Spray-Dried Powder Containing Chitinase and β-1,3-Glucanase with Insecticidal Activity against Ceratitis capitata (Diptera: Tephritidae)

This study focused on obtaining a spray-dried powder containing chitinase and β-1,3-glucanase as active ingredients for the control of agricultural pests. Different carriers were tested in the spray drying of these enzymes. The effectiveness of the application of the enzymes was evaluated against Ceratitis capitata (Diptera: Tephritidae). The combination of maltodextrin (2.5% w/v), gum Arabic (2.5% w/v), and soluble starch (5.0% w/v) as carriers showed the best result of residual activity of β-1,3-glucanase (88.36%) and chitinase (69.82%), with a powder recovery of 45.49%. The optimum conditions for the operational parameters of the spray drying process were: inlet air temperature of 120 °C, drying airflow rate of 1.1 m3/min, feed flow rate of 5.8 mL/min, and nozzle air pressure of 0.4 MPa. The powder produced showed 65.6% efficiency for the control of the fly. These results demonstrated the possibility of using the spray drying process to obtain an enzymatic potential product for biological pest control

Protein kinase cδ deficiency causes mendelian systemic lupus erythematosus with B cell-defective apoptosis and hyperproliferation

International audienceOBJECTIVE: Systemic lupus erythematosus (SLE) is a prototype autoimmune disease that is assumed to occur via a complex interplay of environmental and genetic factors. Rare causes of monogenic SLE have been described, providing unique insights into fundamental mechanisms of immune tolerance. The aim of this study was to identify the cause of an autosomal-recessive form of SLE. METHODS: We studied 3 siblings with juvenile-onset SLE from 1 consanguineous kindred and used next-generation sequencing to identify mutations in the disease-associated gene. We performed extensive biochemical, immunologic, and functional assays to assess the impact of the identified mutations on B cell biology. RESULTS: We identified a homozygous missense mutation in PRKCD, encoding protein kinase δ (PKCδ), in all 3 affected siblings. Mutation of PRKCD resulted in reduced expression and activity of the encoded protein PKCδ (involved in the deletion of autoreactive B cells), leading to resistance to B cell receptor- and calcium-dependent apoptosis and increased B cell proliferation. Thus, as for mice deficient in PKCδ, which exhibit an SLE phenotype and B cell expansion, we observed an increased number of immature B cells in the affected family members and a developmental shift toward naive B cells with an immature phenotype. CONCLUSION: Our findings indicate that PKCδ is crucial in regulating B cell tolerance and preventing self-reactivity in humans, and that PKCδ deficiency represents a novel genetic defect of apoptosis leading to SLE

Resumos concluídos - Medicina

Resumos concluídos - Medicin

Resumos concluídos - Neurociências

Resumos concluídos -  Neurociência