Facilitated news as controlled information flows: The origins, rationale and dilemmas of ‘embedded’ journalism

The article traces the origins, rationale and some of the dilemmas that have emerged in the practice of ‘embedded’ journalism. It argues that the practice emerged as a post-Vietnam response by the US military to the ‘problem’ of independent news coverage of conflicts in which the US was involved. For the post-Vietnam US military, independent news coverage was problematic because it often contradicts the official war narrative and, if left unhindered, undermines public support for the war effort. Since public support is crucial for success in a foreign war, particularly during lengthy engagements, independent news coverage is seen as a threat to the unity of the home front and therefore a threat to the war effort itself. The lesson learned from Vietnam was to restrict independent media access to battle zones, first by denying all access and withdrawing security guarantees to journalists operating in conflict theaters, and then by providing privileged but controlled access to front line units via the practice of facilitated news-gathering known as ‘embedded journalism’. As it turns out, even that practice has a downside, and there is more to the story than the military desire to control the narrative

US failures in strategy and the ‘CNN effect’

Reviewed book by Robert G. Patman Publication date: October, 2011 In this short, but interesting book, Robert Patman argues that US policy failures in the lead up to and aftermath of the October 1993 ‘Blackhawk Down’ incident in Mogadishu facilitated the conditions for the terrorist attacks on the US mainland in 2001. The thesis that the US merely reaped the bad fruit of its foreign policy on 9/11 is not new, but Patman’s approach is

State terror, economic policy, and social-rupture during the Argentine "Proceso," 1976-1981

http://archive.org/details/stateterrorecono00buchN

Allostatic load and ageing; linking the microbiome and nutrition with age related health

Ageing is a process of decline in physiological function and capability over time. It is an anticipated major burden on societal health-care costs due to an increasingly aged global population. Accelerated biological ageing is a feature of age-related morbidities, which also appear to share common underpinning features, including low-grade persistent inflammation, phosphate toxicity, diminished Nrf2 activity, a depleted metabolic capability, depressed mitochondrial biogenesis and a low diversity gut microbiome. Social, psychological, lifestyle and nutritional risk factors can all influence the trajectory of age-related health, as part of an individual's exposome, which reflects the interplay between the genome and the environment. This is manifest as allostatic (over)load reflecting the burden of lifestyle/disease at both a physiological and molecular level. In particular, age-related genomic methylation levels and inflammatory status reflect exposome differences. These features may be mediated by changes in microbial diversity. This can drive the generation of pro-inflammatory factors, such as TMAO, implicated in the ‘diseasome’ of ageing. Additionally, it can be influenced by the ‘foodome’, via nutritional differences affecting the availability of methyl donors required for maintenance of the epigenome and by the provision of nutritionally derived Nrf2 agonists. Both these factors influence age-related physiological resilience and health. This offers novel insights into possible interventions to improve health span, including a rage of emerging senotherapies and simple modifications of the nutritional and environmental exposome. In essence, the emerging strategy is to treat ageing processes common to the diseasome of ageing itself and thus preempt the development or progression of a range of age-related morbidities

Methyl donor nutrients in chronic kidney disease: impact on the epigenetic landscape

Epigenetic alterations, such as those linked to DNA methylation, may potentially provide molecular explanations for complications associated with altered gene expression in illnesses, such as chronic kidney disease (CKD). Although both DNA hypo- and hypermethylation have been observed in the uremic milieu, this remains only a single aspect of the epigenetic landscape and, thus, of any biochemical dysregulation associated with CKD. Nevertheless, the role of uremia-promoting alterations on the epigenetic landscape regulating gene expression is still a novel and scarcely studied field. Although few studies have actually reported alterations of DNA methylation via methyl donor nutrient intake, emerging evidence indicates that nutritional modification of the microbiome can affect one-carbon metabolism and the capacity to methylate the genome in CKD. In this review, we discuss the nutritional modifications that may affect one-carbon metabolism and the possible impact of methyl donor nutrients on the microbiome, CKD, and its phenotype

Generalizing Evidence from Randomized Trials using Inverse Probability of Sampling Weights

Results obtained in randomized trials may not easily generalize to target populations. Whereas in randomized trials the treatment assignment mechanism is known, the sampling mechanism by which individuals are selected to participate in the trial is typically not known and assuming random sampling from the target population is often dubious. We consider an inverse probability of sampling weighted (IPSW) estimator for generalizing trial results to a target population. The IPSW estimator is shown to be consistent and asymptotically normal. A consistent sandwich-type variance estimator is derived and simulation results are presented comparing the IPSW estimator to a previously proposed stratified estimator. The methods are then utilized to generalize results from two randomized trials of HIV treatment to all people living with HIV in the US

Cardiac Performance Measure Compliance in Outpatients The American College of Cardiology and National Cardiovascular Data Registry's PINNACLE (Practice Innovation And Clinical Excellence) Program

ObjectivesWe examined compliance with performance measures for 14,464 patients enrolled from July 2008 through June 2009 into the American College of Cardiology's PINNACLE (Practice Innovation And Clinical Excellence) program to provide initial insights into the quality of outpatient cardiac care.BackgroundLittle is known about the quality of care of outpatients with coronary artery disease (CAD), heart failure, and atrial fibrillation, and whether sex and racial disparities exist in the treatment of outpatients.MethodsThe PINNACLE program is the first, national, prospective office-based quality improvement program of cardiac patients designed, in part, to capture, report, and improve outpatient performance measure compliance. We examined the proportion of patients whose care was compliant with established American College of Cardiology, American Heart Association, and American Medical Association-Physician Consortium for Performance Improvement (ACC/AHA/PCPI) performance measures for CAD, heart failure, and atrial fibrillation.ResultsThere were 14,464 unique patients enrolled from 27 U.S. practices, accounting for 18,021 clinical visits. Of these, 8,132 (56.4%) had CAD, 5,012 (34.7%) had heart failure, and 2,786 (19.3%) had nonvalvular atrial fibrillation. Data from the PINNACLE program were feasibly collected for 24 of 25 ACC/AHA/PCPI performance measures. Compliance with performance measures ranged from being very low (e.g., 13.3% of CAD patients screened for diabetes mellitus) to very high (e.g., 96.7% of heart failure patients with blood pressure assessments), with moderate (70% to 90%) compliance observed for most performance measures. For 3 performance measures, there were small differences in compliance rates by race or sex.ConclusionsFor more than 14,000 patients enrolled from 27 practices in the outpatient PINNACLE program, we found that compliance with performance measures was variable, even after accounting for exclusion criteria, suggesting an important opportunity to improve the quality of outpatient care

Nrf2 in early vascular ageing: calcification, senescence and therapy

Under normal physiological conditions, free radical generation and antioxidant defences are balanced, and reactive oxygen species (ROS) usually act as secondary messengers in a plethora of biological processes. However, when this balance is impaired, oxidative stress develops due to imbalanced redox homeostasis resulting in cellular damage. Oxidative stress is now recognized as a trigger of cellular senescence, which is associated with multiple chronic 'burden of lifestyle' diseases, including atherosclerosis, type-2 diabetes, chronic kidney disease and vascular calcification; all of which possess signs of early vascular ageing. Nuclear factor erythroid 2-related factor 2 (Nrf2), termed the master regulator of antioxidant responses, is a transcription factor found to be frequently dysregulated in conditions characterized by oxidative stress and inflammation. Recent evidence suggests that activation of Nrf2 may be beneficial in protecting against vascular senescence and calcification. Both natural and synthetic Nrf2 agonists have been introduced as promising drug classes in different phases of clinical trials. However, overexpression of the Nrf2 pathway has also been linked to tumorigenesis, which highlights the requirement for further understanding of pathways involving Nrf2 activity, especially in the context of cellular senescence and vascular calcification. Therefore, comprehensive translational pre-clinical and clinical studies addressing the targeting capabilities of Nrf2 agonists are urgently required. The present review discusses the impact of Nrf2 in senescence and calcification in early vascular ageing, with focus on the potential clinical implications of Nrf2 agonists and non-pharmacological Nrf2 therapeutics