ライフサイエンスコーパス: HCO

1 ays important roles in heme-copper oxidases (HCO).

2 ipotent stem cell-derived cardiac organoids (hCOs).

3 emistry carried out in heme-copper oxidases (HCOs).

4 roton-pumping heme-copper oxygen reductases (HCOs).

5 equilibrium data for Sb(III) with Fe(3)O(4)/HCO.

6 nutrient delivery to the inner-most parts of hCOs.

7 o forming a complex vascular-like network in hCOs.

8 d direct hPSC-derived gut tube cultures into HCOs.

9 e criteria, we demonstrate reversible CO(2) /HCO(2) (-) conversion catalyzed by [Pt(depe)(2) ](2+) (d

10 s negligible and the Faradaic efficiency for HCO(2) (-) production is nearly quantitative.

11 L = mu(2):eta(1)-OH(-) (17) and mu(2):eta(2)-HCO(2)(-) (18) and -CN(-) (19).

12 hyl formate and CO(2) to form unidentate L = HCO(2)(-) (5) and HCO(3)(-) (6) products.

13 h direct mass-spectrometric detection of the HCO(2)(-) product.

14 The catalytic reduction of CO(2) to HCO(2)(-) requires a formal transfer of a hydride (two e

15 nversion of C(n) fatty aldehydes to formate (HCO(2)(-)) and the corresponding C(n-1) alk(a/e)nes.

16 of endohedrally coordinated formate ligands (HCO(2)(-)) by 1,2-hydroxyl-functionalized l-glycerate (l

17 ormylation of (-)-menthone (11) with LDA and HCO(2)CH(2)CF(3) avoids loss of configurational integrit

18 uring formylation of menthone with NaOMe and HCO(2)Et led, by a similar strategy, to syntheses of 7-e

19 be cleaved efficiently when treated with 10% HCO(2)H for 0.5 h.

20 These same features (no lag phase for HCO(2)H formation and a lack of equilibration in pulse-c

21 50 mM Na(2)S(2)O(4), 2% HOCH(2)CH(2)SH, 10% HCO(2)H, 95% CF(3)CO(2)H, or irradiation at 365 nm.

22 dation of C(3)H(6)(OCO(2)Li)(2), Li(2)CO(3), HCO(2)Li, CH(3)CO(2)Li accompanied by CO(2) and H(2)O ev

23 Li(2)CO(3), HCO(2)Li, CH(3)CO(2)Li, and C(3)H(6)(OCO(2)Li)(2) accumu

24 mation of C(3)H(6)(OCO(2)Li)(2), Li(2)CO(3), HCO(2)Li, CH(3)CO(2)Li, CO(2), and H(2)O at the cathode,

25 hode on discharge are Li(2)O(2), Li(2)CO(3), HCO(2)Li, CH(3)CO(2)Li, NO, H(2)O, and CO(2).

26 rate and expression of SR, CFTR, and Cl(-) /HCO 3- AE2 and ablated secretin-stimulated biliary secre

27 iferation and increased SR, CFTR, and Cl(-) /HCO 3- AE2 expression.

28 nate anion exchanger 2 (cAMP-->CFTR-->Cl(-) /HCO 3- AE2) signaling that is elevated by biliary hyperp

29 nal role in the adaptive regulation of renal HCO(3(-)) secretion and salt reabsorption.

30 ulation of the mTAL transport of NH(4) (+) , HCO(3) (-) , and NaCl are investigated.

31 H 7.4 and was equally permeable to Cl(-) and HCO(3) (-) .

32 d pH->with increased H(+) buffered by blood [HCO(3) (-) ]->increased CO(2) release from blood->increa

33 essential components of the CCM that deliver HCO(3) (-) accumulated in the chloroplast stroma to CAH3

34 iately promote NH(4) (+) shunting but oppose HCO(3) (-) and NaCl reabsorption in the mTAL, and thus a

35 The roles of the Na(+) /HCO(3) (-) cotransporters NBCn1 and NBCn2 as well as the

36 For CF patients and CF mice, we developed a HCO(3) (-) drinking test to assess the role of the cysti

37 (3) (-) reabsorption during MAlk by opposing HCO(3) (-) efflux via the basolateral anion exchanger AE

38 secretin stimulated pendrin-dependent Cl(-)/HCO(3) (-) exchange.

39 s (CF) do not respond with increased urinary HCO(3) (-) excretion after stimulation with secretin and

40 ne the mechanism of secretin-induced urinary HCO(3) (-) excretion, explain metabolic alkalosis in pat

41 ed the mechanism of secretin-induced urinary HCO(3) (-) excretion.

42 rds that of basolateral liquid, paracellular HCO(3) (-) flux becomes absorptive, tempering the alkali

43 ar pathway could provide a route for passive HCO(3) (-) flux that also modifies ASL pH.

44 These results suggest that HCO(3) (-) flux through the paracellular pathway counter

45 HCO(3) (-) flux through the paracellular pathway may cou

46 -) permeability, and calculated paracellular HCO(3) (-) flux was absorptive.

47 ar HCO(3) (-) permeability, and paracellular HCO(3) (-) flux was negligible.

48 er basal conditions, calculated paracellular HCO(3) (-) flux was secretory.

49 nditions at pH ~6.6, calculated paracellular HCO(3) (-) flux was weakly secretory.

50 re is limited information about paracellular HCO(3) (-) flux, and it remains uncertain whether an aci

51 liquid pH decreased or reversed paracellular HCO(3) (-) flux.

52 late that a series of ion transporters bring HCO(3) (-) from outside the cell to the thylakoid lumen,

53 Cl(-) and HCO(3) (-) had similar paracellular permeabilities in hu

54 acclimation states and the species of C(i) , HCO(3) (-) or CO(2) , that LCI1 transports remain obscur

55 ASL pH to ~7.4 without altering paracellular HCO(3) (-) permeability, and calculated paracellular HCO

56 nized ASL pH to ~7.0, increased paracellular HCO(3) (-) permeability, and paracellular HCO(3) (-) flu

57 al NH(4) (+) uptake during MAc; (2) inhibits HCO(3) (-) reabsorption during MAlk by opposing HCO(3) (

58 Active H(+) and HCO(3) (-) secretion by airway epithelial cells produce

59 counterbalance effects of cellular H(+) and HCO(3) (-) secretion.

60 g the alkaline pH generated by transcellular HCO(3) (-) secretion.

61 ic anhydrase 3 (CAH3) dehydrates accumulated HCO(3) (-) to CO(2), raising the CO(2) concentration for

62 ies, HLA3 clearly plays a meaningful role in HCO(3) (-) transport, but the function of LCI1 has not y

63 To investigate paracellular HCO(3) (-) transport, we studied differentiated primary

64 Previously, HCO(3) (-) transporters have been identified at both the

65 Chlamydomonas CCM, and consists of CO(2) and HCO(3) (-) uptake systems that play distinct roles in lo

66 NH(4) (+) shunting by increasing basolateral HCO(3) (-) uptake to neutralize apical NH(4) (+) uptake

67 combines phosphoenolpyruvate with CO(2) (as HCO(3) (-)), forming oxaloacetate.

68 howed a greatly attenuated or absent urinary HCO(3) (-)-excreting ability.

69 aftor increased the renal ability to excrete HCO(3) (-).

70 e effect of a physiological concentration of HCO(3) (-)/CO(2) (25 mm) on its hyperoxidation.

71 kinetic and MS/MS experiments revealed that HCO(3) (-)/CO(2) increases Prx1 hyperoxidation and inact

72 nt in equilibrated solutions of H(2)O(2) and HCO(3) (-)/CO(2) Indeed, additional experiments and calc

73 The fact that the biologically ubiquitous HCO(3) (-)/CO(2) pair stimulates Prx1 hyperoxidation and

74 hypothesized that the stimulating effect of HCO(3) (-)/CO(2) was due to HCO(4) (-), a peroxide prese

75 rane conductance regulator (CFTR) in urinary HCO(3) (-)excretion and applied it in the patients befor

76 lin 168%, p < 0.05) and PM repair (THAM 87%, HCO(3) 108% of NC likelihood to repair, ns; Forskolin 16

77 the effects of HC on AC activity (THAM 103%, HCO(3) 113% of NC cAMP, ns; Forskolin 168%, p < 0.05) an

78 l operation of Na-H exchange 3 (NHE3) and Cl-HCO(3) [down-regulated in adenoma (DRA) or putative anio

79 d the effect of lipopolysaccharide (LPS), on HCO(3) absorption in isolated perfused rabbit OMCDi.

80 LPS caused a ~ 40% decrease in HCO(3) absorption, providing a mechanism for E. coli pye

81 dissolve proteins in reagents, such as NH(4)HCO(3) and urea, with high efficiency and with an added

82 by one just using a thermo-decomposable NH(4)HCO(3) buffer, eliminating the use of any oil and incomp

83 ic anhydrases (CAs) with the electrogenic Na/HCO(3) cotransporter NBCe1-A speeds transport by regener

84 The Na/HCO(3) cotransporter NBCn1/SLC4A7 can affect glutamate n

85 has an apical V-ATPase and a basolateral Cl:HCO(3) exchanger (kAE1).

86 udy, we examined whether the Na(+)-driven Cl/HCO(3) exchanger NDCBE (Slc4a8) is also upregulated by s

87 se data demonstrate that the Na(+)-driven Cl/HCO(3) exchanger NDCBE is upregulated by chronic acid lo

88 her bacterial cell wall constituents inhibit HCO(3) transport in the outer medullary collecting duct

89 ker in the human SLC4A7 gene encoding the Na/HCO(3) transporter NBCn1 suggest that this pH-regulating

90 (2) to form unidentate L = HCO(2)(-) (5) and HCO(3)(-) (6) products.

91 nic anhydrase-like activities, the non-CO(2)/HCO(3)(-) (intrinsic) intracellular buffering power, or

92 O(4)(-) (log beta(2) = 10.4(-0.4)(+0.4)) and HCO(3)(-) (log beta(2) = 8.3(-0.4)(+0.3)) over other com

93 g the cell to extracellular 1.5% CO(2)/10 mM HCO(3)(-) (pH 7.50) causes pH(i) to fall and pH(S) to ri

94 solved inorganic carbon (DIC) (DIC = CO(2) + HCO(3)(-) + CO(3)(-2)) availability with a carbon-concen

95 Inhibition of HCO(3)(-) absorption by LPS did not require CD14.

96 In contrast, inhibition of HCO(3)(-) absorption by lumen LPS was preserved in TLR2(

97 Inhibition of HCO(3)(-) absorption by TLR2-specific ligands was preser

98 S (ultrapure Escherichia coli K12) decreased HCO(3)(-) absorption in isolated, perfused MTALs from wi

99 hat the effect of basolateral LPS to inhibit HCO(3)(-) absorption in the MTAL through MyD88-dependent

100 e demonstrated that basolateral LPS inhibits HCO(3)(-) absorption in the renal medullary thick ascend

101 e1-A electrogenically cotransports Na(+) and HCO(3)(-) across the basolateral membrane of renal proxi

102 impaired CO(2)-induced stomatal closing and HCO(3)(-) activation of anion channels.

103 ty locus; and RPTPgamma-dependent sensing of HCO(3)(-) adjusts endothelium-mediated vasorelaxation, m

104 Ringer solutions with/without B(OH)(4)(-) or HCO(3)(-) after overexpressing or small interfering RNA

105 CAs) catalyze the hydration of CO(2) forming HCO(3)(-) and a proton, an important reaction for many p

106 n perfused CE in the presence and absence of HCO(3)(-) and acetazolamide (ACTZ) using tissue treated

107 he slow parallel reversible reaction between HCO(3)(-) and amine has also been determined for a numbe

108 tance regulator (CFTR) compromise epithelial HCO(3)(-) and Cl(-) secretion, reduce airway surface liq

109 n HEK293 cells, and relative conductances of HCO(3)(-) and Cl(-) were measured.

110 1 M KOH electrolyte at the interface to form HCO(3)(-) and CO(3)(2-).

111 ission intensity of the dimer is quenched by HCO(3)(-) and H(2)PO(4)(-) but not by Cl(-) and NO(3)(-)

112 stic fibrosis transmembrane regulator, Cl(-)/HCO(3)(-) anion exchanger 2 and AC8, and responded to se

113 suggest that prestin can act as a weak Cl(-)/HCO(3)(-) antiporter and it is proposed that, in additio

114 lasmon resonance (LSPR) is strengthening the HCO(3)(-) bond, further increasing the local pH.

115 ate (HCO(3)(-)) and a multitude of non-CO(2)/HCO(3)(-) buffers.

116 was significantly greater in the presence of HCO(3)(-) but was reduced by ACTZ.

117 e did not fully recover, showing lower blood HCO(3)(-) concentration and more alkaline urine.

118 al pH on the cathode surface is 7.2, and the HCO(3)(-) concentration profile extends a distance of 12

119 CO(3) plus acetazolamide to increase luminal HCO(3)(-) concentration, [HCO(3)(-)], independent of pen

120 ward 1,1,1,2-TeCA depended upon NO(3)(-) and HCO(3)(-) concentration, with complete reactivity loss o

121 ne conductance regulator (CFTR), a Cl(-) and HCO(3)(-) conducting ion channel known to be associated

122 3)(-) in secretory glands is fueled by Na(+)/HCO(3)(-) cotransport mediated by basolateral solute car

123 The renal electrogenic Na(+)/HCO(3)(-) cotransporter (NBCe1-A) contributes to the bas

124 Here, a CO(2) and HCO(3)(-) diffusion-reaction model is developed to exami

125 Because apical HCO(3)(-) exchange depends on cystic fibrosis transmembr

126 ier family 4 member 4 (NBCe1-B) and by Cl(-)/HCO(3)(-) exchange mediated by luminal solute carrier fa

127 ed mutations in ABTS-1, a Na(+)-driven Cl(-)-HCO(3)(-) exchanger that extrudes chloride from cells, l

128 pithelial Na(+) channel, ENaC, and the Cl(-)/HCO(3)(-) exchanger, pendrin, mediate NaCl absorption wi

129 important of which is pendrin, a luminal Cl/HCO(3)(-) exchanger.

130 Our results show that Na(+)-driven Cl(-)-HCO(3)(-) exchangers function with KCCs in generating th

131 In conchocelis, the release of HCO(3)(-) from shell promoted by carbonic anhydrase prov

132 ne encodes an electroneutral Na(+)-dependent HCO(3)(-) importer for which the precise mode of action

133 Secretion of ductal fluid and HCO(3)(-) in secretory glands is fueled by Na(+)/HCO(3)(

134 th the maintenance of a low concentration of HCO(3)(-) in the cytoplasm.

135 on-discriminating photosynthetic fixation of HCO(3)(-) in the high pH and carbon-starved water.

136 etention behavior; some reactive addition of HCO(3)(-) is involved.

137 ium-dependent vasorelaxation only when CO(2)/HCO(3)(-) is present.

138 ransport Na(+) and are expected to move more HCO(3)(-) molecules/turnover were targeted by site-direc

139 It remains unclear whether CO(2), HCO(3)(-) or a combination activates downstream signalli

140 not significantly greater in the presence of HCO(3)(-) or reduced by ACTZ.

141 Geochemical modeling indicated that HCO(3)(-) promoted dissolution accelerated brucite carbo

142 sis (pRTA; usually associated with defective HCO(3)(-) reabsorption in proximal tubule cells) and hyp

143 s to the basolateral step of transepithelial HCO(3)(-) reabsorption in proximal tubule epithelia, con

144 tubule showed that flow-dependent Na(+) and HCO(3)(-) reabsorption is due to a modulation of both NH

145 ar lumen strongly stimulated Cl(-)-dependent HCO(3)(-) secretion and electroneutral transepithelial N

146 hat forms unselective ion channels, restored HCO(3)(-) secretion and increased airway surface liquid

147 R1 is involved in the adaptive regulation of HCO(3)(-) secretion and NaCl reabsorption in the CNT/CCD

148 ivotal role of IRBIT in epithelial fluid and HCO(3)(-) secretion and provide a molecular mechanism by

149 Fluid and HCO(3)(-) secretion are fundamental functions of epithel

150 Without CFTR, airway epithelial HCO(3)(-) secretion is defective, the ASL pH falls and i

151 e and NaHCO(3) to increase pendrin-dependent HCO(3)(-) secretion within the connecting tubule and cor

152 tor mutants slowed but did not abolish CO(2)/HCO(3)(-) signalling, redefining the convergence point o

153 The estimated Na(+):HCO(3)(-) stoichiometry was 1:2.

154 ate hydroxide formation limits reactivity in HCO(3)(-) suspensions.

155 ent anion channel vital for proper Cl(-) and HCO(3)(-) transport across epithelial surfaces provided

156 (+) flux is facilitated by active transport, HCO(3)(-) transport and CA activity, disruption of which

157 llular pH (pH(i)) probe, pHluorin, to report HCO(3)(-) transport and to monitor the small pH(i) chang

158 the internal stores, and facilitated outward HCO(3)(-) transport by the electrogenic sodium bicarbona

159 capacity through the presence of HCO(3)(-), HCO(3)(-) transport, NHE and CA activity.

160 s of CFTR, an anion channel that facilitates HCO(3)(-) transport.

161 ition of HCO(3)(-) transporters, as a single HCO(3)(-) transporter increased modeled A(sat) by 9%.

162 that the best first step is the addition of HCO(3)(-) transporters, as a single HCO(3)(-) transporte

163 that exogenous ABA significantly altered the HCO(3)(-) uptake of Chamydomonas reinhardtii in a light-

164 In high light ABA enhanced HCO(3)(-) uptake, while under low light uptake was dimin

165 In contrast to other salts, HCO(3)(-) was found to play a crucial role acting as a c

166 Furthermore, the HCO(3)(-) wavenumber and peak area increase immediately

167 id/carbamate from the reactions of CO(2) and HCO(3)(-) with the amines are reported.

168 as able to exchange halides for SO(4)(2-) or HCO(3)(-) yet previous analyses of mammalian prestin hav

169 among carbonic acid (H(2)CO(3))/bicarbonate (HCO(3)(-)) and a multitude of non-CO(2)/HCO(3)(-) buffer

170 rtial pressure of CO(2) (or concentration of HCO(3)(-)) and the electron flux through nitrogenase.

171 pon addition of an exogenous proton carrier (HCO(3)(-)) provides evidence that proton-transfer pathwa

172 ), Br(-), NO(2)(-), NO(3)(-), SO(4)(2-), and HCO(3)(-)).

173 situ formation of a bicarbonate counterion (HCO(3)(-)).

174 When used together, NO(3)(-), HCO(3)(-), and DOM closely simulated the photolysis beha

175 a (Ca(2+), Na(+), Mg(2+), K(+), H(+), Cl(-), HCO(3)(-), H(2)PO(4)(-), and HPO(4)(2-)) are distributed

176 r buffering capacity through the presence of HCO(3)(-), HCO(3)(-) transport, NHE and CA activity.

177 Second, NHE3-dependent absorption of HCO(3)(-), measured by single tubule perfusion, was redu

178 d for M(H(2)O)(35-37), with M = I(-), Cl(-), HCO(3)(-), OH(-), tetrabutyl-, tetrapropyl-, and tetrame

179 In the presence of extracellular HCO(3)(-), pH(i) recovered from an acid load 4 times fas

180 This was highly dependent on Na(+) and HCO(3)(-), suggesting a bicarbonate buffer mechanism inv

181 was significantly faster in the presence of HCO(3)(-), was greater on the apical surface, was reduce

182 hibit unusual outward rectification in their HCO(3)(-)-dependent conductance and A(A799G) exhibits re

183 Intrinsic (non-CO(2)/HCO(3)(-)-dependent) buffering power, estimated in the i

184 The RVI was HCO(3)(-)-dependent, that is it was not observed in hepe

185 in HEK-293T cells expressing WT A subunit in HCO(3)(-)-free buffer.

186 efflux and/or pH(i) were measured in BCEC in HCO(3)(-)-free or HCO(3)(-)-rich Ringer, with and withou

187 9V) expression is associated with an unusual HCO(3)(-)-independent conductance that, if associated wi

188 age-clamped oocytes stimulated NBC-mediated, HCO(3)(-)-induced outward currents by >100% for the B an

189 ly 70%) did not alter pHi responses to CO(2)/HCO(3)(-)-rich Ringer, Na(+)-free induced acidification,

190 ) were measured in BCEC in HCO(3)(-)-free or HCO(3)(-)-rich Ringer, with and without niflumic acid (M

191 Here we show that the Ca(2+)/HCO(3)(-)-sensitive enzyme, soluble adenylyl cyclase (sA

192 that endothelial cells express the putative HCO(3)(-)-sensor receptor-type tyrosine-protein phosphat

193 sport, but does not transport B(OH)(4)(-) or HCO(3)(-).

194 and significantly reduced in the presence of HCO(3)(-).

195 ting the normal physiological buffers (24 mm HCO(3)(-)/5%CO(2)) with 10 mm HEPES similarly diminished

196 n CF than normal cells upon increased apical HCO(3)(-)/CO(2) exposure in part because of greater intr

197 ic promoter) in response to increased apical HCO(3)(-)/CO(2) perfusion was higher in normal compared

198 akly basic aqueous buffer solutions of CO(2)/HCO(3)(-)/CO(3)(2-) or HPO(4)(2-)/PO(4)(3-).

199 lpha(1,2)(-/-) mice exhibited a lower blood [HCO(3)(-)] and less Na(+) and K(+) retention than either

200 ion, at least in part by increasing luminal [HCO(3)(-)] and/or pH.

201 Moreover, increasing [HCO(3)(-)] on the apical and basolateral side of Xenopus

202 rent and ENaC abundance rose with increased [HCO(3)(-)] on the apical or the basolateral side, indepe

203 ever, ENaC was more sensitive to changes in [HCO(3)(-)] on the basolateral side of the monolayer.

204 ctivated S-type anion currents, whereas low [HCO(3)(-)](i) at high [CO(2)] and [H(+)] did not.

205 Elevated intracellular [HCO(3)(-)](i) with low [CO(2)] and [H(+)] activated S-ty

206 o increase luminal HCO(3)(-) concentration, [HCO(3)(-)], independent of pendrin.

207 g RPTPgamma-dependent vasorelaxation at low [HCO(3)(-)], RPTPgamma limits increases in cerebral perfu

208 l(-)], and an increase in blood [Na(+)] and [HCO(3)(-)].

209 tially neutralized by addition of NaHCO(3) ([HCO(3)(-)]/[Fe(3+)] < 3).

210 When [HCO(3)(-)]/[Fe(3+)] = 0.5 and 0.6 (initial pH approximat

211 When [HCO(3)(-)]/[Fe(3+)] = 1 (initial pH approximately 2.5),

212 In contrast, when [HCO(3)(-)]/[Fe(3+)] = 2 (initial pH approximately 2.7),

213 process involving apical membrane Na-H, SCFA-HCO(3), and Cl-SCFA exchanges.

214 3 times higher than those of their [NHC(H)][HCO(3)] counterparts 4.

215 mass spectrometry (TGA-MS) of most [NHC(H)][HCO(3)] precursors 4 showed a degradation profile in sta

216 The generation of NHCs from [NHC(H)][HCO(3)] precursors occurred via the formal loss of H(2)C

217 ee NHCs (2), while the synthesis of [NHC(H)][HCO(3)] precursors was directly achieved by anion metath

218 In addition, such [NHC(H)][HCO(3)] precursors were successfully investigated as pre

219 solution, NHC generation from both [NHC(H)][HCO(3)] salts and NHC-CO(2) adducts could be achieved at

220 ically-synthesized precursors such as NHC(H)[HCO(3)] salts or NHC-CO(2) adducts.

221 The [NHC(H)][HCO(3)] salts were next shown to behave as masked NHCs,

222 nz)imidazolium hydrogen carbonates ([NHC(H)][HCO(3)], 4) were independently employed as organic preca

223 ium hydrogen carbonates, denoted as [NHC(H)][HCO(3)].

224 the plasma membrane, orthologs of the Cl(-)/HCO(-)(3) antiporters ae1 and pendrin, and two isoforms

225 x 10(3) m(-1).s(-1), respectively) and that HCO(4) (-) is 250 times more efficient than H(2)O(2) at

226 experiments and calculations uncovered that HCO(4) (-) oxidizes C(P)SOH to C(P)SO(2) (-) with a seco

227 lating effect of HCO(3) (-)/CO(2) was due to HCO(4) (-), a peroxide present in equilibrated solutions

228 can bind to the same nonheme site and confer HCO activity in a heme-nonheme biosynthetic model in myo

229 as been found to vary >500 mV, its impact on HCO activity remains poorly understood.

230 anism in which one H atom moves far from the HCO, almost to dissociation, and then returns to abstrac

231 or the two primary channel products, CH(3) + HCO and H + CH(2)CHO.

232 Cell-cycle reentry in hCO and in vivo required the mevalonate pathway as inhib

233 radical channel C(7)H(15)CHO --> C(7)H(15) + HCO and the molecular channel C(7)H(15)CHO --> C(6)H(12)

234 rt study among 1.25 million adults from 4 US HCOs and included persons with >/=1 clinical encounter d

235 ork suggests that fine-tuning E degrees ' in HCOs and other heme enzymes can modulate their substrate

236 5 K via barrierless recombination of formyl (HCO) and hydroxycarbonyl radicals (HOCO) is reported.

237 While CO, [Formula: see text], HCO, and [Formula: see text] are often abundant species

238 the mechanism of efficient O(2) reduction in HCOs, and the nature of the P(M) intermediate that coupl

239 Heme-copper oxidases (HCOs) are key enzymes in prokaryotes and eukaryotes for

240 essive PMF is known to limit the turnover of HCOs, but the molecular mechanism of this regulatory fee

241 Haem-copper oxidase (HCO) catalyses the natural reduction of oxygen to water

242 Heme-copper oxidases (HCOs) catalyze efficient reduction of oxygen to water in

243 (2)CHO, H + CH(3)CO, H(2) + CH(2)CO, CH(3) + HCO, CH(2) + CH(2)O) and branching ratios (BRs) are dete

244 hat cytochrome bo3 from Escherichia coli, an HCO closely homologous to Complex IV in human mitochondr

245 The cobalt complexes HCo(CO)(4) and HCo(CO)(3)(PR(3)) were the original industrial catalysts

246 The cobalt complexes HCo(CO)(4) and HCo(CO)(3)(PR(3)) were the original indus

247 vious studies have established that C-family HCOs contain a single channel for uptake from the bacter

248 ETV2-expressing cells in hCOs contributed to forming a complex vascular-like netw

249 le in the adsorption of Sb(III) by Fe(3)O(4)/HCO (correlation coefficient R(2) = 0.993).

250 sm of the adsorption of Sb(III) on Fe(3)O(4)/HCO could be described by the synergistic adsorption of

251 barrier imposed by fatty acid metabolism in hCOs could be rescued by simultaneous activation of both

252 The HCO couples with residual methoxy on the surface to yiel

253 Human cortical organoids (hCOs), derived from human embryonic stem cells (hESCs),

254 educed oxy-F33Y-CuBMb, a functional model of HCOs engineered in myoglobin (Mb).

255 firm support for the tyrosyl radical in the HCO enzymatic mechanism.

256 of O-O bond cleavage in heme-copper oxidase (HCO) enzymes, combining experimental and computational i

257 In vitro, HCOs express colonic markers and contained colon-specifi

258 catalyzes the formation of bicarbonate ions (HCO[Formula: see text]), for accumulation of ACC in vesi

259 differentiation of human colonic organoids (HCOs) from hPSCs.

260 groups of burster instances but not for the HCO groups.

261 the oat fractions were 5-CH(3)-H(4)folate, 5-HCO-H(4)folate, and 5,10-CH(+)-H(4)folate.

262 andom number generation to receive intensive HCO-HD (in sessions lasting 6-8 h) or standard HF-HD and

263 m 43 (48%) were randomly assigned to receive HCO-HD and 47 (52%) were randomly assigned to receive HF

264 We therefore aimed to assess whether HCO-HD could increase the frequency of renal recovery in

265 In this phase 2 study, HCO-HD did not improve clinical outcomes for patients wi

266 90 days, 26 infections were reported in the HCO-HD group and 13 infections were reported in the HF-H

267 After 90 days, 24 (56%) patients in the HCO-HD group and 24 (51%) patients in the HF-HD group we

268 serious adverse events were reported in the HCO-HD group and 82 serious adverse events were reported

269 D group, including 14 lung infections in the HCO-HD group and three lung infections in the HF-HD grou

270 ring treatment, nine (21%) patients from the HCO-HD group and two (4%) patients in the HF-HD group di

271 ot support proceeding to a phase 3 study for HCO-HD in these patients.

272 High cutoff haemodialysis (HCO-HD) can remove large quantities of free light chain

273 insights to predict and demonstrate that the HCo(I) (dmpe)2 catalyst system, previously described for

274 Here, we use a biosynthetic model of HCO in myoglobin that selectively binds different non-ha

275 predominant transcellular pathway for Cl and HCO in porcine airway epithelia, and reduced anion perme

276 persons in private healthcare organizations (HCOs) in the United States.

277 Visualizations of HCO instances in a reduced space suggested that there mi

278 Next, transient HCO is made photochemically from formaldehyde.

279 Heme-copper oxidase (HCO) is a class of respiratory enzymes that use a heme-c

280 However, current hCOs lack microvasculature, resulting in limited oxygen

281 in the oxidase activity of Cu- and Fe-bound HCO mimics, respectively, as compared with Zn-bound mimi

282 existing database of half-center oscillator (HCO) model instances of the leech heartbeat CPG.

283 , we use a set of myoglobin-based functional HCO models to investigate the mechanism by which heme E

284 ughput bioengineered human cardiac organoid (hCO) platform, which provides functional contractile tis

285 al translational energy distributions of H + HCO products from S(0) and T(1) are also reported as wel

286 High-throughput proteomics in hCO revealed synergistic activation of the mevalonate pa

287 The Fe(3)O(4)/HCO sorbent appears to be an efficient and environment-f

288 copper and iron, in the heme-copper oxidase (HCO) superfamily is critical to the enzymatic activity o

289 are discussed in relation to O-O cleavage in HCOs, supporting a model in which a peroxo intermediate

290 gs reveal surprising discordance between our hCO system and traditional 2D assays.

291 The Sb(III)/Fe(3)O(4)/HCO system quickly reached adsorption equilibrium within

292 Despite decades of research on HCOs, the role of non-haem metal and the reason for natu

293 ay enable cytochrome bo3, and possibly other HCOs, to maintain a suitable DeltapH under extreme redox

294 (/) epithelia showed markedly reduced Cl and HCO transport.

295 duction potential (E degrees ') of different HCO types has been found to vary >500 mV, its impact on

296 It is determined that HCOs undergo a proton-initiated O-O cleavage mechanism w

297 Following transplantation into mice, HCOs undergo morphogenesis and maturation to form tissue

298 We found that vascularized hCOs (vhCOs) acquired several blood-brain barrier charac

299 A novel adsorbent (Fe(3)O(4)/HCO) was prepared via co-precipitation from a mix of fer

300 P-dependent patterning of human hindgut into HCOs, which will be valuable for studying diseases inclu