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Background Intervertebral disc degeneration (IVDD) is a well-known cause of lower back pain, which is induced by multiple factors including increased apoptosis and decreased survival of nucleus pulposus cells. In this study, we evaluate the effect and potential mechanism of miR-660 on the nucleus pulposus cells apoptosis induced by TNF-α. Methods First, we collected tissue of nucleus pulposus from IVDD and healthy controls. General characteristic of the IVDD and healthy control was also collected. And, we also collected nucleus pulposus cells that stimulated by TNF-α or control. miRNA microarray was performed to identify the differentially expressed miRNAs. Apoptosis rate and miR-660 relative expression was measured after stimulated with different concentration of TNF-α to identify the optimal concentration of TNF-α. Second, we successfully constructed antigomiR-660 to block the miR-660 expression in nucleus pulposus cells and then stimulated with TNF-α (100 ng/ml, 12 h). The apoptosis rates and relative protein expression were then measured again. The target association between miR-660 and SAA1 was confirmed by dual-luciferase reporter. Results There was no significant difference between the age (IVDD: 39 ± 10 years, healthy controls: 36 ± 7 years), BMI and sex between IVDD and healthy controls. Microarray analysis found that miR-660 was significantly up-regulated in IVDD and TNF-α treated groups, which was further identified by PCR. We found that the rate of apoptosis and miR-660 expression increased with TNF-α concentration increased. Finally, TNF-a with 100 ng/ml was used for further experiment. Compared with TNF-α group, TNF-α + antigomiR-660 could significantly down-regulated the apoptosis rate and relative protein (c-Caspase3 and c-Caspase7). Dual-luciferase reporter revealed that miR-660 could directly binding to the SAA1 at 80–87 sites. Compared with TNF-α alone group, TNF-α + antigomiR-660 significantly up-regulated the SAA1 expression (P Conclusion These results indicated that knockdown of miR-660 protected the nucleus pulposus from apoptosis that induced TNF-α via up-regulation of SAA1. Further studies should focus on the role of miR-660 in protecting IVDD in vivo.

Myocardin (MYOCD) plays an important role in cardiovascular disease. However, its underlying impact on atherosclerosis remains to be elucidated. ATP binding cassette transporter A1 (ABCA1), a key membrane-associated lipid transporter which maintains intracellular lipid homeostasis, has a protective function in atherosclerosis progress. The purpose of this study was to investigate whether and how the effect of MYOCD on atherosclerosis is associated with ABCA1 in vascular smooth muscle cells (VSMCs). We found both MYOCD and ABCA1 expression were dramatically decreased in atherosclerotic patient aortas compared to control. MYOCD knockdown inhibited ABCA1 expression in human aortic vascular smooth muscle cells (HAVSMCs), leading to reduced cholesterol efflux and increased intracellular cholesterol contents. MYOCD overexpression exerted the opposite effect. Mechanistically, MYOCD regulates ABCA1 expression in an SRF-dependent manner. Consistently, apolipoprotein E-deficient mice treated with MYOCD shRNA developed more plaques in the aortic sinus, which is associated with reduced ABCA1 expression, increased cholesterol retention in the aorta, and decreased high-density lipoprotein cholesterol levels in the plasma. Our data suggest that MYOCD deficiency exacerbates atherosclerosis by downregulating ABCA1 dependent cholesterol efflux from VSMCs, thereby providing a novel strategy for the therapeutic treatment of atherosclerotic cardiovascular disease.

Conventional gyrocompass alignment methods are based on relatively small azimuth misalignment angles. However, a marine strapdown inertial navigation system may face large azimuth misalignment angle caused by a failed coarse alignment algorithm. This paper provides a novel gyrocompass alignment method to solve the problem. Effects of system parameters are analyzed and the proper scenario of parameter switch based on the classic control theories is derived. Test results show that compared with the conventional methods, our method can accomplish the initial alignment quickly and accurately under large azimuth misalignment angle.

Background: To investigate the clinical effects of stage I repair of skin and soft tissue defects using lateral femoral perforator free flap in pilon fracture surgery. Methods: Fifteen cases of pilon fractures were selected from our hospital between April 2013 and January 2017. There were 8 cases of 43-C1, 4 cases of 43-C2 and 3 cases of 43-C3 fractures, as defined by the Miller AO classification. In all cases, severe contusion of skin and soft tissue around the fracture, skin darkening and necrosis, and tissue edema during surgery, led to difficult closure of incision. The skin and soft tissue defects were repaired at stage I by ipsilateral lateral femoral perforator free flap. Results: Venous crisis occurred in one case, while the other 14 cases survived. During the 6–18 months of follow-up, the function of ankles was satisfactory and the wearing of shoes was not affected by the abnormal foot. The flap color and texture were normal and the protective sensation of the flap recovered. Only a linear scar remained at the donor site and no muscle adhesion occurred. Conclusions: Stage I repair of skin and soft tissue defects using lateral femoral perforator free flap in pilon fracture surgery apparently decreased postoperative infection and protected the blood supply around the fracture. Hence, it was an effective repair method.

Introduction The tripaddle posterior interosseous artery (PIA) flap can be used for multifinger defect resurfacing, but interpatient variations in perforator distribution remain an ongoing challenge when using this approach. This study aims to evaluate the efficacy of 3 different tripaddle PIA perforator flap designs according to the PIA perforator distribution for the repair of 3-finger defects. Methods In accordance with the size of the 3-finger defects and the position of the perforators, a tripaddle flap was designed on the multiple perforators of the descending branch of the PIA in the distal two thirds of the forearm. Patients received 1 of 3 distinct tripaddle PIA perforator flap designs based on perforator distributions of the PIA. Results Three cases of 3-finger defects were repaired with type A trefoil-shaped tripaddle flaps, whereas 4 cases were repaired with type B modified trefoil-shaped tripaddle flaps, and the other 3 cases were repaired with type C chain-shaped tripaddle flaps. All flaps survived except 2 paddles with tip necrosis. After 9.1 months of mean follow-up, 9 of the 10 cases demonstrated satisfactory cosmetic appearance, whereas the last case required a debulking procedure in the second stage. Conclusions The free tripaddle PIA perforator flap is an effective option for repairing 3-finger skin defects. Various flap designs based on the PIA perforator distribution allow for more individualized treatment approaches.