Norway maple (Acer platanoides L), which is among the most invasive tree species in forests of eastern North America, is associated with reduced regeneration of the related native species, sugar maple (Acer saccharum Marsh) and other native flora. To identify traits conferring an advantage to Norway maple, we grew both species through an entire growing season under simulated light regimes mimicking a closed forest understorey vs. a canopy disturbance (gap). Dynamic shade-houses providing a succession of high-intensity direct-light events between longer periods of low, diffuse light were used to simulate the light regimes. We assessed seedling height growth three times in the season, as well as stem diameter, maximum photosynthetic capacity, biomass allocation above- and below-ground, seasonal phenology and phenotypic plasticity. Given the north European provenance of Norway maple, we also investigated the possibility that its growth in North America might be increased by delayed fall senescence. We found that Norway maple had significantly greater photosynthetic capacity in both light regimes and grew larger in stem diameter than sugar maple. The differences in below- and above-ground biomass, stem diameter, height and maximum photosynthesis were especially important in the simulated gap where Norway maple continued extension growth during the late fall. In the gap regime sugar maple had a significantly higher root : shoot ratio that could confer an advantage in the deepest shade of closed understorey and under water stress or browsing pressure. Norway maple is especially invasive following canopy disturbance where the opposite (low root : shoot ratio) could confer a competitive advantage. Considering the effects of global change in extending the potential growing season, we anticipate that the invasiveness of Norway maple will increase in the future.
SUMMARYBALB/c mice were inoculated with Bartonella henselae by both systemic and mucosal routes. Culture analysis of tissues from mice infected intraperitoneally with a high dose of B. henselae yielded positive results 24 hr after infection. However, culture analysis of blood taken between 6 hr and 7 days after infection from groups receiving live B. henselae were negative. Following intraperitoneal infection, B. henselae was detected by polymerase chain reaction in liver and mesenteric lymph nodes by 6 hr and up to 7 days after infection in liver, kidney and spleen tissue. Enzyme-linked immunosorbent assay (ELISA) of serum samples collected as early as 13 days after infection indicated humoral immune responses to B. henselae. Specific humoral responses remained through week 6. Analysis of faecal samples revealed induction of B. henselae-specific immunoglobulin A by day 28 after infection. In addition, B. henselae-specific cellular responses were indicated by a positive delayed-type hypersensitivity and a T helper 1 (Th1) (CD4+ T cell )-type cytokine response following in vitro stimulation of splenocytes. The significance and implications of these data in relation to B. henselae infections are discussed.
In addition to intrinsic genomic and nongenomic alterations, tumor progression is also dependent on the tumor microenvironment (TME, mainly composed of the extracellular matrix (ECM), secreted factors, and bystander immune and stromal cells). In chronic lymphocytic leukemia (CLL), B cells have a defect in cell death; contact with the TME in secondary lymphoid organs dramatically increases the B cells’ survival via the activation of various molecular pathways, including the B cell receptor and CD40 signaling. Conversely, CLL cells increase the permissiveness of the TME by inducing changes in the ECM, secreted factors, and bystander cells. Recently, the extracellular vesicles (EVs) released into the TME have emerged as key arbiters of cross-talk with tumor cells. The EVs’ cargo can contain various bioactive substances (including metabolites, proteins, RNA, and DNA); upon delivery to target cells, these substances can induce intracellular signaling and drive tumor progression. Here, we review recent research on the biology of EVs in CLL. EVs have diagnostic/prognostic significance and clearly influence the clinical outcome of CLL; hence, from the perspective of blocking CLL-TME interactions, EVs are therapeutic targets. The identification of novel EV inhibitors might pave the way to the development of novel combination treatments for CLL and the optimization of currently available treatments (including immunotherapy).
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