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P2X7 receptor antagonism suppresses epileptiform-like activity in an inflammation-primed human iPSC-derived neuron model of drug-resistant epilepsy.
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Department of Physiology and Medical Physics, RCSI University of Medicine and Health Sciences, Dublin, Ireland.
Background And Purpose: Neuroinflammation is increasingly recognised to contribute to drug-resistant epilepsy. Activation of ATP-gated P2X7 receptors has emerged as an important upstream mechanism, and increased P2X7 receptor expression is present in the seizure focus in rodent models and patients. Pharmacological antagonists of P2X7 receptors attenuate seizures in rodents, but this has not been explored in human neural networks.
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Institute of Pathology, University Hospital Schleswig-Holstein, Kiel, Germany.
Mixed neuroendocrine and non-neuroendocrine neoplasms (MiNEN) represent a heterogeneous group of bidirectionally differentiated epithelial malignancies that are, in most cases, highly aggressive. They are defined by the presence of morphologically distinct, yet clonally related, neuroendocrine and non-neuroendocrine components, each comprising at least 30% of the tumor mass according to current guidelines. Tumors that fall within the differential diagnostic spectrum of MiNEN include amphicrine carcinomas-characterized by the co-expression of neuroendocrine and non-neuroendocrine features within the same tumor cell-as well as conventional carcinomas that lack neuroendocrine morphology but exhibit immunohistochemical expression of neuroendocrine markers.
View Article and Find Full Text PDFThe STING/type I interferon axis drives the interplay between marginal zone B cells and T follicular helper cells in Sjögren's disease.
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School of Chinese Medicine, the University of Hong Kong, Hong Kong SAR, China.
Type I interferon (IFN-I) is highly prevalent in autoimmune disorders and is intricately involved in disease pathogenesis, including Sjögren's disease (SjD), also known as Sjögren's syndrome. Although the T follicular helper (Tfh) cell response has been shown to drive SjD development in a mouse model of experimental Sjögren's syndrome (ESS), the connection between IFN-I and the Tfh cell response remains unclear. As the activation of stimulator of interferon genes (STING) induces IFN-I production, we first demonstrated that mice deficient in STING or IFN-I signaling presented diminished Tfh cells and were completely resistant to ESS development.
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Cancer-associated muscle wasting is associated with poor clinical outcomes, but its underlying biology is largely uncharted in humans. Unbiased analysis of the RNAome (coding and non-coding RNAs) with unsupervised clustering using integrative non-negative matrix factorization provides a means of identifying distinct molecular subtypes and was applied here to muscle of patients with colorectal or pancreatic cancer. Rectus abdominis biopsies from 84 patients were profiled using high-throughput next-generation sequencing.
View Article and Find Full Text PDFPML::RARα+ myeloid cells display metabolic alterations that can be targeted to treat resistant/relapse acute promyelocytic leukemias.
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