Publications by authors named "A Gawda"

Epileptogenesis is characterized by intrinsic changes in neuronal firing, resulting in hyperactive neurons and the subsequent generation of seizure activity. These alterations are accompanied by changes in gene transcription networks, first with the activation of early-immediate genes and later with the long-term activation of genes involved in memory. Our objective was to engineer a promoter containing binding sites for activity-dependent transcription factors upregulated in chronic epilepsy (EpiPro) and validate it in multiple rodent models of epilepsy.

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Objective: Development of novel therapies for temporal lobe epilepsy is hindered by a lack of models suitable for drug screening. While testing the hypothesis that "inhibiting inhibitory neurons" was sufficient to induce seizures, it was discovered that a mild electrical kindling protocol of VGAT-Cre mice led to spontaneous motor and electrographic seizures. This study characterizes these seizures and investigates the mechanism.

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Murine macrophages of the J774A.1 line are hydrogen sulphide-producing cells with the primary role of γ-cystathionase (CTH) and secondary role of 3-mercaptopyruvate sulfurtransferase (limited by cysteine availability) and with a negligible role of cystathionine β-synthase (CBS) in HS generation. J774A.

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We have previously reported that the blockage of TrkB and TrkC signaling in primary culture of opossum neocortical cells affects neurogenesis that involves a range of processes including cell proliferation, differentiation, and survival. Here, we studied whether TrkB and TrkC activity specifically affects various types of progenitor cell populations during neocortex formation in the Monodelphis opossum in vivo. We found that the inhibition of TrkB and TrkC activities affects the same proliferative cellular phenotype, but TrkC causes more pronounced changes in the rate of cell divisions.

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Objective: Exposure to air particulate matter (PM) is associated with chronic inflammatory and autoimmune diseases. Macrophages are responsible for the regulation of chronic inflammation. However, whether PM affects macrophage polarization remains unclear.

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