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        <dc:date>2010-08-30T00:00:00Z</dc:date>
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        <item rdf:about="http://www.lipidworld.com/content/9/1/92">
        <title>The assessment of carotid intima media thickness and serum Paraoxonase-1 activity in Helicobacter pylori positive subjects.

</title>
        <description>Background:
The role of inflammation in the pathogenesis and progression of atherosclerosis has been increasingly discussed. Although the seroepidemiological studies have suggested a relationship between Helicobacter pylori (H. pylori) infection and atherosclerosis; the issue is still controversial. It is well known that abnormal lipid profil  is related to atherosclerosis  and the measurement of  carotid-intima media thickness (CIMT) is one of the surrogate marker of atherosclerosis. The serum concentration of high-density lipoprotein (HDL-C) has been known to have an inverse correlation with the development of atherosclerosis. Paraoxonase-1 (PON1) is a major anti-atherosclerotic component of HDL-C. PON1 activity is related to lipid peroxidation and prospective cardiovascular risk. The aim of this study was to investigate CIMT and serum PON1 activities along with lipid parameters in H. pylori positive and negative  subjects.
Methods:
Thirty H. pylori positive subjects and thirty-one negative subjects were enrolled. H. pylori  infection  was  diagnosed by  the  presence  of   positivity  of  stool  H. pylori  antigen  test  or  Carbon 14 labeled urea breath  test. Serum PON1 activity was measured spectrophotometrically. Traditional cardiovascular risk factors were investigated and laboratory analysis included measurement of serum triglycerides (TG), total cholesterol (TC), high-density lipoprotein (HDL-C) and low-density lipoprotein cholesterol (LDL-C). We assessed CIMT  by high-resolution ultrasound of both common carotid arteries.
Results:
We found that the mean and maximum values of right and overall CIMT in H. pylori  positive subjects were significantly thicker than those of H. pylori negative subjects. There was no significant differences in serum HDL-C, LDL-C, TC levels and TC/HDL-C ratios between two groups. Serum TG levels of H. pylori positive subjects were significantly higher than those of H. pylori  negative subjects (p=0.014). We found that  PON1 activities  were significantly lower in H. pylori positive subjects compared with negative subjects. No significantly correlation was observed between PON1 and CIMT values.
Conclusions:
There is an increase in CIMT values in patients with H. pylori  positive compared to H. pylori  negative subjects. PON1 activity decrease significantly in H. pylori positive subjects. However, an association between PON1 and CIMT was not found. These data indicated that H. pylori  may have a role in atherosclerotic processes, however, further studies are needed to evaluate the exact mechanisms.
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&lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=S8ZqQSuu0Z0:BANMjd61bbg:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=S8ZqQSuu0Z0:BANMjd61bbg:TzevzKxY174"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=TzevzKxY174" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=S8ZqQSuu0Z0:BANMjd61bbg:l6gmwiTKsz0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=l6gmwiTKsz0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=S8ZqQSuu0Z0:BANMjd61bbg:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=S8ZqQSuu0Z0:BANMjd61bbg:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?i=S8ZqQSuu0Z0:BANMjd61bbg:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=S8ZqQSuu0Z0:BANMjd61bbg:7Q72WNTAKBA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=7Q72WNTAKBA" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
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        <link>http://rss.neurobiologyoflipids.org/~r/lipidsinhealthanddisease/~3/S8ZqQSuu0Z0/92</link>
                <dc:creator>Halide Akbas</dc:creator>
                <dc:creator>Sebahat Basyigit</dc:creator>
                <dc:creator>Inci Suleymanlar</dc:creator>
                <dc:creator>Didem Kemaloglu</dc:creator>
                <dc:creator>Serkan Koc</dc:creator>
                <dc:creator>Fatih Davran</dc:creator>
                <dc:creator>Ibrahim Demir</dc:creator>
                <dc:creator>Gultekin Suleymanlar</dc:creator>
                <dc:source>Lipids in Health and Disease 2010, 9:92</dc:source>
        <dc:date>2010-08-30T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-511X-9-92</dc:identifier>
        <prism:publicationName>Lipids in Health and Disease</prism:publicationName>
        <prism:issn>1476-511X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>92</prism:startingPage>
        <prism:publicationDate>2010-08-30T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    <feedburner:origLink>http://www.lipidworld.com/content/9/1/92</feedburner:origLink></item>
        <item rdf:about="http://www.lipidworld.com/content/9/1/91">
        <title>Levels of high-density lipoprotein cholesterol (HDL-C) among children with steady-state sickle cell disease</title>
        <description>Background:
The search for sickle cell disease (SCD) prognosis biomarkers is a challenge. These markers identification can help to establish further therapy, later severe clinical complications and with patients follow-up. We attempted to study a possible involvement of levels of high-density lipoprotein cholesterol (HDL-C) in steady-state children with SCD, once that this lipid marker has been correlated with anti-inflammatory, anti-oxidative, anti-aggregation, anti-coagulant and pro-fibrinolytic activities, important aspects to be considered in sickle cell disease pathogenesis.
Methods:
We prospectively analyzed biochemical, inflammatory and hematological biomarkers of 152 steady-state infants with SCD and 132 healthy subjects using immunochemistry, immunoassay and electronic cell counter respectively. Clinical data were collected from patient medical records.
Results:
Of the 152 infants investigated had a significant positive association of high-density lipoprotein cholesterol with hemoglobin (P&lt;0.001), hematocrit (P&lt;0.001) and total cholesterol (P&lt;0.001) and a negative significant association with reticulocytes (P=0.046), leukocytes (P=0.015), monocytes (P=0.004) and platelets (P=0.005), bilirubins [total bilirubin (P&lt;0.001), direct bilirubin (P&lt;0.001) and indirect bilirubin (P&lt;0.001], iron (P&lt;0.001), aminotransferases [aspartate aminotransferase (P=0.004), alanine aminotransferase (P=0.035)], lactate dehydrogenase (P&lt;0.001), urea (P=0.030), alpha 1-antitrypsin (P&lt;0.001), very low-density lipoprotein cholesterol (P=0.003), triglycerides (P=0.005) and hemoglobin S (P=0.002). Low high-density lipoprotein cholesterol concentration was associated with the history of cardiac abnormalities (P=0.025), pneumonia (P=0.033) and blood transfusion use (P=0.025). Lipids and inflammatory markers were associated with the presence of cholelithiasis.
Conclusions:
We hypothesize that some SCD patients can have a specific dyslipidemic subphenotype characterized by low HDL-C with hypertriglyceridemia and high VLDL-C in association with other biomarkers, including those related to inflammation. This represents an important step toward a more reliable clinical prognosis. Additional studies are warranted to test this hypothesis and the probably mechanisms involved in this complex network of markers and their role in SCD pathogenesis.
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/lipidsinhealthanddisease/~4/5nYxvV51Hq0" height="1" width="1"/&gt;</description>
        <link>http://rss.neurobiologyoflipids.org/~r/lipidsinhealthanddisease/~3/5nYxvV51Hq0/91</link>
                <dc:creator>Magda Seixas</dc:creator>
                <dc:creator>Larissa Rocha</dc:creator>
                <dc:creator>Mauricio Carvalho</dc:creator>
                <dc:creator>Jolema Menezes</dc:creator>
                <dc:creator>Isa Lyra</dc:creator>
                <dc:creator>Valma Nascimento</dc:creator>
                <dc:creator>Ricardo Couto</dc:creator>
                <dc:creator>Ajax Atta</dc:creator>
                <dc:creator>Mitermayer Reis</dc:creator>
                <dc:creator>Marilda Goncalves</dc:creator>
                <dc:source>Lipids in Health and Disease 2010, 9:91</dc:source>
        <dc:date>2010-08-27T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-511X-9-91</dc:identifier>
        <prism:publicationName>Lipids in Health and Disease</prism:publicationName>
        <prism:issn>1476-511X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>91</prism:startingPage>
        <prism:publicationDate>2010-08-27T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    <feedburner:origLink>http://www.lipidworld.com/content/9/1/91</feedburner:origLink></item>
        <item rdf:about="http://www.lipidworld.com/content/9/1/90">
        <title>The Gln27Glu Polymorphism in Beta 2-Adrenergic receptor gene is linked to hypertriglyceridemia, hyperinsulinemia and hyperleptinemia in Saudis. </title>
        <description>Background:
beta2-adrenoceptor (beta2AR) gene polymorphism glutamine 27 glutamic acid (Gln27Glu)and Arg16Gly were reported to have an association with obesity and obesity related disorders in some population. We investigated whether the beta2AR (Gln27Glu) gene polymorphism is associated with obesity and other related metabolic parameters in Saudi populations.DesignThree hundred twenty nine unrelated men and women aged 18 to 36 years were randomly selected from Saudi population to study possible association of Gln27Glu in beta2AR gene with body mass index (BMI), anthropometric measurements and other metabolic parameters. The beta2AR polymorphism (Gln27Glu) was identified by sequencing PCR products representing locus of interest. Based on BMI, the subjects were divided into three groups, normal weight, overweight and obese. The genotype and allele frequency were calculated separately for each group.
Results:
The allelic frequency of Glu27 did not differ amongst the three groups, though the Glu27 homozygote (Glu/Glu) were significantly more overweight and had higher concentration of triglyceride, leptin and insulin compared to that in Gln27 heterozygotes and Gln/Gln homozygotes.
Conclusions:
In this study we were able to provide evidence on the influence of Gln27Glu genetic variant of beta2AR gene on  lipid phenotypes, insulin and leptin levels in the Saudi populations.
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&lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=oL5mK91Qma4:e-gEYTlNQlI:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=oL5mK91Qma4:e-gEYTlNQlI:TzevzKxY174"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=TzevzKxY174" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=oL5mK91Qma4:e-gEYTlNQlI:l6gmwiTKsz0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=l6gmwiTKsz0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=oL5mK91Qma4:e-gEYTlNQlI:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=oL5mK91Qma4:e-gEYTlNQlI:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?i=oL5mK91Qma4:e-gEYTlNQlI:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=oL5mK91Qma4:e-gEYTlNQlI:7Q72WNTAKBA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=7Q72WNTAKBA" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/lipidsinhealthanddisease/~4/oL5mK91Qma4" height="1" width="1"/&gt;</description>
        <link>http://rss.neurobiologyoflipids.org/~r/lipidsinhealthanddisease/~3/oL5mK91Qma4/90</link>
                <dc:creator>Maha Daghestani</dc:creator>
                <dc:creator>Arjumand Warsy</dc:creator>
                <dc:creator>Mazin Daghestani</dc:creator>
                <dc:creator>Ali Al-odaib</dc:creator>
                <dc:creator>Abdelmoneim Eldali</dc:creator>
                <dc:creator>Nadia Al-Eisa</dc:creator>
                <dc:creator>Sabah Al-zhrani</dc:creator>
                <dc:source>Lipids in Health and Disease 2010, 9:90</dc:source>
        <dc:date>2010-08-25T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-511X-9-90</dc:identifier>
        <prism:publicationName>Lipids in Health and Disease</prism:publicationName>
        <prism:issn>1476-511X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>90</prism:startingPage>
        <prism:publicationDate>2010-08-25T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    <feedburner:origLink>http://www.lipidworld.com/content/9/1/90</feedburner:origLink></item>
        <item rdf:about="http://www.lipidworld.com/content/9/1/89">
        <title>Dietary olive oil effect on antioxidant status and fatty acid profile in the erythrocyte of 2,4-D- exposed rats</title>
        <description>Background:
Oxidative stress produced by reactive oxygen species (ROS) has been linked to the development of several diseases such as cardiovascular, cancer, and neurodegenerative diseases. This study investigates the possible protective effect of extra virgin olive oil (EVOO), lipophilic fraction (OOLF) and hydrophilic fraction (OOHF) on oxidative stress and fatty acid profile of erythrocytes in 2,4-D treated rats.
Methods:
Male Wistar rats were divided randomly into eight groups: control (C), (2,4-D) at a dose of 5 mg/kg b.w., (2,4-D/EVOO) was given 2,4-D plus EVOO, (2,4-D/OOHF) that received 2,4-D plus hydrophilic fraction, (2,4-D/OOLF) treated with 2,4-D plus lipophilic fraction, (EVOO) that received only EVOO, (OOHF) was given hydrophilic fraction and (OOLF) treated with lipophilic fraction. These components were daily administered by gavages for 4 weeks.
Results:
2,4-D treatment lead to decrease of antioxidant enzyme activities, namely, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) associated with a higher amount of MDA level. Erythrocyte membranes' fatty acid composition was also significantly modified with 2,4-D exposure. EVOO and hydrophilic fraction supplemented to rats with or not 2,4-D treatment enhanced the antioxidant enzyme activities and reduced the MDA level. However, lipophilic fraction did not show any improvement in oxidative damage induced by 2,4-D in spite its richness in MUFA and vitamins.
Conclusion:
EVOO administered to 2,4-D-treated rats protected erythrocyte membranes against oxidative damage by means of preventing excessive lipid peroxidation to increase the MUFA composition and increase maintaining antioxidants enzymes at normal concentrations.
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&lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=wjjLHeGcc6k:18ie37MiXDI:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=wjjLHeGcc6k:18ie37MiXDI:TzevzKxY174"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=TzevzKxY174" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=wjjLHeGcc6k:18ie37MiXDI:l6gmwiTKsz0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=l6gmwiTKsz0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=wjjLHeGcc6k:18ie37MiXDI:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=wjjLHeGcc6k:18ie37MiXDI:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?i=wjjLHeGcc6k:18ie37MiXDI:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=wjjLHeGcc6k:18ie37MiXDI:7Q72WNTAKBA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=7Q72WNTAKBA" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/lipidsinhealthanddisease/~4/wjjLHeGcc6k" height="1" width="1"/&gt;</description>
        <link>http://rss.neurobiologyoflipids.org/~r/lipidsinhealthanddisease/~3/wjjLHeGcc6k/89</link>
                <dc:creator>Amel Nakbi</dc:creator>
                <dc:creator>Wafa Tayeb</dc:creator>
                <dc:creator>Samia Dabbou</dc:creator>
                <dc:creator>Manel Issaoui</dc:creator>
                <dc:creator>Abir Grissa</dc:creator>
                <dc:creator>Nabil Attia</dc:creator>
                <dc:creator>Mohamed Hammami</dc:creator>
                <dc:source>Lipids in Health and Disease 2010, 9:89</dc:source>
        <dc:date>2010-08-25T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-511X-9-89</dc:identifier>
        <prism:publicationName>Lipids in Health and Disease</prism:publicationName>
        <prism:issn>1476-511X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>89</prism:startingPage>
        <prism:publicationDate>2010-08-25T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    <feedburner:origLink>http://www.lipidworld.com/content/9/1/89</feedburner:origLink></item>
        <item rdf:about="http://www.lipidworld.com/content/9/1/88">
        <title>Studies on antidyslipidemic effects of Morinda citrifolia (Noni) fruit, leaves and root extracts</title>
        <description>Background:
The objective of present study was to provide the pharmacological basis for the medicinal use of Morinda citrifolia Linn in dyslipidemia using the aqueous-ethanolic extracts of its fruits (Mc.Cr.F), leaves (Mc.Cr.L) and roots (Mc.Cr.R).
Results:
Mc.Cr.F, Mc.Cr.L and Mc.Cr.R showed antidyslipidemic effects in both triton (WR-1339) and high fat diet-induced dyslipidemic rat models to variable extents. All three extracts caused reduction in total cholesterol and triglyceride levels in triton-induced dyslipidemia. In high fat diet-induced dyslipidemia all these extracts caused significant reduction in total cholesterol, triglyceride, low density lipoprotein-cholesterol (LDL-C), atherogenic index and TC/HDL ratio. Mc.Cr.R extract also caused increase in high density lipoprotein-cholesterol (HDL-C). The Mc.Cr.L and Mc.Cr.R reduced gain in body weight with a reduction in daily diet consumption but Mc.Cr.F had no effect on body weight and daily diet consumption.
Conclusions:
These data indicate that the antidyslipidemic effect of the plant extracts was meditated through the inhibition of biosynthesis, absorption and secretion of lipids. This may be possibly due partly to the presence of antioxidant constituents in this plant. Therefore, this study rationalizes the medicinal use of Morinda citrifolia in dyslipidemia.
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&lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=PH2tca1JjXo:XaK1phg2LqU:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=PH2tca1JjXo:XaK1phg2LqU:TzevzKxY174"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=TzevzKxY174" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=PH2tca1JjXo:XaK1phg2LqU:l6gmwiTKsz0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=l6gmwiTKsz0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=PH2tca1JjXo:XaK1phg2LqU:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=PH2tca1JjXo:XaK1phg2LqU:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?i=PH2tca1JjXo:XaK1phg2LqU:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=PH2tca1JjXo:XaK1phg2LqU:7Q72WNTAKBA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=7Q72WNTAKBA" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/lipidsinhealthanddisease/~4/PH2tca1JjXo" height="1" width="1"/&gt;</description>
        <link>http://rss.neurobiologyoflipids.org/~r/lipidsinhealthanddisease/~3/PH2tca1JjXo/88</link>
                <dc:creator>Saf-ur-Rehman Mandukhail</dc:creator>
                <dc:creator>Nauman Aziz</dc:creator>
                <dc:creator>Anwarul-Hassan Gilani</dc:creator>
                <dc:source>Lipids in Health and Disease 2010, 9:88</dc:source>
        <dc:date>2010-08-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-511X-9-88</dc:identifier>
        <prism:publicationName>Lipids in Health and Disease</prism:publicationName>
        <prism:issn>1476-511X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>88</prism:startingPage>
        <prism:publicationDate>2010-08-20T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    <feedburner:origLink>http://www.lipidworld.com/content/9/1/88</feedburner:origLink></item>
        <item rdf:about="http://www.lipidworld.com/content/9/1/87">
        <title>Cardiac and vascular changes in elderly atherosclerotic mice: the influence of gender</title>
        <description>Background:
Although advanced age is considered a risk factor for several diseases, the impact of gender on age-associated cardiovascular diseases, such as atherosclerotic processes and valvular diseases, remains not completely clarified. The present study was designed to assess aortic valve morphology and function and vascular damage in elderly using the apolipoprotein E knockout (ApoE KO) mouse. Our hypothesis was that advanced age-related cardiovascular changes are aggravated in atherosclerotic male mice.
Methods:
The grade (0 to 4) of aortic regurgitation was evaluated through angiography. In addition, vascular lipid deposition and senescence were evaluated through histochemical analyses in aged male and female ApoE KO mice, and the results were compared to wild-type C57BL/6J (C57) mice.
Results:
Aortic regurgitation was observed in 92% of the male ApoE KO mice and 100% of the male C57 mice. Comparatively, in age-matched female ApoE KO and C57 mice, aortic regurgitation was observed in a proportion of 58% and 53%, respectively. Histological analysis of the aorta showed an outward (positive) remodeling in ApoE KO mice (female: 1.86 +/- 0.15; male: 1.89 +/- 0.68) using C57 groups as reference values. Histochemical evaluation of the aorta showed lipid deposition and vascular senescence only in the ApoE KO group, which were more pronounced in male mice.
Conclusion:
The data show that male gender contributes to the progression of aortic regurgitation and that hypercholesterolemia and male gender additively contribute to the occurrence of lipid deposition and vascular senescence in elderly mice.
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&lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=hJDiRycpW80:8gMU2W29TDw:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=hJDiRycpW80:8gMU2W29TDw:TzevzKxY174"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=TzevzKxY174" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=hJDiRycpW80:8gMU2W29TDw:l6gmwiTKsz0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=l6gmwiTKsz0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=hJDiRycpW80:8gMU2W29TDw:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=hJDiRycpW80:8gMU2W29TDw:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?i=hJDiRycpW80:8gMU2W29TDw:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=hJDiRycpW80:8gMU2W29TDw:7Q72WNTAKBA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=7Q72WNTAKBA" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/lipidsinhealthanddisease/~4/hJDiRycpW80" height="1" width="1"/&gt;</description>
        <link>http://rss.neurobiologyoflipids.org/~r/lipidsinhealthanddisease/~3/hJDiRycpW80/87</link>
                <dc:creator>Thiago Pereira</dc:creator>
                <dc:creator>Breno Nogueira</dc:creator>
                <dc:creator>Leandro Lima</dc:creator>
                <dc:creator>Marcella Porto</dc:creator>
                <dc:creator>Jose Arruda</dc:creator>
                <dc:creator>Elisardo Vasquez</dc:creator>
                <dc:creator>Silvana Meyrelles</dc:creator>
                <dc:source>Lipids in Health and Disease 2010, 9:87</dc:source>
        <dc:date>2010-08-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-511X-9-87</dc:identifier>
        <prism:publicationName>Lipids in Health and Disease</prism:publicationName>
        <prism:issn>1476-511X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>87</prism:startingPage>
        <prism:publicationDate>2010-08-19T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    <feedburner:origLink>http://www.lipidworld.com/content/9/1/87</feedburner:origLink></item>
        <item rdf:about="http://www.lipidworld.com/content/9/1/86">
        <title>Interactions of the apolipoprotein C-III 3238C&gt;G polymorphism and alcohol consumption on serum triglyceride levels</title>
        <description>Background:
Both apolipoprotein (Apo) C-III gene polymorphism and alcohol consumption have been associated with increased serum triglyceride (TG) levels, but their interactions on serum TG levels are not well known. The present study was undertaken to detect the interactions of the ApoC-III 3238C&gt;G (rs5128) polymorphism and alcohol consumption on serum TG levels.
Methods:
A total of 516 unrelated nondrinkers and 514 drinkers aged 15-89 were randomly selected from our previous stratified randomized cluster samples. Genotyping of the ApoC-III 3238C&gt;G was performed by polymerase chain reaction and restriction fragment length polymorphism combined with gel electrophoresis, and then confirmed by direct sequencing. Interactions of the ApoC-III 3238C&gt;G genotype and alcohol consumption was assessed by using a cross-product term between genotypes and the aforementioned factor.
Results:
Serum total cholesterol (TC), TG, high-density lipoprotein cholesterol (HDL-C), ApoA-I and ApoB levels were higher in drinkers than in nondrinkers (P &lt; 0.05-0.001). There was no significant difference in the genotypic and allelic frequencies between the two groups. Serum TG levels in nondrinkers were higher in CG genotype than in CC genotype (P &lt; 0.01). Serum TC, TG, low-density lipoprotein cholesterol (LDL-C) and ApoB levels in drinkers were higher in GG genotype than in CC or CG genotype (P &lt; 0.01 for all). Serum HDL-C levels in drinkers were higher in CG genotype than in CC genotype (P &lt; 0.01). Serum TC, TG, HDL-C and ApoA-I levels in CC genotype, TC, HDL-C, ApoA-I levels and the ratio of ApoA-I to ApoB in CG genotype, and TC, TG, LDL-C, ApoA-I and ApoB levels in GG genotype were higher in drinkers than in nondrinkers (P &lt; 0.05-0.01). But the ratio of ApoA-I to ApoB in GG genotype was lower in drinkers than in nondrinkers (P &lt; 0.01). Multivariate logistic regression analysis showed that the levels of TC, TG and ApoB were correlated with genotype in nondrinkers (P &lt; 0.05 for all). The levels of TC, LDL-C and ApoB were associated with genotype in drinkers (P &lt; 0.01 for all). Serum lipid parameters were also correlated with age, sex, alcohol consumption, cigarette smoking, blood pressure, body weight, and body mass index in both groups.
Conclusions:
This study suggests that the ApoC-III 3238CG heterozygotes benefited more from alcohol consumption than CC and GG homozygotes in increasing serum levels of HDL-C, ApoA-I, and the ratio of ApoA-I to ApoB, and lowering serum levels of TC and TG.
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&lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=nAutcsVdJT8:1ZoJcwpn1BU:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=nAutcsVdJT8:1ZoJcwpn1BU:TzevzKxY174"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=TzevzKxY174" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=nAutcsVdJT8:1ZoJcwpn1BU:l6gmwiTKsz0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=l6gmwiTKsz0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=nAutcsVdJT8:1ZoJcwpn1BU:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=nAutcsVdJT8:1ZoJcwpn1BU:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?i=nAutcsVdJT8:1ZoJcwpn1BU:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=nAutcsVdJT8:1ZoJcwpn1BU:7Q72WNTAKBA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=7Q72WNTAKBA" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/lipidsinhealthanddisease/~4/nAutcsVdJT8" height="1" width="1"/&gt;</description>
        <link>http://rss.neurobiologyoflipids.org/~r/lipidsinhealthanddisease/~3/nAutcsVdJT8/86</link>
                <dc:creator>Yin Ruixing</dc:creator>
                <dc:creator>Li Yiyang</dc:creator>
                <dc:creator>Li Meng</dc:creator>
                <dc:creator>Li Kela</dc:creator>
                <dc:creator>Long Xingjiang</dc:creator>
                <dc:creator>Zhang Lin</dc:creator>
                <dc:creator>Liu Wanying</dc:creator>
                <dc:creator>Wu Jinzhen</dc:creator>
                <dc:creator>Yang Dezhai</dc:creator>
                <dc:creator>Lin Weixiong</dc:creator>
                <dc:source>Lipids in Health and Disease 2010, 9:86</dc:source>
        <dc:date>2010-08-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-511X-9-86</dc:identifier>
        <prism:publicationName>Lipids in Health and Disease</prism:publicationName>
        <prism:issn>1476-511X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>86</prism:startingPage>
        <prism:publicationDate>2010-08-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    <feedburner:origLink>http://www.lipidworld.com/content/9/1/86</feedburner:origLink></item>
        <item rdf:about="http://www.lipidworld.com/content/9/1/85">
        <title>Lipid ratios and appropriate cut off values for prediction of diabetes: a cohort of Iranian men and women</title>
        <description>Background:
Dyslipidemia is a risk factor for incident type 2 diabetes; however, no study has specifically assessed the lipid ratios (i.e. total cholesterol (TC)/high density lipoprotein cholesterol (HDL-C) and triglyceride (TG)/HDL-C) as predictors of diabetes. We aimed to compare the independent association between the different lipid measures with incident diabetes over a median follow up of 6.4 years in Iranian men and women.MethodThe study population consisted of 5201 non diabetic (men = 2173, women = 3028) subjects, aged ≥20 years. The risk factor adjusted odds ratios (ORs) for diabetes were calculated for every 1 standard deviation (SD) change in TC, log-transformed TG, HDL-C, non-HDL-C, TC/HDL-C and log-transformed TG/HDL-C using multivariate logistic regression analysis. Receiver operator characteristic (ROC) curve analysis was used to define the points of the maximum sum of sensitivity and specificity (MAXss) of each lipid measure as a predictor of diabetes.ResultWe found 366 (146 men and 220 women) new diabetes cases during follow-up. The risk-factor-adjusted ORs for a 1 SD increase in TG, TC/HDL-C and TG/HDL-C were 1.23, 1.27 and 1.25 in men; the corresponding risks in females were 1.36, 1.14, 1.39 respectively (all p &lt; 0.05, except TC/HDL-C in females which was marginally significant, p = 0.07). A 1 SD increase of HDL-C only in women decreased the risk of diabetes by 25% [0.75(0.64-0.89)]. In both genders, there was no difference in the discriminatory power of different lipid measures to predict incident diabetes in the risk factor adjusted models (ROC ≈ 82%). TG cutoff values of 1.98 and 1.66 mmol/l; TG/HDL-C cutoff values of 4.7 and 3.7, in men and women, respectively, TC/HDL-C cutoff value of 5.3 in both genders and HDL-C cutoff value of 1.18 mmol/l in women yielded the MAXss for defining the incidence of diabetes.
Conclusion:
TC/HDL-C and TG/HDL-C showed similar performance for diabetes prediction in men population however; among women TG/HDL-C highlighted higher risk than did TC/HDL-C, although there was no difference in discriminatory power. Importantly, HDL-C had a protective effect for incident diabetes only among women.
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&lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=9Vrjh8RRj7Q:FJl766tuhmw:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=9Vrjh8RRj7Q:FJl766tuhmw:TzevzKxY174"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=TzevzKxY174" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=9Vrjh8RRj7Q:FJl766tuhmw:l6gmwiTKsz0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=l6gmwiTKsz0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=9Vrjh8RRj7Q:FJl766tuhmw:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=9Vrjh8RRj7Q:FJl766tuhmw:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?i=9Vrjh8RRj7Q:FJl766tuhmw:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=9Vrjh8RRj7Q:FJl766tuhmw:7Q72WNTAKBA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=7Q72WNTAKBA" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/lipidsinhealthanddisease/~4/9Vrjh8RRj7Q" height="1" width="1"/&gt;</description>
        <link>http://rss.neurobiologyoflipids.org/~r/lipidsinhealthanddisease/~3/9Vrjh8RRj7Q/85</link>
                <dc:creator>Farzad Hadaegh</dc:creator>
                <dc:creator>Masumeh Hatami</dc:creator>
                <dc:creator>Maryam Tohidi</dc:creator>
                <dc:creator>Parvin Sarbakhsh</dc:creator>
                <dc:creator>Navid Saadat</dc:creator>
                <dc:creator>Fereidoun Azizi</dc:creator>
                <dc:source>Lipids in Health and Disease 2010, 9:85</dc:source>
        <dc:date>2010-08-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-511X-9-85</dc:identifier>
        <prism:publicationName>Lipids in Health and Disease</prism:publicationName>
        <prism:issn>1476-511X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>85</prism:startingPage>
        <prism:publicationDate>2010-08-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    <feedburner:origLink>http://www.lipidworld.com/content/9/1/85</feedburner:origLink></item>
        <item rdf:about="http://www.lipidworld.com/content/9/1/84">
        <title>Deoxysphingoid bases as plasma markers in Diabetes mellitus</title>
        <description>Background:
Sphingoid bases are formed from the precursors L-serine and palmitoyl-CoA-a reaction which is catalyzed by the serine-palmitoyltransferase (SPT). SPT metabolizes, besides palmitoyl-CoA also other acyl-CoAs but shows also variability towards the use of other amino acid substrates. The enzyme is also able to metabolize alanine, which results in the formation of an atypical deoxy-sphingoid base (DSB). This promiscuous activity is greatly increased in the case of the sensory neuropathy HSAN1, and pathologically elevated DSB levels have been identified as the cause of this disease. Clinically, HSAN1 shows a pronounced similarity to the diabetic sensory neuropathy (DSN), which is the most common chronic complication of diabetes mellitus. Since serine and alanine metabolism is functionally linked to carbohydrate metabolism by their precursors 3-phosphoglycerate and pyruvate, we were interested to see whether the levels of certain sphingoid base metabolites are altered in patients with diabetes.
Results:
In a case-control study we compared plasma sphingoid base levels between healthy and diabetic individuals. DSB levels were higher in the diabetic group whereas C16 and C18 sphingoid bases were not significantly different. Plasma serine, but not alanine levels were lower in the diabetic group. A subsequent lipoprotein fractionation showed that the DSBs are primarily present in the LDL and VLDL fraction.
Conclusion:
Our results suggest that DSBs are a novel category of plasma biomarkers in diabetes which reflect functional impairments of carbohydrate metabolism. Furthermore, elevated DSB levels as we see them in diabetic patients might also contribute to the progression of the diabetic sensory neuropathy, the most frequent complication of diabetes.
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&lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=SyPZEPOAdro:KHYcuDihVxc:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=SyPZEPOAdro:KHYcuDihVxc:TzevzKxY174"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=TzevzKxY174" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=SyPZEPOAdro:KHYcuDihVxc:l6gmwiTKsz0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=l6gmwiTKsz0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=SyPZEPOAdro:KHYcuDihVxc:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=SyPZEPOAdro:KHYcuDihVxc:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?i=SyPZEPOAdro:KHYcuDihVxc:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=SyPZEPOAdro:KHYcuDihVxc:7Q72WNTAKBA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=7Q72WNTAKBA" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/lipidsinhealthanddisease/~4/SyPZEPOAdro" height="1" width="1"/&gt;</description>
        <link>http://rss.neurobiologyoflipids.org/~r/lipidsinhealthanddisease/~3/SyPZEPOAdro/84</link>
                <dc:creator>Mariana Bertea</dc:creator>
                <dc:creator>Markus Rutti</dc:creator>
                <dc:creator>Alaa Othman</dc:creator>
                <dc:creator>Jaqueline Marti-Jaun</dc:creator>
                <dc:creator>Martin Hersberger</dc:creator>
                <dc:creator>Arnold von Eckardstein</dc:creator>
                <dc:creator>Thorsten Hornemann</dc:creator>
                <dc:source>Lipids in Health and Disease 2010, 9:84</dc:source>
        <dc:date>2010-08-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-511X-9-84</dc:identifier>
        <prism:publicationName>Lipids in Health and Disease</prism:publicationName>
        <prism:issn>1476-511X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>84</prism:startingPage>
        <prism:publicationDate>2010-08-16T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    <feedburner:origLink>http://www.lipidworld.com/content/9/1/84</feedburner:origLink></item>
        <item rdf:about="http://www.lipidworld.com/content/9/1/83">
        <title>Determinants of glycemic control in female diabetic patients: a study from Iran</title>
        <description>Background:
Since microvascular and macrovascular complications are reduced through strict glycemic control, this study carried out to identify the factors that affect glycemic control.
Methods:
A cross-sectional design was carried out to examine the role of demographic, anthropometric, clinical and other relevant characteristics in a sample of 103 female diabetic patients in Tehran, Iran. Personal interviews were conducted to collect data. Then blood sampling collected and the patients were divided into two outcome groups (controlled and uncontrolled diabetes). The groups were compared on the basis of their characteristics using both univariate and multivariate analyses.
Results:
In all 103 patients were entered into the study. The mean age of patients was 46.38 (SD = 11.42) years. Overall, the mean value of HbA1c for the whole sample was 7.5 (SD = 2.35) and 56.3% had HbA1c ≥ 7%. The findings obtained from univariate analysis revealed that there were no significant differences between controlled and uncontrolled patients. However, in multivariate analysis the waist circumference was found to be a significant predictor of increased level of HbA1c (OR = 1.04, 95% CI = 1-1.08, P = 0.04).
Conclusions:
The findings suggest that increased level of HbA1c is associated with waist circumference that is a modifiable factor. It seems that physical activity might be a solution to overcome this health problem. A larger study to identify other factors also is recommended.
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&lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=sI_1__hQOMY:NRZAAj6O3GA:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=sI_1__hQOMY:NRZAAj6O3GA:TzevzKxY174"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=TzevzKxY174" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=sI_1__hQOMY:NRZAAj6O3GA:l6gmwiTKsz0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=l6gmwiTKsz0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=sI_1__hQOMY:NRZAAj6O3GA:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=sI_1__hQOMY:NRZAAj6O3GA:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?i=sI_1__hQOMY:NRZAAj6O3GA:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://rss.neurobiologyoflipids.org/~ff/lipidsinhealthanddisease?a=sI_1__hQOMY:NRZAAj6O3GA:7Q72WNTAKBA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/lipidsinhealthanddisease?d=7Q72WNTAKBA" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/lipidsinhealthanddisease/~4/sI_1__hQOMY" height="1" width="1"/&gt;</description>
        <link>http://rss.neurobiologyoflipids.org/~r/lipidsinhealthanddisease/~3/sI_1__hQOMY/83</link>
                <dc:creator>Zeinab Ghazanfari</dc:creator>
                <dc:creator>Shamsaddin Niknami</dc:creator>
                <dc:creator>Fazlollah Ghofranipour</dc:creator>
                <dc:creator>Bagher Larijani</dc:creator>
                <dc:creator>Hamid Agha-Alinejad</dc:creator>
                <dc:creator>Ali Montazeri</dc:creator>
                <dc:source>Lipids in Health and Disease 2010, 9:83</dc:source>
        <dc:date>2010-08-11T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-511X-9-83</dc:identifier>
        <prism:publicationName>Lipids in Health and Disease</prism:publicationName>
        <prism:issn>1476-511X</prism:issn>
        <prism:volume>9</prism:volume>
        <prism:startingPage>83</prism:startingPage>
        <prism:publicationDate>2010-08-11T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    <feedburner:origLink>http://www.lipidworld.com/content/9/1/83</feedburner:origLink></item>
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<image rdf:about="http://neurobiologyoflipids.org/images/neurobiologyoflipidslogo250x50.jpg"><url>http://neurobiologyoflipids.org/images/neurobiologyoflipidslogo250x50.jpg</url><link>http://neurobiologyoflipids.org/</link><title>Neurobiology of Lipids (ISSN 1683-5506), scholarly expert publication on the role of fats in brain function and nervous system diseases: by scientists for peers and the public</title></image></rdf:RDF>
