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1  under treatment with galactosylsphingosine (psychosine).
2 cytotoxic glycolipid, galactosylsphingosine (psychosine).
3 esidue of beta-galactosyl 1-->1 sphingosine (psychosine).
4 deficient Schwann cells autonomously produce psychosine.
5 orm for developing a medicinal chemistry for psychosine.
6 actolipids, including galactosylceramide and psychosine.
7 egeneration due to accumulation of cytotoxic psychosine.
8 ressive accumulation of the toxic metabolite psychosine.
9 auses accumulation of the toxic sphingolipid psychosine.
10 umulation of galactosylceramide (GalCer) and psychosine.
11  occurred without additional accumulation of psychosine.
12 eading to the accumulation of its metabolite psychosine.
13                                              Psychosine, a lipid-raft-associated sphingolipid that ac
14 he toxic metabolite of galactosylceramidase, psychosine, a potent inhibitor of protein kinase C (PKC)
15 ming cells resulting from an accumulation of psychosine, a toxic substrate of galactosylceramidase an
16                                 Furthermore, psychosine accumulates significantly in the nervous syst
17  the cytotoxic lipid, galactosylsphingosine (psychosine), accumulates in the CNS and peripheral nervo
18 use model of human GLD (twitcher) eliminates psychosine accumulation and cures GLD.
19 o secondary consequences of GALC deficiency (psychosine accumulation and neuroinflammation).
20 hallmarks such as gliosis, globoid cells and psychosine accumulation are present throughout the nervo
21 tivity with carmofur significantly decreases psychosine accumulation in cells from a Krabbe patient a
22 This reaction uncouples GALC deficiency from psychosine accumulation, allowing us to test the long-st
23 esults in a phenotype that includes wasting, psychosine accumulation, and neuroinflammation.
24 eukodystrophy (GLD), mutations in GALC cause psychosine accumulation, inducing demyelination, a neuro
25 gue against a causative relationship between psychosine accumulation, white matter loss and gliosis.
26                                    Exogenous psychosine administration recapitulates many of the mole
27 ease, upon psychosine treatment suggest that psychosine alters the plasma membrane structure by direc
28 sults are consistent with an accumulation of psychosine, an inhibitor of PKC, and suggest that the si
29 r) and sulfatide and their toxic metabolites psychosine and lysosulfatide, respectively.
30 de, which appear to be the primary source of psychosine and lysosulfatide.
31 ebrosidase loss leads to the accumulation of psychosine and subsequent oligodendrocyte cell death, de
32 as lyso-phosphatidylcholine, galactosyl-Sph (psychosine), and lactosyl-Sph at 0.5-10 microM did not s
33 nce sphingolipid classes (e.g., sphingosine, psychosine, and lysosphingomyelin) and molecular species
34 strate galactosylceramide, and the origin of psychosine are poorly understood.
35                        This study identifies psychosine as a pathogenic sphingolipid able to block fa
36                                              Psychosine (beta-galactosylsphingosine), a cationic lyso
37 rofile due to their mechanistic proximity to psychosine biogenesis.
38  phenomenon may provide a mechanism by which psychosine can exert its known inhibitory effect on prot
39 a increased GALC enzyme activity, normalized psychosine concentration, improved myelination, and atte
40 ure, and normalized GALC enzyme activity and psychosine concentration.
41 to restore galactosylceramidase activity and psychosine concentrations to within the normal range.
42                       The glycosphingolipid, psychosine (d-galactosyl-beta-1,1' sphingosine), accumul
43 yde conjugate of beta-galactosylsphingosine (psychosine) found in brain white matter, enhances p140tr
44     We hypothesized that the accumulation of psychosine (galactosyl-sphingosine) in the TWI CNS may r
45 d by the accumulation of a toxic metabolite, psychosine (galactosylsphingosine), which is a substrate
46                            Prior infusion of psychosine greatly attenuated quisqualate-induced behavi
47  psychosine synthesis, confirm the long-held psychosine hypothesis, and provide the impetus to discov
48 tion, allowing us to test the long-standing "psychosine hypothesis." We demonstrate that genetic loss
49 se (GALC) deficiency, accumulating cytotoxic psychosine in nervous systems, and subsequent neuroinfla
50 e knockout mice and the significantly higher psychosine in the brain of the galc(-/-), bgal(+/-) mice
51 ith S202 dose-dependently reduced GalCer and psychosine in the central (CNS) and peripheral (PNS) ner
52  This study underscores the possible role of psychosine in the effect of inducible nitric oxide synth
53 , we have tested neuroprotective efficacy of psychosine in vivo, in a rat model of glutamate excitoto
54 or the progression of neuroinflammation in a psychosine-independent manner.
55                                              Psychosine induced cytokine-mediated nuclear translocati
56 LD may be caused by at least two mechanisms: psychosine-induced demyelination and secondary neuroinfl
57 xpression results, TDAG8 was dispensable for psychosine-induced formation of multinucleated cells.
58 eptor agonist fingolimod (FTY720) attenuates psychosine-induced glial cell death and demyelination bo
59    Myelin-free in vitro analyses showed that psychosine inhibited fast axonal transport through the a
60 verexpression of the sphingolipid metabolite psychosine is a pathogenic factor, but does not fully ac
61                   Here, we show instead that psychosine is generated catabolically through the deacyl
62        Complementary evidence suggested that psychosine is synthesized via an anabolic pathway.
63 presence of lyso-GM3 or its analogue but not psychosine, lactosyl-sphingosine, or lyso-phosphatidylch
64     This study hypothesizes that accumulated psychosine leads to production of cytokines and iNOS exp
65 mary cells that initiate KD with an elevated psychosine level and microglia are required for the prog
66                     On the other hand, brain psychosine level is increased in all twitcher mice, but
67 ological levels of GALC activity and reduced psychosine levels in both the brain and spinal cord, it
68 nduction causes a worse KD phenotype, higher psychosine levels in the rodent brainstem and spinal cor
69                         Glucocerebroside and psychosine levels were not elevated in these specimens,
70 n, persistent GALC expression, nearly normal psychosine levels, and decreased neuroinflammation.
71  GALC activity to the CNS and did not reduce psychosine levels.
72 ith reduced expression of GALC and increased psychosine levels.
73                           This suggests that psychosine maintained or sustained the cytokine-primed e
74           Activation of TDAG8 by its agonist psychosine markedly enhanced dexamethasone-induced apopt
75                                              Psychosine may prove useful in prophylaxis of neurodegen
76  and implicated by overexpression studies in psychosine-mediated inhibition of cytokinesis and in GC-
77 itical role for TDAG8 in immune development, psychosine-mediated inhibition of cytokinesis, and GC-in
78 cultured cells expressing this receptor with psychosine or structurally related glycosphingolipids re
79                                              Psychosine potentiated the LPS-induced production of pro
80                            We found out that psychosine progressively destabilizes plasma membrane, a
81  but not sphingosine 1-phosphate (S1P), PAF, psychosine (Psy), glucosyl-beta1'1-sphingosine (Glu-Sph)
82  cell death-associated gene 8, is a specific psychosine receptor.
83        The ensuing cytotoxic accumulation of psychosine results in diffuse central and peripheral ner
84   In this communication, we demonstrate that psychosine specifically accumulates in LRs in the TWI br
85      Our discovery of a molecular target for psychosine suggests a mechanism for the globoid cell his
86 tal, these data clarify our understanding of psychosine synthesis, confirm the long-held psychosine h
87 inhibits an enzyme several steps upstream of psychosine synthesis, thus altering the balance of other
88 cant, 16.5%, reduction in the GALC substrate psychosine, the abnormal accumulation of which is believ
89 og muscles had significant capacity to store psychosine, the neurotoxin that accumulates in Krabbe di
90  Schwann cells are particularly sensitive to psychosine, thus leading to a demyelinating phenotype.
91  responded in vitro to medium conditioned by psychosine-treated oligodendrocytes, indicating the like
92 , the enzyme lacking in Krabbe disease, upon psychosine treatment suggest that psychosine alters the
93                 However, the accumulation of psychosine was not altered in the brain by LCN2 deficien
94  abnormal accumulation of the GALC substrate psychosine, which is thought to play a pivotal role in d