ライフサイエンスコーパス: galactosamine

1 hosphate group that is partially modified by galactosamine.

2 entrations of lipopolysaccharide (LPS) and D-galactosamine.

3 taining D-chiro-inositol 2a (as pinitol) and galactosamine.

4 ylococcal enterotoxin B in the presence of D-galactosamine.

5 n the abstraction of the C-5 proton from the galactosamine.

6 roxypropyl)methacrylamide copolymers bearing galactosamine.

7 ice sensitized to the effects of LPS by D(+)-galactosamine.

8 from acetaminophen or tumor necrosis factor/galactosamine.

9 -alpha) prevented hepatotoxicity caused by D-galactosamine.

10 an controls after the coinjection of LPS and galactosamine.

11 sugars: cellobiose, mannitol, and N-acetyl-D-galactosamine.

12 the toxic synergism between halothane and D-galactosamine.

13 c shock, with or without pretreatment with D-galactosamine.

14 toxin alone or in combination with 700 mg/kg galactosamine.

15 y administration of lipopolysaccharide and D-galactosamine.

16 ation of both UDP-galactose and UDP-N-acetyl-galactosamine.

17 ons were made in vivo using TNF-alpha with D-galactosamine.

18 uronic acid that is adjacent to N-acetylated galactosamine.

19 Intravenous infusions of D-galactosamine (1.0 to 1.5 gm/kg) did not result in unifo

20 e stages of fragmentation suggested that the galactosamine-1-phosphate was linked to the reducing ter

21 fucose-1-phosphate, glucosamine-1-phosphate, galactosamine-1-phosphate, and N-acetylglucosamine-1-pho

22 thetic clearing agent (biotinylated N-acetyl-galactosamine) 24 and 4 h, respectively, before the admi

23 eat-killed or living N. meningitidis, plus d-galactosamine (400 mg/kg).

24 ffer cells selectively before injection of D-galactosamine (500 mg/kg, intraperitoneally).

25 The human lysosomal enzyme galactosamine-6-sulfatase (GALNS, also known as N-acetyl

26 with B6 mice treated with LPS (100 ng) and D-galactosamine (8 mg).

27 from Kupffer cells causes apoptosis after D-galactosamine administration in the rat.

28 tion assay, nor did it bind to an N-acetyl-D-galactosamine affinity column.

29 ne cluster for the utilization of N-acetyl-D-galactosamine (Aga) and D-galactosamine (Gam).

30 NO donor to rats treated with TNFalpha and D-galactosamine also prevented the increase in caspase-3-l

31 , C3Heb/FeJ mice were treated with 700 mg/kg galactosamine and 100 microgram/kg endotoxin (Gal/ET).

32 -hexosaminidase A for cleavage of N-acetyl-d-galactosamine and conversion to GM3.

33 f repeating disaccharide units of N-acetyl-D-galactosamine and d-glucuronic acid residues, modified w

34 hydrolysis that the polysaccharide contained galactosamine and glucuronic acid.

35 hylococcus aureus enterotoxin B (SEB) with D-galactosamine and had lower plasma levels of tumor necro

36 re induced by intraperitoneal injection of D-galactosamine and lipopolysaccharide in SCID mice.

37 ouse model of acute liver injury caused by D-galactosamine and lipopolysaccharide intoxication.

38 cted from induction of liver injury by D-(+)-galactosamine and lipopolysaccharides or CCl4.

39 Coinjection of D-galactosamine and LPS or staphylococcal enterotoxin B in

40 minal galactosyl groups including N-acetyl-d-galactosamine and N-acetyl-d-lactosamine.

41 viously shown to display stronger binding to galactosamine and N-acetylgalactosamine relative to d-ga

42 ccharides both contain 1,4-linked N-acetyl-d-galactosamine and play an important role in biofilm form

43 wo treatment groups (three rats treated with galactosamine and three with galactosamine+uridine) was

44 ith a variety of carbohydrates (glucosamine, galactosamine, and lactosamine), and the related conjuga

45 The hexosamine monosaccharides, glucosamine, galactosamine, and mannosamine, were derivatized with [C

46 , including bile duct ligation and CCl(4), D-galactosamine, and methylene dianiline toxic liver injur

47 se, d-glucose, d-glucuronic acid, N-acetyl-d-galactosamine, and N-acetyl-d-glucosamine, and all excep

48 Structures bound to glycerol, N-acetyl-d-galactosamine, and N-acetyl-d-lactosamine outline a comm

49 esent, respectively, D-galactose, D-N-acetyl galactosamine, and reducing end), typically found in Glo

50 effect of isomeric amino sugars glucosamine, galactosamine, and their N-acetyl derivatives on parasit

51 y to utilize either N-acetylgalactosamine or galactosamine as sole sources of carbon.

52 ysaccharide or TNFalpha in the presence of d-galactosamine, Bid was cleaved and translocated to mitoc

53 D-galactosamine caused a transient increase in circulating

54 D-galactosamine caused panlobular focal hepatocellular nec

55 umber of other hepatotoxic agents, such as d-galactosamine, CCl4, and thioacetamide, were also ineffe

56 -methyl-d-chiro-inositol) beta-1,4 linked to galactosamine chelated with Mn(2+) (called INS2).

57 followed 24 hours later by a biotin-N-acetyl-galactosamine clearing agent, and 3 hours after that by

58 followed 20 hours later by a biotin-N-acetyl-galactosamine clearing agent, followed 4 hours later by

59 inant enzyme did not utilize glucosamine- or galactosamine-containing acceptors.

60 Galactosamine-containing glycosaminoglycans (GAGs), such

61 F. tularensis containing a phosphate-linked galactosamine could potentially influence its intracellu

62 H and in livers of mice with FH induced by D-galactosamine (D-Gal) and lipopolysaccharide (LPS).

63 The murine D-galactosamine (D-gal) model of tumor necrosis factor alp

64 sitivity to microbial toxins is induced by D-galactosamine (D-Gal).

65 challenges of lipopolysaccharide (LPS) and D-galactosamine (D-Gal).

66 /c mice yields an 85% survival rate in the D-galactosamine (D-gal)/lipolysaccharide (LPS) model of ac

67 LPS) challenge and were susceptible to LPS/D-galactosamine (D-GalN) toxicity.

68 ion of low dose of LPS in combination with d-galactosamine (d-GalN)).

69 l effect of poly(I:C) when sensitized with d-galactosamine (d-GalN), and reduced production of inflam

70 to TSS by using sensitizing agents such as d-galactosamine (d-galN), which skews the disease exclusiv

71 massive apoptotic death of hepatocytes in D-galactosamine (D-GalN)-sensitized mice.

72 evere liver injury and subsequent death of D-galactosamine (D-GalN)-sensitized mice.

73 ity in mice treated with low dose LPS plus d-galactosamine (D-GalN).

74 d with low-dose LPS (1 microgram plus 8 mg D-galactosamine [D-gal] per mouse) and monitored for survi

75 gars like N-acetyl-D-glucosamine, N-acetyl-D-galactosamine, D-glucose and D-galactose, present on the

76 Epimerization of O4 afforded the galactosamine derivative and that of O3 yielded allosami

77 pargyluted N-acetyl glucosamine and N-acetyl galactosamine derivative, respectively.

78 e show that metabolism of peracetyl N-acyl-D-galactosamine derivatives carrying an N-thioglycolyl (Ac

79 hiobutanoyl) (5), and N-methylthioacetyl (6) galactosamine derivatives, N-thioglycolyl-D-glucosamine

80 eated either with hepatotoxic doses of D-(+)-galactosamine (DGAL) or acetaminophen (APAP) or a myotox

81 While 4-O-sulfation of galactosamine dominated, we also detected 6-O-sulfated g

82 An N-trichloroacetyl-protected galactosamine donor performed best for the installation

83 important in the injury process, we used the galactosamine/endotoxin (Gal/ET) model of acute liver fa

84 ury after BDL but eliminated apoptosis after galactosamine/endotoxin in C3HeB/FeJ mice.

85 In galactosamine/endotoxin-treated animals, which developed

86 Galactosamine/ET induced neutrophil accumulation in sinu

87 ly in an experimental toxic state induced by galactosamine exposure in rats.

88 eous hydrofluoric acid and was identified as galactosamine following peracetylation and analysis by g

89 s, protecting rats dosed with TNF alpha plus galactosamine from apoptosis and hepatotoxicity.

90 Injuring hepatocytes with galactosamine further increased matrix metalloproteinase

91 FK866 exhibits a protective effect on D-galactosamine (GaIN)/lipopolysaccharide (LPS) and concan

92 Treatment of C3Heb/FeJ mice with 700 mg/kg galactosamine (Gal) and 100 microg/kg Salmonella abortus

93 However, if galactosamine (Gal) is co-administered with ET, neutroph

94 the identification of a galactose/N-acetyl-D-galactosamine (Gal/GalNAc) lectin in the protozoan host

95 R5 identified several ectodomain O-(N-acetyl galactosamine-galactose-sialic acid) structures.

96 t with a single injection of VLX103 in the d-galactosamine (GalN) and lipopolysaccharide (LPS) model

97 d in an experimental hepatotoxicity study of galactosamine (galN) and the concomitant investigation o

98 odel of acute hepatic failure generated by d-galactosamine (GalN) injection.

99 terminal kinase (JNK) in the ConA and ConA/D-galactosamine (GalN) models of murine liver injury.

100 ium spp. is characterized by the presence of galactosamine (GalN) modifying some of the interior bran

101 isella tularensis subsp. novicida contains a galactosamine (GalN) residue linked to its 1-phosphate g

102 alactan from mycobacteria possesses a single galactosamine (GalN) residue.

103 oinjection of lipopolysaccharide (LPS) and D-galactosamine (GalN) results in hepatic failure in mice.

104 sponder mice were administered LPS following galactosamine (GalN) sensitization.

105 Francisella lipid A contains an unusual galactosamine (GalN) unit, attached to its 1-phosphate m

106 ct the N-acetyl-d-galactosamine (GalNAc) and galactosamine (GalN) utilization pathways and transcript

107 ) alone or LPS together with the hepatotoxin galactosamine (GalN) was performed to identify TNFalpha-

108 with lipopolysaccharides in the presence of galactosamine (GalN), which suppresses NF-kappaB activat

109 ctinomycin D (ActD) and lipopolysaccharide/D-galactosamine (GalN)-induced hepatotoxicity in vitro and

110 of LPS-induced acute liver failure (ALF) in galactosamine (GalN)-sensitized mice, we show that Ron T

111 aride (LPS)-induced acute liver failure in D-galactosamine (GalN)-sensitized mice.

112 the glycosidic bond formation, 6F-N-acetyl-d-galactosamine (GalNAc) (Ac3), was selected for further s

113 sfer of sialic acid to Galbeta1,3 N-acetyl-D-galactosamine (GalNAc) (core-1) in mucin type O-glycosyl

114 omics approach to reconstruct the N-acetyl-d-galactosamine (GalNAc) and galactosamine (GalN) utilizat

115 B3GALNT2 transfers N-acetyl galactosamine (GalNAc) in a beta-1,3 linkage to N-acetyl

116 N-linked sialic acids and O-linked N-acetyl galactosamine (GalNAc) on the membrane of live cells.

117 glH, which transfers three terminal N-acetyl-galactosamine (GalNAc) residues to the carrier polyisopr

118 acetyl (Ac4GalNAc, 3)-through the N-acetyl-D-galactosamine (GalNAc) salvage pathway induced abrogatio

119 lation is the enzymatic addition of N-acetyl galactosamine (GalNAc) to serine and threonine residues

120 -glycan chains consisting of single N-acetyl galactosamine (GalNAc) units rather than the more usual

121 n Pseudomonas was pretreated with N-acetyl D-galactosamine (GalNAc), a binder of PA-I.

122 tures (NA2/NA3) and to repetitive N-acetyl-D-galactosamine (GalNAc), the so-called clustered Tn antig

123 ) chemical synthesis of precursor N-acetyl-D-galactosamine (GalNAc)-PP-Und (2 weeks) and (ii) enzymat

124 eba histolytica is mediated by an N-acetyl D-galactosamine (GalNAc)-specific lectin, a heterodimer of

125 ined only acetylated amino sugar (acetylated galactosamine (GalNAc).

126 Triantennary N-acetyl galactosamine (GalNAc, GN3: ), a high-affinity ligand fo

127 high-affinity ligands (triantennary N-acetyl galactosamine = GalNAc) for hepatocyte-specific asialogl

128 etyl-glucosamine (GlcNAz), and N-azidoacetyl-galactosamine (GalNAz) revealed that 6AzGlcNAc exclusive

129 tion of N-acetyl-D-galactosamine (Aga) and D-galactosamine (Gam).

130 bean agglutinin, which recognizes N-acetyl-d-galactosamine, generated the largest difference in fluor

131 e as well as by N-acetylated glucosamine and galactosamine (GlcNAc and GalNAc) and glycine (GlyNAc).

132 s were obtained for organic extracts for the galactosamine group, sampling/extraction variability bei

133 hydrates (rhamnose, 3-O-methyl rhamnose, and galactosamine) have been demonstrated to be present in B

134 valin A) and independent (lipopolysaccharide/galactosamine) hepatitis and in models of bacterial infe

135 role of Kupffer cells in the mechanism of D-galactosamine hepatotoxicity in rats and determine wheth

136 pport the hypothesis that uridine prevents D-galactosamine hepatotoxicity not only by rescuing the he

137 cosamine hydrochloride, glucosamine sulfate, galactosamine hydrochloride, and mannosamine hydrochlori

138 he N-acetyl-glucosamine residues to N-acetyl-galactosamines (i.e. in chondroitin) still allows the HC

139 A recent model was developed using D-galactosamine in anesthetized dogs.

140 mice (C3Heb/FeJ) were treated with 700 mg/kg galactosamine in combination with 100 microg/kg Salmonel

141 ctosamine, and 1beta-methylseleno-N-acetyl-D-galactosamine in complex biological samples such as huma

142 and metabolism of N-acetylgalactosamine and galactosamine in Escherichia coli.

143 the modification of a lipid A phosphate with galactosamine in Francisella novicida, a model organism

144 Sulfation of the N-acetyl-galactosamines in dermatan-4-sulfate or chondroitin-6-su

145 Recipient animals were either rats with D-galactosamine-induced acute or rats with chronic liver f

146 igh-risk patients, using a murine model of D-galactosamine-induced endotoxic shock.

147 onal defect, and they are resistant to LPS/D-galactosamine-induced endotoxin shock.

148 hibitor in protecting mice from lethal LPS/D-Galactosamine-induced hepatotoxicity.

149 d IL-4Ralpha-deficient mice survived LPS + d-galactosamine-induced lethal toxicity and exhibited decr

150 We report that lipopolysaccharide/galactosamine-induced liver injury depends on hepatocyte

151 haride (LPS) and they are resistant to LPS/D-Galactosamine-induced pathology.

152 In a D-galactosamine-induced rat model of acute liver injury, w

153 osed to LPS and were hypersensitive to LPS/d-galactosamine-induced septic shock.

154 esult, Tpl2(-/-) mice are resistant to LPS/D-galactosamine-induced shock.

155 y, induction of hepatitis in ob/ob mice by D-galactosamine injection led to similar changes in serum

156 transplanted at the same time point after D-galactosamine injection.

157 for 36 hours, during which they received 2 D-galactosamine injections.

158 cells purified with Ep-CAM antibodies from D-galactosamine injured rat liver, a noncarcinogenic model

159 UDP-galactosamine is prepared enzymatically using galactokin

160 ol glycan consisting of D-chiro-inositol and galactosamine isolated from animal tissues with insulin

161 ch is one of the rare natural occurrences of galactosamine lacking an acetyl group on the nitrogen, h

162 free form and in the presence of galactose, galactosamine, lactose, and N-acetyl-lactosamine at high

163 e status in the macrophage-dependent acute D-galactosamine/lipopolysaccaride (D-GalN/LPS) hepatitis m

164 antibody (Jo2), concanavalin A (ConA), or D-galactosamine/lipopolysaccharide (GalN/LPS) administrati

165 herefore, investigated in the TNF-dependent, galactosamine/lipopolysaccharide (GalN/LPS) model of liv

166 it was observed in KO mice challenged with D-galactosamine/lipopolysaccharide.

167 ot observed with any other sugar, including: galactosamine, mannosamine, Glc, GlcNAc, GalNAc, mannose

168 tic shock was investigated using the mouse D-galactosamine model.

169 fic doxorubicin delivery is achievable using galactosamine-modified polymers, and targeting is also s

170 ical requirement of both free sulfhydryl and galactosamine moieties for inhibition of mucin-type O-gl

171 that GlcN is the substrate of choice for the galactosamine moieties of the chondroitin sulfates, inco

172 Glucosamine, but not galactosamine, N-acetylglucosamine, and N-acetylgalactos

173 he non-inhibitory effect on parasite growth, galactosamine, N-acetylglucosamine, and N-acetylgalactos

174 ther, if mice were made LPS-sensitive with D-galactosamine, no differences between leukopenic and nor

175 reover, apoptosis in hepatocytes caused by D-galactosamine occurred before necrosis (6 hours) and was

176 hich proteins are glycosylated with N-acetyl-galactosamine on serine and threonine residues, is regul

177 avenous injection of lipopolysaccharide with galactosamine or Escherichia coli CP9.

178 Mutant mice were also less susceptible to d-galactosamine/p(I:C)-induced sepsis.

179 geting of a polymer bearing doxorubicin with galactosamine (PK2) to the liver.

180 In mice treated with galactosamine plus lipopolysaccharide, glutathione deple

181 pletion were determined in mice treated with galactosamine plus lipopolysaccharide.

182 ce mortality from normally lethal doses of D-galactosamine plus LPS (D-GalN/LPS).

183 tibility to either a lethal challenge with D-galactosamine plus LPS or high dose LPS.

184 BALB/By mice given doses of D-galactosamine plus Staphylococcus aureus enterotoxin B d

185 hepatocyte apoptosis in mice treated with D-galactosamine plus TNF-alpha.

186 RNA expression of three UDP-N-acetyl-alpha-D-galactosamine:polypeptide GalNAc N-acetylgalactosaminylt

187 racting proteins (TLE1, UDP-N-acetyl-alpha-D-galactosamine:polypeptide N-acetylgalactosaminyltransfer

188 g mutations in FGF23 or UDP-N-acetyl-alpha-D-galactosamine:polypeptide N-acetylgalactosaminyltransfer

189 Although 4-sulfation of the N-acetyl-D-galactosamine residue is found to increase significantly

190 tants lacking the arnT gene do not contain a galactosamine residue on their lipid A.

191 A1 and A2 are modified with an alpha-linked galactosamine residue, as shown by NMR spectroscopy and

192 galactose lectin to galactose and N-acetyl-d-galactosamine residues on colonic MUC-2, preventing para

193 ine dominated, we also detected 6-O-sulfated galactosamine residues.

194 re to staphylococcal enterotoxin B without d-galactosamine sensitization.

195 Additionally, galactosamine sensitized mice to a lethal outcome follow

196 orbidity and mortality in a mouse model of d-galactosamine-sensitized endotoxin shock.

197 Administration of 4e to d-galactosamine-sensitized mice challenged with supraletha

198 administration of a PKD inhibitor protects d-galactosamine-sensitized mice from shock-mediated death

199 ified CPS from MO6-24/O when injected into D-galactosamine-sensitized mice was a more immediate induc

200 In D-galactosamine-sensitized mice, however, thioglycolate tr

201 Therefore, using D-galactosamine-sensitized mice, we assessed the lethal po

202 lysaccharide-induced acute liver injury in D-galactosamine-sensitized mice.

203 Using the D-galactosamine-sensitized mouse model to determine endoto

204 atically reduced the lethality of LPS in the galactosamine-sensitized mouse model.

205 ection against lethal SEB challenge in two D-galactosamine-sensitized murine models of SEB intoxicati

206 a-mediated lethality and hepatic injury in D-galactosamine-sensitized NOD mice is apparently due to a

207 Doxorubicin-polymer conjugate without galactosamine showed no targeting.

208 ugars glucosamine, n-acetyl glucosamine, and galactosamine significantly inhibited uptake of apoptoti

209 the M2a marker macrophage galactose N-acetyl-galactosamine specific lectin 1 (MGL1) and localize to i

210 erleukin-6 and lower interleukin-10/N-acetyl-galactosamine specific lectin 1.

211 ng arginase-1, macrophage galactose N-acetyl-galactosamine specific lectin-1, and interleukin-10.

212 Binding of a series of N-acyl derivatives of galactosamine suggests that the 2-substituent of these s

213 n greater quantity than the 4.9-kDa N-acetyl galactosamine-terminating species in all carbon sources.

214 OD) mice are resistant to doses of LPS and D-galactosamine that uniformly produce lethality in C57BL/

215 xose or hexosamine sugar, in addition to the galactosamine that was previously identified.

216 F-antigen (galactose-beta-(1-->3)-N-acetyl-d-galactosamine) that utilizes quantum dot (QD) technology

217 glucosamine-thiazoline (NGT), and N-acetyl-D-galactosamine-thiazoline (GalNGT) at resolutions from 1.

218 jnk1-/- and jnk2-/- mice in vitro and in the galactosamine/TNF (GalN/TNF) liver injury model.

219 ative ability of various acyl derivatives of galactosamine to compete for binding to this modified ca

220 en injections of SR9009 were given LPS and D-galactosamine to induce fulminant hepatitis and MCC950 t

221 Previous work proposed that uridine blocks D-galactosamine toxicity by preventing inhibition of mRNA

222 the gut, have been shown to play a role in D-galactosamine toxicity in rats.

223 dine, a compound that rescues animals from D-galactosamine toxicity, affects Kupffer cells.

224 of approximately 500-fold, in contrast to D-galactosamine-treated LPS-sensitized mice, in which a <

225 iotic treatment was markedly diminished in D-galactosamine-treated mice compared to controls; e.g., i

226 genicity in rabbits and lethal toxicity in D-galactosamine-treated mice shows that toxic effects in t

227 When tested for toxicity in vivo in D-galactosamine-treated mice, the reduced activities of th

228 ats subjected to partial hepatectomy or in D-galactosamine-treated rats.

229 r cell activation by endotoxin early after D-galactosamine treatment as an important event in the mec

230 er cells and prevented apoptosis caused by D-galactosamine treatment in vivo.

231 sistant to recombinant human TNF-alpha and D-galactosamine treatment than B6 mice (p < 0.001).

232 oses of lipopolysaccharide (LPS) following D-galactosamine treatment, have a deficiency in granuloma

233 were detected as early as 2.5 hours after D-galactosamine treatment.

234 blocking apoptosis that occurs early after D-galactosamine treatment.

235 d has been applied to both D-glucosamine and galactosamine trichloroacetimidate donors as well as an

236 -N-substituted benzylidene D-glucosamine and galactosamine trichloroacetimidates.

237 njury by administering Jo2/Fas-antibody or D-galactosamine-tumor necrosis factor alpha (TNFalpha) in

238 bi-functional, synthesising UDP-Gal and UDP-galactosamine (UDP-GalNAc).

239 Introduction of the beta-galactosamine unit required the screening a variety of a

240 135NG) and the other with two O-linked alpha-galactosamine units (RP135digal), were studied by NMR an

241 ction variability being more elevated in the galactosamine+uridine group.

242 ts treated with galactosamine and three with galactosamine+uridine) was compared with sampling/extrac

243 actosamine is prepared by acetylation of UDP-galactosamine using [1-14C]acetate and N-ethoxy-carbonyl

244 PFAA-derivatized mannosamine and galactosamine were successfully transformed into cell-su

245 in the presence of N-acetylgalactosamine or galactosamine, were regulated in vivo by AgaR and posses

246 tes on the CarboPac PA1 column just prior to galactosamine, whereas remaining amino acids and most pe

247 e and cultured in vitro in the presence of D-galactosamine with or without TNF-alpha were found to be

248 etyl-D-glucosamine and UDP-N-[1-14C]acetyl-D-galactosamine with very high specific activities are des

249 the inositol glycan INS-2 (pinitol beta-1-4 galactosamine) with increased phosphorylation in key ups