| 1. |
- Järnum, Hanna, et al.
(författare)
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Longitudinal MRI study of cortical thickness, perfusion, and metabolite levels in major depressive disorder
- 2011
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Ingår i: Acta Psychiatrica Scandinavica. - : Wiley. - 0001-690X .- 1600-0447. ; 124:6, s. 435-446
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To determine whether patients with major depressive disorder (MDD) display morphologic, functional, and metabolic brain abnormalities in limbic-cortical regions at a baseline magnetic resonance (MR) scan and whether these changes are normalized in MDD patients in remission at a follow-up scan. Method: A longitudinal 3.0-Tesla (T) magnetic resonance imaging (MRI) study was carried out with cortical thickness measurements with a surface-based approach, perfusion measurements with three-dimensional (3D) pseudo-continuous arterial spin labeling (pCASL), and spectroscopy (1H-MRS) measurements in the anterior cingulate cortex (ACC) with water as an internal reference adjusted for cerebrospinal fluid content. We examined 23 MDD patients and 26 healthy controls. MDD patients underwent a baseline MRI at inclusion and were invited to a follow-up scan when they were in remission or after a 6-month follow-up period. Results: Major findings were a significantly thinner posterior cingulate cortex in non-remitters than in remitters, a significant decrease in perfusion in the frontal lobes and the ACC in non-remitters compared with healthy controls at baseline and significantly reduced N-acetylaspartate, myo-inositol, and glutamate levels in MDD patients compared with healthy controls at baseline. Conclusion: Using novel MRI techniques, we have found abnormalities in cerebral regions related to cortical-limbic pathways in MDD patients.
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| 2. |
- Järnum, S., et al.
(författare)
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Effects of IdeS on HLA-SAB, C1q-SAB and CDC-XM
- 2018
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Ingår i: American Journal of Transplantation. - : John Wiley & Sons. - 1600-6135 .- 1600-6143. ; 18:S4: Oral Abstracts, s. 370-371
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 3. |
- Safavi, Setareh, et al.
(författare)
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HSP90 inhibition blocks ERBB3 and RET phosphorylation in myxoid/round cell liposarcoma and causes massive cell death in vitro and in vivo
- 2016
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Ingår i: OncoTarget. - : Impact Journals, LLC. - 1949-2553. ; 7:1, s. 433-445
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Tidskriftsartikel (refereegranskat)abstract
- Myxoid sarcoma (MLS) is one of the most common types of malignant soft tissue tumors. MLS is characterized by the FUS-DDIT3 or EWSR1-DDIT3 fusion oncogenes that encode abnormal transcription factors. The receptor tyrosine kinase (RTK) encoding RET was previously identified as a putative downstream target gene to FUS-DDIT3 and here we show that cultured MLS cells expressed phosphorylated RET together with its ligand Persephin. Treatment with RET specific kinase inhibitor Vandetanib failed to reduce RET phosphorylation and inhibit cell growth, suggesting that other RTKs may phosphorylate RET. A screening pointed out EGFR and ERBB3 as the strongest expressed phosphorylated RTKs in MLS cells. We show that ERBB3 formed nuclear and cytoplasmic complexes with RET and both RTKs were previously reported to form complexes with EGFR. The formation of RTK hetero complexes could explain the observed Vandetanib resistence in MLS. EGFR and ERBB3 are clients of HSP90 that help complex formation and RTK activation. Treatment of cultured MLS cells with HSP90 inhibitor 17-DMAG, caused loss of RET and ERBB3 phosphorylation and lead to rapid cell death. Treatment of MLS xenograft carrying Nude mice resulted in massive necrosis, rupture of capillaries and hemorrhages in tumor tissues. We conclude that complex formation between RET and other RTKs may cause RTK inhibitor resistance. HSP90 inhibitors can overcome this resistance and are thus promising drugs for treatment of MLS/RCLS.
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