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Objective At present, cephalomedullary nail is the most frequently used implant in the management of intertrochanteric fractures around the world. The implant design and fixation techniques of the cephalomedullary nail have been continuously improved to ensure uncomplicated bone union during the past decade. However, a degree of reduction loss during bone healing is still not rare in clinical work. Many attributed this complication to misoperation during the surgery and hold that a series of techniques and tips could help to avoid the loss of reduction. However, until now there has been no research to explore whether the reduction loss after the operation can be fully prevented in the best cases. The purposes of the study are as follows: (i) to evaluate the efficiency of the current established CMN techniques; (ii) to quantify the loss of reduction under an appropriately implanted CMN to anatomically realigned intertrochanteric fractures; and (iii) to explore the possible underlying causes for the inevitable loss of reduction. Methods In the retrospective study, 163 consecutive cases with the intertrochanteric fractures fixed with standard cephalomedullary nail technique were reviewed. The anatomical reduction and optimal positioning of the nail were confirmed by postoperative imaging. The fracture types ranged from 31‐A1.1–2.3 according to the OTA/AO fracture classification. One hundred and fifteen cases with stable fracture types (31A1.1–2.1) were allocated to Group A, and 48 cases with unstable 31A2.2–2.3 fracture types were allocated to Group B. The radiological measurements included femoral neck shortening, loss of the neck‐shaft angle, cutout, and cut‐through of the blade. The outcomes between postoperative and 1 year after the operation were evaluated and compared. Results The patients consisted of 66 males and 97 females with an average age of 69.4 (range: 46–78, SD: 14.6) years. At the 1‐year follow‐up, no fixation failure or nonunion was observed in each group. The mean femoral neck shortening and loss of the neck‐shaft angle were 4.47 mm (range: 0.43–17.68, SD: 3.71) and 5.4° (range: 0.51–19.10, SD: 3.58) separately. The mean cutout and cut‐through were 1.84 mm (range: 0.24–11.30, SD: 2.33) and 1.25 mm (range: 0.51–10.29, SD: 1.74). The average femoral neck shortening and loss of the neck‐shaft angle were higher in Group B than Group A. Among the 23 cases with the femoral neck shortening more than 10 mm, 19 cases (16.5%) were from Group A and four cases (8.3%) were from Group B. There were nine (7.8%) cases with the loss of the neck‐shaft angle more than 10° in Group A and six (12.5%) cases in Group B. Conclusions Current established CMN techniques are efficient in treating intertrochanteric femoral fracture. However, even with currently consensual techniques of cephalomedullary nail, the process of fracture healing still risks the loss of reduction, although the migration of the blade could be minimized. This situation may associate with the intrinsic design of the CMN and further improvement is still needed., With currently consensual techniques of cephalomedullary nail, the process of fracture healing still risks the loss of reduction, although the migration of the blade could be minimized.

Wear particles released from prosthetic implants can cause periprosthetic osteolysis, a major cause of implant loosening. The aim of this study was to investigate the effects of the 11R-VIVIT peptide on osteolysis induced by titanium (Ti) particles in vivo. Twenty-four C57BL/J6 mice were divided into 3 groups: sham operation, Ti group, and Ti/VIVIT group. A calvarial osteolysis model was established by implanting Ti particles into mouse calvaria of the Ti and Ti/VIVIT groups. After 2 weeks, 11R-VIVIT peptide (10 mg/kg/day) was intraperitoneally injected into the mice of the Ti/VIVIT group for 14 days. The other 2 groups received saline injection. The calvarial specimens were removed and stained with van Geison staining. The calvarial sagittal suture area was measured to observe bone resorption. The calvarial new bone area was measured to observe bone formation. Compared with the sham group, the area of calvarial new bone and calvarial sagittal suture were higher in the Ti group (P < 0.01). Compared with the Ti group, the area of calvarial new bone was higher and the area of calvarial sagittal suture was lower in the Ti/VIVIT group (P < 0.01). In conclusion, the 11R-VIVIT peptide inhibited bone resorption and enhanced bone formation. This may have contributed to lower wear particle-induced osteolysis. This method could eventually be used to prevent prosthesis loosening after joint replacement and to prolong the life of the prosthesis.

Background Neuroinflammatory responses involve the activation of the interleukin (IL) -1β and IL-18. Processing and activation of the pro-inflammatory IL require NLRP3 inflammasome activation. Rutin can protect spinal cord against damage, but the potential mechanisms underlying remain unknown. Here, we investigated the molecular mechanisms of rutin-mediated neuroprotection in a rat model of spinal cord injury (SCI). Materials and methods One hundred twenty female Sprague–Dawley rats were randomly assigned to four groups: sham group, SCI group, SCI + Rutin50 group, and the SCI + Rutin100 group. The influences of rutin on inflammatory marker levels, histologic alterations, and locomotion scale were analyzed. Results SCI significantly increased the expression of the NLRP3, ASC, IL-1β, IL-18, and tumor necrosis factor-alpha. Rutin significantly reduced the levels of reactive oxygen species, malondialdehyde, NLRP3, ASC, caspase-1, IL-1β, IL-18, and tumor necrosis factor-alpha. Furthermore, rutin administration significantly attenuated histologic alteration and improved locomotion recovery. Conclusions Our data provide clear evidence that rutin attenuates tissue damage and improves locomotion recovery, and the mechanism may be related to the alleviation of inflammation and oxidative stress.

Osteoporosis is characterized by the imbalance of two relatively independent processes-osteoblastogenesis and osteoclastogenesis. Calcineurin (Cn)/nuclear factor of activated T cells (NFAT)(Cn/NFAT) signaling pathway is involved in these two processes in bone metabolism, but its potential as a target to treat osteoporosis needs to be defined. The aim of this study is to investigate the inhibition of polypeptide 11R-VIVIT onCn/NFAT signaling pathway. Rat calvaria (RC) cells were prepared from experimental model of osteoporosis in rat.11R-VIVIT wasused to treat cultured RC cells from wide type (WT) rat or from osteoporosis (OP) rat, we then measured the expressions of NFATc1, osteopontin (OPN), osteocalcin (OC), cytokines, NFκB subunit p65 by real time PCR, western blot or immunofluorescence. Then ALP expression and staining, and alizarin red S (ARS) staining were employed to study the osteoblastodifferentiation. 11R-VIVIT regulates the expression of NFATc1, and some other molecules in Cn/NFAT signaling pathway, such as OPN and OC, at transcriptional level and protein level. Further, it can regulate the expression of inflammatory cytokine like IL-1beta, IL-10 and TNF-alpha and NFκB activity. Further, 11R-VIVIT can accelerate osteoblastodifferentiation of RC cells demonstrated by ALP and ARS staining.11R-VIVIT can stimulate the bone formation by decreasing NFATc1 expression and regulating the expression of inflammation related molecules.

Transforming growth factor-β1 (TGF-β1) plays an important role on fibrogenesis in heart disease. MicroRNAs have exhibited as crucial regulators of cardiac homeostasis and remodeling in various heart diseases. MiR-19a-3p/19b-3p expresses with low levels in the plasma of heart failure patients. The purpose of our study is to determine the role of MiR-19a-3p/19b-3p in regulating autophagy-mediated fibrosis of human cardiac fibroblasts. We elucidate our hypothesis in clinical samples and human cardiac fibroblasts (HCF) to provide valuable basic information. TGF-β1 promotes collagen I α2 and fibronectin synthesis in HCF and that is paralleled by autophagic activation in these cells. Pharmacological inhibition of autophagy by 3-methyladenine decreases the fibrotic response, while autophagy induction of rapamycin increases the response. BECN1 knockdown and Atg5 over-expression either inhibits or enhances the fibrotic effect of TGF-β1 in experimental HCF. Furthermore, miR-19a-3p/19b-3p mimics inhibit epithelial mesenchymal transition (EMT) and extracellular matrix (ECM) prodution and invasion of HCF. Functional studies suggest that miR-19a-3p/19b-3p inhibits autophagy of HCF through targeting TGF-β R II mRNA. Moreover, enhancement of autophagy rescues inhibition effect of miR-19a-3p/19b-3p on Smad 2 and Akt phosphorylation through TGF-β R II signaling. Our study uncovers a novel mechanism that miR-19a-3p/19b-3p inhibits autophagy-mediated fibrogenesis by targeting TGF-β R II.