The current state of sustainable healthcare in Australia.

ObjectiveTo provide the first document map of sustainability and decarbonisation actions across the Australian healthcare sector, as reported in publicly available documents online, and to identify gaps in actions.MethodsHealthcare providers were identified across all state and territories. Structured Google searches between August and December 2022 were followed by document searches.

Value-based public health: Moving beyond value-based health care to support a wellbeing economy.

While value-based health care (VBHC) is transforming Australia's health system, with its focus on patient-centred care and outcomes, it cannot transform Australia's health without policy action to address the social determinants of health. Australia is moving towards a wellbeing economy, but governments have not been explicit in the methods by which the health system will contribute to the development of a wellbeing economy at a macro level. It is also unclear how governments will ensure that approaches to valuing wellbeing will complement current health care innovations in defining and evaluating value in relation to health outcomes.

Australian health policies related to diagnostic imaging: too much of a good thing?

Diagnostic imaging is increasingly being used in Australia to aid clinician diagnostic and therapeutic decision-making. There is concern that this increased use represents an overconsumption of inappropriate health services, which wastes finite resources and may cause direct or indirect harm to the patient. Australian health policies have primarily focused on increasing patient access to diagnostic imaging.

Co-designing a dashboard of predictive analytics and decision support to drive care quality and client outcomes in aged care: a mixed-method study protocol.

Introduction: There is a clear need for improved care quality and quality monitoring in aged care. Aged care providers collect an abundance of data, yet rarely are these data integrated and transformed in real-time into actionable information to support evidence-based care, nor are they shared with older people and informal caregivers. This protocol describes the co-design and testing of a dashboard in residential aged care facilities (nursing or care homes) and community-based aged care settings (formal care provided at home or in the community).

Perturbation of chemical coupling by an endothelial Cx40 mutant attenuates endothelium-dependent vasodilation by KCa channels and elevates blood pressure in mice.

Mutant forms of connexin40 (Cx40) exist in the human population and predispose carriers to atrial fibrillation. Since endothelial expression of Cx40 is important for electrical and chemical communication within the arterial wall, carriers of mutant Cx40 proteins may be predisposed to peripheral arterial dysfunction and dysregulation of blood pressure. We have therefore studied mice expressing either a chemically dysfunctional mutant, Cx40T202S, or wild-type Cx40, with native Cx40, specifically in the endothelium.

Sympathetic overdrive in obesity involves purinergic hyperactivity in the resistance vasculature.

While a close correlation exists in obese humans between sympathetic, adrenergic hyperactivity and structural and functional organ damage, a role for the co-transmitter, ATP, in vascular function remains unexplored. We therefore studied sympathetic nerve-mediated responses of pressurised small mesenteric arteries from control and obese rats. Diet-induced obesity significantly increased the amplitude of vasoconstriction to transmural nerve stimulation (1-10 Hz; P <0.

Diet-induced obesity impairs endothelium-derived hyperpolarization via altered potassium channel signaling mechanisms.

Background: The vascular endothelium plays a critical role in the control of blood flow. Altered endothelium-mediated vasodilator and vasoconstrictor mechanisms underlie key aspects of cardiovascular disease, including those in obesity. Whilst the mechanism of nitric oxide (NO)-mediated vasodilation has been extensively studied in obesity, little is known about the impact of obesity on vasodilation to the endothelium-derived hyperpolarization (EDH) mechanism; which predominates in smaller resistance vessels and is characterized in this study.

Obesity up-regulates intermediate conductance calcium-activated potassium channels and myoendothelial gap junctions to maintain endothelial vasodilator function.

The mechanisms involved in altered endothelial function in obesity-related cardiovascular disease are poorly understood. This study investigates the effect of chronic obesity on endothelium-dependent vasodilation and the relative contribution of nitric oxide (NO), calcium-activated potassium channels (K(Ca)), and myoendothelial gap junctions (MEGJs) in the rat saphenous artery. Obesity was induced by feeding rats a cafeteria-style diet (∼30 kJ as fat) for 16 to 20 weeks, with this model reflecting human dietary obesity etiology.

Heterogeneity in function of small artery smooth muscle BKCa: involvement of the beta1-subunit.

Arteriolar myogenic vasoconstriction occurs when increased stretch or membrane tension leads to smooth muscle cell depolarization and opening of voltage-gated Ca2+ channels. To prevent positive feedback and excessive pressure-induced vasoconstriction, studies in cerebral artery smooth muscle have suggested that activation of large conductance, Ca2+-activated K+ channels (BKCa) provides an opposing hyperpolarizing influence reducing Ca2+ channel activity. We have hypothesized that this mechanism may not equally apply to all vascular beds.

What's where and why at a vascular myoendothelial microdomain signalling complex.

1. Modulation of vascular cell calcium is critical for the control of vascular tone, blood flow and pressure. 2.

Endothelial coordination of cerebral vasomotion via myoendothelial gap junctions containing connexins 37 and 40.

Control of cerebral vasculature differs from that of systemic vessels outside the blood-brain barrier. The hypothesis that the endothelium modulates vasomotion via direct myoendothelial coupling was investigated in a small vessel of the cerebral circulation. In the primary branch of the rat basilar artery, membrane potential, diameter, and calcium dynamics associated with vasomotion were examined using selective inhibitors of endothelial function in intact and endothelium-denuded arteries.

Rhythmicity in arterial smooth muscle.

Many arteries and arterioles exhibit rhythmical contractions which are synchronous over considerable distances. This vasomotion is likely to assist in tissue perfusion especially during periods of altered metabolism or perfusion pressure. While the mechanism underlying vascular rhythmicity has been investigated for many years, it has only been recently, with the advent of imaging techniques for visualizing intracellular calcium release, that significant advances have been made.

Inositol 1,4,5-trisphosphate receptor subtypes are differentially distributed between smooth muscle and endothelial layers of rat arteries.

In blood vessels, the ability to control vascular tone depends on extracellular calcium entry and the release of calcium from inositol 1,4,5-trisphosphate receptor (IP3R)-gated stores located in both the endothelial and smooth muscle cells of the vascular wall. Therefore, we examined mRNA expression and protein distribution of IP3R subtypes in intact aorta, basilar and mesenteric arteries of the rat. IP3R1 mRNA was predominantly expressed in all three arteries.