Väitös (kliininen fysiologia ja isotooppilääketiede): MSc Arghavan Jahandideh
Aika
10.1.2025 klo 12.00 - 16.00
MSc Arghavan Jahandideh esittää väitöskirjansa ”MOLECULAR IMAGING OF AUTOIMMUNE MYOCARDITIS USING NEW PET TRACERS IN EXPERIMENTAL MODELS” julkisesti tarkastettavaksi Turun yliopistossa perjantaina 10.01.2025 klo 12.00 (TYKS, T-sairaala, Risto Lahesmaa -sali, Hämeentie 11, Turku).
Vastaväittäjänä toimii professori Kirsi Timonen (Sairaala Nova, Jyväskylä) ja kustoksena professori Antti Saraste (Turun yliopiston PET-keskus ja TYKS). Tilaisuus on englanninkielinen. Väitöksen alana on kliininen fysiologia ja isotooppilääketiede.
Väitöskirja yliopiston julkaisuarkistossa: https://urn.fi/URN:ISBN:978-951-29-9995-8 (kopioi linkki selaimeen).
***
Tiivistelmä väitöstutkimuksesta:
Myocarditis, an inflammatory heart condition, is difficult to diagnose because its symptoms can mimic many other illnesses. A common tool to detect heart inflammation is positron emission tomography/computed tomography (PET/CT) imaging with a sugar-like tracer called 18F-FDG. However, this tracer can also be taken up by healthy heart muscle, making it difficult to distinguish between healthy and inflamed tissue. To address this problem, my study explored the use of three alternative PET tracers that might more accurately detect active inflammation in the heart.
I tested three PET tracers for their ability to target inflammation in heart tissue in an experimental model of myocarditis: 18F-FOL, which binds to a specific receptor on activated immune cells; [68Ga]Ga-NODAGA-RGD, which targets molecules involved in new blood vessel formation; and [68Ga]Ga-DOTA-Siglec-9, which identifies proteins associated with white blood cell movement. PET/CT imaging showed that all three tracers had high uptake in inflamed heart tissue, whereas there was only minimal background signal in healthy heart tissue. The results were further confirmed with tissue samples of patients with myocarditis associated with sarcoidosis, a chronic systemic autoimmune disease.
This research found that 18F-FOL, [68Ga]Ga-NODAGA-RGD, and [68Ga]Ga-DOTA-Siglec-9 are promising PET tracers to detect active heart inflammation, and encourage further development as a possible diagnostic tools in human myocarditis.
Vastaväittäjänä toimii professori Kirsi Timonen (Sairaala Nova, Jyväskylä) ja kustoksena professori Antti Saraste (Turun yliopiston PET-keskus ja TYKS). Tilaisuus on englanninkielinen. Väitöksen alana on kliininen fysiologia ja isotooppilääketiede.
Väitöskirja yliopiston julkaisuarkistossa: https://urn.fi/URN:ISBN:978-951-29-9995-8 (kopioi linkki selaimeen).
***
Tiivistelmä väitöstutkimuksesta:
Myocarditis, an inflammatory heart condition, is difficult to diagnose because its symptoms can mimic many other illnesses. A common tool to detect heart inflammation is positron emission tomography/computed tomography (PET/CT) imaging with a sugar-like tracer called 18F-FDG. However, this tracer can also be taken up by healthy heart muscle, making it difficult to distinguish between healthy and inflamed tissue. To address this problem, my study explored the use of three alternative PET tracers that might more accurately detect active inflammation in the heart.
I tested three PET tracers for their ability to target inflammation in heart tissue in an experimental model of myocarditis: 18F-FOL, which binds to a specific receptor on activated immune cells; [68Ga]Ga-NODAGA-RGD, which targets molecules involved in new blood vessel formation; and [68Ga]Ga-DOTA-Siglec-9, which identifies proteins associated with white blood cell movement. PET/CT imaging showed that all three tracers had high uptake in inflamed heart tissue, whereas there was only minimal background signal in healthy heart tissue. The results were further confirmed with tissue samples of patients with myocarditis associated with sarcoidosis, a chronic systemic autoimmune disease.
This research found that 18F-FOL, [68Ga]Ga-NODAGA-RGD, and [68Ga]Ga-DOTA-Siglec-9 are promising PET tracers to detect active heart inflammation, and encourage further development as a possible diagnostic tools in human myocarditis.
Viestintä