ライフサイエンスコーパス: HMO

1 HMO administrative data can be used to ascertain NMSC wi

2 HMO composition in these milk samples was analyzed by HP

3 HMO composition was analyzed by high-pressure liquid chr

4 HMO health plan claims data had a higher specificity tha

5 HMO utility by these bacteria employs structure-specific

6 HMOs (n = 131) were queried on how they identify, implem

7 HMOs were measured by high performance liquid chromatogr

8 ore structures was then extended to up to 11 HMOs by 4 robust glycosyltransferases.

9 Comparison of the relative affinities (of 14 HMOs) measured by ESI-MS with the reported specificities

10 Of the 292 HMOs that disclosed their scores in 1998 (including 130

11 patients (4185 had bariatric surgery) from 3 HMO Research Network sites; (2) 23,000 subjects from the

12 A library of 31 HMOs were chemoenzymatically synthesized and characteriz

13 All 4 HMOs showed a significant increase from 15 to 32 weeks o

14 In serum, 4 HMOs [2'-fucosyllactose (2'FL), lactodifucotetraose (LDF

15 oligosaccharides, including an additional 80 HMOs from reanalysis of human milk.

16 Temporal glycoprofiling of acidic HMO consumed during fermentation demonstrated a single c

17 Neutral and acidic HMOs and BMOs were largely separated and enriched with a

18 bsolute quantification of neutral and acidic HMOs by graphitized carbon liquid chromatography-electro

19 e investigated how the maternal diet affects HMO biosynthesis and how any diet-induced HMO alteration

20 ntified the majority of the highest affinity HMO ligands (or isomer sets that contain the highest aff

21 with affinities >500 M(-1) and >/=93% of all HMO ligands (hGal-1-31 of 31 ligands; hGal-3C-25 of 25;

22 t (P < 0.05) on concentrations of almost all HMOs.

23 ed to determine a universal response for all HMOs.

24 Furthermore, altered HMO composition may mediate the impact of maternal prepr

25 M) revealed that treatment of the beta-amino HMOs significantly inhibits bacterial adherence and elim

26 Codes for cases of varicella and of HZ in an HMO were determined in automated databases of inpatients

27 A total of 8,667 adult members of an HMO completed measures of childhood exposure to family d

28 g, were common among the adult members of an HMO in this study.

29 emi-continuous colon simulator, effect of an HMO, 2'-fucosyllactose (2'-FL), on composition of the in

30 nsurance who obtained health care through an HMO.

31 method was validated and applied to analyze HMOs in the human milk obtained from 10 women.

32 iation between maternal prepregnancy BMI and HMO composition was assessed.

33 similar extent in patients with Medicare and HMO or private insurance, and respective mortality rates

34 medical care quality, public reporting, and HMO finances.

35 generally highly supported by physicians and HMOs.

36 Certain bioactive breast milk proteins and HMOs are associated with infant growth and motor and cog

37 Average HMO expenditures on hospital and home-based services dec

38 Because HMOs, gut microbiota, and infant health are interrelated

39 of -amino human milk oligosaccharides (betaA-HMOs).

40 Next, we examined relations between HMO and maternal anthropometric and reproductive indexes

41 nformation on the close relationship between HMO and infant-gut bifidobacteria.

42 e used to determine the relationship between HMO profiles and allergy.

43 -Cox test to explore the association between HMOs and late-onset neonatal sepsis.

44 regression models, the associations between HMOs and (changes in) maternal metabolic parameters were

45 e studies investigating interactions between HMOs and the intestinal microbiome and immunity in infan

46 Relations between HMOs and infant growth and body composition were examine

47 rtum were analyzed for relationships between HMOs, microbiota, and infant morbidity and growth.

48 cardiac procedures than patients covered by HMO and private insurance.

49 Voluntary reporting of quality data by HMOs is ineffective; selective nondisclosure undermines

50 Pay for performance is now commonly used by HMOs, especially those that are situated to assign respo

51 incurred higher expenditures for commercial HMO enrollees for professional, hospital, laboratory, ph

52 Seven commercial HMO standards were used to create calibration curves and

53 the quantities of several low concentration HMOs were determined from a human milk sample.

54 Analysis of consumed HMO structures confirmed the utility of a beta-1,3-galac

55 ever, little is known how B. longum consumes HMO.

56 cal approach to harvest structurally defined HMOs for various applications.

57 By separating different HMO fractions through multidimensional chromatography, w

58 ngs suggest that concentrations of different HMOs vary from one individual to another according to th

59 sion (CSEE), for rapid production of diverse HMOs was reported.

60 HMO catabolic cluster is up-regulated during HMO fermentation and is active on sialylated lacto-N-tet

61 <1 h to complete and consumed <5 ng of each HMO and <0.5 mug of protein.

62 individual, structurally distinct effective HMO, needs further elucidation.

63 s act as a bioactive and prebiotic enriching HMO-utilizing bacteria and cause systematic changes in t

64 ed B. longum subsp. longum are deficient for HMO utilization, although they retain the capacity to fe

65 ighlight the importance of maternal diet for HMO biosynthesis and provide as yet unexplored targets f

66 in 11 international cohorts and analyzed for HMOs by using high-performance liquid chromatography.The

67 udy uncovers a unique antibacterial role for HMOs against a leading neonatal pathogen and expands the

68 liability of the assay, a library of 31 free HMOs, ranging in size from tri- to octasaccharide, was s

69 of simultaneously screening mixtures of free HMOs of known concentration for binding to lectins in vi

70 does not utilize fucose or sialic acid from HMO.

71 All charts from HMO-health plan enrollees in 2007 were reviewed (n = 1,1

72 y NMSC diagnosis, including all records from HMO-enrollee members in 2007.

73 bility to preferentially consume fucosylated HMO suggests a competitive advantage for these unique B.

74 strains additionally metabolized fucosylated HMO.

75 er devoted to the utilization of fucosylated HMO, including genes for import of fucosylated molecules

76 a preference for consumption of fucosylated HMO.

77 A prominent fucosylated HMO, 2'-fucosyllactose, failed to elicit these changes i

78 nce and near-absence of alpha1-2-fucosylated HMOs, respectively.

79 categories of HMOs (total HMOs, fucosylated HMOs, and sialylated HMOs), 51 individual HMOs, and 6 bi

80 Surgeons who work in a group HMO are significantly less likely to provide any charity

81 Inside the gut, HMOs are preferentially bound and catabolized by the ben

82 health care utilization and whether they had HMO or FFS coverage.

83 Higher HMO diversity and evenness at 1 mo were associated with

84 The accessibility of a homogeneous HMO library is essential to solve these issues which hav

85 While B. infantis displayed homogeneous HMO-utilization patterns, B. bifidum were more diverse a

86 s support the hypothesis that differences in HMO composition in mother's milk are associated with inf

87 milk samples to determine the variations in HMO concentrations from women classified as secretors an

88 e aimed to study the presence and changes in HMOs throughout pregnancy and assess associations with m

89 th several HMOs, and multiple differences in HMOs [e.g., lacto-N-neotetrose and DSLNT] were shown bet

90 and can be used to determine differences in HMOs concentrations throughout lactation and among women

91 ere no other differences between patients in HMOs and those in other managed care and fee-for-service

92 Patients with RA in HMOs were less likely to use methotrexate, cyclooxygenas

93 Patients with RA in HMOs were significantly less likely than those in other

94 Patients with RA in HMOs were significantly less likely to use biologic agen

95 On an unadjusted basis, subjects with SLE in HMOs had significantly fewer physician visits (3.1; 95%

96 Subjects with SLE in HMOs utilized substantially less ambulatory care and wer

97 compared health care utilization of those in HMOs and FFS, with and without adjustment for socioecono

98 th people with SLE who were in FFS, those in HMOs were younger (3.3 years), received a diagnosis at a

99 and concentrations are a fundamental tool in HMOs research.

100 and Bifidobacterium bifidum using individual HMO, and compared the global transcriptomes of represent

101 ed HMOs, and sialylated HMOs), 51 individual HMOs, and 6 bioactive proteins (lactalbumin, lactoferrin

102 Relative abundances of several individual HMOs were associated with growth and development, mostly

103 ts HMO biosynthesis and how any diet-induced HMO alterations influence the infant gut microbiome and

104 hat the maternal diet itself might influence HMO composition, we sought to directly determine the eff

105 Instead, HMOs act as a bioactive and prebiotic enriching HMO-util

106 icant reduction in UPEC internalization into HMO-pretreated epithelial cells without observing any si

107 of hGal-3 (hGal-3C) and hGal-7), with known HMO affinities.

108 elines, with higher rates of usage by larger HMOs and by those with higher National Committee on Qual

109 m breve ATCC 15700 showed significantly less HMO catabolic activity compared to B. infantis.

110 with offspring exposed to the neutral Lewis HMO profile, exposure to acidic Lewis HMOs was associate

111 Lewis HMO profile, exposure to acidic Lewis HMOs was associated with a higher risk of allergic disea

112 riptomes of representative isolates on major HMO by RNA-seq.

113 In this manner, HMOs help protect against pathogen colonization and redu

114 limited by the difficulties in manufacturing HMO.

115 ntis efficiently consumes several small mass HMOs and possesses a large gene cluster and other loci d

116 Maternal HMO composition 3 mo after delivery was associated with

117 o determine the association between maternal HMO composition and child growth during the first 5 y of

118 The association between maternal HMO composition and childhood growth may imply a causal

119 determine the relationship between maternal HMO profiles and offspring allergic diseases up to age 1

120 pal well-baby clinics and linked to maternal HMO composition data to test for associations.

121 Profiles/patterns of maternal HMOs were determined using LCA.

122 MS-based analyses, we extracted and measured HMOs from breast milk samples and then correlated their

123 We investigated the mechanisms HMOs deploy to elicit protection in human bladder epithe

124 e maternal diet during lactation alters milk HMO composition, which in turn shapes the functional mil

125 dontal treatment outcome in this group model HMO population.

126 valuated for Cbl deficiency at a staff model HMO were reviewed.

127 HMO-utilization were upregulated by neutral HMO and SL, but not by FL in both species.

128 er to a pattern similar to growth on neutral HMO.

129 lization of pooled HMO is similar to neutral HMO, while transcriptomes for growth on FL were more sim

130 Nineteen HMOs were measured.

131 e, but both codes may be necessary among non-HMO patient populations.

132 his study support our hypothesis that normal HMO concentrations and profiles vary geographically, eve

133 eractions, we unexpectedly uncovered a novel HMO property to directly inhibit the growth of GBS indep

134 an increased absolute abundance of numerous HMOs, including 16 sulfonated HMOs we identified here in

135 nt associations between the concentration of HMO-bound fucose and the abundance of fucosidase (a bact

136 preferentially alter milk concentrations of HMO, including fucosylated species.

137 Little is known about the effects of HMO composition and its changes on the morbidity and gro

138 llision-induced dissociation fingerprints of HMO anions released from the target protein in the gas p

139 However, the underlying mechanisms of HMO in viral protection and the identification of indivi

140 d infant gut and the molecular mechanisms of HMO utilization for the type strain B. longum subsp. inf

141 fect the host, we analyzed the metabolism of HMO 2'-fucosyllactose (2'-FL) in Bifidobacterium longum

142 One-year rates of HMO withdrawal from public disclosure of HEDIS scores fo

143 In the course of our studies of HMO-microbial interactions, we unexpectedly uncovered a

144 sitive associations of absolute abundance of HMOs with DeltaLAZ (P = 0.035), and relative abundance o

145 d associations of the relative abundances of HMOs and concentrations of bioactive proteins with infan

146 I-MS assay for quantifying the affinities of HMOs for lectins was established from the agreement foun

147 nts and comprehensive structural analysis of HMOs.

148 at 6 mo (n = 659) for general categories of HMOs (total HMOs, fucosylated HMOs, and sialylated HMOs)

149 cribe the composition and characteristics of HMOs in Peruvian mothers of these infants.

150 d to examine associations of milk content of HMOs and bioactive proteins at 6 mo postpartum with infa

151 ligns with the vision behind the creation of HMOs, managed care organizations that were once embraced

152 inked glycans express structural elements of HMOs, and thus, the reported synthetic principles will f

153 -MS data and affinities of a small number of HMOs for hGal-1, hGal-3C, and hGal-7 measured by isother

154 The profiles of HMOs produced differ between mothers.

155 -allergy-risk birth cohort, some profiles of HMOs were associated with increased and some with decrea

156 Proponents of HMOs argue that they can lower costs while maintaining a

157 lows accurate and reliable quantification of HMOs and can be used to determine differences in HMOs co

158 n method is introduced for the separation of HMOs by multicapillary gel electrophoresis.

159 Fragmentation spectra of HMOs using collision-induced dissociation were studied t

160 ed the relation between the profit status of HMOs and enrollees' assessments of their care.

161 able to PCMHs that build on the strengths of HMOs while avoiding their mistakes.

162 uggest that specific types and structures of HMOs are sensitive to environmental conditions, protecti

163 quantification, and biofunctional studies of HMOs remain a great challenge due to their diversity and

164 y play a role in regulating the synthesis of HMOs.The results of this study support our hypothesis th

165 e milk samples were more diverse in terms of HMOs than colostrum (Simpson's Reciprocal Diversity Inde

166 The HMO survey indicated that one third of HMOs reported use of ASCO guidelines, with higher rates

167 quantitation of human milk oligosaccharide (HMO) structures employing LC/MS and isotopically labeled

168 Human milk oligosaccharides (HMO) are a diverse range of sugars secreted in breast mi

169 Human milk oligosaccharides (HMO) are believed to have a range of biological activiti

170 Human milk oligosaccharides (HMO) are favorable macromolecules which are, interesting

171 e also found on human milk oligosaccharides (HMO), an abundant and structurally diverse component in

172 utilization of human milk oligosaccharides (HMO).

173 oncentration of human milk oligosaccharides (HMO).

174 Human milk oligosaccharides (HMOs) and bioactive breast milk proteins have many benef

175 ous mixtures of human milk oligosaccharides (HMOs) and bovine milk oligosaccharides (BMOs).

176 iotic nature of human milk oligosaccharides (HMOs) and increasing evidence of direct immunomodulatory

177 ciation between human milk oligosaccharides (HMOs) and late-onset sepsis in very-low-birth-weight inf

178 actions between human milk oligosaccharides (HMOs) and their protein receptors.

179 Human milk oligosaccharides (HMOs) are a family of diverse unconjugated glycans that

180 Human milk oligosaccharides (HMOs) are free glycans naturally present in human milk t

181 Accordingly, human milk oligosaccharides (HMOs) are minimally digested by the infant and persist t

182 rds synthesized human milk oligosaccharides (HMOs) as baby formula additives, and interestingly also

183 a medium using human milk oligosaccharides (HMOs) as the only carbon source purified from breast mil

184 0 g/L GOS - the human milk oligosaccharides (HMOs) concentration is between 5 and 15 g/L--and with a

185 composition of human milk oligosaccharides (HMOs) correlate with infant growth and body composition

186 l library of 74 human milk oligosaccharides (HMOs) derived from results of combined LC-MS/MS experime

187 thirty-two free human milk oligosaccharides (HMOs) for four human galectin proteins, a stable mutant

188 Analysis of human milk oligosaccharides (HMOs) from 6-month-postpartum mothers in two Malawian bi

189 Human milk oligosaccharides (HMOs) function as prebiotics for beneficial bacteria in

190 Human milk oligosaccharides (HMOs) have important nutritional and biological activiti

191 measuring free human milk oligosaccharides (HMOs) in milk samples was developed using multiple react

192 the presence of human milk oligosaccharides (HMOs) in urine of breast-fed, but not formula-fed, neona

193 Human milk oligosaccharides (HMOs) play an important role in the health of an infant

194 Human milk oligosaccharides (HMOs) promote the development of the neonatal intestinal

195 Human milk oligosaccharides (HMOs) shape gut microbiota during infancy by acting as f

196 Human milk oligosaccharides (HMOs) were recently found in serum of normal-weight preg

197 gut microbiota, human milk oligosaccharides (HMOs), and osteoclast and osteoblast biology, young germ

198 onents, such as human milk oligosaccharides (HMOs), is associated with programming of child growth re

199 is composed of human milk oligosaccharides (HMOs), which are resistant to digestion by the infant.

200 multiantennary human milk oligosaccharides (HMOs), which were used to develop a glycan microarray.

201 referred to as human milk oligosaccharides (HMOs).

202 tors, including human milk oligosaccharides (HMOs).

203 a to metabolize Human Milk Oligosaccharides (HMOs).

204 rectly determine the effect maternal diet on HMO and the milk bacteria.

205 ces, the two policies had minimal effects on HMO expenditures for hospital and home-based services.

206 d a modular induction during early growth on HMO and fucosyllactose.

207 ptomes of SC596 during early-stage growth on HMO were more similar to growth on fucosyllactose, trans

208 Thus, the ability to subsist on HMO could demark infant-associated ecotypes potentially

209 B. longum SC596 grew vigorously on HMO, and glycoprofiling revealed a preference for consum

210 ence of the Secretor and Lewis phenotypes on HMOs biosynthesis.

211 Mast cell functions in response to oral HMO treatment were also measured in the passive cutaneou

212 be predicted using Huckel molecular orbital (HMO) localization energy calculations.

213 Health maintenance organization (HMO) administrative databases have been used as sampling

214 visit) in a health maintenance organization (HMO) and a subsequent state law guaranteeing a 48-hour h

215 embers of a health maintenance organization (HMO) and explored the relationship with adult mental hea

216 Health maintenance organization (HMO) and health system administrative databases could be

217 of one U.S. health maintenance organization (HMO) for 1990-1991 through 1999-2000 and of two other HM

218 commercial health maintenance organization (HMO) insurance and the data did not include patients cov

219 es on 1,299 health maintenance organization (HMO) patients aged 30 to 64 who had concurrent medical,

220 rolled in a health maintenance organization (HMO).

221 ple of 252 health maintenance organizations (HMOs) (response rate, 96%) drawn from 41 metropolitan ar

222 s (SLE) in health maintenance organizations (HMOs) and fee-for-service (FFS).

223 or all 384 health maintenance organizations (HMOs) participating in the HEDIS program of the National

224 with RA in health maintenance organizations (HMOs) were significantly less likely to use biologic age

225 embers and Health Maintenance Organizations (HMOs) were surveyed on the value and implementation of A

226 nonprofit health maintenance organizations (HMOs).

227 1990-1991 through 1999-2000 and of two other HMOs for 1996-1997 through 1999-2000.

228 While the parent HMOs lacked antimicrobial and antibiofilm activity, thei

229 ATCC 15697 showed that utilization of pooled HMO is similar to neutral HMO, while transcriptomes for

230 found in Bifidobacterium species to process HMO, and presents detailed information on the close rela

231 Among enrollees in for-profit HMOs, sick enrollees were more likely than healthy enrol

232 Many patients and physicians rejected HMOs as too restrictive, objecting particularly to the c

233 Respondent HMOs valued guidelines for various purposes and used mul

234 Further investigation revealed HMOs, and particularly the sialic acid-containing fracti

235 Mother's HMO composition and infant gut microbiota from 33 Gambia

236 tter mental health care performance for U.S. HMOs.

237 1, hGal-3, hGal-7, and hGal-9 for these same HMOs established using the shotgun human milk glycan mic

238 were extracted from Clalit Health Services (HMO) between July 1, 2008 and July 1, 2012.

239 The levels of several HMOs were highly correlated with each other.

240 mass index were all correlated with several HMOs, and multiple differences in HMOs [e.g., lacto-N-ne

241 tive abundance of fucosylated and sialylated HMOs with language at 18 mo (P < 0.001 and P = 0.033, re

242 total HMOs, fucosylated HMOs, and sialylated HMOs), 51 individual HMOs, and 6 bioactive proteins (lac

243 ty to be confined to specific non-sialylated HMOs and synergistic with a number of conventional antib

244 awian birth cohorts revealed that sialylated HMOs are significantly less abundant in those with sever

245 The sialylated HMOs 3'SL and 3'SLN were associated with fasting glucose

246 This paper describes a simple HMOs extraction and analysis for the simultaneous and ab

247 Higher concentrations of non-3'-SL HMOs were associated with protection against postnatal H

248 But, because disclosure is voluntary, some HMOs could subvert these objectives by refusing to relea

249 Total and specific HMO concentrations were measured by HPLC and compared be

250 Specifically, HMO diversity and the concentration of lacto-N-neo-tetra

251 ce of numerous HMOs, including 16 sulfonated HMOs we identified here in humans for the first time.

252 immune markers, in contrast with sulfonated HMOs, whose expression correlated with suppression of tw

253 rrently quite a few manufacturers synthesize HMOs, however, their analysis is challenging, both in re

254 tio of change, 1.16 [CI, 1.01 to 1.33]) than HMO members.

255 owth on FL were more similar to lactose than HMO in B. bifidum.

256 There has been some evidence that HMO profiles differ in populations, but few studies have

257 is variability.We tested the hypothesis that HMO profiles differ in diverse populations of healthy wo

258 The results of this study suggest that HMO specificities of lectins established using microarra

259 Collectively, our results indicate that HMOs can protect bladder epithelial cells from deleterio

260 confers resistance to HMOs, suggesting that HMOs may function as an alternative substrate to modify

261 The HMO survey indicated that one third of HMOs reported use

262 icaid, Kaiser Permanente California, and the HMO Research Network), starting in 1986 at 1 site and en

263 ut a bleeding event were identified from the HMO Research Network-Stent (HMORN-Stent) Registry.

264 This article reviews the HMO experience and identifies lessons applicable to PCMH

265 on the ability of the strain to utilise the HMO component fucosyllactose.

266 NanH2, encoded within the HMO catabolic cluster is up-regulated during HMO ferment

267 The HMOs composition and concentrations vary significantly a

268 especially since 2'FL and LNnT are among the HMOs now being added to infant formula.

269 More than half the HMOs, representing more than 80% of persons enrolled, us

270 ods that can identify the differences in the HMOs composition and concentrations are a fundamental to

271 four galectins recognize the majority of the HMOs tested (hGal-1 binds thirty-two HMOs, hGal-3C binds

272 Twenty-five of the HMOs tested bind all four galectins, with affinities ran

273 ansion of supplemental benefits available to HMO and PPO Medicare Advantage enrollees, this study ass

274 rge gene cluster and other loci dedicated to HMO metabolism.

275 Genes linked to HMO-utilization were upregulated by neutral HMO and SL,

276 gical variation of infant-borne B. longum to HMO consumption, which resembles B. infantis.

277 ycosyltransferase that confers resistance to HMOs, suggesting that HMOs may function as an alternativ

278 = 659) for general categories of HMOs (total HMOs, fucosylated HMOs, and sialylated HMOs), 51 individ

279 ortion of 3'-sialyllactose (3'-SL) per total HMOs was higher among transmitting than among nontransmi

280 HIV-infected women with total HMOs above the median (1.87 g/L) were less likely to tra

281 arrays may not accurately reflect their true HMO-binding properties and that the use of "in solution"

282 Here, we assess the effect of two HMOs, 2'-fucosyllactose and 6'-sialyllactose, on symptom

283 of the HMOs tested (hGal-1 binds thirty-two HMOs, hGal-3C binds twenty-six, hGal-7 binds thirty-one,

284 the screening libraries of free (unmodified) HMOs against lectins.

285 f Bifidobacterium have been shown to utilize HMOs by conserved, as well as species-specific pathways,

286 elationship between bifidobacteria utilizing HMOs and how the metabolites that are produced could aff

287 ovirus belonging to a recently discovered VA/HMO clade.

288 Astrovirus VA1/HMO-C (VA1; mamastrovirus 9) is a recently discovered as

289 em infections in mammals, and astrovirus VA1/HMO-C is the most prevalent astrovirus in cases of human

290 The discovery of HAstV-VA1/HMO-C-UK1(a) as the cause of encephalitis in this case p

291 We identified an astrovirus, HAstV-VA1/HMO-C-UK1(a), which was highly divergent from human astr

292 this case provides further evidence that VA1/HMO-C viruses, unlike HAstV 1-8, are neuropathic, partic

293 V 1-8) genotypes, but closely related to VA1/HMO-C astroviruses, including one recovered from a case

294 nt-borne B. longum strains exhibited varying HMO growth phenotypes.

295 We investigated whether HMO concentrations are associated with a reduced risk of

296 Whether HMOs have effects on maternal metabolism is unknown.

297 aternal prepregnancy BMI was associated with HMO composition.

298 es and had worse outcomes than patients with HMO or private insurance as the primary payer.

299 Compared with HMOs receiving higher quality-of-care scores, lower-scor

300 Treatment with HMOs also suppressed antigen-induced increases in mouse