ENERGY, ASYMMETRIC DEPENDENCE, AND NATIONAL SECURITY: EXPLAINING HUNGARY AND POLAND’S DIFFERENT RESPONSES TO THE WAR IN UKRAINE

62 pagesOn February 24th, 2022, Russia invaded parts of eastern Ukraine, significantly escalating the war that began in 2014 with the Russian annexation of Crimea. Since the invasion, the European Union (EU) has rallied support from its member countries to support Ukraine with military arms, by imposing sweeping sanctions on Russia, and by continuing to support Ukrainian territorial integrity. Hungary has been a unique exception in the EU, withholding support for Ukraine in a number of ways. Poland, a country with a similar recent political history and ideological leadership, has done the opposite, arguably supporting Ukraine the most of any EU country. This paper uses a most similar systems design method approach to examine what is causing these two countries to respond so differently to the invasion of Ukraine. This paper finds that the difference in each country’s energy infrastructure is the most likely explanation for their difference in response to the war in Ukraine. With these findings, it discusses new factors that international alliances should consider when constructing their security policies

Regulation of insulin-like growth factor-II expression and its role in autocrine growth of human neuroblastoma cells

Insulin-like growth factor-II (IGF-II) is highly expressed in fetal tissues and may act as an autocrine growth factor during early embryogenesis. The SH-SY5Y human neuroblastoma cell line also expresses IGF-II and its receptors and responds to exogenous IGF-II with increased DNA synthesis, cell division, and neuritic outgrowth. For this study, we tested the hypothesis that IGF-II mediates autocrine growth of SH-SY5Y cells in serum-free media. SH-SY5Y cells plated at high densities proliferated in serum-free media, whereas sparsely plated cells did not. IGF-II mRNA levels increased within 24 hours of serum deprivation and were associated with increased immunoreactive IGF-II protein. Exogenous addition of IGF-II increased 3 H-TdR incorporation and cell number in a dose- and time-dependent fashion. By nuclear labelling experiments using 5-Bromo-2′ deoxyuridine (BrdU), we detected a twofold higher percentage of S phase nuclei after a 24-hour incubation in IGF-II. Treatment of SH-SY5Y cells with anti-IGF-II antibodies in serum-free media inhibited cell proliferation, and this inhibition was partially overcome by the addition of increasing concentrations of IGF-II. Collectively, our results indicate that IGF-II mediates an autocrine growth mechanism in SH-SY5Y cells that is associated with increased IGF-II expression. © 1993 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/49884/1/1041550210_ftp.pd

B7-1 drives TGF-β stimulated pancreatic carcinoma cell migration and expression of EMT target genes.

B7-1 proteins are routinely expressed on the surface of antigen presenting cells (APC) and within the innate immune system. They function to establish a biologically optimal and dynamic balance between immune activation and inhibition or self-tolerance. Interactions between B7-1 and its receptors, which include CD28, CTLA4 and PD-L1, contribute to both stimulatory as well as inhibitory or homeostatic regulation. In the current study, we investigated whether the tumor-promoting actions of transforming growth factor beta (TGF-β) disrupted this equilibrium in pancreatic cancer to promote malignant progression and an enhanced means to evade immune detection. The data show that B7-1 is (i) upregulated following treatment of pancreatic carcinoma cells with TGF-β; (ii) induced by TGF-β via both Smad2/3-dependent and independent pathways; (iii) required for pancreatic tumor cell in vitro migration/invasion; and (iv) necessary for TGF-β regulated epithelial-mesenchymal transition (EMT) through induction of Snail family members. Results from the proposed studies provide valuable insights into mechanisms whereby TGF-β regulates both the innate immune response and intrinsic properties of pancreatic tumor growth