The nano-artificial periosteum made of PCL/MgO/AS-IV enhances MC3T3-E1 cell osteogenic differentiation and promotes bone defect repair via the EphB4/EphrinB2 signaling pathway.

Bone regeneration plays a pivotal role in periodontal tissue repair. With advancements in biotechnology materials, the utilization of nanotechnology offers a reliable platform for bone restoration in periodontitis. In this study, we successfully established a long-term bacterial infection model using Porphyromonas gingivalis (P. gingivalis) with MOI = 50. CCK-8 and ROS immunofluorescence results demonstrated that the combined effect of Mg2+ and AS-IV significantly enhanced cell proliferation and effectively suppressed the inflammatory response during bacterial infection. Alkaline phosphatase and alizarin red staining revealed that the synergistic action of Mg2+ and AS-IV notably promoted osteogenic differentiation of MC3T3-E1 cells under P. gingivalis-infected conditions. Considering the properties of these two biomaterials, we fabricated polycaprolactone (PCL) artificial periosteum loaded with MgO and AS-IV using an electrostatic spinning technique. The findings indicated that PCL/MgO/AS-IV artificial periosteum exhibited excellent biocompatibility and hydrophilicity, thereby substantially enhancing cellular adhesion to its surface as well as augmenting cellular value-added rate. Moreover, efficient drug release from the PCL/MgO/AS-IV artificial bone membrane conferred remarkable antimicrobial activity along with in vitro osteogenic potentiality. The in vivo experiments conducted on animals further substantiated the exceptional properties exhibited by PCL/MgO/AS-IV artificial periosteum in bone defect repair. Additionally, it was observed that PCL/MgO/AS-IV artificial periosteum could modulate EphB4-EphrinB2 signaling to enhance osteogenic differentiation under P.gingivalis-infected conditions.This exciting outcome suggests that PCL/MgO/AS-IV artificial periosteum holds great promise as a biomaterial for treating periodontal bone loss.

Reliability and validity of the Chinese version of the Nutritional Form For the Elderly.

OBJECTIVE: The present study aimed to translate the English version of the Nutritional Form For the Elderly into Simplified Chinese, as well as to test the reliability (homogeneity and stability) and validity (content and construct validity) of the Chinese version of the Nutritional Form For the Elderly (NUFFE-CHI). DESIGN: The study adopted a cross-sectional design. The English version of the NUFFE was translated into Simplified Chinese and a questionnaire survey was conducted. The data were analysed with statistical methods to estimate the homogeneity, stability, content and construct validity. SETTING: Jinzhou City, China. SUBJECTS: A total number of 701 community-dwelling older adults answered the questionnaire, including background variables and the NUFFE-CHI. A small group of the participants (n 50) completed the NUFFE-CHI twice for test-retest reliability. RESULTS: Cronbach's α was 0·65 and the split-half reliability was 0·67. Item-to-total correlation analyses showed that the scale has sufficient internal consistency. The test-retest reliability regarding the total scores of NUFFE-CHI was reflected in an intra-class correlation coefficient of 0·88. The intra-class correlation coefficients between the test and retest of the NUFFE-CHI items varied between 0·43 and 0·98. A content validity index of 0·83 explained good content validity. Construct validity was demonstrated in an exploratory factor analysis with a six-factor solution, explaining 57·65 % of the variance. CONCLUSIONS: This first testing of the NUFFE-CHI indicates sufficient evidence for reliability, content and construct validity. Further testing studies regarding homogeneity, concurrent validity, sensitivity and specificity are required before the NUFFE-CHI can be used as a screening instrument in clinical settings and in research.

Silencing of the glypican-3 gene affects the biological behavior of human hepatocellular carcinoma cells.

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer death in the world. The gene glypican-3 (GPC3) is reported to be a potential therapeutic target for HCC. In this study, we use RNA interference with lentiviral vectors to explore the effect of GPC3 silencing on the biological behavior of HCC cells and the potential role of the GPC3 protein in the activation of epithelial-mesenchymal transition (EMT), which relates to HCC cell invasion and migration. Our data suggest that GPC3 silencing leads to a decrease in HCC cell proliferation and to an increase in apoptosis. We demonstrated that GPC3 silencing regulates cell invasion and migration, most probably through the activation of the EMT cellular program. In conclusion, GPC3 is associated with the HCC cell biological behavior, while the relationship between GPC3 and EMT in tumorigenesis of HCC deserves future investigation.

Effects of bortezomib in sensitizing human prostate cancer cell lines to NK-mediated cytotoxicity.

The proteasome inhibitor, bortezomib, has been demonstrated to sensitize tumor cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis. Natural killer (NK) cells represent potent antitumor effector cells. They also express TRAIL. Therefore, we investigated whether bortezomib could sensitize tumor cells to NK cell-mediated killing, and have the same effect in human prostate cancer cell lines (LNCaP and DU145). We found that bortezomib strongly inhibits proliferation in both cell lines. Furthermore, compared with LNCaP cells, DU145 cells are more sensitive to bortezomib-induced apoptosis. However, bortezomib is unable to sensitize these two cell lines to NK cell-mediated killing in short-term assays. In long-term assays, we found that killing mediated by activated NK cells following bortezomib treatment leads to greater antitumor effects than either treatment alone. In addition, treatment with bortezomib causes these cells to upregulate apoptosis-related mRNA as well as death receptors and downregulate the major histocompatibility class (MHC)-I molecule on the cell surface of DU145 cells. In contrast, LNCaP cells are not sensitized by this treatment. Death receptors and the MHC-I molecule did not change in this cell line. These data suggest that bortezomib can be used to sensitize prostate cancer cells to NK cell-mediated killing and improve current cancer therapies. This therapeutic strategy may be more effective in patients with androgen-insensitive prostate cancer.