3,075 research outputs found

    Atlanta Eds and Meds: Collaboration or Competition

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    Metropolitan Atlanta’s universities and hospitals (“Eds and Meds”), with more than 340,000 jobs created, make a larger contribution to the metro area economy than its Fortune 500 headquarters. Its universities have many joint research projects, but major hospitals are much more competitive. Best practice cities showed much more collaboration across the board. This study describes the eleven significant collaborative projects in detail, how and when they were started, the university and medical partners, federal, state and other funding sources. Surprisingly with less than half the hospitals and many major universities participating, significant breakthroughs for global health including COVID-19, EBOLA, HIV-AIDS, cancer, infectious disease, and transplants have been achieved. The pandemic showed major weaknesses in the relationship between public health agencies, hospitals and the public necessary to detect and treat the disease’s impact resulting in Georgia being among the lowest vaccinated states. This research, which includes the collection and analysis of proprietary institutional data and more than 125 interviews with Atlanta stakeholders, finds that more collaboration among Eds and Meds institutions would greatly increase Atlanta’s innovative synergy, economic development and resilience. It includes analysis of best practice cities such as Pittsburgh, San Diego, Baltimore and others that have created a “Grand Plan” between local governments, Eds and Meds and private companies committing to investment and collaboration. The paper closes with several recommendations. Public health agencies, state and local government, university medical and public health schools must learn from the pandemic and develop a strong working relationship in anticipation of the next crisis. State and local governments and chambers of commerce should recognize Eds & Meds as a business cluster similar to supply chain, film and financial technology to promote collaboration, research and job growth. An existing or new organization should take the lead in bringing together potential collaborators. State investment in the Georgia Research Alliance should be restored to prior year levels. Atlanta should learn from best practice cities and create a “grand plan” creating a partnership with Eds & Meds committing to significant expansion of collaborative projects and recruit private partners. Eds & Meds can cooperate to recruit, train and hire citizens for entry level jobs and purchase more goods and services locally to reduce income disparities in the region

    Community detection in temporal multilayer networks, with an application to correlation networks

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    Networks are a convenient way to represent complex systems of interacting entities. Many networks contain "communities" of nodes that are more densely connected to each other than to nodes in the rest of the network. In this paper, we investigate the detection of communities in temporal networks represented as multilayer networks. As a focal example, we study time-dependent financial-asset correlation networks. We first argue that the use of the "modularity" quality function---which is defined by comparing edge weights in an observed network to expected edge weights in a "null network"---is application-dependent. We differentiate between "null networks" and "null models" in our discussion of modularity maximization, and we highlight that the same null network can correspond to different null models. We then investigate a multilayer modularity-maximization problem to identify communities in temporal networks. Our multilayer analysis only depends on the form of the maximization problem and not on the specific quality function that one chooses. We introduce a diagnostic to measure \emph{persistence} of community structure in a multilayer network partition. We prove several results that describe how the multilayer maximization problem measures a trade-off between static community structure within layers and larger values of persistence across layers. We also discuss some computational issues that the popular "Louvain" heuristic faces with temporal multilayer networks and suggest ways to mitigate them.Comment: 42 pages, many figures, final accepted version before typesettin

    Selective vulnerability of inhibitory networks in multiple sclerosis.

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    In multiple sclerosis (MS), a chronic demyelinating disease of the central nervous system, neurodegeneration is detected early in the disease course and is associated with the long-term disability of patients. Neurodegeneration is linked to both inflammation and demyelination, but its exact cause remains unknown. This gap in knowledge contributes to the current lack of treatments for the neurodegenerative phase of MS. Here we ask if neurodegeneration in MS affects specific neuronal components and if it is the result of demyelination. Neuropathological examination of secondary progressive MS motor cortices revealed a selective vulnerability of inhibitory interneurons in MS. The generation of a rodent model of focal subpial cortical demyelination reproduces this selective neurodegeneration providing a new preclinical model for the study of neuroprotective treatments

    Conflict of interest and signal interference lead to the breakdown of honest signalling

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    Animals use signals to coordinate a wide range of behaviours, from feeding offspring to predator avoidance. This poses an evolutionary problem, because individuals could potentially signal dishonestly to coerce others into behaving in ways that benefit the signaller. Theory suggests that honest signalling is favoured when individuals share a common interest and signals carry reliable information. Here, we exploit the opportunities offered by bacterial signalling, to test these predictions with an experimental evolution approach. We show that: (1) a reduced relatedness leads to the relative breakdown of signalling; (2) signalling breaks down by the invasion of mutants that show both reduced signalling and reduced response to signal; (3) the genetic route to signalling breakdown is variable; (4) the addition of artificial signal, to interfere with signal information, also leads to reduced signalling. Our results provide clear support for signalling theory, but we did not find evidence for the previously predicted coercion at intermediate relatedness, suggesting that mechanistic details can alter the qualitative nature of specific predictions. Furthermore, populations evolved under low relatedness caused less mortality to insect hosts, showing how signal evolution in bacterial pathogens can drive the evolution of virulence in the opposite direction to that often predicted by theory

    Histone deacetylase adaptation in single ventricle heart disease and a young animal model of right ventricular hypertrophy.

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    BackgroundHistone deacetylase (HDAC) inhibitors are promising therapeutics for various forms of cardiac diseases. The purpose of this study was to assess cardiac HDAC catalytic activity and expression in children with single ventricle (SV) heart disease of right ventricular morphology, as well as in a rodent model of right ventricular hypertrophy (RVH).MethodsHomogenates of right ventricle (RV) explants from non-failing controls and children born with a SV were assayed for HDAC catalytic activity and HDAC isoform expression. Postnatal 1-day-old rat pups were placed in hypoxic conditions, and echocardiographic analysis, gene expression, HDAC catalytic activity, and isoform expression studies of the RV were performed.ResultsClass I, IIa, and IIb HDAC catalytic activity and protein expression were elevated in the hearts of children born with a SV. Hypoxic neonatal rats demonstrated RVH, abnormal gene expression, elevated class I and class IIb HDAC catalytic activity, and protein expression in the RV compared with those in the control.ConclusionsThese data suggest that myocardial HDAC adaptations occur in the SV heart and could represent a novel therapeutic target. Although further characterization of the hypoxic neonatal rat is needed, this animal model may be suitable for preclinical investigations of pediatric RV disease and could serve as a useful model for future mechanistic studies

    Two-photon Lithography for 3D Magnetic Nanostructure Fabrication

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    Ferromagnetic materials have been utilised as recording media within data storage devices for many decades. Confinement of the material to a two dimensional plane is a significant bottleneck in achieving ultra-high recording densities and this has led to the proposition of three dimensional (3D) racetrack memories that utilise domain wall propagation along nanowires. However, the fabrication of 3D magnetic nanostructures of complex geometry is highly challenging and not easily achievable with standard lithography techniques. Here, by using a combination of two-photon lithography and electrochemical deposition, we show a new approach to construct 3D magnetic nanostructures of complex geometry. The magnetic properties are found to be intimately related to the 3D geometry of the structure and magnetic imaging experiments provide evidence of domain wall pinning at a 3D nanostructured junction

    Conflict of interest and signal interference lead to the breakdown of honest signalling

    Get PDF
    Animals use signals to coordinate a wide range of behaviours, from feeding offspring to predator avoidance. This poses an evolutionary problem, because individuals could potentially signal dishonestly to coerce others into behaving in ways that benefit the signaller. Theory suggests that honest signalling is favoured when individuals share a common interest and signals carry reliable information. Here, we exploit the opportunities offered by bacterial signalling, to test these predictions with an experimental evolution approach. We show that: (1) a reduced relatedness leads to the relative breakdown of signalling; (2) signalling breaks down by the invasion of mutants that show both reduced signalling and reduced response to signal; (3) the genetic route to signalling breakdown is variable; (4) the addition of artificial signal, to interfere with signal information, also leads to reduced signalling. Our results provide clear support for signalling theory, but we did not find evidence for the previously predicted coercion at intermediate relatedness, suggesting that mechanistic details can alter the qualitative nature of specific predictions. Furthermore, populations evolved under low relatedness caused less mortality to insect hosts, showing how signal evolution in bacterial pathogens can drive the evolution of virulence in the opposite direction to that often predicted by theory
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