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Maarika?LiikEmail author Malle?Paris Liina?Vahter Katrin?Gross-Paju Sulev?Haldre 《BMC neurology》2013,13(1):204
Background
Purpose of the study was to investigate alterations in midbrain serotonin transporter (SERT) binding in patients with epilepsy and symptoms of depression compared to patients with epilepsy with no symptoms of depression.Methods
We studied 12 patients with epilepsy (7 patients had focal and 5 had generalized epilepsy syndromes). The presence of self-reported symptoms of depression was assessed using Beck Depression Inventory (BDI) and the Emotional State Questionnaire (EST-Q). The binding potential of the SERT was assessed by performing brain single photon emission tomography (SPET) using the SERT radioligand 2-((2-((dimethylamino)methyl)phenyl)thio)-5-(123)iodophenylamine (123I-ADAM).Results
Seven patients had BDI and EST-Q subscale scores greater than 11 points, which was interpreted as the presence of symptoms of depression. We found that 123I-ADAM binding was not significantly different between patients with epilepsy with and without symptoms of depression. In addition, 123I-ADAM binding did not show a significant correlation to either BDI or EST-Q depression subscale scores and did not differ between patients with focal vs. generalized epilepsy.Conclusion
The results of our study failed to demonstrate alterations of SERT binding properties in patients with epilepsy with or without symptoms of depression.3.
Jürgen Innos Este Leidmaa Mari-Anne Philips Silva Sütt Aet Alttoa Jaanus Harro Sulev Kõks Eero Vasar 《Biochemical and biophysical research communications》2013,430(1):413-418
In mice, the limbic system-associated membrane protein (Lsamp) gene has been implicated in locomotion, anxiety, fear reaction, learning, social behaviour and adaptation. Human data links the LSAMP gene to several psychiatric disorders and completed suicide. Here, we investigated changes in major monoamine systems in mice lacking the Lsamp gene. First, the locomotor and rewarding effects of amphetamine were studied in Lsamp–/– mice and Lsamp+/+ mice. Second, monoamine levels in major brain regions in response to saline and amphetamine injections were measured and, third, the expression levels of dopamine system-related genes in the brain were studied in these mice. Lsamp–/– mice displayed lower sensitivity to amphetamine in the motility box. Likewise, in the place preference test, the rewarding effect of amphetamine was absent in Lsamp–/– mice. In all brain regions studied, Lsamp–/– mice displayed lower serotonin (5-HT) baseline levels, but a greater 5-HT turnover rate, and amphetamine increased the level of 5-HT and lowered 5-HT turnover to a greater extent in Lsamp–/– mice. Finally, Lsamp–/– mice had lower level of dopamine transporter (DAT) mRNA in the mesencephalon. In conclusion, Lsamp-deficiency leads to increased endogenous 5-HT-ergic tone and enhanced 5-HT release in response to amphetamine. Elevated 5-HT function and reduced activity of DAT are the probable reasons for the blunted effects of amphetamine in these mice. Lsamp–/– mice are a promising model to study the neurobiological mechanisms of deviant social behaviour and adaptation impairment observed in many psychiatric disorders. 相似文献
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Phillip J. Dugger Pedro G. Blendinger Katrin Bhning‐Gaese Lackson Chama Marta Correia D. Matthias Dehling Carine Emer Nina Farwig Evan C. Fricke Mauro Galetti Daniel García Ingo Grass Ruben Heleno Fbio A. F. Jacomassa Suelen Moraes Catherine Moran Marcia C. Muoz Eike Lena Neuschulz Larissa Nowak Augusto Piratelli Marco A. Pizo Marta Quitin Haldre S. Rogers Romn A. Ruggera Francisco Saavedra Mariano S. Snchez Rocío Snchez Vinicio Santilln Dana G. Schabo Fernanda Ribeiro da Silva Srgio Timteo Anna Traveset Maximilian G. R. Vollstdt Matthias Schleuning 《Global Ecology and Biogeography》2019,28(2):248-261
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Janeli Viil Katre Maasalu Kristina M?emets-Allas Liis Tamming Kadi L?hmussaar Mikk Tooming Sulev Ingerpuu Aare M?rtson Viljar Jaks 《Arthritis research & therapy》2015,17(1)
IntroductionDupuytren’s contracture (DC) is a chronic fibroproliferative disease of the hand, which is characterized by uncontrolled proliferation of atypical myofibroblasts at the cellular level. We hypothesized that specific areas of the DC tissue are sustaining the cell proliferation and studied the potential molecular determinants that might contribute to the formation of such niches.MethodsWe studied the expression pattern of cell proliferation marker Ki67, phosphorylated AKT (Ak mouse strain thymoma) kinase, DC-associated growth factors (connective tissue growth factor (CTGF), basic fibroblast growth factor (bFGF), insulin-like growth factor 2 (IGF-2)) and extracellular matrix components (laminins, fibronectin, collagen IV) in DC tissue and normal palmar fascia using immunofluorescence microscopy and quantitative real-time polymerase chain reaction (qPCR).ResultsWe found that proliferative cells in the DC nodules were concentrated in the immediate vicinity of small blood vessels and localized predominantly in the myofibroblast layer. Correspondingly, the DC-associated blood vessels contained increased levels of phosphorylated AKT, a hallmark of activated growth factor signaling. When studying the expression of potential activators of AKT signaling we found that the expression of bFGF was confined to the endothelium of the small blood vessels, IGF-2 was present uniformly in the DC tissue and CTGF was expressed in the DC-associated sweat gland acini. In addition, the blood vessels in DC nodules contained increased amounts of laminins 511 and 521, which have been previously shown to promote the proliferation and stem cell properties of different cell types.ConclusionsBased on our findings, we propose that in the DC-associated small blood vessels the presence of growth factors in combination with favorable extracellular matrix composition provide a supportive environment for sustained proliferation of myofibroblasts and thus the blood vessels play an important role in DC pathogenesis.
Electronic supplementary material
The online version of this article (doi:10.1186/s13075-015-0661-y) contains supplementary material, which is available to authorized users. 相似文献8.
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Lidiia?ZhytnikEmail author Katre?Maasalu Ene?Reimann Ele?Prans Sulev?K?ks Aare?M?rtson 《Human genomics》2017,11(1):19
Background
Osteogenesis imperfecta (OI) is a rare bone disorder. In 90% of cases, OI is caused by mutations in the COL1A1/2 genes, which code procollagen α1 and α2 chains. The main aim of the current research was to identify the mutational spectrum of COL1A1/2 genes in Estonian patients. The small population size of Estonia provides a unique chance to explore the collagen I mutational profile of 100% of OI families in the country.Methods
We performed mutational analysis of peripheral blood gDNA of 30 unrelated Estonian OI patients using Sanger sequencing of COL1A1 and COL1A2 genes, including all intron-exon junctions and 5′UTR and 3′UTR regions, to identify causative OI mutations.Results
We identified COL1A1/2 mutations in 86.67% of patients (26/30). 76.92% of discovered mutations were located in the COL1A1 (n = 20) and 23.08% in the COL1A2 (n = 6) gene. Half of the COL1A1/2 mutations appeared to be novel. The percentage of quantitative COL1A1/2 mutations was 69.23%. Glycine substitution with serine was the most prevalent among missense mutations. All qualitative mutations were situated in the chain domain of pro-α1/2 chains.Conclusion
Our study shows that among the Estonian OI population, the range of collagen I mutations is quite high, which agrees with other described OI cohorts of Northern Europe. The Estonian OI cohort differs due to the high number of quantitative variants and simple missense variants, which are mostly Gly to Ser substitutions and do not extend the chain domain of COL1A1/2 products.10.
Ene?ReimannEmail author Sulev?K?ks Xuan?Dung?Ho Katre?Maasalu Aare?M?rtson 《Human genomics》2014,8(1):20