Our project group validated microRNA quantitative measurement methodology together with Medical Faculty of Tuzla BiH by including let-7b, miR-126, miR-9, and miR-19a evaluation in different samples of complex lung cancer model. We included 50 patients and 45 controls. We demonstrated significantly decreased expression levels of let-7b and miR-126 in tumor tissue and surrounding tissue in comparison to corresponding non-tumor tissue or lung tissue from the control group.
COBISS.SI-ID: 30144729
We investigated the regulatory iNKT cells in 47 corticosteroid-naïve patients with sarcoidosis and in 8 control subjects. We used multi-parameter flow cytometry on bronchoalveolar lavage fluid. The frequencies of iNKT cells were significantly lower in patients with sarcoidosis in comparison to control subjects. Moreover, lower invariant NKT cell frequencies in patients with sarcoidosis significantly correlated with exaggerated BALF lymphocytosis and CD4 T cell response.
COBISS.SI-ID: 26317273
Our aim was to compare the quantitative expression levels of genetic factors, which influence regulatory Th1, Th2 and T suppressor cells in non-anaphylactic model of immunotherapy with HDM (mite). We also include the expression of components involved in IgE-mediated signaling. This study was done together with Medical Faculty of Zagreb, Croatia. Thirty-nine HDM-allergic patients who completed a 3- to 5-year course of HDM SCIT, 20 HDM-allergic controls and 25 healthy controls participated in the study. The mRNA levels of T-BET, GATA-3, FOXP3, FcεRI, Syk, PI3K and SHIP were quantified by real-time RT-PCR using PAXGen blood samples. Expression levels of FOXP3 and GATA-3 decreased and T-BET levels increased in both treated patients and in healthy controls compared to untreated patients. The IgE-mediated pathway kinases Syk and PI3K exhibited reduced expression, whereas SHIP phosphatase levels were elevated in both treated patients and healthy controls relative to untreated patients. This immunotherapy resulted in an up regulation of genetic factors significant for regulatory Th1-response and down regulation of genetic factors significant for regulatory Th2-response.
COBISS.SI-ID: 29977049
Our aim was to evaluate whether the expression of FcεRI receptor have a role in the induction of short-term VIT protection. The methodology was based on quantitative real-time RT-PCR by using paired PAXGen blood samples. This study was done together with Pediatric Clinic in Ljubljana. We included 60 adults and 48 children. FcεRI gene expression was assessed at the beginning and just before the first maintenance dose (MD) of 100 μg of ultra-rush VIT (day 5) and at the beginning, during buildup, and just before the first MD of 70 μg and of 100 μg of semi-rush VIT (weeks 1-2 and 5). We showed that FcεRI gene expression was decreased in 34-100% of subjects, with different dynamics between VIT protocols. This suppression of FcεRI expression could be highly relevant for the development of early protective mechanisms.
COBISS.SI-ID: 30233305
Hereditary angioedema (HAE) is a autosomal dominant genetic disease. HAE is caused by mutations affecting the C1 inhibitor gene, SERPING1 and a nationwide survey identified nine unrelated families with HAE in Slovenia, among whom 17 individuals from eight families were recruited for genetic analyses. Genetic studies were carried out using PCR and sequencing to detect SERPING1 mutations in promoter, noncoding exon 1, the 7 coding exons, and exon-intron boundaries. Multiplex ligation-dependent probe amplification was performed in order to search for large deletions/duplications in SERPING1 gene. A mutation responsible for HAE was identified in patients from seven families with the disease. In HAE type I families, one previously reported substitution (Gln67Stop, c.265C)T) and four novel mutations were identified. The new mutations included two missense substitutions, Ser128Phe (c.449C)T) and Glu429Lys (c.1351G)A), together with two frameshift mutations, indel (c.49delGinsTT) and deletion (c.593_594delCT). Both families with HAE type II harbored the two well-known substitutions affecting the arginyl residue at the reactive center in exon 8, Arg444Cys (c.1396C)T) and Arg444His (c.1397G)A), respectively. In one patient only the homozygous variant g.566T)C (c.-21T)C) was identified. Our study identified four novel mutations in the Slovenian HAE population, highlighting the heterogeneity of mutations in the SERPING1 gene causing C1 inhibitor deficiency and HAE.
COBISS.SI-ID: 4586815