Susceptibility of White Spruce Seed Sources to Yellowheaded Spruce Sawfly, \u3ci\u3ePikonema Alaskensis,\u3c/i\u3e(Hymenoptera: Tenthredinidae)

A field caging technique was used to test the susceptibility of 25 white spruce, Picea glauca (Moench) Voss, seed sources to attack by Pikonema alaskensis (Rohwer). No sig- nificant differences were found in the number of eggs laid, number of dessicated eggs, or number of egg slits. Percent oviposition differed significantly within a tree, the south side having more eggs. Bud size differed significantly within trees and between trees but not between seed sources. The number of sawfly eggs laid on a bud could not be related to bud size. There was no significant difference in susceptibility of the seed sources studied to Pikonema alaskensis

Role of the autophagic-lysosomal system on low potassium-induced apoptosis in cultured cerebellar granule cells

Apoptotic and autophagic cell death have been implicated, on the basis of morphological and biochemical criteria, in neuronal loss occurring in neurodegenerative diseases and it has been shown that they may overlap. We have studied the relationship between apoptosis and autophagic cell death in cerebellar granule cells (CGCs) undergoing apoptosis following serum and potassium deprivation. We found that apoptosis is accompanied by an early and marked proliferation of autophagosomal-lysosomal compartments as detected by electron microscopy and immunofluorescence analysis. Autophagy is blocked by hrIGF-1 and forskolin, two well-known inhibitors of CGC apoptosis, as well as by adenovirus-mediated overexpression of Bcl-2. 3-Methyladenine (3-MA) an inhibitor of autophagy, not only arrests this event but it also blocks apoptosis. The neuroprotective effect of 3-MA is accompanied by block of cytochrome c (cyt c) release in the cytosol and by inhibition of caspase-3 activation which, in turn, appears to be mediated by cathepsin B, as CA074-Me, a selective inhibitor of this enzyme, fully blocks the processing of pro-caspase-3. Immunofluorescence analysis demonstratesd that cathepsin B, normally confined inside the lysosomal-endosomal compartment, is released during apoptosis into the cytosol where this enzyme may act as an execution protease. Collectively, these observations indicate that autophagy precedes and is causally connected with the subsequent onset of programmed death

Factors affecting trap catch in pheromone-based monitoring of saddle gall midge Haplodiplosis marginata (Diptera: Cecidomyiidae)

Background: Saddle gall midge, Haplodiplosis marginata (von Roser) (Diptera: Cecidomyiidae), is a pest of cereal crops in Europe. Outbreaks are difficult to predict and effective monitoring tools are required to ensure the effectiveness of pest management options. The female sex pheromone, (R)-2-nonyl butyrate, provides the basis of a highly effective lure for this insect. Here, we demonstrate how the success of this lure can be influenced by parameters such as trap location, lure age, and interference between traps fitted with these lures. Results: A pheromone lure containing (R)-2-nonyl butyrate attracted male midges for at least 9 weeks under field conditions. Pheromone-baited traps performed best when situated away from field margins and below the height of the crop. Interference between nearby traps was evident at distances less than 20 m. Conclusion: The results here offer new insights into the behavioural responses of male H. marginata to the female sex pheromone and provide practical recommendations for the use of H. marginata pheromone traps in the field

Dysregulation of Macrophage-Secreted Cathepsin B Contributes to HIV-1-Linked Neuronal Apoptosis

Chronic HIV infection leads to the development of cognitive impairments, designated as HIV-associated neurocognitive disorders (HAND). The secretion of soluble neurotoxic factors by HIV-infected macrophages plays a central role in the neuronal dysfunction and cell death associated with HAND. One potentially neurotoxic protein secreted by HIV-1 infected macrophages is cathepsin B. To explore the potential role of cathepsin B in neuronal cell death after HIV infection, we cultured HIV-1ADA infected human monocyte-derived macrophages (MDM) and assayed them for expression and activity of cathepsin B and its inhibitors, cystatins B and C. The neurotoxic activity of the secreted cathepsin B was determined by incubating cells from the neuronal cell line SK-N-SH with MDM conditioned media (MCM) from HIV-1 infected cultures. We found that HIV-1 infected MDM secreted significantly higher levels of cathepsin B than did uninfected cells. Moreover, the activity of secreted cathepsin B was significantly increased in HIV-infected MDM at the peak of viral production. Incubation of neuronal cells with supernatants from HIV-infected MDM resulted in a significant increase in the numbers of apoptotic neurons, and this increase was reversed by the addition of either the cathepsin B inhibitor CA-074 or a monoclonal antibody to cathepsin B. In situ proximity ligation assays indicated that the increased neurotoxic activity of the cathepsin B secreted by HIV-infected MDM resulted from decreased interactions between the enzyme and its inhibitors, cystatins B and C. Furthermore, preliminary in vivo studies of human post-mortem brain tissue suggested an upregulation of cathepsin B immunoreactivity in the hippocampus and basal ganglia in individuals with HAND. Our results demonstrate that HIV-1 infection upregulates cathepsin B in macrophages, increases cathepsin B activity, and reduces cystatin-cathepsin interactions, contributing to neuronal apoptosis. These findings provide new evidence for the role of cathepsin B in neuronal cell death induced by HIV-infected macrophages