<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet type="text/xsl" media="screen" href="/~d/styles/rss2full.xsl"?><?xml-stylesheet type="text/css" media="screen" href="http://feeds.feedburner.com/~d/styles/itemcontent.css"?><rss xmlns:media="http://search.yahoo.com/mrss/" xmlns:itunes="http://www.itunes.com/dtds/podcast-1.0.dtd" xmlns:creativeCommons="http://backend.userland.com/creativeCommonsRssModule" xmlns:feedburner="http://rssnamespace.org/feedburner/ext/1.0" version="2.0"><channel><title>PolygenicBlog</title><link>http://polygenicpathways.blogspot.com/</link><atom10:link xmlns:atom10="http://www.w3.org/2005/Atom" rel="self" type="application/rss+xml" href="http://feeds.feedburner.com/Polygenicblog" /><description>Concerning the relationships between genes, risk factors and immunity in Alzheimer's disease, Autism, Bipolar disorder , multiple sclerosis, Parkinson's disease, schizophrenia and chronic fatigue</description><language>en</language><managingEditor>noreply@blogger.com (Chris Carter)</managingEditor><lastBuildDate>Mon, 20 May 2013 22:37:17 PDT</lastBuildDate><generator>Blogger http://www.blogger.com</generator><openSearch:totalResults xmlns:openSearch="http://a9.com/-/spec/opensearch/1.1/">4801</openSearch:totalResults><openSearch:startIndex xmlns:openSearch="http://a9.com/-/spec/opensearch/1.1/">1</openSearch:startIndex><openSearch:itemsPerPage xmlns:openSearch="http://a9.com/-/spec/opensearch/1.1/">25</openSearch:itemsPerPage><feedburner:info uri="polygenicblog" /><atom10:link xmlns:atom10="http://www.w3.org/2005/Atom" rel="hub" href="http://pubsubhubbub.appspot.com/" /><media:thumbnail url="http://www.polygenicpathways.co.uk/disc1.jpg" /><media:keywords>Alzheimer,s,schizophrenia,chronic,fatigue,prostate,cancer,bipolar,disorder,XMRV,Herpes,simplex,virus,multiple,sclerosis,parkinson,s,disease</media:keywords><media:category scheme="http://www.itunes.com/dtds/podcast-1.0.dtd">Science &amp; Medicine/Medicine</media:category><itunes:owner><itunes:email>noreply@blogger.com</itunes:email><itunes:name>Chris Carter</itunes:name></itunes:owner><itunes:author>Chris Carter</itunes:author><itunes:explicit>no</itunes:explicit><itunes:image href="http://www.polygenicpathways.co.uk/disc1.jpg" /><itunes:keywords>Alzheimer,s,schizophrenia,chronic,fatigue,prostate,cancer,bipolar,disorder,XMRV,Herpes,simplex,virus,multiple,sclerosis,parkinson,s,disease</itunes:keywords><itunes:subtitle>PolyBlog</itunes:subtitle><itunes:category text="Science &amp; Medicine"><itunes:category text="Medicine" /></itunes:category><creativeCommons:license>http://creativecommons.org/licenses/by-nc-sa/2.0/</creativeCommons:license><image><link>http://polygenicpathways.blogspot.com/</link><url>http://feeds.feedburner.com/Polygenicblog</url></image><feedburner:emailServiceId>Polygenicblog</feedburner:emailServiceId><feedburner:feedburnerHostname>http://feedburner.google.com</feedburner:feedburnerHostname><item><title>New immune system discovered</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/aHBUkWOQNeA/new-immune-system-discovered.html</link><category>bacteriophage</category><category>Immune system</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Mon, 20 May 2013 22:37:17 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-1575766110116159576</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
"Taking previous research into consideration, we are able to propose the Bacteriophage Adherence to Mucus—or BAM—is a new model of immunity, which emphasizes the important role bacteriophage play in protecting the body from invading pathogens"&lt;br /&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/aHBUkWOQNeA" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-21T06:37:17.616+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/new-immune-system-discovered.html</feedburner:origLink></item><item><title>Type 1 Diabetes May Be Reversible With Immune Suppressor Protein</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/ljV6iz-zgU4/type-1-diabetes-may-be-reversible-with.html</link><category>immunosuppressant</category><category>diabetes</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Mon, 20 May 2013 22:30:59 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-5877703944104900746</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
"A professor in Melbourne, Australia, who is on a mission to find a cure for type 1 diabetes, believes that the answer, or part of it, lies with an immune suppressor protein called CD52. And if it works for type 1 diabetes, then it may well work for other immune disorders, such as multiple sclerosis and rheumatoid arthritis, where disruption in the balance different kinds of T cell in the immune system causes it to attack the body's own healthy tissue."&lt;br /&gt;
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&lt;div class="blogger-post-footer"&gt;pub-5799224524264318&lt;/div&gt;&lt;div class="feedflare"&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/ljV6iz-zgU4" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-21T06:30:59.565+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/type-1-diabetes-may-be-reversible-with.html</feedburner:origLink></item><item><title>Scientists Develop Drug That Improves Memory and Prevents Brain Damage in Mice</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/q0yTjSj12lw/scientists-develop-drug-that-improves.html</link><category>Alzheimer's disease</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Mon, 20 May 2013 06:44:03 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-6899584006024900844</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
A drug developed by scientists at the Salk Institute for Biological Studies, known as J147, improves memory and prevents brain damage in aged mice following short-term treatment. The findings, published May 14 in the journal Alzheimer's Research and Therapy, may pave the way to a new treatment for Alzheimer's disease in humans.J147 was developed at Salk in the laboratory of David Schubert, a professor in the Cellular Neurobiology Laboratory. He and his colleagues bucked the trend within the pharmaceutical industry, which has focused on the biological pathways involved in the formation of amyloid plaques, the dense deposits of protein that characterize the disease. Instead, the Salk team used living neurons grown in laboratory dishes to test whether their new synthetic compounds, which are based upon natural products derived from plants, were effective at protecting brain cells against several pathologies associated with brain aging. From the test results of each chemical iteration of the lead compound, they were able to alter their chemical structures to make them much more potent. Although J147 appears to be safe in mice, the next step will require clinical trials to determine whether the compound will prove safe and effective in humans.&lt;/div&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/q0yTjSj12lw" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-20T14:44:03.722+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/scientists-develop-drug-that-improves.html</feedburner:origLink></item><item><title>Good cholesterol linked to innate immunity: ASM</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/DHNXXkok7u8/good-cholesterol-linked-to-innate.html</link><category>cholesterol</category><category>Innate immune system</category><category>Host-pathogen</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Mon, 20 May 2013 04:35:58 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-4175512099432600861</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;span style="background-color: white; color: #333333; font-family: arial, sans-serif; font-size: 13px; line-height: 17px;"&gt;Trypanosome Lytic Factor (TLF) has emerged as an arm of innate immunity, present only in humans and select non-human primates. TLF was originally discovered in human blood as a minor form of High-density lipoprotein (HDL), (good cholesterol), that kills the African trypanosome, Trypanosoma brucei, making humans resistant to infection. Participants will discuss this finding as well as how understanding these mechanism will provide insights as to other pathogens that TLF should kill, as well as offer potential avenues to therapeutically augment or mimic TLF action.&lt;/span&gt;&lt;span style="background-color: white; color: #333333; font-family: arial, sans-serif; font-size: 13px; line-height: 17px;"&gt;&amp;nbsp;TLF is a mixture of apolipoproteins APOL1 /igm APOA1 and&amp;nbsp;&lt;/span&gt;&lt;span style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"&gt;&amp;nbsp;&lt;/span&gt;&lt;span style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"&gt;haptoglobin-related protein&lt;/span&gt;&lt;span style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"&gt;&amp;nbsp;&lt;/span&gt;&lt;iframe allowfullscreen="" frameborder="0" height="270" src="//www.youtube.com/embed/0Q-81a1Y4x0" width="480"&gt;&lt;/iframe&gt;&lt;br /&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/DHNXXkok7u8" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-20T12:35:58.955+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/good-cholesterol-linked-to-innate.html</feedburner:origLink></item><item><title>BBC News - Sunshine vitamin D 'may treat asthma'</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/BxLR9FBylAA/bbc-news-sunshine-vitamin-d-may-treat.html</link><category>asthma</category><category>Vitamin D</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Mon, 20 May 2013 02:07:25 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-7818994355357936102</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
The amount of time asthma patients spend soaking up the sun may have an impact on the illness, researchers have suggested.

A team at King's College London said low levels of vitamin D, which is made by the body in sunlight, was linked to a worsening of symptoms.

Its latest research shows the vitamin calms an over-active part of the immune system in asthma.&lt;/div&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/BxLR9FBylAA" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-20T10:07:25.368+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/bbc-news-sunshine-vitamin-d-may-treat.html</feedburner:origLink></item><item><title>In US, 20% Of Children Have A Mental Disorder</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/0RD79YWMdt8/in-us-20-of-children-have-mental.html</link><category>child psychiatry</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Sun, 19 May 2013 14:26:44 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-4344300544956454200</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
MNT "Nearly 20% of children in the United States suffer from a mental disorder, and the number has been increasing for over a decade, according to a new report released by the Centers for Disease Control and Prevention (CDC)."&lt;br /&gt;
&lt;br /&gt;
????????????????????????????????????????&lt;/div&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/0RD79YWMdt8" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-19T22:26:44.037+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/in-us-20-of-children-have-mental.html</feedburner:origLink></item><item><title>Ketamine shows significant therapeutic benefit in people with treatment-resistant depression</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/6uojdYH-ADw/ketamine-shows-significant-therapeutic.html</link><category>depression</category><category>Ketamine</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Sun, 19 May 2013 05:34:51 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-3152638726478377544</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&amp;nbsp;"Patients with treatment-resistant major depression saw dramatic improvement in their illness after treatment with ketamine, an anesthetic, according to the largest ketamine clinical trial to-date led by researchers from the Icahn School of Medicine at Mount Sinai. The antidepressant benefits of ketamine were seen within 24 hours, whereas traditional antidepressants can take days or weeks to demonstrate a reduction in depression."&lt;br /&gt;
&lt;br /&gt;
&lt;br /&gt;&lt;/div&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/6uojdYH-ADw" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-19T13:34:51.932+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/ketamine-shows-significant-therapeutic.html</feedburner:origLink></item><item><title>Now we know why old schizophrenia medicine works on antibiotics-resistant bacteria</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/r33FXkPoybU/now-we-know-why-old-scizophrenia.html</link><category>phenothiazene</category><category>Antibacterial</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Sun, 19 May 2013 07:58:01 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-9110880742514350346</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
Thioridazine is known to possess antibacterial effects, although it was not clear how this worked............ "&lt;span style="background-color: white; font-family: Arial, Helvetica, sans-serif; font-size: 13px; line-height: 15px;"&gt;When we treat the bacteria with antibiotics alone, nothing happens -- the bacteria are not even affected. But when we add both thioridazine and antibiotics, something happens: thioridazine weakens the bacterial cell wall by removing glycine (an amino acid) from the cell wall. In the absence of glycine, the antibiotics can attack the weakened cell wall and kill&amp;nbsp;&lt;/span&gt;&lt;em style="background-color: white; font-family: Arial, Helvetica, sans-serif; font-size: 13px; line-height: 15px;"&gt;staphylococcus&lt;/em&gt;&lt;span style="background-color: white; font-family: Arial, Helvetica, sans-serif; font-size: 13px; line-height: 15px;"&gt;&amp;nbsp;bacteria," explains Janne Kudsk Klitgaard, visiting scholar at the Department of Biochemistry and Molecular Biology, University of Southern Denmark".&lt;/span&gt;&lt;br /&gt;
&lt;div class="zemanta-related" style="clear: both; margin-top: 20px; overflow: hidden;"&gt;
&lt;h4 class="zemanta-related-title"&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/r33FXkPoybU" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-19T15:58:01.344+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/now-we-know-why-old-scizophrenia.html</feedburner:origLink></item><item><title>Breathing Emission Particles Turns HDL Cholesterol From 'Good' To 'Bad'</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/iW914xIP63c/breathing-emission-particles-turns-hdl.html</link><category>cholesterol</category><category>Pollution</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Sat, 18 May 2013 23:35:32 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-4170001310971577409</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
MNT: Academic researchers have found that breathing motor vehicle emissions triggers a change in high-density lipoprotein (HDL) cholesterol, altering its cardiovascular protective qualities so that it actually contributes to clogged arteries.In addition to changing HDL from "good" to "bad," the inhalation of emissions activates other components of oxidation, the early cell and tissue damage that causes inflammation, leading to hardening of the arteries, according to the research team, which included scientists from UCLA and other institutions.&lt;/div&gt;
&lt;div class="blogger-post-footer"&gt;pub-5799224524264318&lt;/div&gt;&lt;div class="feedflare"&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/iW914xIP63c" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-19T07:35:32.957+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/breathing-emission-particles-turns-hdl.html</feedburner:origLink></item><item><title>Geographic Variation in the Prevalence of Attention-Deficit/Hyperactivity Disorder: The Sunny Perspective.</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/b900BWNnSKE/geographic-variation-in-prevalence-of.html</link><category>Environment</category><category>ADHD</category><category>circadian</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Sat, 18 May 2013 10:37:16 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-6139424918154694436</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;br /&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
Attention-deficit/hyperactivity disorder (ADHD) is the most common psychiatric disorder of childhood, with average worldwide prevalence of 5.3%, varying by region.&lt;/div&gt;
&lt;h4 style="background-color: white; float: left; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin: 0px 0.25em 0px 0px; text-transform: uppercase;"&gt;
METHODS:&lt;/h4&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
We assessed the relationship between the prevalence of ADHD and solar intensity (SI) (kilowatt hours/square meters/day) on the basis of multinational and cross-state studies. Prevalence data for the U.S. were based on self-report of professional diagnoses; prevalence data for the other countries were based on diagnostic assessment. The SI data were obtained from national institutes.&lt;/div&gt;
&lt;h4 style="background-color: white; float: left; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin: 0px 0.25em 0px 0px; text-transform: uppercase;"&gt;
RESULTS:&lt;/h4&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
In three datasets (across 49 U.S. states for 2003 and 2007, and across 9 non-U.S. countries) a relationship between SI and the prevalence of ADHD was found, explaining 34%-57% of the variance in ADHD prevalence, with high SI having an apparent preventative effect. Controlling for low birth weight, infant mortality, average income (socioeconomic status), latitude, and other relevant factors did not change these findings. Furthermore, these findings were specific to ADHD, not found for the prevalence of autism spectrum disorders or major depressive disorder.&lt;/div&gt;
&lt;h4 style="background-color: white; float: left; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin: 0px 0.25em 0px 0px; text-transform: uppercase;"&gt;
CONCLUSIONS:&lt;/h4&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
In this study we found a lower prevalence of ADHD in areas with high SI for both U.S. and non-U.S. data. This association has not been reported before in the literature. The preventative effect of high SI might be related to an improvement of circadian clock disturbances, which have recently been associated with ADHD. These findings likely apply to a substantial subgroup of ADHD patients and have major implications in our understanding of the etiology and possibly prevention of ADHD by medical professionals, schools, parents, and manufacturers of mobile device&lt;/div&gt;
&lt;/div&gt;
&lt;div class="blogger-post-footer"&gt;pub-5799224524264318&lt;/div&gt;&lt;div class="feedflare"&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/b900BWNnSKE" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-18T18:37:16.913+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/geographic-variation-in-prevalence-of.html</feedburner:origLink></item><item><title>GNbAC1, a humanized monoclonal antibody against the envelope protein of multiple sclerosis-associated endogenous retrovirus: a first-in-humans randomized clinical study.</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/n5YhpwFw8rk/gnbac1-humanized-monoclonal-antibody.html</link><category>Retrovirus</category><category>multiple sclerosis</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Sat, 18 May 2013 06:24:19 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-435664837324605388</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;span style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"&gt;Human endogenous retrovirus (HERV) genes represent about 8% of the human genome. A member of the HERV family W, the Multiple Sclerosis-Associated Retrovirus (MSRV) gene, encodes an envelope protein (Env), which can activate a proinflammatory and autoimmune cascade through its interaction with Toll-like receptor 4. Due to its proinflammatory property and an inhibitory effect on oligodendrocyte precursor cell differentiation, the MSRV-Env protein could play a crucial role in the pathogeny of multiple sclerosis. GNbAC1 is a humanized monoclonal antibody of the immunoglobulin G4 type, which is directed against MSRV-Env. After validation of the MSRV-Env as a therapeutic target in preclinical experimental models, a clinical development program was initiated.&lt;/span&gt;&lt;br /&gt;
&lt;h4 style="background-color: white; float: left; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin: 0px 0.25em 0px 0px; text-transform: uppercase;"&gt;
OBJECTIVE:&lt;/h4&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
This study evaluated the safety profile, pharmacokinetic parameters, and immunogenicity of GNbAC1 in healthy male volunteers.&lt;/div&gt;
&lt;h4 style="background-color: white; float: left; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin: 0px 0.25em 0px 0px; text-transform: uppercase;"&gt;
METHODS:&lt;/h4&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
In this first-in-humans, Phase I, randomized, double-blind, placebo-controlled, dose-escalation study, each subject received a single dose of IV GNbAC1 0.0025, 0.025, 0.15, 0.6, 2, or 6 mg/kg or inactive vehicle (placebo), infused over 1 hour. Tolerability and other laboratory parameters were observed, and regular blood sampling was performed, to study the pharmacokinetic properties and immunogenicity of this monoclonal antibody.&lt;/div&gt;
&lt;h4 style="background-color: white; float: left; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin: 0px 0.25em 0px 0px; text-transform: uppercase;"&gt;
RESULTS:&lt;/h4&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
A total of 33 male subjects (mean age, 44 years) completed the study. GNbAC1 was well tolerated after dosing in all subjects and in each dose cohort. Only minor and nonspecific adverse events (AEs) were recorded; no serious AEs were reported. Pharmacokinetic data show a dose-linear pharmacokinetic profile. The mean elimination half-life ranged between 19 and 26 days, with therapeutically efficient concentrations maintained over a 4-week periods at doses of 2 and 6 mg/kg. No emergence of anti-GNbAC1 antibodies were detected after dosing in any subject over the entire observation period of 64 days.&lt;/div&gt;
&lt;h4 style="background-color: white; float: left; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin: 0px 0.25em 0px 0px; text-transform: uppercase;"&gt;
CONCLUSIONS:&lt;/h4&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
In these healthy male subjects, the safety and pharmacokinetic profiles of GNbAC1 appeared favorable. These findings are expected to allow for the launch of a Phase II development program for this innovative therapeutic approach in patients with multiple sclerosis. ClinicalTrials.gov identifier: NCT01699555.&lt;/div&gt;
&lt;/div&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/n5YhpwFw8rk" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-18T14:24:19.169+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/gnbac1-humanized-monoclonal-antibody.html</feedburner:origLink></item><item><title>Body mass index of low income African-Americans linked to proximity of fast food restaurants</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/_NgWRGqdrBU/body-mass-index-of-low-income-african.html</link><category>obesity</category><category>Fast food</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Sat, 18 May 2013 02:55:33 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-1042283414377709539</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;span style="background-color: white; font-family: Arial, Helvetica, sans-serif; font-size: 13px; line-height: 15px;"&gt;A new study published online in the&lt;/span&gt;&lt;em style="background-color: white; font-family: Arial, Helvetica, sans-serif; font-size: 13px; line-height: 15px;"&gt;American Journal of Public Health&lt;/em&gt;&lt;span style="background-color: white; font-family: Arial, Helvetica, sans-serif; font-size: 13px; line-height: 15px;"&gt;indicates higher BMI associates with residential proximity to a fast food restaurant, and among lower-income African-Americans, the density, or number, of fast food restaurants within two miles of the home&lt;/span&gt;&lt;br /&gt;
&lt;span style="background-color: white; font-family: Arial, Helvetica, sans-serif; font-size: 13px; line-height: 15px;"&gt;&lt;br /&gt;
&lt;/span&gt;&lt;/div&gt;
&lt;div class="blogger-post-footer"&gt;pub-5799224524264318&lt;/div&gt;&lt;div class="feedflare"&gt;
&lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=_NgWRGqdrBU:P2_1VX3SBQ4:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=_NgWRGqdrBU:P2_1VX3SBQ4:-BTjWOF_DHI"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=_NgWRGqdrBU:P2_1VX3SBQ4:-BTjWOF_DHI" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=_NgWRGqdrBU:P2_1VX3SBQ4:dnMXMwOfBR0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?d=dnMXMwOfBR0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=_NgWRGqdrBU:P2_1VX3SBQ4:F7zBnMyn0Lo"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=_NgWRGqdrBU:P2_1VX3SBQ4:F7zBnMyn0Lo" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=_NgWRGqdrBU:P2_1VX3SBQ4:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=_NgWRGqdrBU:P2_1VX3SBQ4:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=_NgWRGqdrBU:P2_1VX3SBQ4:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=_NgWRGqdrBU:P2_1VX3SBQ4:gIN9vFwOqvQ"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=_NgWRGqdrBU:P2_1VX3SBQ4:gIN9vFwOqvQ" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=_NgWRGqdrBU:P2_1VX3SBQ4:FKkp6kN0NBs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=_NgWRGqdrBU:P2_1VX3SBQ4:FKkp6kN0NBs" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/_NgWRGqdrBU" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-18T10:55:33.575+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/body-mass-index-of-low-income-african.html</feedburner:origLink></item><item><title>Nonmelanoma skin cancer is associated with reduced Alzheimer disease risk</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/Z-jzuEGVVgc/nonmelanoma-skin-cancer-is-associated.html</link><category>Alzheimer's disease</category><category>Skin cancer</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Fri, 17 May 2013 11:43:51 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-8239246472037626699</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;span style="background-color: white; font-family: inherit; font-size: inherit; font-style: inherit; line-height: 1.5; text-align: inherit;"&gt;To explore the association of nonmelanoma skin cancer (NMSC) and Alzheimer disease (AD) in the Einstein Aging Study, an epidemiologic study of aging in New York City.&lt;/span&gt;&lt;br /&gt;
&lt;div class="subsection" id="sec-2" style="background-color: white; border: 0px; font-family: Arial, sans-serif; font-size: 13px; line-height: 16px; margin: 0px; outline-style: none; padding: 0px; text-align: justify; vertical-align: baseline;"&gt;
&lt;div id="p-171" style="border: 0px; font-family: inherit; font-size: inherit; font-style: inherit; line-height: 1.5; margin-bottom: 15px; margin-top: 15px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"&gt;
&lt;strong style="border: 0px; font-family: inherit; font-size: inherit; font-style: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"&gt;Methods:&lt;/strong&gt;&amp;nbsp;Community-residing volunteers aged 70 years or older were assessed annually, followed by multidisciplinary diagnostic consensus. Cancer status and type was obtained by self-report. Cox proportional hazards models were used to test associations between NMSC and subsequent risk of developing a neurocognitive disorder. To deduce a biologically specific association between AD and NMSC, we considered 3 nested outcomes groups: only AD (probable or possible AD as the sole diagnosis), any AD (probable AD or possible AD, as well as mixed AD/vascular dementia), and all-cause dementia.&lt;/div&gt;
&lt;/div&gt;
&lt;div class="subsection" id="sec-3" style="background-color: white; border: 0px; font-family: Arial, sans-serif; font-size: 13px; line-height: 16px; margin: 0px; outline-style: none; padding: 0px; text-align: justify; vertical-align: baseline;"&gt;
&lt;div id="p-172" style="border: 0px; font-family: inherit; font-size: inherit; font-style: inherit; line-height: 1.5; margin-bottom: 15px; margin-top: 15px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"&gt;
&lt;strong style="border: 0px; font-family: inherit; font-size: inherit; font-style: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"&gt;Results:&lt;/strong&gt;&amp;nbsp;We followed 1,102 adults with a mean age of 79 years at enrollment. Prevalent NMSC was associated with reduced risk of only AD (hazard ratio = 0.21; 95% confidence interval = 0.051–0.87;&amp;nbsp;&lt;em style="border: 0px; font-family: inherit; font-size: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"&gt;p&lt;/em&gt;&amp;nbsp;= 0.031) among subjects after adjustment for demographics, hypertension, diabetes, and coronary heart disease.&amp;nbsp;&lt;em style="border: 0px; font-family: inherit; font-size: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"&gt;APOE&lt;/em&gt;&amp;nbsp;ε4 genotypes were available in 769 individuals. The association was similar in magnitude, but nonsignificant, when the number of&amp;nbsp;&lt;em style="border: 0px; font-family: inherit; font-size: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"&gt;APOE&lt;/em&gt;ε4 alleles was included in the model. No significant association was found between NMSC and subsequent development of any AD or all-cause dementia.&lt;/div&gt;
&lt;/div&gt;
&lt;div class="subsection" id="sec-4" style="background-color: white; border: 0px; font-family: Arial, sans-serif; font-size: 13px; line-height: 16px; margin: 0px; outline-style: none; padding: 0px; text-align: justify; vertical-align: baseline;"&gt;
&lt;div id="p-173" style="border: 0px; font-family: inherit; font-size: inherit; font-style: inherit; line-height: 1.5; margin-bottom: 15px; margin-top: 15px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"&gt;
&lt;strong style="border: 0px; font-family: inherit; font-size: inherit; font-style: inherit; line-height: inherit; margin: 0px; outline-style: none; padding: 0px; text-align: inherit; vertical-align: baseline;"&gt;Conclusions:&lt;/strong&gt;&amp;nbsp;This population-based longitudinal study shows that individuals older than 70 years with NMSC have a significantly reduced risk of developing AD compared with individuals without NMSC. We deduce Alzheimer-specific neuroprotection, because the effect is attenuated or eliminated when considering less-specific diagnoses such as AD with another diagnosis (any AD) or all-cause dementia.&lt;/div&gt;
&lt;/div&gt;
&lt;div class="zemanta-pixie" style="height: 15px; margin-top: 10px;"&gt;
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&lt;/div&gt;
&lt;div class="blogger-post-footer"&gt;pub-5799224524264318&lt;/div&gt;&lt;div class="feedflare"&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/Z-jzuEGVVgc" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-17T19:43:51.454+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/nonmelanoma-skin-cancer-is-associated.html</feedburner:origLink></item><item><title>EnrichNet: network-based gene set enrichment analysis.</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/lwIJy-ysHZs/enrichnet-network-based-gene-set.html</link><category>Protein–protein interaction</category><category>Databases</category><category>pathways</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Fri, 17 May 2013 04:11:42 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-8259703483012720162</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;br /&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
Assessing functional associations between an experimentally derived gene or protein set of interest and a database of known gene/protein sets is a common task in the analysis of large-scale functional genomics data. For this purpose, a frequently used approach is to apply an over-representation-based enrichment analysis. However, this approach has four drawbacks: (i) it can only score functional associations of overlapping gene/proteins sets; (ii) it disregards genes with missing annotations; (iii) it does not take into account the network structure of physical interactions between the gene/protein sets of interest and (iv) tissue-specific gene/protein set associations cannot be recognized.&lt;/div&gt;
&lt;h4 style="background-color: white; float: left; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin: 0px 0.25em 0px 0px; text-transform: uppercase;"&gt;
RESULTS:&lt;/h4&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
To address these limitations, we introduce an integrative analysis approach and web-application called EnrichNet. It combines a novel graph-based statistic with an interactive sub-network visualization to accomplish two complementary goals: improving the prioritization of putative functional gene/protein set associations by exploiting information from molecular interaction networks and tissue-specific gene expression data and enabling a direct biological interpretation of the results. By using the approach to analyse sets of genes with known involvement in human diseases, new pathway associations are identified, reflecting a dense sub-network of interactions between their corresponding proteins.&lt;/div&gt;
&lt;h4 style="background-color: white; float: left; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin: 0px 0.25em 0px 0px; text-transform: uppercase;"&gt;
AVAILABILITY:&lt;/h4&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
EnrichNet is freely available at &lt;a href="http://www.enrichnet.org/"&gt;http://www.enrichnet.org&lt;/a&gt;&lt;/div&gt;
&lt;/div&gt;
&lt;div class="blogger-post-footer"&gt;pub-5799224524264318&lt;/div&gt;&lt;div class="feedflare"&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/lwIJy-ysHZs" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-17T12:11:42.530+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/enrichnet-network-based-gene-set.html</feedburner:origLink></item><item><title>Does Loss of DNA Methylation and Hydroxymethylation in the Brain Lead to Loss of Memory?</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/H19ocQJnUzU/does-loss-of-dna-methylation-and.html</link><category>epigenetic</category><category>Alzheimer's disease</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Thu, 16 May 2013 14:21:47 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-6434755106222176658</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;br /&gt;&lt;/div&gt;
&lt;div class="blogger-post-footer"&gt;pub-5799224524264318&lt;/div&gt;&lt;div class="feedflare"&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/H19ocQJnUzU" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-16T22:21:47.127+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/does-loss-of-dna-methylation-and.html</feedburner:origLink></item><item><title>In myalgic encephalomyelitis/chronic fatigue syndrome, increased autoimmune activity against 5-HT is associated with immuno-inflammatory pathways and bacterial translocation.</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/u3Jz3O_k0qY/in-myalgic-encephalomyelitischronic.html</link><category>chronic fatigue syndrome</category><category>Autoimmunity</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Wed, 15 May 2013 03:48:40 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-7128795178910496371</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;span style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"&gt;Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is accompanied by activation of immuno-inflammatory pathways, increased bacterial translocation and autoimmune responses to serotonin (5-HT). Inflammation is known to damage 5-HT neurons while bacterial translocation may drive autoimmune responses. This study has been carried out to examine the autoimmune responses to 5-HT in ME/CFS in relation to inflammation and bacterial translocation.&lt;/span&gt;&lt;br /&gt;
&lt;h4 style="background-color: white; float: left; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin: 0px 0.25em 0px 0px; text-transform: uppercase;"&gt;
METHODS:&lt;/h4&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
We examined 5-HT antibodies in 117 patients with ME/CFS (diagnosed according to the centers for disease control and prevention criteria, CDC) as compared with 43 patients suffering from chronic fatigue (CF) but not fulfilling the CDC criteria and 35 normal controls. Plasma interleukin-1 (IL-1), tumor necrosis factor (TNF)α, neopterin and the IgA responses to Gram-negative bacteria were measured. Severity of physio-somatic symptoms was measured using the fibromyalgia and chronic fatigue syndrome rating scale (FF scale).&lt;/div&gt;
&lt;h4 style="background-color: white; float: left; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin: 0px 0.25em 0px 0px; text-transform: uppercase;"&gt;
RESULTS:&lt;/h4&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
The incidence of positive autoimmune activity against 5-HT was significantly higher (p&amp;lt;0.001) in ME/CFS (61.5%) than in patients with CF (13.9%) and controls (5.7%). ME/CFS patients with 5-HT autoimmune activity displayed higher TNFα, IL-1 and neopterin and increased IgA responses against LPS of commensal bacteria than those without 5-HT autoimmune activity. Anti-5-HT antibody positivity was significantly associated with increased scores on hyperalgesia, fatigue, neurocognitive and autonomic symptoms, sadness and a flu-like malaise.&lt;/div&gt;
&lt;h4 style="background-color: white; float: left; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin: 0px 0.25em 0px 0px; text-transform: uppercase;"&gt;
DISCUSSION:&lt;/h4&gt;
&lt;div style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px; margin-bottom: 0.5em;"&gt;
The results show that, in ME/CFS, increased 5-HT autoimmune activity is associated with activation of immuno-inflammatory pathways and increased bacterial translocation, factors which are known to play a role in the onset of autoimmune reactions. 5-HT autoimmune activity could play a role in the pathophysiology of ME/CFS and the onset of physio-somatic symptoms. These results provide mechanistic support for the notion that ME/CFS is a neuro-immune disorder.&lt;/div&gt;
&lt;/div&gt;
&lt;div class="blogger-post-footer"&gt;pub-5799224524264318&lt;/div&gt;&lt;div class="feedflare"&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/u3Jz3O_k0qY" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-15T11:48:40.063+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/in-myalgic-encephalomyelitischronic.html</feedburner:origLink></item><item><title>Molecular characteristics of Human Endogenous Retrovirus type-W in schizophrenia and bipolar disorder.</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/BMglR2bILHM/molecular-characteristics-of-human.html</link><category>Bipolar disorder</category><category>HERV-W</category><category>schizophrenia</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Wed, 15 May 2013 03:32:36 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-6534858850893766093</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;span style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"&gt;Epidemiological and genome-wide association studies of severe psychiatric disorders such as schizophrenia (SZ) and bipolar disorder (BD), suggest complex interactions between multiple genetic elements and environmental factors. The involvement of genetic elements such as Human Endogenous Retroviruses type 'W' family (HERV-W) has consistently been associated with SZ. HERV-W envelope gene (env) is activated by environmental factors and encodes a protein displaying inflammation and neurotoxicity. The present study addressed the molecular characteristics of HERV-W env in SZ and BD. Hundred and thirty-six patients, 91 with BD, 45 with SZ and 73 healthy controls (HC) were included. HERV-W env transcription was found to be elevated in BD (P&amp;lt;10-4) and in SZ (P=0.012) as compared with HC, but with higher values in BD than in SZ group (P&amp;lt;0.01). The corresponding DNA copy number was paradoxically lower in the genome of patients with BD (P=0.0016) or SZ (P&amp;lt;0.0003) than in HC. Differences in nucleotide sequence of HERV-W env were found between patients with SZ and BD as compared with HC, as well as between SZ and BD. The molecular characteristics of HERV-W env also differ from what was observed in Multiple Sclerosis (MS) and may represent distinct features of the genome of patients with BD and SZ. The seroprevalence for Toxoplasma gondii yielded low but significant association with HERV-W transcriptional level in a subgroup of BD and SZ, suggesting a potential role in particular patients. A global hypothesis of mechanisms inducing such major psychoses is discussed, placing HERV-W at the crossroads between environmental, genetic and immunological factors. Thus, particular infections would act as activators of HERV-W elements in earliest life, resulting in the production of an HERV-W envelope protein, which then stimulates pro-inflammatory and neurotoxic cascades. This hypothesis needs to be further explored as it may yield major changes in our understanding and treatment of severe psychotic disorders.&lt;/span&gt;&lt;/div&gt;
&lt;div class="blogger-post-footer"&gt;pub-5799224524264318&lt;/div&gt;&lt;div class="feedflare"&gt;
&lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=BMglR2bILHM:U8qb52QTR64:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=BMglR2bILHM:U8qb52QTR64:-BTjWOF_DHI"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=BMglR2bILHM:U8qb52QTR64:-BTjWOF_DHI" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=BMglR2bILHM:U8qb52QTR64:dnMXMwOfBR0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?d=dnMXMwOfBR0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=BMglR2bILHM:U8qb52QTR64:F7zBnMyn0Lo"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=BMglR2bILHM:U8qb52QTR64:F7zBnMyn0Lo" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=BMglR2bILHM:U8qb52QTR64:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=BMglR2bILHM:U8qb52QTR64:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=BMglR2bILHM:U8qb52QTR64:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=BMglR2bILHM:U8qb52QTR64:gIN9vFwOqvQ"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=BMglR2bILHM:U8qb52QTR64:gIN9vFwOqvQ" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=BMglR2bILHM:U8qb52QTR64:FKkp6kN0NBs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=BMglR2bILHM:U8qb52QTR64:FKkp6kN0NBs" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/BMglR2bILHM" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-15T11:32:36.323+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/molecular-characteristics-of-human.html</feedburner:origLink></item><item><title>dsRNA Sensing During Viral Infection: Lessons from Plants, Worms, Insects, and Mammals</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/AHAr2rd4Rlg/dsrna-sensing-during-viral-infection.html</link><category>Host-pathogen</category><category>Virus</category><category>RNA interference</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Tue, 14 May 2013 22:55:24 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-1609744288311667901</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;span style="color: #333333; font-family: Verdana, Geneva, sans-serif; font-size: 11px; line-height: 15px;"&gt;Host defense systems often rely on direct and indirect pattern recognition to sense the presence of invading pathogens. Patterns can be molecules directly produced by the pathogen or indirectly generated by changes in host parameters as a consequence of infection. Viruses are intracellular pathogens that hijack the cellular machinery to synthesize their own molecules making direct recognition of viral molecules a great challenge. Antiviral systems in prokaryotes and eukaryotes commonly exploit aberrant nucleic acid sensing to recognize virus infection as host and viral nucleic acid metabolism can greatly differ. Indeed, the generation of dsRNA is often associated with viral infection. In this review, we discuss current knowledge on the mechanisms of viral dsRNA sensing utilized by 2 important antiviral defense systems, RNA interference (RNAi) and the vertebrate immune system. The major viral sensors of the vertebrate immune systems are RIG-like receptors, while RNAi pathways depend on Dicer proteins. These 2 families of sensors share a similar helicase domain with high specificity for dsRNA, which is necessary, but not sufficient for efficient recognition by these receptors. Additional intrinsic features to the dsRNA molecule are also necessary for activation of antiviral systems. Studies utilizing synthetic ligands,&amp;nbsp;&lt;/span&gt;&lt;i style="color: #333333; font-family: Verdana, Geneva, sans-serif; font-size: 11px; line-height: 15px;"&gt;in vitro&lt;/i&gt;&lt;span style="color: #333333; font-family: Verdana, Geneva, sans-serif; font-size: 11px; line-height: 15px;"&gt;&amp;nbsp;biochemistry and reporter systems have greatly helped increase our knowledge on intrinsic features of dsRNA recognition. However, characteristics such as subcellular localization are extrinsic to the dsRNA itself, but certainly influence the recognition&amp;nbsp;&lt;/span&gt;&lt;i style="color: #333333; font-family: Verdana, Geneva, sans-serif; font-size: 11px; line-height: 15px;"&gt;in vivo&lt;/i&gt;&lt;span style="color: #333333; font-family: Verdana, Geneva, sans-serif; font-size: 11px; line-height: 15px;"&gt;. Thus, mechanisms of viral dsRNA recognition must address how cellular sensors are recruited to nucleic acids or vice versa. Accessory proteins are likely important for&amp;nbsp;&lt;/span&gt;&lt;i style="color: #333333; font-family: Verdana, Geneva, sans-serif; font-size: 11px; line-height: 15px;"&gt;in vivo&lt;/i&gt;&lt;span style="color: #333333; font-family: Verdana, Geneva, sans-serif; font-size: 11px; line-height: 15px;"&gt;recognition of extrinsic features of viral RNA, but have mostly remained undiscovered due to the limitations of previous strategies. Hence, the identification of novel components of antiviral systems must take into account the complexities involved in viral recognition&amp;nbsp;&lt;/span&gt;&lt;i style="color: #333333; font-family: Verdana, Geneva, sans-serif; font-size: 11px; line-height: 15px;"&gt;in vivo&lt;/i&gt;&lt;span style="color: #333333; font-family: Verdana, Geneva, sans-serif; font-size: 11px; line-height: 15px;"&gt;.&lt;/span&gt;&lt;br /&gt;


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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/AHAr2rd4Rlg" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-15T06:55:24.268+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/dsrna-sensing-during-viral-infection.html</feedburner:origLink></item><item><title>Upregulation of ciliary neurotrophic factor in astrocytes by aspirin: Implications for remyelination in multiple sclerosis</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/6h73t_aEUDY/upregulation-of-ciliary-neurotrophic.html</link><category>myelin</category><category>aspirin</category><category>multiple sclerosis</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Tue, 14 May 2013 14:04:00 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-7918657402647175790</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
Ciliary neurotrophic factor (CNTF) is a promyelinating trophic factor and mechanisms by which CNTF expression could be increased in the brain are poorly understood. Aspirin, acetylsalicylic acid, is one of the most widely-used analgesics. Interestingly, aspirin increased mRNA and protein expression of CNTF in primary mouse and human astrocytes in a dose- and time-dependent manner. Aspirin induced the activation of protein kinase A (PKA), but not protein kinase C (PKC). H-89, an inhibitor of PKA, abrogated aspirin-induced expression of CNTF. The activation of cAMP response element binding (CREB) protein, but not NF-kB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus CRE in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of CNTF gene via the activation of CREB. Furthermore, we demonstrate that aspirin-induced astroglial CNTF was also functionally active and that supernatants of aspirin-treated astrocytes of wild type, but not CNTF null, mice increased myelin-associated proteins in oligodendrocytes and protected oligodendrocytes from TNF-a insult. These results highlight a new and novel myelinogenic property of aspirin, which may be of benefit for multiple sclerosis and other demyelinating disorders.&lt;br /&gt;
&lt;br /&gt;&lt;/div&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/6h73t_aEUDY" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-14T22:04:00.260+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/upregulation-of-ciliary-neurotrophic.html</feedburner:origLink></item><item><title>Virological and Immunological Characteristics of Human Cytomegalovirus Infection Associated with Alzheimer's Disease.</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/lOf1eunNovg/virological-and-immunological.html</link><category>Alzheimer's disease</category><category>cytomegalovirus</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Tue, 14 May 2013 07:59:14 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-4396706731723527386</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;span style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"&gt;Serum, CSF and cryopreserved lymphocytes from subjects in the Rush Alzheimer's Disease Center Religious Orders Study were analyzed for associations between CMV infection and clinical and pathological markers of Alzheimer's Disease (AD). CMV antibody levels were associated with neurofibrillary tangles (NFT). CSF interferon-γ was only detected in seropositive subjects and was significantly associated with NFT. The percentage of senescent T cells (CD4+ or CD8+/CD28-/CD57+) was significantly higher for CMV-seropositive compared to CMV-seronegative subjects, and marginally associated with the pathologic diagnosis of AD (CD4+) or amyloid-β (CD8+). Immunocytochemical analysis showed induction of amyloid-β in human foreskin fibroblasts (HFF) infected with each of 3 clinical CMV strains. In the same subjects there was no association of&amp;nbsp;&lt;/span&gt;&lt;span class="highlight" style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"&gt;HSV-1&lt;/span&gt;&lt;span style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"&gt;&amp;nbsp;antibody levels with CMV antibody levels or clinical or pathological markers of AD.&amp;nbsp;&lt;/span&gt;&lt;span class="highlight" style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"&gt;HSV-1&lt;/span&gt;&lt;span style="background-color: white; font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;"&gt;&amp;nbsp;infection of HFF did not induce amyloid-β. These data support an association of CMV with the development of AD.&lt;/span&gt;&lt;/div&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/lOf1eunNovg" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-14T15:59:14.601+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/virological-and-immunological.html</feedburner:origLink></item><item><title>Animation: Immunology in the Gut Mucosa : Nature Immunology</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/D2XHiaZfufY/animation-immunology-in-gut-mucosa.html</link><category>immunology</category><category>microbiome</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Tue, 14 May 2013 07:16:46 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-6892731853035677707</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
The gut mucosa is the largest and most dynamic immunological environment of the body. It's often the first point of pathogen exposure and many microbes use it as a beachhead into the rest of the body. The gut immune system therefore needs to be ready to respond to pathogens but at the same time it is constantly exposed to innocuous environmental antigens, food particles and commensal microflora which need to be tolerated. Misdirected immune responses to harmless antigens are the underlying cause of food allergies and debilitating conditions such as inflammatory bowel disease. This animation introduces the key cells and molecular players involved in gut immunohomeostasis and disease. From Nature Immunology&lt;/div&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/D2XHiaZfufY" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-14T15:16:46.899+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><media:content url="http://feedproxy.google.com/~r/Polygenicblog/~5/rMJzLMkBUio/federated_f9" fileSize="2649" type="application/x-shockwave-flash" /><itunes:explicit>no</itunes:explicit><itunes:subtitle> The gut mucosa is the largest and most dynamic immunological environment of the body. It's often the first point of pathogen exposure and many microbes use it as a beachhead into the rest of the body. The gut immune system therefore needs to be ready to </itunes:subtitle><itunes:author>Chris Carter</itunes:author><itunes:summary> The gut mucosa is the largest and most dynamic immunological environment of the body. It's often the first point of pathogen exposure and many microbes use it as a beachhead into the rest of the body. The gut immune system therefore needs to be ready to respond to pathogens but at the same time it is constantly exposed to innocuous environmental antigens, food particles and commensal microflora which need to be tolerated. Misdirected immune responses to harmless antigens are the underlying cause of food allergies and debilitating conditions such as inflammatory bowel disease. This animation introduces the key cells and molecular players involved in gut immunohomeostasis and disease. From Nature Immunology pub-5799224524264318</itunes:summary><itunes:keywords>Alzheimer,s,schizophrenia,chronic,fatigue,prostate,cancer,bipolar,disorder,XMRV,Herpes,simplex,virus,multiple,sclerosis,parkinson,s,disease</itunes:keywords><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/animation-immunology-in-gut-mucosa.html</feedburner:origLink><enclosure url="http://feedproxy.google.com/~r/Polygenicblog/~5/rMJzLMkBUio/federated_f9" length="2649" type="application/x-shockwave-flash" /><feedburner:origEnclosureLink>http://c.brightcove.com/services/viewer/federated_f9?isVid=1&amp;isUI=1</feedburner:origEnclosureLink></item><item><title>Association of suicide rates and coal-fired electricity plants by county in North Carolina - Journal of Mood Disorders - </title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/b47RIHdBidw/association-of-suicide-rates-and-coal.html</link><category>depression</category><category>Pollution</category><category>coal</category><category>Suicide</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Tue, 14 May 2013 02:10:10 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-7000352441202792975</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;span style="background-color: white; color: #626262; font-family: verdana, tahoma, helvetica; font-size: 12px; line-height: 19px; text-align: justify;"&gt;Suicide, strongly associated with psychiatric conditions, also correlates with environmental pollution, likely due to quality of life factors which impact mood disorders. This ecological study evaluated the effect of the presence of a coal-fired electricity plant in a county on county suicide rates in North Carolina. Data from the 2000 US Census, 2001-2005 mortality rates from the North Carolina State Center for Health Statistics and the US Environmental Protection Agency were used in multivariable linear regression. Twenty coal plants existed in North Carolina during this study’s period. Only about one third of the population of North Carolina lived in urban areas. Seventy four percent of the population was white, and the mean population per county was nearly 48,000. About 13% of the population lived at or below the poverty level. The median household income of counties was approximately $34,000. County-level suicide rates were higher in North Carolina (12.4/100,000 population) compared to the US population (10.8/100,000). The linear regression model indicated that percent white race, median age of county population and number of coal plants per county explained 25.8% of the variance of county suicide rates. For coal plants, the linear regression model suggests that for each additional coal plant in a given county, there would be an additional 1.96 suicide per 100,000 population. The presence of a coal plant correlated with airborne levels of nickel, mercury, lead, chromium, cadmium, beryllium and arsenic. This is the first study to show that the existence of coal electricity plants is related to population-level suicide rates. Because suicide might be associated with environmental pollution, this study may help inform regulations not only of air pollutants, but also of coal electrical power plant emissions.&lt;/span&gt;&lt;/div&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/b47RIHdBidw" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-14T10:10:10.375+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/association-of-suicide-rates-and-coal.html</feedburner:origLink></item><item><title>Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/ZMLzHM_7w3Q/cross-talk-between-akkermansia.html</link><category>microbiome</category><category>obesity</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Tue, 14 May 2013 01:55:08 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-2672165614864689025</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
Obesity and type 2 diabetes are characterized by altered gut microbiota, inflammation, and gut barrier disruption. Microbial composition and the mechanisms of interaction with the host that affect gut barrier function during obesity and type 2 diabetes have not been elucidated. We recently isolated Akkermansia muciniphila, which is a mucin-degrading bacterium that resides in the mucus layer. The presence of this bacterium inversely correlates with body weight in rodents and humans. However, the precise physiological roles played by this bacterium during obesity and metabolic disorders are unknown. This study demonstrated that the abundance of A. muciniphila decreased in obese and type 2 diabetic mice. We also observed that prebiotic feeding normalized A. muciniphila abundance, which correlated with an improved metabolic profile. In addition, we demonstrated that A. muciniphila treatment reversed high-fat diet-induced metabolic disorders, including fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin resistance. A. muciniphila administration increased the intestinal levels of endocannabinoids that control inflammation, the gut barrier, and gut peptide secretion. Finally, we demonstrated that all these effects required viable A. muciniphila because treatment with heat-killed cells did not improve the metabolic profile or the mucus layer thickness. In summary, this study provides substantial insight into the intricate mechanisms of bacterial (i.e., A. muciniphila) regulation of the cross-talk between the host and gut microbiota. These results also provide a rationale for the development of a treatment that uses &lt;/div&gt;
&lt;div class="blogger-post-footer"&gt;pub-5799224524264318&lt;/div&gt;&lt;div class="feedflare"&gt;
&lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=ZMLzHM_7w3Q:MOZJyMSyALI:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=ZMLzHM_7w3Q:MOZJyMSyALI:-BTjWOF_DHI"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=ZMLzHM_7w3Q:MOZJyMSyALI:-BTjWOF_DHI" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=ZMLzHM_7w3Q:MOZJyMSyALI:dnMXMwOfBR0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?d=dnMXMwOfBR0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=ZMLzHM_7w3Q:MOZJyMSyALI:F7zBnMyn0Lo"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=ZMLzHM_7w3Q:MOZJyMSyALI:F7zBnMyn0Lo" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=ZMLzHM_7w3Q:MOZJyMSyALI:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=ZMLzHM_7w3Q:MOZJyMSyALI:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=ZMLzHM_7w3Q:MOZJyMSyALI:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=ZMLzHM_7w3Q:MOZJyMSyALI:gIN9vFwOqvQ"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=ZMLzHM_7w3Q:MOZJyMSyALI:gIN9vFwOqvQ" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=ZMLzHM_7w3Q:MOZJyMSyALI:FKkp6kN0NBs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=ZMLzHM_7w3Q:MOZJyMSyALI:FKkp6kN0NBs" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/ZMLzHM_7w3Q" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-14T09:55:08.003+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/cross-talk-between-akkermansia.html</feedburner:origLink></item><item><title>The Interaction Of Social Amoeba And Bacteria Defined By Genes</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/-CotqogI5eE/the-interaction-of-social-amoeba-and.html</link><category>genetics</category><category>Host-pathogen</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Mon, 13 May 2013 23:32:54 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-6759808001790890211</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;span style="background-color: white; color: #333333; font-family: Arial, Helvetica; font-size: 14px; line-height: 20px;"&gt;Amoeba eat bacteria and other human pathogens, engulfing and destroying them - or being destroyed by them, but how these single-cell organisms distinguish and respond successfully to different bacterial classes has been largely unexplained.&amp;nbsp;&lt;/span&gt;&lt;br /&gt;
&lt;br style="background-color: white; color: #333333; font-family: Arial, Helvetica; font-size: 14px; line-height: 20px;" /&gt;
&lt;span style="background-color: white; color: #333333; font-family: Arial, Helvetica; font-size: 14px; line-height: 20px;"&gt;In a report in the journal&amp;nbsp;&lt;/span&gt;&lt;i style="background-color: white; color: #333333; font-family: Arial, Helvetica; font-size: 14px; line-height: 20px;"&gt;Current Biology&lt;/i&gt;&lt;span style="background-color: white; color: #333333; font-family: Arial, Helvetica; font-size: 14px; line-height: 20px;"&gt;, researchers from Baylor College of Medicine use the model of the social amoeba -&lt;/span&gt;&lt;i style="background-color: white; color: #333333; font-family: Arial, Helvetica; font-size: 14px; line-height: 20px;"&gt;Dictyostelium discoideum&amp;nbsp;&lt;/i&gt;&lt;span style="background-color: white; color: #333333; font-family: Arial, Helvetica; font-size: 14px; line-height: 20px;"&gt;- to identify the genetic controls on how the amoeba differentiate the different bacteria and respond to achieve their goal of destruction.&lt;/span&gt;&lt;/div&gt;
&lt;div class="blogger-post-footer"&gt;pub-5799224524264318&lt;/div&gt;&lt;div class="feedflare"&gt;
&lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=-CotqogI5eE:htC_2NroseU:yIl2AUoC8zA"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?d=yIl2AUoC8zA" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=-CotqogI5eE:htC_2NroseU:-BTjWOF_DHI"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=-CotqogI5eE:htC_2NroseU:-BTjWOF_DHI" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=-CotqogI5eE:htC_2NroseU:dnMXMwOfBR0"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?d=dnMXMwOfBR0" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=-CotqogI5eE:htC_2NroseU:F7zBnMyn0Lo"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=-CotqogI5eE:htC_2NroseU:F7zBnMyn0Lo" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=-CotqogI5eE:htC_2NroseU:V_sGLiPBpWU"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=-CotqogI5eE:htC_2NroseU:V_sGLiPBpWU" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=-CotqogI5eE:htC_2NroseU:qj6IDK7rITs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?d=qj6IDK7rITs" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=-CotqogI5eE:htC_2NroseU:gIN9vFwOqvQ"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=-CotqogI5eE:htC_2NroseU:gIN9vFwOqvQ" border="0"&gt;&lt;/img&gt;&lt;/a&gt; &lt;a href="http://feeds.feedburner.com/~ff/Polygenicblog?a=-CotqogI5eE:htC_2NroseU:FKkp6kN0NBs"&gt;&lt;img src="http://feeds.feedburner.com/~ff/Polygenicblog?i=-CotqogI5eE:htC_2NroseU:FKkp6kN0NBs" border="0"&gt;&lt;/img&gt;&lt;/a&gt;
&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/-CotqogI5eE" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-14T07:32:54.573+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/the-interaction-of-social-amoeba-and.html</feedburner:origLink></item><item><title>Circadian patterns of gene expression in the human brain and disruption in major depressive disorder</title><link>http://feedproxy.google.com/~r/Polygenicblog/~3/Gs_8PxySpeY/circadian-patterns-of-gene-expression.html</link><category>depression</category><category>circadian</category><category>clock.</category><author>noreply@blogger.com (Chris Carter)</author><pubDate>Mon, 13 May 2013 23:17:57 PDT</pubDate><guid isPermaLink="false">tag:blogger.com,1999:blog-9080680274793928567.post-2899858319213110380</guid><description>&lt;div dir="ltr" style="text-align: left;" trbidi="on"&gt;
&lt;span style="background-color: white; color: #333333; font-family: Arial, sans-serif; font-size: 14px; line-height: 21px; text-align: justify;"&gt;A cardinal symptom of major depressive disorder (MDD) is the disruption of circadian patterns. However, to date, there is no direct evidence of circadian clock dysregulation in the brains of patients who have MDD. Circadian rhythmicity of gene expression has been observed in animals and peripheral human tissues, but its presence and variability in the human brain were difficult to characterize. Here, we applied time-of-death analysis to gene expression data from high-quality postmortem brains, examining 24-h cyclic patterns in six cortical and limbic regions of 55 subjects with no history of psychiatric or neurological illnesses (“controls”) and 34 patients with MDD. Our dataset covered ∼12,000 transcripts in the dorsolateral prefrontal cortex, anterior cingulate cortex, hippocampus, amygdala, nucleus accumbens, and cerebellum. Several hundred transcripts in each region showed 24-h cyclic patterns in controls, and &amp;gt;100 transcripts exhibited consistent rhythmicity and phase synchrony across regions. Among the top-ranked rhythmic genes were the canonical clock genes&amp;nbsp;&lt;/span&gt;&lt;em style="background-color: white; border: 0px; color: #333333; font-family: Arial, sans-serif; font-size: 14px; line-height: 21px; margin: 0px; outline-style: none; padding: 0px; text-align: justify; vertical-align: baseline;"&gt;BMAL1(ARNTL), PER1-2-3, NR1D1(REV-ERBa), DBP, BHLHE40 (DEC1)&lt;/em&gt;&lt;span style="background-color: white; color: #333333; font-family: Arial, sans-serif; font-size: 14px; line-height: 21px; text-align: justify;"&gt;, and&lt;/span&gt;&lt;em style="background-color: white; border: 0px; color: #333333; font-family: Arial, sans-serif; font-size: 14px; line-height: 21px; margin: 0px; outline-style: none; padding: 0px; text-align: justify; vertical-align: baseline;"&gt;BHLHE41(DEC2)&lt;/em&gt;&lt;span style="background-color: white; color: #333333; font-family: Arial, sans-serif; font-size: 14px; line-height: 21px; text-align: justify;"&gt;. The phasing of known circadian genes was consistent with data derived from other diurnal mammals. Cyclic patterns were much weaker in the brains of patients with MDD due to shifted peak timing and potentially disrupted phase relationships between individual circadian genes. This transcriptome-wide analysis of the human brain demonstrates a rhythmic rise and fall of gene expression in regions outside of the suprachiasmatic nucleus in control subjects. The description of its breakdown in MDD suggests potentially important molecular targets for treatment of mood disorders.&lt;/span&gt;&lt;/div&gt;
&lt;div class="blogger-post-footer"&gt;pub-5799224524264318&lt;/div&gt;&lt;div class="feedflare"&gt;
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&lt;/div&gt;&lt;img src="http://feeds.feedburner.com/~r/Polygenicblog/~4/Gs_8PxySpeY" height="1" width="1"/&gt;</description><app:edited xmlns:app="http://www.w3.org/2007/app">2013-05-14T07:17:57.110+01:00</app:edited><thr:total xmlns:thr="http://purl.org/syndication/thread/1.0">0</thr:total><feedburner:origLink>http://polygenicpathways.blogspot.com/2013/05/circadian-patterns-of-gene-expression.html</feedburner:origLink></item><media:credit role="author">Chris Carter</media:credit><media:rating>nonadult</media:rating><media:description type="plain">PolyBlog</media:description></channel></rss>
