Background: Accurate thymoma staging via computed tomography (CT) images is difficult even for experienced thoracic doctors. Here we developed a preoperative staging tool differentiating Masaoka-Koga (MK) stage I patients from stage II patients using CT images. Methods: CT images of 174 thymoma patients were retrospectively selected. Two chest radiologists independently assessed the images. Variables with statistical differences in univariate analysis were adjusted for age, sex, and smoking history in multivariate logical regression to determine independent predictors of the thymoma stage. We established a deep learning (DL) 3D-DenseNet model to distinguish the MK stage I and stage II thymomas. Furthermore, we compared two different methods to label the regions of interest (ROI) in CT images. Results: In routine CT images, there were statistical differences (P<0.05) in contour, necrosis, cystic components, and the degree of enhancement between stage I and II disease. Multivariate logical regression showed that only the degree of enhancement was an independent predictor of the thymoma stage. The area under the receiver operating characteristic curve (AUC) of routine CT images for classifying thymoma as MK stage I or II was low (AUC =0.639). The AUC of the 3D-DenseNet model showed better performance with a higher AUC (0.773). ROIs outlined by segmentation labels performed better (AUC =0.773) than those outlined by bounding box labels (AUC =0.722). Conclusions: Our DL 3D-DenseNet may aid thymoma stage classification, which may ultimately guide surgical treatment and improve outcomes. Compared with conventional methods, this approach provides improved staging accuracy. Moreover, ROIs labeled by segmentation is more recommendable when the sample size is limited.

Background: Cemented or uncemented total hip replacement (CTR or UTR) for femoral neck fractures (AO/OTA type 31B/C) is a relatively common procedure in elderly individuals. The recent literature is limited regarding long-term outcomes following CTR versus UTR in the Asian population. Methods: Using our institutional database, we performed long-term outcome analysis on 268 patients with femoral neck fractures (AO/OTA type 31B/C) who had undergone a primary UTR or CTR (CTR: n = 132, mean age, 67.43 ± 6.51 years; UTR: n = 136, mean age, 67.65 ± 6.13 years) during 2007–2014, and these patients were followed until 2019. Follow-up occurred 1, 3, 6, and 12 months postoperatively and yearly thereafter. The primary endpoint was the Harris hip score (HHS); the secondary endpoint was the incidence of orthopaedic complications. Results: The mean follow-up time was 62.5 months (range, 50.1–76.1 months). At the final follow-up, the HHS was 79.39 ± 16.92 vs 74.18 ± 17.55 (CTR vs UTR, respectively, p = 0.011). Between-group significant differences were observed regarding the incidence of prosthesis revision, prosthesis loosening, and periprosthetic fracture (7.6% [95% CI, 6.4–8.2] for CTR vs 16.9% [95% CI, 14.7–17.3] for UTR, p = 0.020; 9.8% [95% CI, 8.3–10.7] for CTR vs 19.9% [95% CI, 18.2–20.9] for UTR, p = 0.022; 5.3% [95% CI, 4.4–6.7] for CTR vs 13.2% [95% CI, 12.1–13.8] for UTR, p = 0.026, respectively). Conclusion: CTR showed superiority to UTR by improving the HHS and decreasing the incidence of orthopaedic complications. Our findings need to be confirmed in a prospective, randomized controlled study to verify whether they can be applicable to a broader population.

Lung adenocarcinoma (LUAD) remains one of the leading causes of death in patients with cancer. The association of CD155 with CD96 transmits an inhibitory signal and suppresses antitumor immune response. This study investigates the effect of CD155/CD96 on immune suppression in LUAD. We demonstrate that LUAD patients with high CD155 expression suffer from immune suppression and experience a poor prognosis, which coincides with an inhibited AKT-mTOR signaling pathway in CD8 T cells and subsequently up-regulated CD96 expression. Moreover, the inhibition effect can be reversed by CD96 blocking antibody. High CD155 expression inhibited the release of IFNγ from CD8 cells. Moreover, Blocking CD96 restored IFNγ production in CD8 T cells and neutralized the inhibition of IFNγ production in CD8 T cells mediated by CD155. Animal experiments showed that CD155-mediated LUAD growth might depend on its suppression antitumor immune response in the tumor microenvironment in PDX mice. In conclusion, our results suggest that LUAD cells suppress antitumor immune response in the tumor microenvironment through CD155/CD96. CD155/CD96 could be a potential therapeutic target for LUAD patients. Abbreviations: LUAD: lung adenocarcinoma; IFNγ: interferon gamma; PDX: patient-derived xenograft; NSCLC: non-small cell lung cancer; PRR: poliovirus receptor–related; MDSCs: myeloid-derived suppressor cells; PRR: poliovirus receptor–related; STR: short tandem repeat; IRS: immunoreactive score; SI: staining intensity; PP: percentage of positive cells; RT-PCR: reverse transcription-polymerase chain reaction; PBS: phosphate-buffered saline; PBMCs: peripheral blood mononuclear cells; SDS–PAGE: sodium dodecyl sulfate-polyacrylamide gel electrophoresis; rCD155: recombinant human CD155; LUAD cells: lung adenocarcinoma cells; TILs: tumor-infiltrating lymphocytes; GzmB: granzyme B; IL-2 (Interleukin-2); TNF-α : tumor necrosis factor-alpha; PI: propidium Iodide; PDX: patient-derived xenograft; TIGIT: T cell immunoreceptor with Igand ITIM domains; WBC: white blood cells; MFI: mean fluorescence intensity; HPF: high power field