ライフサイエンスコーパス: AGE

1 AGE and LPS, alone or in combination, stimulated IL-6, I

2 AGE deposition and RAGE expression were noted in animals

3 AGE increases sterol regulatory element binding protein

4 AGE modifications to Ara h 1 and Ara h 3 can be found in

5 AGE modifications were found on Ara h 1 and Ara h 3 in b

6 AGE reversed 67% of the transcriptome alteration induced

7 AGE-mediated autophagy is inhibited by suppression of PI

8 AGE-mediated autophagy is partially suppressed by inhibi

9 AGEs and other alarmins inadvertently prime innate signa

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

11 AGEs have been associated with insulin resistance, oxida

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

13 AGEs improve prediction of RFL and its major structural

14 AGEs were loge-transformed, combined in a z-score, and t

15 The complete 10-AGE panel is associated with three-step Early Treatment

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

17 Norovirus was detected in 302 of 1465 (21%) AGE cases and 52 of 826 (6%) healthy controls.

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

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

20 portion of their ASC content and accumulated AGEs.

21 From December 2011 to November 2012, active AGE surveillance was performed at 6 geographically diver

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

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

24 Although AGE-mediated lipogenesis is affected by autophagy inhibi

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

26 minotransferase, aspartate aminotransferase, AGEs and insulin levels.

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

28 modulatory effect of aminoguanidine (AG), an AGE inhibitor, in various stages of experimental periodo

29 Here we report a study of an AGE outbreak in an elementary school in December 2014 ca

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

31 stology, immunohistochemistry of the AGE and AGE receptor (RAGE), and gene expression of tumor necros

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 CM/MIS, there was no difference in AOPP and AGE concentrations between these two groups of patients.

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

36 ent oxidation and 28 different glycation and AGE modifications by mass spectrometry in a variety of s

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

38 P. gingivalis LPS and AGE in combination caused significantly greater expressi

39 However, the mechanisms of ASC oxidation and AGE formation in the human lens are poorly understood.

40 a 12-T magnetic field, and gelation rate and AGE content were measured.

41 ediator-related symptoms had lower AOPPs and AGEs as compared to patients without symptoms.

42 Serum levels of AOPPs and AGEs in 34 patients with mastocytosis (23 CM/MIS and 11

43 AOPPs and AGEs were inversely correlated with the severity of symp

44 resulting in lower blood levels of AOPPs and AGEs.

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

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

47 As well as AGE-OVA, a crude glycation product in thermal incubation

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

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

50 Interaction between AGE-modified plaque components and immune cells is belie

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

52 patients with diabetes, yet the link between AGEs and inflammatory and fibrogenic activity in nonalco

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

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

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

56 modern diet include excessive nutrient-bound AGEs, such as neurotoxic methyl-glyoxal derivatives (MG)

57 ynurenine-mediated ASC oxidation followed by AGE formation may be an important mechanism for lens agi

58 humans is both preventable and reversible by AGE reduction, a therapeutic strategy that includes AGE

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

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

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

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

63 ospitalizations from rotavirus and all-cause AGE.

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

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

66 ologically and chemically well-characterized AGE markers.

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

68 mporal correlations between high circulating AGEs and impaired cognition, as well as insulin sensitiv

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

70 atabase, we estimated the consumption of CML AGE in the prospective NIH-AARP Diet and Health Study an

71 eatic cancer and the mediating effect of CML AGE on the association between red meat consumption and

72 N()-(carboxymethyl)lysine (CML) AGE is one of the major biologically and chemically well

73 dy and evaluated the association between CML-AGE consumption and pancreatic cancer and the mediating

74 Dietary CML-AGE consumption was associated with modestly increased r

75 With the use of a published food CML-AGE database, we estimated the consumption of CML AGE in

76 ), which attenuated after adjustment for CML-AGE consumption (HR: 1.20; 95% CI: 0.95, 1.53).

77 The consumption of red meat, which is CML-AGE rich, has been positively associated with pancreatic

78 in the fifth and the first quintiles of CML-AGE consumption, we observed increased pancreatic cancer

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

80 ower content of potential harmful compounds (AGEs).

81 Critically, AGE accumulation is also directly affected by our lifest

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

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

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

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

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

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

88 Dietary AGEs are an important contributor to the AGE pool in the

89 To determine whether dietary AGEs promote AD, we evaluated WT mice pair-fed three die

90 uctures rely on agarose-gel electrophoresis (AGE) for separation.

91 generation of advanced glycation endproduct (AGE) modifications.

92 lar ECs with advanced glycation endproducts (AGE), a metabolite commonly elevated in diabetic patient

93 Advanced glycation endproducts (AGEs) accumulate in patients with diabetes, yet the link

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

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

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

97 Advanced glycation endproducts (AGEs), a pathogenic factor implicated in diabetes and ot

98 ion of NO by advanced glycation endproducts (AGEs), which accumulate on tissue proteins as a function

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

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

101 Five AGEs were measured in serum collected at enrollment and

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

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

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

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

106 and immunohistochemistry of the receptor for AGE (RAGE).

107 Receptor for AGE was demonstrated to selectively interact with AGE-mo

108 the expression of its receptor, receptor for AGE.

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

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

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

112 ascorbate (ASC) oxidation products can form AGEs in proteins.

113 kynurenines to photooxidize ASC and to form AGEs in lens proteins.

114 Overall, the added set of four AGEs enhances the association of the original panel with

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

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

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

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

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

120 visiting the ED with acute gastroenteritis (AGE) for the 2012 and 2013 seasons at 7 medical institut

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

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

123 40% of severe endemic acute gastroenteritis (AGE) in children <5 years of age in the United States, t

124 causing outbreaks of acute gastroenteritis (AGE) in China.

125 Acute gastroenteritis (AGE) is a common and impactful disease, typically manage

126 is a leading cause of acute gastroenteritis (AGE).

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

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

129 scosity, faster gelation rates, and a higher AGE-specific fluorescence.

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

131 % of acute gastroenteritis hospitalizations [AGE] among children aged <5 years).

132 arly ondansetron and probiotics in improving AGE outcomes.

133 ults clearly identify the active compound in AGE as allicin.

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

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

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

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

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

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

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

141 uction, a therapeutic strategy that includes AGE reduction may offer a new strategy to combat the epi

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

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

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

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

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

147 significantly reduced periodontal bone loss, AGE deposition, and expressions of TNF-alpha and RAGE bu

148 Low AGE diets decreased insulin resistance (mean difference

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

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

151 ce pair-fed three diets throughout life: low-AGE (MG(-)), MG-supplemented low-AGE (MG(+)), and regula

152 t life: low-AGE (MG(-)), MG-supplemented low-AGE (MG(+)), and regular (Reg) chow.

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

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

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

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

157 s was analyzed for the presence of the major AGEs N(epsilon)-(carboxymethyl)lysine (CML), VCAM-1, neu

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

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

160 presented higher phenolic levels (435.08 mg AGE 100 g(-1)) and elevated antioxidant capacity in all

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

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

163 irus cases (11%), and 804 rotavirus-negative AGE controls.

164 irus cases (14%) and 2559 rotavirus-negative AGE controls.

165 avirus-positive cases and rotavirus-negative AGE controls.

166 rotavirus cases and 1811 rotavirus-negative AGE controls.

167 No AGE modifications were found on Ara h 2.

168 Norovirus AGE cases were 2.8-fold more likely than norovirus-negat

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

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

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

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

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

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

175 ovide further insights into the chemistry of AGE formation and will be helpful to find specific marke

176 monocytes was performed with combinations of AGE and P. gingivalis LPS.

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

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

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

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

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

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

183 derstand the complex mechanistic pathways of AGE formation, it is crucial to extend the knowledge on

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

185 serves as a proxy for tissue accumulation of AGEs.

186 and glucose whereas only limited amounts of AGEs were released.

187 This review will discuss the contribution of AGEs to the cancer phenotype, with a particular emphasis

188 increased brain amyloid-beta42, deposits of AGEs, gliosis, and cognitive deficits, accompanied by su

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 A similar formation of AGEs was observed in UVA-irradiated lenses from human ID

192 esults underline the potential importance of AGEs in development of CVD.

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

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

195 However, the presence of AGEs within atrial tissue of atrial fibrillation (AF) pa

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

197 e changes and the potential biologic role of AGEs in promoting cancer, opportunities exist for collab

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

199 Furthermore, compared with native OVA, AGE-OVA and Pyr-OVA induced higher IgE production in mic

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

201 NF-kappaB, and represses the polyol pathway, AGEs production, and hyperlipidemia.

202 cs may improve patient outcomes in pediatric AGE.

203 ne use of probiotics in outpatient pediatric AGE.

204 RT1, nicotinamide phosphoribosyltransferase, AGE receptor 1, and PPARgamma.

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

206 and sucrose as potential precursors of plant AGEs.

207 ar events, and triglycerides), higher plasma AGE z-scores were associated with higher risk of inciden

208 idence of an association between high plasma AGEs and increased cardiovascular risk remains inconclus

209 In conclusion, high plasma AGEs were associated with incident cardiovascular events

210 rmediates in advanced glycation end product (AGE) formation.

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

212 Advanced glycation end products (AGE) have been found in inflamed gingival tissue and hav

213 e effect of advanced glycation end products (AGE) in the presence and absence of Porphyromonas gingiv

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

215 Advanced glycation end-products (AGE) are reactive metabolites produced as a by-product o

216 Advanced glycation end products (AGEs) accumulate in T2DM, resulting in inflammation, oxi

217 release of advanced glycation end products (AGEs) and antioxidant capacity of puffed cereals was stu

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

219 Advanced glycation end products (AGEs) are a heterogeneous group of compounds present in

220 e so-called advanced glycation end products (AGEs) are formed, including proteins with various glycat

221 he roles of advanced glycation end products (AGEs) are investigated.

222 Advanced glycation end products (AGEs) are involved in the inflammatory process and are c

223 Advanced glycation end products (AGEs) contribute to lens protein pigmentation and cross-

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

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

226 idation and advanced glycation end products (AGEs) had been shown to give rise to colored and fluores

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

228 a role for advanced glycation end products (AGEs) in cardiovascular disease (CVD), particularly in t

229 Presence of advanced glycation end products (AGEs) in the heart induces a proinflammatory phenotype.

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

231 far unknown advanced glycation end products (AGEs) of creatinine.

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

233 in collagen advanced glycation end products (AGEs) originally measured near to the time of the Diabet

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

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

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

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

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

239 phages with advanced glycation end products (AGEs), which accumulate in diabetic nerve tissue, increa

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

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

242 (AOPPs) and advanced glycation end products (AGEs).

243 oduction of advanced glycation end products (AGEs).

244 lycotoxins [advanced glycation end products (AGEs)].

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

246 fluorescent advanced glycation end-products (AGEs).

247 mulation of advanced glycation end-products (AGEs).

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

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

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

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

252 th color in a subset of samples, but several AGEs exhibited a strong correlation with product color i

253 Skin AGEs are robust long-term markers of microvascular disea

254 It has been suggested that some AGEs could have immunostimulatory effects.

255 The data identify a specific AGE (MG) as a modifiable risk factor for AD and MS, poss

256 ith sample color was verified for a specific AGE, carboxymethyllysine, by ELISA, thus validating the

257 elucidate the specific residues and specific AGE modifications found in raw and roasted peanuts and o

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

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

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

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

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

263 loproteinase 3 (Timp3), we hypothesized that AGEs induce TACE through nicotinamide adenine dinucleoti

264 These data indicate that AGEs are at least partially responsible for the color se

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

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

267 objective of this study was to determine the AGE content, as measured by Nepsilon-carboxymethyllysine

268 How has the AGE paradigm for the tissue complications of aging and d

269 roving cellular viability and inhibiting the AGE-RAGE axis.

270 aphy, histology, immunohistochemistry of the AGE and AGE receptor (RAGE), and gene expression of tumo

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

272 ulation was related to the inhibition of the AGE-RAGE axis to resume cell-matrix interactions and mai

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

274 ary AGEs are an important contributor to the AGE pool in the body.

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

276 loses significance after adjustment for the AGEs.

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

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

279 n autofluorescence (SAF; a measure of tissue AGE levels) on people aged >55 years with and without T2

280 inal studies may help confirm whether tissue AGE accumulation is associated with brain atrophy in T2D

281 We aimed to study whether tissue AGE accumulation is associated with T2DM-related brain a

282 type of reactive aldehyde that gives rise to AGE modification.

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

284 hway, and TACE was induced after exposure to AGEs.

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

286 the addition of four originally unavailable AGEs (i.e., glucosepane [GSPNE], hydroimidazolones of me

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

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

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

290 In vitro, AGE exposure decreased Sirt1 and Timp3 in hepatic stella

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

292 d S-allylcystein, a compound associated with AGE's neuroprotective effect against damage induced by c

293 ing the use of these agents in children with AGE in developed countries.

294 of intravenous rehydration in children with AGE in emergency-department-based trials.

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

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

297 of age hospitalized or visiting the ED with AGE symptoms from November 2009-June 2010 and from Novem

298 as demonstrated to selectively interact with AGE-modified rAra h 1.

299 937 children <5 years of age presenting with AGE had their stools collected and tested for rotavirus

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