ライフサイエンスコーパス: TPN

1 TPN administration in wild-type mice resulted in several

2 TPN also up-regulated phosphorylated (p)-beta-catenin (S

3 TPN causes depression of mucosal immunity compared with

4 TPN causes global intestinal barrier failure, but elemen

5 TPN causes peptides to associate and dissociate faster o

6 TPN duration ranged from 2 to 252 months.

7 TPN significantly changed the amount of T1Rs, GLM recept

8 TPN significantly down-regulated E-cadherin and beta-cat

9 TPN use, if correctly indicated, is a clinical sign of i

10 TPN was initiated in 40 adult patients and continued for

11 TPN(Q) inhibits the ROMK1 and GIRK1/4 inward-rectifier K

12 TPN-Y1/K12/Q13 and mono-iodo-TPN-Y1/K12/Q13 ([(127)I]TPN

13 TPNs receive input from gustatory receptor neurons and r

14 is not related to serum Ab, because 10 of 13 TPN-fed mice shed virus into their nasal secretions desp

15 er of hemodialysis days [6.20; (2.67-14.4)], TPN duration [2.87; (1.40-5.90)], and mean number of red

16 er of hemodialysis days [3.84; (1.75-8.40)], TPN duration [11.0; (5.52-21.7)] and mean number of red

17 acing their variable region with that from a TPN-sensitive channel.

18 Our data indicate that a TPN-assisted mechanism of peptide selection relies on di

19 IEL changes in phenotype and function after TPN administration.

20 ncreased risk of mortality even >1.5 y after TPN use.

21 mutagenesis studies on both the channel and TPN(Q) together strongly suggest that to block the K(+)

22 discharge, post-operative complication, and TPN requirement.

23 +/- 0.18 attomoles/microL in the control and TPN groups, respectively.

24 10 received daily GH, systemic insulin, and TPN.

25 idino Yellow into TPNs revealed that RPM and TPN motoneurons are indeed interdigitated in T17-S1.

26 ed a complete concordance with CRT, TAP, and TPN but not with calnexin.

27 at the physical interaction between TAP2 and TPN is disrupted by benzene, a compound known to interfe

28 Ileal bacteria from TEN and TPN piglets were also examined for their ability to grow

29 was equally complex in the ileum of TEN and TPN piglets, but profiles clustered according to mode of

30 DNA were observed between the treatments and TPN alone (SEN: 15-59% increase; GLP-2: 14-84% increase;

31 re identical, as was the use of antibiotics, TPN, and enteral feedings.

32 Although both N-domains act as TPN-docking sites, various studies suggest a functional

33 nt deprivation, to study this interaction as TPN results in mucosal atrophy due to decreased IEC prol

34 ble TNF-alpha signaling from IECs attenuates TPN-induced mucosal atrophy.

35 on, not the composition of the diet, because TPN solution fed orally via gastrostomy instead of i.v.

36 interaction or the complex formation between TPN and MHC I.

37 We found that the interaction between TPN(Q) and the ROMK1 channel is a bimolecular reaction,

38 of 120% to 130% of calories is delivered by TPN.

39 d, jugular and portal catheters, were fed by TPN for 7 days.

40 is essential for high-affinity inhibition by TPN and that variability in the region underlies the gre

41 t processes may occur in humans nourished by TPN and may thereby contribute to intestinal dysfunction

42 el transplants and tissue growth from cells, TPN will be a temporary measure rather than a lifetime r

43 in association with TAP and two chaperones, TPN and CRT.

44 determined long-term survival after clinical TPN use in a consecutive cohort who were attending an ac

45 Evening infusions of calcium-containing TPN eliminated the nocturnal rise in serum PTH, increase

46 In the present study, the TPN derivative, TPN-Y1/K12/Q13, has been synthesized and radiolabeled to

47 ity but retain high affinity, we derivatized TPN(Q) by replacing histidine 12 with lysine.

48 Two different TPN feeding strategies were compared: hypocaloric feedin

49 hat are unable to conformationally disengage TPN from class I molecules are excluded from the reperto

50 on dysfunction in ADHD emphasize altered DMN-TPN interactions.

51 a priori hypothesis, we observed reduced DMN-TPN segregation co-occurring with structural abnormaliti

52 ating glucagon-like peptide 2 (GLP-2) during TPN.

53 but not GH, prevented mucosal atrophy during TPN, although GH elevated plasma IGF-I and increased bod

54 factorial design and maintained with either TPN or PN for 7 d.

55 GIRK1 subunit confers the high affinity for TPN.

56 crosis factor-alpha is a critical factor for TPN-associated epithelial barrier dysfunction, and both

57 Treatment for 10 d with calcium-free TPN restored the nocturnal rise in serum PTH and increas

58 follow-up, including 8 who were weaned from TPN after intestinal transplantation.

59 IL-7 mice given TPN, however, maintained IEL proliferation, and sustaine

60 oxidized by air, which significantly hinders TPN binding to the channels.

61 sed clinically to sustain patients; however, TPN is associated with profound mucosal atrophy, which m

62 rogen balance in comparison with hypocaloric TPN.

63 [(125)I]TPN-Y1/K12/Q13 binds in a saturable, time-dependent, and

64 aken together, they demonstrate that [(125)I]TPN-Y1/K12/Q13 represents the first high specific activi

65 12/Q13 and mono-iodo-TPN-Y1/K12/Q13 ([(127)I]TPN-Y1/K12/Q13) inhibit with high affinity rat but not h

66 ls decreased significantly in both IV and IG TPN groups versus the chow or complex enteral diet group

67 were randomized to receive chow, IV TPN, IG TPN, or an isocaloric, complex enteral diet.

68 y with IV TPN and partial impairment with IG TPN and provide a cytokine-mediated explanation for redu

69 Intragastric (IG) TPN maintains antiviral defenses but only partially pres

70 In TPN group, average energy intake was significantly highe

71 4 h were significantly higher (P < 0.001) in TPN recipients (5.0 +/- 0.9 pmol/L) than in healthy volu

72 eflects titration of histidine residue 12 in TPN(Q) by extracellular protons, since it largely vanish

73 Methionine residue 13 in TPN interacts with residue F148 in the channel, located

74 (+25%) and intestinal blood volume (+51%) in TPN-fed piglets.

75 EEN group versus 64.4% (95% CI 54.2-73.6) in TPN group (P = 0.040).

76 er parathyroid gland function is abnormal in TPN recipients.

77 e, ERp57 failed to associate with H chain in TPN-deficient.220 cells.

78 ic channels indicate that the differences in TPN sensitivity between rat and human Kir1.1 channels ar

79 lfated monosaccharides were also enriched in TPN samples.

80 due to oxidation of M13, we replaced M13 in TPN with fourteen different residues.

81 ression and phosphorylation were measured in TPN-fed pigs acutely (4 h) infused with GLP-2.

82 thesis that the lack of enteral nutrients in TPN might select commensal or pathogenic bacteria that u

83 matory state and mucosal atrophy observed in TPN-treated mice.

84 To overcome the reduction in TPN affinity due to oxidation of M13, we replaced M13 in

85 e, enhances the regularity of PTH release in TPN recipients.

86 The methionine residue in TPN can be oxidized by air, which significantly hinders

87 ed that TNF-alpha plays an important role in TPN-associated EBF dysfunction.

88 The interaction surface in TPN(Q) is primarily formed by its alpha helix rather tha

89 associated bacteria (100 colonies tested) in TPN compared with 33% of mucus-associated bacteria (100

90 We conclude that in TPN-fed neonatal pigs, GLP-2 acutely stimulates intestin

91 ation of intestinal substrate utilization in TPN-fed piglets.

92 e significantly greater with GLP-2 infusion (TPN alone: 25 +/- 9 pmol/L; SEN: 29 +/- 10 pmol/L; GLP-2

93 uorescein (CT-FITC) or Diamidino Yellow into TPNs revealed that RPM and TPN motoneurons are indeed in

94 Intragastric TPN partially preserved this respiratory immunity.

95 of gut ischemia, the IV-TPN and intragastric TPN groups showed a higher death rate than the chow and

96 en the complex enteral diet and intragastric TPN groups.

97 tes) eliminated any benefits of intragastric TPN on survival.

98 produce GALT atrophy, but only intragastric TPN preserves established antiviral immunity.

99 eral diet group (n = 5) and the intragastric TPN group (n = 5) after 30 minutes of gut ischemia and 1

100 ere randomized to chow, IV-TPN, intragastric TPN, or complex enteral diet for 5 days' feeding.

101 Intravenous TPN caused greater bacterial translocation in all small

102 epleting diets (intragastric and intravenous TPN) would impair immunity against bacterial pneumonia.

103 elemental diet) 307 kcal/kg/day, intravenous TPN (parenteral diet) 307 kcal/kg/day via jugular venous

104 nd was lost in animals receiving intravenous TPN.

105 This protection is lost with intravenous TPN, partially preserved with a chemically defined enter

106 TPN-Y1/K12/Q13 and mono-iodo-TPN-Y1/K12/Q13 ([(127)I]TPN-Y1/K12/Q13) inhibit with hig

107 e association of ERp57 with mouse class I is TPN dependent and parallels that of CRT and not calnexin

108 ps significantly in mice receiving IG and IV TPN in association with reduced IgA levels, whereas IL-1

109 mpairments in mucosal immunity induced by IV TPN.

110 one mice were randomized to receive chow, IV TPN, IG TPN, or an isocaloric, complex enteral diet.

111 t groups, whereas IL-10 decreased only in IV TPN mice.

112 After 5 days of IV TPN, mice received 0, 1, 2, or 3 days of BBS IV three ti

113 ases significantly only in mice receiving IV TPN.

114 h severely impaired mucosal immunity with IV TPN and partial impairment with IG TPN and provide a cyt

115 were randomized to chow or intravenous (IV) TPN.

116 In experiment 2, IV-TPN significantly increased pulmonary and hepatic 125I a

117 Mice were randomized to chow, IV-TPN, intragastric TPN, or complex enteral diet for 5 day

118 d for PMNs, the authors hypothesized that IV-TPN may affect organ injury after gut ischemia-reperfusi

119 After 30 minutes of gut ischemia, the IV-TPN and intragastric TPN groups showed a higher death ra

120 ntly reduced the death rate compared with IV-TPN after 15 minutes of I/R.

121 This derivative-denoted tertiapin-KQ (TPN(KQ))-not only is practically insensitive to extracel

122 signaling plays a central role in mediating TPN-induced mucosal atrophy without intact epidermal gro

123 Using a mouse TPN model, removing enteral nutrition leads to decreased

124 Using a mouse TPN model, we explored the relative roles of TNFR1 vs. T

125 s were significantly abrogated in MyD88(-/-) TPN mice.

126 th a Ki value very similar to that of native TPN.

127 However, unlike native TPN, TPN(Q) is nonoxidizable by air.

128 and the nodes of the task positive network (TPN).

129 del entitled Toxicologic Prediction Network (TPN) to assess chronic hepatotoxicity based on subchroni

130 de network (DMN) and task-positive networks (TPNs), would co-occur with structural abnormalities in c

131 connections with two task positive networks (TPNs): frontoparietal network and ventral attention netw

132 y three classes of taste projection neurons (TPNs) in Drosophila melanogaster distinguished by their

133 st 50% of nutritional needs on PoD 5, and no TPN for more than consecutive 48 hours.

134 utrition (Control) or intravenous nutrition (TPN).

135 total or supplemental parenteral nutrition (TPN or PN, respectively).

136 deprivation via total parenteral nutrition (TPN) administration leads to local mucosal inflammatory

137 tients beginning total parenteral nutrition (TPN) and whether a 3-d regimen of TPN would further incr

138 equire long-term total parenteral nutrition (TPN) for intestinal failure and 15% to 40% of adults on

139 Total parenteral nutrition (TPN) is an invasive and advanced rescue feeding techniqu

140 Total parenteral nutrition (TPN) is commonly used clinically to sustain patients; ho

141 Total parenteral nutrition (TPN) leads a loss of epithelial barrier function, declin

142 t deprivation or total parenteral nutrition (TPN) led to a loss of intestinal epithelial barrier func

143 and intragastric total parenteral nutrition (TPN) produce GALT atrophy, but only intragastric TPN pre

144 emically defined total parenteral nutrition (TPN) to genetically normal, immune ICR mice by the i.v.

145 are dependent on total parenteral nutrition (TPN) to prevent hypoglycemia and provide a sufficient en

146 rms of survival, total parenteral nutrition (TPN) weaning, and complications.

147 ventilation and total parenteral nutrition (TPN) were measured for > or = 15 min by using indirect c

148 atients received total parenteral nutrition (TPN) with caloric intake 20% to 30% above their resting

149 ory of long-term total parenteral nutrition (TPN) with TPN-related cholestatic liver disease.

150 ion (NJEEN) with total parenteral nutrition (TPN), after pancreaticoduodenectomy (PD), in terms of po

151 ial reference to total parenteral nutrition (TPN), an area in which I have been involved from 1937 un

152 fection, days of total parenteral nutrition (TPN), and days of injectable narcotic therapy (all over

153 factors such as total parenteral nutrition (TPN), blood product transfusions, invasive procedures, c

154 uding rats given total parenteral nutrition (TPN), IGF-I more potently stimulates mucosal growth than

155 lized a model of total parenteral nutrition (TPN), or enteral nutrient deprivation, to study this int

156 deprivation, or total parenteral nutrition (TPN), resulting in intestinal mucosal atrophy and decrea

157 ce that received total parenteral nutrition (TPN), which deprives the animals of enteral nutrients, d

158 l with long-term total parenteral nutrition (TPN), while others develop life-threatening complication

159 Total parenteral nutrition (TPN), with the complete removal of enteral nutrition, re

160 LD but developed total parenteral nutrition (TPN)-induced liver failure.

161 eficiency (one), Total Parenteral Nutrition (TPN)-related (one), cryptogenic cirrhosis (one), and hep

162 ith the need for total parenteral nutrition (TPN).

163 by the method of total parenteral nutrition (TPN).

164 complications of total parenteral nutrition (TPN).

165 tients receiving total parenteral nutrition (TPN).

166 r 7 days by oral total parenteral nutrition (TPN; elemental diet) 307 kcal/kg/day, intravenous TPN (p

167 ression would attenuate many of the observed TPN-associated IEL changes.

168 enteral nutrition with the administration of TPN is associated with a loss of intestinal epithelial b

169 Administration of TPN upregulated the downstream nuclear factor-B and myos

170 enteral nutrition, reverses complications of TPN and avoids intestinal transplantation in the majorit

171 ients with life-threatening complications of TPN.

172 Leptin concentrations increased after 3 d of TPN, from 356 +/- 300 to 794 +/- 600 pmol/L (P < 0.05) i

173 20 (11 women and 9 men) completed all 3 d of TPN.

174 fection (P <.01), (3) 2.7 additional days of TPN (P <.0001), (4) 2.6 additional days of injectable na

175 support and nitrogen balance after 5 days of TPN.

176 Not surprisingly, this alanine derivative of TPN(Q) binds to the channel with much lower affinity.

177 repeat lengthening led to discontinuation of TPN in almost half of these carefully selected patients

178 n mechanistic insights into the functions of TPN.

179 unify our understanding of the functions of TPN.

180 an average of 1.5 y after the initiation of TPN.

181 IEL cytokine expression in a mouse model of TPN.

182 es with class I molecules in the presence of TPN.

183 rect calorimetry and 1.5 g/kg/day protein of TPN.

184 Provision of TPN to a goal of 25 kcal/kg was not associated with more

185 nutrition (TPN) and whether a 3-d regimen of TPN would further increase plasma leptin concentrations

186 These findings reveal a critical role of TPN for ER retention of empty class I molecules.

187 To evaluate the in vivo role of TPN, we have generated Tpn mutant mice.

188 g cells in the nasal passages and spleens of TPN-fed mice was unaffected, while both the number and t

189 The stability of TPN(Q) allows us to investigate how it interacts with th

190 Survival after the clinical use of TPN >6 mo is unknown.

191 58% in 437 patients with a first-time use of TPN at an average of 1.5 y after the initiation of TPN.

192 the region underlies the great variation of TPN affinities among eukaryotic Kir channels.

193 Activation of TPNs influences innate feeding behavior, whereas inhibit

194 Sixty-nine percent of patients are off TPN at most recent follow-up, including 8 who were weane

195 nctioning and the patient was completely off TPN.

196 y equal to or better than quality of life on TPN and children report quality of life similar to norma

197 icantly higher in IFN-gamma knockout mice on TPN compared to C57BL/6 mice that received TPN.

198 via GLM could be a strategy for patients on TPN.

199 Rats on TPN received vehicle, GH, or IGF-I.

200 channel is a bimolecular reaction, i.e., one TPN(Q) molecule binds to one channel.

201 al unit acting as a docking site for optimal TPN/MHC I recruitment, whereas three distinct highly con

202 patients undergoing PD to NJEEN (n = 103) or TPN (n = 101).

203 d by total enteral nutrition (TEN; n = 6) or TPN (n = 5) were compared with the use of 16S ribosomal

204 mice were provided either enteral feeding or TPN.

205 nulation and were given enteral nutrition or TPN for 7 days.

206 Oral TPN caused gut barrier failure only in the ileal segment

207 by bilateral muscles: the transversus penis (TPN) and retractor penis magnus (RPM).

208 one of these muscles, the transversus penis (TPN), were localized by using the retrograde tracer bioc

209 strongly suggest that to block the K(+) pore TPN(Q) plugs its alpha helix into the vestibule of the K

210 ve significant clinical potential to prevent TPN-associated atrophy.

211 TLR4 blockade significantly prevented TPN-associated atrophy by preserving proliferation and p

212 GLM significantly prevented TPN-associated intestinal atrophy (2.5-fold increase in

213 Tertiapin-Q (TPN(Q)), a honey bee toxin derivative, inhibits inward-r

214 patients received standard TPN, 10 received TPN plus daily injections of GH, and 10 received daily G

215 One group received TPN without chow, and controls received standard chow.

216 Adult C57BL/6 mice received TPN or enteral diet for 7 days.

217 n TPN compared to C57BL/6 mice that received TPN.

218 We conclude that in VLBW infants receiving TPN, normoglycemia was maintained during reduced glucose

219 F-alpha blockade in wild-type mice receiving TPN confirmed that soluble TNF-alpha signaling is respon

220 phy in TLR4 knockout (TLR4KO) mice receiving TPN.

221 In critically ill patients receiving TPN, indirect calorimetry, if available, remains the mos

222 Experimental rats receiving TPN were able to process infused glucose completely at r

223 Twenty-six patients requiring TPN were enrolled in this prospective, nonintervention s

224 ere the following: transection or resection (TPN alone), +/- SEN (days 4-6), and +/- GLP-2 (100 mug .

225 N-domain binds to the TM region of a single TPN molecule, which recruits one MHC I molecule to TAP1

226 after surgery: 10 patients received standard TPN, 10 received TPN plus daily injections of GH, and 10

227 lay an important role in development of such TPN-associated IEL changes.

228 We propose that TAP/TPN complex formation is driven by hydrophobic interacti

229 esulting in greater significance of the TAP2/TPN interaction for MHC loading.

230 ultifactorial complex that includes tapasin (TPN), a membrane protein that tethers empty class I glyc

231 examined interactions in a soluble tapasin (TPN)/HLA-B*0801 complex to gain mechanistic insights int

232 ide-loading complex (PLC), to which tapasin (TPN) recruits MHC class I (MHC I) and accessory chaperon

233 roid gland function is abnormal in long-term TPN recipients, which may contribute to disturbances in

234 Tertiapin (TPN), a small protein toxin originally isolated from hon

235 In this respect, tertiapin (TPN), a 21 amino acid peptide isolated from bee venom, h

236 o the channel with even higher affinity than TPN(Q) at extracellular pH 7.6.

237 In the present study we found that TPN(Q) inhibition of the channels is profoundly affected

238 Results show that TPN acts as a chaperone by increasing the ratio of activ

239 We also show that TPN sensitivity can be readily conferred onto some Kir c

240 Our study showed that TPN administration led to significant changes in IEL phe

241 Previous work shows that TPN results in a loss of intestinal epithelial cell-deri

242 We suggest that TPN influences presentation of antigenic peptides accord

243 The TPN-associated downregulation of junctional protein expr

244 uption in the segregation of the DMN and the TPN at rest may be mediated through both a direct pathwa

245 ncreased functional connectivity between the TPN and SN appears to be associated with reduced perform

246 nectivity was also observed between both the TPN and DMN and nodes associated with the Salience Netwo

247 Control rats consuming the TPN solution by mouth ingested glucose at 42 mmol/day an

248 mTBI patients with memory complaints for the TPN.

249 oup to 0.44 +/- 0.11 attomoles/microL in the TPN group (P <.05).

250 c pathogen, was specifically enriched in the TPN ileum (P < 0.05).

251 Baseline plasma leptin in the TPN patients ranged from 62.5 to 1625 pmol/L ( +/- SD: 4

252 concentrations were moderately higher in the TPN recipients than in healthy volunteers, and values ob

253 itrate-induced hypocalcemia was lower in the TPN recipients, consistent with secondary hyperparathyro

254 d through an indirect pathway that links the TPN and DMN through nodes of the SN.

255 unted for 96% of the T17-S1 motoneurons: the TPN, RPM, caudifemoralis (CF), and cloacal sphincter (SC

256 of increased FC between various nodes of the TPN and DMN, and through an indirect pathway that links

257 The advantages of the TPN are further demonstrated through two novel applicati

258 d gain a more accurate representation of the TPN motoneuron pool.

259 onation of the histidine residue reduces the TPN(Q)-ROMK1 binding energy by 1.6 kcal/mol.

260 In the present study, the TPN derivative, TPN-Y1/K12/Q13, has been synthesized and

261 Motoneurons projecting to the TPN lie in spinal segments trunk 17 and sacral 1 (T17-S1

262 ritional factors, glutamine was added to the TPN solution.

263 the GH and insulin groups compared with the TPN only group.

264 muscle protein net balance compared with the TPN only group.

265 The TPNs essential for conditioned aversion project to the s

266 d could be a contributing mechanism for this TPN-associated loss of EC proliferation.

267 when enteral nutrients were withheld in this TPN piglet model.

268 BBS prevents this TPN-induced GALT atrophy, depressed gastrointestinal and

269 Thus, TPN administration is associated with significant expans

270 ed that EGF signaling is preserved in TLR4KO-TPN mice and prevents mucosal atrophy.

271 Bcl-2 was significantly increased in TLR4KO-TPN mice, while Bax decreased 10-fold.

272 increased, and TNF-alpha decreased in TLR4KO-TPN versus wild-type (WT)-TPN mice.

273 were 15-fold higher in WT-TPN versus TLR4KO-TPN mice.

274 lpha blockade, but not in TNFR1KO or TNFR2KO TPN groups.

275 ed whether some supplement could be added to TPN to avoid this GALT atrophy and lower the incidence o

276 ific contributions of TNF-alpha signaling to TPN-induced mucosal atrophy remain unclear.

277 (+) channels with affinities very similar to TPN.

278 However, unlike native TPN, TPN(Q) is nonoxidizable by air.

279 Moreover, two TPN classes are absolutely required for conditioned tast

280 n decreased 1.7-fold compared with wild-type TPN mice.

281 junctional protein losses in mice undergoing TPN.

282 Using TPN-treated IEC-specific ADAM17-deficient mice, the pres

283 ne (LDD) for renal protection, vasopressors, TPN, and enteral feeding.

284 fe-threatening complications or fail to wean TPN.

285 These findings suggest a mechanism by which TPN results in observed IEL changes.

286 ss of the epithelial barrier associated with TPN.

287 findings of mucosal atrophy associated with TPN.

288 microbiota (but distinct from controls) with TPN.

289 egulatory cells significantly decreased with TPN in WT mice.

290 GLM led to a loss of EBF with TPN (60% increase in FITC-dextran permeability, 40% decl

291 atory cytokines significantly increased with TPN.

292 hanges were observed in MyD88(-/-) mice with TPN administration.

293 Loss of luminal nutrients with TPN administration may widely affect intestinal taste se

294 findings, the loss of EC proliferation with TPN may well be due to a loss of total beta-catenin, as

295 The marked decline in IEC proliferation with TPN was nearly prevented in TLR4KO mice, and intestinal

296 tokine expression changes significantly with TPN administration.

297 barrier function declined significantly with TPN compared to controls.

298 g-term total parenteral nutrition (TPN) with TPN-related cholestatic liver disease.

299 robiota were Firmicutes-dominant, whereas WT TPN mice were Proteobacteria-domiant.

300 ecreased in TLR4KO-TPN versus wild-type (WT)-TPN mice.

301 sitive crypt cells were 15-fold higher in WT-TPN versus TLR4KO-TPN mice.