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This essay discusses modernisation from the point of view of the reformist drive to create increased opportunities for consumption in state socialist society from the 1960s onward. Within these reforms competition was a means to accelerate entrepreneurialism and creativity that were needed to reorient production to better fulfil the need for increased consumption. Competition was essentially a market-type of behaviour in a non-market-oriented society. In the urge to revitalise the communist system, the use of market models grew over time and eventually competition contributed to the gradual transformation of values widely across society and became a significant factor openly questioning the basis of the whole system.

This book presents a comprehensive reassessment of Europe in the Cold War period, 1945-91. Contrary to popular belief, it shows that relations between East and West were based not only on confrontation and mutual distrust, but also on collaboration. The authors reveal that - despite opposing ideologies - there was in fact considerable interaction and exchange between different Eastern and Western actors (such states, enterprises, associations, organisations and individuals) irrespective of the Iron Curtain. This book challenges both the traditional understanding of the East-West juxtaposition and the relevancy of the Iron Curtain. Covering the full period, and taking into account a range of spheres including trade, scientific-technical co-operation, and cultural and social exchanges, it reveals how smaller countries and smaller actors in Europe were able to forge and implement their agendas within their own blocs. The books suggests that given these lower-level actors engaged in mutually beneficial cooperation, often running counter to the ambitions of the bloc-leaders, the rules of Cold War interaction were not, in fact, exclusively dictated by the superpowers. Notes on Contributors Glossary of Terms and Abbreviations List of tables Acknowledgments Introduction: The Cold War from a New Perspective - Sari Autio-Sarasmo and Katalin Miklóssy 1. The Soviet Union’s Acquisition of Western Technology after Stalin: Some Thoughts on People and Connections - Philip Hanson 2. Economic Interest in Soviet Post-War Policy on Finland - Tatiana Androsova 3. CoCom and Neutrality: Western Export Control Policies, Finland and the Cold War, 1949–1958 - Niklas Jensen-Eriksen 4. Knowledge through the Iron Curtain - Soviet Scientific-Technical Cooperation with Finland and West Germany - Sari Autio-Sarasmo 5. Learning from the French: The Modernisation of Soviet Winemaking, 1956-1961 - Jeremy Smith 6. Soft Contacts through the Iron Curtain - Riikka Nisonen-Trnka 7. Internal Transfer of Cybernetics and Informality in the Soviet Union: The Case of Lithuania - Eglė Rindzevičiūtė 8. New Advantages of Old Kinship Ties. Finnish–Hungarian Interactions in the 1970s - Katalin Miklóssy 9. Soviet Women, Cultural Exchange and the Women’s International Democratic Federation - Melanie Ilic 10. Overcoming Cold War Boundaries at the World Youth Festivals - Pia Koivunen 11. Room to Manoeuvre? National Interests and Coalition-Building in the CMEA, 1969–1974 - Suvi Kansikas Bibliography Index Sari Autio-Sarasmo is a Senior Researcher at the Aleksanteri Institute (Finnish Centre of Russian and Eastern European Studies), University of Helsinki and Adjunct Professor at the University of Tampere, Finland. Katalin Miklóssy is a Researcher at the Aleksanteri Institute, University of Helsinki and Adjunct Professor at the University of Helsinki, Finland.

This chapter investigates how two small countries, situated on opposite sides of the Iron Curtain, developed a new type of interaction during the 1970s. The decade can be characterized by the détente in East-West relations, with the general relaxation culminating in the negotiation process leading to the Helsinki Conference on Security and Cooperation in Europe (CSCE). The CSCE brought a significant change to the Cold War bipolarity by introducing a safe arena where representatives of Eastern and Western countries could meet more freely. The CSCE provided an institutional framework for multilateralism that particularly served the interests of the small countries with limited elbowroom. For these countries, the CSCE offered – for the first time in the Cold War period – the opportunity to cross the Iron Curtain and establish political contacts that were not regulated by the bloc-leader superpowers. By performing actively on this multilateral stage, these countries were able to further their national aims more effectively. Therefore, keeping the CSCE process alive just to maintain this arena of interaction became a goal that was shared in common by the smaller countries.

From the perspective of historiography, the collapse of the communist system in Eastern Europe in 1989 and the disintegration of the Soviet Union in 1991 were perceived as the beginning of a new era that would bring fundamental changes in the interpretation of this period. It seemed that the epoch of grand narratives of law-governed historical processes had also come to an end. Francis Fukuyama even declared the end of history, now that the struggle of the Cold War had culminated in the victory of the righteous, Western liberal democracy and market economy. Almost the same conclusion was reached by Karl Popper, who claimed that the notion of history as a suprapersonal power with its own direction had suffered a decisive defeat with the termination of the Cold War.1 There were high hopes of an impending revolution in historiography due to the supposedly vanishing bipolar mindset and to the opening of the Eastern archives, providing scholars with new evidence.2 The end of the Cold War thus represented a unique opportunity to expand our understanding of the Cold War era. In practice, however, the newly available materials seldom generated new approaches, or even new research questions.

Objective Accumulation of mitochondria underlies T-cell dysfunction in systemic lupus erythematosus (SLE). Mitochondrial turnover involves endosomal traffic regulated by HRES-1/Rab4, a small GTPase that is overexpressed in lupus T cells. Therefore, we investigated whether (1) HRES-1/Rab4 impacts mitochondrial homeostasis and (2) Rab geranylgeranyl transferase inhibitor 3-PEHPC blocks mitochondrial accumulation in T cells, autoimmunity and disease development in lupus-prone mice. Methods Mitochondria were evaluated in peripheral blood lymphocytes (PBL) of 38 SLE patients and 21 healthy controls and mouse models by flow cytometry, microscopy and western blot. MRL/lpr mice were treated with 125 μg/kg 3-PEHPC or 1 mg/kg rapamycin for 10 weeks, from 4 weeks of age. Disease was monitored by antinuclear antibody (ANA) production, proteinuria, and renal histology. Results Overexpression of HRES-1/Rab4 increased the mitochondrial mass of PBL (1.4-fold; p=0.019) and Jurkat cells (2-fold; p=0.000016) and depleted the mitophagy initiator protein Drp1 both in human (−49%; p=0.01) and mouse lymphocytes (−41%; p=0.03). Drp1 protein levels were profoundly diminished in PBL of SLE patients (−86±3%; p=0.012). T cells of 4-week-old MRL/lpr mice exhibited 4.7-fold over-expression of Rab4A (p=0.0002), the murine homologue of HRES-1/Rab4, and depletion of Drp1 that preceded the accumulation of mitochondria, ANA production and nephritis. 3-PEHPC increased Drp1 (p=0.03) and reduced mitochondrial mass in T cells (p=0.02) and diminished ANA production (p=0.021), proteinuria (p=0.00004), and nephritis scores of lupus-prone mice (p<0.001). Conclusions These data reveal a pathogenic role for HRES-1/Rab4-mediated Drp1 depletion and identify endocytic control of mitophagy as a treatment target in SLE.

HRES-1/Rab4 is a small GTPase that regulates endocytic recycling. It has been colocalized to mitochondria and the mechanistic target of rapamycin (mTOR), a suppressor of autophagy. Since the autophagosomal membrane component microtubule-associated protein light chain 3 (LC3) is derived from mitochondria, we investigated the impact of HRES-1/Rab4 on the formation of LC3(+) autophagosomes, their colocalization with HRES-1/Rab4 and mitochondria, and the retention of mitochondria during autophagy induced by starvation and rapamycin. HRES-1/Rab4 exhibited minimal baseline colocalization with LC3, which was enhanced 22-fold upon starvation or 6-fold upon rapamycin treatment. Colocalization of HRES-1/Rab4 with mitochondria was increased >2-fold by starvation or rapamycin. HRES-1/Rab4 overexpression promoted the colocalization of mitochondria with LC3 upon starvation or rapamycin treatment. A dominant-negative mutant, HRES-1/Rab4(S27N) had reduced colocalization with LC3 and mitochondria upon starvation but not rapamycin treatment. A constitutively active mutant, HRES-1/Rab4(Q72L) showed diminished colocalization with LC3 but promoted the partitioning of mitochondria with LC3 upon starvation or rapamycin treatment. Phosphorylation-resistant mutant HRES-1/Rab4(S204Q) showed diminished colocalization with LC3 but increased partitioning to mitochondria. A newly discovered C-terminally truncated native isoform, HRES-1/Rab4(1-121), showed enhanced localization to LC3 and mitochondria without starvation or rapamycin treatment. HRES-1/Rab4(1-121) increased the formation of LC3(+) autophagosomes in resting cells, while other isoforms promoted autophagosome formation upon starvation. HRES-1/Rab4, HRES-1/Rab4(1-121), HRES-1/Rab4(Q72L) and HRES-1/Rab4(S204Q) promoted the accumulation of mitochondria during starvation. The specificity of HRES-1/Rab4-mediated mitochondrial accumulation is indicated by its abrogation by dominant-negative HRES-1/Rab4(S27N) mutation. The formation of interconnected mitochondrial tubular networks was markedly enhanced by HRES-1/Rab4(Q72L) upon starvation, which may contribute to the retention of mitochondria during autophagy. The present study thus indicates that HRES-1/Rab4 regulates autophagy through promoting the formation of LC3(+) autophagosomes and the preservation of mitochondria.

HRES-1/Rab4 is a small GTPase that regulates endocytic recycling. It has been colocalized to mitochondria and the mechanistic target of rapamycin (mTOR), a suppressor of autophagy. Since the autophagosomal membrane component microtubule-associated protein light chain 3 (LC3) is derived from mitochondria, we investigated the impact of HRES-1/Rab4 on the formation of LC3.sup.+ autophagosomes, their colocalization with HRES-1/Rab4 and mitochondria, and the retention of mitochondria during autophagy induced by starvation and rapamycin. HRES-1/Rab4 exhibited minimal baseline colocalization with LC3, which was enhanced 22-fold upon starvation or 6-fold upon rapamycin treatment. Colocalization of HRES-1/Rab4 with mitochondria was increased >2-fold by starvation or rapamycin. HRES-1/Rab4 overexpression promoted the colocalization of mitochondria with LC3 upon starvation or rapamycin treatment. A dominant-negative mutant, HRES-1/Rab4.sup.S27N had reduced colocalization with LC3 and mitochondria upon starvation but not rapamycin treatment. A constitutively active mutant, HRES-1/Rab4.sup.Q72L showed diminished colocalization with LC3 but promoted the partitioning of mitochondria with LC3 upon starvation or rapamycin treatment. Phosphorylation-resistant mutant HRES-1/Rab4.sup.S204Q showed diminished colocalization with LC3 but increased partitioning to mitochondria. A newly discovered C-terminally truncated native isoform, HRES-1/Rab4.sup.1-121, showed enhanced localization to LC3 and mitochondria without starvation or rapamycin treatment. HRES-1/Rab4.sup.1-121 increased the formation of LC3.sup.+ autophagosomes in resting cells, while other isoforms promoted autophagosome formation upon starvation. HRES-1/Rab4, HRES-1/Rab4.sup.1-121, HRES-1/Rab4.sup.Q72L and HRES-1/Rab4.sup.S204Q promoted the accumulation of mitochondria during starvation. The specificity of HRES-1/Rab4-mediated mitochondrial accumulation is indicated by its abrogation by dominant-negative HRES-1/Rab4.sup.S27N mutation. The formation of interconnected mitochondrial tubular networks was markedly enhanced by HRES-1/Rab4.sup.Q72L upon starvation, which may contribute to the retention of mitochondria during autophagy. The present study thus indicates that HRES-1/Rab4 regulates autophagy through promoting the formation of LC3.sup.+ autophagosomes and the preservation of mitochondria.