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1 dition of oligomycin A, phosphocreatine, and creatine phosphokinase.
2 ach ferredoxin, ovalbumin, and rabbit muscle creatine phosphokinase.
3 ty population in either group were increased creatine phosphokinase (52 [19%] of 269 patients in the
4 ce, and zinc supplementation decreased serum creatine phosphokinase activities and eliminated the dif
7 ns of these factors, which lacked detectable creatine phosphokinase and ATPase activities, creatine p
9 min) induced an elevation in serum levels of creatine phosphokinase and myocardial injury characteriz
10 ick end labeling, (iii) a reduction in serum creatine phosphokinase, and (iv) improved weight gain.
11 rdiac lipid peroxidation, elevation of serum creatine phosphokinase, and functional changes in the is
12 age, disease duration, skin score, levels of creatine phosphokinase, and presence of tendon friction
13 ete blood count and electrolyte, creatinine, creatine phosphokinase, and troponin T levels were norma
15 CKM Glu83Gly (rs11559024) with constitutive creatine phosphokinase (CK) levels, CK variation, and in
16 ffect was an asymptomatic increase in plasma creatine phosphokinase concentration (200 mg, n=5; 400 m
17 ed a transient increase in the muscle enzyme creatine phosphokinase (CPK) 4 weeks after gene transfer
18 eficiency on muscle cells and the release of creatine phosphokinase (CPK) as a sequela of that defici
21 R (EC 1.5.1.3); (ii) transferase activity of creatine phosphokinase (EC 2.7.3.2) and hexokinase (EC 2
22 s treatment-related adverse events occurred (creatine phosphokinase elevation attributed to antilipid
23 (6.8%) and included asthenia, AST elevation, creatine phosphokinase elevation, and decreased appetite
25 treatment is associated with moderate serum creatine phosphokinase elevations in up to 12% of patien
26 3 pravastatin and 7 placebo patients due to creatine phosphokinase elevations; no cases of mild or s
27 and one patient at 20 mg/kg, increased blood creatine phosphokinase in two patients at 20 mg/kg, and
28 in the placebo and vemurafenib group), blood creatine phosphokinase increase (30 [12%] vs one [<1%]),
29 patients: lymphopenia in two patients, blood creatine phosphokinase increase in one patient, aminotra
30 ted the association of elevated troponin and creatine phosphokinase isoenzyme levels with mortality a
31 sthetic effects on extrarenal injury (plasma creatine phosphokinase, lactate dehydrogenase, and hemat
32 two groups (all p > 0.05), whereas the peak creatine phosphokinase level was significantly reduced i
34 ck had lower ejection fractions, higher peak creatine phosphokinase levels (P < .0001), and more dise
35 f three recipients tested had elevated serum creatine phosphokinase levels and detectable serum myogl
38 the development of new pathologic Q waves or creatine phosphokinase-MB isoenzyme elevation >8 x upper
39 e transcripts including muscle mitochondrial creatine phosphokinase, muscle glycogen phosphorylase, h
40 h autoimmune disorder (n=3), increased blood creatine phosphokinase (n=2), and increased aspartate am
41 [11%] in treatment group B), increased blood creatine phosphokinase (one [1%] vs four [4%]), and hypo
42 uch as age, diabetes, smoking history, serum creatine phosphokinase, or electrocardiographic findings
43 infarct size (p < 0.001), cardiac release of creatine phosphokinase (p < 0.001), and apoptotic cell d
45 ction both in myocardial damage, assessed by creatine phosphokinase release, and in endothelial cell
49 dividuals had eye defects or elevated muscle creatine phosphokinase, separating the TMTC3 COB phenoty
50 laboratory values, including increased blood creatine phosphokinase (seven [8%]), increased alanine a
52 ethnicity, skin score, serum creatinine and creatine phosphokinase values, hypothyroidism, and cardi
53 stry appeared to be normal with exception of creatine phosphokinase, which peaked at 7 days after inf
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