On the Security and Privacy Challenges of Virtual Assistants.

Since the purchase of Siri by Apple, and its release with the iPhone 4S in 2011, virtual assistants (VAs) have grown in number and popularity. The sophisticated natural language processing and speech recognition employed by VAs enables users to interact with them conversationally, almost as they would with another human. To service user voice requests, VAs transmit large amounts of data to their vendors; these data are processed and stored in the Cloud. The potential data security and privacy issues involved in this process provided the motivation to examine the current state of the art in VA research. In this study, we identify peer-reviewed literature that focuses on security and privacy concerns surrounding these assistants, including current trends in addressing how voice assistants are vulnerable to malicious attacks and worries that the VA is recording without the user's knowledge or consent. The findings show that not only are these worries manifold, but there is a gap in the current state of the art, and no current literature reviews on the topic exist. This review sheds light on future research directions, such as providing solutions to perform voice authentication without an external device, and the compliance of VAs with privacy regulations.

Issues facing the future health care workforce: the importance of demand modelling.

This article examines issues facing the future health care workforce in Australia in light of factors such as population ageing. It has been argued that population ageing in Australia is affecting the supply of health care professionals as the health workforce ages and at the same time increasing the demand for health care services and the health care workforce.However, the picture is not that simple. The health workforce market in Australia is influenced by a wide range of factors; on the demand side by increasing levels of income and wealth, emergence of new technologies, changing disease profiles, changing public health priorities and a focus on the prevention of chronic disease. While a strong correlation is observed between age and use of health care services (and thus health care workforce), this is mediated through illness, as typified by the consistent finding of higher health care costs in the months preceding death.On the supply side, the health workforce is highly influenced by policy drivers; both national policies (eg funded education and training places) and local policies (eg work place-based retention policies). Population ageing and ageing of the health workforce is not a dominant influence. In recent years, the Australian health care workforce has grown in excess of overall workforce growth, despite an ageing health workforce. We also note that current levels of workforce supply compare favourably with many OECD countries. The future of the health workforce will be shaped by a number of complex interacting factors.Market failure, a key feature of the market for health care services which is also observed in the health care labour market - means that imbalances between demand and supply can develop and persist, and suggests a role for health workforce planning to improve efficiency in the health services sector. Current approaches to health workforce planning, especially on the demand side, tend to be highly simplistic. These include historical allocation methods, such as the personnel-to-population ratios which are essentially circular in their rationale rather than evidence-based. This article highlights the importance of evidence-based demand modelling for those seeking to plan for the future Australian health care workforce. A model based on population health status and best practice protocols for health care is briefly outlined.

A work force model to support the adoption of best practice care in chronic diseases - a missing piece in clinical guideline implementation.

The development and implementation of an evidence-based approach to health workforce planning is a necessary step to achieve access to best practice chronic disease management. In its absence, the widely reported failure in implementation of clinical best practice guidelines is almost certain to continue. This paper describes a demand model to estimate the community-based primary care health workforce consistent with the delivery of best practice chronic disease management and prevention. The model takes a geographic region as the planning frame and combines data about the health status of the regional population by disease category and stage, with best practice guidelines to estimate the clinical skill requirement or competencies for the region. The translation of the skill requirement into a service requirement can then be modelled, incorporating various assumptions about the occupation group to deliver nominated competencies. The service requirement, when compared with current service delivery, defines the gap or surplus in services. The results of the model could be used to inform service delivery as well as a workforce supply strategy.

Calcium events in smooth muscles and their interstitial cells; physiological roles of sparks.

The observation of spontaneous sporadic releases of packets of stored calcium made 20 years ago has opened up a number of new concepts in smooth muscle physiology: (1) the calcium release sites are ryanodine and inositol 1,4,5-trisphosphate (IP3) receptor channels which contribute to cell-wide increases in [Ca2+]i in response to cell depolarization, activation of IP3-generating receptors, or other stimuli; (2) changes in [Ca2+]i act back on the cell membrane to activate or modulate K+, Cl- and cation channel activity so affecting contraction, in arterial smooth muscle for example affecting blood pressure; (3) IP3 production is voltage dependent and is believed to contribute to pacemaker potentials and to refractory periods which control the rhythmical motility of many hollow organs. Most smooth muscle tissues contain interstitial cells (ICs) in addition to contractile smooth muscle cells (SMCs). The interactions of these internal mechanisms, and in turn the interactions of SMCs and ICs in various smooth muscle tissues, are major factors in determining the unique physiological profiles of individual smooth muscles.

Phospholipase C, but not InsP3 or DAG, -dependent activation of the muscarinic receptor-operated cation current in guinea-pig ileal smooth muscle cells.

1. In visceral smooth muscles, both M(2) and M(3) muscarinic receptor subtypes are found, and produce two major metabolic effects: adenylyl cyclase inhibition and PLCbeta activation. Thus, we studied their relevance for muscarinic cationic current (mI(CAT)) generation, which underlies cholinergic excitation. Experiments were performed on single guinea-pig ileal cells using patch-clamp recording techniques under conditions of weakly buffered [Ca(2+)](i) (either using 50 microm EGTA or 50-100 microm fluo-3 for confocal fluorescence imaging) or with [Ca(2+)](i) 'clamped' at 100 nm using 10 mm BAPTA/CaCl(2) mixture. 2. Using a cAMP-elevating agent (1 microm isoproterenol) or a membrane-permeable cAMP analog (10 microm 8-Br-cAMP), we found no evidence for mI(CAT) modulation through a cAMP/PKA pathway. 3. With low [Ca(2+)](i) buffering, the PLC blocker U-73122 at 2.5 microm almost abolished mI(CAT), in some cases without any significant effect on [Ca(2+)](i). When [Ca(2+)](i) was buffered at 100 nm, U-73122 reduced both carbachol- and GTPgammaS-induced mI(CAT) maximal conductances (IC(50)=0.5-0.6 microm) and shifted their activation curves positively. 4. U-73343, a weak PLC blocker, had no effect on GTPgammaS-induced mI(CAT), but weakly inhibited carbachol-induced current, possibly by competitively inhibiting muscarinic receptors, since the inhibition could be prevented by increasing the carbachol concentration to 1 mm. Aristolochic acid and D-609, which inhibit PLA(2) and phosphatidylcholine-specific PLC, respectively, had no or very small effects on mI(CAT), suggesting that these enzymes were not involved. 5. InsP(3) (1 microm) in the pipette or OAG (20 microm) applied externally had no effect on mI(CAT) or its inhibition by U-73122. Ca(2+) store depletion (evoked by InsP(3), or by combined cyclopiazonic acid, ryanodine and caffeine treatment) did not induce any significant current, and had no effect on mI(CAT) in response to carbachol when [Ca(2+)](i) was strongly buffered to 100 nm. 6. It is concluded that phosphatidylinositol-specific PLC modulates mI(CAT) via Ca(2+) release, but also does so independently of InsP(3), DAG, Ca(2+) store depletion or a rise of [Ca(2+)](i). Our present results explain the previously established 'permissive' role of the M(3) receptor subtype in mI(CAT) generation, and provide a new insight into the molecular mechanisms underlying the shifts of the cationic conductance activation curve.