Coupling Soybean Cyst Nematode Damage to CROPGRO-Soybean

The soybean cyst nematode (SCN) Heterodera glycines Ichinohe is responsible for substantial economic losses in soybean (Glycine max L. Merr.) production throughout the U.S. Results from past efforts to quantify the severity of crop damage resulting from SCN are often subject to variable experimental conditions resulting from differences in weather, soil type, and cultivar. Because of the difficulty in accounting for these variables, a process–oriented crop growth simulation model was chosen as a platform for studying the dynamics of SCN damage and for transferring knowledge between crop production scenarios. The objective of this study was to develop and evaluate hypotheses for coupling SCN damage to the process–oriented crop growth model CROPGRO–Soybean. A monomolecular function was used to relate daily SCN damage to initial population density of SCN eggs. The equation was incorporated into the crop model in order to test two hypotheses of how SCN damage occurs. The first hypothesis was that SCN reduce daily photosynthesis (Pg), while the second hypothesis was that SCN reduce daily potential root water uptake (RWU). Canopy biomass data collected in 1997 and 1998 from a site in Iowa were used to estimate damage function parameters for two distinct coupling points, one applied to reduce daily photosynthesis (Pg) and the other applied to reduce daily potential root water uptake (RWU). Function parameters were estimated by minimizing the log transformation of root mean square error (RMSE) between predicted and measured canopy biomass collected every 2 weeks during the season in Iowa. Biomass data collected in 1997 and 1998 from an independent site in Missouri were used to validate the SCN damage models. The minimum root mean squared errors (RMSE) of canopy and grain biomass were 0.245 and 0.198 log10(kg ha–1), respectively, for the RWU coupling point, and 0.238 and 0.193 log10(kg ha–1), respectively, for the Pg coupling point at the independent site in Missouri. The damage functions transferred very well to the independent site. Validation showed that the Pg coupling point represented the variability of both canopy and final yield data slightly better than the RWU coupling point

Soybean Cyst Nematode Reduces Soybean Yield Without Causing Obvious Aboveground Symptoms

Field experiments were conducted at locations in northern and southern Illinois, central Iowa, and central Missouri from 1997 to 1999 to investigate the effects of Heterodera glycines on soybean growth, development, and yield. A wide range of infestation levels was present at all locations. Two locally adapted cultivars, one resistant to H. glycines, were grown at each location. Cultivars were planted in alternating four-row strips with 76 cm between rows. For each cultivar, 20 1-m-long single-row plots were sampled every 2 weeks starting 4 weeks after planting. Infection by H. glycines reduced plant height and leaf and stem weight on the resistant cultivars in the first 12 weeks after planting, and delayed pod and seed development 12 to 14 weeks after planting. Biomass accumulation was not reduced on the susceptible cultivars until 10 weeks after planting; reduction in pod and seed development occurred throughout the reproductive stages. Susceptible cultivars produced significantly lower yields than resistant cultivars, but the yield reductions were not accompanied by visually detectable symptoms

A Standard Greenhouse Method for Assessing Soybean Cyst Nematode Resistance in Soybean: SCE08 (Standardized Cyst Evaluation 2008)

The soybean cyst nematode (SCN), Heterodera glycines Ichinohe, is distributed throughout the soybean [Glycine max (L.) Merr.] production areas of the United States and Canada (Fig. 1) (26). SCN remains the most economically important pathogen of soybean in North America; the most recent estimate of soybean yield reduction in North America due to SCN totaled 34,659,000 metric tons during 2006 (34)

Elpusztított emlékhelyek

A Magyar Királyi Csendőrségnek négy emlékhelye volt, közülük hármat Budapesten helyezték el a két világháború között, a negyediket Nyitra vármegyében a dualizmus időszakában hozták létre

Separate loci underlie resistance to root infection and leaf scorch during soybean sudden death syndrome

Soybean [Glycine max (L.) Merr.] cultivars show differences in their resistance to both the leaf scorch and root rot of sudden death syndrome (SDS). The syndrome is caused by root colonization by Fusarium virguliforme (ex. F. solani f. sp. glycines). Root susceptibility combined with reduced leaf scorch resistance has been associated with resistance to Heterodera glycines HG Type 1.3.6.7 (race 14) of the soybean cyst nematode (SCN). In contrast, the rhg1 locus underlying resistance to Hg Type 0 was found clustered with three loci for resistance to SDS leaf scorch and one for root infection. The aims of this study were to compare the inheritance of resistance to leaf scorch and root infection in a population that segregated for resistance to SCN and to identify the underlying quantitative trait loci (QTL). “Hartwig”, a cultivar partially resistant to SDS leaf scorch, F. virguliforme root infection and SCN HG Type 1.3.6.7 was crossed with the partially susceptible cultivar “Flyer”. Ninety-two F5-derived recombinant inbred lines and 144 markers were used for map development. Four QTL found in earlier studies were confirmed. One contributed resistance to leaf scorch on linkage group (LG) C2 (Satt277; P = 0.004, R 2 = 15%). Two on LG G underlay root infection at R8 (Satt038; P = 0.0001 R 2 = 28.1%; Satt115; P = 0.003, R 2 = 12.9%). The marker Satt038 was linked to rhg1 underlying resistance to SCN Hg Type 0. The fourth QTL was on LG D2 underlying resistance to root infection at R6 (Satt574; P = 0.001, R 2 = 10%). That QTL was in an interval previously associated with resistance to both SDS leaf scorch and SCN Hg Type 1.3.6.7. The QTL showed repulsion linkage with resistance to SCN that may explain the relative susceptibility to SDS of some SCN resistant cultivars. One additional QTL was discovered on LG G underlying resistance to SDS leaf scorch measured by disease index (Satt130; P = 0.003, R 2 = 13%). The loci and markers will provide tagged alleles with which to improve the breeding of cultivars combining resistances to SDS leaf scorch, root infection and SCN HG Type 1.3.6.7

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.