Background: To explore whether radiomics combined with computed tomography (CT) images can be used to establish a model for differentiating high grade (International Society of Urological Pathology [ISUP] grade III–IV) from low-grade (ISUP I–II) clear cell renal cell carcinoma (ccRCC). Methods: For this retrospective study, 3-phase contrast-enhanced CT images were collected from 227 patients with pathologically confirmed ISUP-grade ccRCC (155 cases in the low-grade group and 72 cases in the high-grade group). First, we delineated the largest dimension of the tumor in the corticomedullary and nephrographic CT images to obtain the region of interest. Second, variance selection, single variable selection, and the least absolute shrinkage and selection operator were used to select features in the corticomedullary phase, nephrographic phase, and 2-phase union samples, respectively. Finally, a model was constructed using the optimal features, and the receiver operating characteristic curve and area under the curve (AUC) were used to evaluate the predictive performance of the features in the training and validation queues. A Z test was employed to compare the differences in AUC values. Results: The support vector machine (SVM) model constructed using the screening features for the 2-stage joint samples can effectively distinguish between high- and low-grade ccRCC, and obtained the highest prediction accuracy. Its AUC values in the training queue and the validation queue were 0.88 and 0.91, respectively. The results of the Z test showed that the differences between the 3 groups were not statistically significant. Conclusion: The SVM model constructed by CT-based radiomic features can effectively identify the ISUP grades of ccRCC.

Background Osteosarcoma, a common primary malignant tumor, occurs in children and adolescents with a poor prognosis. The current treatment methods are various, while the five‐year survival rate of patients has not been significantly improved. As a member of the programmed death factor (PDCD) family, programmed death factor 10 (PDCD10) plays a role in regulating cell apoptosis. Several studies of PDCD10 in CCM and cancers have been reported before. However, there are no relevant research reports on the effects of PDCD10 on osteosarcoma. Methods We used bioinformatics analysis, IHC, and clinical data to confirm the expression of PDCD10 and its correlation with prognosis in osteosarcoma. Then, we used shRNAs and cDNA to knock down or overexpress PDCD10 in U2OS and MG63 cell lines. A series of function assays such as CCK8, Wound healing test, Plate cloning formation assay, and Transwell were done to confirm how PDCD10 affects osteosarcoma. Animal assays were done to confirm the conclusions in cell lines. At last, WB was used to measure the protein expression levels of apoptosis and the EMT pathway. Results PDCD10 was highly expressed in patients with osteosarcoma and correlated with prognosis; PDCD10 knockdown inhibited osteosarcoma growth, proliferation, migration, and invasion; PDCD10 overexpression promoted osteosarcoma growth, proliferation, migration, and invasion. In vivo experiments confirmed the conclusions in cell lines; PDCD10 inhibited apoptosis and activated the EMT pathway. Conclusions In this study, it was found that PDCD10 was highly expressed in patients with osteosarcoma, and it was closely related to patient prognosis. PDCD10 inhibited tumor cell apoptosis and promoted tumor progression by activating the EMT pathway. These findings may provide a potential target for gene therapy of osteosarcoma.

Background: Although several effective therapies are available for the treatment of postmenopausal osteoporosis (PMO), the most common type of primary osteoporosis (OP). More effective and acceptable drugs to cure postmenopausal osteoporosis were needed. NaHS, the donor of H2S, may be one of the drugs to treat PMO, but its role and mechanism are still unclear. Methods：Ovariectomized mice and Sham operation mice, BMMs and RAW264.7 cell lines were used to illustrate the in vivo and in vitro effects of NaHS on the osteoclast differentiation. On the other hand, molecular and histological methods were applied to evaluate the osteoclast differentiation and investigate the in vivo and in vitro mechanism. Results: Phenotypically, NaHS treatment can increase the bone mineral density and bone quality of osteoporosis models induced by ovariectomy (OVX) in mice. Mechanistically, NaHS inhibited the nuclear translocation of p65 by inhibiting the ubiquitination and proteasome degradation of IkB-α. Conclusions: NaHS protects against OVX-induced bone loss by inhibiting osteoclastic bone resorption. It plays an important role in inhibiting osteoclast differentiation and protecting against bone loss in PMO and it is potential for preventing and treating PMO.