<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.plefa.com/?rss=yes"><title>Prostaglandins, Leukotrienes and Essential Fatty Acids</title><description>Prostaglandins, Leukotrienes and Essential Fatty Acids RSS feed: Current Issue. The role of lipids, including essential fatty acids and their prostaglandin, leukotriene and other derivatives, is now evident in almost 
all areas of biomedical science. Cell membrane behaviour and cell signalling in all tissues are highly dependent on the lipid constituents 
of cells.  Prostaglandins, Leukotrienes and Essential Fatty Acids  aims to cover all aspects of the roles of lipids in cellular, 
organ and whole organism function, and places a particular emphasis on human studies. Papers concerning all medical specialties are published. 
Much of the material is particularly relevant to the development of novel treatments for disease. 
 
   
To order this journal online, 
visit  http://intl.elsevierhealth.com/journals/plef 
</description><link>http://www.plefa.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:issn>0952-3278</prism:issn><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:publicationDate>February 2010</prism:publicationDate><prism:copyright> © 2010 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.plefa.com/article/PIIS0952327810000244/abstract?rss=yes"/><rdf:li rdf:resource="http://www.plefa.com/article/PIIS0952327810000207/abstract?rss=yes"/><rdf:li rdf:resource="http://www.plefa.com/article/PIIS0952327810000025/abstract?rss=yes"/><rdf:li rdf:resource="http://www.plefa.com/article/PIIS0952327809002038/abstract?rss=yes"/><rdf:li rdf:resource="http://www.plefa.com/article/PIIS0952327809001756/abstract?rss=yes"/><rdf:li rdf:resource="http://www.plefa.com/article/PIIS0952327810000190/abstract?rss=yes"/><rdf:li rdf:resource="http://www.plefa.com/article/PIIS0952327809002063/abstract?rss=yes"/><rdf:li rdf:resource="http://www.plefa.com/article/PIIS0952327809002075/abstract?rss=yes"/><rdf:li rdf:resource="http://www.plefa.com/article/PIIS0952327809002051/abstract?rss=yes"/><rdf:li rdf:resource="http://www.plefa.com/article/PIIS0952327809002026/abstract?rss=yes"/><rdf:li rdf:resource="http://www.plefa.com/article/PIIS0952327809001999/abstract?rss=yes"/><rdf:li rdf:resource="http://www.plefa.com/article/PIIS0952327809001975/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.plefa.com/article/PIIS0952327810000244/abstract?rss=yes"><title>Editorial Board</title><link>http://www.plefa.com/article/PIIS0952327810000244/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0952-3278(10)00024-4</dc:identifier><dc:source>Prostaglandins, Leukotrienes and Essential Fatty Acids 82, 2 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:issueIdentifier>S0952-3278(10)X0003-5</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>i</prism:startingPage><prism:endingPage>i</prism:endingPage></item><item rdf:about="http://www.plefa.com/article/PIIS0952327810000207/abstract?rss=yes"><title>Society News</title><link>http://www.plefa.com/article/PIIS0952327810000207/abstract?rss=yes</link><description></description><dc:title>Society News</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.plefa.2010.01.002</dc:identifier><dc:source>Prostaglandins, Leukotrienes and Essential Fatty Acids 82, 2 (2010)</dc:source><dc:date>2010-02-05</dc:date><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:publicationDate>2010-02-05</prism:publicationDate><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:issueIdentifier>S0952-3278(10)X0003-5</prism:issueIdentifier><prism:section>ISSFAL Society Section</prism:section><prism:startingPage>63</prism:startingPage><prism:endingPage>67</prism:endingPage></item><item rdf:about="http://www.plefa.com/article/PIIS0952327810000025/abstract?rss=yes"><title>Isoprostane nomenclature: More suggestions</title><link>http://www.plefa.com/article/PIIS0952327810000025/abstract?rss=yes</link><description>What’s in a name? that which we call a roseBy any other name would smell as sweet;   William Shakespeare, Romeo and Juliet 1594</description><dc:title>Isoprostane nomenclature: More suggestions</dc:title><dc:creator>Robert C. Murphy, Eoin Fahy</dc:creator><dc:identifier>10.1016/j.plefa.2010.01.001</dc:identifier><dc:source>Prostaglandins, Leukotrienes and Essential Fatty Acids 82, 2 (2010)</dc:source><dc:date>2010-01-21</dc:date><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:publicationDate>2010-01-21</prism:publicationDate><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:issueIdentifier>S0952-3278(10)X0003-5</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>69</prism:startingPage><prism:endingPage>70</prism:endingPage></item><item rdf:about="http://www.plefa.com/article/PIIS0952327809002038/abstract?rss=yes"><title>Isoprostane nomenclature: Inherent problems may cause setbacks for the development of the isoprostanoid field</title><link>http://www.plefa.com/article/PIIS0952327809002038/abstract?rss=yes</link><description>Abstract: Do we have to bother about the isoprostane nomenclature? The widely accepted IUPAC isoprostane nomenclature provides an unambiguous and systematic terminology to name all theoretical possible isoprostanes. However, the currently accepted nomenclature system provides an unnatural framework which is not well suited to address certain biologically relevant questions. Artificial categorization of isoprostanoids into prostanoid families disrupts prostaglandin-ring core structures needed to describe biogenetic precursor–product relationships. In addition, the IUPAC system defines isoprostanoid families which comprise chemically heterogeneous isoprostanoids which largely differ in their physicochemical properties from those of the corresponding prostaglandins. As a result of this, alternative nomenclature systems such as the phytoprostane nomenclature system overcoming some inherent problems of the IUPAC nomenclature are still in use. However, different naming of isoprostanoids especially the classification of prostanoid family names has created considerable confusion. Therefore, a cautionary note on the current use of different nomenclature systems is necessary.</description><dc:title>Isoprostane nomenclature: Inherent problems may cause setbacks for the development of the isoprostanoid field</dc:title><dc:creator>Martin J. Mueller</dc:creator><dc:identifier>10.1016/j.plefa.2009.11.007</dc:identifier><dc:source>Prostaglandins, Leukotrienes and Essential Fatty Acids 82, 2 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:issueIdentifier>S0952-3278(10)X0003-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>71</prism:startingPage><prism:endingPage>81</prism:endingPage></item><item rdf:about="http://www.plefa.com/article/PIIS0952327809001756/abstract?rss=yes"><title>A cautionary note on the correct structure assignment of phytoprostanes and the emergence of a new prostane ring system</title><link>http://www.plefa.com/article/PIIS0952327809001756/abstract?rss=yes</link><description>Abstract: Considerable confusion exists about the correct structural representation of phytoprostanes (PhytoP). Improper use of the different nomenclature systems leads to incorrect structure assignment of PhytoP, which results in wrong synthetic approaches to these molecules and may lead to wrong rationalization of biological activity. A new prostane ring system was found, which is proposed to be termed L1-PhytoP or L2-IsoP, respectively.</description><dc:title>A cautionary note on the correct structure assignment of phytoprostanes and the emergence of a new prostane ring system</dc:title><dc:creator>Ullrich Jahn, Jean-Marie Galano, Thierry Durand</dc:creator><dc:identifier>10.1016/j.plefa.2009.10.005</dc:identifier><dc:source>Prostaglandins, Leukotrienes and Essential Fatty Acids 82, 2 (2010)</dc:source><dc:date>2010-01-25</dc:date><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:publicationDate>2010-01-25</prism:publicationDate><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:issueIdentifier>S0952-3278(10)X0003-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>83</prism:startingPage><prism:endingPage>86</prism:endingPage></item><item rdf:about="http://www.plefa.com/article/PIIS0952327810000190/abstract?rss=yes"><title>The Effects of EPA, DHA, and Aspirin Ingestion on Plasma Lysophospholipids and Autotaxin</title><link>http://www.plefa.com/article/PIIS0952327810000190/abstract?rss=yes</link><description>Abstract: Lysophophatidylcholine (LPC) and lysophosphatidic acid (LPA) are potent lysolipid mediators increasingly linked with atherosclerosis and inflammation. A current model proposing that plasma LPA is produced when LPC is hydrolyzed by the enzyme autotaxin has not been rigorously investigated in human subjects. We conducted a clinical trial of eicosapentaenoic acid/docosahexaenoic acid (EPA/DHA) and aspirin ingestion in normal volunteers. Fasting blood samples were drawn at baseline and after 4-week supplementation with EPA/DHA (3.4g/d) with and without aspirin (650mg). Plasma LPC and LPA species and autotaxin activity were measured. EPA-LPC and DHA-LPC concentrations increased significantly with EPA/DHA supplementation whereas EPA- and DHA-LPA did not. Autotaxin activity was unaffected by any treatment, and aspirin had no effect on any endpoint. Taken together, our data demonstrate that plasma LPC, but not LPA, species can be dynamically regulated by dietary supplementation, and argue against a simple model of LPA generation via LPC hydrolysis.</description><dc:title>The Effects of EPA, DHA, and Aspirin Ingestion on Plasma Lysophospholipids and Autotaxin</dc:title><dc:creator>R.C. Block, R. Duff, P. Lawrence, L. Kakinami, J.T. Brenna, G.C. Shearer, N. Meednu, S. Mousa, A. Friedman, W.S. Harris, Mark Larson, S. Georas</dc:creator><dc:identifier>10.1016/j.plefa.2009.12.005</dc:identifier><dc:source>Prostaglandins, Leukotrienes and Essential Fatty Acids 82, 2 (2010)</dc:source><dc:date>2010-01-27</dc:date><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:publicationDate>2010-01-27</prism:publicationDate><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:issueIdentifier>S0952-3278(10)X0003-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>87</prism:startingPage><prism:endingPage>95</prism:endingPage></item><item rdf:about="http://www.plefa.com/article/PIIS0952327809002063/abstract?rss=yes"><title>Prophylactic and therapeutic effects of Mytilus edulis fatty acids on adjuvant-induced arthritis in male Wistar rats</title><link>http://www.plefa.com/article/PIIS0952327809002063/abstract?rss=yes</link><description>Abstract: Lipid-rich fractions from the flesh tissue of Mytilus edulis were obtained by solvent extraction and chromatographic separation, and tested for anti-inflammatory (AI) activity in vitro and in vivo. Inhibition of leukotriene production by isolated human neutrophils in response to calcium ionophore stimulation in the presence of exogenous arachidonic acid substrate was demonstrated for the hydrolysed triglyceride fraction of the crude lipid extract. This fraction was subsequently tested for in vivo AI activity using the mycobacterial adjuvant-induced polyarthritis rat model. The hydrolysed triglyceride fraction showed significant AI activity when dosed therapeutically (10mg/kgBW/day, p.o., for 6 days from the onset of arthritis), decreasing body weight loss by 55% and hind paw swelling by 65% compared to the arthritic control. The (non-hydrolysed) crude lipid extract was effective when dosed prophylactically (30mg/kgBW/day, p.o., for 16 days starting on day −2 of arthritigen inoculation). Structural analysis by GC and GC–MS revealed in the extracts an abundance of EPA (20:5n-3) and DHA (22:6n-3) (37% of total fatty acids), along with a small quantity of a rare anti-inflammatory n-3 analogue of arachidonic acid, namely 7, 11, 14, 17-eicosatetraenoic acid (20:4n-3).</description><dc:title>Prophylactic and therapeutic effects of Mytilus edulis fatty acids on adjuvant-induced arthritis in male Wistar rats</dc:title><dc:creator>Sarah McPhee, Lynn D. Hodges, Paul F.A. Wright, Paul M. Wynne, Nicolette Kalafatis, Theodore A. Macrides</dc:creator><dc:identifier>10.1016/j.plefa.2009.12.003</dc:identifier><dc:source>Prostaglandins, Leukotrienes and Essential Fatty Acids 82, 2 (2010)</dc:source><dc:date>2010-01-14</dc:date><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:publicationDate>2010-01-14</prism:publicationDate><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:issueIdentifier>S0952-3278(10)X0003-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>97</prism:startingPage><prism:endingPage>103</prism:endingPage></item><item rdf:about="http://www.plefa.com/article/PIIS0952327809002075/abstract?rss=yes"><title>Effect of conjugated linoleic acid on body fat, tumor necrosis factor alpha and resistin secretion in spontaneously hypertensive rats</title><link>http://www.plefa.com/article/PIIS0952327809002075/abstract?rss=yes</link><description>Abstract: Conjugated linoleic acid (CLA) is a naturally occurring group of dienoic derivaties of linoleic acid found mainly in beef and dairy products. CLA has been reported to reduce body fat, as well as to possess anticarcinogenic, antiatherogenic and procatabolic activities in animals. The objective of this study was to evaluate the effect of CLA supplementation to spontaneously hypertensive rats (SHR) on body fat, biochemical parameters of serum related tumor necrosis factor alpha (TNF-α) and resistin secretion. Thirty rats were divided in three groups, the first group of spontaneously hypertensive rats received a standard diet (V-SHR group, n=10), a second group of SHR was fed 1.5% of conjugated linoleic acid (CLA-SHR group, n=10) and the third was the control, non-hypertensive group (KW, n=10) also on a standard diet including 7.5% of sunflower oil during eight weeks.After CLA diet administration, spontaneously hypertensive rats showed a significant reduction in blood pressure, serum glucose, cholesterol and triacylglycerols, together with reduction of index of body fat, pericardic, abdominal and epididymal adipose tissue. These effects were accompanied by a decrease in the secretion of TNF-α and resistin.</description><dc:title>Effect of conjugated linoleic acid on body fat, tumor necrosis factor alpha and resistin secretion in spontaneously hypertensive rats</dc:title><dc:creator>Guillermo Hernández-Díaz, Alfonso Alexander-Aguilera, Agustin Arzaba-Villalba, Ida Soto-Rodríguez, Hugo S. García</dc:creator><dc:identifier>10.1016/j.plefa.2009.12.004</dc:identifier><dc:source>Prostaglandins, Leukotrienes and Essential Fatty Acids 82, 2 (2010)</dc:source><dc:date>2010-01-14</dc:date><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:publicationDate>2010-01-14</prism:publicationDate><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:issueIdentifier>S0952-3278(10)X0003-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>105</prism:startingPage><prism:endingPage>109</prism:endingPage></item><item rdf:about="http://www.plefa.com/article/PIIS0952327809002051/abstract?rss=yes"><title>Age-related changes of n-3 and n-6 polyunsaturated fatty acids in the anterior cingulate cortex of individuals with major depressive disorder</title><link>http://www.plefa.com/article/PIIS0952327809002051/abstract?rss=yes</link><description>Abstract: Accumulating evidence finds a relative deficiency of peripheral membrane fatty acids in persons with affective disorders such as unipolar and bipolar depression. Here we sought to investigate whether postmortem brain fatty acids within the anterior cingulate cortex (BA-24) varied according to the presence of major depression at the time of death. Using capillary gas chromatography we measured fatty acids in a depressed group (n=12), and in a control group without lifetime history of psychiatric diagnosis (n=14). Compared to the control group, the depressed group showed significantly lower concentrations of numerous saturated and polyunsaturated fatty acids including both the n-3 and n-6 fatty acids. Additionally, significant correlations between age at death and precursor (or metabolites) in the n-3 fatty acid pathway were demonstrated in the depressed group but not in control subjects. In the n-6 fatty acid family, the ratio of 20:3(n-6)/18:2(n-6) was higher in patients than in control groups, whereas the ratio of 20:4(n-6)/20:3(n-6) was relatively decreased in patients. Lastly, a significant negative correlation between age and the ratio of 20:4(n-6) to 22:6(n-3) was found in patients, but not in controls. Taken together, decreases in 22:6(n-3) may be caused, at least in part, by the diminished formation of 20:5(n-3), which is derived from 20:4(n-3) through a Δ5 desaturase reaction. The present findings from postmortem brain tissue raise the possibility that an increased ratio of 20:4(n-6) to 22:6(n-3) may provide us with a biomarker for depression. Future research should further investigate these relationships.</description><dc:title>Age-related changes of n-3 and n-6 polyunsaturated fatty acids in the anterior cingulate cortex of individuals with major depressive disorder</dc:title><dc:creator>Sarah M. Conklin, Caroline A. Runyan, Sherry Leonard, Ravinder D. Reddy, Matthew F. Muldoon, Jeffrey K. Yao</dc:creator><dc:identifier>10.1016/j.plefa.2009.12.002</dc:identifier><dc:source>Prostaglandins, Leukotrienes and Essential Fatty Acids 82, 2 (2010)</dc:source><dc:date>2010-01-08</dc:date><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:publicationDate>2010-01-08</prism:publicationDate><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:issueIdentifier>S0952-3278(10)X0003-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>111</prism:startingPage><prism:endingPage>119</prism:endingPage></item><item rdf:about="http://www.plefa.com/article/PIIS0952327809002026/abstract?rss=yes"><title>Cloning, purification and characterization of non-human primate 12/15-lipoxygenases</title><link>http://www.plefa.com/article/PIIS0952327809002026/abstract?rss=yes</link><description>Abstract: The enzyme 15-lipoxygenase-1 (15-LO-1) possesses mainly 15-LO activity and has so far only been described in human cells and rabbit reticulocytes. The animal ortholog, except rabbit reticulocytes, is an enzyme with predominantly a 12-lipoxygenase activity, commonly referred to as 12/15-LO. We describe herein the characterization of the 12/15-LOs in Macaca mulatta (rhesus monkey) and in Pongo pygmaeus (orang-utan). The rhesus and the orang-utan enzymes have mainly 12-lipoxygenase and 15-lipoxygenase activity, respectively, and they display 94% and 98% identity to the human 15-LO-1 protein. The rhesus enzyme was functionally different from the human enzyme with respect to substrate utilization in that anandamide was used differently and that the rhesus enzymes positional specificity could be affected by the substrate concentration. Furthermore, genomic data indicate that chimpanzees express an enzyme with mainly 15-lipoxygenase activity whereas marmosets express an enzyme with mainly 12-LO activity. Taken together, the switch during evolution from a 12-lipoxygenating enzyme in lower primates to a 15-lipoxygenating enzyme in higher primates and man might be of importance for the biological function of this enzyme.</description><dc:title>Cloning, purification and characterization of non-human primate 12/15-lipoxygenases</dc:title><dc:creator>M. Johannesson, L. Backman, H.-E. Claesson, P.K.A. Forsell</dc:creator><dc:identifier>10.1016/j.plefa.2009.11.006</dc:identifier><dc:source>Prostaglandins, Leukotrienes and Essential Fatty Acids 82, 2 (2010)</dc:source><dc:date>2010-01-27</dc:date><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:publicationDate>2010-01-27</prism:publicationDate><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:issueIdentifier>S0952-3278(10)X0003-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>121</prism:startingPage><prism:endingPage>129</prism:endingPage></item><item rdf:about="http://www.plefa.com/article/PIIS0952327809001999/abstract?rss=yes"><title>Hypertonic environment elicits cyclooxygenase-2-driven prostaglandin E2 generation by colon cancer cells: Role of cytosolic phospholipase A2-α and kinase signaling pathways</title><link>http://www.plefa.com/article/PIIS0952327809001999/abstract?rss=yes</link><description>Abstract: Cyclooxygenase (COX)-2-derived prostaglandin (PG)E2 controls many aspects of colon cancer development, modulating from apoptosis resistance and cell proliferation to angiogenesis, invasion, and metastasis. Here, we investigated the role of different phospholipases (PL)A2 in supplying arachidonic acid (AA) for COX-2-dependent PGE2 generation and signaling pathways involved in activation of colon cancer cells by a physiologically relevant stimulus. To emulate the hypertonic environment found physiologically in colon, the human colon cancer cell line Caco-2 was maintained in hypertonic complete DMEM medium. Human colon cancer cell line Caco-2 exposed to a hypertonic environment responded with marked AA release, COX-2 induction and PGE2 generation. Selective secretory (s)PLA2 and calcium-independent (i)PLA2 inhibitors did not modify PGE2 generation, while either COX-2 or cytosolic (c)PLA2 inhibitors completely inhibited PGE2 generation. cPLA2-α was responsible for AA supply for PGE2 generation, but had no role in COX-2 induction. Mitogen-activated protein (MAP) kinases, ERK 1/2, p38, and JNK, participated in the signaling events that lead to PGE2 generation by modulating AA release, but only ERK 1/2 was involved in COX-2 upregulation. Our results indicate that hypertonic stress activates PGE2 generation by Caco-2 cells through a mechanism dependent on MAP kinase-regulated AA mobilization, increased cPLA2-α activity, and COX-2 induction.</description><dc:title>Hypertonic environment elicits cyclooxygenase-2-driven prostaglandin E2 generation by colon cancer cells: Role of cytosolic phospholipase A2-α and kinase signaling pathways</dc:title><dc:creator>Luciana B. Gentile, Bruno Piva, Bianca C. Capizzani, Luiz G.B. Furlaneto, Luciana S. Moreira, Daniel Zamith-Miranda, Bruno L. Diaz</dc:creator><dc:identifier>10.1016/j.plefa.2009.11.005</dc:identifier><dc:source>Prostaglandins, Leukotrienes and Essential Fatty Acids 82, 2 (2010)</dc:source><dc:date>2009-12-10</dc:date><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:publicationDate>2009-12-10</prism:publicationDate><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:issueIdentifier>S0952-3278(10)X0003-5</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>131</prism:startingPage><prism:endingPage>139</prism:endingPage></item><item rdf:about="http://www.plefa.com/article/PIIS0952327809001975/abstract?rss=yes"><title>The very low density lipoprotein receptor is not necessary for maintaining brain polyunsaturated fatty acid concentrations</title><link>http://www.plefa.com/article/PIIS0952327809001975/abstract?rss=yes</link><description>Abstract: Polyunsaturated fatty acids (PUFA), especially docosahexaenoic and arachidonic acids, as well as cholesterol are important for neural development and maintaining brain function. However, in contrast to cholesterol, the brain is unable to synthesize the required amounts of these PUFA de novo and requires a constant supply from plasma. Suggested pools of uptake include plasma unesterified PUFA or the uptake of PUFA-containing lipoproteins via lipoprotein receptors into endothelial cells of the blood brain barrier. Our study tested whether the very low density lipoprotein receptor (VLDLr) is necessary for maintaining brain PUFA and cholesterol concentrations. Moreover, since VLDLr knockout (VLDLr−/−) mice have been reported to have behavioural deficits, this study asked the question whether altered brain PUFA and cholesterol concentrations might be related to these deficits. VLDLr−/− and wild-type mice had ad libitum access to chow. At 7 weeks of age the mice were sacrificed, and the cortex, cerebellum, hippocampus, and the remainder of the brain were isolated for total fatty acid and cholesterol analyses. There were no differences in total lipid PUFA or cholesterol concentrations in any of the four brain regions between VLDLr−/− and wild-type mice. These findings demonstrate that the VLDLr is not necessary for maintaining brain PUFA concentrations and suggest that other mechanisms to transport PUFA into the brain must exist.</description><dc:title>The very low density lipoprotein receptor is not necessary for maintaining brain polyunsaturated fatty acid concentrations</dc:title><dc:creator>Tupur Rahman, Ameer Y. Taha, Byung Jun Song, Sarah K. Orr, Zhen Liu, Chuck T. Chen, Richard P. Bazinet</dc:creator><dc:identifier>10.1016/j.plefa.2009.11.003</dc:identifier><dc:source>Prostaglandins, Leukotrienes and Essential Fatty Acids 82, 2 (2010)</dc:source><dc:date>2010-01-27</dc:date><prism:publicationName>Prostaglandins, Leukotrienes and Essential Fatty Acids</prism:publicationName><prism:publicationDate>2010-01-27</prism:publicationDate><prism:volume>82</prism:volume><prism:number>2-3</prism:number><prism:issueIdentifier>S0952-3278(10)X0003-5</prism:issueIdentifier><prism:section>Short Communication</prism:section><prism:startingPage>141</prism:startingPage><prism:endingPage>145</prism:endingPage></item></rdf:RDF>