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1 brain damage during ischemia due to enhanced lactic acidosis.
2 and catecholamines were responsible for the lactic acidosis.
3 t rate and systemic vascular resistance, and lactic acidosis.
4 elay, lethargy, severe hypotonia, and modest lactic acidosis.
5 ctate, making them specialized for detecting lactic acidosis.
6 in body fat distribution, dyslipidemia, and lactic acidosis.
7 es, branched-chain ketoaciduria, and primary lactic acidosis.
8 e, global neurodevelopmental regression, and lactic acidosis.
9 rdynamic, tachycardic state with progressive lactic acidosis.
10 dead space ventilation and exercise-induced lactic acidosis.
11 ed to hypovolemia, tissue hypoperfusion, and lactic acidosis.
12 erature, heart rate, oxygen consumption, and lactic acidosis.
13 ive to treatment and causing oxygen debt and lactic acidosis.
14 PDH worsens exercise performance and induces lactic acidosis.
15 minal pain and metabolic decompensation with lactic acidosis.
16 ety events of interest were hypoglycemia and lactic acidosis.
17 DG metabolism, were relatively unaffected by lactic acidosis.
18 ed lifespan of Ndufs4-KO mice and attenuated lactic acidosis.
19 mplex II deficiency, were found to have mild lactic acidosis.
20 ab work was significant for leukocytosis and lactic acidosis.
21 was strongly associated with the presence of lactic acidosis.
22 aprevir-ritonavir-dasabuvir may cause type B lactic acidosis.
23 epatic metabolism, intestinal infarction and lactic acidosis.
24 and CotH expression, an effect not seen with lactic acidosis.
25 gram, marked elevation of serum enzymes, and lactic acidosis.
26 year-old man who died with linezolid-induced lactic acidosis.
27 and serologic evidence of liver failure and lactic acidosis.
28 not been associated with increased rates of lactic acidosis.
29 genase enzyme activity but most did not have lactic acidosis.
30 aired kidney function because of concerns of lactic acidosis.
31 in was not associated with increased risk of lactic acidosis.
32 vival of cells after exposure to hypoxia and lactic acidosis.
33 lls is abolished by simultaneous exposure to lactic acidosis.
34 ng the origins and treatment of pathological lactic acidosis.
35 nd hyperglycemia, possibly mediated by brain lactic acidosis.
36 e molecule used by sensory neurons to detect lactic acidosis.
39 ondrial inner membrane to undergo fusion and lactic acidosis after the loss of outer membrane fusion.
40 mino acid supplies, glucose deprivation, and lactic acidosis, all of which pose challenges for protei
41 rine metabolite studies showed hypoglycemia, lactic acidosis, altered Krebs cycle function and dysreg
42 e characterized by fetal growth retardation, lactic acidosis, aminoaciduria, cholestasis, and abnorma
43 An infant presented with fatal infantile lactic acidosis and cardiomyopathy, and was found to hav
44 , aminoaciduria, cholestasis, iron overload, lactic acidosis and early death (GRACILE syndrome), and
45 drome patients in having intermittent severe lactic acidosis and early-onset neurodevelopmental probl
46 ion who were taking stavudine presented with lactic acidosis and elevated levels of aminotransferases
47 Both affected individuals presented with lactic acidosis and evidence of multiple mitochondrial r
48 three families with children suffering from lactic acidosis and hyperpyruvatemia revealed a causal l
50 ses up to 100-fold, possibly contributing to lactic acidosis and hypoglycemia in patients with severe
51 ative epidermis but rapidly died of systemic lactic acidosis and hypoglycemia, indicating excessive g
53 Q(10) deficiency who presented with neonatal lactic acidosis and later developed multisytem disease i
58 with failure to thrive, developmental delay, lactic acidosis and severe encephalopathy suggestive of
60 en use in five severely septic patients with lactic acidosis and six healthy volunteers before and af
61 ds harboring mitochondrial encephalomyopathy lactic acidosis and stroke A3243G tRNA((Leu)UUR) gene mu
62 her the mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (A3243G MELAS)
63 such as mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) and myo
64 of the mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) phenoty
65 suggestive of mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) syndrom
66 osis (ALS), mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS), dermat
67 romes including mitochondrial encephalopathy lactic acidosis and stroke-like episodes (MELAS), matern
69 tation causing mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS); the tR
70 tients with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes syndrome (MELAS
72 MELAS (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes) and MIDD syndr
73 Melas (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes) is one of a gr
74 (Mitochondrial Myopathy, Encephalopathy with Lactic Acidosis and Stroke-like episodes) syndrome, the
76 ssociated with mitochondrial encephalopathy, lactic acidosis and stroke-like episodes, but were docum
79 muscle and, therefore, is proposed to detect lactic acidosis and to transduce angina and muscle ische
80 erum fibrinogen, elevated prothrombin time), lactic acidosis, and hepatic steatosis were characterist
84 d Ca accumulation, attenuated sepsis-related lactic acidosis, and improved left ventricular function.
89 hildren present with a fatal encephalopathy, lactic acidosis, and severe mtDNA depletion in muscle.
90 nd drugs interacting with metformin to cause lactic acidosis, and showed both to induce effects on th
91 ssociated with a clinical triad of myopathy, lactic acidosis, and sideroblastic anemia in predominant
92 h as mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke (MELAS), neuropathy, ataxia,
93 experiment to mitochondrial encephalopathy, lactic acidosis, and stroke-like episode (MELAS)-associa
94 tient carrying the myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) A3243G
95 the mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndro
96 underlying mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndro
99 dy the elusive mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes-associated A32
101 tion causes mitochondrial encephalomyopathy, lactic acidosis, and stroke-like symptoms (MELAS) and 2%
106 Since Coffin-Lowry syndrome and neonatal lactic acidosis are associated with mutations in the hum
107 ver toxicity, hypersensitivity reactions and lactic acidosis are recognized as acute events with pote
108 a has many manifestations, of which coma and lactic acidosis are the best independent predictors of a
109 opathy, peripheral neuropathy, myopathy, and lactic acidosis associated with deficiencies of multiple
110 who presented with exercise intolerance and lactic acidosis associated with severe deficiency of com
112 at 32 degrees C attenuated the shock-related lactic acidosis but caused metabolic acidosis, most like
113 ndrial toxicity (i.e., neuropathy, myopathy, lactic acidosis), but these side effects are rarely repo
114 fever, tachycardia, oxygen consumption, and lactic acidosis, but it does not prevent the development
116 ever, the dominant theory in the field, that lactic acidosis causes muscle fatigue, is unlikely to te
117 to occur in a variety of diseases including lactic acidosis, Cowden Syndrome, and several cancers.
125 nly has been assumed that the development of lactic acidosis during sepsis results from a deficit in
126 sive myocardial thickening, hyperalaninemia, lactic acidosis, exercise intolerance, and persistent ad
128 were significantly (P < 0.05) protected from lactic acidosis, glutamate buildup, and diminished HCO(3
129 severe neurological dysfunction, congenital lactic acidosis, growth retardation, and early death.
130 d multi-organ derangement with leukocytosis, lactic acidosis, haemolytic anaemia and hyperbilirubinem
131 ated individuals who presented at birth with lactic acidosis, hypotonia, feeding difficulties, and de
132 al MCT1 may contribute to the development of lactic acidosis in brain pathologies, and suggest target
134 pertaining to metformin, kidney disease, and lactic acidosis in humans between 1950 and June 2014.
138 e role played by the tumor microenvironment, lactic acidosis in particular, on the uptake by tumor ce
141 e patients with severe exercise intolerance, lactic acidosis in the resting state (in four patients),
143 cultures with concurrent vasopressors and/or lactic acidosis increased (P < .001 for all methods), wh
145 pplied pharmacokinetic modeling to show that lactic acidosis inhibits FDG uptake by cancer cells in v
152 , it is known to induce metformin-associated lactic acidosis (MALA), a severe medical condition with
155 ghei malaria, (ii) respiratory distress with lactic acidosis occurs during P. berghei malaria, and (i
156 logies, anaerobic glycolysis produces severe lactic acidosis of brain tissue leading to brain cell da
157 at express ASICs an extra sensitivity to the lactic acidosis of local ischemia compared to acidity ca
158 ith serious metabolic complications, such as lactic acidosis, pancreatitis, and peripheral neuropathy
160 Our findings reveal that the condition of lactic acidosis present in solid tumors inhibits canonic
162 Blood data were consistent with extreme lactic acidosis, reduced glomerular filtration, and stre
163 trovirals are well characterized and include lactic acidosis related to nucleoside reverse transcript
165 fection who all presented with severe type B lactic acidosis shortly after starting treatment with om
166 nificantly associated with the occurrence of lactic acidosis (specificity: 92.9%; sensitivity: 67.1%;
167 ome (mitochondrial myopathy, encephalopathy, lactic acidosis, stroke-like episodes) is a rare, multis
169 cytochrome c oxidase deficiency and hepatic lactic acidosis that accompanies this disorder is unknow
173 h a clinical spectrum ranging from infantile lactic acidosis to childhood (cardio)myopathy and late-o
174 bit rapid weight loss and suffer from severe lactic acidosis, ultimately leading to early mortality u
175 alpha alpha Hb (n = 6) resulted in hypoxia, lactic acidosis, ventricular arrhythmias, and decreased
178 s associated with hemodynamic depression and lactic acidosis, which appeared (illustrative echocardio
179 mitochondrial myopathy, encephalopathy, and lactic acidosis with stroke-like episodes (MELAS) and Pa
180 hold causes mitochondrial encephalomyopathy, lactic acidosis with stroke-like episodes (MELAS) syndro