Cognitive decline leading to dementia, accompanied by the accumulation of amyloid-beta (Aβ) in neuritic plaques together with the appearance of neurofibrillary tangles (NFT) composed of hyperphosphorylated tau protein (tau), are previously noted hallmarks of Alzheimer’s disease (AD). We previously discovered hypervascularity in brain specimens from AD patients and consistent with this observation, we demonstrated that overexpression of Aβ drives cerebrovascular neoangiogenesis leading to hypervascularity and…
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Stem cell homeostasis requires coordinated fate decisions among stem cells that are often widely distributed within a tissue at varying distances from their stem cell niche. This requires a mechanism to ensure robust fate decisions within a population of stem cells. Here, we show that, in the Drosophila hematopoietic organ, the lymph gland (LG), gap junctions form a network that coordinates fate…
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Klebsiella pneumoniae has been implicated in wide-ranging nosocomial outbreaks, causing severe infections without effective treatments due to antibiotic resistance. Here, we performed genome sequencing of 70 extensively drug resistant clinical isolates, collected from Brasília’s hospitals (Brazil) between 2010 and 2014. The majority of strains (60 out of 70) belonged to a single clonal complex (CC), CC258, which has become distributed worldwide…
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In land plants and algae, cellulose is important for strengthening cell walls and preventing breakage due to physical forces. Though our understanding of cellulose production by cellulose synthase enzymes (CESAs) has seen significant advances for several land plant and bacterial species, functional characterization of this fundamental protein is absent in red algae. Here we identify CESA gene candidates in the…
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Huntington disease is an inherited neurodegenerative disorder that affects 1 in 7,500 individuals in the Western world. It is characterized by involuntary movements, cognitive disorders including dementia, eventually leading to death. The cause of Huntington disease is a mutation in the HTT gene, which produces the toxic mutant huntingtin protein. One of the strategies presented in this publication, consists of modulating the level of a post-transcriptional modification of mutant huntingtin, called palmitoylation (the addition of a palmitic acid onto a protein).
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The Mizumoto lab studies the fundamental mechanisms of how our brain develops. In particular, they focus on the specific cellular interface called synapses that the nerve cells use to send and receive information. The number and position of synapses are tightly controlled because it is essential for our brains to function properly. To uncover the genetic and molecular mechanisms underlying precise control of synapse number and position, they use non-parasitic nematode (C. elegans) as an experimental model.
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The claustrum is a brain region implicated in a wide variety of functions - from attention, to sleep, to impulsivity, to consciousness itself. Remarkably, we know relatively little about how this brain region is organized, and understanding this organization can provide critical insight into how such diverse functions emerge from this single region. In our work, we used high-throughput techniques to map the molecular, cellular, and circuit organization of the claustrum. In doing so, we discovered distinct types of excitatory neurons that likely play different roles in claustrum function.
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The Levings lab is working to understand the biological properties of regulatory T cells (Tregs) and develop ways to use them as an immunoregulatory cell therapy. In this paper, they developed an optimized method to genome engineer human Tregs in order to remove or introduce genes of interest. They then used this method to knock out FOXP3, a key Treg lineage transcription factor. They were surprised to find that deleting FOXP3 had a relatively minimal effect on various aspects of Treg biology, including patterns of protein expression, DNA methylation and mRNA expression.
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The Role of Mitochondrial Apoptotic Pathway in Islet Amyloid-Induced β-Cell Death

Islet amyloid, formed by aggregation of human islet amyloid polypeptide (hIAPP), contributes to β-cell death in type 2 diabetes. We previously showed that extracellular hIAPP aggregates promote Fas-mediated β-cell apoptosis. Here, we tested if hIAPP aggregates can trigger the mitochondrial apoptotic pathway (MAP). hIAPP aggregation in Ad-hIAPP transduced INS-1 and human islet β-cells promoted cytochrome c release, caspase-9 activation and apoptosis, which were reduced…
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Exposure of blood to a foreign surface in the form of a diagnostic or therapeutic biomaterial device or implanted cells or tissues, elicits an immediate, evolutionarily conserved thrombo-inflammatory response by the host. Primarily designed to protect against invading organisms following an injury, this innate response features instantaneous activation of several blood-borne, highly interactive and well-orchestrated cascades and cellular events that…
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