Executive pay and performance: did bankers’ bonuses cause the crisis?

This paper examines the pay-performance relationship between executive cash compensation (including bonuses) and company performance for a sample of large UK companies, focusing particularly on the financial services industry, since incentive misalignment has been blamed as one of the factors causing the global financial crisis of 2007–2008. Although we find that pay in the financial services sector is high, the cash-plus-bonus pay-performance sensitivity of financial firms is not significantly higher than in other sectors. Consequently, we conclude that it unlikely that incentive structures could be held responsible for inducing bank executives to focus on short-term results.

Collagen or collagen-related peptide cause (Ca2+)i elevation and increased tyrosine phosphorylation in human megakaryocytes.

Since megakaryocytes are the cellular precursors of platelets we have investigated whether they share responses to platelet agonists, in particular collagen. Although previous studies have reported responses to thrombin in non-human megakaryocytes, through studies of single cell calcium responses and protein tyrosine-phosphorylation we demonstrate for the first time that both isolated human megakaryocytes and CD41/61-positive megakaryocytes derived in culture from CD34+ cells share responses to the platelet agonists collagen, collagen-related peptide and thrombin. The responses to either collagen or CRP were seen only in the most mature megakaryocytes and not in megakaryocyte-like cell lines, suggesting that the response to collagen is a characteristic developed late during megakaryocyte differentiation. These primary cells offer the opportunity to use many molecular and cellular techniques to study and manipulate signalling events in response to platelet receptor agonists, which cannot be performed in the small, anucleate platelet itself.

Protease-activated receptor 2 sensitizes the transient receptor potential vanilloid 4 ion channel to cause mechanical hyperalgesia in mice

Exacerbated sensitivity to mechanical stimuli that are normally innocuous or mildly painful (mechanical allodynia and hyperalgesia) occurs during inflammation and underlies painful diseases. Proteases that are generated during inflammation and disease cleave protease-activated receptor 2 (PAR2) on afferent nerves to cause mechanical hyperalgesia in the skin and intestine by unknown mechanisms. We hypothesized that PAR2-mediated mechanical hyperalgesia requires sensitization of the ion channel transient receptor potential vanilloid 4 (TRPV4). Immunoreactive TRPV4 was coexpressed by rat dorsal root ganglia (DRG) neurons with PAR2, substance P (SP) and calcitonin gene-related peptide (CGRP), mediators of pain transmission. In PAR2-expressing cell lines that either naturally expressed TRPV4 (bronchial epithelial cells) or that were transfected to express TRPV4 (HEK cells), pretreatment with a PAR2 agonist enhanced Ca2+ and current responses to the TRPV4 agonists phorbol ester 4alpha-phorbol 12,13-didecanoate (4alphaPDD) and hypotonic solutions. PAR2-agonist similarly sensitized TRPV4 Ca2+ signals and currents in DRG neurons. Antagonists of phospholipase Cbeta and protein kinases A, C and D inhibited PAR2-induced sensitization of TRPV4 Ca2+ signals and currents. 4alphaPDD and hypotonic solutions stimulated SP and CGRP release from dorsal horn of rat spinal cord, and pretreatment with PAR2 agonist sensitized TRPV4-dependent peptide release. Intraplantar injection of PAR2 agonist caused mechanical hyperalgesia in mice and sensitized pain responses to the TRPV4 agonists 4alphaPDD and hypotonic solutions. Deletion of TRPV4 prevented PAR2 agonist-induced mechanical hyperalgesia and sensitization. This novel mechanism, by which PAR2 activates a second messenger to sensitize TRPV4-dependent release of nociceptive peptides and induce mechanical hyperalgesia, may underlie inflammatory hyperalgesia in diseases where proteases are activated and released.

Is missing orographic gravity wave drag near 60°S the cause of the stratospheric zonal wind biases in chemistry–climate models?

Nearly all chemistry–climate models (CCMs) have a systematic bias of a delayed springtime breakdown of the Southern Hemisphere (SH) stratospheric polar vortex, implying insufficient stratospheric wave drag. In this study the Canadian Middle Atmosphere Model (CMAM) and the CMAM Data Assimilation System (CMAM-DAS) are used to investigate the cause of this bias. Zonal wind analysis increments from CMAMDAS reveal systematic negative values in the stratosphere near 608S in winter and early spring. These are interpreted as indicating a bias in the model physics, namely, missing gravity wave drag (GWD). The negative analysis increments remain at a nearly constant height during winter and descend as the vortex weakens, much like orographic GWD. This region is also where current orographic GWD parameterizations have a gap in wave drag, which is suggested to be unrealistic because of missing effects in those parameterizations. These findings motivate a pair of free-runningCMAMsimulations to assess the impact of extra orographicGWDat 608S. The control simulation exhibits the cold-pole bias and delayed vortex breakdown seen in the CCMs. In the simulation with extra GWD, the cold-pole bias is significantly reduced and the vortex breaks down earlier. Changes in resolved wave drag in the stratosphere also occur in response to the extra GWD, which reduce stratospheric SH polar-cap temperature biases in late spring and early summer. Reducing the dynamical biases, however, results in degraded Antarctic column ozone. This suggests that CCMs that obtain realistic column ozone in the presence of an overly strong and persistent vortex may be doing so through compensating errors.

Training pharmacists to deliver a complex information technology intervention (PINCER) using the principles of educational outreach and root cause analysis

Objective: To describe the training undertaken by pharmacists employed in a pharmacist-led information technology-based intervention study to reduce medication errors in primary care (PINCER Trial), evaluate pharmacists’ assessment of the training, and the time implications of undertaking the training. Methods: Six pharmacists received training, which included training on root cause analysis and educational outreach, to enable them to deliver the PINCER Trial intervention. This was evaluated using self-report questionnaires at the end of each training session. The time taken to complete each session was recorded. Data from the evaluation forms were entered onto a Microsoft Excel spreadsheet, independently checked and the summary of results further verified. Frequencies were calculated for responses to the three-point Likert scale questions. Free-text comments from the evaluation forms and pharmacists’ diaries were analysed thematically. Key findings: All six pharmacists received 22 hours of training over five sessions. In four out of the five sessions, the pharmacists who completed an evaluation form (27 out of 30 were completed) stated they were satisfied or very satisfied with the various elements of the training package. Analysis of free-text comments and the pharmacists’ diaries showed that the principles of root cause analysis and educational outreach were viewed as useful tools to help pharmacists conduct pharmaceutical interventions in both the study and other pharmacy roles that they undertook. The opportunity to undertake role play was a valuable part of the training received. Conclusions: Findings presented in this paper suggest that providing the PINCER pharmacists with training in root cause analysis and educational outreach contributed to the successful delivery of PINCER interventions and could potentially be utilised by other pharmacists based in general practice to deliver pharmaceutical interventions to improve patient safety.

Does political proximity to the U.S. cause terror?

We analyze the impact of political proximity to the United States on the occurrence and severity of terror. Employing panel data for 116 countries over the period 1975–2001 we find that countries voting in line with the U.S. are victims of more and deadlier attacks.

Cox-dependent fatty acid metabolites cause pain through activation of the irritant receptor TRPA1.

Prostaglandins (PG) are known to induce pain perception indirectly by sensitizing nociceptors. Accordingly, the analgesic action of nonsteroidal anti-inflammatory drugs (NSAIDs) results from inhibition of cyclooxygenases and blockade of PG biosynthesis. Cyclopentenone PGs, 15-d-PGJ(2), PGA(2), and PGA(1), formed by dehydration of their respective parent PGs, PGD(2), PGE(2), and PGE(1), possess a highly reactive alpha,beta-unsaturated carbonyl group that has been proposed to gate the irritant transient receptor potential A1 (TRPA1) channel. Here, by using TRPA1 wild-type (TRPA1(+/+)) or deficient (TRPA1(-/-)) mice, we show that cyclopentenone PGs produce pain by direct stimulation of nociceptors via TRPA1 activation. Cyclopentenone PGs caused a robust calcium response in dorsal root ganglion (DRG) neurons of TRPA1(+/+), but not of TRPA1(-/-) mice, and a calcium-dependent release of sensory neuropeptides from the rat dorsal spinal cord. Intraplantar injection of cyclopentenone PGs stimulated c-fos expression in spinal neurons of the dorsal horn and evoked an instantaneous, robust, and transient nociceptive response in TRPA1(+/+) but not in TRPA1(-/-) mice. The classical proalgesic PG, PGE(2), caused a slight calcium response in DRG neurons, increased c-fos expression in spinal neurons, and induced a delayed and sustained nociceptive response in both TRPA1(+/+) and TRPA1(-/-) mice. These results expand the mechanism of NSAID analgesia from blockade of indirect nociceptor sensitization by classical PGs to inhibition of direct TRPA1-dependent nociceptor activation by cyclopentenone PGs. Thus, TRPA1 antagonism may contribute to suppress pain evoked by PG metabolites without the adverse effects of inhibiting cyclooxygenases.

Dominant β-catenin mutations cause intellectual disability with recognizable syndromic features

The recent identification of multiple dominant mutations in the gene encoding β-catenin in both humans and mice has enabled exploration of the molecular and cellular basis of β-catenin function in cognitive impairment. In humans, β-catenin mutations that cause a spectrum of neurodevelopmental disorders have been identified. We identified de novo β-catenin mutations in patients with intellectual disability, carefully characterized their phenotypes, and were able to define a recognizable intellectual disability syndrome. In parallel, characterization of a chemically mutagenized mouse line that displays features similar to those of human patients with β-catenin mutations enabled us to investigate the consequences of β-catenin dysfunction through development and into adulthood. The mouse mutant, designated batface (Bfc), carries a Thr653Lys substitution in the C-terminal armadillo repeat of β-catenin and displayed a reduced affinity for membrane-associated cadherins. In association with this decreased cadherin interaction, we found that the mutation results in decreased intrahemispheric connections, with deficits in dendritic branching, long-term potentiation, and cognitive function. Our study provides in vivo evidence that dominant mutations in β-catenin underlie losses in its adhesion-related functions, which leads to severe consequences, including intellectual disability, childhood hypotonia, progressive spasticity of lower limbs, and abnormal craniofacial features in adults

The power of the bond between cause and effect

This article presents a treatment of Jay Wright Forrester's life and achievements. The concentration is on the intellectual provenance, emergence and growth of system dynamics.

On the cause of a magnetospheric flux transfer event

We present a detailed investigation of a magnetospheric flux transfer event (FTE) seen by the Active Magnetospheric Tracer Explorer (AMPTE) UKS and IRM satellites around 1046 UT on October 28, 1984. This event has been discussed many times previously in the literature and has been cited as support for a variety of theories of FTE formation. We make use of a model developed to reproduce ion precipitations seen in the cusp ionosphere. The analysis confirms that the FTE is well explained as a brief excursion into an open low-latitude boundary layer (LLBL), as predicted by two theories of magnetospheric FTEs: namely, that they are bulges in the open LLBL due to reconnection rate enhancements or that they are indentations of the magnetopause by magnetosheath pressure increases (but in the presence of ongoing steady reconnection). The indentation of the inner edge of the open LLBL that these two models seek to explain is found to be shallow for this event. The ion model reproduces the continuous evolution of the ion distribution function between the sheath-like population at the event center and the surrounding magnetospheric populations; it also provides an explanation of the high-pressure core of the event as comprising field lines that were reconnected considerably earlier than those that are draped over it to give the event boundary layer. The magnetopause transition parameter is used to isolate a field rotation on the boundaries of the core, which is subjected to the tangential stress balance test. The test identifies this to be a convecting structure, which is neither a rotational discontinuity (RD) nor a contact discontinuity, but could possibly be a slow shock. In addition, evidence for ion reflection off a weak RD on the magnetospheric side of this structure is found. The event structure is consistent in many ways with features predicted for the open LLBL by analytic MHD theories and by MHD and hybrid simulations. The de Hoffman-Teller velocity of the structure is significantly different from that of the magnetosheath flow, indicating that it is not an indentation caused by a high-pressure pulse in the sheath but is consistent with the motion of newly opened field lines (different from the sheath flow because of the magnetic tension force) deduced from the best fit to the ion data. However, we cannot here rule out the possibility that the sheath flow pattern has changed in the long interval between the two satellites observing the FTE and subsequently emerging into the magnetosheath; thus this test is not conclusive in this particular case. Analysis of the fitted elapsed time since reconnection shows that the core of the event was reconnected in one pulse and the event boundary layer was reconnected in a subsequent pulse. Between these two pulses is a period of very low (but nonzero) reconnection rate, which lasts about 14 mins. Thus the analysis supports, but does not definitively verify, the concept that the FTE is a partial passage into an open LLBL caused by a traveling bulge in that layer produced by a pulse in reconnection rate.

Does fertilizer type and method of application cause significant differences in essential oil yield and composition in rosemary (Rosmarinus officinalis L.)?

Organic fertilizers based on seaweed extract potentially have beneficial effects on many crop plants. Herewe investigate the impact of organic fertilizer on Rosmarinus officinalis measured by both yield and oilquality. Plants grown in a temperature-controlled greenhouse with a natural photoperiod and a controlledirrigation system were treated with seaweed fertilizer and an inorganic fertilizer of matching mineralcomposition but with no organic content. Treatments were either by spraying on to the foliage or wateringdirect to the compost. The essential oil was extracted by hydro-distillation with a Clevenger apparatusand analysed by gas-chromatography mass-spectrometry (GC–MS) and NMR. The chemical composi-tions of the plants were compared, and qualitative differences were found between fertilizer treatmentsand application methods. Thus sprayed seaweed fertilizer showed a significantly higher percentage of�-pinene, �-phellandrene, �-terpinene (monoterpenes) and 3-methylenecycloheptene than other treat-ments. Italicene, �-bisabolol (sesquiterpenes), �-thujene, and E-isocitral (monoterpenes) occurred insignificantly higher percentages for plants watered with the seaweed extract. Each was significantly dif-ferent to the inorganic fertilizer and to controls. The seaweed treatments caused a significant increasein oil amount and leaf area as compared with both inorganic treatments and the control regardless ofapplication method.