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1 aprevir-ritonavir-dasabuvir may cause type B lactic acidosis.
2 t rate and systemic vascular resistance, and lactic acidosis.
3 elay, lethargy, severe hypotonia, and modest lactic acidosis.
4 ctate, making them specialized for detecting lactic acidosis.
5 in body fat distribution, dyslipidemia, and lactic acidosis.
6 es, branched-chain ketoaciduria, and primary lactic acidosis.
7 e, global neurodevelopmental regression, and lactic acidosis.
8 rdynamic, tachycardic state with progressive lactic acidosis.
9 dead space ventilation and exercise-induced lactic acidosis.
10 ed to hypovolemia, tissue hypoperfusion, and lactic acidosis.
11 erature, heart rate, oxygen consumption, and lactic acidosis.
12 epatic metabolism, intestinal infarction and lactic acidosis.
13 ive to treatment and causing oxygen debt and lactic acidosis.
14 and CotH expression, an effect not seen with lactic acidosis.
15 gram, marked elevation of serum enzymes, and lactic acidosis.
16 year-old man who died with linezolid-induced lactic acidosis.
17 mplex II deficiency, were found to have mild lactic acidosis.
18 and serologic evidence of liver failure and lactic acidosis.
19 not been associated with increased rates of lactic acidosis.
20 genase enzyme activity but most did not have lactic acidosis.
21 aired kidney function because of concerns of lactic acidosis.
22 ab work was significant for leukocytosis and lactic acidosis.
23 in was not associated with increased risk of lactic acidosis.
24 vival of cells after exposure to hypoxia and lactic acidosis.
25 lls is abolished by simultaneous exposure to lactic acidosis.
26 ng the origins and treatment of pathological lactic acidosis.
27 nd hyperglycemia, possibly mediated by brain lactic acidosis.
28 e molecule used by sensory neurons to detect lactic acidosis.
29 brain damage during ischemia due to enhanced lactic acidosis.
30 and catecholamines were responsible for the lactic acidosis.
33 ondrial inner membrane to undergo fusion and lactic acidosis after the loss of outer membrane fusion.
34 rine metabolite studies showed hypoglycemia, lactic acidosis, altered Krebs cycle function and dysreg
35 e characterized by fetal growth retardation, lactic acidosis, aminoaciduria, cholestasis, and abnorma
36 An infant presented with fatal infantile lactic acidosis and cardiomyopathy, and was found to hav
37 drome patients in having intermittent severe lactic acidosis and early-onset neurodevelopmental probl
38 ion who were taking stavudine presented with lactic acidosis and elevated levels of aminotransferases
39 Both affected individuals presented with lactic acidosis and evidence of multiple mitochondrial r
40 three families with children suffering from lactic acidosis and hyperpyruvatemia revealed a causal l
42 Q(10) deficiency who presented with neonatal lactic acidosis and later developed multisytem disease i
45 with failure to thrive, developmental delay, lactic acidosis and severe encephalopathy suggestive of
47 en use in five severely septic patients with lactic acidosis and six healthy volunteers before and af
48 ds harboring mitochondrial encephalomyopathy lactic acidosis and stroke A3243G tRNA((Leu)UUR) gene mu
49 her the mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (A3243G MELAS)
50 such as mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) and myo
51 of the mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) phenoty
52 suggestive of mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) syndrom
53 osis (ALS), mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS), dermat
54 romes including mitochondrial encephalopathy lactic acidosis and stroke-like episodes (MELAS), matern
55 tation causing mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS); the tR
57 MELAS (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes) and MIDD syndr
58 Melas (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes) is one of a gr
59 (Mitochondrial Myopathy, Encephalopathy with Lactic Acidosis and Stroke-like episodes) syndrome, the
60 ssociated with mitochondrial encephalopathy, lactic acidosis and stroke-like episodes, but were docum
62 muscle and, therefore, is proposed to detect lactic acidosis and to transduce angina and muscle ische
63 erum fibrinogen, elevated prothrombin time), lactic acidosis, and hepatic steatosis were characterist
65 d Ca accumulation, attenuated sepsis-related lactic acidosis, and improved left ventricular function.
70 hildren present with a fatal encephalopathy, lactic acidosis, and severe mtDNA depletion in muscle.
71 ssociated with a clinical triad of myopathy, lactic acidosis, and sideroblastic anemia in predominant
72 h as mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke (MELAS), neuropathy, ataxia,
73 tient carrying the myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) A3243G
74 the mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) syndro
75 underlying mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndro
78 tion causes mitochondrial encephalomyopathy, lactic acidosis, and stroke-like symptoms (MELAS) and 2%
82 Since Coffin-Lowry syndrome and neonatal lactic acidosis are associated with mutations in the hum
83 ver toxicity, hypersensitivity reactions and lactic acidosis are recognized as acute events with pote
84 a has many manifestations, of which coma and lactic acidosis are the best independent predictors of a
85 opathy, peripheral neuropathy, myopathy, and lactic acidosis associated with deficiencies of multiple
86 who presented with exercise intolerance and lactic acidosis associated with severe deficiency of com
88 at 32 degrees C attenuated the shock-related lactic acidosis but caused metabolic acidosis, most like
89 ndrial toxicity (i.e., neuropathy, myopathy, lactic acidosis), but these side effects are rarely repo
90 fever, tachycardia, oxygen consumption, and lactic acidosis, but it does not prevent the development
92 ever, the dominant theory in the field, that lactic acidosis causes muscle fatigue, is unlikely to te
93 to occur in a variety of diseases including lactic acidosis, Cowden Syndrome, and several cancers.
100 nly has been assumed that the development of lactic acidosis during sepsis results from a deficit in
101 sive myocardial thickening, hyperalaninemia, lactic acidosis, exercise intolerance, and persistent ad
102 were significantly (P < 0.05) protected from lactic acidosis, glutamate buildup, and diminished HCO(3
103 severe neurological dysfunction, congenital lactic acidosis, growth retardation, and early death.
104 ated individuals who presented at birth with lactic acidosis, hypotonia, feeding difficulties, and de
105 al MCT1 may contribute to the development of lactic acidosis in brain pathologies, and suggest target
106 pertaining to metformin, kidney disease, and lactic acidosis in humans between 1950 and June 2014.
111 e patients with severe exercise intolerance, lactic acidosis in the resting state (in four patients),
112 cultures with concurrent vasopressors and/or lactic acidosis increased (P < .001 for all methods), wh
119 , it is known to induce metformin-associated lactic acidosis (MALA), a severe medical condition with
121 ghei malaria, (ii) respiratory distress with lactic acidosis occurs during P. berghei malaria, and (i
122 logies, anaerobic glycolysis produces severe lactic acidosis of brain tissue leading to brain cell da
123 at express ASICs an extra sensitivity to the lactic acidosis of local ischemia compared to acidity ca
124 ith serious metabolic complications, such as lactic acidosis, pancreatitis, and peripheral neuropathy
125 Our findings reveal that the condition of lactic acidosis present in solid tumors inhibits canonic
126 trovirals are well characterized and include lactic acidosis related to nucleoside reverse transcript
128 fection who all presented with severe type B lactic acidosis shortly after starting treatment with om
129 ome (mitochondrial myopathy, encephalopathy, lactic acidosis, stroke-like episodes) is a rare, multis
131 cytochrome c oxidase deficiency and hepatic lactic acidosis that accompanies this disorder is unknow
134 h a clinical spectrum ranging from infantile lactic acidosis to childhood (cardio)myopathy and late-o
135 alpha alpha Hb (n = 6) resulted in hypoxia, lactic acidosis, ventricular arrhythmias, and decreased
138 s associated with hemodynamic depression and lactic acidosis, which appeared (illustrative echocardio
139 mitochondrial myopathy, encephalopathy, and lactic acidosis with stroke-like episodes (MELAS) and Pa
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