Reduced complexity on-line estimation of hidden Markov model parameters

In this paper we propose and study low complexity algorithms for on-line estimation of hidden Markov model (HMM) parameters. The estimates approach the true model parameters as the measurement noise approaches zero, but otherwise give improved estimates, albeit with bias. On a nite data set in the high noise case, the bias may not be signi cantly more severe than for a higher complexity asymptotically optimal scheme. Our algorithms require O(N3) calculations per time instant, where N is the number of states. Previous algorithms based on earlier hidden Markov model signal processing methods, including the expectation-maximumisation (EM) algorithm require O(N4) calculations per time instant.

Predicting reduced driver alertness on monotonous highways : a driving simulator study

Impaired driver alertness increases the likelihood of drivers’ making mistakes and reacting too late to unexpected events while driving. This is particularly a concern on monotonous roads, where a driver’s attention can decrease rapidly. While effective countermeasures do not currently exist, the development of in-vehicle sensors opens avenues for monitoring driving behavior in real-time. The aim of this study is to predict drivers’ level of alertness through surrogate measures collected from in-vehicle sensors. Electroencephalographic activity is used as a reference to evaluate alertness. Based on a sample of 25 drivers, data was collected in a driving simulator instrumented with an eye tracking system, a heart rate monitor and an electrodermal activity device. Various classification models were tested from linear regressions to Bayesians and data mining techniques. Results indicated that Neural Networks were the most efficient model in detecting lapses in alertness. Findings also show that reduced alertness can be predicted up to 5 minutes in advance with 90% accuracy, using surrogate measures such as time to line crossing, blink frequency and skin conductance level. Such a method could be used to warn drivers of their alertness level through the development of an in-vehicle device monitoring, in real-time, drivers' behavior on highways.

Reduced motor facilitation during action observation in schizophrenia : a mirror neuron deficit?

Impairments in social cognitive functioning are well documented in schizophrenia, however the neural basis of these deficits is unclear. A recent explanatory model of social cognition centers upon the activity of mirror neurons, which are cortical brain cells that become active during both the performance and observation of behavior. Here, we test for the first time whether mirror neuron functioning is reduced in schizophrenia. Fifteen individuals with schizophrenia or schizoaffective disorder and fifteen healthy controls completed a transcranial magnetic stimulation (TMS) experiment designed to assess mirror neuron activation. While patients demonstrated no abnormalities in cortical excitability, motor facilitation during action observation, putatively reflecting mirror neuron activity, was reduced in schizophrenia. Dysfunction within the mirror neuron system may contribute to the pathophysiology of schizophrenia.

Estimating the impact of reduced inertia on frequency stability due to large-scale wind penetration in Australian electricity network

Large-scale integration of non-inertial generators such as wind farms will create frequency stability issues due to reduced system inertia. Inertia based frequency stability study is important to predict the performance of power system with increased level of renewables. This paper focuses on the impact large-scale wind penetration on frequency stability of the Australian Power Network. MATLAB simulink is used to develop a frequency based dynamic model utilizing the network data from a simplified 14-generator Australian power system. The loss of generation is modeled as the active power disturbance and minimum inertia required to maintain the frequency stability is determined for five-area power system.

Retinal tissue thickness is reduced in diabetic peripheral neuropathy

Aim Retinal tissue integrity in relation to diabetic neuropathy is not known. The aim of this study was to investigate retinal tissue thickness in relation to diabetic peripheral neuropathy (DPN) with and without diabetic retinopathy (DR). Methods Full retinal thickness at the parafoveal and perifoveal macula and neuro-retinal thickness around the optic nerve head (ONH) and at the macula was examined using spectral domain optical coherence tomography. The eye on the hand-dominant side of 85 individuals with type 1 diabetes and 66 individuals with type 2 diabetes, with or without DR and DPN, were compared to the eyes (n=45) of age-matched non-diabetic controls. Diabetic neuropathy was defined as Neuropathy Disability Score (NDS) ≥3 on a scale of 0-10. A general linear model was used to examine the relationship between diabetic neuropathy and foveal, parafoveal and perifoveal retinal thickness and neuro-retinal thickness, in relation to DR status, age, gender, HbA1c levels and duration of diabetes. A p-value of <0.05 was considered statistically significant. Results Perifoveal retinal thickness is reduced with increasing severity of neuropathy, especially in the inferior hemisphere (p=0.004); this effect was not related to age (p=0.088). For every unit increase in NDS score, the inferior perifoveal retinal thickness reduced by 1.64 μm. Neuro-retinal thickness around the ONH decreased with increasing severity of neuropathy (p<0.014 for average and hemisphere thicknesses); for every unit increase in NDS, neuro-retinal thickness around the ONH reduced by 1.23 μm. Retinal thickness in the parafovea was increased in the absence of DR (p<0.017 for average and hemisphere thicknesses). Neuro-retinal thickness at the macula was inversely related to age alone (p<0.001). All retinal parameters, except the inferior perifovea, reduced with advancing age (p<0.007 for all). Conclusions Diabetic neuropathy is associated with changes in full retinal thickness and neuro-retinal layers. This may represent a second threat to vision integrity, in addition to the better-characterised retinopathy. This study provides new knowledge about the anatomical aspects of the retinal tissue in relation to neuropathy and retinopathy.

Interaction of erythrocyte eicosapentaenoic acid and physical activity predicts reduced risk of mild cognitive impairment

Objectives To evaluate relationships between self-reported physical activity, proportions of long-chain omega-3 polyunsaturated fatty acids (LCn3) in erythrocyte content (percentage of total fatty acids) and risk of mild cognitive impairment (MCI) in older adults. Method A cross-sectional study was conducted. Community-dwelling male and female (n = 84) participants over the age of 65 years with and without MCI were tested for erythrocyte proportions of the LCn3s eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Physical activity was measured using a validated questionnaire. Results The interaction between erythrocyte EPA, but not DHA, and increased physical activity was associated with increased odds of a non-MCI classification. Conclusion An interaction between physical activity and erythrocyte EPA content (percentage of fatty acids) significantly predicted MCI status in older adults. Randomised control trials are needed to examine the potential for supplementation with EPA in combination with increased physical activity to mitigate the risk of MCI in ageing adults.

Surface engineering of reduced graphene oxide for controllable ambipolar flash memories

Tunable charge-trapping behaviors including unipolar charge trapping of one type of charge carrier and ambipolar trapping of both electrons and holes in a complementary manner is highly desirable for low power consumption multibit flash memory design. Here, we adopt a strategy of tuning the Fermi level of reduced graphene oxide (rGO) through self-assembled monolayer (SAM) functionalization and form p-type and n-type doped rGO with a wide range of manipulation on work function. The functionalized rGO can act as charge-trapping layer in ambipolar flash memories, and a dramatic transition of charging behavior from unipolar trapping of electrons to ambipolar trapping and eventually to unipolar trapping of holes was achieved. Adjustable hole/electron injection barriers induce controllable Vth shift in the memory transistor after programming operation. Finally, we transfer the ambipolar memory on flexible substrates and study their charge-trapping properties at various bending cycles. The SAM-functionalized rGO can be a promising candidate for next-generation nonvolatile memories.

Rotational cryptanalysis of round-reduced Keccak

In this paper we attack round-reduced Keccak hash function with a technique called rotational cryptanalysis. We focus on Keccak variants proposed as SHA-3 candidates in the NIST’s contest for a new standard of cryptographic hash function. Our main result is a preimage attack on 4-round Keccak and a 5-round distinguisher on Keccak-f[1600] permutation — the main building block of Keccak hash function.

Reduced intensity conditioning for allogeneic hematopoietic stem cell transplant determines the kinetics of acute Graft-Versus-Host Disease

Background Preparative myeloablative conditioning regimens for allogeneic hematopoietic stem-cell transplantation (HSCT) may control malignancy and facilitate engraftment but also contribute to transplant related mortality, cytokine release, and acute graft-versus-host disease (GVHD). Reduced intensity conditioning (RIC) regimens have decreased transplant related mortality but the incidence of acute GVHD, while delayed, remains unchanged. There are currently no in vivo allogeneic models of RIC HSCT, limiting studies into the mechanism behind RIC-associated GVHD. Methods We developed two RIC HSCT models that result in delayed onset GVHD (major histocompatibility complex mismatched (UBI-GFP/BL6 [H-2b]→BALB/c [H-2d]) and major histocompatibility complex matched, minor histocompatibility mismatched (UBI-GFP/BL6 [H-2b]→BALB.B [H-2b])) enabling the effect of RIC on chimerism, dendritic cell (DC) chimerism, and GVHD to be investigated. Results In contrast with myeloablative conditioning, we observed that RIC-associated delayed-onset GVHD is characterized by low production of tumor necrosis factor-α, maintenance of host DC, phenotypic DC activation, increased T-regulatory cell numbers, and a delayed emergence of activated donor DC. Furthermore, changes to the peritransplant milieu in the recipient after RIC lead to the altered activation of DC and the induction of T-regulatory responses. Reduced intensity conditioning recipients suffer less early damage to GVHD target organs. However, as donor cells engraft, activated donor DC and rising levels of tumor necrosis factor-α are associated with a later onset of severe GVHD. Conclusions Delineating the mechanisms underlying delayed onset GVHD in RIC HSCT recipients is vital to improve the prediction of disease onset and allow more targeted interventions for acute GVHD.

Experimentally reduced hip-abductor muscle strength and frontal-plane biomechanics during walking

Researchers have postulated that reduced hip-abductor muscle strength may have a role in the progression of knee osteoarthritis by increasing the external knee-adduction moment. However, the relationship between hip-abductor strength and frontal-plane biomechanics remains unclear. To experimentally reduce hip-abduction strength and observe the subsequent changes in frontal-plane biomechanics. Descriptive laboratory study. Research laboratory. Eight healthy, recreationally active men (age = 27 ± 6 years, height = 1.75 ± 0.11 m, mass = 76.1 ± 10.0 kg). All participants underwent a superior gluteal nerve block injection to reduce the force output of the hip-abductor muscle group. Maximal isometric hip-abduction strength and gait biomechanical data were collected before and after the injections. Gait biomechanical variables collected during walking consisted of knee- and hip-adduction moments and impulses and the peak angles of contralateral pelvic drop, hip adduction, and ipsilateral trunk lean. Hip-abduction strength was reduced after the injection (P = .001) and remained lower than baseline values at the completion of the postinjection gait data collection (P = .02). No alterations in hip- or knee-adduction moments (hip: P = .11; knee: P = .52) or impulses (hip: P = .16; knee: P = .41) were found after the nerve block. Similarly, no changes in angular kinematics were observed for contralateral pelvic drop (P = .53), ipsilateral trunk lean (P = .78), or hip adduction (P = .48). A short-term reduction in hip-abductor strength was not associated with alterations in the frontal-plane gait biomechanics of young, healthy men. Further research is needed to determine whether a similar relationship is true in older adults with knee osteoarthritis.

Property law reforms in Queensland: Is the regulatory burden on land transactions reduced?

The reduction of unnecessary regulation was a clear policy objective of the Queensland government during 2014. In the area of property sales significant reforms were introduced from 1 December 2014. This article examines the key aspects of these reforms and whether there has been a reduction in red tape for sellers and buyers of land.

N-ethyl-N-nitrosourea (ENU) induced mutations within the Klotho gene lead to ectopic calcification and reduced lifespan in mouse models

Ectopic calcification (EC), which is the pathological deposition of calcium and phosphate in extra-skeletal tissues, may be associated with hypercalcaemic and hyperphosphataemic disorders, or it may occur in the absence of metabolic abnormalities. In addition, EC may be inherited as part of several monogenic disorders and studies of these have provided valuable insights into the metabolic pathways regulating mineral metabolism. For example, studies of tumoural calcinosis, a disorder characterised by hyperphosphataemia and progressive EC, have revealed mutations of fibroblast growth factor 23 (FGF23), polypeptide N-acetyl galactosaminyltransferase 3 (GALNT3) and klotho (KL), which are all part of a phosphate-regulating pathway. However, such studies in humans are limited by the lack of available large families with EC, and to facilitate such studies we assessed the progeny of mice treated with the chemical mutagen N-ethyl-N-nitrosourea (ENU) for EC. This identified two mutants with autosomal recessive forms of EC, and reduced lifespan, designated Ecalc1 and Ecalc2. Genetic mapping localized the Ecalc1 and Ecalc2 loci to a 11.0 Mb region on chromosome 5 that contained the klotho gene (Kl), and DNA sequence analysis identified nonsense (Gln203Stop) and missense (Ile604Asn) Kl mutations in Ecalc1 and Ecalc2 mice, respectively. The Gln203Stop mutation, located in KL1 domain, was severely hypomorphic and led to a 17-fold reduction of renal Kl expression. The Ile604Asn mutation, located in KL2 domain, was predicted to impair klotho protein stability and in vitro expression studies in COS-7 cells revealed endoplasmic reticulum retention of the Ile604Asn mutant. Further phenotype studies undertaken in Ecalc1 (kl203X/203X) mice demonstrated elevations in plasma concentrations of phosphate, FGF23 and 1,25-dihydroxyvitamin D. Thus, two allelic variants of Kl that develop EC and represent mouse models for tumoural calcinosis have been established. © 2015 Esapa et al.