Life sciences Journal Impact Factor & Information

Publisher: Elsevier

Current impact factor: 2.70

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.702
2013 Impact Factor 2.296
2012 Impact Factor 2.555
2011 Impact Factor 2.527
2010 Impact Factor 2.451
2009 Impact Factor 2.56
2008 Impact Factor 2.583
2007 Impact Factor 2.257
2006 Impact Factor 2.389
2005 Impact Factor 2.512
2004 Impact Factor 2.158
2003 Impact Factor 1.944
2002 Impact Factor 1.824
2001 Impact Factor 1.758
2000 Impact Factor 1.808
1999 Impact Factor 1.774
1998 Impact Factor 1.937
1997 Impact Factor 2.275
1996 Impact Factor 2.352
1995 Impact Factor 2.345
1994 Impact Factor 2.5
1993 Impact Factor 2.381
1992 Impact Factor 2.053

Impact factor over time

Impact factor

Additional details

5-year impact 2.67
Cited half-life >10.0
Immediacy index 0.69
Eigenfactor 0.02
Article influence 0.69
ISSN 1879-0631

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: In this study, we investigated the effects of Bax-inhibiting peptide (Bip)-V5, an anti-apoptosis membrane-permeable peptide, on the 6-hydroxydopamine (6-OHDA) induced Parkinson's disease (PD) model rats. Materials and methods: Rats were randomly divided into five groups: Control, 6-OHDA only, Vehicle+6-OHDA, zVAD+6-OHDA, and V5+6-OHDA, that rats were preadministrated with different reagents before 6-OHDA administration. Key findings: The result showed that intrastriatal preadministration of Bip-V5 significantly decreased the amphetamine-induced rotation of the 6-OHDA model rats and the loss of the nigral dopaminergic (DA) neurons. Moreover, Bip-V5 intrastriatal preadministration not only significantly decreased the expression of activated caspase 9 and activated caspase 3 but also decreased the enhanced expression of AIF and its nuclear translocation in the SNpc. The results in our study provide the first experimental evidence that both caspase-dependent and AIF-dependent apoptosis pathways are involved in the loss of the nigral DA neurons caused by intrastriatal administration of 6-OHDA, and intrastriatal preadministration of Bip-V5 can inhibit the above two apoptosis pathways to protect the nigral DA neurons. Significance: Our results provide a new idea that Bax-inhibiting peptide may be a promising preventive or therapeutic method for PD.
    Life sciences 11/2015; DOI:10.1016/j.lfs.2015.11.019
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aim: Eukaryotic translation initiation factors 3a (eIF3a) is involved in regulating cell cycle, cell division, growth and differentiation. Previous studies suggest a role of eIF3a on fibrosis disease and cellular proliferation and differentiation of fibroblasts. The present study aims to investigate the role of eIF3a on hypoxia-induced right ventricular (RV) remodeling and underlying mechanism. Main methods: RV remodeling was induced by hypoxia (10% O2, 3weeks) in rats. Primary cardiac fibroblasts were cultured in vitro and their proliferation was investigated by MTS and EdU incorporation method. eIF3a knockdown was conducted by eIF3a siRNA. The expression/level of TGF-β1, eIF3a, p27 and α-SMA, collagen-I, collagen-III, ANP and BNP were analyzed by ELISA, real-time PCR or Western blot. Key findings: The expression of eIF3a was obviously increased in right ventricle of RV remodeling rats accompanied by up-regulation of α-SMA and collagens. In cultured cardiac fibroblasts, application of exogenous TGF-β1-induced cellular proliferation and differentiation concomitantly with up-regulation of eIF3a expression and down-regulation of p27 expression. The effects of TGF-β1-induced proliferation and up-regulation of α-SMA and collagen in cardiac fibroblasts were abolished by eIF3a siRNA. eIF3a siRNA reversed TGF-β1 induced down-regulation of p27 expression. Significance: The eIF3a plays a crucial role in hypoxia-induced RV remodeling by regulating TGF-β1-induced proliferation and differentiation of cardiac fibroblasts, which is mediated via eIF3a/p27 pathway.
    Life sciences 11/2015; DOI:10.1016/j.lfs.2015.11.020
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: Doxorubicin is a widely used anthracycline derivative anticancer drug. Unfortunately, the clinical use of doxorubicin has the serious drawback of cardiotoxicity. In this study, we investigated whether baicalein, a bioflavonoid, can prevent doxorubicin-induced cardiotoxicity in vivo and we delineated the possible underlying mechanisms. Main methods: Male BALB/c mice were treated with either intraperitoneal doxorubicin (15mg/kg divided into three equal doses for 15days) and/or oral baicalein (25 and 50mg/kg for 15days). Serum markers of cardiac injury, histology of heart, parameters related to myocardial oxidative stress, apoptosis and inflammation were investigated. Key findings: Treatment with baicalein reduced doxorubicin-induced elevation of serum creatine kinase-MB isoenzyme (CK-MB), lactate dehydrogenase (LDH), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and ameliorated the histopathological damage. Baicalein restored the doxorubicin-induced decrease in both enzymatic and non-enzymatic myocardial antioxidants and increased the myocardial expression of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1). Further studies showed that baicalein could inverse the Bax/Bcl-2 ratio, suppress doxorubicin-induced p53, cleaved caspase-3 and PARP expression and prevented doxorubicin-induced DNA damage. Baicalein treatment also interferes with doxorubicin-induced myocardial NF-κB signaling through inhibition of IκBα phosphorylation and nuclear translocation of p65 subunit. Doxorubicin elevated iNOS and nitrites levels were also significantly decreased in baicalein treated mice. However, we did not find any significant change (p>0.05) in the myocardial TNF-α and IL-6 levels in control and treated animals. Significance: Our finding suggests that baicalein might be a promising molecule for the prevention of doxorubicin-induced cardiotoxicity.
    Life sciences 11/2015; DOI:10.1016/j.lfs.2015.11.018
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: Glucocorticoids, such as dexamethasone, are widely used anti-inflammatory drugs. Their use is frequently associated with the development of steroid- associated diabetes. Pancreatic β-cell dysfunction has been suggested to be one of the main causes of steroid-associated diabetes. However, the mechanism is not fully understood. Glycogen synthase kinase-3β (GSK-3β) is a multifunctional serine/threonine kinase and plays an important role in energy metabolism, cell growth and apoptosis. Therefore, the contribution of GSK-3β in dexamethasone-induced pancreatic β-cell apoptosis was determined in the present study. Main methods: The effect of dexamethasone treatment on rat pancreatic β-cell line (INS-1) apoptosis (determined by TUNEL and Flow Cytometry), generation of reactive oxidative stress (ROS), and the phosphorylation status of GSK-3β was determined. The inhibitory effect of GSK-3β inhibitor-lithium chloride (LiCl) on dexamethasone-induced β-cell apoptosis was also evaluated. Key findings: Dexamethasone (0.1μM) treatment induced INS-1 apoptosis, which was associated with increased GSK-3β activation and increased NOX4-derived ROS generation. Pretreatment of INS-1 with LiCl inhibited dexamethasone induced ROS generation and INS-1 apoptosis. Significance: This study provides a new mechanism of Dex induced pancreatic β cell apoptosis and may serve as a new therapeutic option for treating GCs induced diabetes.
    Life sciences 11/2015; 144. DOI:10.1016/j.lfs.2015.11.017
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: Sepsis patients and other patients in the critical care settings are at very high risk of mortality due to the primary illness. However, a fraction of patients, even after showing initial clinical improvement, deteriorates relentlessly at later stages. Increasingly, it is being identified that this is mostly due to dysfunction of the neurological system. Main methods: We obtained peripheral nerve biopsies from the sural nerve from ICU patients. Nav1.6 expression was significantly diminished. The expression of cellular membrane anchoring protein for Nav1.6, ankyrin, remained unaffected, suggesting that genomic repression may be responsible for the diminished expression of the sodium channels. We examined the expression of two regulatory transcription factors: (a) a positive regulator YY1 that binds to the promoter region of sodium channels and (b) an upstream negative neuronal regulator REST. Key findings: REST expression was significantly elevated, while YY1 expression was diminished. Finally, we also observed that the cholinergic synthetic enzyme acyltransferase was also significantly diminished in sensory nerve lysates. Finally, circulating antibodies was detected in the peripheral blood against all the major sodium channels Nav1.6, 1.8 and 1.9, which contribute to the development and propagation of action potentials. Significance: This may potentially explain why its dysfunction affects neurological functions across all systems of the body during critical illness. The underlying mechanism of why the expression of the REST transcriptional factor is affected in critical illnesses remains our future goals of investigation.
    Life sciences 11/2015; DOI:10.1016/j.lfs.2015.11.008
  • [Show abstract] [Hide abstract]
    ABSTRACT: Stem cells are characterized by their capacity for self-renewal and their ability to differentiate into specific cell types under the influence of their microenvironment. These cells are potent therapeutic tools to treat various regenerative diseases based on their ability to produce a therapeutic protein or restore natural tissue function with minimal side effects. However, a major problem that must be overcome is to find a suitable stem cell delivery system. Cell encapsulation is a novel concept in which cells are immobilized inside a biocompatible and semi-permeable natural or synthetic matrix. The purpose of encapsulation is to protect the cell from the host's immune system, improve cell expansion and maintain cell viability, self-renewal potency and direct cell differentiation toward a desired lineage. This review will provide an overview of the application of encapsulation technology for phenotypic and functional improvement of stem cells and using these encapsulated cells to treat various diseases.
    Life sciences 11/2015; 143. DOI:10.1016/j.lfs.2015.11.007
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: To investigate the effects of sevoflurane inhalation on β-amyloid (Aβ)-induced cognitive disorders and hippocampal oxidative stress in rat models. Materials and methods: Cognitive dysfunction is induced by hippocampal injection of Aβ1-40 (10μg in 2μl) for 22days. To explore the effect of sevoflurane inhalation on Aβ1-40 induced cognitive disorder, two doses of sevoflurane inhalation are used: 1.3% (Aβ+S1) and 2.6% (Aβ+S2). Sham operation (Sham, for operation control), saline injection (Control, for injection control) and 30% oxygen inhalation after Aβ1-40 injection (Aβ+O2, for inhalation control) were used as controls. All rats were further tested in electrical Y-maze and Morris water maze. Serum S100β levels, hippocampal superoxide dismutase (SOD) activity, S100β expression and malonyldialdehyde (MDA) concentrations were further quantified. Key findings: Rats in Aβ+O2, Aβ+S1 and Aβ+S2 group had lower number of correct actions in the electrical Y maze task, longer escape latencies, less time exploring the original platform, elevated serum S100β levels, depressed hippocampal SOD activity, S100β expression and higher MDA concentrations compared to control group (p<0.05). Such difference was not significant between Aβ+S1 and Aβ+O2 rats. Rats in Aβ+S2 group, however, showed significantly impaired performances compared to Aβ+S1 group (p<0.05). Significance: Sevoflurane (2.6%) can aggravate the Aβ-induced cognitive dysfunction, possibly via the intracerebral oxidative stress response.
    Life sciences 11/2015; DOI:10.1016/j.lfs.2015.11.002
  • [Show abstract] [Hide abstract]
    ABSTRACT: Organochlorine pesticides (OCPs) are persistent and bioaccumulative environmental contaminants with potential neurotoxic effects. The growing body of evidence has demonstrated that prenatal exposure to organochlorines (OCs) is associated with impairment of neuropsychological development. The hypothesis is consistent with recent studies emphasizing the correlation of environmental as well as genetic factors to the pathophysiology of neurodevelopmental and neurobehavioral defects. It has been suggested that maternal exposure to OCPs results in impaired motor and cognitive development in newborns and infants. Moreover, in utero exposure to these compounds contributes to the etiology of autism. Although impaired neurodevelopment occurs through prenatal exposure to OCs, breastfeeding causes postnatal toxicity in the infants. Parkinson's disease (PD) is another neurological disorder, which has been associated with exposure to OCs, leading to α-synuclein accumulation and depletion of dopaminergic neurons. The study aimed to review the potential association between pre- and post-natal exposure to OCs and impaired neurodevelopmental processes during pregnancy and neuropsychological diseases such as PD, behavioral alterations, seizures and autism.
    Life sciences 11/2015; DOI:10.1016/j.lfs.2015.11.006
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: Endothelin-1 (ET-1) is an autocrine inhibitor of collecting duct (CD) Na(+) and water reabsorption. CD ET-1 production is increased by a high salt diet and is important in promoting a natriuretic response. The mechanisms by which a high salt diet enhances CD ET-1 are being uncovered. In particular, elevated tubule fluid flow, as occurs in salt loading, enhances CD ET-1 synthesis. Tubule fluid solute content and interstitial osmolality can also be altered by a high salt diet, however their effect on CD ET-1 alone, or in combination with flow, is poorly understood. Main methods: ET-1 mRNA production by a mouse inner medullary CD cell line (mIMCD3) in response to changing flow and/or osmolality was assessed. Key findings: Flow or hyperosmolality (using NaCl, mannitol or urea) individually caused an ~2-fold increase in ET-1 mRNA, while flow and hyperosmolality together increased ET-1 mRNA by ~14 fold. The hyperosmolality effect alone and the synergistic effect of flow + hyperosmolality was inhibited by chelation of intracellular Ca(2+), however were not altered by blockade of downstream Ca(2+)-signaling pathways (calcineurin or NFATc), inhibition of cellular Ca(2+) entry channels (purinergic receptors or polycystin-2), or blockade of the epithelial Na(+) channel. Inhibition of NFAT5 with rottlerin or NFAT5 siRNA greatly reduced the stimulatory effect of osmolality alone and osmolality + flow on mIMCD3 ET-1 mRNA levels. Significance: Both flow and osmolality individually and synergistically stimulate mIMCD3 ET-1 mRNA content. These findings may be relevant to explaining high salt diet induction of CD ET-1 production.
    Life sciences 11/2015; DOI:10.1016/j.lfs.2015.10.037
  • [Show abstract] [Hide abstract]
    ABSTRACT: Coffee is consumed worldwide with greater than a billion cups of coffee ingested every day. Epidemiological studies have revealed an association of coffee consumption with reduced incidence of a variety of chronic diseases as well as all-cause mortality. Current research has primarily focused on the effects of coffee or its components on various organ systems such as the cardiovascular system, with relatively little attention on skeletal muscle. Summary of current literature suggests that coffee has beneficial effects on skeletal muscle. Coffee has been shown to induce autophagy, improve insulin sensitivity, stimulate glucose uptake, slow the progression of sarcopenia, and promote the regeneration of injured muscle. Much more research is needed to reveal the full scope of benefits that coffee consumption may exert on skeletal muscle structure and function.
    Life sciences 11/2015; DOI:10.1016/j.lfs.2015.11.005
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    ABSTRACT: Aims: This study aims to investigate the effect of allicin on motor functions and histopathologic changes after spinal cord injury and the mechanism underlying its neuroprotective effects. Main methods: The motor function of rats was evaluated with the Basso, Beattie, and Bresna test. Histopathologic changes were evaluated by hematoxylin and eosin and Nissl staining. Spinal cord oxidative stress markers were determined by measuring glutathione and malondialdehyde content and superoxide dismutase activity using commercial kits. Inflammatory factors were determined by measuring tumor necrosis factor-α, interleukin-1β and interleukin-6 using ELISA assay. Apoptosis was examined using TUNEL staining. The effect of allicin on Nrf2 protein levels and localization was assessed using immunofluorescence staining and Western blotting analysis. Key findings: Results demonstrated that allicin accelerated the motor functional recovery and protected neuron damage against spinal cord injury (SCI). SCI-induced oxidative stress, inflammatory response and cell apoptosis in the spinal cord were also prevented by allicin. In addition, we observed that SCI increased Nrf2 nuclear expression, and allicin treatment further increased Nrf2 nuclear translocation in neurons and astrocytes. siRNA-mediated Nrf2 gene knockdown completely blocked the effect of allicin on spinal cord tissue. Significance: Our finding suggests that allicin promotes the recovery of motor function after SCI in rats, and this effect may be related to its anti-oxidant, anti-inflammatory and anti-apoptotic effects. Allicin mediated Nrf2 nuclear translocation may be involved in the protective effect as well.
    Life sciences 11/2015; 143. DOI:10.1016/j.lfs.2015.11.001
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: Iron overload in animal models and humans increases oxidative stress and induces cardiomyopathy. It has been suggested that the vasculature is also damaged, but the impacts on vascular reactivity and the underlying mechanisms remain poorly understood. In this study, we aimed to identify possible changes in the vascular reactivity of aortas from iron overloaded rats and investigate the underlying mechanisms. Main methods: Rats were treated with 100mg/kg/day iron-dextran, ip, five days a week for four weeks and compared to a saline-injected group. Key findings: Chronic iron administration increased serum iron and transferrin saturation with significant deposition in the liver. Additionally, iron overload significantly increased the vasoconstrictor response in aortic rings as assessed in vitro, with reduced influence of endothelial denudation or L-NAME incubation on the vascular reactivity. In vitro assay with DAF-2 indicated reduced NO production in the iron overload group. Iron overload-induced vascular hyperactivity was reversed by incubation with tiron, catalase, apocynin, allopurinol and losartan. Moreover, malondialdehyde was elevated in the plasma, and O2(•-) generation and NADPH oxidase subunit (p22phox) expression were increased in the aortas of iron-loaded rats. Significance: Our results demonstrated that chronic iron overload is associated with altered vascular reactivity and the loss of endothelial modulation of the vascular tone. This iron loading-induced endothelial dysfunction and reduced nitric oxide bioavailability may be a result of increased production of reactive oxygen species and local renin-angiotensin system activation.
    Life sciences 11/2015; 143. DOI:10.1016/j.lfs.2015.10.034
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    ABSTRACT: MicroRNAs (miRNAs) are small non-coding RNAs, with a length of 18 to 24 nucleotides that play a regulatory role in several cellular processes. Since their discovery, they have been identified in cells, tissues, organs, and body fluids and their potential as molecular biomarkers for the diagnosis of various pathologic conditions has been explored. However, little is known about the origin of the extracellular miRNAs and what factors influence the levels of circulating miRNAs. This information could help the refinement of miRNAs as more effective biomarkers. Additionally, the identification of the origin of miRNAs may prove to be very useful in the association of particular miRNAs with specific pathologies. This review aims to gather information concerning the origin of miRNAs in plasma and serum, as well as to assess their potential to be use as biomarkers for these peripheral blood fractions.
    Life sciences 11/2015; 143. DOI:10.1016/j.lfs.2015.10.029
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    ABSTRACT: Aims: Opioid addiction is associated with long-term adaptive changes in the brain that involve protein expression. The carboxyl-terminal of the μ opioid receptor (MOR-C) is important for receptor signal transduction under opioid treatment. However, the proteins that interact with MOR-C after chronic morphine exposure remain unknown. The brain cDNA library of chronic morphine treatment rats was screened using rat MOR-C to investigate the regulator of opioids dependence in the present study. Main methods: The brain cDNA library from chronic morphine-dependent rats was constructed using the SMART (Switching Mechanism At 5' end of RNA Transcript) technique. Bacterial two-hybrid system was used to screening the rat MOR-C interacting proteins from the cDNA library. RT-qPCR and immunoblotting were used to determine the variation of MOR-C interacting proteins in rat brain after chronic morphine treatment. Column overlay assays, immunocytochemistry and coimmunoprecipitation were used to demonstrate the interaction of MOR-C and p75NTR-associated cell death executor (NADE). Key findings: 21 positive proteins, including 19 known proteins were screened to interact with rat MOR-C. Expression of several of these proteins was altered in specific rat brain regions after chronic morphine treatment. Among these proteins, NADE was confirmed to interact with rat MOR-C by in vitro protein-protein binding and coimmunoprecipitation in Chinese hamster ovary (CHO) cells and rat brain with or without chronic morphine treatment. Significance: Understanding the rat MOR-C interacting proteins and the proteins variation under chronic morphine treatment may be critical for determining the pathophysiological basis of opioid tolerance and addiction.
    Life sciences 11/2015; 143. DOI:10.1016/j.lfs.2015.10.032
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    ABSTRACT: Aims: Morphine strongly induces reactive oxygen species (ROS). The deleterious actions of morphine can be countered by antioxidant system. In the present study, we investigated the expression levels of nine antioxidant genes in human SH-SY5Y cells treated with morphine. Main methods: The cells were treated with three final concentrations of morphine (1, 5, and 10μmol) for four exposure times (1h, 24h, 72h and 18days). The mRNA levels were determined using quantitative real-time RCR. Key findings: Based on the alterations of mRNA levels, the genes might be categorized into three different groups: In the first group, the mRNA levels of the CAT, SOD1 and GSTM3 genes were significantly down-regulated in all examined experimental conditions. In the second group, the mRNA levels of SOD2, NQO1, GSTM2 and GSTO1 were initially increased and then decreased. In the third group, the mRNA levels of NQO2 and GSTP1, were initially increased and then reached to the control levels. The number of down-regulated genes were significantly increased as a function of exposure time (χ(2)=7.52, P=0.006). We investigated the effect of morphine (10μmol) in the absence and presence of N-acetyl-cysteine (NAC, 1mmol). The mRNA levels revealed significant differences between cells exposed to morphine and cells co-treated with morphine plus NAC. In cases that morphine increased the level of mRNAs, morphine plus NAC, result in decreased mRNA levels and vice versa. Significance: These findings suggested that there are different pathways for regulation of antioxidant genes after SH-SY5Y cells exposed to morphine and morphine might act through inducing ROS.
    Life sciences 11/2015; DOI:10.1016/j.lfs.2015.11.014