Aims: This is the first study carried out to describe the role of fetal microchimerism (FM) in the pathogenesis of uterine cancer. The prevalence and concentration of male fetal microchimeric cells (FMCs) were examined in endometrial tissues in relation to subtypes of uterine cancer, and the histological grade and stage of the tumor. FM occurrence was analyzed in relation to risk factors including hypertension, obesity, type 2 diabetes, dyslipidemia, age at cancer diagnosis and patient pregnancy history. The prevalence and concentration of FMCs were examined in endometrial tissues using real-time polymerase chain reaction, SRY and b-globin sequences as markers for male fetal FMCs and total DNA. The studied group involved 47 type 1 endometrial cancers, 28 type 2 endometrial cancers and 41 benign uterine diseases. Results: While the prevalence of FM was decreased only in type 1 endometrial cancer, compared to benign uterine disorders (38.3% vs.70.7%; OR = 0.257, 95% CI: 0.105 to 0.628, p = 0.003), FMC concentrations did not differ within examined groups. The lower FM prevalence was detected in low grade (grade 1 and grade 2) endometrioid cancer (38.3% vs. 70.7%, OR = 0.256, 95% CI: 0.105 to 0.627, p = 0.003) and in FIGO 1 tumors (40.7% vs. 70.7%, OR= 0.285, 95% CI: 0.120 to 0.675, p = 0.004). No correlation between FM prevalence or FMC concentrations and risk factors was demonstrated. Conclusions: A lower prevalence of male FM seemed to be associated with better prognoses in uterine cancer based on tumor subtype, histological grade and stage of the tumor. and Ilona Hromadnikova, Katerina Kotlabova, Petra Pirkova, Pavla Libalova, Zdenka Vernerova, Bohuslav Svoboda, Eduard Kucera
Cíl studie: Cílem studie bylo zjištění vztahů mezi manifestací tinnitu, nálezem na sluchových evokovaných potenciálech a genetickým pozadím u receptoru pro gamaaminomáselnou kyselinu typu A (GABA(A) receptor), podporující desinhibiční hypotézu vzniku tinnitu. Soubor a metodika: Bylo vyšetřeno 131 pacientů z hlediska sluchové ztráty, provedena kvantifikace tinnitu, sluchové evokované potenciály střední latence (MLR) a kmenové sluchové evokované potenciály (BAEP) a dále stanovení genotypu (CA)n repetitivní sekvence pro beta‑3 podjednotku GABA(A) receptoru. Následně byly hledány vztahy mezi jednotlivými výsledky a manifestací tinnitu. Výsledky: Byla nalezena korelace tinnitus skóre s amplitudovým poměrem vln V/III v BAEP (R = 0,22, p < 0,001) a s průměrným sluchovým prahem (R = 0,22, p = 0,17). Rovněž byla nalezena korelace tinnitus skóre s amplitudou vlny PA v MLR (R = 0,31–0,37; p < 0,001). Výsledky MLR neukázaly žádný vztah k průměrnému sluchovému prahu. U skupiny s kratší anamnézou tinnitu (méně než devět měsíců) byl prokázán rozdíl v manifestaci tinnitu na genotypu pro (CA)n repetitivní sekvenci genu pro beta‑3 podjednotku GABA(A) receptoru (p = 0,002). Tento výsledek byl rovněž konzistentní s rozložením amplitudy vlny PA v dané subpopulaci. Závěr: Tyto výsledky svědčí o existenci dvou hlavních regulačních mechanizmů vzniku tinnitu: první, který je závislý na velikosti sluchové ztráty, je na úrovni mozkového kmene, zatímco druhý je na úrovni korové s možnou souvislostí s genotypem (CA)n repetitivní sekvence pro beta‑3 podjednotku GABA(A) receptoru., Study aim:Study objective was to explore associations between manifestation of tinnitus, auditory evoked potentials and genetic background of gamma‑aminobutyric acid type A (GABA(A) receptors) to support the disinhibited feedback hypothesis of tinnitus generation. Materials and methods: A population of 131 patients was assessed for severity of hearing loss, quantification of tinnitus, mid‑latency responses (MLR) and brainstem auditory evoked potentials (BAEP), and (CA)n tandem repeat polymorphism in GABA(A) Beta‑3 subunit gene to establish any correlation with manifestation of tinnitus. Results: It was observed that tinnitus score correlates with V/III amplitude ratio in BAEP (R = 0.22, p < 0.001) and with mean pure tone audiometry (PTA) threshold (R = 0.22, p = 0.017). Analysis of the MLR results showed a significant correlation between the PA wave amplitude and the tinnitus score (R = 0.31–0.37; p < 0.001). MLR result analysis showed no statistically significant correlation between the wave amplitudes and the mean auditory threshold. An analysis of a subgroup with shorter clinical history (less than nine months) revealed a statistically significant difference in the tinnitus score in relation to the genotype of (CA)n tandem repeat of the GABRß3 receptor subunit gene (p = 0.002). This result was also consistent with the distribution of the PA wave amplitude in the given subpopulation. Conclusion: Our findings indicate existence of two main regulatory mechanisms of tinnitus generation: first, the brainstem mechanism is dependent on the severity of the hearing loss; second, the cortical mechanism is likely to be dependent on the genotype of (CA)n tandem repeat in GABA(A) beta‑3 subunit gene., and J. Rottenberg, M. Zallmann, R. Kostrica, M. Jurajda, T. Talach