Time-Domain Blind ICI Compensation in Coherent Optical FBMC/OQAM System.

A blind discrete-cosine-transform-based phase noise compensation (BD-PNC) is proposed to compensate the inter-carrier-interference (ICI) in the coherent optical offset-quadrature amplitude modulation (OQAM)-based filter-bank multicarrier (CO-FBMC/OQAM) transmission system. Since the phase noise sample can be approximated by an expansion of the discrete cosine transform (DCT) in the time-domain, a time-domain compensation model is built for the transmission system. According to the model, phase noise compensation (PNC) depends only on its DCT coefficients. The common phase error (CPE) compensation is firstly performed for the received signal. After that, a pre-decision is made on a part of compensated signals with low decision error probability, and the pre-decision results are used as the estimated values of transmitted signals to calculate the DCT coefficients. Such a partial pre-decision process reduces not only decision error but also the complexity of the BD-PNC method while keeping almost the same performance as in the case of the pre-decision of all compensated signals. Numerical simulations are performed to evaluate the performance of the proposed scheme for a 30 GBaud CO-FBMC/OQAM system. The simulation results show that its bit error rate (BER) performance is improved by more than one order of magnitude through the mitigation of the ICI in comparison with the traditional blind PNC scheme only aiming for CPE compensation.

Recombinant BMP 4/7 fusion protein induces differentiation of bone marrow stem cells.

Bone morphogenetic proteins (BMPs) induce differentiation of mesenchymal cells to cartilage and bone. We cloned BMP4 and BMP7 cDNAs from human placenta and fetal cartilage cells, respectively, and used an Escherichia coli expression system to produce recombinant BMP4 and BMP4/7 proteins. Differentiation of primary cultures of bone marrow stem cells (BMSC) treated with BMP4 or BMP4/7 was evaluated by Von Kossa staining and by determining alkaline phosphatase activity and osteocalcin level. BMP4/7-induced BMSC differentiation more potently than BMP4. We showed that BMP4/7 fusion protein expressed in E. coli is biologically active and is a novel strategy to treat bone injury in a clinical setting.

miR-196 acts as a tumor suppressor in osteosarcoma by targeting HOXA9.

Abnormal expression of microRNAs (miRNAs) has been found in most cancer types. Therefore, the discovery of miRNAs could help us to understand the mechanism of tumor initiation and development. The purpose of this study was to investigate the significance of miR-196 in osteosarcoma (OS) and to identify its target genes. We found miR-196 expression was significantly reduced in OS tissues and cell lines (Saos-2 and MG-63) as compared to normal tissues and cell line. The OS cell line proliferation and migration abilities were inhibited by miR-196 overexpression but promoted by miR-196 downregulation in vitro. Moreover, we revealed that miR-196 could bind to the 3'-untranslated region (3'-UTR) of homeobox A9 (HOXA9) and inhibit HOXA9 expression in OS cell lines. Furthermore, knockdown the expression of HOXA9 resulted in decreased proliferation and migration which was similar to that observed with miR-196 overexpression in OS cell lines. In summary, miR-196 inhibits proliferation and migration of OS cell lines through regulating HOXA9, which might be a useful target for OS treatment.

Inactivation of the Rho-ROCK signaling pathway to promote neurologic recovery after spinal cord injuries in rats.

BACKGROUND: After injury, axonal regeneration of the adult central nervous system (CNS) is inhibited by myelin-derived growth-suppressing proteins. These axonal growth inhibitory proteins are mediated via activation of Rho, a small GTP-binding protein. The activated form of Rho, which is bound to GTP, is the direct activator of Rho kinase (ROCK) through serial downstream effector proteins to inhibit axonal regeneration. The objective of this study was to observe the therapeutic effect of inactivation of the Rho-ROCK signaling pathway to promote neurologic recovery after spinal cord injuries in rats. METHODS: One hundred and twenty adult female Sprague-Dawley rats were randomly divided into three groups. Laminectomies alone were conducted in 40 rats in the sham group. Laminectomies and spinal cord transections were performed in 40 rats in the control group (treated with normal saline administered intraperitoneally). Laminectomies and spinal cord transections were performed in 40 rats in the fasudil-treated group (treated with fasudil administered intraperitoneally). Neurologic recovery was evaluated before surgery and 3 days, and 1, 2, 3, and 4 weeks after surgery using the Basso-Beattie-Bresnahan (BBB) scale of hind limb movement. At the same time, the expression of RhoA mRNA was determined with RT-PCR. Histopathologic examinations and immunofluorescence staining of NF were performed 1 month after surgery. RESULTS: Compared with the control group, the BBB scores of the fasudil-treated group were significantly increased and the expression of RhoA mRNA was significantly decreased. In the fasudil-treated group, a large number of NF-positive regenerating fibers was observed; some fibers crossed the slit of the lesion. CONCLUSION: Inactivation of the Rho-ROCK signaling pathway promotes CNS axonal regeneration and neurologic recovery after spinal cord injuries in rats.