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A high frequency of MetS has previously been reported in RA patients [ 59- 61].
There were significant differences of frequency of MetS according to residence, educational level, occupation, smoking, and nutrition status.
G-allele carriers have also been reported to have reduced frequency of MetS and the subsequent IL-18 levels were suggested to be of genetic origin [ 32].
The frequency of low HDL-c was significantly higher in CAD patients (P < 0.05), while the frequency of MetS and other components of MetS showed no difference between the CAD and non-CAD groups (all P > 0.05).
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We found that DDM group carried a higher frequency of Met allele (53.9%).
However, few studies have assessed the frequency of MET mutations in primary breast cancer.
Although the frequency of MET amplification in cases of EGFR-TKI resistance was initially reported to be 20% [ 7], this has varied by approximately 5 11% in follow-up studies [ 6, 14, 19].
Interestingly, in a recent report a higher frequency of MET gene copy number elevations was observed in TNBC compared with other breast cancer subtypes, which is in line with our findings (Gonzalez-Angulo et al, 2012).
Firstly, the average Met frequency in the set of proteins containing oxidised Met is 0.027 as compared to the other amino acids (AA) in the complete proteome where it is 0.025 [ 25], and hence is nearly the same; we also noted that none of the 50 Arabidopsis proteins with the highest frequency of Met occurrence (0.09) contained any oxidised Met residues.
The frequencies of Met-BDNF genotype (G/G vs. G/A or A/A) were not different between ON, MCI, and AD subjects (Fisher's Exact Test p = 0.36).
DDM group carried the highest frequencies of Met allele (53.9%) compared to HC group (39.3%) and NDDM group (38.8%).
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