Technology and Biological Weapons: Future Threats

Ye

The Glass Ceiling Women Face: An Examination and Proposals for Development of Future Women Entrepreneurs

As of 2007, there were an estimated 10.4 million businesses in the United States that were owned and operated by women. The number of women-owned firms has continued to grow at around twice the rate of all firms for the past two decades (Center for Women’s Business Research, 2008). On the other hand, women comprise only 15.4 percent of corporate officers in Fortune 500 companies (Catalyst, 2007b) and, in 2003, held only 14.8 percent of board seats in the Fortune 500 (Catalyst, 2007a).To better understand the glass ceiling faced by both female entrepreneurs and women leaders, the research on women’s issues is examined from a number of different vantage points. Women’s entrepreneurship and women’s leadership research on leadership, decision-making, and gender differences was examined to discover commonalities. Then female single-sex education literature was reviewed for insights on developmental issues that might influence future women entrepreneurs and leaders. In this exploration of research, it was found that both women entrepreneurs and women leaders in the corporate environment tend toward the same leadership styles and ways of interacting with others; they also experience a lack of role models and possible lack of self-efficacy.The literature on single-sex education provides observations that young women may thrive in environments in which there are fewer male competitors, hold less stereotyped views on gender, hold higher aspirations, may have greater opportunities for training of leadership skills, and may have increased self-confidence that may be the result of exposure to successful women role models. Implications for future research are explored and suggestions are provided to meet the needs of developing women entrepreneurs

A paradigm shift in the CBW proliferation problem: devising effective restraint on the evolving biochemical threat

In den vergangenen drei Jahrzehnten ist das akkumulierte Wissen über die Mechanismen und Funktionen biologischer Systeme durch wissenschaftliche und technologische Entwicklungen explosionsartig gewachsen. Der vorliegende Forschungsbericht untersucht die Wechselwirkung von naturwissenschaftlicher Forschung, insbesondere in der Biotechnologie und Molekularbiologie, und politischem Steuerungshandeln im Bereich der Rüstungskontrolle. Vor dem Hintergrund der gegenwärtigen Krise der Genfer Verhandlungen über ein Verifikationsprotokoll zum "Übereinkommen über das Verbot der Entwicklung, Herstellung und Lagerung bakteriologischer (biologischer) Waffen und Toxinwaffen" (BWÜ) ist es dringend erforderlich, den Handlungsbedarf für die Rüstungskontrollpolitik neu zu bestimmen. Die Verfasser untersuchten die Missbrauchsmöglichkeiten neuer Forschungserkenntnisse und Technologieentwicklungen für die Herstellung von Biowaffen auf der Grundlage einer naturwissenschaftlichen Analyse. In der Studie konnten besondere Risikobereiche identifiziert und sichtbar gemacht werden, die für die Rüstungskontrollpolitik und für Verifikationssysteme zu biologischen Waffen von grundlegender Bedeutung sind. Hierbei traten deutliche Hinweise auf einen Paradigmenwechsel bei den Proliferationsgefahren für biologische und chemische Waffen zutage: Lag die Hauptgefahr bisher im Einsatz modifizierter Mikroorganismen, um Infektionskrankheiten auszulösen, so steht nun die Möglichkeit im Vordergrund, biochemische Agenzien als Waffen zu benutzen, um gezielt die Funktionsweise und Interaktion biologischer Systeme im menschlichen Körper anzugreifen. Im Zentrum der Untersuchung standen zwei lebenswichtige, miteinander verbundene physiologische Systeme - das Nerven- und das Immunsystem, die eine doppelte Verletzbarkeit durch Manipulationen aufweisen und somit eine grundsätzliche Relevanz für die biochemische Rüstungskontrolle besitzen. Eine Analyse dieser Systeme im Kontext jüngster Entwicklungen in den Lebenswissenschaften (Life Sciences) verdeutlicht, dass ein Großteil des gestiegenen Wissens einen dual-use-Charakter hat und somit für nicht-friedliche Zwecke missbraucht werden kann, sofern die Verbotsnormen des BWÜ in dem kommenden Jahrzehnten nicht angepasst werden. (ICD2

Comparison of Transmittance and Reflectance Pulse Oximetry in Anesthetized Dogs

Objectives: The tongue is the standard site for placement of a pulse oximeter probe but is difficult to access during certain procedures such as dental and ophthalmic procedures and computerized tomography of the head. The aim of this study was to evaluate the performance of a new-generation reflectance pulse oximeter using the tail and tibia as sites for probe attachment. Materials and Methods: A total of 100 client-owned dogs that underwent anesthesia for various reasons were premedicated with butorphanol (n = 50; 0.2 mg/kg; group BUT) or butorphanol and dexmedetomidine (n = 50; 5 μg/kg; group DEX), administered intravenously. Anesthesia was induced with propofol and maintained with sevoflurane. A transmittance pulse oximeter probe was placed on the tongue and served as the reference standard. A reflectance probe was randomly placed on the tail base or the proximal tibia, and the position changed after testing. Signals from three consecutive measurements were obtained at each position. Failure was defined as “no signal,” “low signal,” or a pulse difference >10/min compared with the ECG heart rate. Data were analyzed using chi-square test, Wilcoxon matched-pair signed-rank test, and Bland-Altman analysis. P < 0.05 was considered significant. Results: In both groups (BUT and DEX), failure rate was higher when the tibia and tail were used as probe sites compared with the tongue. In both groups, the failure rate was higher for the tibia than for the tail. Dexmedetomidine-induced vasoconstriction increased failure rate at all probe positions. Clinical Significance: The tail base, but not the tibia, is an acceptable position for reflectance pulse oximeter probes in dogs. The tongue remains the probe site of choice, if accessible

Lifestyle factors and high-risk atherosclerosis: Pathways and mechanisms beyond traditional risk factors

Despite major efforts to reduce atherosclerotic cardiovascular disease (ASCVD) burden with conventional risk factor control, significant residual risk remains. Recent evidence on non-traditional determinants of cardiometabolic health has advanced our understanding of lifestyle-disease interactions. Chronic exposure to environmental stressors like poor diet quality, sedentarism, ambient air pollution and noise, sleep deprivation and psychosocial stress affect numerous traditional and non-traditional intermediary pathways related to ASCVD. These include body composition, cardiorespiratory fitness, muscle strength and functionality and the intestinal microbiome, which are increasingly recognized as major determinants of cardiovascular health. Evidence points to partially overlapping mechanisms, including effects on inflammatory and nutrient sensing pathways, endocrine signalling, autonomic function and autophagy. Of particular relevance is the potential of low-risk lifestyle factors to impact on plaque vulnerability through altered adipose tissue and skeletal muscle phenotype and secretome. Collectively, low-risk lifestyle factors cause a set of phenotypic adaptations shifting tissue cross-talk from a proinflammatory milieu conducive for high-risk atherosclerosis to an anti-atherogenic milieu. The ketone body ß-hydroxybutyrate, through inhibition of the NLRP-3 inflammasome, is likely to be an intermediary for many of these observed benefits. Adhering to low-risk lifestyle factors adds to the prognostic value of optimal risk factor management, and benefit occurs even when the impact on conventional risk markers is discouragingly minimal or not present. The aims of this review are (a) to discuss novel lifestyle risk factors and their underlying biochemical principles and (b) to provide new perspectives on potentially more feasible recommendations to improve long-term adherence to low-risk lifestyle factors

High-Risk Atherosclerosis and Metabolic Phenotype: The Roles of Ectopic Adiposity, Atherogenic Dyslipidemia, and Inflammation

Current algorithms for assessing risk of atherosclerotic cardiovascular disease (ASCVD) and, in particular, the reliance on low-density lipoprotein (LDL) cholesterol in conditions where this measurement is discordant with apoB and LDL-particle concentrations fail to identify a sizeable part of the population at high risk for adverse cardiovascular events. This results in missed opportunities for ASCVD prevention, most notably in those with metabolic syndrome, prediabetes, and diabetes. There is substantial evidence that accumulation of ectopic fat and associated metabolic traits are markers for and pathogenic components of high-risk atherosclerosis. Conceptually, the subset of advanced lesions in high-risk atherosclerosis that triggers vascular complications is closely related to a set of coordinated high-risk traits clustering around a distinct metabolic phenotype. A key feature of this phenotype is accumulation of ectopic fat, which, coupled with age-related muscle loss, creates a milieu conducive for the development of ASCVD: atherogenic dyslipidemia, nonresolving inflammation, endothelial dysfunction, hyperinsulinemia, and impaired fibrinolysis. Sustained vascular inflammation, a hallmark of high-risk atherosclerosis, impairs plaque stabilization in this phenotype. This review describes how metabolic and inflammatory processes that are promoted in large measure by ectopic adiposity, as opposed to subcutaneous adipose tissue, relate to the pathogenesis of high-risk atherosclerosis. Clinical biomarkers indicative of these processes provide incremental information to standard risk factor algorithms and advanced lipid testing identifies atherogenic lipoprotein patterns that are below the discrimination level of standard lipid testing. This has the potential to enable improved identification of high-risk patients who are candidates for therapeutic interventions aimed at prevention of ASCVD