RESUMEN
OBJECTIVES: Emissions from road traffic, power generation and industry were substantially reduced during pandemic lockdown periods globally. Thus, we analysed reductions in traffic-related air pollution in Australian capital cities during March-April 2020 and then modelled the mortality benefits that could be realised if similar reductions were sustained by structural policy interventions. STUDY DESIGN: Satellite, air pollution monitor and land use observations were used to estimate ground-level nitrogen dioxide (NO2) concentrations in all Australian capital cities during: (a) a typical year with no prolonged air pollution events; (b) a hypothetical sustained reduction in NO2 equivalent to the COVID-19 lockdowns. METHODS: We use the WHO recommended NO2 exposure-response coefficient for mortality (1.023, 95 % CI: 1.008-1.037, per 10 µg/m3 annual average) to assess gains in life expectancy and population-wide years of life from reduced exposure to traffic-related air pollution. RESULTS: We attribute 1.1 % of deaths to anthropogenic NO2 exposures in Australian cities, corresponding to a total of 13,340 years of life lost annually. Although COVID-19-related reductions in NO2 varied widely between Australian cities during April 2020, equivalent and sustained reductions in NO2 emissions could reduce NO2-attributable deaths by 27 %, resulting in 3348 years of life gained annually. CONCLUSIONS: COVID-19 mobility restrictions reduced NO2 emissions and population-wide exposures in Australian cities. When sustained to the same extent by policy interventions that reduce fossil fuel consumption by favouring the uptake of electric vehicles, active travel and public transport, the health, mortality and economic benefits will be measurable in Australian cities.
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Contaminantes Atmosféricos , Contaminación del Aire , COVID-19 , Humanos , Contaminantes Atmosféricos/análisis , Ciudades , Emisiones de Vehículos , Dióxido de Nitrógeno/análisis , COVID-19/prevención & control , Australia/epidemiología , Control de Enfermedades Transmisibles , Contaminación del Aire/análisis , Material Particulado/análisis , Monitoreo del Ambiente/métodosRESUMEN
BACKGROUND: Visceral adipose tissue (VAT) is associated with greater obesity-related metabolic disturbance. Many studies have reported preferential loss of VAT with weight loss. OBJECTIVE: This systematic review looks for factors associated with preferential loss of VAT relative to subcutaneous abdominal fat (SAT) during weight loss. DESIGN: Medline and Embase were searched for imaging-based measurements of VAT and subcutaneous abdominal adipose tissue (SAT) before and after weight loss interventions. We examine for factors that influences the percentage change in VAT versus SAT (%deltaV/%deltaS) with weight loss. Linear regression analyses were performed on the complete data set and on subgroups of studies. Factors examined included percentage weight loss, degree of caloric restriction, exercise, initial body mass index (BMI), gender, time of follow-up and baseline VAT/SAT. RESULTS: There were 61 studies with a total of 98 cohort time points extracted. Percentage weight loss was the only variable that influenced %deltaV/%deltaS (r=-0.29, P=0.005). Modest weight loss generated preferential loss of VAT, but with greater weight loss this effect was attenuated. The method of weight loss was not an influence with one exception. Very-low-calorie diets (VLCDs) provided exceptional short-term (<4 weeks) preferential VAT loss. But this effect was lost by 12-14 weeks. CONCLUSIONS: Visceral adipose tissue is lost preferentially with modest weight loss, but the effect is attenuated with greater weight loss. Acute caloric restriction, using VLCD, produces early preferential loss of VAT. These observations may help to explain the metabolic benefits of modest weight loss.
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Grasa Intraabdominal/fisiopatología , Obesidad/terapia , Grasa Subcutánea Abdominal/fisiopatología , Pérdida de Peso/fisiología , Distribución de la Grasa Corporal , Índice de Masa Corporal , Dieta Reductora , Ejercicio Físico/fisiología , Femenino , Humanos , Masculino , Obesidad/fisiopatologíaRESUMEN
OBJECTIVE: To identify the proportion of weight lost as fat-free mass (FFM) by various weight loss interventions. METHODS: Medline and Embase were systematically searched for reliable measurements of FFM before and after weight loss of >10 kg and eligible data were pooled. In a fixed effect model of % FFM loss/weight loss (%FFML), linear regression analysis was used to determine the influence of degree of caloric restriction, exercise, magnitude of weight loss, initial body mass index (BMI) and type of surgery. RESULTS: Data were included from 26 cohorts treated with dietary and behavioral interventions and 29 cohorts of bariatric surgery patients. The degree of caloric restriction was positively associated with %FFML (r (2)=0.31, P=0.006) and in three randomized controlled trials exercise was shown to decrease %FFML. Compared with laparoscopic adjustable gastric banding (LAGB), biliopancreatic diversion (BPD) and roux en Y gastric bypass (RYGB) caused greater log(e) (natural log) %FFML (r (2)=0.453, P<0.001). Differences in log(e) %FFML between surgical procedures were independent of initial BMI and magnitude of weight loss. CONCLUSIONS: The degree of caloric restriction, exercise and rate of weight loss influence the proportion of weight lost as FFM after non-surgical interventions. For surgical interventions, BPD and RYGB result in greater %FFML than LAGB.
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Composición Corporal/fisiología , Dieta Reductora , Obesidad , Pérdida de Peso/fisiología , Absorciometría de Fotón , Ejercicio Físico , Femenino , Humanos , Modelos Lineales , Masculino , Obesidad/dietoterapia , Obesidad/cirugía , Obesidad/terapia , Ensayos Clínicos Controlados Aleatorios como AsuntoRESUMEN
The nature of the pathogen-host relationship is recognized as being a dynamic coevolutionary process where the immune system has required ongoing adaptation and improvement to combat infection. Under survival pressure from sophisticated immune responses, adaptive processes for microbes, including viruses, have manifested as immune evasion strategies. This paper proposes a theory that virus immune evasion can be broadly classified into 'acquisition' or 'erroneous replication' strategies. Acquisition strategies are characteristic of large genome dsDNA viruses, which (i) replicate in the cell nucleus; (ii) have acquired host genes that can be used to directly manipulate responses to infection; (iii) are often latent for the lifetime of the host; and (iv) have little or no serious impact on health. Alternatively, erroneous replication strategies are characteristic of small genome RNA viruses, which are recognized as being the cause of many serious diseases in humans. It is proposed that this propensity for disease is due to the cytoplasmic site of replication and truncated temporal relationship with the host, which has limited or removed the evolutionary opportunity for RNA viruses to have acquired host genes. This has resulted in RNA viruses relying on error-prone replication strategies which, while allowing survival and persistence, are more likely to lead to disease due to the lack of direct viral control over potentially host-deleterious inflammatory and immune responses to infection.