Joint data assimilation of satellite reflectance and net ecosystem exchange data constrains ecosystem carbon fluxes at a high-elevation subalpine forest

We utilized an ecosystem process model (SIPNET, simplified photosynthesis and evapotranspiration model) to estimate carbon fluxes of gross primary productivity and total ecosystem respiration of a high-elevation coniferous forest. The data assimilation routine incorporated aggregated twice-daily measurements of the net ecosystem exchange of CO2 (NEE) and satellite-based reflectance measurements of the fraction of absorbed photosynthetically active radiation (fAPAR) on an eight-day timescale. From these data we conducted a data assimilation experiment with fifteen different combinations of available data using twice-daily NEE, aggregated annual NEE, eight-day f AP AR, and average annual fAPAR. Model parameters were conditioned on three years of NEE and fAPAR data and results were evaluated to determine the information content from the different combinations of data streams. Across the data assimilation experiments conducted, model selection metrics such as the Bayesian Information Criterion and Deviance Information Criterion obtained minimum values when assimilating average annual fAPAR and twice-daily NEE data. Application of wavelet coherence analyses showed higher correlations between measured and modeled fAPAR on longer timescales ranging from 9 to 12 months. There were strong correlations between measured and modeled NEE (R2, coefficient of determination, 0.86), but correlations between measured and modeled eight-day fAPAR were quite poor (R2 = −0.94). We conclude that this inability to determine fAPAR on eight-day timescale would improve with the considerations of the radiative transfer through the plant canopy. Modeled fluxes when assimilating average annual fAPAR and annual NEE were comparable to corresponding results when assimilating twice-daily NEE, albeit at a greater uncertainty. Our results support the conclusion that for this coniferous forest twice-daily NEE data are a critical measurement stream for the data assimilation. The results from this modeling exercise indicate that for this coniferous forest, average annuals for satellite-based fAPAR measurements paired with annual NEE estimates may provide spatial detail to components of ecosystem carbon fluxes in proximity of eddy covariance towers. Inclusion of other independent data streams in the assimilation will also reduce uncertainty on modeled values.

Mens rea in joint enterprise: a role for endorsement?

This paper argues that the problems commonly associated with the joint enterprise doctrine might be alleviated by supplementing the cognitive mens rea standard of foresight with a volitional element that looks to how the defendant related to the foreseen risk. A re-examination of the case law suggests that a mens rea conception of foresight plus endorsement might be within interpretative reach. The paper considers possible objections to such a development but ultimately rejects them. It concludes that it is not necessary to wait for Parliament to put in place reforms: joint enterprise is a creature of the common law, and the common law is able to tame it unaided.

Spontaneous facial mimicry is modulated by joint attention and autistic traits

Joint attention (JA) and spontaneous facial mimicry (SFM) are fundamental processes in social interactions, and they are closely related to empathic abilities. When tested independently, both of these processes have been usually observed to be atypical in individuals with autism spectrum conditions (ASC). However, it is not known how these processes interact with each other in relation to autistic traits. This study addresses this question by testing the impact of JA on SFM of happy faces using a truly interactive paradigm. Sixty-two neurotypical participants engaged in gaze-based social interaction with an anthropomorphic, gaze-contingent virtual agent. The agent either established JA by initiating eye contact or looked away, before looking at an object and expressing happiness or disgust. Eye tracking was used to make the agent's gaze behavior and facial actions contingent to the participants' gaze. SFM of happy expressions was measured by Electromyography (EMG) recording over the Zygomaticus Major muscle. Results showed that JA augments SFM in individuals with low compared with high autistic traits. These findings are in line with reports of reduced impact of JA on action imitation in individuals with ASC. Moreover, they suggest that investigating atypical interactions between empathic processes, instead of testing these processes individually, might be crucial to understanding the nature of social deficits in autism

The N-terminal SH2 domain of Syk is required for (hem)ITAM, but not integrin, signaling in mouse platelets

We have used a novel knockin mouse to investigate the effect of disruption of phosphotyrosine binding of the N-terminal SH2 domain of Syk on platelet activation by GPVI, CLEC-2, and integrin αIIbβ3. The Syk(R41Afl/fl) mouse was crossed to a PF4-Cre(+) mouse to induce expression of the Syk mutant in the megakaryocyte/platelet lineage. Syk(R41Afl/fl;PF4-Cre) mice are born at approximately 50% of the expected frequency and have a similar phenotype to Syk(fl/fl;PF4-Cre) mice, including blood-lymphatic mixing and chyloascites. Anastomosis of the venous and lymphatic vasculatures can be seen in the mesenteric circulation accounting for rapid and continuous mixing of the 2 vasculatures. Platelet activation by CLEC-2 and GPVI is abolished in Syk(R41Afl/fl;PF4-Cre) platelets. Syk phosphorylation on Tyr519/20 is blocked in CLEC-2-stimulated platelets, suggesting a model in which binding of Syk via its N-terminal SH2 domain regulates autophosphorylation. In contrast, outside-in signaling by integrin αIIbβ3 is not altered, but it is inhibited in the presence of inhibitors of Src and Syk tyrosine kinases. These results demonstrate that αIIbβ3 regulates Syk through an ITAM-independent pathway in mice and provide novel insight into the course of events underlying Syk activation and hemITAM phosphorylation by CLEC-2.

Towards anomaly detection for increased security in multibiometric systems: spoofing-resistant 1-median fusion eliminating outliers

Multibiometrics aims at improving biometric security in presence of spoofing attempts, but exposes a larger availability of points of attack. Standard fusion rules have been shown to be highly sensitive to spoofing attempts – even in case of a single fake instance only. This paper presents a novel spoofing-resistant fusion scheme proposing the detection and elimination of anomalous fusion input in an ensemble of evidence with liveness information. This approach aims at making multibiometric systems more resistant to presentation attacks by modeling the typical behaviour of human surveillance operators detecting anomalies as employed in many decision support systems. It is shown to improve security, while retaining the high accuracy level of standard fusion approaches on the latest Fingerprint Liveness Detection Competition (LivDet) 2013 dataset.

A joint state and parameter estimation scheme for nonlinear dynamical systems

We present a novel algorithm for concurrent model state and parameter estimation in nonlinear dynamical systems. The new scheme uses ideas from three dimensional variational data assimilation (3D-Var) and the extended Kalman filter (EKF) together with the technique of state augmentation to estimate uncertain model parameters alongside the model state variables in a sequential filtering system. The method is relatively simple to implement and computationally inexpensive to run for large systems with relatively few parameters. We demonstrate the efficacy of the method via a series of identical twin experiments with three simple dynamical system models. The scheme is able to recover the parameter values to a good level of accuracy, even when observational data are noisy. We expect this new technique to be easily transferable to much larger models.

Stimulation of "stress-regulated" mitogen-activated protein kinases (stress-activated protein kinases/c-Jun N-terminal kinases and p38-mitogen-activated protein kinases) in perfused rat hearts by oxidative and other stresses.

"Stress-regulated" mitogen-activated protein kinases (SR-MAPKs) comprise the stress-activated protein kinases (SAPKs)/c-Jun N-terminal kinases (JNKs) and the p38-MAPKs. In the perfused heart, ischemia/reperfusion activates SR-MAPKs. Although the agent(s) directly responsible is unclear, reactive oxygen species are generated during ischemia/reperfusion. We have assessed the ability of oxidative stress (as exemplified by H2O2) to activate SR-MAPKs in the perfused heart and compared it with the effect of ischemia/reperfusion. H2O2 activated both SAPKs/JNKs and p38-MAPK. Maximal activation by H2O2 in both cases was observed at 0.5 mM. Whereas activation of p38-MAPK by H2O2 was comparable to that of ischemia and ischemia/reperfusion, activation of the SAPKs/JNKs was less than that of ischemia/reperfusion. As with ischemia/reperfusion, there was minimal activation of the ERK MAPK subfamily by H2O2. MAPK-activated protein kinase 2 (MAPKAPK2), a downstream substrate of p38-MAPKs, was activated by H2O2 to a similar extent as with ischemia or ischemia/reperfusion. In all instances, activation of MAPKAPK2 in perfused hearts was inhibited by SB203580, an inhibitor of p38-MAPKs. Perfusion of hearts at high aortic pressure (20 kilopascals) also activated the SR-MAPKs and MAPKAPK2. Free radical trapping agents (dimethyl sulfoxide and N-t-butyl-alpha-phenyl nitrone) inhibited the activation of SR-MAPKs and MAPKAPK2 by ischemia/reperfusion. These data are consistent with a role for reactive oxygen species in the activation of SR-MAPKs during ischemia/reperfusion.

The p38-MAPK inhibitor, SB203580, inhibits cardiac stress-activated protein kinases/c-Jun N-terminal kinases (SAPKs/JNKs).

SB203580 is a recognised inhibitor of p38-MAPKs. Here, we investigated the effects of SB203580 on cardiac SAPKs/JNKs. The IC50 for inhibition of p38-MAPK stimulation of MAPKAPK2 was approximately 0.07 microM, whereas that for total SAPK/JNK activity was 3-10 microM. SB203580 did not inhibit immunoprecipitated JNK1 isoforms. Three peaks of SAPK/JNK activity were separated by anion exchange chromatography, eluting in the isocratic wash (44 kDa), and at 0.08 M (46 and 52 kDa) and 0.15 M NaCl (54 kDa). SB203580 (10 microM) completely inhibited the 0.15 M NaCl activity and partially inhibited the 0.08 M NaCl activity. Since JNK1 antibodies immunoprecipitate the 46 kDa activity, this indicates that SB203580 selectively inhibits 52 and 54 kDa SAPKs/JNKs.

Activation of c-Jun N-terminal kinases and p38-mitogen-activated protein kinases in human heart failure secondary to ischaemic heart disease.

Three well-characterized mitogen-activated protein kinase (MAPK) subfamilies are expressed in rodent and rabbit hearts, and are activated by pathophysiological stimuli. We have determined and compared the expression and activation of these MAPKs in donor and failing human hearts. The amount and activation of MAPKs was assessed in samples from the left ventricles of 4 unused donor hearts and 12 explanted hearts from patients with heart failure secondary to ischaemic heart disease. Total MAPKs or dually phosphorylated (activated) MAPKs were detected by Western blotting and MAPK activities were measured by in gel kinase assays. As in rat heart, c-Jun N-terminal kinases (JNKs) were detected in human hearts as bands corresponding to 46 and 54 kDa; p38-MAPK(s) was detected as a band corresponding to approximately 40 kDa, and extracellularly regulated kinases, ERK1 and ERK2, were detected as 44- and 42-kDa bands respectively. The total amounts of 54 kDa JNK, p38-MAPK and ERK2 were similar in all samples, although 46-kDa JNK was reduced in the failing hearts. However, the mean activities of JNKs and p38-MAPK(s) were significantly higher in failing heart samples than in those from donor hearts (P<0.05). There was no significant difference in phosphorylated (activated) ERKs between the two groups. In conclusion, JNKs, p38-MAPK(s) and ERKs are expressed in the human heart and the activities of JNKs and p38-MAPK(s) were increased in heart failure secondary to ischaemic heart disease. These data indicate that JNKs and p38-MAPKs may be important in human cardiac pathology.

Up-regulation of c-jun mRNA in cardiac myocytes requires the extracellular signal-regulated kinase cascade, but c-Jun N-terminal kinases are required for efficient up-regulation of c-Jun protein.

Cardiac hypertrophy, an important adaptational response, is associated with up-regulation of the immediate early gene, c- jun, which encodes the c-Jun transcription factor. c-Jun may feed back to up-regulate its own transcription and, since the c-Jun N-terminal kinase (JNK) family of mitogen-activated protein kinases (MAPKs) phosphorylate c-Jun(Ser-63/73) to increase its transactivating activity, JNKs are thought to be the principal factors involved in c- jun up-regulation. Hypertrophy in primary cultures of cardiac myocytes is induced by endothelin-1, phenylephrine or PMA, probably through activation of one or more of the MAPK family. These three agonists increased c- jun mRNA with the rank order of potency of PMA approximately endothelin-1>phenylephrine. Up-regulation of c- jun mRNA by endothelin-1 was attenuated by inhibitors of protein kinase C (GF109203X) and the extracellular signal-regulated kinase (ERK) cascade (PD98059 or U0126), but not by inhibitors of the JNK (SP600125) or p38-MAPK (SB203580) cascades. Hyperosmotic shock (0.5 M sorbitol) powerfully activates JNKs, but did not increase c- jun mRNA. These data suggest that ERKs, rather than JNKs, are required for c- jun up-regulation. However, endothelin-1 and phenylephrine induced greater up-regulation of c-Jun protein than PMA and phosphorylation of c-Jun(Ser-63/73) correlated with the level of c-Jun protein. Up-regulation of c-Jun protein by endothelin-1 was attenuated by inhibitors of protein kinase C and the ERK cascade, probably correlating with a primary input of ERKs into transcription. In addition, SP600125 inhibited the phosphorylation of c-Jun(Ser-63/73), attenuated the increase in c-Jun protein induced by endothelin-1 and increased the rate of c-Jun degradation. Thus whereas ERKs are the principal MAPKs required for c- jun transcription, JNKs are necessary to stabilize c-Jun for efficient up-regulation of the protein.

Joint use of attribute importance rankings and non-attendance data in choice experiments

The joint and alternative uses of attribute non-attendance and importance ranking data within discrete choice experiments are investigated using data from Lebanon examining consumers’ preferences for safety certification in food. We find that both types of information; attribute non-attendance and importance rankings, improve estimates of respondent utility. We introduce a method of integrating both types of information simultaneously and find that this outperforms models where either importance ranking or non-attendance data are used alone. As in previous studies, stated non-attendance of attributes was not found to be consistent with respondents having zero marginal utility for those attributes

Inexpensive footwear decreases joint loading in elderly women with knee osteoarthritis

Recent literature has highlighted that the flexibility of walking barefoot reduces overload in individuals with knee osteoarthritis (OA). As such, the aim of this study was to evaluate the effects of inexpensive, flexible, non-heeled footwear (Moleca (R)) as compared with a modern heeled shoes and walking barefoot on the knee adduction moment (KAM) during gait in elderly women with and without knee OA. The gait of 45 elderly women between 60 and 70 years of age was evaluated. Twenty-one had knee OR graded 2 or 3 according to Kellgren and Lawrence`s criteria, and 24 who had no OA comprised the control group (CG). The gait conditions were: barefoot, Moleca (R), and modern heeled shoes. Three-dimensional kinematics and ground reaction forces were measured to calculate KAM by inverse dynamics. For both groups, the Moleca (R) provided peak KAM and KAM impulse similar to barefoot walking. For the OA group, the Moleca (R) reduced KAM even more as compared to the barefoot condition during midstance. On the other hand, the modern heeled shoes increased this variable in both groups. Inexpensive, flexible, and non-heeled footwear provided loading on the knee joint similar to a barefoot gait and significant overload decreases in elderly women with and without knee OA, compared to modern heeled shoes. During midstance, the Moleca (R) also allowed greater reduction in the knee joint loads as compared to barefoot gait in elderly women with knee OA, with the further advantage of providing external foot protection during gait. (C) 2011 Elsevier B.V. All rights reserved.