<?xml version="1.0" encoding="utf-8" standalone="yes"?><rss version="2.0" xmlns:atom="http://www.w3.org/2005/Atom"><channel><title>Abstract on Michael’s Domain</title><link>https://jeltsch.org/en/tags/abstract/</link><description>Recent content in Abstract on Michael’s Domain</description><generator>Hugo</generator><language>en-us</language><copyright>Copyright © 2002 - 2026 Michael Jeltsch.</copyright><lastBuildDate>Fri, 24 Jul 2026 00:18:18 +0300</lastBuildDate><atom:link href="https://jeltsch.org/en/tags/abstract/index.xml" rel="self" type="application/rss+xml"/><item><title>Finnish abstract of our recent work about PSA (Prostate-specific antigen) in Duodecim</title><link>https://jeltsch.org/en/finnish_abstract_of_our_recent_work_about_psa_prostate_specific_antigen_in_duodecim/</link><pubDate>Sun, 25 Aug 2019 00:00:00 +0000</pubDate><guid>https://jeltsch.org/en/finnish_abstract_of_our_recent_work_about_psa_prostate_specific_antigen_in_duodecim/</guid><description>&lt;p&gt;There is a nice Finnish language abstract about our recent finding that PSA (Prostate-specific antigen) activates VEGF-C and VEGF-D in the Finnish medical journal &lt;strong&gt;Duodecim&lt;/strong&gt;: Eturauhassyövän merkkiaine PSA aktivoi syövän leviämiseen osallistuvia veri- ja imusuonikasvutekijöitä (
 &lt;a href="https://www.duodecimlehti.fi/lehti/2019/15/duo15024" target="_blank" rel="noopener noreferrer nofollow"&gt;https://www.duodecimlehti.fi/lehti/2019/15/duo15024&amp;nbsp;






 
 
 
 &lt;svg class="svg-inline--fa fas fa-up-right-from-square fa-2xs" fill="currentColor" aria-hidden="true" role="img" viewBox="0 0 512 512" overflow="visible"&gt;&lt;use href="#fas-up-right-from-square"&gt;&lt;/use&gt;&lt;/svg&gt;&lt;/a&gt;
 ). Given the dominant position of the English language in medical science (and life science in general). &lt;strong&gt;Duodecim&lt;/strong&gt; is arguably the only relevant, remaining Finnish language medical journal. &lt;strong&gt;Duodecim&lt;/strong&gt; is the publication of the homonymous Association of Finnish Medical Doctors.&lt;/p&gt;</description></item><item><title>Essentials facts about VEGF-C in lymphology</title><link>https://jeltsch.org/en/essentials_facts_about_vegf_c_in_lymphology/</link><pubDate>Fri, 05 May 2017 00:00:00 +0000</pubDate><guid>https://jeltsch.org/en/essentials_facts_about_vegf_c_in_lymphology/</guid><description>&lt;p&gt;&lt;strong&gt;Essentials facts about VEGF-C in lymphology&lt;/strong&gt;&lt;/p&gt;
&lt;p&gt;Dr. Michael Jeltsch, Adjunct Professor, University of Helsinki &amp;amp; Wihuri Research Institute, Finland, 
 &lt;a href="mailto:michael@jeltsch.org"&gt;michael@jeltsch.org&lt;/a&gt;
&lt;/p&gt;
&lt;p&gt;Vascular endothelial growth factor C (VEGF-C) is essential for the development and growth of the lymphatic vasculature. Together with VEGF-D, it forms the lymphatic subgroup within the VEGF family of growth factors, whose other members (PlGF, VEGF/VEGF-A, VEGF-B) are primarily responsible for the growth and function of blood vessels. VEGF-C was discovered as a ligand of the tyrosine kinase receptor VEGFR-3 (1) and its specific effect on lymph vessels was first described in 1997 (2,3). About one-third of hereditary lymphedema cases in humans result from mutations in genes involved in VEGF-C signaling (4). The complete absence of VEGF-C leads to death during embryogenesis (5). Likely for this reason, clinical cases of hereditary lymphedema are characterised by a partial inactivation of the signal transduction. VEGFR-3 (6) is affected in most cases, but mutations of the hereditary lymphedema are described or suspected for all components of the VEGF-C signal transduction described below, partly within a multifactorial inheritance.&lt;/p&gt;</description></item></channel></rss>