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 was analyzed by high-pressure liquid chr

3 HMO health plan claims data had a higher specificity tha

4 HMO utility by these bacteria employs structure-specific

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

6 cian mental health professionals per 100,000 HMO members, and the ratio of full-time-equivalent nonph

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

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

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

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

11 than 1500 g were up-to-date at each of the 3 HMOs compared with 69% to 73% of those weighing 1500 to

12 A library of 31 HMOs were chemoenzymatically synthesized and characteriz

13 Of the 329 HMOs that publicly disclosed HEDIS scores in 1997, 161 p

14 the Medicare fee-for-service system, 48,380 HMO enrollees before enrollment, and 23,870 HMO enrollee

15 HMO enrollees before enrollment, and 23,870 HMO enrollees after disenrollment.

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

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

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

21 ed to determine a universal response for all HMOs.

22 lished to foster a scientific exchange among HMO-based researchers.

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

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

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

26 nsurance who obtained health care through an HMO.

27 t each site: MWM, 3-fold; MAM, 1.7-fold; and HMO, 3.1-fold.

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

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

30 generally highly supported by physicians and HMOs.

31 nts were as likely to undergo angiography as HMO patients but more likely than Medicaid and uninsured

32 choice of subspecialty training increased as HMO penetration increased from 0 to 0.15.

33 n exposure data derived from these automated HMO vaccination databases.

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

35 Among women undergoing BCS, HMO enrollees were significantly more likely to receive

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

37 regression to model the association between HMO enrollment and presence of physical and depressive s

38 Collaboration between HMO-based research centers and researchers from academia

39 in relative risk of dying were found between HMO and FFS groups (relative risk, 0.96; 95% confidence

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 Relations between HMOs and infant growth and body composition were examine

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

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

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

46 are increasingly delegated responsibility by HMOs for utilization management and quality assurance.

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

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

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

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

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

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

53 By separating different HMO fractions through multidimensional chromatography, w

54 on and of having neither an IPA nor a direct HMO contract.

55 care physicians had at least 1 IPA or direct HMO contract.

56 characteristics of dependency at discharge, HMO patients were more likely than FFS patients to be se

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

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

59 Separate analyses were conducted for each HMO and for each vaccine type administered between 1991

60 type, geographic region, and the method each HMO used to collect data.

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 During the period of our study, elderly HMO enrollees did not appear to have systematic access p

64 aRs, HLA antigens, and monokines, elutriated HMOs and U937 cells were transfected with an adenovirus-

65 itionally, a subpopulation of Nef-expressing HMOs underwent apoptosis.

66 Nef-expressing HMOs, treated with lipopolysaccharide (LPS) or phorbol 1

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

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

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

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

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

72 does not utilize fucose or sialic acid from HMO.

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

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

75 Beneficiaries who disenrolled from HMOs re-enrolled at about the time that their level of u

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

77 strains additionally metabolized fucosylated HMO.

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

79 a preference for consumption of fucosylated HMO.

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 Lower expenditures in areas with high HMO market shares may indicate that traditional Medicare

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

85 an FFS patients to be sent to nursing homes (HMO, 41.8%; FFS, 27.9%; P=.001) and less likely to be di

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

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

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

89 e percentages undergoing BCS were similar in HMO and FFS settings overall (HMO, 38.4%; FFS, 36.8%; di

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

91 Treatment of early-stage breast cancer in HMOs often differs from local FFS patterns, but not in a

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

93 ptoms were 16% less likely to be enrolled in HMOs than in fee-for-service plans after adjustment for

94 Patient enrollment in HMOs grew from 285503 to 3028881.

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

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

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

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

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

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

101 be enrolled in fee-for-service plans than in HMOs.

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

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

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

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

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

107 th physician-diagnosed asthma within a large HMO, Kaiser Permanente, NW Region.

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 ef expression in human monocytes/macrophage (HMO) and U937 on the levels of FcgammaRs, HLA antigens,

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

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

113 limited by the difficulties in manufacturing HMO.

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

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

116 a on system-wide (Medicare and non-Medicare) HMO market share in these areas.

117 dontal treatment outcome in this group model HMO population.

118 ontrol in diabetic patients in a group-model HMO.

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

120 characteristics for 30 staff and group model HMOs.

121 ores were highest for staff- and group-model HMOs.

122 37 months of follow-up (median, 30.4 months, HMO; 31.1 months, FFS) from the date of hospital admissi

123 All the IPAs contracted with multiple HMOs for the full range of primary and specialty care ph

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

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

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

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

128 etween enrollees in for-profit and nonprofit HMOs, for-profit HMOs are rated less favorably than nonp

129 For nonprofit HMOs, there was only one significant difference between

130 HMOs are rated less favorably than nonprofit HMOs by patients who have self-reported fair or poor hea

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

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

133 iography was performed in 86% of FFS, 80% of HMO, 61% of Medicaid and 75% of uninsured patients.

134 In a community cohort of HMO members, generalized social anxiety disorder was rar

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 utilization of human milk oligosaccharides (HMO).

155 oncentration of human milk oligosaccharides (HMO).

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

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

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

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

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

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

162 0 g/L GOS - the human milk oligosaccharides (HMOs) concentration is between 5 and 15 g/L--and with a

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

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

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

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

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

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

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

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

171 tors, including human milk oligosaccharides (HMOs).

172 referred to as human milk oligosaccharides (HMOs).

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

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

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

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

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

178 or terminated from a contract with an IPA or HMO, but 87% of office-based primary care physicians had

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

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

181 f both groups had do-not-resuscitate orders (HMO, 25.4%; FFS, 27.9%; P=.68).

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

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

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

185 of care in health maintenance organization (HMO) and fee-for-service (FFS) settings.

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

187 in a single health maintenance organization (HMO) and presented with myocardial infarction at 1 of 19

188 tients, and Health Maintenance Organization (HMO) enrollees with either leukemia or lymphoma are sign

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

190 icians in a health maintenance organization (HMO) in April 1997 to assess their knowledge of the risk

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

192 oportion of health maintenance organization (HMO) members enrolled in investor-owned plans has increa

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

194 s capitated health maintenance organization (HMO) patients made up 16.0% of the total admissions but

195 Health maintenance organization (HMO) penetration (possible range, 0.0 to 1.0; higher val

196 ation about health maintenance organization (HMO) penetration in 1995 was available.

197 rom a large health-maintenance organization (HMO) to predict asthma-related hospitalization and emerg

198 base of the health maintenance organization (HMO) was used to assess the use of beta-agonists by mete

199 group-model health maintenance organization (HMO) were used to perform a population-based analysis of

200 of a large health maintenance organization (HMO), as were various self-reported measures of health c

201 vice (FFS), health maintenance organization (HMO), Medicaid and uninsured.

202 up practice health maintenance organization (HMO).

203 ession in a health maintenance organization (HMO).

204 of a large health maintenance organization (HMO).

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

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

207 s in large health maintenance organizations (HMOs) is still lacking.

208 ty data on health maintenance organizations (HMOs) might improve public accountability, inform consum

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

210 West Coast health maintenance organizations (HMOs) participating in the Vaccine Safety DataLink (VSD)

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

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

213 roup model health maintenance organizations (HMOs), and to compare the psychiatrist-to-member ratio w

214 nonprofit health maintenance organizations (HMOs).

215 ompared to health maintenance organizations (HMOs).

216 models of health maintenance organizations (HMOs).

217 nrolled in health maintenance organizations (HMOs).

218 1990-1991 through 1999-2000 and of two other HMOs for 1996-1997 through 1999-2000.

219 ere similar in HMO and FFS settings overall (HMO, 38.4%; FFS, 36.8%; difference, 1.6% [95% CI, 0.0%-3

220 Investor-owned HMOs deliver lower quality of care than not-for-profit p

221 farction, 59.2% of members in investor-owned HMOs vs 70.6% in not-for-profit plans received a beta-bl

222 diagnosed at late stages than FFS patients (HMO, 7.6%; FFS, 10.8%; difference, -3.2% [95% confidence

223 therapy but, again, results varied by plan (HMO, 69.0%; FFS, 63.7%; difference, 5.3% [95% CI, 2.9%-7

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

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

226 in for-profit and nonprofit HMOs, for-profit HMOs are rated less favorably than nonprofit HMOs by pat

227 Compared with not-for-profit HMOs, investor-owned plans had lower rates for all 14 qu

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

229 of these plans compared with not-for-profit HMOs.

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

231 Respondent HMOs valued guidelines for various purposes and used mul

232 ionals per 100,000 members in the responding HMOs was 6.8 and 22.9, respectively.

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

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

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

236 1, hGal-3, hGal-7, and hGal-9 for these same HMOs established using the shotgun human milk glycan mic

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

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

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

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

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

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

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

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

245 were more likely to undergo angiography than HMO (odds ratio [OR] 1.27, 95% confidence interval [CI]

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

247 f both depressive and physical symptoms than HMO enrollees.

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

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

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

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

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

253 The HMO enrollees were less likely to have breast cancer dia

254 The HMO Research Network has recently been established to fo

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

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

257 participation rates (ranging from 53% at the HMO to 77% at the academic center) and consent rates for

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

259 4 years (as a percentage of all women in the HMO aged 50-64 years) and of low-yield examinations (ie,

260 y 1983 and were continuously enrolled in the HMO until 30 June 1995.

261 e-for-service group, whereas the rate in the HMO-disenrollment group after disenrollment was 180 perc

262 The rate of use of inpatient services in the HMO-enrollment group during the year before enrollment w

263 Sixteen percent of the HMO population presented with a breast symptom during th

264 Members of the HMO who were identified during the period October 1991 t

265 ained from the cost accounting system of the HMO.

266 tial adult cases were found by reviewing the HMO pharmacy records for dispensation of antidepressant

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

268 r year, and the total cost of RA care to the HMO was $703,053.

269 was observed for the MAM program, while the HMO had nearly 3 times more clonidine than antidepressan

270 It varied among the 19 clinics within the HMO but was nowhere higher than 150/100,000.

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

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

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

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

275 For privately insured patients in this HMO, the requirement of modest, fixed copayments for eme

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

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

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

279 show marked selection biases with respect to HMO enrollment and disenrollment.

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

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

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

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

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

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

286 harged to rehabilitation hospitals or units (HMO, 16.2%; FFS, 23.4%; P=.03).

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

288 These youth were randomized to usual HMO care (n = 49) or usual care plus a 15-session group

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

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

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

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

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

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

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

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

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

298 a regression model, increases in system-wide HMO market share were associated with declines in both P

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

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

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