Idiosyncratic Risk and Volatility Bounds, or Can Models with Idiosyncratic Risk Solve the Equity Premium Puzzle?

This paper uses Hansen and Jagannathan's (1991) volatility bounds to evaluate models with idiosyncratic consumption risk. I show that idiosyncratic risk does not change the volatility bounds at all when consumers have CRRA preferences and the distribution of the idiosyncratic shock is independent of the aggregate state. Following Mankiw (1986), I then show that idiosyncratic risk can help to enter the bounds when idiosyncratic uncertainty depends on the aggregate state of the economy. Since individual consumption data are not reliable, I compute an upper bound of the volatility bounds using individual income data and assume that agents have to consume their endowment. I find that the model does not pass the Hansen and Jagannathan test even for very volatile idiosyncratic income data

Electromechanical mapping versus positron emission tomography and single photon emission computed tomography for the detection of myocardial viability in patients with ischemic cardiomyopathy

AbstractObjectivesWe compared catheter-based electromechanical mapping (NOGA system, Biosense-Webster, Haifa, Israel) with positron emission tomography (PET) and single photon emission computed tomography (SPECT) for prediction of reversibly dysfunctional myocardium (RDM) and irreversibly dysfunctional myocardium (IDM) in patients with severe left ventricular dysfunction. Furthermore, we established the optimal discriminatory value of NOGA measurements for distinction between RDM and IDM.BackgroundThe NOGA system can detect viable myocardium but has not been used for prediction of post-revascularization contractile function in patients with ischemic cardiomyopathy.MethodsTwenty patients (19 males, age [mean ± SD] 60 ± 16 years, ejection fraction [EF] 29 ± 6%) underwent viability testing with NOGA and PET or SPECT before revascularization. Left ventricular function was studied at baseline and six months after revascularization.ResultsThe EF increased to 34 ± 13% at six months (p < 0.05 vs. baseline). The 58 RDM and 57 IDM regions differed with regard to unipolar voltage amplitude (UVA) (9.2 ± 3.9 mV vs. 7.6 ± 4.0 mV, p < 0.05), normalized UVA (106 ± 54% vs. 75 ± 39%, p < 0.05), and tracer uptake (76 ± 17% vs. 60 ± 20%, p < 0.05). The NOGA local shortening did not distinguish between RDM and IDM (6.4 ± 5.8% vs. 5.4 ± 6.6%). By receiver operating characteristic curve analysis, myocardial tracer uptake had better diagnostic performance than UVA (area under curve [AUC] ± SE: 0.82 ± 0.04 vs. 0.63 ± 0.05, p < 0.05) and normalized UVA (AUC ± SE: 0.70 ± 0.05, p < 0.05). Optimal threshold was defined as the value yielding sensitivity = specificity for prediction of RDM. Sensitivity and specificity were 59% at a UVA of 8.4 mV, 65% at a normalized UVA of 83%, and 78% at a tracer uptake of 69%.ConclusionsThe NOGA system may discriminate RDM from IDM with optimal discriminatory values for UVA and normalized UVA of 8.4 mV and 83%, respectively. However, the diagnostic performance does not reach the level obtained by PET and SPECT in patients with severe heart failure

Pyramiding of scald resistance genes in four spring barley MAGIC populations

Genome-Wide Association Studies (GWAS) of four Multi-parent Advanced Generation Inter-Cross (MAGIC) populations identified nine regions on chromosomes 1H, 3H, 4H, 5H, 6H and 7H associated with resistance against barley scald disease. Three of these regions are putatively novel resistance Quantitative Trait Loci (QTL). Barley scald is caused by Rhynchosporium commune, one of the most important barley leaf diseases that are prevalent in most barley-growing regions. Up to 40% yield losses can occur in susceptible barley cultivars. Four MAGIC populations were generated in a Nordic Public-Private Pre-breeding of spring barley project (PPP Barley) to introduce resistance to several important diseases. Here, these MAGIC populations consisting of six to eight founders each were tested for scald resistance in field trials in Finland and Iceland. Eight different model covariate combinations were compared for GWAS studies, and the models that deviated the least from the expected p-values were selected. For all QTL, candidate genes were identified that are predicted to be involved in pathogen defence. The MAGIC progenies contained new haplotypes of significant SNP-markers with high resistance levels. The lines with successfully pyramided resistance against scald and mildew and the significant markers are now distributed among Nordic plant breeders and will benefit development of disease-resistant cultivars

A Novel QTL for Powdery Mildew Resistance in Nordic Spring Barley (Hordeum vulgare L. ssp. vulgare) Revealed by Genome-Wide Association Study

The powdery mildew fungus, Blumeria graminis f. sp. hordei is a worldwide threat to barley (Hordeum vulgare L. ssp. vulgare) production. One way to control the disease is by the development and deployment of resistant cultivars. A genome-wide association study was performed in a Nordic spring barley panel consisting of 169 genotypes, to identify marker-trait associations significant for powdery mildew. Powdery mildew was scored during three years (2012–2014) in four different locations within the Nordic region. There were strong correlations between data from all locations and years. In total four QTLs were identified, one located on chromosome 4H in the same region as the previously identified mlo locus and three on chromosome 6H. Out of these three QTLs identified on chromosome 6H, two are in the same region as previously reported QTLs for powdery mildew resistance, whereas one QTL appears to be novel. The top NCBI BLASTn hit of the SNP markers within the novel QTL predicted the responsible gene to be the 26S proteasome regulatory subunit, RPN1, which is required for innate immunity and powdery mildew-induced cell death in Arabidopsis. The results from this study have revealed SNP marker candidates that can be exploited for use in marker-assisted selection and stacking of genes for powdery mildew resistance in barley