Effectiveness of vagus nerve stimulation for drug-resistant generalized epilepsy in children aged six and younger.

Background: To explore a novel scoring system to evaluate the efficacy of vagus nerve stimulation (VNS) in children with drug-resistant generalized epilepsy (DRGE) aged six and younger.

Basic Procedures: The data of twelve children with DRGE under the age of 6 years who accepted VNS and have been followed up for at least 3 years were retrospectively reviewed. The outcome was evaluated with the McHugh Classification System and a novel scoring system we proposed.

Discovery of imidazopyrrolopyridines derivatives as novel and selective inhibitors of JAK2.

Herein, we describe the design, synthesis, and structure-activity relationships of a series of imidazopyrrolopyridines derivatives that selectively inhibit Janus kinase 2 (JAK2). These screening cascades revealed that 6k was a preferred compound, with IC values of 10 nM for JAK2. Moreover, 6k was a selective JAK2 inhibitor with 19-fold, >30-fold and >30-fold selectivity over JAK1, JAK3 and TYK2 respectively.

Whole Exome Sequencing of Multiple Atypical Meningiomas in a Patient without History of Neurofibromatosis Type II: A Case Report.

BACKGROUND The pathogenesis of sporadic multiple meningiomas in the patients without history of neurofibromatosis type II remains unclear. We report whole exome sequencing (WES) of 2 metachronous multiple meningiomas of the same patient. CASE REPORT A 39-year-old female had a 5-month history of headache and her magnetic resonance imaging (MRI) revealed a significantly enhanced intracranial space-occupying pathology with dura tail sign and skull invasion.

Janus kinases (JAKs): The efficient therapeutic targets for autoimmune diseases and myeloproliferative disorders.

The Janus kinases or JAKs are a family of intracellular tyrosine kinases that play an essential role in the signaling of numerous cytokines that have been implicated in the pathogenesis of autoimmune diseases and myeloproliferative disorders. JAKs are activated upon ligand induced receptor homo- or heterodimerization, which results in the immediate phosphorylation of tyrosine residues and the phosphotyrosines then serve as docking sites for cytoplasmic signal transducer and activator of transcription (STAT) proteins which become phosphorylated by the JAKs upon recruitment to the receptor complex. The phosphorylated STAT proteins dimerize and travel to the cellular nucleus, where they act as transcription factors.

Disproportionately large communicating fourth ventricle: two case reports.

Background: Management of the disproportionately large communicating fourth ventricle is still problematic.

Case Presentation: Two cases of disproportionately large communicating fourth ventricle were treated successfully. One was a case of a 51-year-old Han Chinese woman with a complaint of headache and dizziness of 1 year's duration.

IDH1 overexpression induced chemotherapy resistance and IDH1 mutation enhanced chemotherapy sensitivity in Glioma cells in vitro and in vivo.

Isocitrate dehydrogenase (IDH) is of great importance in cell metabolism and energy conversion. IDH mutation in glioma cells is reported to be associated with an increased overall survival. However, effects biological behavior of therapy of gliomas are unclear.

Mechanisms underlying the biological changes induced by isocitrate dehydrogenase-1 mutation in glioma cells.

Isocitrate dehydrogenase 1 (IDH1) mutation has been reported to be associated with an increased overall survival in patients with glioma in a number of studies. Previous studies have focused on the mutation rate and possible metabolic pathways of the mutated IDH1 gene. However, the effects of IDH1 mutation on the biological behavior of glioma cells and the associated mechanisms, as well as the possible effects they may have on clinical therapy, have not been studied.

Advances and prospects of anginex as a promising anti-angiogenesis and anti-tumor agent.

Anginex, a novel artificial cytokine-like peptide (βpep-25), is designed by using basic folding principles and incorporating short sequences from the β-sheet domains of anti-angiogenic agents, including platelet factor-4 (PF4), interleukin-8 (IL-8), and bactericidal-permeability increasing protein 1 (BP1). Anginex can specially block the adhesion and migration of the angiogenically activated endothelial cells (ECs), leading to apoptosis and ultimately to the inhibition of angiogenesis and tumor growth. In vitro and in vivo studies have proved its inhibitory effects on the formation of new blood vessels and tumor growth even though the mechanism is not clear.

Anti-angiogenesis and anti-tumor effects of AdNT4-anginex.

Anginex is a novel artificial peptide that can inhibit angiogenesis. AdNT4-anginex was constructed by inserting the artificial anginex gene into a recombinant adenoviral vector. We demonstrated that AdNT4-anginex inhibited migration of human endothelial cells, angiogenesis and tumor growth in in vitro and in vivo studies.