ライフサイエンスコーパス: galactosamine

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

2 hosphate group that is partially modified by 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 -alpha) prevented hepatotoxicity caused by D-galactosamine.

9 an controls after the coinjection of LPS and galactosamine.

10 the toxic synergism between halothane and D-galactosamine.

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

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

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

14 from acetaminophen or tumor necrosis factor/galactosamine.

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

16 y administration of lipopolysaccharide and D-galactosamine.

17 r a peptide, d-biotin, BODIPY, or N-acetyl-d-galactosamine.

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

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

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

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

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

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

24 In DMSO solution, imines derived from d-galactosamine, [(2R,3R,4R,5R,6R)-3-amino-6-hydroxymethyl

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

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

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

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

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

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

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

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

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

34 fficiently assembled by rapid synthesis of d-galactosamine and AAT building blocks from cheap and abu

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

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

37 hydrolysis that the polysaccharide contained galactosamine and glucuronic acid.

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

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

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

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

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

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

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

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

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

47 data showed that the oligo-alpha-(1 -> 4)-d-galactosamines and their N-acetylated derivatives allowe

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

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

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

51 sugars, including glucosamine, mannosamine, galactosamine, and muramic acid, as laboratory standards

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

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

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

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

56 lkyl glycosides (O- and S- d-galactosides, d-galactosamines, and l-fucose), delivering consistent iso

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

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

59 revealed a partial substitution of N-acetyl-galactosamine by the keto sugar 2-acetamido-2,6-dideoxy-

60 D-galactosamine caused a transient increase in circulating

61 D-galactosamine caused panlobular focal hepatocellular nec

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

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

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

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

66 uctural analysis of the apo Ega3 and an Ega3-galactosamine complex, at 1.76 and 2.09 angstrom resolut

67 ctoside, biotinylated oligo-alpha-(1 -> 4)-d-galactosamines comprising from two to six GalN units wer

68 d hepatocellular PMR induced with TNF plus D-galactosamine, concanavalin A, Jo2 anti-Fas agonist anti

69 method structured the challenging furanosyl galactosamine configuration, facilitated further concise

70 nical trial evaluated olezarsen, an N-acetyl-galactosamine-conjugated antisense oligonucleotide targe

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

72 Galactosamine-containing glycosaminoglycans (GAGs), such

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

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

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

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

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

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

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

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

81 s induced by lipopolysaccharide (LPS) plus D-galactosamine (D-Galn), and concanavalin A (ConA) to ide

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 In galactosamine/endotoxin-treated animals, which developed

99 Galactosamine/ET induced neutrophil accumulation in sinu

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

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

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

103 Injuring hepatocytes with galactosamine further increased matrix metalloproteinase

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 This study examines the role of SphK1 in D-galactosamine (GalN)/lipopolysaccharide (LPS)-induced AL

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

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

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

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

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

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

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

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

134 ugation of synthetic triantennary N-acetyl-d-galactosamine (GalNAc) to small interfering RNA (siRNA)

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

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

137 ing RNAs conjugated to triantennary N-acetyl galactosamine (GalNAc), the ligand recognized by the asi

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

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

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

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

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

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

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

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

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

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

148 types, and hepatocyte-selective tri-N-acetyl galactosamine (GN)-conjugated siRNAs were then used to e

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 verse agonists reduced mortality in an LPS/d-galactosamine-induced fulminant hepatitis mouse model.

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

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

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

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

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

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

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

173 4th (4S) and 6th (6S) positions of n-acetyl-galactosamine inhibits outgrowth in several types of cen

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

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

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

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

178 UDP-galactosamine is prepared enzymatically using galactokin

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

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

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

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

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

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

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

186 Acute liver failure was induced with Galactosamine-LPS and in both models animals were treate

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

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

189 d is employed to cross-link the BMT with the galactosamine-modified antibody.

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

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

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

193 The galactosamine moiety bound to ribosomal proteins and blo

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

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

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

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

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

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

200 of in vivo rat livers with ALF induced by d-galactosamine over 48 hours, and the stiffness change wa

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

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

203 In mice treated with galactosamine plus lipopolysaccharide, glutathione deple

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 Additionally, galactosamine sensitized mice to a lethal outcome follow

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

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

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

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

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

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

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

226 ve against lipopolysaccharide challenge in D-galactosamine-sensitized mice.

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

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

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

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

231 Doxorubicin-polymer conjugate without galactosamine showed no targeting.

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

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

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

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

236 lso uncovered the molecular determinants for galactosamine specificity and substrate binding at the -

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

238 new strategy for the assembly of protected d-galactosamine synthons.

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

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

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

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

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

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

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

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

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

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

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

250 s the Golgi-localized polypeptide N-acetyl-d-galactosamine-transferase 2 isoenzyme.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

265 tosyltransferases toward uridine-diphosphate-galactosamine (UDP-GalN), which is not a commonly used s

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

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

268 135NG) and the other with two O-linked alpha-galactosamine units (RP135digal), were studied by NMR an

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

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

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

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

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

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

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

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

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