Impact Assessment of African Agricultural Technology Development and Transfer: Synthesis of Findings and Lessons Learned

Research and Development/Tech Change/Emerging Technologies, Downloads July 2008 - June 2009: 13,

And Tommy Goes, Too

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The management of tree genetic resources and the livelihoods of rural communities in the tropics: non-timber forest products, smallholder agroforestry practices and tree commodity crops

Products and services provided by trees in forests and farmland support the needs and promote the wellbeing of hundreds of millions of people in the tropics. Value depends on managing both the diversity of tree species present in landscapes and the genetic variation within these species. The benefits from trees and their genetic resources are, however, often not well quantified because trade is frequently outside formal markets, there is a multiplicity of species and ways in which trees are used and managed, and genetic diversity within species is frequently not given proper consideration. We review here what is known about the value of trees to rural communities through considering three production categories: non-timber products harvested from trees in natural and managed forests and woodlands; the various products and services obtained from a wide range of trees planted and/or retained in smallholders’ agroforestry systems; and the commercial products harvested from cultivated tree commodity crops. Where possible, we focus on the role of intra-specific genetic variation in providing support to livelihoods, and for each of the three production categories we also consider wider conservation and sustainability issues, including the linkages between categories in terms of management. Challenges to ‘conventional wisdom’ on tree resource use, value and management – such as in the posited links between commercialisation, cultivation and conservation – are highlighted, and constraints and opportunities to maintain and enhance value are described

Economic outcomes associated with deep surgical site infection in patients with an open fracture of the lower limb

Aims The aim of this study was to estimate economic outcomes associated with deep surgical site infection (SSI) in patients with an open fracture of the lower limb. Patients and Methods A total of 460 patients were recruited from 24 specialist trauma hospitals in the United Kingdom Major Trauma Network. Preference-based health-related quality-of-life outcomes, assessed using the EuroQol EQ-5D-3L and the 6-Item Short-Form Health Survey questionnaire (SF-6D), and economic costs (£, 2014/2015 prices) were measured using participant-completed questionnaires over the 12 months following injury. Descriptive statistics and multivariate regression analysis were used to explore the relationship between deep SSI and health utility scores, quality-adjusted life-years (QALYs), and health and personal social service (PSS) costs. Results Deep SSI was associated with lower EQ-5D-3L derived QALYs (adjusted mean difference -0.102, 95% confidence interval (CI) -0.202 to 0.001, p = 0.047) and increased health and social care costs (adjusted mean difference £1950; 95% CI £1383 to £5285, p = 0.250) versus patients without deep SSI over the 12 months following injury. Conclusion Deep SSI may lead to significantly impaired health-related quality of life and increased economic costs. Our economic estimates can be used to inform clinical and budgetary service planning and can act as reference data for future economic evaluations of preventive or treatment interventions

Legionella pneumophila strain 130b evades macrophage cell death independent of the effector SidF in the absence of flagellin

International audienceThe human pathogen Legionella pneumophila must evade host cell death signaling to enable replication in lung macrophages and to cause disease. After bacterial growth, however, L. pneumophila is thought to induce apoptosis during egress from macrophages. The bacterial effector protein, SidF, has been shown to control host cell survival and death by inhibiting pro-apoptotic BNIP3 and BCL-RAMBO signaling. Using live-cell imaging to follow the L. pneumophila-macrophage interaction, we now demonstrate that L. pneumophila evades host cell apoptosis independent of SidF. In the absence of SidF, L. pneumophila was able to replicate, cause loss of mitochondria membrane potential, kill macrophages, and establish infections in lungs of mice. Consistent with this, deletion of BNIP3 and BCL-RAMBO did not affect intracellular L. pneumophila replication, macrophage death rates, and in vivo bacterial virulence. Abrogating mitochondrial cell death by genetic deletion of the effectors of intrinsic apoptosis, BAX, and BAK, or the regulator of mitochondrial permeability transition pore formation, cyclophilin-D, did not affect bacterial growth or the initial killing of macrophages. Loss of BAX and BAK only marginally limited the ability of L. pneumophila to efficiently kill all macrophages over extended periods. L. pneumophila induced killing of macrophages was delayed in the absence of capsase-11 mediated pyroptosis. Together, our data demonstrate that L. pneumophila evades host cell death responses independently of SidF during replication and can induce pyroptosis to kill macrophages in a timely manner

Potential prebiotic substrates modulate composition, metabolism, virulence and inflammatory potential of an in vitro multi-species oral biofilm

Background: Modulation of the commensal oral microbiota constitutes a promising preventive/therapeutic approach in oral healthcare. The use of prebiotics for maintaining/restoring the health-associated homeostasis of the oral microbiota has become an important research topic. Aims: This study hypothesised that in vitro 14-species oral biofilms can be modulated by (in)direct stimulation of beneficial/commensal bacteria with new potential prebiotic substrates tested at 1 M and 1%((w/v)), resulting in more host-compatible biofilms with fewer pathogens, decreased virulence and less inflammatory potential. Methods: Established biofilms were repeatedly rinsed with N-acetyl-D-glucosamine, alpha-D-lactose, D-(+)-trehalose or D-(+)-raffinose at 1 M or 1%((w/v)). Biofilm composition, metabolic profile, virulence and inflammatory potential were eventually determined. Results: Repeated rinsing caused a shift towards a more health-associated microbiological composition, an altered metabolic profile, often downregulated virulence gene expression and decreased the inflammatory potential on oral keratinocytes. At 1 M, the substrates had pronounced effects on all biofilm aspects, whereas at 1%((w/v)) they had a pronounced effect on virulence gene expression and a limited effect on inflammatory potential. Conclusion: Overall, this study identified four new potential prebiotic substrates that exhibit different modulatory effects at two different concentrations that cause in vitro multi-species oral biofilms to become more host-compatible

Physical Properties of Emission-Line Galaxies at z ~ 2 from Near-Infrared Spectroscopy with Magellan FIRE

We present results from near-infrared spectroscopy of 26 emission-line galaxies at z ~ 2 obtained with the FIRE spectrometer on the Magellan Baade telescope. The sample was selected from the WISP survey, which uses the near-infrared grism of the Hubble Space Telescope Wide Field Camera 3 to detect emission-line galaxies over 0.3 < z < 2.3. Our FIRE follow-up spectroscopy (R~5000) over 1.0-2.5 micron permits detailed measurements of physical properties of the z~2 emission-line galaxies. Dust-corrected star formation rates for the sample range from ~5-100 M_sun yr-1. We derive a median metallicity for the sample of ~0.45 Z_sun, and the estimated stellar masses range from ~10^8.5 - 10^9.5 M_sun. The average ionization parameters measured for the sample are typically much higher than what is found for local star-forming galaxies. We derive composite spectra from the FIRE sample, from which we infer typical nebular electron densities of ~100-400 cm^-3. Based on the location of the galaxies and composite spectra on BPT diagrams, we do not find evidence for significant AGN activity in the sample. Most of the galaxies as well as the composites are offset in the BPT diagram toward higher [O III]/H-beta at a given [N II]/H-alpha, in agreement with other observations of z > 1 star-forming galaxies, but composite spectra derived from the sample do not show an appreciable offset from the local star-forming sequence on the [O III]/H-beta versus [S II]/H-alpha diagram. We infer a high nitrogen-to-oxygen abundance ratio from the composite spectrum, which may contribute to the offset of the high-redshift galaxies from the local star-forming sequence in the [O III]/H-beta versus [N II]/H-alpha diagram. We speculate that the elevated nitrogen abundance could result from substantial numbers of Wolf-Rayet stars in starbursting galaxies at z~2. (Abridged)Comment: Accepted for publication in Ap

Myosin VI-Dependent Actin Cages Encapsulate Parkin-Positive Damaged Mitochondria.

Mitochondrial quality control is essential to maintain cellular homeostasis and is achieved by removing damaged, ubiquitinated mitochondria via Parkin-mediated mitophagy. Here, we demonstrate that MYO6 (myosin VI), a unique myosin that moves toward the minus end of actin filaments, forms a complex with Parkin and is selectively recruited to damaged mitochondria via its ubiquitin-binding domain. This myosin motor initiates the assembly of F-actin cages to encapsulate damaged mitochondria by forming a physical barrier that prevents refusion with neighboring populations. Loss of MYO6 results in an accumulation of mitophagosomes and an increase in mitochondrial mass. In addition, we observe downstream mitochondrial dysfunction manifesting as reduced respiratory capacity and decreased ability to rely on oxidative phosphorylation for energy production. Our work uncovers a crucial step in mitochondrial quality control: the formation of MYO6-dependent actin cages that ensure isolation of damaged mitochondria from the network

Regulation of prion gene expression by transcription factors SP1 and metal transcription factor-1

Prion diseases are associated with the conformational conversion of the host-encoded cellular prion protein into an abnormal pathogenic isoform. Reduction in prion protein levels has potential as a therapeutic approach in treating these diseases. Key targets for this goal are factors that affect the regulation of the prion protein gene. Recent in vivo and in vitro studies have suggested a role for prion protein in copper homeostasis. Copper can also induce prion gene expression in rat neurons. However, the mechanism involved in this regulation remains to be determined. We hypothesized that transcription factors SP1 and metal transcription factor-1 (MTF-1) may be involved in copper-mediated regulation of human prion gene. To test the hypothesis, we utilized human fibroblasts that are deleted or overexpressing the Menkes protein (MNK), a major mammalian copper efflux protein. Menkes deletion fibroblasts have high intracellular copper, whereas Menkes overexpressed fibroblasts have severely depleted intracellular copper. We have utilized this system previously to demonstrate copper-dependent regulation of the Alzheimer amyloid precursor protein. Here we demonstrate that copper depletion in MNK overexpressed fibro-blasts decreases cellular prion protein and PRNP gene levels. Conversely, expression of transcription factors SP1 and/or MTF-1 significantly increases prion protein levels and up-regulates prion gene expression in copper-replete MNK deletion cells. Furthermore, siRNA "knockdown" of SP1 or MTF-1 in MNK deletion cells decreases prion protein levels and down-regulates prion gene expression. These data support a novel mechanism whereby SP1 and MTF-1 act as copper-sensing transcriptional activators to regulate human prion gene expression and further support a role for the prion protein to function in copper homeostasis. Expression of the prion protein is a vital component for the propagation ofprion diseases; thus SP1 and MTF-1 represent new targets in the devel-opment of key therapeutics toward modulating the expression of the cellular prion protein and ultimately the prevention of prion disease

Star Formation at 4<z<64 < z < 6 From the Spitzer Large Area Survey with Hyper-Suprime-Cam (SPLASH)

Using the first 50% of data collected for the Spitzer Large Area Survey with Hyper-Suprime-Cam (SPLASH) observations on the 1.8 deg$^2$ Cosmological Evolution Survey (COSMOS) we estimate the masses and star formation rates of 3398 $M_*>10^{10}M_\odot$ star-forming galaxies at $4 < z < 6$ with a substantial population up to $M_* \gtrsim 10^{11.5} M_\odot$. We find that the strong correlation between stellar mass and star formation rate seen at lower redshift (the "main sequence" of star-forming galaxies) extends to $z\sim6$. The observed relation and scatter is consistent with a continued increase in star formation rate at fixed mass in line with extrapolations from lower-redshift observations. It is difficult to explain this continued correlation, especially for the most massive systems, unless the most massive galaxies are forming stars near their Eddington-limited rate from their first collapse. Furthermore, we find no evidence for moderate quenching at higher masses, indicating quenching either has not occurred prior to $z \sim 6$ or else occurs rapidly, so that few galaxies are visible in transition between star-forming and quenched.Comment: ApJL, accepte