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Summary: Background. Severe combined immunodeficiency (SCID) is a form of immunodeficiencies (PID), caused by molecular defects. These defects can restrict the development and function of lymphocytes. Early diagnosis and treatment of SCID can lead to disease-free survival. This study aims to investigate some of the possible underlying genetic defects in a group of Egyptian infants and children with clinical and immunological profiles suggestive of SCID. Methods. This study included eighty patients who showed clinical warning signs of immunodeficiency. Subjects were thoroughly examined clinically. Laboratory evaluation included immunoglobulins serum levels and flow cytometric assessment of immune cells. This testing showed an altered immune profile in thirty patients. They had decreased T and/or B lymphocytes or natural killer cells. DNA extraction was done for those cases. The coding regions of the RAG1 gene and RAG2 gene was investigated for hot spot mutations by sequencing technique guided by the patient clinical evaluation, inheritance pattern, immunophenotyping by flow cytometric analysis of lymphocyte subsets, and serum immunoglobulins level detection. Results. Results showed novel and previously reported variants (mutation, polymorphism), they were found in 18 cases which include variants in the RAG1 gene (E880K, A960A, H249R, S913R, K820R, V782G), and variants in the RAG2 gene (P501T, L514M, rs10836573, cDNA.2129A>T). Conclusions. To evaluate SCID patients completely, mutation gene analysis is highly required and recommended.

Soybean aphid, Aphis glycines Matsumura (Hemiptera: Aphidae), a major pest of soybean in the Midwest U.S., is primarily controlled with insecticides, but aphid-resistant plants are becoming available for growers. However, aphid populations can still occasionally build to economically damaging levels on resistant plants, which require treatment with insecticides to protect yields. To determine if resistant plants alter soybean aphid susceptibility to foliar insecticides, aphid populations were monitored over two years from 2014 to 2015 in field experiments with near isogenic soybean lines that were either susceptible or resistant to aphids. Field plots of each soybean line were either untreated or treated with an organophosphate (i.e., chlorpyrifos), a pyrethroid (i.e., λ-cyhalothrin), or a mixture of pyrethrum and azadirachtin. Greenhouse bioassays were also conducted with near isogenic lines and two of the insecticides to examine potential interactions under more controlled conditions. In field plots, organophosphate and pyrethroid treatments significantly reduced cumulative aphid days on at least one soybean line each year; additive effects between resistant plants and insecticides were most common. However, significant synergistic interactions between resistant plants and insecticide were found for λ-cyhalothrin in 2015. On chlorpyrifos-treated plants, a synergistic interaction occurred in 2014 and an antagonistic interaction occurred in 2015, but aphid populations did not exceed those of untreated resistant plants. Interactions between aphid-resistant plants and foliar insecticides were variable, but these tactics generally appear compatible for integrated pest management programs. Growers could benefit from additive and synergistic interactions, and the only documented instance of antagonism had a relatively small effect. [ABSTRACT FROM AUTHOR]

Host-plant resistance (HPR) is an important tool for pest management, affording both economic and environmental benefits. The mechanisms of aphid resistance in soybean are not well understood, but likely involve the induction of the jasmonic acid (JA) pathway, and possibly other phytohormone signals involved in plant defense responses. Despite the efficacy of aphid resistance in soybean, virulent aphids have overcome this resistance through mostly unknown mechanisms. Here, we have used metabolomic tools to define the role of plant phytohormones, especially the JA pathway, in regulating interactions between aphid-resistant soybean and virulent aphids. We hypothesized that virulent aphids avoid or suppress the JA pathway to overcome aphid resistance. Our results suggested that aphid-resistant soybean increased accumulation of JA-isoleucine (JA-Ile) only when infested with avirulent aphids; virulent aphids did not cause induction of JA-Ile. Further, applying JA-Ile to aphid-resistant soybean reduced subsequent virulent aphid populations. The concentrations of other phytohormones remained unchanged due to aphid feeding, highlighting the importance of JA-Ile in this interaction. These results increase our knowledge of soybean resistance mechanisms against soybean aphids and contribute to our understanding of aphid virulence mechanisms, which will in turn promote the durability of HPR., (© The Author(s) 2020. Published by Oxford University Press on behalf of Entomological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)