Research progress on black phosphorus hybrids hydrogel platforms for biomedical applications.

Hydrogels, also known as three-dimensional, flexible, and polymer networks, are composed of natural and/or synthetic polymers with exceptional properties such as hydrophilicity, biocompatibility, biofunctionality, and elasticity. Researchers in biomedicine, biosensing, pharmaceuticals, energy and environment, agriculture, and cosmetics are interested in hydrogels. Hydrogels have limited adaptability for complicated biological information transfer in biomedical applications due to their lack of electrical conductivity and low mechanical strength, despite significant advances in the development and use of hydrogels. The nano-filler-hydrogel hybrid system based on supramolecular interaction between host and guest has emerged as one of the potential solutions to the aforementioned issues. Black phosphorus, as one of the representatives of novel two-dimensional materials, has gained a great deal of interest in recent years owing to its exceptional physical and chemical properties, among other nanoscale fillers. However, a few numbers of publications have elaborated on the scientific development of black phosphorus hybrid hydrogels extensively. In this review, this review thus summarized the benefits of black phosphorus hybrid hydrogels and highlighted the most recent biological uses of black phosphorus hybrid hydrogels. Finally, the difficulties and future possibilities of the development of black phosphorus hybrid hydrogels are reviewed in an effort to serve as a guide for the application and manufacture of black phosphorus -based hydrogels. Recent applications of black phosphorus hybrid hydrogels in biomedicine.

Bone marrow mesenchymal stem cells could reduce the toxic effects of hexavalent chromium on the liver by decreasing endoplasmic reticulum stress-mediated apoptosis via SIRT1/HIF-1α signaling pathway in rats.

This study focused on the effect of bone marrow mesenchymal stem cells (BMSCs) on the repair of rat liver injury induced by Cr (VI). Twenty-four Wistar rats were randomly divided into the control, model and cell therapy group, with 8 rats in each group. Potassium dichromate solution containing 0, 0.4 and 0.4 mg/kg·bw Cr (VI) was administered 5 times a week for 30 days. At the end of treatment, rats in the cell therapy group were administered 1 × 107 BMSCs. Two weeks later, serum alanine and aspartate aminotransferase levels in the cell therapy group were significantly improved compared with those in the model group, CM-Dil-labeled BMSCs were localized in rat livers. Compared with the model group, in the cell therapy group the number of apoptotic hepatocytes by TUNEL assay, MDA content, the expression of HIF-1α, endoplasmic reticulum (ER) stress-mediated apoptosis-related proteins including Grp78, CHOP, Cleaved-Caspase-12, ATF6, and Bax was significantly lower, and SOD activity, the expression of SIRT1 and Bcl-2 was significantly higher. It is suggested that BMSCs are localized in livers and reduce the toxic effects of Cr (VI) on the liver, and the possible mechanism may be related to the mechanisms of BMSCs decreasing ER stress-mediated hepatocyte apoptosis via the SIRT1/HIF-1α signaling pathway.

The efficacy of oral versus intravenous tranexamic acid in reducing blood loss after primary total knee and hip arthroplasty: A meta-analysis.

BACKGROUND: Blood management after arthroplasties has become a serious problem. The objective is to perform a meta-analysis to compare the efficacy and safety between oral tranexamic acid (TXA) and intravenous TXA for blood management in total knee and hip arthroplasty. METHODS: We systematically searched randomized controlled trials (RCTs) from Medline, Embase, and the Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science and Google scholar. Eligibility criteria: Patients: adult patients with end-stage joint osteoarthritis, rheumatoid arthritis, and osteonecrosis of the femoral head, who prepared for TJA; Interventions: The experiential group received the intravenous form of TXA; Comparisons: Oral form of TXA; Outcomes: Total blood loss, hemoglobin reduction, transfusion requirements, duration of hospitalization, and thrombotic complications including deep vein thrombosis (DVT) and pulmonary embolism (PE); Study design: Randomized control trials (RCTs) and non-RCT. Meta-analysis results were collected and analyzed by the software STATA 11.0. After testing for heterogeneity between studies, data were aggregated for random-effects models when necessary. RESULTS: Four RCTs and 2 non-RCTs were included in the meta-analysis. The present meta-analysis revealed that there were no significant differences regarding total blood loss (WMD = -25.013, 95% CI: -51.002 to 0.977, P = .059), postoperative hemoglobin decline (WMD = -0.090, 95% CI: -0.205 to 0.024, P = .122), or transfusion rate (RD = -0.039, 95% CI: -0.080 to 0.002, P = .062) between the 2 groups. CONCLUSION: Oral TXA shows comparable efficacy to that of the intravenous forms after total knee and hip arthroplasty. Due to the limited quality of evidence currently available, higher quality RCTs is necessary.

Knockdown of ANRIL aggravates H2O2-induced injury in PC-12 cells by targeting microRNA-125a.

Spinal cord injury (SCI) is a devastating and common neurological disorder which causes local oxidative damage. The study aimed to investigate the underlying role of ANRIL in H2O2-induced cell injury of rat PC-12 cells. Cell injury was evaluated on the basis of cell viability, migration, invasion and apoptosis. The effect of ANRIL on H2O2-induced cell injury was estimated after cell transfection. Then, the interaction between ANRIL and miR-125a was explored by qRT-PCR and estimation of cell injury. Predicted by TargetScan, the possible target gene of miR-125a was verified. After that, the effects of aberrantly expressed target gene on cell viability, migration, invasion and apoptosis as well as phosphorylation of key kinases involved in JAK/STAT and ERK/MAPK pathways were evaluated. Results revealed that H2O2-induced PC-12 cell injury could be aggravated by ANRIL suppression. ANRIL appeared to act as a sponge of miR-125a, and ANRIL suppression promoted H2O2-induced cell injury by up-regulation of miR-125a. MCL-1 was a target of miR-125a, and MCL-1 was negatively correlated with miR-125a. Subsequent experiments showed the effect of MCL-1 silence on H2O2-induced PC-12 cell injury was the same as ANIRL suppression. MCL-1 attenuated H2O2-induced PC-12 cell injury by activating JAK/STAT and ERK/MAPK pathways. These findings suggested that knockdown of ANRIL aggravates H2O2-induced injury in PC-12 cells by targeting miR-125a. This might provide novel insights in the role of ANRIL in pathogenesis of oxidative damage during SCI.

Enhanced antitumor immunity is elicited by adenovirus-mediated gene transfer of CCL21 and IL-15 in murine colon carcinomas.

The chemokine CCL21 is a potent chemoattractant for T cells and dendritic cells. IL-15 elicits powerful antitumor immune responses through the stimulation of natural killer cells. We constructed a CCL21/IL-15-expressing adenovirus (Ad-CCL21-IL-15) and evaluated its antitumor effects in vitro and in vivo. We found that the intratumoral injection of Ad-CCL21-IL-15 into murine colon carcinomas significantly inhibited tumor growth. Splenocytes from mice treated with Ad-CCL21-IL-15 developed tumor-specific cytotoxic T cells and were protected from subsequent challenges with tumor cells. This study indicates that providing cancer therapy by combining CCL21 and IL-15 can induce antitumor immune responses and is an effective strategy for cancer immunotherapy.