Hacking Nuclear Command and Control

Executive Summary This paper will analyse the threat of cyber terrorism in regard to nuclear weapons. Specifically, this research will use open source knowledge to identify the structure of nuclear command and control centres, how those structures might be compromised through computer network operations, and how doing so would fit within established cyber terrorists' capabilities, strategies, and tactics. If access to command and control centres is obtained, terrorists could fake or actually cause one nuclear-armed state to attack another, thus provoking a nuclear response from another nuclear power. This may be an easier alternative for terrorist groups than building or acquiring a nuclear weapon or dirty bomb themselves. This would also act as a force equaliser, and provide terrorists with the asymmetric benefits of high speed, removal of geographical distance, and a relatively low cost. Continuing difficulties in developing computer tracking technologies which could trace the identity of intruders, and difficulties in establishing an internationally agreed upon legal framework to guide responses to computer network operations, point towards an inherent weakness in using computer networks to manage nuclear weaponry. This is particularly relevant to reducing the hair trigger posture of existing nuclear arsenals. All computers which are connected to the internet are susceptible to infiltration and remote control. Computers which operate on a closed network may also be compromised by various hacker methods, such as privilege escalation, roaming notebooks, wireless access points, embedded exploits in software and hardware, and maintenance entry points. For example, e-mail spoofing targeted at individuals who have access to a closed network, could lead to the installation of a virus on an open network. This virus could then be carelessly transported on removable data storage between the open and closed network. Information found on the internet may also reveal how to access these closed networks directly. Efforts by militaries to place increasing reliance on computer networks, including experimental technology such as autonomous systems, and their desire to have multiple launch options, such as nuclear triad capability, enables multiple entry points for terrorists. For example, if a terrestrial command centre is impenetrable, perhaps isolating one nuclear armed submarine would prove an easier task. There is evidence to suggest multiple attempts have been made by hackers to compromise the extremely low radio frequency once used by the US Navy to send nuclear launch approval to submerged submarines. Additionally, the alleged Soviet system known as Perimetr was designed to automatically launch nuclear weapons if it was unable to establish communications with Soviet leadership. This was intended as a retaliatory response in the event that nuclear weapons ha

Reduction of carbon dioxide and organic carbonyls by hydrosilanes catalysed by the perrhenate anion

The simple perrhenate salt [N(hexyl)4][(ReO4)] acts as a catalyst for the reduction of organic carbonyls and carbon dioxide by primary and secondary hydrosilanes. In the case of CO2, this results in the formation of methanol equivalents via silylformate and silylacetal intermediates. Furthermore, the addition of alkylamines to the reaction mixture favours catalytic amine N-methylation over methanol production under certain conditions. DFT analysis of the mechanism of CO2 reduction shows that the perrhenate anion activates the silylhydride forming a hypervalent silicate transition state such that the CO2 can directly cleave a Si–H bond

Runx1 stabilizes the mammary epithelial cell phenotype and prevents epithelial to mesenchymal transition

Runx1 is a well characterized transcription factor essential for hematopoietic differentiation and Runx1 mutations are the cause of leukemias. Runx1 is highly expressed in normal epithelium of most glands and recently has been associated with solid tumors. Notably, the function of Runx1 in the mammary gland and how it is involved in initiation and progression of breast cancer is still unclear. Here we demonstrate the consequences of Runx1 loss in normal mammary epithelial and breast cancer cells. We first observed that Runx1 is decreased in tumorigenic and metastatic breast cancer cells. We also observed loss of Runx1 expression upon induction of epithelial-mesenchymal transition (EMT) in MCF10A (normal-like) cells. Furthermore depletion of Runx1 in MCF10A cells resulted in striking changes in cell shape, leading to mesenchymal cell morphology. The epithelial phenotype could be restored in breast cancer cells by re-expressing Runx1. Analyses of breast tumors and patient data revealed that low Runx1 expression is associated with poor prognosis and decreased survival. We addressed mechanisms for the function of Runx1 in maintaining the epithelial phenotype and find Runx1 directly regulates E-cadherin; and serves as a downstream transcription factor mediating TGFbeta signaling. We also observed through global gene expression profiling of growth factor depleted cells that induction of EMT and loss of Runx1 is associated with activation of TGFbeta and WNT pathways. Thus these findings have identified a novel function for Runx1 in sustaining normal epithelial morphology and preventing EMT and suggest Runx1 levels could be a prognostic indicator of tumor progression

Runx1 stabilizes the mammary epithelial cell phenotype and prevents epithelial to mesenchymal transition

Runx1 is a well characterized transcription factor essential for hematopoietic differentiation and Runx1 mutations are the cause of leukemias. Runx1 is highly expressed in normal epithelium of most glands and recently has been associated with solid tumors. Notably, the function of Runx1 in the mammary gland and how it is involved in initiation and progression of breast cancer is still unclear. Here we demonstrate the consequences of Runx1 loss in normal mammary epithelial and breast cancer cells. We first observed that Runx1 is decreased in tumorigenic and metastatic breast cancer cells. We also observed loss of Runx1 expression upon induction of epithelial-mesenchymal transition (EMT) in MCF10A (normal-like) cells. Furthermore depletion of Runx1 in MCF10A cells resulted in striking changes in cell shape, leading to mesenchymal cell morphology. The epithelial phenotype could be restored in breast cancer cells by re-expressing Runx1. Analyses of breast tumors and patient data revealed that low Runx1 expression is associated with poor prognosis and decreased survival. We addressed mechanisms for the function of Runx1 in maintaining the epithelial phenotype and find Runx1 directly regulates E-cadherin; and serves as a downstream transcription factor mediating TGFbeta signaling. We also observed through global gene expression profiling of growth factor depleted cells that induction of EMT and loss of Runx1 is associated with activation of TGFbeta and WNT pathways. Thus these findings have identified a novel function for Runx1 in sustaining normal epithelial morphology and preventing EMT and suggest Runx1 levels could be a prognostic indicator of tumor progression

Analysis of baseline by treatment interactions in a drug prevention and health promotion program for high school male athletes B

Abstract This paper investigates baseline by treatment interactions (BTI) of a randomized anabolic steroid prevention program delivered to high school football players. Baseline by treatment interactions occur when a participant's score on an outcome variable is associated with both their pretreatment standing on the outcome variable and the treatment itself. The program was delivered to 31 high school football teams (Control=16, Treatment=15) in Oregon and Washington over the course of 3 years (Total N=3207). Although most interactions were nonsignificant, consistent baseline by treatment interactions were obtained for knowledge of the effects of steroid use and intentions to use steroids. Both of these interactions were beneficial in that they increased the effectiveness of the program for participants lower in knowledge and higher in intentions at baseline.

Endometrial CXCL13 Expression Is Cycle Regulated in Humans and Aberrantly Expressed in Humans and Rhesus Macaques With Endometriosis

C-X-C ligand 13 (CXCL13), a regulator of mucosal immunity, is secreted by human endometrial epithelium and may be involved in embryo implantation. However, cyclic expression of human endometrial CXCL13 in health and disease is not well studied. This study examines cycle stage-specific endometrial CXCL13 expression in normal humans when compared to those with biopsy-confirmed, stage 1 to 4 endometriosis using real-time reverse transcriptase, real-time polymerase chain reaction and immunohistochemistry. Eutopic endometrial CXCL13 expression was also compared between normal, control Rhesus macaques, and macaques with advanced endometriosis. In healthy women, CXLC13 messenger RNA expression was minimal in the proliferative phase and maximal in the secretory phase. However, in the presence of endometriosis, proliferative-phase endometrial expression markedly increased in both humans and rhesus subjects (P < .05). The cross-species and cross-stage concordance suggests a pathophysiologic role for CXCL13 in endometriosis and its use as a biomarker for disease

Self-consistent modelling of the Milky Way's Nuclear Stellar Disc

© 2022 The Author(s) Published by Oxford University Press on behalf of Royal Astronomical Society. This is the accepted manuscript version of an article which has been published in final form at https://doi.org/10.1093/mnras/stac639The Nuclear Stellar Disc (NSD) is a flattened high-density stellar structure that dominates the gravitational field of the Milky Way at Galactocentric radius $30\lesssim R\lesssim 300$ pc. We construct axisymmetric self-consistent equilibrium dynamical models of the NSD in which the distribution function is an analytic function of the action variables. We fit the models to the normalised kinematic distributions (line-of-sight velocities + VIRAC2 proper motions) of stars in the NSD survey of Fritz et al., taking the foreground contamination due to the Galactic Bar explicitly into account using an $N$-body model. The posterior marginalised probability distributions give a total mass of $M_{\rm NSD} = 10.5^{+1.1}_{-1.0} \times10^8 \,{\rm M_\odot}$, roughly exponential radial and vertical scale-lengths of $R_{\rm disc} = 88.6^{+9.2}_{-6.9}$ pc and $H_{\rm disc}=28.4^{+5.5}_{-5.5}$ pc respectively, and a velocity dispersion $\sigma \simeq 70$ km/s that decreases with radius. We find that the assumption that the NSD is axisymmetric provides a good representation of the data. We quantify contamination from the Galactic Bar in the sample, which is substantial in most observed fields. Our models provide the full 6D (position+velocity) distribution function of the NSD, which can be used to generate predictions for future surveys. We make the models publicly available as part of the software package AGAMA.Peer reviewedFinal Accepted Versio