Evaluation of full thread screw and different fixation configurations in Pauwels type III femoral neck fracture.

Objectives: The purpose of this study is to evaluate the value of full thread screw and different fixation configurations in Pauwels type III femoral neck fracture. Methods: A total of 40 artificial femoral model specimens were chosen, and Pauwels type III femoral neck fracture was simulated upon osteotomy at 80°. According to random number table, models were divided into four groups (10 cases in each group): Group A received the paralleled fixation with three partial thread screws (PTSs), group B received the crossed fixation with three PTSs, group C received the paralleled fixation with two full thread screws (FTSs) and one PTS, and group D received the crossed fixation with two FTSs and one PTS. Changes including the model rigidity, axial displacement in fatigue test and limit loads for Pauwels type III femoral neck fracture models were analyzed through MTS 858 Mini Bionix Ⅱ test system. Results: Among four groups, the model rigidity, axial displacement in fatigue test and limit loads were the highest in group D, and they were the lowest in group A. However, the model rigidity, axial displacement in fatigue test and limit loads between group B and group C showed no statistically significant difference (P＞0.05). Eventually, all the specimens were displaced along the fracture lines while the femoral head was split at varying degrees. After splits, the removal rate of fixation screws in group A (60.0 %) and group C (40.0 %) was significantly higher than that of group B (10.0 %) and group D (0 %) (P＜0.05), but it showed no statistically significant difference between group A and group C, and between group B and group D (P＞0.05). Conclusions: The crossed fixation configuration with two FTSs and one PTS in group D is proven to be more effective, which can go against the shear stress, tension and introversion in Pauwels type III femoral neck fracture models.

Controllable Synthesis, Formation Mechanism, and Photocatalytic Activity of Tellurium with Various Nanostructures.

Telluriums (Te) with various nanostructures, including particles, wires, and sheets, are controllably synthesized by adjusting the content of polyvinylpyrrolidone (PVP) in a facile solvothermal reaction. Te nanostructures all have complete grain sizes with excellent crystallinity and mesopore structures. Further, the formation mechanisms of Te nanostructures are proposed to be that the primary nuclei of Te are released from the reduction of TeO32- using N2H4·H2O, and then grow into various nanostructures depending on the different content of PVP. These nanostructures of Te all exhibit the photocatalytic activities for the degradation of MB and H2 production under visible light irradiation, especially Te nanosheets, which have the highest efficiencies of degradation (99.8%) and mineralization (65.5%) at 120 min. In addition, compared with pure Te nanosheets, the rate of H2 production increases from 412 to 795 µmol∙h-1∙g-1 after the introduction of Pt, which increases the output by nearly two times. The above investigations indicate that Te with various nanostructures is a potential photocatalyst in the field of degradation of organic pollutants and H2 fuel cells.

CircRNA PTPRM Promotes Non-Small Cell Lung Cancer Progression by Modulating the miR-139-5p/SETD5 Axis.

Introduction: Circular RNAs (circRNAs) are important regulators in various cancers, especially hepatocellular carcinoma. However, the role of circ RNA PTPRM (circPTPRM) in the development of non-small-cell lung cancer (NSCLC) remains unclear. Methods: We collected 26 clinical specimens (corresponding to 26 normal lung tissues) of lung adenocarcinoma and the expression of mir-139-5p and circPTPRM were first detected. Cell proliferation was detected by EdU method, invasion/migration ability of cells was evaluated by transwell method. And the correlation between circPTPRM and mir-139-5p was detected by luciferase reporter gene and RNA pull-down assay. Finally, we verified our hypothesis with BALB/c nude mice. Results: Through bioinformatics software, we found that circPTPRM was negatively correlated with mir-139-5p, and then we used human adenocarcinoma tissue samples to further verify their relationship and get the same result. EdU method, transwell method, and luciferase assay, RNA pull-down assay were applied, and the results show that the knockdown of circPTPRM inhibit proliferation, migration, and invasion of cells can be reversed by mir-139-5p inhibitor. Next, we used Starbase v2.0 to identify the target site of miR-139-5p and focused on SET domain containing 5 (SETD5). We derive the hypothesis by verifying the relationship between miR-139-5p and SETD5 that circPTPRM may interact with miR-139-5p/SETD5 axis. At last, we evaluated the effects of circPTPRM, SETD5, and miR-139-5p on tumor growth in vivo using BALB/c nude mice to prove the hypothesis. Conclusion: We thus conclude that circPTPRM promotes the progression of NSCLC by regulating the miR-139-5p/SETD5 axis.

Osteoporosis in patients with rheumatoid arthritis is associated with serum immune regulatory cellular factors.

OBJECTIVE: Osteoporosis (OP) is a comorbidity of rheumatoid arthritis (RA) that largely causes disability. This study discussed the expression patterns of serum immunoregulatory factors and their clinical significance in RA patients complicated with OP. METHODS: A total of 116 RA patients were enrolled. Bone mineral density (BMD) was measured using dual energy X-ray absorptiometry to allocate patients to OP group (N = 62) and non-OP group (N = 54). CRP, rheumatoid factor, IgG, IgA, and IgM were detected using rate nephelometry. Erythrocyte sedimentation rate (ESR) and bone metabolic indexes were detected using Microsed automatic ESR analyzer and Cobas e601 automated immunoassay systems and reagents. IL-17, IL-6, TNF-α, IL-10, and IL-4 levels were determined using ELISA kit and their prediction values on OP were analyzed using the ROC curve. Influencing factors of OP incidence were analyzed using logistic regression model. RESULTS: RA patients with OP showed increased age, disease course, tender and swollen joints, ESR, CRP, DAS28 scores, ß-CTX, IL-17, IL-6, and TNF-α, and decreased 25(OH)D3, IL-10, and IL-4. DAS28 was positively correlated with IL-17, IL-6, and TNF-α, and negatively correlated with IL-10 and IL-4. DAS28, IL-17, IL-10, and IL-4 were independently correlated with OP in RA patients. The combination of DAS28, IL-17, IL-10, and IL-4 can better predict the incidence of OP complication in RA patients. CONCLUSION: IL-17, IL-6, TNF-α, IL-10, and IL-4 were associated with disease activity of RA patients complicated with OP. A combination of DAS28, IL-17, IL-10, and IL-4 might predict OP incidence in RA patients.

Long non-coding RNA LINC00265 promotes proliferation, apoptosis, and inflammation of chondrocytes in osteoarthritis by sponging miR-101-3p.

Long non-coding RNAs (lncRNAs) play a part in a wide variety of diseases, including osteoarthritis (OA). This study was designed to investigate the biological role of lncRNA LINC00265 in OA and its underlying mechanisms. We examined the levels of LINC00265 and miR-101-3p using RT-qPCR, inflammatory factors using ELISA, and caspase-3, c-caspase-3, Bcl-2, Bax, and MMP-13 levels using Western blot in normal and OA chondrocytes, analysed the relationship between LINC00265 and miR-101-3p using bioinformatics analysis and luciferase reporter assays, performed loss- and gain-of-function analyses. The results showed that (1) LINC00265 expression was increased in OA chondrocytes, (2) si-LINC00265 inhibited OA chondrocyte apoptosis and inflammation, and (3) LINC00265 overexpression promoted normal and OA chondrocyte apoptosis and inflammation. Furthermore, we predicted and confirmed that miR-101-3p was a target of LINC00265. LINC00265 negatively regulated miR-101-3p in OA chondrocytes and LINC00265 promoted OA and normal chondrocyte apoptosis via miR-101-3p. Overall, lncRNA LINC00265 regulates chondrocyte apoptosis by acting as a sponge of miR-101-3p in OA.

MicroRNA-140-5p represses chondrocyte pyroptosis and relieves cartilage injury in osteoarthritis by inhibiting cathepsin B/Nod-like receptor protein 3.

Osteoarthritis (OA) is a degenerative joint disease. Dysregulated microRNA (miRNA) expressions are implicated in OA progression. Consequently, the current study set out to investigate the mechanism of miR-140-5p in OA cartilage injury. Firstly, the murine and cell models of OA were established, and cartilage tissues of OA mice were observed using hematoxylin and eosin staining and safranin O staining. Chondrocyte pyroptosis was further assessed using immunohistochemical and Calcein-AM/PI staining. The levels of gasdermin-D (GSDMD)-N, cleaved caspase-1, interleukin (IL)-1ß, and IL-18 in cartilage tissues and cells were determined using Western blot and enzyme-linked immunosorbent assay kits. The targeting relationship between miR-140-5p and cathepsin B (CTSB) was verified using a dual-luciferase assay. Moreover, the binding of CTSB and Nod-like receptor protein 3 (NLRP3) was detected using co-immunoprecipitation assay. Lastly, the effects of NLRP3 activation and CTSB overexpression on chondrocyte pyroptosis were documented. It was found that OA induction aggravated cartilage tissue injury and enhanced chondrocyte pyroptosis. miR-140-5p was poorly-expressed in OA models, and miR-140-5p over-expression alleviated chondrocyte pyroptosis, as evidenced by decreased GSDMD-N, cleaved caspase-1, IL-1ß, and IL-18 levels. miR-140-5p targeted the CTSB gene, whereas CTSB further bound to NLRP3 and activated the NLRP3 inflammasome. Additionally, CTSB over-expression or NLRP3 activation reversed the inhibitory effect of miR-140-5p on chondrocyte pyroptosis. Collectively, our findings revealed that miR-140-5p repressed chondrocyte pyroptosis and alleviated OA cartilage injury via inhibition of the CTSB/NLRP3. This study may confer a theoretical basis for the treatment of OA cartilage injury.

Identification of Key Gene Signatures Associated With Bone Metastasis in Castration-Resistant Prostate Cancer Using Co-Expression Analysis.

About 80-90% of castration-resistant prostate cancer (CRPC) patients would develop bone metastasis. However, the molecular mechanisms of bone metastasis are still not clear. This study aimed to detect the differences between the tumor and normal samples in bone after metastatic colonization. Four transcriptional datasets (GSE32269, GSE101607, GSE29650, and GSE74685) were obtained from the GEO database. 1983 differentially expressed genes (DEGs) were first identified between tumor and normal marrow samples in GSE32269. Most of the top 10 up-regulated DEGs are related with prostate cancer, and the top 10 down-regulated DEGs are mainly related with bone development. Seven co-expression modules were then detected based on the 1469 DEGs shared by the four datasets. Three of them were found highly preserved among the four datasets. Enrichment analysis showed that the three modules were respectively enriched in Cell adhesion molecules (CAMs), Leukocyte transendothelial migration and cell cycle, which might play significantly important roles in the tumor development in bone marrow. Ten, 17, and 99 hub genes for each module were then identified. And four genes (C3AR1, IL10RA, LY86, and MS4A6A) were detect to be tightly related to progression of bone metastatic CRPC. ROC curve was plotted and AUC was calculated to distinguish tumor and normal bone marrow samples as well as bone and non-bone metastatic CRPCs. The present study identified key genes and modules involved in bone metastatic CRPCs, which may provide new insights and biomarkers for understanding of the molecular mechanisms of bone metastatic CRPC.