Traces and routes of old roads on Carpathian Foothills escarpment

Ewolucja sieci komunikacyjnej jest odzwierciedleniem przemian społecznych i gospodarczych zachodzących na Pogórzu Karpackim. Pierwotna sieć głównych szlaków komunikacyjnych uzależniona była ściśle od warunków terenowych. Wraz z rozwojem gospodarczym regionu i postępem technicznym zaczęto budować drogi na terenach wcześniej uznanych za niekorzystne. Nowe drogi poprowadzono blisko sieci osadniczej zlokalizowanej w dolinach. W efekcie najstarsze główne trakty wytyczone pierwotnie po wierzchowinach zostały zdegradowane do roli dojazdów do pól bądź całkowicie wyłączone z użytkowania. Występujące współcześnie w krajobrazie Pogórza opuszczone wcięcia drogowe starych szlaków są jedyny śladem dawnego układu komunikacyjnego.Road network evolution reflects social and economical transformation on Carpathians Foothills. Original network of main communication routes was strictly conditioned by the local relief. Along with economical and technological development new roads were built - on the areas previously considered as impassable. They were led along the valleys where the settlement was located. In effect the oldest main roads, which were originally led across the tophills, are today degraded to access roads or even completely excluded from use. Abandoned road cuts found today on foothills landscape are the traces of old communication network

Akt is transferred to the nucleus of cells treated with apoptin, and it participates in apoptin-induced cell death

Abstract. Objectives: The phosphatidylinositol 3-kinase (PI3-K)/Akt pathway is well known for the regulation of cell survival, proliferation, and some metabolic routes. Meterials and Methods: In this study, we document a novel role for the PI3-K/Akt pathway during cell death induced by apoptin, a tumour-selective inducer of apoptosis. Results: We show for the first time that apoptin interacts with the p85 regulatory subunit, leading to constitutive activation of PI3-K. The inhibition of PI3-K activation either by chemical inhibitors or by genetic approaches severely impairs cell death induced by apoptin. Downstream of PI3-K, Akt is activated and translocated to the nucleus together with apoptin. Direct interaction between apoptin and Akt is documented. Co-expression of nuclear Akt significantly potentiates cell death induced by apoptin. Thus, apoptin-facilitated nuclear Akt, in contrast to when in its cytoplasmic pool, appears to be a positive regulator, rather than repressor of apoptosis. Conclusions: Our observations indicate that PI3-K/Akt pathways have a dual role in both survival and cell death processes depending on the stimulus. Nuclear Akt acts as apoptosis stimulator rather than as a repressor, as it likely gains access to a new set of substrates in the nucleus. The implicated link between survival and cell death pathways during apoptosis opens new pharmacological opportunities to modulate apoptosis in cancer, for example through the manipulation of Akt's cellular localization

Correction of Writing disorders of the 1st year pupils with Phonetically Phonemic Disorders

Abstract. Objectives: The phosphatidylinositol 3-kinase (PI3-K)/Akt pathway is well known for the regulation of cell survival, proliferation, and some metabolic routes. Meterials and Methods: In this study, we document a novel role for the PI3-K/Akt pathway during cell death induced by apoptin, a tumour-selective inducer of apoptosis. Results: We show for the first time that apoptin interacts with the p85 regulatory subunit, leading to constitutive activation of PI3-K. The inhibition of PI3-K activation either by chemical inhibitors or by genetic approaches severely impairs cell death induced by apoptin. Downstream of PI3-K, Akt is activated and translocated to the nucleus together with apoptin. Direct interaction between apoptin and Akt is documented. Co-expression of nuclear Akt significantly potentiates cell death induced by apoptin. Thus, apoptin-facilitated nuclear Akt, in contrast to when in its cytoplasmic pool, appears to be a positive regulator, rather than repressor of apoptosis. Conclusions: Our observations indicate that PI3-K/Akt pathways have a dual role in both survival and cell death processes depending on the stimulus. Nuclear Akt acts as apoptosis stimulator rather than as a repressor, as it likely gains access to a new set of substrates in the nucleus. The implicated link between survival and cell death pathways during apoptosis opens new pharmacological opportunities to modulate apoptosis in cancer, for example through the manipulation of Akt's cellular localization