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Flexor tendon injuries and tendinopathy are very common but remain challenging in clinical treatment. Exosomes‐based cell‐free therapy appears to be a promising strategy for tendon healing, while limited studies have evaluated its impacts on tenocyte biology. The objective of this study was to characterize a novel purified exosome product (PEP) derived from plasma, as well as to explore its cellular effects on canine tenocyte biology. The transmission electron microscope revealed that exosomes of PEP present cup‐shaped structures with the diameters ranged from 80 to 141 nm, and the NanoSight report presented that their size mainly concentrated around 100 nm. The enzyme‐linked immunosorbent assay kits analysis showed that PEP was positive for CD63 and AChE expression, and the cellular uptake of exosomes internalized into tenocyte cytoplasm was observed. The cell growth assays displayed that tenocyte proliferation ability was enhanced by PEP solution in a dose‐dependent manner. Tenogenic phenotype was preserved as is evident by that tendon‐related genes expression (SCX, COL1A, COL3A1, TNMD, DCN, and MKX) were expressed insistently in a high level, while tenocytes were treated with 5% PEP solution. Furthermore, migration capability was maintained and total collagen deposition was increased. More interesting, dexamethasone‐induced cellular apoptosis was attenuated during the incubation of tenocytes with a 5% PEP solution. These findings will provide the basic understandings about the PEP, and support the potential use of this biological strategy for tendon healing.

Uncertainties of renewable energy sources like wind power are one of the considerable challenges of prosumer microgrids. To meet the grid codes requirements regarding the voltage stability of wind farm integration, finding the balance between providing the demanding dynamic performance of the voltage and reactive power, and at the same time decreasing the investment on centralized reactive power compensation device, becomes an important research topic. This paper compares the effects of the static synchronous compensator (STATCOM) and static VAR compensator (SVC) on transient voltage stability at the point of common coupling (PCC) of a doubly fed induction generator (DFIG)-based wind farm. And a new fast coordinated control scheme of STATCOM and DFIG is proposed for minimizing the capacity of centralized reactive power compensation device and making the best use of the reactive power control capability of DFIG. The simulation results based on test system show that STATCOM, even with less capacity, can contribute more reactive power than SVC for voltage stability, especially during the serious voltage drop transient stage, and perform a faster voltage recovery time after fault than SVC, proved to be a more economic choice; The proposed coordinated control scheme can not only improve the transient voltage stability, but also help reducing the capacity of STATCOM, so that the cost of investments in wind farms would be reduced.

Most kidney cancers are renal cell carcinomas (RCC). RCC lacks early warning signs and 70 % of patients with RCC develop metastases. Among them, 50 % of patients having skeletal metastases developed a dismal survival of less than 10 % at 5 years. Therefore, exploring the key driving proteins and pathways involved in RCC bone metastasis could benefit patients’ therapy and prolong their survival. We examined the difference between the OS-RC-2 cells and the OS-RC-2-BM5 cells (subpopulation from OS-RC-2) of RCC with proteomics. Then we employed Western-blot, immunohistochemistry and the clinical database (oncomine) to screen and verify the key proteins and then we analyzed the functions and the related pathways of selected key proteins with system biology approaches. Our proteomic data revealed 26 significant changed spots (fold change <0.5 and >1.9, P < 0.05) between two cells. The Western blotting results validated for these identified spots were consistent with the proteomics’. From the public clinical database, 23 out of 26 proteins were connected with RCC metastases and 9 out of 23 with survival time directly (P < 0.05). Finally, only 8 out of 9 proteins had significantly positive results in tissues of RCC patients with bone metastasis compared with primary tumor (P < 0.05). System biology analyzing results showed these eight proteins mainly distributed in oxidative phosphorylation which indicates that mitochondria dysfunction played the critical role to regulate cells metastasis. Our article used a variety of experimental techniques to find eight proteins which abnormally regulated mitochondrial function to achieve a successful induction for RCC metastasis to bone.Electronic supplementary materialThe online version of this article (doi:10.1007/s10585-015-9731-4) contains supplementary material, which is available to authorized users.

Mitochondrial dysfunction contributes to osteoarthritis (OA) onset and progress.Mitochondrial dynamics, coupled with mitophagy, is critical for the maintenance of mitochondrial fitness, involving many cellular processes, such as proliferation and apoptosis. Excessive mechanical stress induces chondrocyte apoptosis; however, the effects of mechanical stress on mitochondrial dynamics remain elusive. In this study, we performed fluorescence staining, flow cytometry, transmission electron microscope, Western blot analysis, and RNA-sequencing to assess the effects of different strength of mechanical stimulation on mitochondrial functions of chondrocyte treated with interleukin-1β (IL-1β). We found that moderate mechanical stress reduced the IL-1β-induced apoptosis by maintaining mitochondrial function and scavenging the reactive oxygen species, while excessive mechanical stress induced strong mitochondrial dysfunction and apoptosis. Moreover, RNAsequencing revealed that mitophagy and mitochondrial dynamics were involved in the regulation of mechanical stress on chondrocyte biology. In addition to the elevated mitophagy, moderate mechanical stress also promoted mitochondrial dynamics by enhancing the expression of MFN1/2 and OPA1 and the translocation of dynamin-related protein 1 from the cytoplasm to the mitochondria. However, an uncoupling of mitochondrial dynamics, characterized by strongly elevated fission, resulted in the unfavorable apoptosis of excessive mechanical stress-stimulated chondrocytes. This study revealed the effects of mechanical stress upon mitochondrial dynamics in chondrocyte.

With the increasing participation of wind generation in the power system, a wind power plant (WPP) with an energy storage system (ESS) has become one of the options available for a black-start power source. In this article, a method for the energy storage configuration used for black-start is proposed. First, the energy storage capacity for starting a single turbine was determined. Then, a hierarchical planning model was established. This model did not consider the starting efficiency of the WPP, but it did consider the layout of the energy storage in the WPP and the balance of the terminal voltage when starting the WPP. Finally, the feasibility and value of the proposed method and model were verified in a 49.5 MW WPP with an ESS (a power rating of 2.24 MW and energy capacity of about 1.68 MWh). The result suggests that configuring an ESS with a small capacity on the side of the turbine can achieve black-start for a WPP with an ESS as the power source.