Life Sciences (LIFE SCI)
Life Sciences is an international weekly journal publishing reports on research in biomedical areas. Articles are encouraged that emphasize the molecular, cellular and functional aspects of Cardiovascular & Autonomic Mechanisms; Drug Metabolism; Endocrinology; Growth Factors and Neoplasia; Immunology; Neuroscience and Toxicology. The Journal publishes original research rapidly. Although full-length manuscripts are favored, shorter submissions are also considered. These shorter articles must be of the same high quality as full-length articles, and should contain information from topical and fast-moving fields in order to merit more rapid communication. Mini-reviews on topics of wide interest to investigators in the life sciences are also published. All articles are rigorously reviewed. The Journal favors publication of papers where modern scientific technologies are used to explain molecular, cellular and physiological mechanisms. Articles that merely report observations are rarely accepted. Recommendations from the Declaration of Helsinki or NIH guidelines for care and use of laboratory animals must be adhered to. Articles should be written at a level accessible to readers who are non-specialists in the topic of the article themselves, but who are interested in the research.
- Impact factor2.53Show impact factor historyHide impact factor history
- WebsiteLife Sciences website
Other titlesLife sciences (New York, N.Y.: 1973), Life sciences
Material typePeriodical, Internet resource
Document typeJournal / Magazine / Newspaper, Internet Resource
- Author can archive a pre-print version
- Author can archive a post-print version
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- Pre-print can not be deposited for The Lancet
Publications in this journal
Article: A review on factors affected Marital Adjustment among parents of autistic children and gender effects[show abstract] [hide abstract]
ABSTRACT: We aimed to systematically review studies that examine factors affecting marital adjustment among parents of children with disabilities, especially the autistic children. Besides, we emphasized the effects of gender on marital adjustments among the parents. There were at least 20 articles reviewed. The related journal articles on factor affecting marital adjustments were downloaded with cut off limit from 1992 to 2012. The articles were then analyzed and organized according to the definitions of marital adjustments and various factor affecting marital adjustments. We found there was no conclusive evidence regarding the factors affecting the marital among parents of autistics children. There was conclusive evidence from the reviewed literature regarding gender effect, yet the number of article supporting it was small. Mothers of autistics children were more affected in the marital adjustments as compared to fathers. Finally, with conclusion we then suggest for future interventional study. [AlHorany, AK, Hassan . SA, Bataineh, MZ. Universiti Putra Malaysia (UPM), 43400, UPM Serdang, Selangor Darul Ehsan, Malaysia. Life Sci J 2013;10(1):400-405]. (ISSN:Life Sciences 03/2013; 10.
Article: The antiproliferative activity of 3-deoxyanthocyanins extracted from red sorghum (Sorghum bicolor) bran through P53-dependent and Bcl-2 gene expression in breast cancer cell line[show abstract] [hide abstract]
ABSTRACT: Aims: The aim of this study was to investigate the anti proliferative activity of 3-deoxyanthocyanin extracted from red sorghum bran on human breast cancer cell line MCF 7. The confirmatory tests were carried out in vitro through the expression studies of p53 and bcl 2 genes in MCF 7 cells. Method: The 3-deoxyanthocyanins were isolated from red sorghum bran and cytotoxic studies were performed in MCF 7 cell line by MTT assay. The mRNA expression levels of p53 and bcl 2 genes were performed using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) analysis in MCF 7 cells. Key findings: On cytotoxic studies, the present data indicates sorghum anthocyanins, which showed 84.09% of inhibition in the proliferation of MCF 7 cells, and the CTC50 value was 300 μg/ml. The sorghum 3-deoxyanthocyanins induced apoptosis in MCF 7 was mediated by stimulation of the p53 gene and down regulation of the bcl 2 gene. Significance: The significance of our work was the anthocyanin isolated from red sorghum bran inhibits the proliferation of human breast cancer cell line. © 2013 Elsevier Inc. All rights reserved.Life Sciences 01/2013; 92 (2013)(/10.1016/j.lfs.2013.01.006):379–382.
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Article: Mevinolin enhances osteogenic genes (ALP, type I collagen and osteocalcin), CD44, CD47 and CD51 expression during osteogenic differentiation.[show abstract] [hide abstract]
ABSTRACT: In this study, we evaluated the effect of mevinolin on the expressions of osteogenic genes and surface molecules expression during osteogenesis. D1 cells were cultured in osteogenic differentiation medium (ODM) for 6 days, treated with mevinolin for 2 days, and then subjected to alizarin red S staining, MTT assays, alkaline phosphatase (ALP) activity determinations, energy dispersive X-ray spectrophotometry (EDX), real-time PCR, Western blot, fluorescence microscopy and FACS analysis. Mevinolin is commonly prescribed and widely used to lower cholesterol levels, and offers an important, effective approach to the treatment of hypercholesterolemia and arteriosclerosis. However, the direct effect of mevinolin on osteogenesis in vitro has not been clarified. ODM has been previously shown to increase the osteoblast differentiation of D1 cells. In the present study, we investigated the expressions of osteogenic genes and surface molecules during osteoblast differentiation induced by mevinolin. We found that the induction of ALP, type I collagen, osteocalcin, CD44, CD47 and CD51 by mevinolin is responsible for the osteoblastic differentiation of D1 cells. Our data show that mevinolin enhances the expressions of proteins and surface molecules related to osteogenesis.Life Sciences 02/2009; 84(9-10):290-5.
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ABSTRACT: Diabetic nephropathy is a serious complication for patients with diabetes mellitus. Approximately 30-40% of patients with type I and 15% with type II diabetes mellitus develop end stage renal disease. The study was designed to evaluate the impact of tocotrienol on renal function and reno-inflammatory cascade in streptozotocin-induced diabetes. Streptozotocin (STZ)-induced diabetic rats were treated with tocotrienol (25, 50 and 100 mg/kg), alpha-tocopherol (100 mg/kg) or with vehicle form 5th to 8th weeks. After 8 weeks, urine albumin excretion, urine output, serum creatinine, blood urea nitrogen, creatinine and urea clearance were measured. Cytoplasmic and nuclear fractions of kidney was prepared for the quantification of oxidative-nitrosative stress (lipid peroxidation, superoxide dismutase, catalase, non protein thiols, total nitric oxide), tumor necrosis factor-alpha (TNF-alpha), tissue growth factor-1beta (TGF-beta1), p65 subunit of NFkappabeta and caspase-3. After 8 weeks of STZ injection, the rats produced significant alteration in renal function, increased oxidative-nitrosative stress, TNF-alpha, TGF-beta1, caspase-3 activity in cytoplasmic lysate and active p65 subunit of NFkappabeta in nuclear lysate of kidney of diabetic rats. Interestingly, co-administration of tocotrienol significantly and dose-dependently prevented biochemical and molecular changes associated with diabetes. Tocotrienol (100 mg/kg) was demonstrated to be more effective than alpha-tocopherol (100 mg/kg). Moreover, diabetic rats treated with insulin-tocotrienol combination produced more pronounced effect on molecular parameters as compared to their respective groups. Taken together, the data reveal that tocotrienol modulates the release of profibrotic cytokines, oxidative stress, ongoing chronic inflammation and apoptosis and thus exerts a marked renoprotective effect.Life Sciences 01/2009; 84(9-10):296-301.
Article: Norcantharidin reduced cyclins and cytokines production in human peripheral blood mononuclear cells.[show abstract] [hide abstract]
ABSTRACT: To evaluate potential agents of therapeutic value in tissue inflammation, we studied norcantharidin (NCTD) and its derivatives for their effects on immune responses of human peripheral blood mononuclear cells (PBMC) in vitro. PBMC proliferation was evaluated by tritiated thymidine uptake method. The production and gene expression of cytokines were determined with enzyme immunoassays (EIA) and reverse transcription-polymerase chain reaction (RT-PCR), respectively. Five derivatives from NCTD had no significant effect on cell proliferation in PBMC. NCTD inhibited PBMC proliferation induced by phytohemagglutinin (PHA) with a 50% inhibitory concentration (IC(50)) 42.1+/-2.3 microM. The inhibitory action of NCTD did not involve direct cytotoxicity. To localize the point in the PBMC proliferation where arrest occurred, a set of key regulatory events leading to the cell proliferation, including cell cycle progression, production and gene expression of interleukin-2 (IL-2), IL-4, IL-10, and interferon-gamma (IFN-gamma) and cyclins was examined. Data demonstrated NCTD arrested the cell cycle progression of activated PBMC from the G1 transition to the S phase. The cyclin D3, E, A, and B transcripts and protein production in PHA-treated PBMC was reduced by NCTD. Whereas NCTD exerted no effect on IL-4 and IFN-gamma production, it significantly alleviated the production and mRNA expression of IL-2 and IL-10 in activated PBMC. The suppressant effects of NCTD on proliferation of PBMC activated by PHA therefore appear to be mediated, at least in part, through inhibition of cyclins and IL-2 production and arrest of cell cycle progression in the cells.Life Sciences 01/2009; 84(7-8):218-26.
Article: Differential analyses of angiogenesis and expression of growth factors in micro- and macrovascular endothelial cells of type 2 diabetic rats.[show abstract] [hide abstract]
ABSTRACT: This study observed the relationship of angiogenesis and differential expression of growth factors and their receptors in micro- and macrovascular endothelial cells of diabetic and normal rats. Myocardial microvascular endothelial cells (MMVEC) and aortic endothelial cells (AEC) were isolated from type 2 diabetic-Goto-Kakizaki (GK) rats and age-matched normal Wistar rats. In vitro and in vivo Angiogenesis assay were used to observe the difference between GK rats and Wistar rats. mRNA and protein expression were analyzed by Real-time RT-PCR and Western blotting. MMVEC but not AEC of diabetic rats had reduced abilities of angiogenesis in vitro. Real-time RT-PCR showed increased mRNA levels of VEGF, fms-like tyrosine kinase (Flt-1) and kinase insert domain containing receptor (Flk-1) in GK-MMVEC, but not the hypoxia-inducible factor-1alpha (Hif-1alpha), basic fibroblast growth factor (bFGF), fibroblast growth factor receptor 1 (FGFR1), Angiopoietin-1(Ang-1), Angiopoietin-2(Ang-2), Tie-1 and Tie-2. In contrast, Western blotting showed decreased protein levels of VEGF and receptors, including the phosphorylation of receptors. No significant differences in the expression of theses genes were observed between AEC from diabetic and control rats. Anti-rat VEGF antibodies inhibited MMVEC angiogenic function including cell proliferation, adhesion, migration, scratch wound healing and capillary-like tube formation. The in vivo angiogenesis assay had similar results. These result indicated that decreased expression of VEGF and its receptors caused by post-transcription disorder in MMVEC may be responsible for diabetic impaired cardiac angiogenesis.Life Sciences 01/2009; 84(7-8):240-9.
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ABSTRACT: Hippocampal cholinergic hypofunction is known to be involved in the cognitive deficits of Alzheimer's disease, but the detailed mechanisms remain to be elucidated. In order to establish an in vitro hippocampal cholinergic neuronal model for the relevant mechanistic studies, we have characterized a widely used hippocampal neuronal cell line, HT22, a sub-line derived from parent HT4 cells that were originally immortalized from primary mouse hippocampal neuronal culture. Western blot and immunocytochemistry were used to examine expression of cholinergic markers in HT22 cells. High potassium-evoked [(3)H]ACh release was used to evaluate the cholinergic functional properties of the cells. We found that HT22 cells express essential cholinergic markers, such as the high affinity choline transporter, choline acetyltransferase, vesicular acetylcholine transporter, and muscarinic acetylcholine receptors. Exposure of HT22 cells to high potassium evoked [(3)H]ACh release in a dose-dependent manner. In addition, the [(3)H]ACh release was significantly potentiated when presynaptic autoreceptors were blocked. Our results suggest that HT22 cells possess functional cholinergic properties, and can be used for an in vitro model for defining the mechanisms in cognitive deficits of Alzheimer's disease.Life Sciences 01/2009; 84(9-10):267-71.
Article: Possible involvement of activation of P53/P21 and demethylation of RUNX 3 in the cytotoxicity against Lovo cells induced by 5-Aza-2'-deoxycytidine.[show abstract] [hide abstract]
ABSTRACT: In our model, we aimed to explore the cytotoxicity of 5-Aza-2'-deoxycytidine (5-Aza-CdR) against the colorectal cell line, Lovo, and further characterize the possible mechanisms. After Lovo cells were treated with 5-Aza-CdR at different concentrations for different periods of time, the cell viability was examined using an MTT assay and apoptosis was examined using both flow cytometry and DNA laddering. To examine the mechanisms by which Lovo cells respond to 5-Aza-CdR, we measured both caspase 3 activity as well as DNA damage. Western blotting and RT-PCR assays were used to assess the changes in the expression levels of P53, P21(Waf1/Cip1), runt-related transcription factor 3 (RUNX 3), DNA methyltransferases (DNMTs) and matrix metalloproteinases (MMPs). Additionally, we performed gelatin zymography to examine the effects of 5-Aza-CdR on metastasis. We observed that the growth and survival advantages of Lovo cells were overcome with 5-Aza-CdR treatment at limited concentrations. Mechanistic exploration demonstrated that 5-Aza-CdR was incorporated into the DNA to induce DNA damage in Lovo cells, which was evidenced by activation of P53, P21(Waf1/Cip1) and a caspase-independent cell apoptosis pathway. Also, further experiments preliminarily suggested that 5-Aza-CdR results in the deletion of DNMT 3a and DNMT 3b, but not DNMT 1, which reactivates the expression of RUNX 3. Finally, our data revealed that 5-Aza-CdR potentially reduces the activity and expression of MMP 2. These data greatly enhance our understanding of how human cancer cells respond to 5-Aza-CdR and also reveal a new role for 5-Aza-CdR in improving patient outcome in human colorectal cancer.Life Sciences 01/2009; 84(9-10):311-20.
Article: Protective effect of caffeic acid against beta-amyloid-induced neurotoxicity by the inhibition of calcium influx and tau phosphorylation.[show abstract] [hide abstract]
ABSTRACT: The progressive accumulation of beta-amyloid peptide (Abeta), in the form of senile plaques, has been recognized as one of the major causes of Alzheimer's disease (AD) pathology. Increased production of Abeta and the aggregation of Abeta to oligomers have been reported to trigger neurotoxicity, oxidative damage and inflammation. Furthermore, Abeta-induced tau hyperphosphorylation and neurotoxicity are downstream of Abeta. Therefore, we studied the possible neuroprotective effects of caffeic acid against Abeta-induced toxicity. Treatment of PC12 cells with 10 microM Abeta (25-35) for 24 h significantly decreased the cell viability; this was accompanied by an increase in intracellular calcium levels and tau phosphorylation with GSK-3beta (glycogen synthase kinase-3beta) activation (phosphorylation). However, pretreatment of the PC12 cells with 10 and 20 microg/ml of caffeic acid, for 1 h prior to Abeta, significantly reversed the Abeta-induced neurotoxicity by attenuating the elevation of intracellular calcium levels and tau phosphorylation. Taken together, these results suggest that caffeic acid protected the PC12 cells against Abeta-induced toxicity. In addition, the neuroprotective mechanisms of caffeic acid against Abeta attenuated intracellular calcium influx and decreased tau phosphorylation by the reduction of GSK-3beta activation.Life Sciences 01/2009; 84(9-10):257-62.
Article: Minocycline prevents Abeta(25-35)-induced reduction of somatostatin and neprilysin content in rat temporal cortex.[show abstract] [hide abstract]
ABSTRACT: Tetracyclines have been demonstrated to inhibit formation of beta-amyloid (Abeta) aggregates and to disassemble preformed fibrils. Minocycline, a semi-synthetic second-generation tetracycline, can reverse Abeta-induced impairment of cognitive functions. Since somatostatin is involved in cognition and we recently showed that Abeta(25-35) lowers somatostatin expression in the rat temporal cortex, our aim here was to analyze the effects of minocycline on somatostatin immunoreactivity and mRNA levels in the temporal cortex of Abeta(25-35)-infused and healthy rats. Moreover, since brain levels of neprilysin, an Abeta-degrading enzyme, decrease with age, favoring the appearance of senile neuritic plaques, we tested whether minocyline could affect neprilysin expression. Wistar rats were thus injected with minocycline twice on the first day of treatment. On the following day, and during 14 days, Abeta(25-35) or vehicle were administered. Minocycline was injected once again on days 13 and 14. All animals were sacrificed 24 h after the last drug injection. Minocycline abrogated the Abeta(25-35)-induced decrease of somatostatin-like immunoreactive content, somatostatin mRNA levels, phosphorylated-CREB content and neprilysin levels. Minocycline alone enhanced these targets. Our findings indicate that minocycline prevents the deleterious effects of Abeta(25-35) on SRIF and neprilysin expression in the rat temporal cortex and that it has protective effects per se on these parameters.Life Sciences 01/2009; 84(7-8):205-10.
Article: Multifunctional effect of epigallocatechin-3-gallate (EGCG) in downregulation of gelatinase-A (MMP-2) in human breast cancer cell line MCF-7.[show abstract] [hide abstract]
ABSTRACT: The tumor inhibiting property of green tea polyphenol epigallocatechin-3-gallate (EGCG) is well documented. Studies reveal that matrix-metalloproteinases (MMPs) play pivotal roles in tumor invasion through degradation of basement membranes and extracellular matrix (ECM). We studied the effect of EGCG on matrixmetalloproteinases-2 (MMP-2), the factors involved in activation, secretion and signaling molecules that might be involved in the regulation of MMP-2 in human breast cancer cell line, MCF-7. MCF-7 was treated with EGCG (20 muM, 24 h), the effect of EGCG on MMP-2 expression, activity and its regulatory molecules were studied by gelatin zymography, Western blot, quantitative and semi-quantitative real time RT-PCR, immunoflourescence and cell adhesion assay. EGCG treatment reduced the activity, protein expression and mRNA expression level of MMP-2. EGCG treatment reduced the expression of focal adhesion kinase (FAK), membrane type-1-matrix metalloproteinase (MT1-MMP), nuclear factor-kappa B (NF-kB), vascular endothelial growth factor (VEGF) and reduced the adhesion of MCF-7 cells to ECM, fibronectin and vitronectin. Real time RT-PCR revealed a reduced expression of integrin receptors alpha5, beta1, alphav and beta3 due to EGCG treatment. Down regulation of expression of MT1-MMP, NF-kB, VEGF and disruption of functional status of integrin receptors may indicate decreased MMP-2 activation; low levels of FAK expression might indicate disruption in FAK-induced MMP-2 secretion and decrease in activation of phosphatidyl-inositol-3-kinase (PI-3K), extracellular regulated kinase (ERK) indicates probable hindrance in MMP-2 regulation and induction. We propose EGCG as potential inhibitor of expression and activity of pro-MMP-2 by a process involving multiple regulatory molecules in MCF-7.Life Sciences 01/2009; 84(7-8):194-204.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
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