies in celebration of the IUBMB 2015 Miami Winter Symposium, featuring articles from Biofactors, Biotechnology and Applied Biochemistry, and IUBMB Life.

2015 BioFactors Young Investigator Award

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On behalf of the IUBMB, BioFactors and Wiley, it is with great pleasure and honor that we announce Shilpa Thakur as the recipient of the 2015 BioFactors - Wiley Young Investigator Award for her article, Regulation at multiple levels controls the expression of folate transporters in liver cells in conditions of ethanol exposure and folate deficiency.

Shilpa Thakur is a Ph.D student in the Department of Biochemistry, Post Graduate Institute of Medical Education and Research, in Chandigarh, India. She completed her Bachelor’s and Masters' degree in Biotechnology and thereafter joined the Ph.D program under the guidance of Dr. Jyotdeep Kaur, Additional Professor in the Department of Biochemistry. As a part of her thesis work, Dr. Thakur has examined various regulatory mechanisms underlying the effects of folate deficiency and ethanol exposure on folate transport, and has gained expertise in the field of molecular biology and epigenetics during her Ph.D tenure. Presently, Dr. Thakur’s laboratory is focusing on folate deficiency and epigenetic regulation of some imprinting genes.

Shilpa Thakur will be honored with the 2015 BioFactors - Wiley Young Investigator Award at the 23rd International Union for Biochemistry and Molecular Biology (IUBMB) Congress and 44th Annual Meeting of the Brazilian Society for Biochemistry and Molecular Biology in Foz do Iguaçu, Brazil from August 24th to 28th, 2015, and her award-winning article will be FREELY available online through the conference.

Please join us in congratulating Shipla Thakur as the recipient of the annual BioFactors– Wiley Young Investigator Award!

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2014 Impact Factor:
BioFactors is pleased to announce its 2014 Impact Factor has increased to 4.592!

2015 Release of Journal Citation Reports®
Source: Thomson Reuters 2014 Citation Data

Open Access Highlight

Click below to read this OnlineOpen Review Article in BioFactors for FREE:

Novel insights on interactions between folate and lipid metabolism
Robin P. da Silva, Karen B. Kelly, Ala Al Rajabi, René L. Jacobs
Volume 40, Issue 3, May/June 2014

Folate is an essential B vitamin required for the maintenance of AdoMet-dependent methylation. The liver is responsible for many methylation reactions that are used for post-translational modifications of proteins, methylation of DNA, and the synthesis of hormones, creatine, carnitine, and phosphatidylcholine. Conditions where methylation capacity is compromised, including folate deficiency, are associated with impaired phospatidylcholine synthesis resulting in non-alcoholic fatty liver disease and steatohepatitis. Read the full article FREE!

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