Strategies for proteomic analysis of blood glycated proteins

Comunicaciones a congreso

Labeling of bifidobacterium longum cells with 13C-substituted leucine for quantitative proteomic analyses

Comunicaciones a congreso

Quantitative analysis of protein glycation in clinical samples

Comunicaciones a congreso

The cell envelope proteome of bifidobacterium longum in a vitro bile environment

Comunicaciones a congreso

Glycated platelets proteome

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Quaking RNA bindings proteins as mediator of oncolytic HSV vectors in huma hepatoma cells

Comunicaciones a congreso

The Most Massive Ultra-Compact Dwarf Galaxy in the Virgo Cluster

We report on the properties of the most massive ultra-compact dwarf galaxy (UCD) in the nearby Virgo Cluster of galaxies using imaging from the Next Generation Virgo Cluster Survey (NGVS) and spectroscopy from Keck/DEIMOS. This object (M59-UCD3) appears to be associated with the massive Virgo galaxy M59 (NGC 4621), has an integrated velocity dispersion of 78 km/s, a dynamical mass of $3.7\times10^8 M_\odot$, and an effective radius ($R_e$) of 25 pc. With an effective surface mass density of $9.4\times10^{10} M_\odot/kpc^2$, it is the densest galaxy in the local Universe discovered to date, surpassing the density of the luminous Virgo UCD, M60-UCD1. M59-UCD3 has a total luminosity of $M_{g'}=-14.2$ mag, and a spectral energy distribution consistent with an old (14 Gyr) stellar population with [Fe/H]=0.0 and [$\alpha$/Fe]=+0.2. We also examine deep imaging around M59 and find a broad low surface brightness stream pointing towards M59-UCD3, which may represent a tidal remnant of the UCD progenitor. This UCD, along with similar objects like M60-UCD1 and M59cO, likely represents an extreme population of tidally stripped galaxies more akin to larger and more massive compact early-type galaxies than to nuclear star clusters in present-day dwarf galaxies.Comment: 6 pages, 4 figures, 1 table, accepted for publication in ApJ Letter

Experimental Zika Virus Infection in the Pregnant Common Marmoset Induces Spontaneous Fetal Loss and Neurodevelopmental Abnormalities.

During its most recent outbreak across the Americas, Zika virus (ZIKV) was surprisingly shown to cause fetal loss and congenital malformations in acutely and chronically infected pregnant women. However, understanding the underlying pathogenesis of ZIKV congenital disease has been hampered by a lack of relevant in vivo experimental models. Here we present a candidate New World monkey model of ZIKV infection in pregnant marmosets that faithfully recapitulates human disease. ZIKV inoculation at the human-equivalent of early gestation caused an asymptomatic seroconversion, induction of type I/II interferon-associated genes and proinflammatory cytokines, and persistent viremia and viruria. Spontaneous pregnancy loss was observed 16-18 days post-infection, with extensive active placental viral replication and fetal neurocellular disorganization similar to that seen in humans. These findings underscore the key role of the placenta as a conduit for fetal infection, and demonstrate the utility of marmosets as a highly relevant model for studying congenital ZIKV disease and pregnancy loss

New insights into the genetic etiology of Alzheimer’s disease and related dementias

Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele