Biogenesis, structure, and immune-suppressive effects of virus-like particles of a Drosophila parasitoid, Leptopilina victoriae.

Drosophila melanogaster larvae are attacked by virulent strains of parasitoid wasps. Females of Leptopilina heterotoma produce virus-like particles (VLPs) that efficiently destroy lamellocytes, a major larval immune effector cell type. We report here that L. victoriae, a closely related wasp species, also produces VLPs that trigger immune suppression responses in fly hosts. We compare the ability of immune suppression of the two parasitoids using a mutant host strain hopscotch(Tumorous-lethal) (hop(Tum-l)). hop(Tum-l) larvae have two defects of hematopoietic origin: overproliferation of hemocytes and constitutive encapsulation of self-tissue by lamellocytes. The encapsulation phenotype is suppressed weakly by L. victoriae and strongly by L. heterotoma. In vitro studies on hop(Tum-l) lamellocytes show that VLP-containing fluid from either wasp species induces lamellocyte lysis, but with different kinetics. Previously undocumented precursors of L. victoriae VLPs are synthesized in the long gland and are first visible within canals connecting secretory cells to the long gland lumen. VLP assembly occurs in the lumen. VLPs show multiple electron-dense projections surrounding a central core. Maturing particles appear segmented, singly or in arrays, embedded in the reservoir matrix. In sections, mature particles are pentagonal or hexagonal; the polygon vertices extending into spikes. Our results suggest that L. victoriae is likely to promote immune suppression by an active mechanism that is mediated by VLPs, similar to that used by L. heterotoma.

Carotid intima-media thickness and plaque assessment by trained medical residents: validation and preliminary testing of a training protocol.

BACKGROUND: Training of nonsonographer physicians or staff members is needed to implement carotid intima-media thickness (CIMT) and plaque screening by ultrasound for the assessment of subclinical atherosclerosis. The purpose of this study was to determine the effect of formal training on CIMT assessment and plaque detection by medical residents. METHODS: A medical resident (R1) was trained using an abbreviated American Society of Echocardiography CIMT protocol. CIMT and plaque assessment by R1 were compared against an expert scanner on 60 subjects using a portable US system. A second medical resident (R2) was then trained on the CIMT protocol focusing on plaque visualization after the results of the first phase of the study were analyzed, and the results were compared against an expert on an additional 10 subjects. RESULTS: In the first phase of the study, a total of 106 images (94% interpretable) were available for CIMT and plaque assessment by both R1 and the expert. CIMT measurements were bioequivalent within the limits of ultrasound resolution, with 88% agreement. Variability on plaque presence was high, with only 53% agreement. R2 and the expert each scanned 10 new subjects twice, from whom 40 images were available for interpretation. R2 demonstrated CIMT agreement (93%) comparable with that observed in phase 1 but with greatly improved plaque agreement (100%). Intraobserver variability during phase 2 for both R2 and the expert was extremely low. CONCLUSIONS: Medical residents can undergo rapid training for CIMT measurement and plaque visualization to detect subclinical atherosclerosis compared with an expert.