ライフサイエンスコーパス: acidosis

1 pyramidal neurons (HPNs) exposed to low pH (acidosis).

2 sorineural deafness and distal renal tubular acidosis.

3 H expression, an effect not seen with lactic acidosis.

4 normal defense of blood pH during whole-body acidosis.

5 I deficiency, were found to have mild lactic acidosis.

6 arked elevation of serum enzymes, and lactic acidosis.

7 d man who died with linezolid-induced lactic acidosis.

8 e crucial for the activation of eEF2K during acidosis.

9 the cytoplasm of cancer cells based on tumor acidosis.

10 and accelerated recovery from intracellular acidosis.

11 subtype alterations and magnified metabolic acidosis.

12 ocampal pyramidal neuron cultures exposed to acidosis.

13 emolytic anemias and/or distal renal tubular acidosis.

14 es hypertension, hyperkalemia, and metabolic acidosis.

15 hat mouse VSNs reliably detect extracellular acidosis.

16 btype distribution, resulting in more severe acidosis.

17 hagy by elevated CO2 was not attributable to acidosis.

18 umor and invade into the normal tissue using acidosis.

19 loss, hypertonic dehydration, and metabolic acidosis.

20 on of eEF2K promotes cancer cell death under acidosis.

21 bility and oligomer structure in response to acidosis.

22 can be accomplished by monitoring associated acidosis.

23 ses could adequately normalize ketonemia and acidosis.

24 erkalemia, hyperaldosteronism, and metabolic acidosis.

25 of blood glucose decrease and resolution of acidosis.

26 d anions were the leading cause of metabolic acidosis.

27 rologic evidence of liver failure and lactic acidosis.

28 ut how tumor cells adapt their metabolism to acidosis.

29 en associated with increased rates of lactic acidosis.

30 channels that are activated by extracellular acidosis.

31 demineralization allows compensation of the acidosis.

32 enzyme activity but most did not have lactic acidosis.

33 idney function because of concerns of lactic acidosis.

34 apilla, and chronic hyperchloremic metabolic acidosis.

35 to hypoxia and 13% exclusively sensitive to acidosis.

36 ion and excitation in response to hypoxia or acidosis.

37 al under disease relevant conditions such as acidosis.

38 erential sensitivity to either hypoxia or to acidosis.

39 of S427L in mediating proximal renal tubular acidosis.

40 yperparathyroidism, and distal renal tubular acidosis.

41 lation can cause hypercapnia and hypercapnic acidosis.

42 th hyperkalemia and hyperchloremic metabolic acidosis.

43 30 min in pH 6.5 medium, provided a model of acidosis.

44 sue damage despite more pronounced metabolic acidosis.

45 oncentration (p = 0.001), a marker of tissue acidosis.

46 on transport, causing proximal renal tubular acidosis.

47 nel activation and respiratory and metabolic acidosis.

48 th of which were associated with peritumoral acidosis.

49 icarbonate, particularly in patients without acidosis.

50 ptic current and to the detection of painful acidosis.

51 with markers of volume depletion and severe acidosis.

52 was significant for leukocytosis and lactic acidosis.

53 whole cohort and in patients with metabolic acidosis.

54 ive kidney disease, even among those without acidosis.

55 ever, lowering Vts may result in respiratory acidosis.

56 -ritonavir-dasabuvir may cause type B lactic acidosis.

57 metabolism, intestinal infarction and lactic acidosis.

58 nd tumorigenic properties of CSCs induced by acidosis.

59 ensated hypercapnia, 20,463; and hypercapnic acidosis, 122,245) were included in analysis.

60 rds (68%) were sensitive to both hypoxia and acidosis, 19% were exclusively sensitive to hypoxia and

61 sue space for monitoring extracellular tumor acidosis, a prognostic factor in tumor pathophysiology.

62 ine urine but do not exhibit overt metabolic acidosis, a renal phenotype similar to that of the Atpbv

63 vitro and in vivo experiments document that acidosis accounts for a net increase in tumor sensitivit

64 his study, we demonstrate that extracellular acidosis activates and sensitizes the human irritant rec

65 Crude rates of hyperchloremic acidosis, acute kidney injury, and hospital mortality al

66 e compared the development of hyperchloremic acidosis, acute kidney injury, and survival among those

67 Indeed, acidosis alone is sufficient to induce the increase in C

68 Hypercapnic acidosis also directly reduced DNA binding of the nuclea

69 udy period; 1,609 met criteria for metabolic acidosis and 145 had normal acid-base values.

70 transmission, mice inhaled CO2 to induce an acidosis and activate acid sensing ion channels.

71 l and pathological processes associated with acidosis and alkalinization.

72 Therefore, because acidosis and alkalosis are associated with altered PTH s

73 and mineral metabolism, correcting metabolic acidosis and anemia, achieving excellent blood pressure

74 Further, mice given BHB developed clinical acidosis and became extremely susceptible to mucormycosi

75 re severe inflammation, shock, and metabolic acidosis and by worse clinical outcomes.

76 infant presented with fatal infantile lactic acidosis and cardiomyopathy, and was found to have profo

77 atients in having intermittent severe lactic acidosis and early-onset neurodevelopmental problems wit

78 h affected individuals presented with lactic acidosis and evidence of multiple mitochondrial respirat

79 Hypercapnic acidosis and IkappaBalpha-SuperRepressor transgene overe

80 findings highlight the influence that tumor acidosis and metabolism exert on each other.

81 Routine blood tests showed lactic acidosis and mild elevation of the creatine kinase level

82 All case subjects presented with lactic acidosis and nine developed hypertrophic cardiomyopathy.

83 6v1b1 were reported to exhibit a compensated acidosis and normal hearing.

84 afferents, in which they sense extracellular acidosis and other metabolites released during ischemia

85 ated Na(+) channels playing a role in tissue acidosis and pain.

86 ministering HCO3 (-) after FPI prevented the acidosis and reduced the extent of neurodegeneration.

87 (SLC4A4) is linked to proximal renal tubular acidosis and results in impaired transport function, sug

88 ilure to thrive, developmental delay, lactic acidosis and severe encephalopathy suggestive of a mitoc

89 Mitochondrial myopathy with lactic acidosis and sideroblastic anemia (MLASA) is an oxidativ

90 tive of mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome, howe

91 LS), mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS), dermatomyosit

92 ncluding mitochondrial encephalopathy lactic acidosis and stroke-like episodes (MELAS), maternally in

93 (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes) and MIDD syndromes (m

94 (+) efflux with oncogenic Raf or Ras induces acidosis and synthetic lethality.

95 s experienced faster correction of metabolic acidosis and tended to be more rapidly weaned off catech

96 on, we found that CO2 inhalation caused BNST acidosis and that acidosis was sufficient to depolarize

97 childhood can lead to significant metabolic acidosis and that compensation with bone buffering does

98 responsible for the main types of metabolic acidosis and the outcome.

99 derness, severe hepatic cytolysis, metabolic acidosis, and hemodynamic dysfunction.

100 emia, hyperkalemia, hypercalcemia, metabolic acidosis, and increased serum lithium concentrations, ad

101 reased glycolysis, glutaminolysis and lactic acidosis, and neurotransmitter imbalances.

102 ventilation under normocapnia or hypercapnic acidosis, and nuclear factor-kappaB activation, animal s

103 key TRPA1 failed to respond to extracellular acidosis, and protons even inhibited rodent TRPA1.

104 present with a fatal encephalopathy, lactic acidosis, and severe mtDNA depletion in muscle.

105 ed with a clinical triad of myopathy, lactic acidosis, and sideroblastic anemia in predominantly Midd

106 is, growth hormone deficiency, renal tubular acidosis, and small for gestational age with no catch-up

107 ying mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome.

108 with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes.

109 ding mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes (MELAS).

110 entially more sensitive to either hypoxia or acidosis, and thus may evoke different and more specific

111 Metformin poisoning with lactic acidosis appears to be amenable to extracorporeal treatm

112 anges in Na(V) kinetics during extracellular acidosis are as yet unknown.

113 ot all gene defects that cause renal tubular acidosis are associated with hypercalciuria and nephroca

114 growth factor (NGF) receptor trkA and tissue acidosis are critically linked to inflammation-associate

115 Hypoxia and acidosis are inherent stress factors of the tumor microe

116 Diverse effects of hypercapnic acidosis are mediated via inhibition of nuclear factor-k

117 ncentration defects and distal renal tubular acidosis as a result of impaired V-ATPase activity.

118 s were associated with chronic extracellular acidosis (as indicated by the marker LAMP2 near/at the p

119 activated during peripheral inflammation and acidosis associated with various neuronal disorders, suc

120 ow pH may thus contribute to inflammation in acidosis-associated pathologies such as atherosclerosis

121 tertile had higher adjusted odds of incident acidosis at 1 year (adjusted odds ratio, 2.56; 95% CI, 1

122 The first presented with acute lactic acidosis at 3 weeks of age and developed severe developm

123 Among participants without acidosis at baseline, the adjusted hazard ratio for thos

124 odies, in response to hypoxia ( mmHg) and to acidosis at pH 6.8.

125 The degree of acidosis at presentation appears to determine final VA;

126 erential sensory transduction of hypoxia and acidosis at the level of glomus cells.

127 suggesting stretch activates and hypercapnic acidosis blocks stretch-mediated activation of ADAM17.

128 egrees C attenuated the shock-related lactic acidosis but caused metabolic acidosis, most likely resu

129 Patients with lactic and unmeasured anions acidosis, but not those with hyperchloremic acidosis, ha

130 Finally, an induction of acidosis by treatment with kainic acid or pH 6.0 medium

131 Because acidosis can activate acid sensing ion channels (ASICs),

132 severalfold during inflammation, where local acidosis can occur.

133 Severe symptoms include seizures, lactic acidosis, cardiac arrhythmia, and death within days of b

134 e assessed in vitro (i.e., in the absence of acidosis/circulating inflammatory mediators) was increas

135 adequate tissue perfusion and for preventing acidosis, coagulopathy, and hypothermia, referred to as

136 Hypercapnic acidosis, common in mechanically ventilated patients, ha

137 ed and severe intraoperative hypercapnia and acidosis, compared with open surgery.

138 O generation, particularly under hypoxic and acidosis conditions.

139 Acidosis could be a universal marker for cancer imaging

140 ese data suggest that under disease relevant acidosis, DAMPs and lactic acid induce the secretion of

141 II score, mechanical ventilation, metabolic acidosis, delirium on the prior day, and coma are risk f

142 Genetic deletion of GPR4 disrupted acidosis-dependent activation of RTN neurons, increased

143 with blood pH </= 7.15, persistent metabolic acidosis despite adequate supportive measures and antido

144 Lactic acidosis developed during continuous infusion of linezol

145 efractory to inotropic agents, and metabolic acidosis developed in the patient within 2 hours.

146 levels who might benefit from alkali before acidosis develops.

147 might benefit from oral alkali before overt acidosis develops.

148 renal acid excretion in distal renal tubular acidosis (dRTA) may lead to nephrocalcinosis and renal f

149 use autosomal-recessive distal renal tubular acidosis (dRTA).

150 when defective, causes distal renal tubular acidosis (dRTA).

151 man ATP6V1B1 gene cause distal renal tubular acidosis (dRTA; OMIM #267300) often associated with sens

152 ents with critical tissue hypoxia and lactic acidosis due to anemia.

153 Among children with lactic acidosis due to severe anemia, transfusion of longer-sto

154 tients developed metformin-associated lactic acidosis during follow-up.

155 The results suggest that transient acidosis during retrieval renders the memory of an avers

156 Hypercapnic acidosis during the first 24 hours of intensive care adm

157 th elevated carbon dioxide], and hypercapnic acidosis) during the first 24 hours of ICU stay.

158 Here we show that extracellular acidosis elicits activation of eEF2K in vivo, leading to

159 Heliox improves respiratory acidosis, encephalopathy, and the respiratory rate more

160 dary outcomes included time to resolution of acidosis, episodes of treatment failures, and incidences

161 ocardial thickening, hyperalaninemia, lactic acidosis, exercise intolerance, and persistent adrenergi

162 BHB-related acidosis exerted a direct effect on both GRP78 and CotH

163 back inhibition, likely to prevent metabolic acidosis from occurring.

164 Here, we show that glioma hypoxia and acidosis functionally cooperate in inducing HIF transcri

165 with compensated hypercapnia and hypercapnic acidosis had higher Acute Physiology and Chronic Health

166 acidosis, but not those with hyperchloremic acidosis, had an increased mortality compared to patient

167 supplementation trials, correcting metabolic acidosis has a strikingly broad array of potential benef

168 Local acidosis has been demonstrated in ischemic tissues and a

169 eleterious effects of acidosis, treatment of acidosis has been tested very little, especially with re

170 diagnosis of inherited distal renal tubular acidosis has no identified causative mutations in curren

171 lammatory mediators and correcting metabolic acidosis, high-volume hemofiltration (HVHF) might halt t

172 dividuals who presented at birth with lactic acidosis, hypotonia, feeding difficulties, and deafness.

173 lmonary disorders in relation to respiratory acidosis, impaired gas exchange, systemic congestion, re

174 e trial testing whether correcting metabolic acidosis improves clinical outcomes has not been conduct

175 e 1,000 muatm by 2100 - inducing respiratory acidosis in fish that must be corrected through branchia

176 ro by reducing hypoxia-induced extracellular acidosis in HT-29 and HeLa cell lines.

177 at hTRPA1 acts as a sensor for extracellular acidosis in human sensory neurons and should thus be tak

178 ing to metformin, kidney disease, and lactic acidosis in humans between 1950 and June 2014.

179 A signaling, diazepam provoked intracellular acidosis in macrophage, leading to impaired cytokine pro

180 The overall incidence of lactic acidosis in metformin users varies across studies from a

181 Data suggesting an increased risk of lactic acidosis in metformin-treated patients with chronic kidn

182 cus for cross-sensitization between AITC and acidosis in nociceptive neurons.

183 vitro studies demonstrate the involvement of acidosis in OCL activation and the implication of transi

184 Given the presence of acidosis in pathological states, our objective was to te

185 t of compensated hypercapnia and hypercapnic acidosis in patients receiving mechanical ventilation.

186 g the effects of hypercapnia and hypercapnic acidosis in patients requiring mechanical ventilation.

187 sites of chemotransduction of hypoxaemia and acidosis in peripheral arterial chemoreceptors.

188 ty during hypoglycaemia to prevent a serious acidosis in poorly controlled diabetes.

189 Mussels showed an extracellular acidosis in response to OA and copper individually which

190 ted fear behavior depends on chemosensing of acidosis in the amygdala via the acid-sensing ion channe

191 hese data suggest that diabetes causes local acidosis in the BM that in turn increases osteoclast act

192 o studies confirm the establishment of local acidosis in the diabetic bone marrow (BM) as well as the

193 se findings suggest the involvement of brain acidosis in the etiopathogenesis of Alzheimer disease, a

194 arterial CO2 levels and prevents respiratory acidosis in the face of increased metabolism.

195 sms are responsible for the hyperkalemia and acidosis in this model.

196 d suggests an important role for respiratory acidosis in triggering the fatal arrhythmia underlying S

197 Tactics to reduce respiratory acidosis include reductions in ventilation circuit dead

198 s with concurrent vasopressors and/or lactic acidosis increased (P < .001 for all methods), whereas t

199 In mice, diet-induced chronic acidosis increased alpha-ICs and decreased beta-ICs.

200 Chronic acidosis increases alpha-ICs at the expense of beta-ICs,

201 by growth factor quantitative PCR array that acidosis increases expression of mRNA encoding SDF1 (or

202 Lactic acidosis, induced by the addition of 25 mm lactic acid,

203 r, Hif1a deletion in all CCD cells prevented acidosis-induced IC subtype distribution, resulting in m

204 sor in mammalian brain and a key mediator of acidosis-induced neuronal damage following cerebral isch

205 nts demonstrate a critical role for ASIC1 in acidosis-induced reactive oxidative species and NF-kappa

206 Hypercapnic acidosis inhibited canonical nuclear factor-kappaB signa

207 Since acidosis is a hallmark of tumor development, progression

208 Acidosis is also a key feature of the inflammatory micro

209 erence and the strong ion gap) suggests that acidosis is also due in part to the presence of an unkno

210 Together, these results suggest that acidosis is an important and previously overlooked regul

211 Acidosis is an important complication of AKI and CKD.

212 Linezolid-induced lactic acidosis is associated with diminished global oxygen con

213 Metabolic acidosis is associated with increased urinary calcium ex

214 Metabolic acidosis is associated with poor outcomes in CKD.

215 these individuals with subclinical metabolic acidosis is challenging, but recent results suggest that

216 LAMP2 upregulation by acidosis is confirmed both in vitro and in vivo.

217 Metabolic acidosis is not uncommon in CKD and is linked with bone

218 ficiently by the adaptive immune system when acidosis is triggered during infection.

219 Lactic acidosis (LA) frequently occurs after heart transplantat

220 Extracellular tumor acidosis largely results from an exacerbated glycolytic

221 rinary diversion may cause chronic metabolic acidosis, leading to long-term bone loss in patients wit

222 ic conditions, such as ischemic stroke where acidosis leads to widespread death of glia and subsequen

223 primary aldosteronism, distal renal tubular acidosis, Liddle's disease, apparent mineralocorticoid e

224 (SD) length of time to achieve resolution of acidosis (low vs standard dose: 16.5 [7.2] vs 17.2 [7.7]

225 During metabolic acidosis (MAc), AE3 speeds initial acidification, but li

226 fication during the early phase of metabolic acidosis (MAc), not just in neurons but, surprisingly, i

227 luate safety (cardiac arrhythmia, persistent acidosis, major vessel thrombosis and bleeding, and deat

228 known to induce metformin-associated lactic acidosis (MALA), a severe medical condition with poor pr

229 c acidosis that occurs with injury, and this acidosis may have detrimental clinical effects.

230 Local acidosis may promote inflammation at ischemic and inflam

231 d excretion in CKD, with potential metabolic acidosis, may contribute to the progression of CKD.

232 the prevalence and risk factors of metabolic acidosis, mechanisms of acid-mediated organ injury, resu

233 othermia (median temperature <34 degrees C), acidosis (median pH <7.2), and/or coagulopathy.

234 Mechanistically, ASIC1 is required for acidosis-mediated signaling through calcium influx.

235 ell senses the acidic signal to activate the acidosis-mediated signaling.

236 depletion of LAMP2 is sufficient to increase acidosis-mediated toxicity.

237 related lactic acidosis but caused metabolic acidosis, most likely resulting from reduced carbohydrat

238 tient in the doxorubicin alone group (lactic acidosis [n=1]).

239 ercapnic respiratory failure and respiratory acidosis nonresponsive to noninvasive ventilation.

240 Therefore, as extracellular acidosis occurs during infection by various micro-organi

241 t/vtx mice do not recapitulate the metabolic acidosis of dRTA patients, they provide a new genetic mo

242 was to establish the effects of hypercapnic acidosis on mitogen-activated protein kinase (MAPK) acti

243 o studies examined the effect of hypercapnic acidosis on specific nuclear factor-kappaB canonical pat

244 We aim to examine the effect of hypercapnic acidosis on the nuclear factor-kappaB pathway in the set

245 The effect of hypercapnic acidosis on the p50/p65 nuclear factor-kappaB heterodime

246 derlying mechanisms of action of hypercapnic acidosis on this pathway is unclear.

247 was no longer associated with hyperchloremic acidosis or acute kidney injury after controlling for to

248 oride load and development of hyperchloremic acidosis or acute kidney injury is less clear, and furth

249 including chemotherapeutic dosing, degree of acidosis or base deficit achieved, and peak temperature

250 to neuronal membranes in response to either acidosis or neuronal depolarization provides two novel m

251 ociated with profound hypoxemia, respiratory acidosis, or hemodynamic compromise.

252 hospital mortality was higher in hypercapnic acidosis patients (odds ratio, 1.74; 95% CI, 1.62-1.88)

253 The mortality was higher in hypercapnic acidosis patients when compared with other groups, with

254 temic arterial pressure 31 +/- 1 mm Hg), and acidosis (pH 7.02 +/- 0.02).

255 rameters such as oxygen (pO2), extracellular acidosis (pHe), and concentration of interstitial inorga

256 inary calcium excretion induced by metabolic acidosis predominantly results from increased mobilizati

257 Proximal renal tubular acidosis (pRTA) is a rare, recessively-inherited disease

258 onate-wasting disease proximal renal tubular acidosis (pRTA).

259 eria was met: severe hyperkalemia, metabolic acidosis, pulmonary edema, blood urea nitrogen level hig

260 Hypercapnic acidosis reduced E. coli inflammation and lung injury in

261 s with concurrent vasopressors and/or lactic acidosis remained stable (P = .098).

262 amics, microvascular indices and measures of acidosis, renal function, and pulmonary edema were follo

263 Extracellular acidosis resulting from intense metabolic activities in

264 se events (hyperglycaemia or ketosis without acidosis) resulting in hospital admission occurred in th

265 who all presented with severe type B lactic acidosis shortly after starting treatment with ombitasvi

266 tochondrial myopathy, encephalopathy, lactic acidosis, stroke-like episodes) is a rare, multisystem d

267 g sensitivity to physical (membrane stretch, acidosis, temperature) and chemical stimuli (signaling l

268 chaemic core had a more severe intracellular acidosis than hypoperfused tissue recruited to the final

269 ptide technology to target the extracellular acidosis that characterizes solid tumors.

270 1 gene) of ALS enters a progressive state of acidosis that is associated with several metabolic (horm

271 rauma patients, may exacerbate the metabolic acidosis that occurs with injury, and this acidosis may

272 us, triggered by heat shock or physiological acidosis, that depends on the expression of ribosomal in

273 In patients with hypercapnic acidosis, the mortality increased with increasing PCO2 u

274 In patients with metabolic acidosis, the results were similar.

275 Lactic acidosis--the strongest prognostic indicator in adults w

276 ptive response of tumor cells to hypoxia and acidosis through increased internalization of lipoprotei

277 nical spectrum ranging from infantile lactic acidosis to childhood (cardio)myopathy and late-onset pr

278 portance of careful metabolic control of the acidosis to prevent and manage this infection.

279 ments ventilation in response to hypercapnic acidosis to restore normal pH and PCO2Tac1-Pet1 axonal b

280 Pre-malignant cells must adapt to acidosis to thrive in this hostile microenvironment.

281 n, higher fluid balance, obesity, hypoxemia, acidosis, tobacco use, emergent hematoma evacuation, and

282 from perifused human parathyroid cells, and acidosis transiently increased PTH secretion.

283 cumulated evidence of deleterious effects of acidosis, treatment of acidosis has been tested very lit

284 instem slices of wild-type mice, respiratory acidosis triggered robust elevations in [Ca(2+) ]i in as

285 hypertension with hyperkalemia and metabolic acidosis, unmasked a complex multiprotein system that re

286 xcretion is important in the pathogenesis of acidosis, urine ammonium excretion might be a better and

287 detector of noxious stimuli, including heat, acidosis, vanilloid compounds and lipids.

288 e-volume fluid resuscitation, hyperchloremic acidosis was documented in 523 (11%).

289 The duration of hypercapnia and acidosis was longer in thoracoscopy compared with that i

290 Metabolic acidosis was one of the earliest complications to be rec

291 Metabolic acidosis was prevented in the 4-aminopyridine group.

292 CO2 inhalation caused BNST acidosis and that acidosis was sufficient to depolarize BNST neurons and i

293 ine and bilirubin concentrations, and severe acidosis were all managed safely and effectively.

294 7] hours; P = .73) and rate of resolution of acidosis were also similar in the groups.

295 No cases of lactic acidosis were observed.

296 ma, seizures, new vision deficits, metabolic acidosis with blood pH </= 7.15, persistent metabolic ac

297 t association of hypercapnia and hypercapnic acidosis with hospital mortality.

298 as Rhcg(-/-) mice developed severe metabolic acidosis with reduced ammonuria and high mortality.

299 easured anions, and hyperchloremic metabolic acidosis with that of patients without acid-base disorde

300 eed for resuscitation 10 min after birth, or acidosis within 1 h of birth.