Symposium lectures on-line

Most of the lectures of the Symposium were published on-line. You can find the video presentations at the top of each lecture abstract. We hope to complete the whole on-line program in the near feature.

Pictures of Semmelweis Symposium 2008

You can find the pictures of all the three days of Semmelweis Symposium 2008 here.

Lecture of Prof. Sándor Kovács

You can find the whole video-presentation of Prof. Sándor Kovács at "Lectures" on the following page.

Summary

More than 500 participants from 20 countries attended Semmelweis Symposium 2008. You can find a detailed summary of the event here. A summary of press echo in the Hungarian media you can find here.

Poster abstracts

You can find the poster abstracts of Semmelweis Symposium 2008 here.

Scientific Program - printable version

You can download the printable version of the Scientific Program here.

Cardiovascular pharmacogenomics course

According to the program of Semmelweis Symposium, Peter Pokreisz (Katholieke Universiteit Leuven, Belgium) will give a lecture (in Hungarian) on cGMP regulatory mechanisms in cardiology at 18:00 Wednesday, 26 November.

Abstract submission period extended

The deadline for abstract submission was extended until 18 November 2008. More detailes on the Abstract submission form.

On-line registration

Participation in the program of Semmelweis Symposium 2008 is free.
However, completion the on-line registration form is required to attend the Symposium.

Abstract submission for poster presentation

Abstracts for poster presentation are welcome to the Semmelweis Symposium. Deadline for abstract submission  is 15 November. More detailes on the Abstract Submission Form.

PhD course registration

Semmelweis Symposium 2008 was accredited by the School of Doctoral Studies of Semmelweis University. Students attending all the three days of the Symposium will get 2 PhD credits.

OFTEX registration

Semmelweis Symposium 2008 was registred to the OFTEX system. Colleagues attending all the three days of the Symposium will get 20 OFTEX credits. For detailed information look for SE-TK/2008-07/00383 at www.oftex.hu .

Final program

The final program of the Symposium has been completed. For detailes visit to the Scientific Program pages.

Current trends in Cardiology

This year cardiology is in the focus of Semmelweis Symposium. The members of the Heart Center take the opportunity to kindly invite you to this event.

Purpose: Ghrelin is a newly discovered gastrointestinal endocrine regulatory peptide with multiple functions. Its production has recently been described in various tissues including the myocardium where it may have cardioprotective effects. However, contradictory data are available on the vascular actions of ghrelin in different organs and species. The aim of this study was to characterize the direct effect of the peptide on canine coronary bed and to evaluate the role of the 1a-type growth hormone secretagouge receptor (GHS-R1a) in the effect of ghrelin on coronary arterioles. Methods: Presence of GHS-R1a in the coronary arterioles was investigated with immunohistochemistry. Vascular responses to ghrelin (30-100-300 nM) of isolated and cannulated canine coronary arterioles (n=16, mean inner diameter +/- SEM: 210 +/- 16 microm) were recorded by videomicroscopy as changes of vessel diameter with or without preconstriction evoked by the thromboxane mimetic agent U46619 (1 microM). Experiments were also performed in the presence of the GHS-R1a antagonist D-Lys3-GHRP-6. Results: Positive immunostaining for GHS-R1a was detected in the wall of small intramural coronary arteries and arterioles. On coronary arterioles with spontaneous tone ghrelin did not elicit significant effect on vessel diameter. However, in the case of elevated vascular tone (25+/-4% decrease in diameter) ghrelin evoked significant vasoconstriction with a maximum of 33+/-9 % of the effect of U46619 (p<0.05) which was not abolished by the blockade of GHS-R1a. Conclusions: The results suggest that ghrelin induces tone-dependent constriction of canine coronary arterioles. This effect – despite their presence in coronary arterioles – is likely not mediated by GHS-R1a.