Asthma and protracted bronchitis : who fares better during an acute respiratory infection?

Aim Acute respiratory infections (ARI) are common in children, and symptoms range from days to weeks. The aim of this study was to determine if children with asthma have more severe ARI episodes compared with children with protracted bronchitis and controls. Methods Parents prospectively scored their child's next ARI using the Canadian acute respiratory illness and flu scale (CARIFS) and a validated cough diary (on days 1–7, 10 and 14 of illness). Children were age- and season-matched. Results On days 10 and 14 of illness, children with protracted bronchitis had significantly higher median CARIFS when compared with children with asthma and healthy controls. On day 14, the median CARIFS were: asthma = 4.1 (interquartile range (IQR) 4.0), protracted bronchitis = 19.6 (IQR 25.8) and controls = 4.1 (IQR 5.25). The median cough score was significantly different between groups on days 1, 7, 10 and 14 (P < 0.001). A significantly higher proportion of children with protracted bronchitis (63%) were still coughing at day 14 in comparison with children with asthma (24%) and healthy controls (26%). Conclusion Children with protracted bronchitis had the most severe ARI symptoms and higher percentage of respiratory morbidity at day 14 in comparison with children with asthma and healthy controls.

Liability in negligence and the failure to disclose multiple risks in surgery : I would have been willing to run the risk

It has been 21 years since the decision in Rogers v Whitaker and the legal principles concerning informed consent and liability for negligence are still strongly grounded in this landmark High Court decision. This paper considers more recent developments in the law concerning the failure to disclose inherent risks in medical procedures, focusing on the decision in Wallace v Kam [2013] HCA 19. In this case, the appellant underwent a surgical procedure that carried a number of risks. The surgery itself was not performed in a sub-standard way, but the surgeon failed to disclose two risks to the patient, a failure that constituted a breach of the surgeon’s duty of care in negligence. One of the undisclosed risks was considered to be less serious than the other, and this lesser risk eventuated causing injury to the appellant. The more serious risk did not eventuate, but the appellant argued that if the more serious risk had been disclosed, he would have avoided his injuries completely because he would have refused to undergo the procedure. Liability was disputed by the surgeon, with particular reference to causation principles. The High Court of Australia held that the appellant should not be compensated for harm that resulted from a risk he would have been willing to run. We examine the policy reasons underpinning the law of negligence in this specific context and consider some of the issues raised by this unusual case. We question whether some of the judicial reasoning adopted in this case, represents a significant shift in traditional causation principles.

Securing medical devices Part B : what’s available for nasogastric tubes?

This article is the second part of a two-part series examining securement options for commonly used therapeutic devices in the adult intensive care unit. Part A focused on endotracheal device securement.1 This article addresses nasogastric tube (NGT) securement options and with the aim of identifying the available range of NGT securement devices in Australia as a resource for clinicians seeking to explore options for tube stabilisation. Nasogastric feeding or gastric decompression tubes are commonly inserted via the nostril/nares. The National Pressure Ulcer Advisory Panel (NPUAP) 2011 position statement on mucosal pressure injuries, highlighted that mucosal tissues are vulnerable to pressure from devices.2 Securing of these devices sometimes leads to pressure-related injury to the internal mucosa due to difficulty visualising the mucosa and failure to reposition the nasogastric tube to relieve the pressure in a particular area.3 The nasal orifice is much smaller than the oral cavity and regular tube position changes are vital to minimise the risk of mucosal damage and ulcer development.

An acute growth factor treatment that preserves function after spinal cord contusion injury

Inflammation of the spinal cord after traumatic spinal cord injury leads to destruction of healthy tissue. This “secondary degeneration” is more damaging than the initial physical damage and is the major contributor to permanent loss of functions. In our previous study we showed that combined delivery of two growth factors, vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF), significantly reduced secondary degeneration after hemi-section injury of the spinal cord in the rat. Growth factor treatment reduced the size of the lesion cavity at 30d compared to control animals and further reduced the cavity at 90d in treated animals while in control animals the lesion cavity continued to increase in size. Growth factor treatment also reduced astrogliosis and reduced macroglia/macrophage activation around the injury site. Treatment with individual growth factors alone had similar effects to control treatments. The present study investigated whether growth factor treatment would improve locomotor behaviour after spinal contusion injury, a more relevant preclinical model of spinal cord injury. The growth factors were delivered for the first 7d to the injury site via osmotic minipump. Locomotor behaviour was monitored at 1-28d after injury using the BBB score and at 30d using automated gait analysis. Treated animals had BBB scores of 18; Control animals scored 10. Treated animals had significantly reduced lesion cavities and reduced macroglia/macrophage activation around the injury site. We conclude that growth factor treatment preserved spinal cord tissues after contusion injury, thereby allowing functional recovery. This treatment has the potential to significantly reduce the severity of human spinal cord injuries.

Unidentified vehicle in multi-vehicle accident - failure to notify Nominal Defendant no bar to proceedings against it

In Kumar v Suncorp Metway Insurance Limited [2004] QSC 381 Douglas J examined s37 of the Motor Accident Insurance Act 1994 (Qld) in the context of an accident involving multiple insurers when a notice of accident had not been given to the Nominal Defendant

Failure of discontinuous railhead edges due to plastic strain accumulation

Railhead is perhaps the highest stressed civil infrastructure due to the passage of heavily loaded wheels through a very small contact patch. The stresses at the contact patch cause yielding of the railhead material and wear. Many theories exist for the prediction of these mechanisms of continuous rails; this process in the discontinuous rails is relatively sparingly researched. Discontinuous railhead edges fail due to accumulating excessive plastic strains. Significant safety concern is widely reported as these edges form part of Insulated Rail Joints (IRJs) in the signalling track circuitry. Since Hertzian contact is not valid at a discontinuous edge, 3D finite element (3DFE) models of wheel contact at a railhead edge have been used in this research. Elastic–plastic material properties of the head hardened rail steel have been experimentally determined through uniaxial monotonic tension tests and incorporated into a FE model of a cylindrical specimen subject to cyclic tension load- ing. The parameters required for the Chaboche kinematic hardening model have been determined from the stabilised hysteresis loops of the cyclic load simulation and imple- mented into the 3DFE model. The 3DFE predictions of the plastic strain accumulation in the vicinity of the wheel contact at discontinuous railhead edges are shown to be affected by the contact due to passage of wheels rather than the magnitude of the loads the wheels carry. Therefore to eliminate this failure mechanism, modification to the contact patch is essential; reduction in wheel load cannot solve this problem.

Acute resistance exercise increases the expression of chemotactic factors within skeletal muscle

Intense resistance exercise causes mechanical loading of skeletal muscle, followed by muscle adaptation. Chemotactic factors likely play an important role in these processes. Purpose We investigated the time course of changes in the expression and tissue localization of several key chemotactic factors in skeletal muscle during the early phase of recovery following resistance exercise. Methods Muscle biopsy samples were obtained from vastus lateralis of eight untrained men (22+-0.5 yrs) before and 2, 4 and 24 h after three sets of leg press, squat and leg extension at 80% 1 RM. Results Monocyte chemotactic protein-1 (95×), interleukin-8 (2,300×), IL-6 (317×), urokinase-type plasminogen activator (15×), vascular endothelial growth factor (2×) and fractalkine (2.5×) mRNA was significantly elevated 2 h post-exercise. Interleukin-8 (38×) and interleukin-6 (58×) protein was also significantly elevated 2 h post-exercise, while monocyte chemotactic protein-1 protein was significantly elevated at 2 h (22×) and 4 h (21×) post-exercise. Monocyte chemotactic protein-1 and interleukin-8 were expressed by cells residing in the interstitial space between muscle fibers and, in some cases, were co-localized with CD68+ macrophages, PAX7+ satellite cells and blood vessels. However, the patterns of staining were inconclusive and not consistent. Conclusion In conclusion, resistance exercise stimulated a marked increase in the mRNA and protein expression of various chemotactic factors in skeletal muscle. Myofibers were not the dominant source of these factors. These findings suggest that chemotactic factors regulate remodeling/adaptation of skeletal muscle during the early phase of recovery following resistance exercise.

Performance evaluation of three-level Z-source inverters under semiconductor-failure conditions

This paper evaluates and proposes various compensation methods for three-level Z-source inverters under semiconductor-failure conditions. Unlike the fault-tolerant techniques used in traditional three-level inverters, where either an extra phase-leg or collective switching states are used, the proposed methods for three-level Z-source inverters simply reconfigure their relevant gating signals so as to ride-through the failed semiconductor conditions smoothly without any significant decrease in their ac-output quality and amplitude. These features are partly attributed to the inherent boost characteristics of a Z-source inverter, in addition to its usual voltage-buck operation. By focusing on specific types of three-level Z-source inverters, it can also be shown that, for the dual Z-source inverters, a unique feature accompanying it is its extra ability to force common-mode voltage to zero even under semiconductor-failure conditions. For verifying these described performance features, PLECS simulation and experimental testing were performed with some results captured and shown in a later section for visual confirmation.

A typology of technological enablers of website service failure prevention

An increasing range of services are now offered via online applications and e-commerce websites. However, problems with online services still occur at times, even for the best service providers due to the technical failures, informational failures, or lack of required website functionalities. Also, the widespread and increasing implementation of web services means that service failures are both more likely to occur, and more likely to have serious consequences. In this paper we first develop a digital service value chain framework based on existing service delivery models adapted for digital services. We then review current literature on service failure prevention, and provide a typology of technolo- gies and approaches that can be used to prevent failures of different types (functional, informational, system), that can occur at different stages in the web service delivery. This makes a contribution to theory by relating specific technologies and technological approaches to the point in the value chain framework where they will have the maximum impact. Our typology can also be used to guide the planning, justification and design of robust, reliable web services.

Failure of amino acid homeostasis causes cell death following proteasome inhibition

The ubiquitin-proteasome system targets many cellular proteins for degradation and thereby controls most cellular processes. Although it is well established that proteasome inhibition is lethal, the underlying mechanism is unknown. Here, we show that proteasome inhibition results in a lethal amino acid shortage. In yeast, mammalian cells, and flies, the deleterious consequences of proteasome inhibition are rescued by amino acid supplementation. In all three systems, this rescuing effect occurs without noticeable changes in the levels of proteasome substrates. In mammalian cells, the amino acid scarcity resulting from proteasome inhibition is the signal that causes induction of both the integrated stress response and autophagy, in an unsuccessful attempt to replenish the pool of intracellular amino acids. These results reveal that cells can tolerate protein waste, but not the amino acid scarcity resulting from proteasome inhibition.

The impact of prolonged hyperinsulinaemia on glucose transport in equine skeletal muscle and digital lamellae

REASONS FOR PERFORMING STUDY An increased incidence of metabolic disease in horses has led to heightened recognition of the pathological consequences of insulin resistance (IR). Laminitis, failure of the weight-bearing digital lamellae, is an important consequence. Altered trafficking of specialised glucose transporters (GLUTs) responsible for glucose uptake, are central to the dysregulation of glucose metabolism and may play a role in laminitis pathophysiology. OBJECTIVES We hypothesised that prolonged hyperinsulinaemia alters the regulation of glucose transport in insulin-sensitive tissue and digital lamellae. Our objectives were to compare the relative protein expression of major GLUT isoforms in striated muscle and digital lamellae in healthy horses and during hyperinsulinaemia. STUDY DESIGN Randomised, controlled study. METHODS Prolonged hyperinsulinaemia and lamellar damage were induced by a prolonged-euglycaemic hyperinsulinaemic clamp (p-EHC) or a prolonged-glucose infusion (p-GI) and results were compared to electrolyte-treated controls. GLUT protein expression was examined with immunoblotting. RESULTS Lamellar tissue contained more GLUT1 protein than skeletal muscle (p = 0.002) and less GLUT4 than the heart (p = 0.037). During marked hyperinsulinaemia and acute laminitis (induced by the p-EHC), GLUT1 protein expression was decreased in skeletal muscle (p = 0.029) but unchanged in the lamellae, while novel GLUTs (8; 12) were increased in the lamellae (p = 0.03), but not skeletal muscle. However, moderate hyperinsulinaemia and subclinical laminitis (induced by the p-GI) did not cause differential GLUT protein expression in the lamellae vs. control horses. CONCLUSIONS The results suggest that lamellar tissue functions independently of insulin and that IR may not be an essential component of laminitis aetiology. Marked differences in GLUT expression exist between insulin-sensitive and insulin-independent tissues during metabolic dysfunction in horses. The different expression profiles of novel GLUTs during acute and subclinical laminitis may be important to disease pathophysiology and require further investigation.

Artemisinin-induced parasite dormancy : a plausible mechanism for treatment failure

Background Artemisinin-combination therapy is a highly effective treatment for uncomplicated falciparum malaria but parasite recrudescence has been commonly reported following artemisinin (ART) monotherapy. The dormancy recovery hypothesis has been proposed to explain this phenomenon, which is different from the slower parasite clearance times reported as the first evidence of the development of ART resistance. Methods In this study, an existing P. falciparum infection model is modified to incorporate the hypothesis of dormancy. Published in vitro data describing the characteristics of dormant parasites is used to explore whether dormancy alone could be responsible for the high recrudescence rates observed in field studies using monotherapy. Several treatment regimens and dormancy rates were simulated to investigate the rate of clinical and parasitological failure following treatment. Results The model output indicates that following a single treatment with ART parasitological and clinical failures occur in up to 77% and 67% of simulations, respectively. These rates rapidly decline with repeated treatment and are sensitive to the assumed dormancy rate. The simulated parasitological and clinical treatment failure rates after 3 and 7 days of treatment are comparable to those reported from several field trials. Conclusions Although further studies are required to confirm dormancy in vivo, this theoretical study adds support for the hypothesis, highlighting the potential role of this parasite sub-population in treatment failure following monotherapy and reinforcing the importance of using ART in combination with other anti-malarials.

Artemisinin induced dormancy in Plasmodium falciparum : duration, recovery rates and implications in treatment failure

Background Despite the remarkable activity of artemisinin and its derivatives, monotherapy with these agents has been associated with high rates of recrudescence. The temporary arrest of the growth of ring-stage parasites (dormancy) after exposure to artemisinin drugs provides a plausible explanation for this phenomenon. Methods Ring-stage parasites of several Plasmodium falciparum lines were exposed to different doses of dihydroartemisinin (DHA) alone or in combination with mefloquine. For each regime, the proportion of recovering parasites was determined daily for 20 days. Results Parasite development was abruptly arrested after a single exposure to DHA, with some parasites being dormant for up to 20 days. Approximately 50% of dormant parasites recovered to resume growth within the first 9 days. The overall proportion of parasites recovering was dose dependent, with recovery rates ranging from 0.044% to 1.313%. Repeated treatment with DHA or with DHA in combination with mefloquine led to a delay in recovery and an ∼10-fold reduction in total recovery. Strains with different genetic backgrounds appeared to vary in their capacity to recover. Conclusions These results imply that artemisinin-induced arrest of growth occurs readily in laboratory-treated parasites and may be a key factor in P. falciparum malaria treatment failure.

Integrating the impact of climate into event based failure models for water pipes

This paper presents an event-based failure model to predict the number of failures that occur in water distribution assets. Often, such models have been based on analysis of historical failure data combined with pipe characteristics and environmental conditions. In this paper weather data have been added to the model to take into account the commonly observed seasonal variation of the failure rate. The theoretical basis of existing logistic regression models is briefly described in this paper, along with the refinements made to the model for inclusion of seasonal variation of weather. The performance of these refinements is tested using data from two Australian water authorities.