Soybean White Mold: What Have We Learned Since 1992?

White mold, sometimes called Sclerotinia stem rot, remains an important disease of soybean in the midwest. Although other pathogens and pests are more consistent problems, management of white mold usually entails an integrated and often complicated integration of management practices. A white mold management system may fail if one weak link in chain exists. White mold causes direct yield loss, but yield potential may be lost in the absence of the disease if growers have made management adjustments that result in lower yield potential. White mold is best managed by an integrated approach of selecting soybean varieties with the highest level of resistance and adjusting cultural practices to minimize environmental factors that favor disease development. An alternative approach entails a coordinated crop management plan that matches the level of resistance in a soybean cultivar. Most crop management tactics for white mold are linked to speed and extinct of crop canopy closure. No single tactic will completely control white mold

A step toward control of bean pod mottle virus: Identifying field tolerance

So, have you been wondering what to do about all those soybean plants that have mottled leaves? Populations of bean leaf beetles, the insect that efficiently transmits bean pod mottle virus, have been very high. The last issue of the ICM newsletter told you to expect potential yield reductions this fall and reduced seed quality evidenced by seeds that are stained (hilum bleeding). But there may be some soybean cultivars/accessions that are not so bad. We have known for some time that soybean cultivars can vary significantly in response to disease caused by the virus

An Integrated Approach to Control Sclerotinia Stem Rot (White Mold) in Soybean

While brown stem rot, Phytophthora root rot, sudden death syndrome and the soybean cyst nematode generally are regarded as the most significant diseases of soybean in the North Central States, Sclerotinia stem rot, also called white mold, has been a problem in Minnesota, Wisconsin and Michigan for many years. Beginning in 1992, and again in 1994, Sclerotinia stem rot developed throughout the northern range of the North Central Region. Nationally, the disease is considered to be minor because it has not involved a high percentage of the national soybean acreage. Possibly this situation has changed and Sclerotinia stem rot will be an annual threat to soybean production in more of the Region. Chamberlain (1951) was the first to make a detailed report on Sclerotinia stem rot in the mid-west after he observed localized, but severe outbreaks of the disease in lllinois in 1946. Chamberlain (1951) summarized his findings by the following quote; \u27There appears to be no ready explanation as to why Sclerotinia stem rot, certainly one of the least prevalent of soybean diseases, can cause such severe but localized damage . After almost 50 years, more is known about factors that impact on the incidence and severity of this disease, but an element of mystery still remains as to why sudden outbreaks occur

Influence of Aphanomyces Root Rot on Alfalfa Health and Forage Yields

Maximum alfalfa performance is achieved when grown on deep, well drained soils, while severe stand and yield losses can occur on soils that are imperfectly drained (Wing, 1909; Alva et al., 1985). In Wisconsin, nearly half of all forage production is on soils that are classified as somewhat poorly drained

Recent study brings good news about the soybean aphid

Increased activity of bean leaf beetles and soybean aphids in Iowa soybean fields has challenged many of us over the last five years. Not just because of the sap feeding and leaf defoliation that can cause significant yield loss but also because we are dealing with another yield robber that we often can\u27t see. Iowa soybean fields can be infected with bean pod mottle and soybean {m}osaic viruses that are transmitted by bean leaf beetles and soybean aphids, respectively. The challenge that we are dealing with is, first of all, we can\u27t always see that we have a virus in soybean, and yield loss caused by viruses can occur even when symptoms are not apparent

Vascular endothelial cells cultured from patients with cerebral or uncomplicated malaria exhibit differential reactivity to TNF.

Plasmodium falciparum malaria is a major cause of morbidity and mortality in African children, and factors that determine the development of uncomplicated (UM) versus cerebral malaria (CM) are not fully understood. We studied the ex vivo responsiveness of microvascular endothelial cells to pro-inflammatory stimulation and compared the findings between CM and UM patients. In patients with fatal disease we compared the properties of vascular endothelial cells cultured from brain tissue to those cultured from subcutaneous tissue, and found them to be very similar. We then isolated, purified and cultured primary endothelial cells from aspirated subcutaneous tissue of patients with CM (EC(CM) ) or UM (EC(UM) ) and confirmed the identity of the cells before analysis. Upon TNF stimulation in vitro, EC(CM) displayed a significantly higher capacity to upregulate ICAM-1, VCAM-1 and CD61 and to produce IL-6 and MCP-1 but not RANTES compared with EC(UM) . The shedding of endothelial microparticles, a recently described parameter of severity in CM, and the cellular level of activated caspase-3 were both significantly greater in EC(CM) than in EC(UM) . These data suggest that inter-individual differences in the endothelial inflammatory response to TNF may be an additional factor influencing the clinical course of malaria

Cation distribution and mixing thermodynamics in Fe/Ni thiospinels

The structural analogy between Ni-doped greigite minerals (Fe3S4) and the (Fe, Ni)S clusters present in biological enzymes has led to suggestions that these minerals could have acted as catalysts for the origin of life. However, little is known about the distribution and stability of Ni dopants in the greigite structure. We present here a theoretical investigation of mixed thiospinels (Fe1−xNix)3S4, using a combination of density functional theory (DFT) calculations and Monte Carlo simulations. We find that the equilibrium distribution of the cations deviates significantly from a random distribution: at low Ni concentrations, Ni dopants are preferably located in octahedral sites, while at higher Ni concentrations the tetrahedral sites become much more favourable. The thermodynamic mixing behaviour between greigite and polydymite (Ni3S4) is dominated by the stability field of violarite (FeNi2S4), for which the mixing enthalpy exhibits a deep negative minimum. The analysis of the free energy of mixing shows that Ni doping of greigite is very unstable with respect to the formation of a separate violarite phase. The calculated variation of the cubic cell parameter with composition is found to be non-linear, exhibiting significant deviation from Vegard’s law, but in agreement with experiment

The Role of Animal Models for Research on Severe Malaria

In light of the recent controversies over the role of animal models for research into the development of new treatments for severe malaria, particularly cerebral disease, a group of scientists came together to discuss the relative merits of a range of animal models and their overlap with the complex clinical syndromes of human disease. While it was not possible to fully resolve differences over the utility of the Plasmodium berghei ANKA model of experimental cerebral malaria, the meeting did bring the two research communities closer together to identify further work to provide information needed to validate the model and revitalise the development of other animal models displaying features of human pathology. The driving force behind this was the desire to ensure better translation of experimental findings into effective treatments for severe malaria

The Role of Animal Models for Research on Severe Malaria

The Role of Animal Models for Research on Severe Malari

A case of feline gastrointestinal eosinophilic sclerosing fibroplasia associated with phycomycetes

Feline gastrointestinal eosinophilic sclerosing fibroplasia (FGESF) is a recently described inflammatory condition of domestic cats with unknown aetiology. A proportion of cases of FGESF are associated with bacteria, but antibiotic treatment is ineffective. It has been hypothesized that genetically predisposed cats may develop FGESF in response to the introduction of bacteria or other antigens into the intestinal wall. A 9- month-old male Persian cat presented with a history of marked acute haematemesis. A mass (10 cm diameter) was detected within the pylorus and proximal duodenum and this was not surgically accessible. On necropsy examination the duodenal wall was seen to be markedly thickened with extensive mucosal ulceration. Microscopically, there were haphazardly oriented trabecular bands of dense eosinophilic collagen,separated by wide, clear areas containing variable numbers of fibroblasts, eosinophils, mast cells, neutrophils,macrophages, lymphocytes and plasma cells. Numerous pleomorphic, non-parallel walled, sparsely septate hyphae, characteristic of phycomycetes, were present within the collagen matrix. Colonies of gram-positive and gram-negative rods were also present within the lesion. This is the first description of FGESF with intralesional fungi