The construction of a Solanum habrochaites LYC4 introgression line population and the identification of QTLs for resistance to Botrytis cinerea

Tomato (Solanum lycopersicum) is susceptible to grey mold (Botrytis cinerea). Partial resistance to this fungus has been identified in accessions of wild relatives of tomato such as Solanum habrochaites LYC4. In a previous F2 mapping study, three QTLs conferring resistance to B. cinerea (Rbcq1, Rbcq2 and Rbcq4a) were identified. As it was probable that this study had not identified all QTLs involved in resistance we developed an introgression line (IL) population (n = 30), each containing a S. habrochaites introgression in the S. lycopersicum cv. Moneymaker genetic background. On average each IL contained 5.2% of the S. habrochaites genome and together the lines provide an estimated coverage of 95%. The level of susceptibility to B. cinerea for each of the ILs was assessed in a greenhouse trial and compared to the susceptible parent S. lycopersicum cv. Moneymaker. The effect of the three previously identified loci could be confirmed and seven additional loci were detected. Some ILs contains multiple QTLs and the increased resistance to B. cinerea in these ILs is in line with a completely additive model. We conclude that this set of QTLs offers good perspectives for breeding of B. cinerea resistant cultivars and that screening an IL population is more sensitive for detection of QTLs conferring resistance to B. cinerea than the analysis in an F2 population

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Soil carbon of hedgerows and ‘ghost’ hedgerows

Agroforestry can contribute significantly to carbon sequestration in agricultural lands, as carbon accumulates both in tree biomass and the soil. One of the oldest, yet declining, forms of agroforestry in Europe are hedgerow-bordered fields. An analysis of historical maps of our study area in Belgium shows that 70% of the hedgerow network was cleared since 1960, creating a large number of 'ghost' hedgerows. We selected arable fields next to hedgerows, 'ghost' hedgerows and grass strips to study how hedgerow trees influence SOC stocks and how much of these are still present after hedgerow clearing. SOC stocks to a depth of 23 cm reached up to 81.7 +/- 28.8 Mg C ha(-1) in hedgerows, storing a considerably larger amount of soil carbon compared to grass strips (56.6 +/- 14.5 Mg C ha(-1)). These built-up stocks were completely gone in 'ghost' hedgerows (57.9 +/- 14.1 Mg C ha(-1)). In the fields adjacent to hedgerows, SOC stocks were only slightly (and insignificantly) increased compared to stocks in fields with grass strips (56.4 +/- 6.3 vs 55.6 +/- 5.0 Mg C ha(-1)) with an exponential decay up to 30 m from the margin. This trend was still limitedly detectable in 'ghost' hedgerowbordered fields, however stocks were not elevated anymore (53.9 +/- 6.1 Mg C ha(-1)). Since 1960, 4 957 +/- 1 664 Mg C from the soil alone were released back into the atmosphere due to hedgerow removal in the study area. The implementation of a strict hedgerow conservation policy would thus be a highly effective climate change mitigation measure in agricultural landscapes

QTL mapping of insect resistance components of Solanum galapagense

Key message: QTLs for insect resistance parameters, trichome type IV development, and more than 200 non-volatile metabolites, including 76 acyl sugars, all co-locate at the end of Chromosome 2 of Solanum galapagense. Abstract: Host plant resistance is gaining importance as more and more insecticides are being banned due to environmental concerns. In tomato, resistance towards insects is found in wild relatives and has been attributed to the presence of glandular trichomes and their specific phytochemical composition. In this paper, we describe the results from a large-scale QTL mapping of data from whitefly resistance tests, trichome phenotyping and a comprehensive metabolomics analysis in a recombinant inbred line population derived from a cross between the cultivated Solanum lycopersicum and the wild relative S. galapagense, which is resistant to a range of pest insects. One major QTL (Wf-1) was found to govern the resistance against two different whitefly species. This QTL co-localizes with QTLs for the presence of trichomes type IV and V, as well as all 76 acyl sugars detected and about 150 other non-volatile phytochemicals, including methyl esters of the flavonols myricetin and quercetin. Based on these results, we hypothesize that Wf-1 is regulating the formation of glandular trichome type IV on the leaf epidermis, enabling the production and accumulation of bioactive metabolites in this type of trichomes.</p

QTL mapping of insect resistance components of Solanum galapagense

Key message: QTLs for insect resistance parameters, trichome type IV development, and more than 200 non-volatile metabolites, including 76 acyl sugars, all co-locate at the end of Chromosome 2 of Solanum galapagense. Abstract: Host plant resistance is gaining importance as more and more insecticides are being banned due to environmental concerns. In tomato, resistance towards insects is found in wild relatives and has been attributed to the presence of glandular trichomes and their specific phytochemical composition. In this paper, we describe the results from a large-scale QTL mapping of data from whitefly resistance tests, trichome phenotyping and a comprehensive metabolomics analysis in a recombinant inbred line population derived from a cross between the cultivated Solanum lycopersicum and the wild relative S. galapagense, which is resistant to a range of pest insects. One major QTL (Wf-1) was found to govern the resistance against two different whitefly species. This QTL co-localizes with QTLs for the presence of trichomes type IV and V, as well as all 76 acyl sugars detected and about 150 other non-volatile phytochemicals, including methyl esters of the flavonols myricetin and quercetin. Based on these results, we hypothesize that Wf-1 is regulating the formation of glandular trichome type IV on the leaf epidermis, enabling the production and accumulation of bioactive metabolites in this type of trichomes.</p

Antiinflammatory therapy with canakinumab for atherosclerotic disease

BACKGROUND: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. METHODS: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P=0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P=0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P=0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P=0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P=0.31). CONCLUSIONS: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. Copyright © 2017 Massachusetts Medical Society