Objective To evaluate the biomechanical effects of using a new injectable calcium phosphate cement to consolidate the fixation of osteoporotic intertrochanteric fracture.Method Five matchod pairs of human cadaver femora were used to produce the model of intertrochanteric fracture.All fractures were fixed with dynamic hip screws(DHS),and divided into two groups.In the CPC consolidation group of each pair,CPC was used to grout the hip screw and to fill the posteromedial defect.All femora were subjected to biomechanical test.Results Under the loading of 500 N,in the CPC consolidation group,the mean axial stiffness is(691.93±18.90)N/mm and the horizontal shear stiffness is(5553.84±27.47)N/mm.The mean lateral and medial strength is(5.15±0.35)MPa and(4.13±0.24)MPa.The torsion stiffness was 0.41 and the ultimate loading is(3580±286)N.In the control group,the mean axiak stiffness is(453.45±19.75)N/mm,the horizontal shear stiffness is(3848.87±22.63)N/mm,the mean lateral and medial strength is(3.12±0.37)MPa and(1.80±0.21)MPa,and,the torsion stiffness is 0.35 and the ultimate loading is(2512±189)N.Consolidation fixation with CPC increased each of the biomechanical efficiency(P＜0.05).Conclusions CPC consolidation of osteoprotic femoral head and the medial defect of intertrochanteric fracture can significantly improve the overall stability and decrease the rate of postoperative complication.

Pulmonary fibrosis (PF) is a pathological change caused by repeated injuries and repair dysfunction of the alveolar epithelium. Our previous study revealed that the residues Asn3 and Asn4 of peptide DR8 (DHNNPQIR-NH₂) could be modified to improve stability and antifibrotic activity, and the unnatural hydrophobic amino acids α-(4-pentenyl)-Ala and d-Ala were considered in this study. DR3penA (DHα-(4-pentenyl)-ANPQIR-NH₂) was verified to have a longer half-life in serum and to significantly inhibit oxidative damage, epithelial-mesenchymal transition (EMT) and fibrogenesis in vitro and in vivo. Moreover, DR3penA has a dosage advantage over pirfenidone through the conversion of drug bioavailability under different routes of administration. A mechanistic study revealed that DR3penA increased the expression of aquaporin 5 (AQP5) by inhibiting the upregulation of miR-23b-5p and the mitogen-activated protein kinase (MAPK) pathway, indicating that DR3penA may alleviate PF by regulating MAPK/miR-23b-5p/AQP5. Safety evaluation showed that DR3penA is a peptide drug without obvious toxicity or acute side effects and has significantly improved safety compared to DR8. Thus, our findings suggest that DR3penA, as a novel and low-toxic peptide, has the potential to be a leading compound for PF therapy, which provides a foundation for the development of peptide drugs for fibrosis-related diseases.

The antimicrobial peptide APKGVQGPNG (named YD), a natural peptide originating from Bacillus amyloliquefaciens CBSYD1, exhibited excellent antibacterial and antioxidant properties in vitro. These characteristics are closely related to inflammatory responses which is the central trigger for liver fibrosis. However, the therapeutic effects of YD against hepatic fibrosis and the underlying mechanisms are rarely studied. In this study, we show that YD improved liver function and inhibited the progression of liver fibrosis by measuring the serum transaminase activity and the expression of α-smooth muscle actin and collagen I in carbon tetrachloride-induced mice. Then we found that YD inhibited the level of miR-155, which plays an important role in inflammation and liver fibrosis. Bioinformatics analysis and luciferase reporter assay indicate that Casp12 is a new target of miR-155. We demonstrate that YD significantly decreases the contents of inflammatory cytokines and suppresses the NF-κB signaling pathway. Further studies show that transfection of the miR-155 mimic in RAW264.7 cells partially reversed the YD-mediated CASP12 upregulation, the downregulated levels of inflammatory cytokines, and the inactivation of the NF-κB pathways. Collectively, our study indicates that YD reduces inflammation through the miR-155–Casp12–NF-κB axis during liver fibrosis and provides a promising therapeutic candidate for hepatic fibrosis.