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  1. +0 −27 Peslyak-P1.html
  2. +2 −0 readme.md
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-<!DOCTYPE html PUBLIC "-//W3C//DTD XHTML 1.0 Transitional//EN"
- "http://www.w3.org/TR/xhtml1/DTD/xhtml1-transitional.dtd">
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-<html xmlns="http://www.w3.org/1999/xhtml" xml:lang="en" lang="en">
-<head>
- <meta http-equiv="Content-Type" content="text/html; charset=utf-8"/>
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- <title>Peslyak Psoriasis Paper</title>
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-<body>
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-<h1>Model of Pathogenesis of Psoriasis</h1>
-<h2>Mikhail Peslyak</h2>
-<p>With additional notes, editorial, and annotations by Duane Johnson. Last updated Jan 9, 2012.</p>
-
-<div id="introduction">
- <h2>Introduction</h2>
- <p id="intro1">The self-renewal of the Epidermis is a normal process: New cells are born in the basal layer. They mature, vary, and migrate toward the outside and form the external cornified layer. Then they die away and exfoliate. The standard lifecycle of an epidermal cell for areas of skin with average thickness (the renewal period) is 20-25 days. Psoriasis accelerates self-renewal--cells live only 4-10 days (Baker 2000, Iizuka 2004, Weinstein 1985). Cells migrating outside have no time to differentiate and they aren't quite functional. Psoriatic plaques have a red shade--they are tender, covered by white flakes due to the accelerated loss of cells, and they are much thicker.</p>
- <p id="intro2">Psoriasis isn't contagious. There are various types of psoriasis (codes are given according to ICD-10): <a href="http://apps.who.int/classifications/icd10/browse/2010/en#/L40.0">vulgaris or plaque (L40.0)</a>, <a href="http://apps.who.int/classifications/icd10/browse/2010/en#/L40.8">flexural or inverse (L40.83-4)</a>, <a href="http://apps.who.int/classifications/icd10/browse/2010/en#/L40.8">erythrodermic (L40.85)</a>, <a href="http://apps.who.int/classifications/icd10/browse/2010/en#/L40.1">pustular (L40.1-3, L40.82)</a>, <a href="http://apps.who.int/classifications/icd10/browse/2010/en#/L40.4">guttate (L40.4)</a>. Chronic plaque psoriasis (CPs) is the most frequent type (more than 80% of total number of cases). Up to 15% of psoriatics also suffer from <a href="http://apps.who.int/classifications/icd10/browse/2010/en#/L40.5">psoriatic arthritis (L40.5)</a>. Psoriasis is present in about 2-3% of the human population (120-180 million people). 4-6 million people are newly diagnosed with psoriasis every year. The disease can appear at birth or in extreme old age. Psoriasis is a chronic disease, so there are periods of aggravation and remission. Sometimes there appears to be no cause for periods of remission, and sometimes aggravation can be decreased as a result of treatment. Serious psoriasis can result in disability. The onset and progress of psoriasis is similar in men and women. African Americans, Indians, Chinese and Japanese suffer from psoriasis less frequently, however, and Eskimos don't suffer from psoriasis at all (Piruzian 2006, Giardina 2004).</p>
- <p id="intro3">Psoriasis is registered in the "Online Mendelian Inheritance in Man" as <a href="http://omim.org/entry/177900">OMIM*177900</a>. Psoriasis is a disease with a hereditary predisposition: concordance between uniovular twins is 70%. If one parent suffers from psoriasis, children are diagnosed with the disease in 15-25% of cases; if both parents suffer from psoriasis children are diagnosed with the disease in more than 40-60% of cases. The interrelation of <a href="http://omim.org/entry/142840#0001">allele HLA-Cw*0602</a> (chromosome 6p21) and psoriasis of the first type (characterized by its early beginning) has been demonstrated (Weisenseel 2002). This allele is found in more than 60% of psoriatics (not more than 15% of healthy people). Locuses of other chromosomes have weaker interrelations (Piruzian 2006, Giardina 2004). Psoriasis never manifests only in the presence of genetic defects--external exposure is necessary for the beginning and maintenance of psoriasis. Infections, skin traumas, stress, reaction to medications, climatic changes and other causes can provoke the onset of psoriasis or its aggravation (Molochkov 2007, Bos 2005, Fry 2007b, Gudjonsson 2004).</p>
- <p id="intro4">Accelerated proliferation of keratinocytes (skin cells) is likely to be caused by erroneous actions of various antibacterial protection mechanisms of the skin. The influence of beta-hemolitic streptococci (first of all causing tonsillar infections) on the initialization and aggravation of psoriasis is avowed (Molochkov 2007, Khairutdinov 2007, Baker 2006a, Baker 2003, Baker 2000, Fry 2007b, Gudjonsson 2004). There is no uniform point of view on etiology and pathogenesis of psoriasis. Researchers offer various models (Baltabaev 2005, Korotkii & Peslyak 2005, Khardikova 2000, Baker 2000, Baker 2006b, Bos 2005, Danilenko 2008, Gudjonsson 2004, Gyurcsovics 2003, Iizuka 2004, Lowes 2007, Majewski 2003, Nestle 2005b, Nickoloff 2000, Sabat 2007).</p>
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2 readme.md
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# What is this project? #
An attempt to make sense of a very interesting paper on [Psoriasis](http://en.wikipedia.org/wiki/Psoriasis) called "[Model of pathogenesis of psoriasis](http://arxiv.org/abs/1110.0584)", published first in Russian, and then in English.
+The online version of these notes can be accessed [here](http://canadaduane.github.com/peslyak-psoriasis-paper/Peslyak-P1.html).
+
## Is it a retranslation? ##
Not really. While I have taken editorial liberties in making certain places sound more like colloquial English, I'm not really attempting a retranslation. For starters, I don't know Russian. And secondarily, I don't know the author. Rather, I want to be more of a student of Mikhail Peslyak's paper, and so this project is an attempt to understand enough of his paper so that I can make sense of it, and perhaps help myself or others who have psoriatic symptoms (e.g. arthritic, epidermic, or otherwise).

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