179 resultados para Rural Wireless Channels, Channel Measurements, Weather Effects
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Heat islands are a significant problem in urban spaces worldwide. The phenomenon occurs when air and surface temperatures in urban areas significantly exceed those experienced in nearby rural areas. There are two main causes of heat islands. The first is the use of highly absorptive construction materials in buildings and infrastructure, which soak up heat and radiate it back into the immediate surroundings. These materials, including but not limited to concrete, steel, asphalt and stone, are usually impermeable and so do not embody moisture that could dissipate some of the absorbed heat. The second cause relates to urban form, where the canyon-like configurations of buildings and streets channel and trap heat from the sun. In both cases, an absence of greenery and other soft landscaping can compound the problem by lowering capacity for cooling through shading and evotranspiration. Incidences of heat islands increase as urban areas swell in size and cover more land area, making the phenomenon an unwelcome side effect of global trends towards increased urbanisation. Heat islands create serious problems, including increased energy demand for cooling, declining air quality and heat stress for people and animals. In very severe cases, heat islands can compound the effects of high urban temperatures, leading to increased human mortality...
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A loss of function mutation in the TRESK K2P potassium channel (KCNK18), has recently been linked with typical familial migraine with aura. We now report the functional characterisation of additional TRESK channel missense variants identified in unrelated patients. Several variants either had no apparent functional effect, or they caused a reduction in channel activity. However, the C110R variant was found to cause a complete loss of TRESK function, yet is present in both sporadic migraine and control cohorts, and no variation in KCNK18 copy number was found. Thus despite the previously identified association between loss of TRESK channel activity and migraine in a large multigenerational pedigree, this finding indicates that a single non-functional TRESK variant is not alone sufficient to cause typical migraine and highlights the genetic complexity of this disorder. Migraine is a common, disabling neurological disorder with a genetic, environmental and in some cases hormonal component. It is characterized by attacks of severe, usually unilateral and throbbing headache, can be accompanied by nausea, vomiting and photophobia and is clinically divided into two main subtypes, migraine with aura (MA) when a migraine is accompanied by transient and reversible focal neurological symptoms and migraine without aura (MO)1. The multifactorial and clinical heterogeneity of the disorder have considerably hindered the identification of common migraine susceptibility genes and most of our current understanding comes from the studies of familial hemiplegic migraine (FHM), a rare monogenic autosomal dominant form of MA2. So far, the three susceptibility genes that have been convincingly identified in FHM families all encode ion channels or transporters: CACNA1A encoding the α1 subunit of the Cav2.1 calcium channel3, SCN1A encoding the Nav1.1 sodium channel4 and ATP1A2 encoding the α2 subunit of the Na+/K+ pump5. It is believed that mutations in these genes may lead to increased efflux of glutamate and potassium in the synapse and thereby cause migraine by rendering the brain more susceptible to cortical spreading depression (CSD)6 which is thought to play a role in initiating a migraine attack7,8. However, these genes have not to date been implicated in common forms of migraine9. Nevertheless, current opinion suggests that typical migraine, like FHM, is also disorder of neuronal excitability, ion homeostasis and neurotransmitter release10,11,12. Mutations in the SLC4A4 gene encoding the sodium-bicarbonate cotransporter NBCe1, have recently been implicated in several different forms of migraine13, and a variety of genes involved in glutamate homeostasis (PGCP, MTDH14 and LRP115) and a cation channel (TRPM8)15 have also recently been implicated in migraine via genome-wide association studies. Ion channels are therefore highly likely to play an important role in the pathogenesis of typical migraine. TRESK (KCNK18), is a member of the two-pore domain (K2P) family of potassium channels involved in the control of cellular electrical excitability16. Regulation of TRESK activity by the calcium-dependent phosphatase calcineurin17, as well as its expression in dorsal root ganglia (DRG)18 and trigeminal ganglia (TG)19,20 has led to a proposed role for this channel in a variety of pain pathways. In a recent study, a frameshift mutation (F139Wfsx24) in TRESK was identified in a large multigenerational pedigree where it co-segregated perfectly with typical MA and a significant genome-wide linkage LOD score of 3.0. Furthermore, functional analysis revealed that this mutation caused a complete loss of TRESK function and that the truncated subunit was also capable of down regulating wild-type channel function. This therefore highlighted KCNK18 as potentially important candidate gene and suggested that TRESK dysfunction might play a possible role in the pathogenesis of familial migraine with visual aura20. Additional screening for KCNK18 mutations in unrelated sporadic migraine and control cohorts also identified a number of other missense variants; R10G, A34V, C110R, S231P and A233V20. The A233V variant was found only in the control cohort, whilst A34V was identified in a single Australian migraine proband for which family samples were not available, but it was not detected in controls. By contrast, the R10G, C110R, and S231P variants were found in both migraineurs and controls in both cohorts. In this study, we have investigated the functional effect of these variants to further probe the potential association of TRESK dysfunction with typical migraine.
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The calcium-activated potassium ion channel gene (KCNN3) is located in the vicinity of the familial hemiplegic migraine type 2 locus on chromosome 1q21.3. This gene is expressed in the central nervous system and plays a role in neural excitability. Previous association studies have provided some, although not conclusive, evidence for involvement of this gene in migraine susceptibility. To elucidate KCNN3 involvement in migraine, we performed gene-wide SNP genotyping in a high-risk genetic isolate from Norfolk Island, a population descended from a small number of eighteenth century Isle of Man ‘Bounty Mutineer’ and Tahitian founders. Phenotype information was available for 377 individuals who are related through the single, well-defined Norfolk pedigree (96 were affected: 64 MA, 32 MO). A total of 85 SNPs spanning the KCNN3 gene were genotyped in a sub-sample of 285 related individuals (76 affected), all core members of the extensive Norfolk Island ‘Bounty Mutineer’ genealogy. All genotyping was performed using the Illumina BeadArray platform. The analysis was performed using the statistical program SOLAR v4.0.6 assuming an additive model of allelic effect adjusted for the effects of age and sex. Haplotype analysis was undertaken using the program HAPLOVIEW v4.0. A total of four intronic SNPs in the KCNN3 gene displayed significant association (P < 0.05) with migraine. Two SNPs, rs73532286 and rs6426929, separated by approximately 0.1 kb, displayed complete LD (r 2 = 1.00, D′ = 1.00, D′ 95% CI = 0.96–1.00). In all cases, the minor allele led to a decrease in migraine risk (beta coefficient = 0.286–0.315), suggesting that common gene variants confer an increased risk of migraine in the Norfolk pedigree. This effect may be explained by founder effect in this genetic isolate. This study provides evidence for association of variants in the KCNN3 ion channel gene with migraine susceptibility in the Norfolk genetic isolate with the rarer allelic variants conferring a possible protective role. This the first comprehensive analysis of this potential candidate gene in migraine and also the first study that has utilised the unique Norfolk Island large pedigree isolate to implicate a specific migraine gene. Studies of additional variants in KCNN3 in the Norfolk pedigree are now required (e.g. polyglutamine variants) and further analyses in other population data sets are required to clarify the association of the KCNN3 gene and migraine risk in the general outbred population.
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Background Migraine is a polygenic multifactorial disease, possessing environmental and genetic causative factors with multiple involved genes. Mutations in various ion channel genes are responsible for a number of neurological disorders. KCNN3 is a neuronal small conductance calcium-activated potassium channel gene that contains two polyglutamine tracts, encoded by polymorphic CAG repeats in the gene. This gene plays a critical role in determining the firing pattern of neurons and acts to regulate intracellular calcium channels. Methods The present association study tested whether length variations in the second (more 3') polymorphic CAG repeat in exon 1 of the KCNN3 gene, are involved in susceptibility to migraine with and without aura (MA and MO). In total 423 DNA samples from unrelated individuals, of which 202 consisted of migraine patients and 221 non-migraine controls, were genotyped and analysed using a fluorescence labelled primer set on an ABI310 Genetic Analyzer. Allele frequencies were calculated from observed genotype counts for the KCNN3 polymorphism. Analysis was performed using standard contingency table analysis, incorporating the chi-squared test of independence and CLUMP analysis. Results Overall, there was no convincing evidence that KCNN3 CAG lengths differ between Caucasian migraineurs and controls, with no significant difference in the allelic length distribution of CAG repeats between the population groups (P = 0.090). Also the MA and MO subtypes did not differ significantly between control allelic distributions (P > 0.05). The prevalence of the long CAG repeat (>19 repeats) did not reach statistical significance in migraineurs (P = 0.15), nor was there a significant difference between the MA and MO subgroups observed compared to controls (P = 0.46 and P = 0.09, respectively), or between MA vs MO (P = 0.40). Conclusion This association study provides no evidence that length variations of the second polyglutamine array in the N-terminus of the KCNN3 channel exert an effect in the pathogenesis of migraine.
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Structurally novel compounds able to block voltage-gated Ca2+ channels (VGCCs) are currently being sought for the development of new drugs directed at neurological disorders. Fluorescence techniques have recently been developed to facilitate the analysis of VGCC blockers in a multi-well format. By utilising the small cell lung carcinoma cell line, NCI-H146, we were able to detect changes in intracellular Ca2+ concentration ([Ca2+]i) using a fluorescence microplate reader. NCI-H146 cells have characteristics resembling those of neuronal cells and express multiple VGCC subtypes, including those of the L-, N- and P-type. We found that K+-depolarisation of fluo-3 loaded NCI-H146 cells causes a rapid and transient increase in fluorescence, which was readily detected in a 96-well plate. Extracts of Australian plants, including those used traditionally as headache or pain treatments, were tested in this study to identify those affecting Ca2+ influx following membrane depolarisation of NCI-H146 cells. We found that E. bignoniiflora, A. symphyocarpa and E. vespertilio caused dose-dependent inhibition of K+-depolarised Ca2+ influx, with IC50 values calculated to be 234, 548 and 209 μg/ml, respectively. This data suggests an effect of these extracts on the function of VGCCs in these cells. Furthermore, we found similar effects using a fluorescence laser imaging plate reader (FLIPR) that allows simultaneous measurement of real-time fluorescence in a multi-well plate. Our results indicate that the dichloromethane extract of E. bignoniiflora and the methanolic extract of E. vespertilio show considerable promise as antagonists of neuronal VGCCs. Further analysis is required to characterise the function of the bioactive constituents in these extracts and determine their selectivity on VGCC subtypes.
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As Earth's climate is rapidly changing, the impact of ambient temperature on health outcomes has attracted increasing attention in the recent time. Considerable number of excess deaths has been reported because of exposure to ambient hot and cold temperatures. However, relatively little research has been conducted on the relation between temperature and morbidity. The aim of this study was to characterize the relationship between both hot and cold temperatures and emergency hospital admissions in Brisbane, Australia, and to examine whether the relation varied by age and socioeconomic factors. It aimed to explore lag structures of temperature–morbidity association for respiratory causes, and to estimate the magnitude of emergency hospital admissions for cardiovascular diseases attributable to hot and cold temperatures for the large contribution of both diseases to the total emergency hospital admissions. A time series study design was applied using routinely collected data of daily emergency hospital admissions, weather and air pollution variables in Brisbane during 1996–2005. Poisson regression model with a distributed lag non-linear structure was adopted to assess the impact of temperature on emergency hospital admissions after adjustment for confounding factors. Both hot and cold effects were found, with higher risk of hot temperatures than that of cold temperatures. Increases in mean temperature above 24.2oC were associated with increased morbidity, especially for the elderly ≥ 75 years old with the largest effect. The magnitude of the risk estimates of hot temperature varied by age and socioeconomic factors. High population density, low household income, and unemployment appeared to modify the temperature–morbidity relation. There were different lag structures for hot and cold temperatures, with the acute hot effect within 3 days after hot exposure and about 2-week lagged cold effect on respiratory diseases. A strong harvesting effect after 3 days was evident for respiratory diseases. People suffering from cardiovascular diseases were found to be more vulnerable to hot temperatures than cold temperatures. However, more patients admitted for cardiovascular diseases were attributable to cold temperatures in Brisbane compared with hot temperatures. This study contributes to the knowledge base about the association between temperature and morbidity. It is vitally important in the context of ongoing climate change. The findings of this study may provide useful information for the development and implementation of public health policy and strategic initiatives designed to reduce and prevent the burden of disease due to the impact of climate change.
The health effects of temperature : current estimates, future projections, and adaptation strategies
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Climate change is expected to be one of the biggest global health threats in the 21st century. In response to changes in climate and associated extreme events, public health adaptation has become imperative. This thesis examined several key issues in this emerging research field. The thesis aimed to identify the climate-health (particularly temperature-health) relationships, then develop quantitative models that can be used to project future health impacts of climate change, and therefore help formulate adaptation strategies for dealing with climate-related health risks and reducing vulnerability. The research questions addressed by this thesis were: (1) What are the barriers to public health adaptation to climate change? What are the research priorities in this emerging field? (2) What models and frameworks can be used to project future temperature-related mortality under different climate change scenarios? (3) What is the actual burden of temperature-related mortality? What are the impacts of climate change on future burden of disease? and (4) Can we develop public health adaptation strategies to manage the health effects of temperature in response to climate change? Using a literature review, I discussed how public health organisations should implement and manage the process of planned adaptation. This review showed that public health adaptation can operate at two levels: building adaptive capacity and implementing adaptation actions. However, there are constraints and barriers to adaptation arising from uncertainty, cost, technologic limits, institutional arrangements, deficits of social capital, and individual perception of risks. The opportunities for planning and implementing public health adaptation are reliant on effective strategies to overcome likely barriers. I proposed that high priorities should be given to multidisciplinary research on the assessment of potential health effects of climate change, projections of future health impacts under different climate and socio-economic scenarios, identification of health cobenefits of climate change policies, and evaluation of cost-effective public health adaptation options. Heat-related mortality is the most direct and highly-significant potential climate change impact on human health. I thus conducted a systematic review of research and methods for projecting future heat-related mortality under different climate change scenarios. The review showed that climate change is likely to result in a substantial increase in heatrelated mortality. Projecting heat-related mortality requires understanding of historical temperature-mortality relationships, and consideration of future changes in climate, population and acclimatisation. Further research is needed to provide a stronger theoretical framework for mortality projections, including a better understanding of socioeconomic development, adaptation strategies, land-use patterns, air pollution and mortality displacement. Most previous studies were designed to examine temperature-related excess deaths or mortality risks. However, if most temperature-related deaths occur in the very elderly who had only a short life expectancy, then the burden of temperature on mortality would have less public health importance. To guide policy decisions and resource allocation, it is desirable to know the actual burden of temperature-related mortality. To achieve this, I used years of life lost to provide a new measure of health effects of temperature. I conducted a time-series analysis to estimate years of life lost associated with changes in season and temperature in Brisbane, Australia. I also projected the future temperaturerelated years of life lost attributable to climate change. This study showed that the association between temperature and years of life lost was U-shaped, with increased years of life lost on cold and hot days. The temperature-related years of life lost will worsen greatly if future climate change goes beyond a 2 °C increase and without any adaptation to higher temperatures. The excess mortality during prolonged extreme temperatures is often greater than the predicted using smoothed temperature-mortality association. This is because sustained period of extreme temperatures produce an extra effect beyond that predicted by daily temperatures. To better estimate the burden of extreme temperatures, I estimated their effects on years of life lost due to cardiovascular disease using data from Brisbane, Australia. The results showed that the association between daily mean temperature and years of life lost due to cardiovascular disease was U-shaped, with the lowest years of life lost at 24 °C (the 75th percentile of daily mean temperature in Brisbane), rising progressively as temperatures become hotter or colder. There were significant added effects of heat waves, but no added effects of cold spells. Finally, public health adaptation to hot weather is necessary and pressing. I discussed how to manage the health effects of temperature, especially with the context of climate change. Strategies to minimise the health effects of high temperatures and climate change can fall into two categories: reducing the heat exposure and managing the health effects of high temperatures. However, policy decisions need information on specific adaptations, together with their expected costs and benefits. Therefore, more research is needed to evaluate cost-effective adaptation options. In summary, this thesis adds to the large body of literature on the impacts of temperature and climate change on human health. It improves our understanding of the temperaturehealth relationship, and how this relationship will change as temperatures increase. Although the research is limited to one city, which restricts the generalisability of the findings, the methods and approaches developed in this thesis will be useful to other researchers studying temperature-health relationships and climate change impacts. The results may be helpful for decision-makers who develop public health adaptation strategies to minimise the health effects of extreme temperatures and climate change.
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Cold-formed steel Lipped Channel Beams (LCB) with web openings are commonly used as floor joists and bearers in building structures. Shear behaviour of these beams is more complicated and their shear capacities are considerably reduced by the presence of web openings. Hence detailed numerical and experimental studies of simply supported LCBs under a mid-span load with aspect ratios of 1.0 and 1.5 were undertaken to investigate the shear behaviour and strength of LCBs with web openings. Experimental and numerical results showed that the current design rules in cold-formed steel structures design codes are very conservative. Improved design equations were therefore proposed for the shear strength of LCBs with web openings based on both experimental and numerical results. This research showed a significant reduction in shear capacities of LCBs when large web openings are included for the purpose of locating building services. A cost effective method of eliminating such detrimental effects of large circular web openings was also therefore investigated using experimental and numerical studies. For this purpose LCBS were reinforced using plate, stud, transverse and sleeve stiffeners with varying sizes and thicknesses that were welded and screw-fastened to the web of LCBs. These studies showed that plate stiffeners were the most suitable. Suitable screw-fastened plate stiffener arrangements with optimum thicknesses were then proposed for LCBs with web openings to restore their original shear capacities. This paper presents the details of finite element analyses and experiments of LCBs with web openings in shear, and the development of improved shear design rules. It then describes the experimental and numerical studies to determine the optimum plate stiffener arrangements and the results. The proposed shear design rules in this paper can be considered for inclusion in the future versions of cold-formed steel design codes.
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Objective: The objective of the study was to explore whether and how rural culture influences type II diabetes management and to better understand the social processes that rural people construct in coping with diabetes and its complications. In particular, the study aimed to analyse the interface and interactions between rural people with type II diabetes and the Australian health care system, and to develop a theoretical understanding that reflects constructs that may be more broadly applicable. Methods: The study applied constructivist grounded theory methods within an interpretive interactionist framework. Data from 39 semi-structured interviews with rural and urban type II diabetes patients and a mix of rural health care providers were analysed to develop a theoretical understanding of the social processes that define diabetes management in that context. Results: The analysis suggests that although type II diabetes imposes limitations that require adjustment and adaptation, these processes are actively negotiated by rural people within the environmental context to fit the salient social understandings of autonomy and self-reliance. Thus, people normalized self-reliant diabetes management behaviours because this was congruent with the rural culture. Factors that informed the actions of normalization were relationships between participants and health care professionals, support, and access to individual resources. Conclusions: The findings point to ways in which rural self-reliance is conceived as the primary strategy of diabetes management. People face the paradox of engaging with a health care system that at the same time maximizes individual responsibility for health and minimizes the social support by which individuals manage the condition. The emphasis on self-reliance gives some legitimacy to a lack of prevention and chronic care services. Success of diabetes management behaviours is, however, contingent on relative resources. Where there is good primary care, there develops a number of downstream effects including a sense of empowerment to manage difficult rural environmental circumstances. This has particular bearing on health outcomes for people with fewer resources.
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This thesis analyses the performance bounds of amplify-and-forward relay channels which are becoming increasingly popular in wireless communication applications. The statistics of cascaded Nakagami-m fading model which is a major obstacle in evaluating the outage of wireless networks is analysed using Mellin transform. Furthermore, the upper and the lower bounds for the ergodic capacity of the slotted amplify-and-forward relay channel, for finite and infinite number of relays are derived using random matrix theory. The results obtained will enable wireless network designers to optimize the network resources, benefiting the consumers.
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Capacity of current and future high data rate wireless communications depend significantly on how well changes in the wireless channel are predicted and tracked. Generally, this can be estimated by transmitting known symbols. However, this increases overheads if the channel varies over time. Given today’s bandwidth demand and the increased necessity for mobile wireless devices, the contributions of this research are very significant. This study has developed a novel and efficient channel tracking algorithm that can recursively update the channel estimation for wireless broadband communications reducing overheads, therefore increasing the speed of wireless communication systems.
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Background Whilst resistance training has been proven to convey considerable benefits to older people; immediately post-exercise there may be elevated transient risks for cardiac events and falls. Objectives and Measurements We assessed the acute effects of eccentrically-biased (EB) and conventional (CONV) resistance exercise on: platelet number, activation and granule exocytsosis; and mean velocity of centre of pressure displacement (Vm). Design, Setting, Participants and Intervention Ten older adults (7 males, 3 females; 69 ± 4 years) participated in this randomised controlled cross-over study in which they performed EB and CONV training sessions that were matched for total work and a control condition. Results Immediately post-exercise there was a statistically significant difference in platelet count between the control condition, in which it fell (pre 224 ± 35 109/L; post 211 ± 30 109/L: P < 0.05) and CONV in which it increased (pre 236 ± 55 109/L; post 242 ± 51 109/L: P > 0.05). There was no change in platelet activation and granule exocytsosis or Vm following EB and CONV. Conclusions Overall, while minor differences between regimens were observed, no major adverse effect on parameters of platelet function or centre of pressure displacement were observed acutely following either regimen. Eccentrically-biased and conventional resistance exercise training regimens do not appear to present an elevated acute risk in the context of changes to platelet function contributing to a cardiac event or postural stability increasing falls risk for apparently healthy older adults.
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Dengue virus (DENV) transmission in Australia is driven by weather factors and imported dengue fever (DF) cases. However, uncertainty remains regarding the threshold effects of high-order interactions among weather factors and imported DF cases and the impact of these factors on autochthonous DF. A time-series regression tree model was used to assess the threshold effects of natural temporal variations of weekly weather factors and weekly imported DF cases in relation to incidence of weekly autochthonous DF from 1 January 2000 to 31 December 2009 in Townsville and Cairns, Australia. In Cairns, mean weekly autochthonous DF incidence increased 16.3-fold when the 3-week lagged moving average maximum temperature was <32 °C, the 4-week lagged moving average minimum temperature was ≥24 °C and the sum of imported DF cases in the previous 2 weeks was >0. When the 3-week lagged moving average maximum temperature was ≥32 °C and the other two conditions mentioned above remained the same, mean weekly autochthonous DF incidence only increased 4.6-fold. In Townsville, the mean weekly incidence of autochthonous DF increased 10-fold when 3-week lagged moving average rainfall was ≥27 mm, but it only increased 1.8-fold when rainfall was <27 mm during January to June. Thus, we found different responses of autochthonous DF incidence to weather factors and imported DF cases in Townsville and Cairns. Imported DF cases may also trigger and enhance local outbreaks under favorable climate conditions.
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BACKGROUND Dengue fever (DF) outbreaks often arise from imported DF cases in Cairns, Australia. Few studies have incorporated imported DF cases in the estimation of the relationship between weather variability and incidence of autochthonous DF. The study aimed to examine the impact of weather variability on autochthonous DF infection after accounting for imported DF cases and then to explore the possibility of developing an empirical forecast system. METHODOLOGY/PRINCIPAL FINDS Data on weather variables, notified DF cases (including those acquired locally and overseas), and population size in Cairns were supplied by the Australian Bureau of Meteorology, Queensland Health, and Australian Bureau of Statistics. A time-series negative-binomial hurdle model was used to assess the effects of imported DF cases and weather variability on autochthonous DF incidence. Our results showed that monthly autochthonous DF incidences were significantly associated with monthly imported DF cases (Relative Risk (RR):1.52; 95% confidence interval (CI): 1.01-2.28), monthly minimum temperature ((o)C) (RR: 2.28; 95% CI: 1.77-2.93), monthly relative humidity (%) (RR: 1.21; 95% CI: 1.06-1.37), monthly rainfall (mm) (RR: 0.50; 95% CI: 0.31-0.81) and monthly standard deviation of daily relative humidity (%) (RR: 1.27; 95% CI: 1.08-1.50). In the zero hurdle component, the occurrence of monthly autochthonous DF cases was significantly associated with monthly minimum temperature (Odds Ratio (OR): 1.64; 95% CI: 1.01-2.67). CONCLUSIONS/SIGNIFICANCE Our research suggested that incidences of monthly autochthonous DF were strongly positively associated with monthly imported DF cases, local minimum temperature and inter-month relative humidity variability in Cairns. Moreover, DF outbreak in Cairns was driven by imported DF cases only under favourable seasons and weather conditions in the study.
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Wireless networked control systems (WNCSs) have been increasingly deployed in industrial applications. As they require timely data packet transmissions, it is difficult to make efficient use of the limited channel resources, particularly in contention based wireless networks in the layered network architecture. Aiming to maintain the WNCSs under critical real-time traffic condition at which the WNCSs marginally meet the real-time requirements, a cross-layer design (CLD) approach is presented in this paper to adaptively adjust the control period to achieve improved channel utilization while still maintaining effective and timely packet transmissions. The effectiveness of the proposed approach is demonstrated through simulation studies.