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Träfflista för sökning "L773:0753 3322 srt2:(2005-2009)"

Sökning: L773:0753 3322 > (2005-2009)

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1.
  • Cao, Y (författare)
  • Tumor angiogenesis and therapy
  • 2005
  • Ingår i: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. - 0753-3322. ; 5959 Suppl 2, s. S340-S343
  • Tidskriftsartikel (refereegranskat)
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  • Fjaeraa Alfredsson, Christina, et al. (författare)
  • Effect of ellagic acid on proliferation, cell adhesion and apoptosis in SH-SY5Y human neuroblastoma cells
  • 2009
  • Ingår i: Biomedicine and Pharmacotherapy. - : Elsevier. - 0753-3322 .- 1950-6007. ; 63:4, s. 254-261
  • Tidskriftsartikel (refereegranskat)abstract
    • Ellagic acid, a polyphenolic compound found in berries, fruits and nuts, has been shown to possess growth-inhibiting and apoptosis promoting activities in cancer cell lines in vitro. The objective of this study was to investigate the effect of ellagic acid in human neuroblastoma SH-SY5Y cells. In cultures of SH-SY5Y cells incubated with ellagic acid, time- and concentration-dependent inhibitory effects on cell number were demonstrated.Ellagic acid induced cell detachment, decreased cell viability and induced apoptosis as measured by DNA strand breaks. Ellagic acid-induced alterations in cell cycle were also observed. Simultaneous treatment with all-trans retinoic acid did not rescue the cells from ellagic acid effects. Furthermore, the results suggested that pre-treatment with all-trans retinoic acid to induce differentiation and cell cycle arrest did not rescue the cells from ellagic acid-induced cell death.
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  • Hardell, Lennart, 1944-, et al. (författare)
  • Decreased survival in pancreatic cancer patients with high concentrations of organochlorines in adipose tissue
  • 2007
  • Ingår i: Biomedicine and Pharmacotherapy. - : Elsevier BV. - 0753-3322 .- 1950-6007. ; 61:10, s. 659-664
  • Tidskriftsartikel (refereegranskat)abstract
    • We analysed adipose tissue concentrations of persistent organic pollutants (POPs) in 21 cases with exocrine pancreatic cancer. The comparison group consisted of 59 subjects. Significantly increased concentrations of polychlorinated biphenyls (PCBs), hexachlorobenzene (HCB), sum of chlordanes and polybrominated diphenylethers (PBDEs) were found in the cases. For 1,1,-dichloro-2,2-bis(p-chlorophenyl)-ethylene (p,p'-DDE) no significant difference was seen. For PCBs no odds ratio (OR) could be calculated since all cases had concentration>median in controls used as a cut-off. HCB yielded OR=53.0, 95% confidence interval (CI)=4.64-605 and sum of chlordanes OR=18.4, 95% CI=2.71-124 whereas OR was not significantly increased for p,p'-DDE or PBDEs. Body mass index (BMI) at the time of tissue sampling was significantly lower for the cases. This might have influenced the results. Using BMI one year previously or decreasing the concentrations of POPs with the same percentage as weight loss among the cases did not change the results. Survival of the cases was shorter in the group with the concentration of POPs>median among cases, significantly so for the sum of PCBs (147 vs. 294 days), p,p'-DDE (134 vs. 302 days), and sum of chlordanes (142 vs. 294 days) in the high and low group, respectively. The results were based on a low number of cases and should be interpreted with caution.
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7.
  • Hellman, Lars (författare)
  • Regulation of IgE homeostasis, and the identification of potential targets for therapeutic intervention
  • 2007
  • Ingår i: Biomedicine and Pharmacotherapy. - : Elsevier BV. - 0753-3322 .- 1950-6007. ; 61:1, s. 34-49
  • Forskningsöversikt (refereegranskat)abstract
    • Atopic allergies have increased during the past 20-30 years in frequency quite dramatically and in many countries have reached almost epidemic proportions. Allergies have thereby become one of the major medical issues of the western world. Inummoglobulin E (IgE) is here a central player. IgE is the Ig class that is present in the lowest concentration in human plasma. IgG is, for example, 10000 to 1 million times more abundant than IgE. However, despite of its low plasma levels IgE is a very important inducer of inflammation, due to its interaction with high-affinity receptors on mast cell and basophils. IgE has been conserved as a single active gene in all placental mammals studied, and the expression of this gene is under a very stringent control, most likely due to its very potent inflammatory characteristics. IgE expression is being regulated at many levels: by cytokines, switch region length, positive and negatively acting transcription factors and suppressors of cytokine signaling (SOCS). In addition, the plasma half-life differs markedly for IgG and IgE, with 21 and 2.5 days, respectively. This review summarizes the rapid progress in our understanding of the complex network of regulatory mechanisms acting on IgE and also how this new information may help us in our efforts to control IgE-mediated inflammatory conditions.
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  • Irigaray, P., et al. (författare)
  • Lifestyle-related factors and environmental agents causing cancer : an overview
  • 2007
  • Ingår i: Biomedicine and Pharmacotherapy. - : Elsevier BV. - 0753-3322 .- 1950-6007. ; 61:10, s. 640-658
  • Forskningsöversikt (refereegranskat)abstract
    • The increasing incidence of a variety of cancers after the Second World War confronts scientists with the question of their origin. In Western countries, expansion and ageing of the population as well as progress in cancer detection using new diagnostic and screening tests cannot fully account for the observed growing incidence of cancer. Our hypothesis is that environmental factors play a more important role in cancer genesis than it is usually agreed. (1) Over the last 2-3 decades, alcohol consumption and tobacco smoking in men have significantly decreased in Western Europe and North America. (2) Obesity is increasing in many countries, but the growing incidence of cancer also concerns cancers not related to obesity nor to other known lifestyle-related factors. (3) There is evidence that the environment has changed over the time period preceding the recent rise in cancer incidence, and that this change, still continuing, included the accumulation of many new carcinogenic factors in the environment. (4) Genetic susceptibility to cancer due to genetic polymorphism cannot have changed over one generation and actually favours the role of exogenous factors through gene-environment interactions. (5) Age is not the unique factor to be considered since the rising incidence of cancers is seen across all age categories, including children, and adolescents. (6) The fetus is specifically vulnerable to exogenous factors. A fetal exposure during a critical time window may explain why current epidemiological studies may still be negative in adults. We therefore propose that the involuntary exposure to many carcinogens in the environment, including microorganisms (viruses, bacteria and parasites), radiations (radioactivity, UV and pulsed electromagnetic fields) and many xenochemicals, may account for the recent growing incidence of cancer and therefore that the risk attributable to environmental carcinogen may be far higher than it is usually agreed. Of major concern are: outdoor air pollution by carbon particles associated with polycyclic aromatic hydrocarbons; indoor air pollution by environmental tobacco smoke, formaldehyde and volatile organic compounds such as benzene and 1,3 butadiene, which may particularly affect children and food contamination by food additives and by carcinogenic contaminants such as nitrates, pesticides, dioxins and other organochlorines. In addition, carcinogenic metals and metalloids, pharmaceutical medicines and some ingredients and contaminants in cosmetics may be involved. Although the risk fraction attributable to environmental factors is still unknown, this long list of carcinogenic and especially mutagenic factors supports our working hypothesis according to which numerous cancers may in fact be caused by the recent modification of our environment. (C) 2007 Elsevier Masson SAS. All rights reserved.
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