Serological evidence of Ebola virus exposure in dogs from affected communities in Liberia: A preliminary report.

Filoviruses such as Ebola virus (EBOV) cause outbreaks of viral hemorrhagic fevers for which no FDA-approved vaccines or drugs are available. The 2014-2016 EBOV outbreak in West Africa infected approximately 30,000 people, killing more than 11,000 and affecting thousands more in areas still suffering from the effects of civil wars. Sierra Leone and Liberia reported EBOV cases in every county demonstrating the efficient spread of this highly contagious virus in the well-connected societies of West Africa.

Tet2 loss leads to hypermutagenicity in haematopoietic stem/progenitor cells.

TET2 is a dioxygenase that catalyses multiple steps of 5-methylcytosine oxidation. Although TET2 mutations frequently occur in various types of haematological malignancies, the mechanism by which they increase risk for these cancers remains poorly understood. Here we show that Tet2 mice develop spontaneous myeloid, T- and B-cell malignancies after long latencies.

Combined Loss of Tet1 and Tet2 Promotes B Cell, but Not Myeloid Malignancies, in Mice.

TET1/2/3 are methylcytosine dioxygenases that regulate cytosine hydroxymethylation. Tet1/2 are abundantly expressed in HSC/HPCs and are implicated in hematological malignancies. Tet2 deletion in mice causes myeloid malignancies, while Tet1-null mice develop B cell lymphoma after an extended period of latency.

The TET2 interactors and their links to hematological malignancies.

Ten-eleven translocation (TET) family proteins are dioxygenases that oxidize 5-methylcytosine to 5-hydroxymethylcytosine, 5-formylcytosine, and 5-carboxylcytosine in DNA, early steps of active DNA demethylation. TET2, the second member of TET protein family, is frequently mutated in patients with hematological malignancies, leading to aberrant DNA methylation profiling and decreased 5hmC levels. Located in the nucleus and acting as a DNA-modifying enzyme, TET2 is thought to exert its function via TET2-containing protein complexes.

Science café course: an innovative means of improving communication skills of undergraduate biology majors.

To help bridge the increasing gap between scientists and the public, we developed an innovative two-semester course called Science Café. In this course, undergraduate biology majors learn to develop communication skills to be better able to explain science concepts and current developments in science to non-scientists. Students develop and host outreach events on various topics relevant to the community, thereby increasing interactions between budding scientists and the public.

Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice.

ASXL1 is mutated/deleted with high frequencies in multiple forms of myeloid malignancies, and its alterations are associated with poor prognosis. De novo ASXL1 mutations cause Bohring-Opitz syndrome characterized by multiple congenital malformations. We show that Asxl1 deletion in mice led to developmental abnormalities including dwarfism, anophthalmia, and 80% embryonic lethality.

Combined estradiol and lithium increase ER-alpha mRNA in embryonic C57BL/6J primary hippocampal cultures.

Estrogen replacement therapy (ERT) is commonly prescribed during menopause. Post-menopausal women also tend to suffer from bipolar disorders and as a result are prescribed mood stabilizers - in addition to ERT. There is a paucity of data on how combined hormones and mood stabilizers interact in regulating gene expression that led us to hypothesize that in primary cultures of mixed brain cells predominated by glia, combined 17beta-estradiol (E2) and lithium chloride (LiCl) (E2÷LiCl) will alter estrogen receptor-alpha (ER-alpha) mRNA expression.

Lithium enhances cortical mRNA expression in ovariectomized C57BL/6J mice.

The hippocampus and cortex of the mammalian brain are regions involved in learning and long-term memory. Estrogen and lithium affect similar learning and memory molecular processes. We hypothesized that in ovariectomized mice lithium treatment will enhance genetic factors in the brain that are involved in neuroprotection, learning and memory.

Alzheimer's beta-amyloid peptide blocks vascular endothelial growth factor mediated signaling via direct interaction with VEGFR-2.

Beta-amyloid peptides (Abeta) are the major constituents of senile plaques and cerebrovascular deposits in the brains of Alzheimer's disease patients. We have shown previously that soluble forms of Abeta are anti-angiogenic both in vitro and in vivo. However, the mechanism of the anti-angiogenic activity of Abeta peptides is unclear.

CD40/CD40L interaction induces Abeta production and increases gamma-secretase activity independently of tumor necrosis factor receptor associated factor (TRAF) signaling.

CD40, a member of tumor necrosis factor receptor superfamily, and its cognate ligand CD40L are both elevated in the brain of Alzheimer's disease (AD) patients compared to controls. We have shown that pharmacological or genetic interruption of CD40/CD40L interaction results in mitigation of AD-like pathology in vivo in transgenic AD mouse models, and in vitro. Recently, we showed that CD40L stimulation could increase Abeta levels via NFkappaB signaling, presumably through TRAFs.

Estradiol and lithium chloride specifically alter NMDA receptor subunit NR1 mRNA and excitotoxicity in primary cultures.

Glutamate facilitates calcium influx via NMDAR, and excess calcium influx increases excitotoxicity--a pathological characteristic of neurological diseases. Both 17beta-estradiol (E2) and lithium influence NMDAR expression/signaling and excitotoxicity. This led us to hypothesize that combined E2 and lithium will alter NMDAR expression and excitotoxicity.