Winning War in a Globalized World: Utilizing Women & Gender Initiatives in 21st Century Conflict

Three thousand years of recorded history has reserved warfighting for men and, in 2017, we continue to rely on ideas of hegemonic masculinity to understand who participates in war. However, women have played a vital role in the context of warfare from its inception. In the twenty-first century, women’s service is critical to the types of conflicts militaries regularly confront – specifically, counter insurgency and peacekeeping operations. The intersection of gender and security today provides new routes to peaceful prosperity globally. Applying gender initiatives to militaries – whether it means creating a gender balanced force, the integration of women into combat arms, or the adoption of gender perspectives by male soldiers – could fundamentally shift culture and revolutionize the organization. Indeed, the structure of armed forces, the demographics of military elites, and the soldier’s orientation to operational imperatives will all change as a result. Taking seriously the concept of gender in the military context, as I argue in this paper, constitutes a Revolution in Military Affairs (RMA). This alternative understanding of how militaries approach war, in direct opposition to how militaries have engaged historically, bring new possibilities to the forefront. In this paper, I will review the literature on RMA and introduce a re-conceptualized RMA to include gender and culture as critical variables. Concrete examples from the Iraq and Afghanistan wars will illustrate the significant advantages this new paradigm brings, from increased operational effectiveness to the maintenance of security in a globalized world

Overexpression of extracellular superoxide dismutase reduces acute radiation induced lung toxicity

BACKGROUND: Acute RT-induced damage to the lung is characterized by inflammatory changes, which proceed to the development of fibrotic lesions in the late phase of injury. Ultimately, complete structural ablation will ensue, if the source of inflammatory / fibrogenic mediators and oxidative stress is not removed or attenuated. Therefore, the purpose of this study is to determine whether overexpression of extracellular superoxide dismutase (EC-SOD) in mice ameliorates acute radiation induced injury by inhibiting activation of TGFβ1 and downregulating the Smad 3 arm of its signal transduction pathway. METHODS: Whole thorax radiation (single dose, 15 Gy) was delivered to EC-SOD overexpressing transgenic (XRT-TG) and wild-type (XRT-WT) animals. Mice were sacrificed at 1 day, 1 week, 3, 6, 10 and 14 weeks. Breathing rates, right lung weights, total/differential leukocyte count, activated TGFβ1 and components of its signal transduction pathway (Smad 3 and p-Smad 2/3) were assessed to determine lung injury. RESULTS: Irradiated wild-type (XRT-WT) animals exhibited time dependent increase in breathing rates and right lung weights, whereas these parameters were significantly less increased (p < 0.05) at 3, 6, 10 and 14 weeks in irradiated transgenic (XRT-TG) mice. An inflammatory response characterized predominantly by macrophage infiltration was pronounced in XRT-WT mice. This acute inflammation was significantly attenuated (p < 0.05) in XRT-TG animals at 1, 3, 6 and 14 weeks. Expression of activated TGFβ1 and components of its signal transduction pathway were significantly reduced (p < 0.05) at later time-points in XRT-TG vs. XRT-WT. CONCLUSION: This study shows that overexpression of EC-SOD confers protection against RT-induced acute lung injury. EC-SOD appears to work, in part, via an attenuation of the macrophage response and also decreases TGFβ1 activation with a subsequent downregulation of the profibrotic TGFβ pathway

Conceptualizing the civil-military gap: a research note

The authors suggest that scholars mean very different things when they refer to the civil-military gap. To illustrate the point, the authors conceptualize the gap in terms of four distinct ideal types and show that scholars have referred to each variant as the civil-military gap at different times. Though the authors recognize that the four ideal types-cultural, demographic, policy preference, and institutional-are not always mutually exclusive, the authors suggest that they are divergent enough to warrant consideration as distinct variants and that their specification can enhance the civil-military relations literature by helping scholars identify and untangle the causes and effects of the gap

Overexpression of extracellular superoxide dismutase reduces acute radiation induced lung toxicity

Abstract Background Acute RT-induced damage to the lung is characterized by inflammatory changes, which proceed to the development of fibrotic lesions in the late phase of injury. Ultimately, complete structural ablation will ensue, if the source of inflammatory / fibrogenic mediators and oxidative stress is not removed or attenuated. Therefore, the purpose of this study is to determine whether overexpression of extracellular superoxide dismutase (EC-SOD) in mice ameliorates acute radiation induced injury by inhibiting activation of TGFβ1 and downregulating the Smad 3 arm of its signal transduction pathway. Methods Whole thorax radiation (single dose, 15 Gy) was delivered to EC-SOD overexpressing transgenic (XRT-TG) and wild-type (XRT-WT) animals. Mice were sacrificed at 1 day, 1 week, 3, 6, 10 and 14 weeks. Breathing rates, right lung weights, total/differential leukocyte count, activated TGFβ1 and components of its signal transduction pathway (Smad 3 and p-Smad 2/3) were assessed to determine lung injury. Results Irradiated wild-type (XRT-WT) animals exhibited time dependent increase in breathing rates and right lung weights, whereas these parameters were significantly less increased (p vs. XRT-WT. Conclusion This study shows that overexpression of EC-SOD confers protection against RT-induced acute lung injury. EC-SOD appears to work, in part, via an attenuation of the macrophage response and also decreases TGFβ1 activation with a subsequent downregulation of the profibrotic TGFβ pathway.</p