In addition, at the beginning of the present study, we expected that skewness or kurtosis would help distinguish the three subgroups like other tumors. However, the distinction was not accomplished with skewness and kurtosis. We presume that the patterns of the histogram graphs of AIS, MIA and invasive adenocarcinoma might vary too much to provide separation among the subgroups. The present study demonstrates that even in patients with invasive adenocarcinoma, for which the median extent of invasion was 9.8 mm, 97.7% had DFS for 5 years. A good prognosis of invasive adenocarcinoma shown as pure GGN may be explained, in part, by the difference in the predominant subtypes. All invasive adenocarcinomas in our study were lepidic, acinar or papillary predominant tumors, which are known to show good prognosis as compared with micropapillary or solid predominant tumors. Travis et al. concluded that all histologic subtypes other than lepidic predominant adenocarcinoma show solid nodules on CT. However, as seen in Fig. 2, well-organized and well-differentiated acinar or papillary predominant adenocarcinomas can also be seen as pure GGNs. Our study was limited inherently by its retrospective design, and we may have had a selection bias. However, we tried to include as many patients as possible for whom the pathologic assessment of the whole tumor was feasible. We also included GGNs with #5mm solid component on CT scans as well as pure GGNs with the insight that the nonmucinous type of MIA can appear as a partsolid nodule consisting of a predominant ground-glass component and a small central solid component measuring 5 mm or less. As a result, we excluded the patients for whom only a small fragment of a tumor was available for diagnosis only or in whom the entire tumor was not available for surgical reasons, and 3 AIS and 8 MIAs having,5 mm solid component could be included for analysis. Another potential limitation is that the pathologic invasive component was evaluated in a subjective manner. Thunnissen et al. assessed the reproducibility of invasion of lung adenocarcinoma among an international group of pulmonary Acetylcorynoline pathologists, and concluded that there is fair reproducibility distinguishing invasive from in-situ patterns. Nevertheless, we tried to reduce inter-observer and intra-observer variability by using virtual microscopy. Recent related studies showed that virtual microscopy is a reliable and more reproducible technology. Also in our study, digital pathology offered a rigorous and reproducible method for quantifying invasive and noninvasive components of histopathology. In conclusion, quantitative analysis of CT imaging metrics can help distinguish invasive adenocarcinoma from pre-invasive or minimally invasive adenocarcinoma shown as GGN with Danshensu little solid component on CT scans. This inflammatory phenotype was also seen in murine models overexpressing IL-36a in basal keratinocytes which develop age-dependent inflammatory skin lesions with features of human psoriasis like acanthosis, hyperkeratosis, inflammatory cell infiltrates and enhanced cytokine production. In this mouse model, IL-36a enhances the production of proinflammatory cytokines IL-17A, IL-23p19 and TNF-a in skin inflammation, cytokines which are also involved in rheumatoid arthritis. The blockade of TNF-a or IL-23p19 diminished clinical signs like epidermal thickness, inflammation and cytokine production. In addition, an induction of IL-36 cytokines in IL-17A and TNF-a stimulated primary human keratinocytes.