Zobrazeno 1 - 10
of 66
pro vyhledávání: '"You-Hai Xu"'
Publikováno v:
Journal of Lipid Research, Vol 51, Iss 7, Pp 1643-1675 (2010)
Glycosphingolipids (GSLs) and gangliosides are a group of bioactive glycolipids that include cerebrosides, globosides, and gangliosides. These lipids play major roles in signal transduction, cell adhesion, modulating growth factor/hormone receptor, a
Externí odkaz:
https://doaj.org/article/91e3df29f42841f188f0c3281ac43a3d
Publikováno v:
Journal of Lipid Research, Vol 47, Iss 10, Pp 2161-2170 (2006)
The reversibility and regression of histological and biochemical findings in a mouse model of Gaucher disease (4L/PS-NA) was evaluated using a liver-enriched activator protein promoter control of a tetracycline-controlled transcriptional activation-r
Externí odkaz:
https://doaj.org/article/3354632ee8594277b74b607115d08af1
Autor:
Sonya Barnes, You-Hai Xu, Wujuan Zhang, Benjamin Liou, Kenneth D R Setchell, Liming Bao, Gregory A Grabowski, Ying Sun
Publikováno v:
PLoS ONE, Vol 9, Iss 12, p e116023 (2014)
Gaucher disease is a lysosomal storage disease caused by defective activity of acid β-glucosidase (GCase), which leads to the accumulation of its major substrates, glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph) in many cells. To modulate
Externí odkaz:
https://doaj.org/article/a5023a320f5b4a29baac1320c8929196
Autor:
Ying Sun, Wujuan Zhang, You-Hai Xu, Brian Quinn, Nupur Dasgupta, Benjamin Liou, Kenneth D R Setchell, Gregory A Grabowski
Publikováno v:
PLoS ONE, Vol 8, Iss 3, p e57560 (2013)
Gaucher disease results from GBA1 mutations that lead to defective acid β-glucosidase (GCase) mediated cleavage of glucosylceramide (GC) and glucosylsphingosine as well as heterogeneous manifestations in the viscera and CNS. The mutation, tissue, an
Externí odkaz:
https://doaj.org/article/17503a5132614b3282b08cc38f30eecf
Autor:
Nupur Dasgupta, You-Hai Xu, Sunghee Oh, Ying Sun, Li Jia, Mehdi Keddache, Gregory A Grabowski
Publikováno v:
PLoS ONE, Vol 8, Iss 10, p e74912 (2013)
Gaucher disease type 1, an inherited lysosomal storage disorder, is caused by mutations in GBA1 leading to defective glucocerebrosidase (GCase) function and consequent excess accumulation of glucosylceramide/glucosylsphingosine in visceral organs. En
Externí odkaz:
https://doaj.org/article/3906fe1689964fcda5bef74993202cc5
Autor:
He-Sheng, He, Gui-Ping, Su, Jun-Ping, Yao, Shang-Hao, Liu, You-Hai, Xu, Yu-Qiong, Yang, Dong-Ping, Huang
Publikováno v:
Zhongguo shi yan xue ye xue za zhi. 28(5)
To investigate the clinical characteristics, diagnosis and treatment methods of patients with myeloid sarcoma(MS). Methods: The clinical data, laboratory examination, clinical pathology and treatment methods of 15 patients with MS treated in the Fi
Autor:
Kristin Bowden, Teddy Chan, Hong Du, Gregory A. Grabowski, Gordon A. Francis, You-Hai Xu, Joshua A. Dubland
Publikováno v:
Arteriosclerosis, Thrombosis, and Vascular Biology. 38:1191-1201
Objective— To explore the role of LAL (lysosomal acid lipase) in macrophage cholesterol efflux and whole-body reverse cholesterol transport. Approach and Results— Immortalized peritoneal macrophages from lal −/− mice showed reduced expression
Publikováno v:
PLoS ONE, Vol 5, Iss 5, p e10750 (2010)
Gaucher disease type 1 is caused by the defective activity of the lysosomal enzyme, acid beta-glucosidase (GCase). Regular infusions of purified recombinant GCase are the standard of care for reversing hematologic, hepatic, splenic, and bony manifest
Externí odkaz:
https://doaj.org/article/c45b576b8543436fb958adc8e5ba658e
Publikováno v:
PLoS ONE, Vol 4, Iss 10, p e7320 (2009)
Gaucher disease is a lysosomal storage disease caused by mutations in acid beta-glucosidase (GCase) leading to defective hydrolysis and accumulation of its substrates. Two L-type calcium channel (LTCC) blockers-verapamil and diltiazem-have been repor
Externí odkaz:
https://doaj.org/article/7cda69c23fb843328e199b586fe8076b
Publikováno v:
Zhongguo shi yan xue ye xue za zhi. 26(2)
To explore the individualized treatment for patient with chronic phase chronic myeloid leukemia(CML-CP).The clinical data and treatment process of one CML-CP patient which intolerated to nilotinib were analyzed.Nilotinib was given to the patient once