ライフサイエンスコーパス: AGE

1 AGE alter tissue function via direct effects on ECM and

2 AGE increases sterol regulatory element binding protein

3 AGE is increased in adipose tissue from diabetic compare

4 AGE reversed 67% of the transcriptome alteration induced

5 AGE-IAPP, like normal IAPP, is capable of interacting wi

6 AGE-mediated autophagy is inhibited by suppression of PI

7 AGE-mediated autophagy is partially suppressed by inhibi

8 AGEs and other alarmins inadvertently prime innate signa

9 AGEs are also formed in the presence of a high concentra

10 AGEs have been identified in all organisms, and their co

11 AGEs improve prediction of RFL and its major structural

12 In total, 19 AGE modification sites corresponding to 11 proteins were

13 n AGE hospitalizations, and 36% (IQR, 28-46) AGE mortality.

14 patterns were complex but reproducible: 789 AGE-modified peptides in 772 proteins were detected in t

15 influenced by plant age, the abundance of 96 AGE sites in 71 proteins was significantly affected in a

16 agy and M1 polarization of macrophages after AGEs (advanced glycation endproducts) treatment, blockin

17 res the potential role of antibodies against AGE-modified proteins in pathogenesis of different chron

18 is study, we detected autoantibodies against AGE-modified proteins with ELISA in plasma samples of 91

19 between the levels of autoantibodies against AGEs and diabetes mellitus (DM 44% vs 24.4%; p = 0.05).

20 ing the production of autoantibodies against AGEs.

21 ibitory activity of fermented flours against AGEs formation was generally reduced.

22 the advanced glycation end-product-albumin (AGE-albumin) from activated macrophages is critical in b

23 Although AGE-mediated lipogenesis is affected by autophagy inhibi

24 The contents of two amide-AGEs in human serum albumin and apolipoprotein A-II were

25 minotransferase, aspartate aminotransferase, AGEs and insulin levels.

26 nd glyoxal hydroimidazolones (P = 0.049), an AGE measured in skin biopsy collagen, in DCCT.

27 stage 3 at baseline, 1, and 5 years using an AGE reader (DiagnOptics).

28 Using an AGE Reader, we measured the sAF at the first visit of 34

29 s measured 5 y (median value) later using an AGE Reader.

30 products (AGEs) in food items and to analyze AGEs in a selection of food items commonly consumed in a

31 Glycated collagen 1 and AGE-modified ECM regulate adipocyte glucose uptake and e

32 Dietary AGEs and AGE-forming sugars might be the missing link, a hypothes

33 We propose that a diet high in AGEs and AGE-forming sugars results in misinterpretation of a thr

34 The AIA circuit and AGE-1, an insulin-regulated PI3 kinase, signal to AWC to

35 gastroenteritis (AGE) hospitalizations, and AGE deaths among children <5 years old.

36 he rapid declines in rotavirus infection and AGE in vaccinated and unvaccinated age groups within 1 y

37 Associations between protein intake and AGE-RAGE biomarkers were examined using linear regressio

38 , we found sustained impact on rotavirus and AGE hospitalizations and deaths.

39 egression was performed with dicarbonyls and AGEs as dependent variables, and dietary GI or GL as mai

40 Dicarbonyls and AGEs were measured in the fasting state by ultra-perform

41 the endogenous formation of dicarbonyls and AGEs.

42 Exposure of BMVECs to high glucose and AGEs led to significant augmentation of ICAM and VCAM ex

43 Pericytes exposed to hyperglycemia and AGEs displayed diminished expression of integrin alpha1,

44 ratios, tissue oxidative stress levels, and AGEs and RAGE levels in pulmonary and renal endothelial

45 s, and increased tissue oxidative stress and AGEs-RAGE levels in pulmonary and renal endothelial cell

46 iki' (450 MPa/5 min) showed the highest anti-AGE activity (12.37 mg/mL).

47 riod 2, overall AGE and norovirus-associated AGE incidence was 51.8/100 PY (95% CI, 48.8-54.9) and 6.

48 this is true for sporadic medically-attended AGE are limited.

49 scavenger receptors RAGE or CD36, attenuated AGE-ECM inhibition of adipocyte glucose uptake.

50 ata were derived from ongoing hospital-based AGE surveillance from January 2009 to December 2014.

51 Interactions between AGEs and their receptors, including advanced glycation e

52 iovascular disease, the relationship between AGEs and cardiovascular disease in patients with CKD is

53 Our recent study showed that both AGE and FruArg significantly attenuate lipopolysaccharid

54 ts could be modulated by treatment with both AGE and FruArg.

55 rovirus prevalence among tested specimens by AGE-coded outpatient encounters and inpatient discharges

56 ides and makes interpretation of a causative AGE at a specific amino acid residue difficult.

57 n, seasonal peaks of rotavirus and all-cause AGE were dwarfed.

58 ry-confirmed infections and 50 427 all-cause AGE-associated hospital admissions were averted in 2013-

59 (July 2000 through June 2015) and all-cause AGE-associated hospitalizations (July 2007 through June

60 ine (RR, 0.74; 95% CI, .65-.84) in all-cause AGE-associated hospitalizations in 2013-2014, compared w

61 ospitalizations from rotavirus and all-cause AGE.

62 ue oxidative stress levels, endothelial cell AGEs and RAGE levels, pulmonary and renal cell apoptosis

63 injury linked to increased endothelial cell AGEs and RAGE levels.

64 In chronic renal failure, higher circulating AGE levels result from increased formation and decreased

65 ods high in protein may increase circulating AGE concentrations.

66 lecule-1, 8-isoprostane, leptin, circulating AGEs and receptor for AGEs were reduced after consumptio

67 orts the implementation of ELISA in food CML/AGEs screening.

68 N (e)-(Carboxyethyl)lysine (CEL) is a common AGE associated with AD patients and occurs at either Lys

69 ower content of potential harmful compounds (AGEs).

70 s multiyear analysis of laboratory-confirmed AGE surveillance from 4 VAMCs demonstrates dynamic intra

71 ased functional ingredients in controlling d-AGEs formation.

72 f dietary advanced glycation end-products (d-AGEs), dicarbonyls and acrylamide.

73 retreatment with Myr significantly decreased AGEs-induced inflammatory cytokine expression, limited a

74 We detected AGE as one of the potent inducers of autophagy compared

75 to reduce AGE accumulation, such as dietary AGE restriction, may reduce cardiovascular risk in CKD,

76 We determined whether changing dietary AGE intake could modulate insulin sensitivity and secret

77 Hence, a restriction in dietary AGE content may be an effective strategy to decrease dia

78 associations were not independent of dietary AGE intake.

79 The presented dietary AGE database opens the possibility to further quantify a

80 Dietary AGEs and AGE-forming sugars might be the missing link, a

81 glycated, 48 advanced glycation endproduct (AGE-) modified, and 20 oxidized/carbonylated peptides re

82 Advanced glycation endproducts (AGEs) and their precursors (dicarbonyls) are associated

83 Advanced glycation endproducts (AGEs) are believed to play a significant role in the pat

84 Advanced glycation endproducts (AGEs) are formed in a series of non-enzymatic reactions

85 rmination of advanced glycation endproducts (AGEs) in food items and to analyze AGEs in a selection o

86 ri) and late advanced glycation endproducts (AGEs) together with free radicals via autoxidation of gl

87 f AGEs, increasing the breakdown of existing AGEs, or inhibiting AGE-induced inflammation.

88 Aged garlic extract (AGE) is widely used as a dietary supplement on account o

89 Five AGEs were measured in serum collected at enrollment and

90 PEF efficiently reduced fluorescent AGE formation in breads compared with TEF.

91 ed the formation of overall free fluorescent AGEs and pentosidine.

92 CAP attenuated the formation of fluorescent AGEs (38.5%), Dityrosine (44.6%), N-formylkynurenine (42

93 d for annual changes in hospitalizations for AGE and rotavirus; 2012 was excluded as a transition yea

94 reby children aged <5 years hospitalized for AGE have stool sample tested for rotavirus antigen, was

95 the expression of its receptor, receptor for AGE.

96 d glycation end products (AGEs) receptor for AGEs (RAGE) pathway, and (3) enalapril (which has antiox

97 yl-lysine (CML) and the soluble receptor for AGEs (sRAGE) in 2439 participants from the Health, Aging

98 D-MSCs) with or without soluble receptor for AGEs (sRAGE).

99 e, leptin, circulating AGEs and receptor for AGEs were reduced after consumption of low AGE diets wit

100 ization for all-cause acute gastroenteritis (AGE) and rotavirus-specific AGE at a large referral hosp

101 trategies in the U.S. Acute gastroenteritis (AGE) burden, etiology, and severity in adults is not wel

102 are used to estimate acute gastroenteritis (AGE) disease burden.

103 urden of diarrhea and acute gastroenteritis (AGE) due to norovirus in a lower-middle-income community

104 tavirus and all-cause acute gastroenteritis (AGE) during the first 10 years since vaccine licensure,

105 e hospitalized due to acute gastroenteritis (AGE) during the first 3 rotavirus seasons after RV5 vacc

106 zations for all-cause acute gastroenteritis (AGE) during the first year after introduction.

107 ased surveillance for acute gastroenteritis (AGE) hospitalizations and emergency department (ED) visi

108 We compared all-cause acute gastroenteritis (AGE) hospitalizations and rotavirus-associated hospitali

109 tion on rotavirus and acute gastroenteritis (AGE) hospitalizations and to estimate vaccine effectiven

110 rus hospitalizations, acute gastroenteritis (AGE) hospitalizations, and AGE deaths among children <5

111 cted surveillance for acute gastroenteritis (AGE) in 3 Kenyan hospitals.

112 ing cause of epidemic acute gastroenteritis (AGE) in the U.S, with most outbreaks occurring during wi

113 epidemic and endemic acute gastroenteritis (AGE) worldwide.

114 ant cause of epidemic acute gastroenteritis (AGE), yet the burden of endemic disease in adults has no

115 etes nor CKD, which may be explained by high AGE formation in diabetes and decreased excretion in CKD

116 y and fibrogenic responses in mice on a high AGEs diet.

117 by 0.8 mg . kg(-1) . min(-1) after the high-AGE diet (P = 0.086).

118 low-AGE dietary period than during the high-AGE period (all P < 0.05), which was confirmed by change

119 We found the highest AGE levels in high-heat processed nut or grain products,

120 % of acute gastroenteritis hospitalizations [AGE] among children aged <5 years).

121 We chemically synthesized glycated IAPP (AGE-IAPP) to mimic the consequence of this hormone pepti

122 , 2016-June 30, 2018, we actively identified AGE inpatient cases and non-AGE inpatient controls throu

123 The number of identified AGE-modified and oxidized residues increased slightly af

124 -dimensional trajectory of immune aging (IMM-AGE) that describes a person's immune status better than

125 We show that the IMM-AGE score predicted all-cause mortality beyond well-esta

126 avirus hospitalizations, 36% (IQR, 23-47) in AGE hospitalizations, and 36% (IQR, 28-46) AGE mortality

127 rient-matched diets that were high or low in AGE content were alternately consumed for 2 wk and separ

128 s of age, the median percentage reduction in AGE hospitalizations was 38% overall and 41%, 30%, and 4

129 We observed a significant reduction in AGE-associated in-hospital morbidity and mortality follo

130 We propose that a diet high in AGEs and AGE-forming sugars results in misinterpretation

131 The Western diet is high in AGEs, which are derived from cooked meat, oils, and chee

132 Our findings suggest that diets low in AGEs may be an effective strategy for improving cardiome

133 A diet that is low in AGEs may reduce the risk of type 2 diabetes by increasin

134 olecular pattern molecules (DAMPs) including AGEs, HMGB1, S100s, and DNA.

135 al evidence that high-protein diets increase AGEs is lacking.

136 f MG, we showed that low doses of MG induced AGEs formation and tumour growth in vivo, both of which

137 Aged garlic inhibited AGEs by 56.4% compared to 33.5% for an equivalent concen

138 he breakdown of existing AGEs, or inhibiting AGE-induced inflammation.

139 genesis is affected by autophagy inhibitors, AGE-mediated autophagy is not influenced by lipogenesis

140 L), and advanced glycosylation-modified LDL (AGE-LDL) in circulating ICs were associated with the fou

141 C. difficile and norovirus were leading AGE pathogens in outpatient and hospitalized US Veterans

142 otein cross-linking and higher cross-linking AGE levels.

143 es revealed that the levels of cross-linking AGEs were significantly higher in the glycated chaperone

144 related with levels of protein-cross-linking AGEs.

145 Low AGE diets decreased insulin resistance (mean difference

146 meta-analysis to determine the effect of low AGE diets in reducing cardiometabolic risk factors.

147 r AGEs were reduced after consumption of low AGE diets with increased adiponectin and sirtuin-1.

148 d by 1.3 mg . kg(-1) . min(-1) after the low-AGE diet (P = 0.004), whereas it showed a tendency to de

149 umed less CML, CEL, and MG-H1 during the low-AGE dietary period than during the high-AGE period (all

150 This was associated with lower AGE levels in the negative-GGap group (79%), lower proin

151 vegetables, butter and coffee had the lowest AGE content.

152 iated with serum concentrations of the major AGE carboxymethyl-lysine (CML) and the soluble receptor

153 itable for the quantification of three major AGEs in food items.

154 In mammals, AGEs are continuously formed during the life of the orga

155 sing data from 2 teaching hospitals, monthly AGE and rotavirus admissions by age were examined 40 mon

156 Moreover, AGE-IAPP can induce normal IAPP to expedite its aggregat

157 We implemented a multisite AGE surveillance platform in 4 Veterans Affairs Medical

158 s cases was compared with rotavirus-negative AGE controls.

159 ively identified AGE inpatient cases and non-AGE inpatient controls through prospective screening of

160 t and community-acquired inpatient norovirus AGE at 4 Veterans Affairs Medical Centers (VAMC) (Atlant

161 imately half of sporadic pediatric norovirus AGE cases were caused by GII.4 norovirus.

162 Serum AOPPs, but not AGEs, were significantly higher in patients with mastocy

163 gnitive and functional abilities than did NU-AGE participants (women: 64%; mean age: 70 y; n = 151).

164 y Population for Healthy Aging in Europe (NU-AGE)] was carried out in older Europeans to investigate

165 n percent of DRIE participants and 22% of NU-AGE participants were dehydrated (serum osmolality >300

166 our Elders; living in long-term care) or NU-AGE (Dietary Strategies for Healthy Ageing in Europe; li

167 The NU-AGE trial was registered at clinicialtrials.gov as NCT01

168 Overall, 12% of AGE inpatient cases had ICU stays and 2% died; 3 deaths

169 Accumulation of AGE-modifications alters protein structure and function,

170 Norovirus was a significant cause of AGE in this community, especially among children <2 year

171 n vigilant for bacterial and viral causes of AGE year-round.

172 , stool specimens collected within 7 days of AGE symptom onset for clinician-requested diagnostic tes

173 015), we used an expanded case definition of AGE (by adding >/=2 vomiting episodes without diarrhea o

174 This study aims to unveil effects of AGE and FruArg on gene expression regulation in LPS stim

175 Moreover, we newly report enrichment of AGE-RAGE signaling pathway in diabetic complications, IL

176 e adipocyte glucose uptake and expression of AGE scavenger receptors and Rho signaling mediators, inc

177 Therefore, the inhibition of AGE-albumin from activated macrophages could be a succes

178 is important to understand the mechanism of AGE-mediated signaling leading to the activation of auto

179 ermine the role and underlying mechanisms of AGE in regulating human ECM-adipocyte metabolic crosstal

180 d implicate hDia1 as a potential mediator of AGE-ECM-adipocyte metabolic crosstalk.

181 a1-42, which results in a complex mixture of AGE-modified peptides and makes interpretation of a caus

182 t not glycoxidation, as the major pathway of AGE formation.

183 he general metabolic background, pathways of AGE formation, and the status of plant anti-oxidative/an

184 diseases; our data confirms the presence of AGE-autoantibodies in patients with CAD and that in para

185 s urinary AGE is most likely a reflection of AGE accumulation and degradation in tissues, where they

186 The sensitivity of AGE codes was similar (54% and 58%) in both populations

187 is known about specific molecular targets of AGE and its bioactive components, including N-alpha-(1-d

188 was estimated using FFQs and the content of AGEs measured in commonly consumed foods.

189 we review the various deleterious effects of AGEs in CKD that lead to cardiovascular complications an

190 6]-gingerol from ginger inhibit formation of AGEs and suppress the receptor for advanced glycation en

191 Inhibition of AGEs or RAGE deletion in hepatocytes in vivo reversed th

192 MPa/5 min) was the most potent inhibitor of AGEs in the BSA-GLU model (6.52 mg/mL on average) relati

193 tomatoes were the most potent inhibitors of AGEs in BSA-GLU (7.20mg/mL) and BSA-MGO (9.53mg/mL) mode

194 d AGER1 downregulation, lowered the level of AGEs, and improved proinflammatory and fibrogenic respon

195 nd [6]-gingerol also decreased the levels of AGEs and CML levels, via Nrf2 pathway, enhancing GSH/GSS

196 The GCF levels of AGEs are higher in CP patients with type-2 DM compared t

197 The aim was to assess the levels of AGEs in the GCF of CP patients with and without type-2 D

198 The GCF was collected and levels of AGEs were assessed using standard techniques.

199 Levels of AGEs were detected in all the patients.

200 The mean GCF levels of AGEs were significantly higher among patients in group-1

201 The mean GCF levels of AGEs were significantly higher among patients in group-2

202 yoxal are found to be the main precursors of AGEs and N(epsilon)-(carboxymethyl)lysine (CML) found to

203 However, the role of AGEs in age-related molecular alterations in plants is s

204 Diet is a major source of AGEs, and foods high in protein may increase circulating

205 reducing exogenous and endogenous sources of AGEs, increasing the breakdown of existing AGEs, or inhi

206 rovirus: 291) and inpatients >=65 years old (AGE: 459; C. difficile: 91; norovirus: 26).

207 ot associated with any of the dicarbonyls or AGEs.

208 00 population was highest among outpatients (AGE: 2715; C. difficile: 285; norovirus: 291) and inpati

209 During period 2, overall AGE and norovirus-associated AGE incidence was 51.8/100

210 Thus, the knowledge of the plant AGE patterns and the underlying pathways of their format

211 and sucrose as potential precursors of plant AGEs.

212 T-elevation acute coronary syndrome (POPular AGE): the randomised, open-label, non-inferiority trial.

213 Tissue advanced glycation end product (AGE) accumulation has been proposed as a marker of cumul

214 hesis of the advanced glycation end product (AGE) methylglyoxal-derived imidazolium crosslink (MODIC)

215 Advanced glycation end-product (AGE) formation is increased in diabetes.

216 Advanced glycation end products (AGE) accumulate in diabetic patients and aging people be

217 fluorescence advanced glycated end-products (AGE) and a reduced amount of alpha-dicarbonyl compounds

218 Advanced glycation end products (AGEs) accumulate in tissues with age and in conditions s

219 Advanced glycation end products (AGEs) accumulated during long-term hyperglycemia are inv

220 fluorescent advanced glycation end products (AGEs) and Amadori adducts were determined.

221 ormation of advanced glycation end products (AGEs) and reactive oxygen species (ROS), both of which d

222 t levels of advanced glycation end products (AGEs) are higher in the gingival crevicular fluid (GCF)

223 ecursor for advanced glycation end products (AGEs) due to its protein glycation reactions, which are

224 nditions or advanced glycation end products (AGEs) ex vivo resulted in significant abnormalities in m

225 al (MG) and advanced glycation end products (AGEs) formation in cancer cells.

226 sumption of advanced glycation end products (AGEs) has increased because of modern food processing an

227 ly measures advanced glycation end products (AGEs) in the skin and is a risk indicator for diabetes c

228 iets low in advanced glycation end products (AGEs) on cardiometabolic parameters are conflicting.

229 Advanced glycation end products (AGEs) promote adverse health effects and may contribute

230 tive stress-advanced glycation end products (AGEs) receptor for AGEs (RAGE) pathway, and (3) enalapri

231 nyls) yield advanced glycation end products (AGEs) that can alter the structures and functions of pro

232 ciations of advanced glycation end products (AGEs) with renal function loss (RFL) and its structural

233 Advanced glycation end products (AGEs), a heterogeneous group of compounds formed by none

234 ormation of advanced glycation end products (AGEs), also originating from alpha-dicarbonyl products o

235 ny types of advanced glycation end products (AGEs), formed through the reactions of an amino group of

236 GE ligands, Advanced Glycation End products (AGEs), HMGB1, and S100 proteins, have all been shown to

237 ys included advanced glycation end products (AGEs), phosphatidylcholines, sphingolipids, saturated/un

238 s including advanced glycation end products (AGEs), S100 proteins, and HMGB1.

239 ormation of advanced glycation end products (AGEs), the activity of angiotensin-converting (ACE) and

240 recursor of advanced glycation end products (AGEs), which result in protein dysfunction, glycation of

241 mice and on advanced glycation end products (AGEs)-induced H9c2 cardiomyocytes.

242 s accumulate advanced glycated end products (AGEs).

243 ormation of advanced glycation end products (AGEs).

244 oduction of advanced glycation end products (AGEs).

245 g early and advanced glycation end products (AGEs).

246 Advanced glycation end-products (AGEs) accumulate during prolonged hyperglycemia, but the

247 ormation of advanced glycation end-products (AGEs) and the activity of angiotenisn-converting enzyme

248 Advanced glycation end-products (AGEs) are also present in foods.

249 Resulting advanced glycation end-products (AGEs) contribute to pathogenesis of diabetes mellitus an

250 fluorescent advanced glycation end-products (AGEs) in vitro of raw and roasted buckwheat flours was s

251 es generate Advanced Glycation End-products (AGEs), including N(epsilon)-carboxymethyllysine (CML) fo

252 ormation of advanced glycation end-products (AGEs).

253 fluorescent advanced glycation end-products (AGEs).

254 proteomics approach to identify and quantify AGE modification sites in plasma proteins by reversed ph

255 indings suggest that interventions to reduce AGE accumulation, such as dietary AGE restriction, may r

256 emergency department visits due to rotavirus AGE were reduced by a median of 67% overall and 71%, 59%

257 ivated M1 macrophages synthesize and secrete AGE-albumin, which induced the skeletal muscle cell deat

258 Skin AGEs measured as skin autofluorescence (SAF) are a nonin

259 ate the association between dietary and skin AGEs in the Rotterdam Study, a population-based cohort o

260 gastroenteritis (AGE) and rotavirus-specific AGE at a large referral hospital in Lusaka.

261 F) are a noninvasive reflection of long-term AGE accumulation in tissues.

262 sites might be useful to predict long term, AGE-related complications in diabetic patients, such as

263 These data demonstrate that AGE-modification of ECM contributes to adipocyte insulin

264 rcular dichroism spectra also indicated that AGE-IAPP exhibited faster conformational changes from ra

265 Our data revealed that AGE-IAPP formed amyloid faster than normal IAPP, and hig

266 the first time, we provide data showing that AGE induces several cell signaling cascades, like NF-kap

267 nking mechanism in the lens and suggest that AGE-mediated cross-linking of alpha-crystallin-client co

268 These findings suggests that AGE and FruArg are capable of alleviating oxidative stre

269 In summary, this study elucidates that AGEs induces autophagy and modulates macrophage polariza

270 European Study of Atherosclerosis), and the AGE-RS (Age, Gene/Environment Susceptibility-Reykjavik S

271 To fill this gap, we describe the AGE-modified proteome ofBrassica napusand characterize i

272 ence of the early glycated precursors of the AGE-modified protein residues indicated autoxidative gly

273 and therapeutic strategies that focus on the AGE-RAGE axis to prevent vascular complications in patie

274 The AGEs can be formed via degradation of early glycation in

275 d renal injury by reducing activation of the AGEs-RAGE pathway in endothelial cells in both organs.

276 In this study, we show that the AGEs clearance receptor AGER1 was downregulated in patie

277 atients with CAD and that in parallel to the AGEs themselves, they may have a potential role in conco

278 vascular complications and the role of these AGEs in diabetic nephropathy.

279 ults suggest that dAGEs can influence tissue AGE accumulation and possibly thereby age-related diseas

280 ent in the diet (dAGEs) contribute to tissue AGEs is unclear.

281 further quantify actual dietary exposure to AGEs and to explore its physiological impact on human he

282 Collectively, prolonged exposure to AGEs in the liver promotes an AGER1/RAGE imbalance and c

283 Taken together, AGE-albumin from activated macrophages is critical for b

284 or autophagosomes, is shown to increase upon AGE stimulation.

285 ), which was confirmed by changes in urinary AGE excretion.

286 This urinary AGE is most likely a reflection of AGE accumulation and

287 Dietary, plasma and urinary AGEs N(euro)-(carboxymethyl)lysine (CML), N(euro)-(carbo

288 We validated AGE-related codes in pediatric and adult populations usi

289 han normal IAPP, and higher-molecular-weight AGE-IAPP oligomers were also observed in the early stage

290 Whether AGEs present in the diet (dAGEs) contribute to tissue AG

291 opose the "false alarm" hypothesis, in which AGEs that are present in or formed from the food in our

292 Over 11 seasons, 6954 children with AGE were enrolled and submitted a stool specimen (2187 h

293 eness (VE) was estimated using children with AGE who test negative for rotavirus as controls for the

294 The proportion of children with AGE who tested positive for rotavirus declined from 53%

295 of age hospitalized or visiting the ED with AGE were enrolled from January 2006 through June 2016.

296 937 children <5 years of age presenting with AGE had their stools collected and tested for rotavirus

297 Children from 15 days to 17 years with AGE symptoms were recruited from the outpatient, emergen

298 of necroptosis depends upon glycolysis with AGEs and ROS playing a role.

299 rates of virus shedding in children without AGE symptoms.

300 pounds interact with blood proteins yielding AGEs.