Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human immunodeficiency virus (HIV)-1 infection is often complicated with neurologic disorders, but the pathogenesis of HIV-1 encephalopathy is incompletely understood. Tat (HIV-1 transactivator protein) is released from HIV-1-infected cells and has been detected in the sera and cerebrospinal fluid of HIV-1-infected patients. Tat, along with increased inflammatory cytokines such as interferon-gamma (IFN-gamma), have been implicated in the pathogenesis of HIV-1-associated blood-brain barrier dysfunction. The present study examined the effects of Tat and IFN-gamma on human brain microvascular endothelial cells (HBMECs), which constitute the blood-brain barrier. Tat produced cytotoxicity of HBMECs, but required IFN-gamma. IFN-gamma treatment of HBMECs up-regulates vascular endothelial growth factor receptor-2 (VEGFR2/KDR), which is known to be the receptor for Tat. Tat activated KDR in the presence of IFN-gamma, and Tat-mediated cytopathic changes involve its interaction with KDR and phosphatidylinositol 3-kinase (PI3K). Further understanding and characterization of Tat-HBMEC interactions should help us understand HIV-1 neuropathogenesis and develop strategies to prevent HIV-1 encephalopathy.
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PMID:Human immunodeficiency virus type 1 tat-mediated cytotoxicity of human brain microvascular endothelial cells. 1460 71

CEACAM1 is the founder molecule of the family of 'carcinoembryonic antigen-related cell adhesion molecules' and part of the immunoglobulin superfamily. Due to its role as a coreceptor to many other receptors (e.g. Toll-like receptor 2, Toll-like receptor 4, T-cell receptor, B-cell receptor, epidermal growth factor receptor and vascular endothelial growth factor receptor) and its different isoforms, CEACAM1 is a multifunctional protein with an impact on proliferation and differentiation of multiple cell types. Although different modes of action in other tissues are described, the role of CEACAM1 in the developing brain remains elusive. Here we report for the first time that CEACAM1 is expressed ontogenetically in oligodendrocytes of the developing rat brain, and that CEACAM1 expression has a spatiotemporal relation to myelination. In addition, CEACAM1 expression is altered in a model of hyperoxia- and inflammation-induced encephalopathy of prematurity, a myelination disorder of children born preterm. Furthermore, primary oligodendrocytes stimulated with CEACAM1 show increased myelination. Therefore, we postulate that CEACAM1 is, at least in part, involved in hyperoxia- and inflammation-induced disruption of myelination, but may also play a role in intact myelination as it is ontogenetically expressed in myelinating oligodendrocytes.
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PMID:CEACAM1 expression in oligodendrocytes of the developing rat brain shows a spatiotemporal relation to myelination and is altered in a model of encephalopathy of prematurity. 2365 19

Apatinib is an orally administered small-molecule vascular endothelial growth factor receptor-2 inhibitor that has demonstrated encouraging anticancer activity across a broad range of malignancies, including gastric cancer, non-small-cell lung cancer, breast cancer, and hepatocellular carcinoma. We report a case of probable apatinib-induced hyperammonemic encephalopathy in a 69-year-old male. The patient received apatinib as targeted therapy for hepatocellular carcinoma and presented with acute confusion and hypersomnolence after four days of medication initiation. He showed improvement on drug withdrawal; then he resumed apatinib with a half dose and had a recurrence. Possible underlying mechanisms that include direct neuronal effect and antiangiogenic properties are discussed. We would like to draw attention to the potential risk of vascular endothelial growth factor receptor-tyrosine kinase inhibitors induced hyperammonemic encephalopathy even with a low dosage. Clinicians should be aware of any unexplained neurological syndrome after the initiation of apatinib in patients with hepatocellular carcinoma.
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PMID:Apatinib-induced hyperammonemic encephalopathy. 3106 89