Evidence for a climate signal in trends of global crop yield variability over the past 50 years

Low variability of crop production from year to year is desirable for many reasons, including reduced income risk and stability of supplies. Therefore, it is important to understand the nature of yield variability, whether it is changing through time, and how it varies between crops and regions. Previous studies have shown that national crop yield variability has changed in the past, with the direction and magnitude dependent on crop type and location. Whilst such studies acknowledge the importance of climate variability in determining yield variability, it has been assumed that its magnitude and its effect on crop production have not changed through time and, hence, that changes to yield variability have been due to non-climatic factors. We address this assumption by jointly examining yield and climate variability for three major crops (rice, wheat and maize) over the past 50 years. National yield time series and growing season temperature and precipitation were de-trended and related using multiple linear regression. Yield variability changed significantly in half of the crop–country combinations examined. For several crop–country combinations, changes in yield variability were related to changes in climate variability.

Femto-chemometrics: the signal processing of fast pulse transients

Traditional chemometrics techniques are augmented with algorithms tailored specifically for the de-noising and analysis of femtosecond duration pulse datasets. The new algorithms provide additional insights on sample responses to broadband excitation and multi-moded propagation phenomena.

Theory and generalization of Monte Carlo models of the BOLD signal source

The dependency of the blood oxygenation level dependent (BOLD) signal on underlying hemodynamics is not well understood. Building a forward biophysical model of this relationship is important for the quantitative estimation of the hemodynamic changes and neural activity underlying functional magnetic resonance imaging (fMRI) signals. We have developed a general model of the BOLD signal which can model both intra- and extravascular signals for an arbitrary tissue model across a wide range of imaging parameters. The model of the BOLD signal was instantiated as a look-up-table (LuT), and was verified against concurrent fMRI and optical imaging measurements of activation induced hemodynamics. Magn Reson Med, 2008. © 2008 Wiley-Liss, Inc.

Corticospinal tract integrity and lesion volume play different roles in chronic hemiparesis and its improvement through motor practice

Background. Initial evidence suggests that the integrity of the ipsilesional corticospinal tract (CST) after stroke is strongly related to motor function in the chronic state but not the treatment gain induced by motor rehabilitation. Objective. We examined the association of motor status and treatment benefit by testing patients with a wide range of severity of hemiparesis of the left and right upper extremity. Method. Diffusion tensor imaging was performed in 22 patients beyond 12 months after onset of stroke with severe to moderate hemiparesis. Motor function was tested before and after 2 weeks of modified constraint-induced movement therapy. Results. CST integrity, but not lesion volume, correlated with the motor ability measures of the Wolf Motor Function Test and the Motor Activity Log. No differences were found between left and right hemiparesis. Motor performance improved significantly with the treatment regime, and did so equally for patients with left and right arm paresis. However, treatment benefit was not associated with either CST integrity or lesion volume. Conclusion. CST integrity correlated best in this small trial with chronic long-term status but not treatment-induced improvements. The CST may play a different role in the mechanisms mediating long-term outcome compared to those underlying practice-induced gains after a chronic plateau in motor function.

A Kind of Integrity: explorations in history and drama

All of our knowledge of history is mediated in one way or another. Even the experience of first hand witnesses are, it may be argued, subject to semiotic influences such as physical and emotional position, attitudinal point of view and accuracy of recall. A great deal of historical knowledge is acquired through dramatised versions of historical events. As the characters who actually took part in historical events become the dramatis personae of re-enacted accounts, their stories are edited not only to meet dramatic necessities but the social, psychological and cultural needs of both storytellers and audience. The process of popularising history in this way thus becomes as much about the effects of events on people as the events themselves. This chapter describes and analyses the way in which four historical events have formed the basis of school based drama workshops that explore this process. The Player in Tom Stoppard’s ‘Rosencrantz and Guildenstern Are Dead’ posits that actors do on stage what others are supposed to do off, which, he claims, ‘is a kind of integrity.’ The chapter discusses how drama may be used to explore not only stories from history but how those stories may be mediated and so become open to multiple interpretations. The process of dramatising events from history provides opportunities to develop and exercise a critical literacy that is concerned not so much with either fact or empathy as with interrogating both why and how stories are told. Thus, the experience of exploring the symbiotic relationship between drama and history is dependent on an internal logic which may indeed be perceived as a kind of integrity.

An enhanced model for small-signal analysis of the phase-shifted full-bridge converter

This paper presents an in-depth critical discussion and derivation of a detailed small-signal analysis of the Phase-Shifted Full-Bridge (PSFB) converter. Circuit parasitics, resonant inductance and transformer turns ratio have all been taken into account in the evaluation of this topology’s open-loop control-to-output, line-to-output and load-to-output transfer functions. Accordingly, the significant impact of losses and resonant inductance on the converter’s transfer functions is highlighted. The enhanced dynamic model proposed in this paper enables the correct design of the converter compensator, including the effect of parasitics on the dynamic behavior of the PSFB converter. Detailed experimental results for a real-life 36V-to-14V/10A PSFB industrial application show excellent agreement with the predictions from the model proposed herein.1

On the application of optimal wavelet filter banks for ECG signal classification

This paper discusses ECG signal classification after parametrizing the ECG waveforms in the wavelet domain. Signal decomposition using perfect reconstruction quadrature mirror filter banks can provide a very parsimonious representation of ECG signals. In the current work, the filter parameters are adjusted by a numerical optimization algorithm in order to minimize a cost function associated to the filter cut-off sharpness. The goal consists of achieving a better compromise between frequency selectivity and time resolution at each decomposition level than standard orthogonal filter banks such as those of the Daubechies and Coiflet families. Our aim is to optimally decompose the signals in the wavelet domain so that they can be subsequently used as inputs for training to a neural network classifier.

Towards (more) integrity in academia: transcending neo-liberal assumption of research and knowledge creation and the “rules” supressing academic freedom

European researchers across heterogeneous disciplines voice concerns and argue for new paths towards a brighter future regarding scientific and knowledge creation and communication. Recently, in biological and natural sciences concerns have been expressed that major threats are intentionally ignored. These threats are challenging Europe’s future sustainability towards creating knowledge that effectively deals with emerging social, environmental, health, and economic problems of a planetary scope. Within social science circles however, the root cause regarding the above challenges, have been linked with macro level forces of neo-liberal ways of valuing and relevant rules in academia and beyond which we take for granted. These concerns raised by heterogeneous scholars in natural and the applied social sciences concern the ethics of today’s research and academic integrity. Applying Bourdieu’s sociology may not allow an optimistic lens if change is possible. Rather than attributing the replication of neo-liberal habitus in intentional agent and institutional choices, Bourdieu’s work raises the importance of thoughtlessly internalised habits in human and social action. Accordingly, most action within a given paradigm (in this case, neo-liberalism) is understood as habituated, i.e. unconsciously reproducing external social fields, even ill-defined ways of valuing. This essay analyses these and how they may help critically analyse the current habitus surrounding research and knowledge production, evaluation, and communication and related aspects of academic freedom. Although it is acknowledged that transformation is not easy, the essay presents arguments and recent theory paths to suggest that change nevertheless may be a realistic hope once certain action logics are encouraged.

Evidence of a topographic signal in surface soil moisture derived from ENVISAT ASAR wide swath data

The susceptibility of a catchment to flooding is affected by its soil moisture prior to an extreme rainfall event. While soil moisture is routinely observed by satellite instruments, results from previous work on the assimilation of remotely sensed soil moisture into hydrologic models have been mixed. This may have been due in part to the low spatial resolution of the observations used. In this study, the remote sensing aspects of a project attempting to improve flow predictions from a distributed hydrologic model by assimilating soil moisture measurements are described. Advanced Synthetic Aperture Radar (ASAR) Wide Swath data were used to measure soil moisture as, unlike low resolution microwave data, they have sufficient resolution to allow soil moisture variations due to local topography to be detected, which may help to take into account the spatial heterogeneity of hydrological processes. Surface soil moisture content (SSMC) was measured over the catchments of the Severn and Avon rivers in the South West UK. To reduce the influence of vegetation, measurements were made only over homogeneous pixels of improved grassland determined from a land cover map. Radar backscatter was corrected for terrain variations and normalized to a common incidence angle. SSMC was calculated using change detection. To search for evidence of a topographic signal, the mean SSMC from improved grassland pixels on low slopes near rivers was compared to that on higher slopes. When the mean SSMC on low slopes was 30–90%, the higher slopes were slightly drier than the low slopes. The effect was reversed for lower SSMC values. It was also more pronounced during a drying event. These findings contribute to the scant information in the literature on the use of high resolution SAR soil moisture measurement to improve hydrologic models.

Decomposition of surface electromyographic signal using Hidden Markov Model

The detection of physiological signals from the motor system (electromyographic signals) is being utilized in the practice clinic to guide the therapist in a more precise and accurate diagnosis of motor disorders. In this context, the process of decomposition of EMG (electromyographic) signals that includes the identification and classification of MUAP (Motor Unit Action Potential) of a EMG signal, is very important to help the therapist in the evaluation of motor disorders. The EMG decomposition is a complex task due to EMG features depend on the electrode type (needle or surface), its placement related to the muscle, the contraction level and the health of the Neuromuscular System. To date, the majority of researches on EMG decomposition utilize EMG signals acquired by needle electrodes, due to their advantages in processing this type of signal. However, relatively few researches have been conducted using surface EMG signals. Thus, this article aims to contribute to the clinical practice by presenting a technique that permit the decomposition of surface EMG signal via the use of Hidden Markov Models. This process is supported by the use of differential evolution and spectral clustering techniques. The developed system presented coherent results in: (1) identification of the number of Motor Units actives in the EMG signal; (2) presentation of the morphological patterns of MUAPs in the EMG signal; (3) identification of the firing sequence of the Motor Units. The model proposed in this work is an advance in the research area of decomposition of surface EMG signals.

Long-latency reductions in gamma power predict hemodynamic changes that underlie the negative BOLD signal

Studiesthat use prolonged periods of sensory stimulation report associations between regional reductions in neural activity and negative blood oxygenation level-dependent (BOLD) signaling. However, the neural generators of the negative BOLD response remain to be characterized. Here, we use single-impulse electrical stimulation of the whisker pad in the anesthetized rat to identify components of the neural response that are related to “negative” hemodynamic changes in the brain. Laminar multiunit activity and local field potential recordings of neural activity were performed concurrently withtwo-dimensional optical imaging spectroscopy measuring hemodynamic changes. Repeated measurements over multiple stimulation trials revealed significant variations in neural responses across session and animal datasets. Within this variation, we found robust long-latency decreases (300 and 2000 ms after stimulus presentation) in gammaband power (30 – 80 Hz) in the middle-superficial cortical layers in regions surrounding the activated whisker barrel cortex. This reduction in gamma frequency activity was associated with corresponding decreases in the hemodynamic responses that drive the negative BOLD signal. These findings suggest a close relationship between BOLD responses and neural events that operate over time scales that outlast the initiating sensory stimulus, and provide important insights into the neurophysiological basis of negative neuroimaging signals.

Growth factor receptor-bound protein 2 contributes to (hem)immunoreceptor tyrosine-based activation motif-mediated signaling in platelets

Rationale: Platelets are anuclear cell fragments derived from bone marrow megakaryocytes (MKs) that safeguard vascular integrity but may also cause pathological vessel occlusion. One major pathway of platelet activation is triggered by 2 receptors that signal through an (hem)immunoreceptor tyrosine-based activation motif (ITAM), the activating collagen receptor glycoprotein (GP) VI and the C-type lectin-like receptor 2 (CLEC-2). Growth factor receptor–bound protein 2 (Grb2) is a ubiquitously expressed adapter molecule involved in signaling processes of numerous receptors in different cell types, but its function in platelets and MKs is unknown. Objective: We tested the hypothesis that Grb2 is a crucial adapter protein in (hem)immunoreceptor tyrosine-based activation motif signaling in platelets. Methods and Results: Here, we show that genetic ablation of Grb2 in MKs and platelets did not interfere with MK differentiation or platelet production. However, Grb2-deficiency severely impaired glycoprotein VI–mediated platelet activation because of defective stabilization of the linker of activated T-cell (LAT) signalosome and activation of downstream signaling proteins that resulted in reduced adhesion, aggregation, and coagulant activity on collagen in vitro. Similarly, CLEC-2–mediated signaling was impaired in Grb2-deficient platelets, whereas the cells responded normally to stimulation of G protein–coupled receptors. In vivo, this selective (hem)immunoreceptor tyrosine-based activation motif signaling defect resulted in prolonged bleeding times but affected arterial thrombus formation only after concomitant treatment with acetylsalicylic acid, indicating that defective glycoprotein VI signaling in the absence of Grb2 can be compensated through thromboxane A2–induced G protein–coupled receptor signaling pathways. Conclusions: These results reveal an important contribution of Grb2 in (hem)immunoreceptor tyrosine-based activation motif signaling in platelets in hemostasis and thrombosis by stabilizing the LAT signalosome.

GPVI and CLEC-2 in hemostasis and vascular integrity

The glycoprotein VI (GPVI)-FcR gamma-chain complex initiates powerful activation of platelets by the subendothelial matrix proteins collagen and laminin through an immunoreceptor tyrosine-based activation motif (ITAM)-regulated signaling pathway. ITAMs are characterized by two YxxL sequences separated by 6-12 amino acids and are found associated with several classes of immunoglobulin (Ig) and C-type lectin receptors in hematopoietic cells, including Fc receptors. Cross-linking of the Ig GPVI leads to phosphorylation of two conserved tyrosines in the FcR gamma-chain ITAM by Src family tyrosine kinases, followed by binding and activation of the tandem SH2 domain-containing Syk tyrosine kinase and stimulation of a downstream signaling cascade that culminates in activation of phospholipase Cgamma2 (PLCgamma2). In contrast, the C-type lectin receptor CLEC-2 mediates powerful platelet activation through Src and Syk kinases, but regulates Syk through a novel dimerization mechanism via a single YxxL motif known as a hemITAM. CLEC-2 is a receptor for podoplanin, which is expressed at high levels in several tissues, including type 1 lung alveolar cells, lymphatic endothelial cells, kidney podocytes and some tumors, but is absent from vascular endothelial cells and platelets. In this article, we compare the mechanism of platelet activation by GPVI and CLEC-2 and consider their functional roles in hemostasis and other vascular processes, including maintenance of vascular integrity, angiogenesis and lymphogenesis.

Regulation of early steps of GPVI signal transduction by phosphatases: a systems biology approach

We present a data-driven mathematical model of a key initiating step in platelet activation, a central process in the prevention of bleeding following Injury. In vascular disease, this process is activated inappropriately and causes thrombosis, heart attacks and stroke. The collagen receptor GPVI is the primary trigger for platelet activation at sites of injury. Understanding the complex molecular mechanisms initiated by this receptor is important for development of more effective antithrombotic medicines. In this work we developed a series of nonlinear ordinary differential equation models that are direct representations of biological hypotheses surrounding the initial steps in GPVI-stimulated signal transduction. At each stage model simulations were compared to our own quantitative, high-temporal experimental data that guides further experimental design, data collection and model refinement. Much is known about the linear forward reactions within platelet signalling pathways but knowledge of the roles of putative reverse reactions are poorly understood. An initial model, that includes a simple constitutively active phosphatase, was unable to explain experimental data. Model revisions, incorporating a complex pathway of interactions (and specifically the phosphatase TULA-2), provided a good description of the experimental data both based on observations of phosphorylation in samples from one donor and in those of a wider population. Our model was used to investigate the levels of proteins involved in regulating the pathway and the effect of low GPVI levels that have been associated with disease. Results indicate a clear separation in healthy and GPVI deficient states in respect of the signalling cascade dynamics associated with Syk tyrosine phosphorylation and activation. Our approach reveals the central importance of this negative feedback pathway that results in the temporal regulation of a specific class of protein tyrosine phosphatases in controlling the rate, and therefore extent, of GPVI-stimulated platelet activation.