20 research outputs found
Metahistorical Scepticism in Aleksei Goldenveizerβs Chronicle of Everyday Life in Kyiv, 1917β1921
The article was submitted on 19.07.2018.This article analyzes the memoir of a Russian-speaking Jewish lawyer, Aleksei Goldenveiser (1890β1979), as a source on the history of Kyiv during the revolutionary period (1917β1921). His work stands out among other reminiscences about the Revolution in Ukraine because of the authorβs unprecedented attention to details of everyday life, along with his self-identification as simply an apolitical resident of Kyiv. Especially striking is the authorβs satirical, even acerbic, tone in the description of all the political regimes that came to power in Kyiv during the Revolution: Ukrainian, White, and Bolshevik. This article proposes to conceptualize Goldenveizerβs position as metahistorical skepticism or as a strategy of conscious resistance to grand narratives, which is grounded in identification with the local and a focus on everydayness. It argues the Goldenveizer developed this narrative strategy following the failure, in the summer of 1917, of the political project of a civic, multinational, and urban identity. Although Goldenveizer served on the Executive Committee of United Civic Organizations in Kyiv and, briefly, on the Small Rada of the Ukrainian Central Rada, he felt like an outsider in politics of the day and described it as an astute bystander rather than participant. Because of this position, he was the first to note the reversal of imperial hierarchies and the creation of a new category: βnational minorities.β At the same time, Goldenveizer consistently attempted in his memoir to check his own political and cultural biases, as one can see in his ambiguous treatment of the Ukrainian language and the Ukrainian national movement.Π‘ΡΠ°ΡΡΡ ΠΏΠΎΡΠ²ΡΡΠ΅Π½Π° Π°Π½Π°Π»ΠΈΠ·Ρ Π²ΠΎΡΠΏΠΎΠΌΠΈΠ½Π°Π½ΠΈΠΉ ΡΡΡΡΠΊΠΎΡΠ·ΡΡΠ½ΠΎΠ³ΠΎ Π΅Π²ΡΠ΅ΠΉΡΠΊΠΎΠ³ΠΎ Π°Π΄Π²ΠΎΠΊΠ°ΡΠ° ΠΠ»Π΅ΠΊΡΠ΅Ρ ΠΠΎΠ»ΡΠ΄Π΅Π½Π²Π΅ΠΉΠ·Π΅ΡΠ° (1890β1979) ΠΊΠ°ΠΊ ΠΈΡΡΠΎΡΠ½ΠΈΠΊΠ° ΠΏΠΎ ΠΈΡΡΠΎΡΠΈΠΈ ΠΠΈΠ΅Π²Π° ΡΠ΅Π²ΠΎΠ»ΡΡΠΈΠΎΠ½Π½ΠΎΠ³ΠΎ ΠΏΠ΅ΡΠΈΠΎΠ΄Π° (1917β1921). ΠΠ³ΠΎ ΡΡΡΠ΄ Π²ΡΠ΄Π΅Π»ΡΠ΅ΡΡΡ ΡΡΠ΅Π΄ΠΈ Π΄ΡΡΠ³ΠΈΡ
Π²ΠΎΡΠΏΠΎΠΌΠΈΠ½Π°Π½ΠΈΠΉ ΠΎ ΡΠ΅Π²ΠΎΠ»ΡΡΠΈΠΈ Π½Π° Π£ΠΊΡΠ°ΠΈΠ½Π΅ Π±Π»Π°Π³ΠΎΠ΄Π°ΡΡ Π±Π΅ΡΠΏΡΠ΅ΡΠ΅Π΄Π΅Π½ΡΠ½ΠΎΠΌΡ Π²Π½ΠΈΠΌΠ°Π½ΠΈΡ ΠΊ Π΄Π΅ΡΠ°Π»ΡΠΌ ΠΏΠΎΠ²ΡΠ΅Π΄Π½Π΅Π²Π½ΠΎΠΉ ΠΆΠΈΠ·Π½ΠΈ, Π° ΡΠ°ΠΊΠΆΠ΅ ΡΠ°ΠΌΠΎΠΈΠ΄Π΅Π½ΡΠΈΡΠΈΠΊΠ°ΡΠΈΠΈ Π°Π²ΡΠΎΡΠ° ΠΏΡΠΎΡΡΠΎ ΠΊΠ°ΠΊ Π°ΠΏΠΎΠ»ΠΈΡΠΈΡΠ½ΠΎΠ³ΠΎ ΠΆΠΈΡΠ΅Π»Ρ ΠΠΈΠ΅Π²Π°. Π‘Π°ΡΠΈΡΠΈΡΠ΅ΡΠΊΠΈΠΉ, Π΄Π°ΠΆΠ΅ ΠΆΠ΅Π»ΡΠ½ΡΠΉ ΡΠΎΠ½ Π°Π²ΡΠΎΡΠ° ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎ Π·Π°ΠΌΠ΅ΡΠ΅Π½ Π² ΠΎΠΏΠΈΡΠ°Π½ΠΈΡΡ
Π²ΡΠ΅Ρ
ΠΏΠΎΠ»ΠΈΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠ΅ΠΆΠΈΠΌΠΎΠ², ΠΊΠΎΡΠΎΡΡΠ΅ ΠΏΡΠΈΡ
ΠΎΠ΄ΠΈΠ»ΠΈ ΠΊ Π²Π»Π°ΡΡΠΈ Π² ΠΠΈΠ΅Π²Π΅ Π²ΠΎ Π²ΡΠ΅ΠΌΡ ΡΠ΅Π²ΠΎΠ»ΡΡΠΈΠΈ: ΡΠΊΡΠ°ΠΈΠ½ΡΠΊΠΎΠ³ΠΎ, Π±Π΅Π»ΠΎΠ³ΠΎ ΠΈ Π±ΠΎΠ»ΡΡΠ΅Π²ΠΈΡΡΡΠΊΠΎΠ³ΠΎ. ΠΠ²ΡΠΎΡ ΠΏΡΠ΅Π΄Π»Π°Π³Π°Π΅Ρ ΠΊΠΎΠ½ΡΠ΅ΠΏΡΡΠ°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°ΡΡ ΠΏΠΎΠ·ΠΈΡΠΈΡ ΠΠΎΠ»ΡΠ΄Π΅Π½Π²Π΅ΠΉΠ·Π΅ΡΠ° ΠΊΠ°ΠΊ Β«ΠΌΠ΅ΡΠ°ΠΈΡΡΠΎΡΠΈΡΠ΅ΡΠΊΠΈΠΉ ΡΠΊΠ΅ΠΏΡΠΈΡΠΈΠ·ΠΌΒ», ΠΈΠ»ΠΈ ΡΡΡΠ°ΡΠ΅Π³ΠΈΡ ΡΠΎΠ·Π½Π°ΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ ΡΠΎΠΏΡΠΎΡΠΈΠ²Π»Π΅Π½ΠΈΡ Π±ΠΎΠ»ΡΡΠΈΠΌ Π½Π°ΡΡΠ°ΡΠΈΠ²Π°ΠΌ, ΠΊΠΎΡΠΎΡΠ°Ρ Π±Π°Π·ΠΈΡΡΠ΅ΡΡΡ Π½Π° ΠΈΠ΄Π΅Π½ΡΠΈΡΠΈΠΊΠ°ΡΠΈΠΈ Ρ Π»ΠΎΠΊΠ°Π»ΡΠ½ΡΠΌ ΠΈ ΡΠΎΠΊΡΡΠ΅ Π½Π° ΠΏΠΎΠ²ΡΠ΅Π΄Π½Π΅Π²Π½ΠΎΡΡΠΈ. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ ΠΠΎΠ»ΡΠ΄Π΅Π½Π²Π΅ΠΉΠ·Π΅Ρ Π²ΡΡΠ°Π±ΠΎΡΠ°Π» ΡΡΡ Π½Π°ΡΡΠ°ΡΠΈΠ²Π½ΡΡ ΡΡΡΠ°ΡΠ΅Π³ΠΈΡ ΠΏΠΎΡΠ»Π΅ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΡ Π»Π΅ΡΠΎΠΌ 1917 Π³. ΠΏΠΎΠ»ΠΈΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΏΡΠΎΠ΅ΠΊΡΠ° Π³ΡΠ°ΠΆΠ΄Π°Π½ΡΠΊΠΎΠΉ ΠΌΠ½ΠΎΠ³ΠΎΠ½Π°ΡΠΈΠΎΠ½Π°Π»ΡΠ½ΠΎΠΉ Π³ΠΎΡΠΎΠ΄ΡΠΊΠΎΠΉ ΠΈΠ΄Π΅Π½ΡΠΈΡΠ½ΠΎΡΡΠΈ. Π₯ΠΎΡΡ ΠΠΎΠ»ΡΠ΄Π΅Π½Π²Π΅ΠΉΠ·Π΅Ρ Π±ΡΠ» ΡΠ»Π΅Π½ΠΎΠΌ ΠΡΠΏΠΎΠ»Π½ΠΈΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ ΠΊΠΎΠΌΠΈΡΠ΅ΡΠ° ΠΠ±ΡΠ΅Π΄ΠΈΠ½Π΅Π½Π½ΡΡ
ΠΎΠ±ΡΠ΅ΡΡΠ²Π΅Π½Π½ΡΡ
ΠΎΡΠ³Π°Π½ΠΈΠ·Π°ΡΠΈΠΉ ΠΠΈΠ΅Π²Π°, Π° ΡΠ°ΠΊΠΆΠ΅ ΠΠ°Π»ΠΎΠΉ ΡΠ°Π΄Ρ Π£ΠΊΡΠ°ΠΈΠ½ΡΠΊΠΎΠΉ ΡΠ΅Π½ΡΡΠ°Π»ΡΠ½ΠΎΠΉ ΡΠ°Π΄Ρ, Π² ΠΏΠΎΠ»ΠΈΡΠΈΠΊΠ΅ ΡΠΎΠ³ΠΎ Π²ΡΠ΅ΠΌΠ΅Π½ΠΈ ΠΎΠ½ ΡΡΠ²ΡΡΠ²ΠΎΠ²Π°Π» ΡΠ΅Π±Ρ Π°ΡΡΡΠ°ΠΉΠ΄Π΅ΡΠΎΠΌ ΠΈ ΠΎΠΏΠΈΡΡΠ²Π°Π» Π΅Π΅ ΠΊΠ°ΠΊ Π½Π°Π±Π»ΡΠ΄Π°ΡΠ΅Π»ΡΠ½ΡΠΉ ΠΏΠΎΡΡΠΎΡΠΎΠ½Π½ΠΈΠΉ, Π° Π½Π΅ ΡΡΠ°ΡΡΠ½ΠΈΠΊ. ΠΠ»Π°Π³ΠΎΠ΄Π°ΡΡ ΡΠ°ΠΊΠΎΠΉ ΠΏΠΎΠ·ΠΈΡΠΈΠΈ ΠΎΠ½ ΠΏΠ΅ΡΠ²ΡΠΌ ΠΎΠ±ΡΠ°ΡΠΈΠ» Π²Π½ΠΈΠΌΠ°Π½ΠΈΠ΅ Π½Π° ΠΏΠΎΠ»Π½ΡΡ ΠΏΠ΅ΡΠ΅ΡΡΠ°Π½ΠΎΠ²ΠΊΡ ΠΈΠΌΠΏΠ΅ΡΡΠΊΠΈΡ
ΠΈΠ΅ΡΠ°ΡΡ
ΠΈΠΉ ΠΈ ΡΠΎΠ·Π΄Π°Π½ΠΈΠ΅ Π½ΠΎΠ²ΠΎΠΉ ΠΊΠ°ΡΠ΅Π³ΠΎΡΠΈΠΈ Β«Π½Π°ΡΠΈΠΎΠ½Π°Π»ΡΠ½ΡΡ
ΠΌΠ΅Π½ΡΡΠΈΠ½ΡΡΠ²Β». Π ΡΠΎ ΠΆΠ΅ Π²ΡΠ΅ΠΌΡ ΠΠΎΠ»ΡΠ΄Π΅Π½Π²Π΅ΠΉΠ·Π΅Ρ ΠΏΠΎΡΡΠΎΡΠ½Π½ΠΎ ΡΡΠ°ΡΠ°Π»ΡΡ Π½Π΅ Π΄ΠΎΠΏΡΡΡΠΈΡΡ, ΡΡΠΎΠ±Ρ Π΅Π³ΠΎ ΠΊΡΠ»ΡΡΡΡΠ½ΡΠ΅ ΠΈ ΠΏΠΎΠ»ΠΈΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΡΠ΅Π΄ΠΏΠΎΡΡΠ΅Π½ΠΈΡ ΡΠ΄Π΅Π»Π°Π»ΠΈ ΡΠ΅ΠΊΡΡ ΠΎΠ΄Π½ΠΎΡΡΠΎΡΠΎΠ½Π½ΠΈΠΌ, ΡΡΠΎ ΠΏΡΠΈΠ²Π΅Π»ΠΎ ΠΊ Π½Π΅ΠΎΠ΄Π½ΠΎΠ·Π½Π°ΡΠ½ΠΎΠΉ ΠΎΡΠ΅Π½ΠΊΠ΅ ΡΠΊΡΠ°ΠΈΠ½ΡΠΊΠΎΠ³ΠΎ ΡΠ·ΡΠΊΠ° ΠΈ ΡΠΊΡΠ°ΠΈΠ½ΡΠΊΠΎΠ³ΠΎ Π½Π°ΡΠΈΠΎΠ½Π°Π»ΡΠ½ΠΎΠ³ΠΎ Π΄Π²ΠΈΠΆΠ΅Π½ΠΈΡ
Cell competition in intratumoral and tumor microenvironment interactions
Tumors are complex cellular and acellular environments within which cancer clones are under continuous selection pressures. Cancer cells are in a permanent mode of interaction and competition with each other as well as with the immediate microenvironment. In the course of these competitive interactions, cells share information regarding their general state of fitness, with less-fit cells being typically eliminated via apoptosis at the hands of those cells with greater cellular fitness. Competitive interactions involving exchange of cell fitness information have implications for tumor growth, metastasis, and therapy outcomes. Recent research has highlighted sophisticated pathways such as Flower, Hippo, Myc, and p53 signaling, which are employed by cancer cells and the surrounding microenvironment cells to achieve their evolutionary goals by means of cell competition mechanisms. In this review, we discuss these recent findings and explain their importance and role in evolution, growth, and treatment of cancer. We further consider potential physiological conditions, such as hypoxia and chemotherapy, that can function as selective pressures under which cell competition mechanisms may evolve differently or synergistically to confer oncogenic advantages to cancer
Antigen presentation plays positive roles in the regenerative response to cardiac injury in zebrafish
In contrast to adult mammals, adult zebrafish can fully regenerate injured cardiac tissue, and this regeneration process requires an adequate and tightly controlled immune response. However, which components of the immune response are required during regeneration is unclear. Here, we report positive roles for the antigen presentation-adaptive immunity axis during zebrafish cardiac regeneration. We find that following the initial innate immune response, activated endocardial cells (EdCs), as well as immune cells, start expressing antigen presentation genes. We also observe that T helper cells, a.k.a. Cd4(+) T cells, lie in close physical proximity to these antigen-presenting EdCs. We targeted Major Histocompatibility Complex (MHC) class II antigen presentation by generating cd74a; cd74b mutants, which display a defective immune response. In these mutants, Cd4(+) T cells and activated EdCs fail to efficiently populate the injured tissue and EdC proliferation is significantly decreased. cd74a; cd74b mutants exhibit additional defects in cardiac regeneration including reduced cardiomyocyte dedifferentiation and proliferation. Notably, Cd74 also becomes activated in neonatal mouse EdCs following cardiac injury. Altogether, these findings point to positive roles for antigen presentation during cardiac regeneration, potentially involving interactions between activated EdCs, classical antigen-presenting cells, and Cd4(+) T cells
Pleiotropic effects of laminar flow and statins depend on the KrΓΌppel-like factor-induced lncRNA MANTIS
AIMS: To assess the functional relevance and therapeutic potential of the pro-angiogenic long non-coding RNA MANTIS in vascular disease development. METHODS AND RESULTS: RNA sequencing, CRISPR activation, overexpression, and RNAi demonstrated that MANTIS, especially its Alu-element, limits endothelial ICAM-1 expression in different types of endothelial cells. Loss of MANTIS increased endothelial monocyte adhesion in an ICAM-1-dependent manner. MANTIS reduced the binding of the SWI/SNF chromatin remodelling factor BRG1 at the ICAM-1 promoter. The expression of MANTIS was induced by laminar flow and HMG-CoA-reductase inhibitors (statins) through mechanisms involving epigenetic rearrangements and the transcription factors KLF2 and KLF4. Mutation of the KLF binding motifs in the MANTIS promoter blocked the flow-induced MANTIS expression. Importantly, the expression of MANTIS in human carotid artery endarterectomy material was lower compared with healthy vessels and this effect was prevented by statin therapy. Interestingly, the protective effects of statins were mediated in part through MANTIS, which was required to facilitate the atorvastatin-induced changes in endothelial gene expression. Moreover, the beneficial endothelial effects of statins in culture models (spheroid outgrowth, proliferation, telomerase activity, and vascular organ culture) were lost upon knockdown of MANTIS. CONCLUSION: MANTIS is tightly regulated by the transcription factors KLF2 and KLF4 and limits the ICAM-1 mediated monocyte adhesion to endothelial cells and thus potentially atherosclerosis development in humans. The beneficial effects of statin treatment and laminar flow are dependent on MANTIS