Is your wiring system safe and energy efficient? (1993)

Electricity is a safe and convenient source of energy for heat, light and power in your home and on your farm, provided it is distributed in correctly sized and properly protected conductors. Good wiring systems are safe and energy-efficient

Installing lightning arresters for equipment protection

"Statistical data which show that lightning damages more than $100 million worth of equipment and property in the U.S. each year should move us toward precautionary action. All too often, however, we think about installing protective equipment only when we hear those first claps of thunder. While nothing can be done to eliminate lightning, something can be done to eliminate the damage that it brings to electrical wiring and electrical equipment. In fact, good protection can be obtained at a very low cost."--First page.Kenneth L. McFate and Fred M. Crawford (Department of Agricultural Engineering, College of Agriculture)Revised 1/7

Side-to-Side Knee Strength Imbalances and Increased Odds of Reporting Injury in Military Special Forces Operators

Please see the pdf version of the abstract

Is your wiring system safe and energy efficient?

"Electricity is a safe and convenient source of energy for heat, light and power in your home and on your farm, provided it is distributed in correctedly sized and properly protected conductors. Good wiring systems are safe and energy efficient."--First page.K.L. McFate (Department of Agricultural Engineering), F.M. Crawford (Extension Agricultural Engineer, College of Agriculture)Revised 1/82/8

Sub-Sets of Cancer Stem Cells Differ Intrinsically in Their Patterns of Oxygen Metabolism

PMCID: PMC3640080This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Oxygen Consumption Can Regulate the Growth of Tumors, a New Perspective on the Warburg Effect

The unique metabolism of tumors was described many years ago by Otto Warburg, who identified tumor cells with increased glycolysis and decreased mitochondrial activity. However, "aerobic glycolysis" generates fewer ATP per glucose molecule than mitochondrial oxidative phosphorylation, so in terms of energy production, it is unclear how increasing a less efficient process provides tumors with a growth advantage.We carried out a screen for loss of genetic elements in pancreatic tumor cells that accelerated their growth as tumors, and identified mitochondrial ribosomal protein L28 (MRPL28). Knockdown of MRPL28 in these cells decreased mitochondrial activity, and increased glycolysis, but paradoxically, decreased cellular growth in vitro. Following Warburg's observations, this mutation causes decreased mitochondrial function, compensatory increase in glycolysis and accelerated growth in vivo. Likewise, knockdown of either mitochondrial ribosomal protein L12 (MRPL12) or cytochrome oxidase had a similar effect. Conversely, expression of the mitochondrial uncoupling protein 1 (UCP1) increased oxygen consumption and decreased tumor growth. Finally, treatment of tumor bearing animals with dichloroacetate (DCA) increased pyruvate consumption in the mitochondria, increased total oxygen consumption, increased tumor hypoxia and slowed tumor growth.We interpret these findings to show that non-oncogenic genetic changes that alter mitochondrial metabolism can regulate tumor growth through modulation of the consumption of oxygen, which appears to be a rate limiting substrate for tumor proliferation

Modeling Core Metabolism in Cancer Cells: Surveying the Topology Underlying the Warburg Effect

BACKGROUND: Alterations on glucose consumption and biosynthetic activity of amino acids, lipids and nucleotides are metabolic changes for sustaining cell proliferation in cancer cells. Irrevocable evidence of this fact is the Warburg effect which establishes that cancer cells prefers glycolysis over oxidative phosphorylation to generate ATP. Regulatory action over metabolic enzymes has opened a new window for designing more effective anti-cancer treatments. This enterprise is not trivial and the development of computational models that contribute to identifying potential enzymes for breaking the robustness of cancer cells is a priority. METHODOLOGY/PRINCIPAL FINDINGS: This work presents a constraint-base modeling of the most experimentally studied metabolic pathways supporting cancer cells: glycolysis, TCA cycle, pentose phosphate, glutaminolysis and oxidative phosphorylation. To evaluate its predictive capacities, a growth kinetics study for Hela cell lines was accomplished and qualitatively compared with in silico predictions. Furthermore, based on pure computational criteria, we concluded that a set of enzymes (such as lactate dehydrogenase and pyruvate dehydrogenase) perform a pivotal role in cancer cell growth, findings supported by an experimental counterpart. CONCLUSIONS/SIGNIFICANCE: Alterations on metabolic activity are crucial to initiate and sustain cancer phenotype. In this work, we analyzed the phenotype capacities emerged from a constructed metabolic network conformed by the most experimentally studied pathways sustaining cancer cell growth. Remarkably, in silico model was able to resemble the physiological conditions in cancer cells and successfully identified some enzymes currently studied by its therapeutic effect. Overall, we supplied evidence that constraint-based modeling constitutes a promising computational platform to: 1) integrate high throughput technology and establish a crosstalk between experimental validation and in silico prediction in cancer cell phenotype; 2) explore the fundamental metabolic mechanism that confers robustness in cancer; and 3) suggest new metabolic targets for anticancer treatments. All these issues being central to explore cancer cell metabolism from a systems biology perspective

Co-operation, Contestation and Complexity in Post-Conflict Security Sector Reform

Security Sector Reform (SSR) remains a key feature of peacebuilding interventions and is usually undertaken by a state alongside national and international partners. External actors engaged in SSR tend to follow a normative agenda that often has little regard for the context in post-conflict societies. Despite recurrent criticism, SSR practices of international organisations and bilateral donors often remain focused on state institutions, and often do not sufficiently attend to alternative providers of security or existing normative frameworks of security. This article provides a critical overview of existing research and introduces the special issue on “Co-operation, Contestation and Complexity in Post-Conflict Security Sector Reform”. We explore three aspects that add an important piece to the puzzle of what constitutes effective SSR. First, the variation of norm adoption, norm contestation and norm imposition in post-conflict countries that might explain the mixed results in terms of peacebuilding. Second, the multitude of different security actors within and beyond the state which often leads to multiple patterns of co-operation and contestation within reform programmes. And third, how both the multiplicity of and tension between norms and actors further complicate efforts to build peace or, as complexity theory would posit, influence the complex and non-linear social system that is the conflict-affected environment