A conceptual framework for climate change, health and wellbeing in NSW, Australia.

Changes in natural hazards related to climate change are evident in New South Wales (NSW), Australia, and are projected to become more frequent and intense. The impacts of climate change may adversely affect health and wellbeing, directly via extreme weather events such as heatwaves, storms and floods, and indirectly via impacts on food security, air and water quality, and other environmental amenities. The NSW Government's Climate Change Policy Framework recognises the need to reduce the effects of climate change on health and wellbeing.

Climate change, health and wellbeing: challenges and opportunities in NSW, Australia.

The NSW (New South Wales) Climate Change Policy Framework, launched by the NSW Government in 2016, recognises that climate change presents risks to health and wellbeing. Risks to health and wellbeing come from direct impacts of extreme weather events, and from indirect impacts through effects on air, water, food and ecosystems. Responding to these challenges offers an opportunity to protect and promote health by enhancing environmental amenities, and building adaptive capacity and resilience in populations and systems.

A Comparison of the Health Effects of Ambient Particulate Matter Air Pollution from Five Emission Sources.

This article briefly reviews evidence of health effects associated with exposure to particulate matter (PM) air pollution from five common outdoor emission sources: traffic, coal-fired power stations, diesel exhaust, domestic wood combustion heaters, and crustal dust. The principal purpose of this review is to compare the evidence of health effects associated with these different sources with a view to answering the question: Is exposure to PM from some emission sources associated with worse health outcomes than exposure to PM from other sources? Answering this question will help inform development of air pollution regulations and environmental policy that maximises health benefits. Understanding the health effects of exposure to components of PM and source-specific PM are active fields of investigation.

Childhood interstitial lung diseases in immunocompetent children in Australia and New Zealand: a decade's experience.

Background: Childhood interstitial lung disease (chILD) represents a rare heterogeneous group of respiratory disorders. In the absence of randomized controlled clinical trials, global collaborations have utilized case series with an aim to standardising approaches to diagnosis and management. Australasian data are lacking.

Childhood interstitial lung disease: A systematic review.

Objectives: Childhood interstitial lung disease (chILD) is a group of rare chronic and complex disorders of variable pathology. There has been no systematic review of published chILD research. This study aimed to describe chILD classification systems, epidemiology, morbidity, treatments, outcomes, and the impact of chILD on families and the burden on health services.

Bone marrow-derived HL mitigates bone marrow-derived CETP-mediated decreases in HDL in mice globally deficient in HL and the LDLr.

The objective of this study was to determine the combined effects of HL and cholesteryl ester transfer protein (CETP), derived exclusively from bone marrow (BM), on plasma lipids and atherosclerosis in high-fat-fed, atherosclerosis-prone mice. We transferred BM expressing these proteins into male and female double-knockout HL-deficient, LDL receptor-deficient mice (HL(-/-)LDLr(-/-)). Four BM chimeras were generated, where BM-derived cells expressed 1) HL but not CETP, 2) CETP and HL, 3) CETP but not HL, or 4) neither CETP nor HL.

Childhood interstitial lung disease due to surfactant protein C deficiency: frequent use and costs of hospital services for a single case in Australia.

Background: Rare chronic diseases of childhood are often complex and associated with multiple health issues. Such conditions present significant demands on health services, but the degree of these demands is seldom reported. This study details the utilisation of hospital services and associated costs in a single case of surfactant protein C deficiency, an example of childhood interstitial lung disease.

Specific dietary polyphenols attenuate atherosclerosis in apolipoprotein E-knockout mice by alleviating inflammation and endothelial dysfunction.

Objective: Animal and clinical studies have suggested that polyphenols in fruits, red wine, and tea may delay the development of atherosclerosis through their antioxidant and anti-inflammatory properties. We investigated whether individual dietary polyphenols representing different polyphenolic classes, namely quercetin (flavonol), (-)-epicatechin (flavan-3-ol), theaflavin (dimeric catechin), sesamin (lignan), or chlorogenic acid (phenolic acid), reduce atherosclerotic lesion formation in the apolipoprotein E (ApoE)(-/-) gene-knockout mouse.

Methods And Results: Quercetin and theaflavin (64-mg/kg body mass daily) significantly attenuated atherosclerotic lesion size in the aortic sinus and thoracic aorta (P<0.

Leukocyte-derived hepatic lipase increases HDL and decreases en face aortic atherosclerosis in LDLr-/- mice expressing CETP.

In addition to hepatic expression, cholesteryl ester transfer protein (CETP) and hepatic lipase (HL) are expressed by human macrophages. The combined actions of these proteins have profound effects on HDL structure and function. It is not known how these HDL changes influence atherosclerosis.

Anti-atherosclerotic and anti-diabetic properties of probucol and related compounds.

Probucol is a diphenolic compound with anti-oxidant and anti-inflammatory properties that reduces atherosclerosis and restenosis. Unfortunately, adverse effects on blood lipoproteins and cardiac electrophysiology have curtailed its use as a drug. Compounds related to probucol that have improved efficacy without the adverse effects offer promise as novel therapies of cardiovascular disease.

High-density lipoproteins: an emerging target in the prevention of cardiovascular disease.

High-density lipoproteins (HDLs) have been well established to protect against the development of atherosclerotic cardiovascular disease. It has become apparent that in addition to the promotion of reverse cholesterol transport, HDLs possess a number of additional functional properties that may contribute to their beneficial influence on the arterial wall. A number of exciting therapeutic strategies have been developed that target HDL and its ability to protect against the development of atherosclerotic plaque.

What is so special about apolipoprotein AI in reverse cholesterol transport?

An initial step in reverse cholesterol transport is the movement of unesterified cholesterol from peripheral cells to high-density lipoproteins (HDLs). This transfer usually occurs in extracellular spaces, such as the subendothelial space of a vessel wall, and is promoted by the interaction of lipid-free or lipid-poor apolipoprotein (apo)AI with ATP binding cassette A1 cellular transporters on macrophages (MPhi). Because HDL does not interact with MPhi ATP binding cassette A1 and apoAI is not synthesized by macrophages, this apoAI must be generated from spherical HDL.

Formation of high density lipoproteins containing both apolipoprotein A-I and A-II in the rabbit.

Human plasma HDLs are classified on the basis of apolipoprotein composition into those that contain apolipoprotein A-I (apoA-I) without apoA-II [(A-I)HDL] and those containing apoA-I and apoA-II [(A-I/A-II)HDL]. ApoA-I enters the plasma as a component of discoidal particles, which are remodeled into spherical (A-I)HDL by LCAT. ApoA-II is secreted into the plasma either in the lipid-free form or as a component of discoidal high density lipoproteins containing apoA-II without apoA-I [(A-II)HDL].

Apolipoprotein E enhances hepatic lipase-mediated hydrolysis of reconstituted high-density lipoprotein phospholipid and triacylglycerol in an isoform-dependent manner.

This study compares the kinetics of hepatic lipase (HL)-mediated phospholipid and triacylglycerol hydrolysis in spherical, reconstituted high-density lipoproteins (rHDL) that contain either apolipoprotein E2 (apoE2), apoE3, apoE4, or apoA-I as the sole apolipoprotein. HL-mediated phospholipid hydrolysis was assessed by incubating various concentrations of rHDL that contained only cholesteryl esters (CE) in their core, (E2/CE)rHDL, (E3/CE)rHDL, (E4/CE)rHDL, and (A-I/CE)rHDL, with a constant amount of HL. The rate of phospholipid hydrolysis was determined as the formation of nonesterified fatty acid mass.