ular distribution of the proteins, but found out no correlation between them. Instead, the staining intensity shows a strong correlation with EGFR mutation status. Therefore, the staining of “the membrane and/or cytoplasm” was equally and jointly considered in our scoring system. The high activity of EGFR protein in lung cancer is due to the activation mutations, but the gene amplifications may also play a significant role. In this study, 334/399 cases of NSCLC were demonstrated to have elevated expression of EGFR protein by using monoclonal antibody, the rate much higher than standard detection at genetic level. It remains to be further investigated if this elevated expression of EGFR in some cases without detectable mutations is mediated by ampification of its gene or other alternative mechanisms. Whether or not the TKIs can be empirically applied to these patients needs to be verified by additional experimental studies and clinical trials. In summary, according to our analyses of EGFR mutation status by IHC, patients with a score of 3+ had a perfect PPV, and may accept the TKI treatment directly without need for a confirmatory molecular-based assay. Patients with a score of 0 had a high NPV. However, samples with 
score 1+ or 2+ are unreliable and need further verification of EGFR mutation status by molecular-based assay. Therefore, by using our diagnostic algorithm, in nearly half of all patients, an applicability of TKI therapy could be determined by immunohistochemistry and more complex, expensive molecular test be avoided. Samples with score 0 in IHC-based assay with the two EGFR mutation-specific antibodies should be The New Algorithm Detecting EGFR Status by IHC further tested for expression of total EGFR using EGFR monoclonal antibody, in order to further reduce the false negative rate. Take together, compared with using IHC-based assay alone, this integrated approach combining IHCand molecular-based assays demonstrates a higher sensitivity, specificity and k value,and is thus more practical for the patients screened for a possible TKI therapy. Our diagnostic algorithm may potentially optimize therapeutic options, reduce costs and save time. were undetectable with mutation-specific antibodies in certain cases, even though the mutations were identified 16678548 by molecular-based assay in the cases. ~~ Microbial translocation has been described as associated with chronic inflammation in both HIV-infected and hepatitis -infected patients. The mechanism of microbial translocation is positively correlated with the level of the bacterial product, lipopolysaccharide, and is indirectly reflected by the presence of soluble CD14, a plasma biomarker of monocyte/macrophage activation. In HIV-infected patients, several studies reported that high sCD14 plasma levels predict disease progression and are positively correlated with all-cause mortality. Higher levels of the inflammatory biomarkers, C-reactive protein and interleukine-6, have been also previously associated with an increased risk of mortality or opportunistic diseases in large PF-562271 randomized clinical trials. Similarly, the role of sCD14 has been reported 23446639 in patients infected with HBV or HCV, as well as an association between high sCD14 plasma levels and cirrhosis; thus, the presence of sCD14 can predict progression to end-stage liver disease. However, there are scarce data on the role and predictive value in the development of liver fibrosis of inflammatory biomarkers as high-sensitivity CRP