On 2-edge-connected [a,b]-factors of graphs with Ore-type condition

AbstractLet a⩾2 and t⩾2 be two integers. Suppose that G is a 2-edge-connected graph of order |G|⩾2(t+1)((a-2)t+a)+t-1 with minimum degree at least a. Then G has a 2-edge-connected [a,at]-factor if every pair of non-adjacent vertices has degree sum at least 2|G|/(1+t). This lower bound is sharp. As a consequence, we have Ore-type conditions for the existence of a 2-edge-connected [a,b]-factor in graphs

Path factors in claw-free graphs

AbstractA graph G is called claw-free if G has no induced subgraph isomorphic to K1,3. We prove that if G is a claw-free graph with minimum degree at least d, then G has a path factor such that the order of each path is at least d+1

Inhibition of KDM1A activity restores adult neurogenesis and improves hippocampal memory in a mouse model of Kabuki syndrome.

To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked DownloadKabuki syndrome (KS) is a rare cause of intellectual disability primarily caused by loss-of-function mutations in lysine-specific methyltransferase 2D (KMT2D), which normally adds methyl marks to lysine 4 on histone 3. Previous studies have shown that a mouse model of KS (Kmt2d +/βGeo ) demonstrates disruption of adult neurogenesis and hippocampal memory. Proof-of-principle studies have shown postnatal rescue of neurological dysfunction following treatments that promote chromatin opening; however, these strategies are non-specific and do not directly address the primary defect of histone methylation. Since lysine-specific demethylase 1A (LSD1/KDM1A) normally removes the H3K4 methyl marks added by KMT2D, we hypothesized that inhibition of KDM1A demethylase activity may ameliorate molecular and phenotypic defects stemming from KMT2D loss. To test this hypothesis, we evaluated a recently developed KDM1A inhibitor (TAK-418) in Kmt2d +/βGeo mice. We found that orally administered TAK-418 increases the numbers of newly born doublecortin (DCX)+ cells and processes in the hippocampus in a dose-dependent manner. We also observed TAK-418-dependent rescue of histone modification defects in hippocampus both by western blot and chromatin immunoprecipitation sequencing (ChIP-seq). Treatment rescues gene expression abnormalities including those of immediate early genes such as FBJ osteosarcoma oncogene (Fos) and FBJ osteosarcoma oncogene homolog B (Fosb). After 2 weeks of TAK-418, Kmt2d +/βGeo mice demonstrated normalization of hippocampal memory defects. In summary, our data suggest that KDM1A inhibition is a plausible treatment strategy for KS and support the hypothesis that the epigenetic dysregulation secondary to KMT2D dysfunction plays a major role in the postnatal neurological disease phenotype in KS.United States Department of Health & Human Services National Institutes of Health (NIH) - USA Louma G. Foundation, USA Walter Zaitzeff Fund, USA Icelandic Research Fund, Iceland Takeda Pharmaceutical Company Lt

Luxury Perfusion Syndrome Confirmed by Sequential Studies of Regional Cerebral Blood Flow and Volume after Extracranial to Intracranial Bypass Surgery: Case Report

Abstract We report a case of luxury perfusion syndrome with temporary neurological deterioration after extracranial to intracranial bypass surgery. A preoperative computed tomographic scan showed no detectable infarct, and the measurement of regional cerebral blood flow showed severe depression of ipsilateral hemispheric perfusion. The patient developed temporary neurological deterioration after bypass surgery, with no recognizable pathological signs on postoperative computed tomographic and angiographic studies. Regional cerebral blood flow and volume were more elevated during the period of neurological deterioration than after the subsequent recovery. This strongly suggests that excessive blood flow directed into chronically ischemic brain through a graft may induce a luxury perfusion syndrome resulting in neurological deterioration