Obesity is a major influence on the development and course of cardiovascular diseases and affects physical and social functioning and quality of life. The importance of effective interventions to reduce obesity and related health risks has increased in recent decades because the number of adults and children who are obese has reached epidemic proportions. To prevent the development of overweight and obesity throughout the life course, population-based strategies that improve social and physical environmental contexts for healthful eating and physical activity are essential. Population-based approaches to obesity prevention are complementary to clinical preventive strategies and also to treatment programs for those who are already obese. This American Heart Association scientific statement aims: 1) to raise awareness of the importance of undertaking population-based initiatives specifically geared to the prevention of excess weight gain in adults and children; 2) to describe considerations for undertaking obesity prevention overall and in key risk subgroups; 3) to differentiate environmental and policy approaches to obesity prevention from those used in clinical prevention and obesity treatment; 4) to identify potential targets of environmental and policy change using an ecological model that includes multiple layers of influences on eating and physical activity across multiple societal sectors; and 5) to highlight the spectrum of potentially relevant interventions and the nature of evidence needed to inform population-based approaches. The evidence-based experience for population-wide approaches to obesity prevention is highlighted.

https://www.commed.vcu.edu/Chronic_Disease/2008/obesityRx_AHA.pdf

Population-Based Prevention of Obesity : The Need for Comprehensive Promotion of Healthful Eating, Physical Activity, and Energy Balance A Scientific Statement From American Heart Association Council on Epidemiology and Prevention, Interdisciplinary Committee for Prevention (Formerly the Expert Panel on Population and Prevention Science)

Obesity and its repercussions constitute an important source of morbidity, impaired quality of life and its complications can have a major bearing on life expectancy. The present article summarizes the most important co-morbidities of obesity and their prevalence. Furthermore, it describes classification and grading systems that can be used to assess the individual and combined impact of co-morbid conditions on mortality risk. The literature was screened for assessment tools that can be deployed in the quantification of morbidity and mortality risk in individual patients. Thirteen specific domains have been identified that account for morbidity and mortality in obesity. Cardiovascular disease (CVD) and cancer account for the greatest mortality risk associated with obesity. The King’s Criteria and Edmonton Obesity Staging System (EOSS) were identified as useful tools for the detection and monitoring of individual patient mortality risk in obesity care. The stark facts on the complications of obesity should be capitalized on to improve patient management and knowledge and referred to in the wider dissemination of public health messages aimed at improving primary prevention.

Morbidity and mortality associated with obesity.

In this report we describe experiments to investigate a simple virulence model in which Pseudomonas aeruginosa PAO1 rapidly paralyzes and kills the nematode Caenorhabditis elegans . Our results imply that hydrogen cyanide is the sole or primary toxic factor produced by P. aeruginosa that is responsible for killing of the nematode. Four lines of evidence support this conclusion. First, a transposon insertion mutation in a gene encoding a subunit of hydrogen cyanide synthase ( hcnC ) eliminated nematode killing. Second, the 17 avirulent mutants examined all exhibited reduced cyanide synthesis, and the residual production levels correlated with killing efficiency. Third, exposure to exogenous cyanide alone at levels comparable to the level produced by PAO1 killed nematodes with kinetics similar to those observed with bacteria. The killing was not enhanced if hcnC mutant bacteria were present during cyanide exposure. And fourth, a nematode mutant ( egl-9 ) resistant to P. aeruginosa was also resistant to killing by exogenous cyanide in the absence of bacteria. A model for nematode killing based on inhibition of mitochondrial cytochrome oxidase is presented. The action of cyanide helps account for the unusually broad host range of virulence of P. aeruginosa and may contribute to the pathogenesis in opportunistic human infections due to the bacterium.

Pseudomonas aeruginosa PAO1 kills Caenorhabditis elegans by cyanide poisoning.

Abbreviations and symbols used in this guideline 

Executive summary 

Summary of recommendations 

Section 1 Introduction 

Section 2 Methodology of guideline production 

Section 3 Normal values and definitions

https://thorax.bmj.com/content/thoraxjnl/72/Suppl_1/ii1.full.pdf

BTS Guideline for Oxygen Use in Adults in Healthcare and Emergency Settings

Pulmonary hypertension (PH) frequently complicates the course of patients with various forms of chronic lung disease (CLD). CLD-associated PH (CLD-PH) is invariably associated with reduced functional ability, impaired quality of life, greater oxygen requirements and an increased risk of mortality. The aetiology of CLD-PH is complex and multifactorial, with differences in the pathogenic sequelae between the diverse forms of CLD. Haemodynamic evaluation of PH severity should be contextualised within the extent of the underlying lung disease, which is best gauged through a combination of physiological and imaging assessment. Who, when, if and how to screen for PH will be addressed in this article, as will the current state of knowledge with regard to the role of treatment with pulmonary vasoactive agents. Although such therapy cannot be endorsed given the current state of findings, future studies in this area are strongly encouraged.

https://erj.ersjournals.com/content/erj/53/1/1801914.full.pdf

Pulmonary hypertension in chronic lung disease and hypoxia.

https://www.amjmed.com/article/S0002-9343(03)00565-5/pdf

Obesity-associated hypoventilation in hospitalized patients: prevalence, effects, and outcome.

Pseudomonas aeruginosa is a persistent pathogen in the airways of patients with cystic fibrosis or bronchiectasis from other causes and appears to have evolved strategies to survive the inflammatory response of the host. We hypothesized that the secreted hemolytic phospholipase C (PLC) of P. aeruginosa (PlcHR) would decrease neutrophil respiratory burst activity. We found that while intact wild-type P. aeruginosa cells stimulated moderate respiratory burst activity from human neutrophils, an isogenic mutant pseudomonas (DeltaHR strain) containing a targeted deletion of the plcHR operon induced a much more robust oxidative burst from neutrophils. In contrast, a second pseudomonas mutant (DeltaN) containing a disruption in the gene encoding the nonhemolytic PLC (PlcN) was not different from the wild type in stimulating neutrophil O2.- production. Readdition of purified PlcHR to the DeltaHR strain suppressed neutrophil O2.- production to levels stimulated by wild-type bacteria. Interestingly, purified PlcHR decreased phorbol myristate acetate (PMA)- but not formyl methionyl-leucyl-proline (fMLP)-induced respiratory burst activity, suggesting interference by PlcHR with a protein kinase C (PKC)-specific signaling pathway. Accordingly, the PKC inhibitor bisindolylmaleimide inhibited the oxidative burst induced by either PMA or intact pseudomonas, but not by fMLP, whereas the p38 kinase inhibitor SB-203580 fully inhibited the respiratory burst induced by fMLP or the PlcHR-replete wild-type bacteria, but not PMA or the PlcHR-deficient DeltaHR bacterial mutant. We conclude that expression of PlcHR by P. aeruginosa suppresses bacterium-induced neutrophil respiratory burst by interfering with a PKC-dependent, non-p38 kinase-dependent pathway.

https://iai.asm.org/content/iai/67/5/2371.full.pdf

Sogol Nowbar

Papers

Obesity-associated hypoventilation in hospitalized patients: prevalence, effects, and outcome.

Pseudomonas aeruginosa hemolytic phospholipase C suppresses neutrophil respiratory burst activity

A 60-Year-old Man With Septic Arthritis and Hypotension After a Fall