39,159 research outputs found

    The effects of soil moisture, soil texture, and host orientation on the ability of Heterorhabditis bacteriophora (Rhabditida: Heterorhabditidae) to infect Galleria mellonella (Lepidoptera: Pyralidae)

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    Abstract Entomopathogenic nematodes (EPN) demonstrate potential as a biological control for soil dwelling insects. However, edaphic factors, such as soil moisture and texture impact the efficacy of EPN on a host. The objectives were to examine the effects of soil texture and moisture on 1) the infection rate of Galleria mellonella L. by EPN and; 2) the ability of H. bacteriophora (Poinar) to move through the soil to find a host at different orientations. Soil textures consisted of sand, a sand/silt/peat mixture, and a silt/peat mixture at 50% and 100% moisture. A general linear model was used to evaluate infection rates and EPN movement. Both soil moisture (p \u3c 0.05) and texture (p \u3c 0.05) had significant effects on nematodes infection rates of G. mellonella. Texture, moisture, and host orientation did not significantly affect (p \u3e 0.05) the ability of EPN to find a host. While EPN were able to find a host within a variety of soil types, soils that held more water had higher infection rates than soils that held less water, suggesting that moisture may be a key component in facilitating infection by EPN. By understanding the factors that influence the ability of EPN to find and infect a host, improved bio-control programs using EPN can be developed

    Is Self-Abortion a Fundamental Right?

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    CSF sTREM2: Marking the tipping point between preclinical AD and dementia?

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    Biomarkers for Alzheimer's disease (AD) have improved our understanding of the temporal sequence of biological events that lead to AD dementia (Jack et al, 2013). AD is characterized neuropathologically by amyloid plaques comprised of the amyloid‐β peptide and neurofibrillary tangles comprised of tau. Brain amyloid deposition, as evidenced by a decline in amyloid‐β peptide 42 (Aβ42) in the cerebrospinal fluid (CSF) or by binding of amyloid PET ligands, is thought to be a key initiating event in AD and begins many years prior to the onset of dementia. A rise in CSF tau and phosphorylated tau in the setting of Aβ deposition appears to reflect neurodegeneration and also begins years prior to the onset of dementia but after Aβ deposition has begun to accumulate. Individuals with “preclinical AD,” that is, normal cognition but abnormal AD biomarkers, have a much higher risk for developing AD dementia but may remain cognitively normal for years (Vos et al, 2013). While deposition of amyloid and formation of tau tangles are necessary for AD to occur, it is likely that additional events involving inflammation or other processes contribute to crossing the tipping point from preclinical AD to AD dementia. Current efforts are aimed at defining the biomarker(s) that best predict the transition from cognitive normality to abnormality. A biomarker that is closely associated with the onset of cognitive decline could help us to understand the biological events that connect amyloid deposition and tangle formation to cognitive decline and could have significant practical value in AD diagnosis and clinical trial design
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