ライフサイエンスコーパス: acidosis

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

2 ) or through lactic acid infusion (metabolic acidosis).

3 n channel that is activated by extracellular acidosis.

4 factor that responds to fermentation-induced acidosis.

5 al pH has long been used to identify ruminal acidosis.

6 toacids; and 'A', a high anion gap metabolic acidosis.

7 e on milk and during weaning can cause rumen acidosis.

8 lves using our model of feed induced ruminal acidosis.

9 upon protonation arising from intracellular acidosis.

10 in plasma from patients with severe malaria acidosis.

11 % of patients, respectively, and may lead to acidosis.

12 el family and are modulated by extracellular acidosis.

13 span of Ndufs4-KO mice and attenuated lactic acidosis.

14 hypertension and hyperkalemia with metabolic acidosis.

15 r effectively and safely corrected metabolic acidosis.

16 tant channel was unaffected by extracellular acidosis.

17 ongly associated with the presence of lactic acidosis.

18 sorineural deafness and distal renal tubular acidosis.

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

20 and accelerated recovery from intracellular acidosis.

21 d anions were the leading cause of metabolic acidosis.

22 lation can cause hypercapnia and hypercapnic acidosis.

23 icarbonate, particularly in patients without acidosis.

24 ptic current and to the detection of painful acidosis.

25 with markers of volume depletion and severe acidosis.

26 was significant for leukocytosis and lactic acidosis.

27 whole cohort and in patients with metabolic acidosis.

28 ive kidney disease, even among those without acidosis.

29 ever, lowering Vts may result in respiratory acidosis.

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

31 metabolism, intestinal infarction and lactic acidosis.

32 nd tumorigenic properties of CSCs induced by acidosis.

33 can permit accurate in vivo visualization of acidosis.

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

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

36 alphaICs, even when stimulated by metabolic acidosis.

37 arked elevation of serum enzymes, and lactic acidosis.

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

39 to the femoral circulation, worsening fetal acidosis.

40 e crucial for the activation of eEF2K during acidosis.

41 the cytoplasm of cancer cells based on tumor acidosis.

42 OMCDi dysfunction and pyelonephritis-induced acidosis.

43 te residues at distal NT and is disrupted by acidosis.

44 mechanism for E. coli pyelonephritis-induced acidosis.

45 n of the imaging signals triggered by tumour acidosis.

46 ncreases ASIC-mediated neuronal death during acidosis.

47 consistent with a diagnosis of renal tubular acidosis.

48 econdary to high concentrate feeds and rumen acidosis.

49 likely compensating for a chronic metabolic acidosis.

50 tion of why severe ketosis is accompanied by acidosis.

51 n in the ventilatory response to hypercapnic acidosis.

52 nce of several genera in calves with induced acidosis.

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

54 Metabolic acidosis, a complication of chronic kidney disease, caus

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

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

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

58 othelial dysfunction (L-arginine), metabolic acidosis (alanine and lactate), and disease severity (ph

59 id supplies, glucose deprivation, and lactic acidosis, all of which pose challenges for protein proce

60 Hypercapnic acidosis also directly reduced DNA binding of the nuclea

61 Chronic metabolic acidosis also stimulates ammoniagenesis that increases a

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

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

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

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

66 aciduria, cholestasis, iron overload, lactic acidosis and early death (GRACILE syndrome), and Bjornst

67 can present with severe hypoglycemia, lactic acidosis and hypertriglyceridemia.

68 Hypercapnic acidosis and IkappaBalpha-SuperRepressor transgene overe

69 r safely and effectively corrected metabolic acidosis and improved subjective and objective measures

70 njection of gemcitabine increased intratumor acidosis and increased cell death.

71 ms of affected family members include lactic acidosis and low serum methionine levels.

72 the development of hyperchloremic metabolic acidosis and may reduce the need for vasopressors.

73 6v1b1 were reported to exhibit a compensated acidosis and normal hearing.

74 Hyperchloraemic acidosis and respiratory and neurological dysfunction in

75 with fatal infantile cardiomyopathy, lactic acidosis and respiratory failure.

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

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

78 LAS (mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes) syndrome.

79 exceeds the level predicted by the sustained acidosis and the acute CO(2)/H(+) chemoreflex, suggestin

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

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

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

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

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

85 cancer cells, leading to decreased hypoxia, acidosis, and nutrient depletion.

86 mplicated in tumor metastasis, renal tubular acidosis, and osteoporosis.

87 nd neurological dysfunction, hyperchloraemic acidosis, and reduction in haemoglobin concentration.

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

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

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

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

92 ated mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes.

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

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

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

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

97 ospective studies identify chronic metabolic acidosis as an independent and modifiable risk factor fo

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

99 C is a valuable tool to noninvasively assess acidosis associated with both central and peripheral inn

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

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

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

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

104 icating the liver's response to feed induced acidosis at the transcriptome level.

105 Treatment of chronic metabolic acidosis attenuates these adaptive responses; reduces le

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

107 In this study, we induced ruminal acidosis by feeding a highly processed, starch-rich diet

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

109 Severe local acidosis causes tissue damage and pain, and is one of th

110 erve muscle oxygenation and reduce metabolic acidosis compared with CLE at the same average work rate

111 O generation, particularly under hypoxic and acidosis conditions.

112 Eighty-seven patients (44.8%) had lactic acidosis defined as an arterial blood pH less than 7.35

113 Lactic acidosis developed during continuous infusion of linezol

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

115 levels who might benefit from alkali before acidosis develops.

116 might benefit from oral alkali before overt acidosis develops.

117 etention, leading us to conclude that tissue acidosis does not mediate the hypoxia selectivity of [(6

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

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

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

121 characterized by hyperglycemia and metabolic acidosis due to the accumulation of ketone bodies, which

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

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

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

125 rements and Main Results: During respiratory acidosis, electrodialysis reduced plasma chloride concen

126 During metabolic acidosis, electrodialysis reduced plasma chloride concen

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

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

129 (NSF), which associates with ASIC1a-NT under acidosis, facilitating RIPK1 interaction with ASIC1a-CT.

130 slower compensatory response to respiratory acidosis (final pH = 7.29 +/- 0.03; P < 0.001).

131 ile one had fatal cardiomyopathy with lactic acidosis following a febrile illness.

132 The extracellular acidosis found in solid tumors triggers pHLIP to transit

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

134 (pRTA), a disease characterized by metabolic acidosis, growth retardation, ocular abnormalities, and

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

136 Independent induction of tissue acidosis had no direct effect on [(64)Cu][Cu(ATSM)] phar

137 Calves with induced ruminal acidosis had significantly lower ruminal pH in compariso

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

139 -organ derangement with leukocytosis, lactic acidosis, haemolytic anaemia and hyperbilirubinemia.

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

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

142 sociated with the development of hypercapnic acidosis (HCA).

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

144 to cellular stresses, such as heat shock or acidosis, HSP27 oligomers can dissociate into dimers and

145 ions of CKD, such as hyperkalemia, metabolic acidosis, hyperphosphatemia, vitamin D deficiency, secon

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

147 nd and demonstrated the areas of significant acidosis, hypoxia, and elevated Pi content.

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

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

150 Metabolic acidosis in CKD stimulates production of intrakidney par

151 diagnosis and precision management of rumen acidosis in dairy calves.

152 agnosis and preventative management of rumen acidosis in dairy calves.

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

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

155 played by the tumor microenvironment, lactic acidosis in particular, on the uptake by tumor cells of

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

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

158 ty of veverimer as a treatment for metabolic acidosis in patients with chronic kidney disease.

159 nd source of metabolic acids contributing to acidosis in patients with severe falciparum malaria.

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

161 ng in the liver resultant from the prolonged acidosis in post weaning calves, which may facilitate fu

162 nscriptome changes associated with prolonged acidosis in post weaning calves.

163 rstand the health risks of prolonged ruminal acidosis in post weaning calves.

164 ular changes associated with prolonged rumen acidosis in post weaning young calves are largely unknow

165 pH-sensitive PET tracer specifically detects acidosis in regions associated with sepsis-driven proinf

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

167 entral to the development of coma and lactic acidosis in severe falciparum malaria.

168 ntly to the pathogenesis of life-threatening acidosis in severe falciparum malaria.

169 asured plasma acids strongly associated with acidosis in severe malaria.

170 Acidosis in severe Plasmodium falciparum malaria is asso

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

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

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

174 on was caused by SO(2) -induced local tissue acidosis in the lung and airways.

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

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

177 other deleterious consequences of metabolic acidosis including progression of chronic kidney disease

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

179 , in particular, through direct sensation of acidosis induced by CO(2) levels.

180 (E575/H578) in the pore turret abolished the acidosis-induced decrease of current amplitude, without

181 to suppress cellular metabolism and prevent acidosis-induced DNA damage.

182 otic effects on tracer pharmacokinetics from acidosis-induced hypocontractility, parallel studies use

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

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

185 Hypercapnic acidosis induces mitochondrial dysfunction and impairs t

186 he tumor microenvironment and indicates that acidosis induces potentially therapeutically actionable

187 Four of them were fed the acidosis-inducing diet (Treated) and the rest of the fou

188 at saline may cause hyperchloremic metabolic acidosis, inflammation, hypotension, acute kidney injury

189 hich areas within a tumor are acidic and how acidosis influences gene expression to promote invasion.

190 Hypercapnic acidosis inhibited canonical nuclear factor-kappaB signa

191 Acidosis is a fundamental feature of the tumor microenvi

192 Since acidosis is a hallmark of ischemic tissue and tumors, th

193 Since acidosis is a hallmark of tumor development, progression

194 Acidosis is a key driver for many diseases, including ca

195 Acidosis is also a key feature of the inflammatory micro

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

197 Acidosis is an important complication of AKI and CKD.

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

199 Acidosis is associated with E. coli induced pyelonephrit

200 Metabolic acidosis is associated with increased urinary calcium ex

201 Metabolic acidosis is associated with poor outcomes in CKD.

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

203 sets of neurons influence their responses to acidosis is not known.

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

205 The acidosis is usually attributed to the 'acidic' nature of

206 Carbon dioxide (CO(2)), via effects on local acidosis, is one of the most potent regulators of cerebr

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

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

209 NH(4) Cl-induced metabolic acidosis (MAc) substantially increases protein expressio

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

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

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

213 pectroscopy of untreated liver tumors showed acidosis (mean extracellular pH, 6.78 +/- 0.09) compared

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

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

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

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

218 Indeed, the outcome of lactic acidosis might depend on the prompt initiation of renal

219 In response to acidosis, MondoA shows preferential binding to just two

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

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

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

223 Extracellular acidosis occurs in pathological states including cardiac

224 eased in-hospital mortality were severity of acidosis (odds ratio [OR] 2.10 for a 7-mEq/L increase in

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

226 Acidosis of the tumor microenvironment leads to cancer i

227 tients with CKD, untreated chronic metabolic acidosis often leads to an accelerated reduction in GFR.

228 , implying the direct effect of feed-induced acidosis on both the rumen microbial community and liver

229 ganization, indicating the impact of ruminal acidosis on liver development in young calves.

230 The effects of acidosis on macroscopic current amplitude and deactivati

231 phogenesis, indicating the impact of ruminal acidosis on rumen epithelium development.

232 to understand the role of prolonged ruminal acidosis on rumen microbial community or host health in

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

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

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

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

237 Lithium caused acidosis only in one mouse strain, whereas hypercalcemia

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

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

240 hrough reduction of ventilation (respiratory acidosis) or through lactic acid infusion (metabolic aci

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

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

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

244 that their response to moderate hypercapnic acidosis (pH 7.4 to ~7.2) was markedly reduced by antago

245 Tumor oxygenation (pO(2)), acidosis (pH) and interstitial inorganic phosphate conce

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

247 Among lactic acidosis-positive patients, however, in-ICU death was le

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

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

250 ions in SLC4A4 causes proximal renal tubular acidosis (pRTA), a disease characterized by metabolic ac

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

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

253 mechanism was sensitive to pH; extracellular acidosis reduced both hERG1a and1b channel open time and

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

255 ood data were consistent with extreme lactic acidosis, reduced glomerular filtration, and stress.

256 deployed for severe hypoxemia or hypercapnic acidosis refractory to conventional ventilator managemen

257 e tracts in post-weaning calves with ruminal acidosis remain largely unexplored.

258 Extracellular acidosis resulting from intense metabolic activities in

259 molecular weight proteinuria, renal tubular acidosis (RTA), aminoaciduria, and hypercalciuria.

260 te 20-40 mL/min per 1.73 m(2)) and metabolic acidosis (serum bicarbonate 12-20 mmol/L), who had compl

261 of 20-40 mL/min per 1.73 m(2)) and metabolic acidosis (serum bicarbonate concentration of 12-20 mmol/

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

263 cromolecular strategy for integrating tumour acidosis should enable improved cancer detection, survei

264 Calves with induced ruminal acidosis showed significantly less weight gain over the

265 tly associated with the occurrence of lactic acidosis (specificity: 92.9%; sensitivity: 67.1%; area u

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

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

268 ogenous acid, resulting in chronic metabolic acidosis that increases the risk of disease progression

269 ral sodium bicarbonate therapy for metabolic acidosis that only neutralises accumulated acid.

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

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

272 We therefore conclude that lactic acidosis-the combination of lactate ion buildup and acid

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

274 pH (pHe) of tissues in vivo, allowing tumor acidosis to be used as a diagnostic biomarker.

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

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

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

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

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

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

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

282 ts with chronic kidney disease and metabolic acidosis, veverimer safely and effectively corrected met

283 e ventilatory response to graded hypercapnic acidosis vs. controls.

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

285 Using isolated perfused rat hearts, acidosis was induced using an ammonium pre-pulse method,

286 Respiratory acidosis was never detected, although a mild metabolic a

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

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

289 Acidosis was subsequently sustained for 12-14 hours.

290 One such signal is acidosis, which increases MondoA activity and also drive

291 in feed, which subsequently may cause rumen acidosis while on milk and during weaning.

292 ney stone disorders, including renal tubular acidosis with deafness, Bartter syndrome, primary hypero

293 rmalities in PBC, including increased muscle acidosis with exercise linked to the antimitochondrial a

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

295 ure (PaO2/FIO2 < 85 mm Hg and/or respiratory acidosis with pH < 7.25) who were successfully treated w

296 uses mitochondrial encephalomyopathy, lactic acidosis with stroke-like episodes (MELAS) syndrome, the

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

298 ortant association of tumor microenvironment acidosis with tumor cell invasion, relatively little is

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

300 This study expands our understanding of acidosis within the tumor microenvironment and indicates