Stroke results in the disruption of tissue architecture and is the third leading cause of death in the United States1. Transplanting scaffolds containing stem cells into the injured areas of the brain has been proposed as a treatment strategy2, and carbon nanotubes show promise in this regard, with positive outcomes when used as scaffolds in neural cells3,4 and brain tissues5. Here, we show that pretreating rats with amine-modified single-walled carbon nanotubes can protect neurons and enhance the recovery of behavioural functions in rats with induced stroke. Treated rats showed less tissue damage than controls and took longer to fall from a rotating rod, suggesting better motor functions after injury. Low levels of apoptotic, angiogenic and inflammation markers indicated that aminemodified single-walled carbon nanotubes protected the brains of treated rats from ischaemic injury.

Alzheimer's disease (AD) is characterized by the deposition of aggregated beta-amyloid (Aβ), which triggers a cellular stress response called the unfolded protein response (UPR). The UPR signaling pathway is a cellular defense system for dealing with the accumulation of misfolded proteins but switches to apoptosis when endoplasmic reticulum (ER) stress is prolonged. ER stress is involved in neurodegenerative diseases including AD, but the molecular mechanisms of ER stress-mediated Aβ neurotoxicity still remain unknown. Here, we show that treatment of Aβ triggers the UPR in the SK-N-SH human neuroblastoma cells. Aβ mediated UPR pathway accompanies the activation of protective pathways such as Grp78/Bip and PERK-eIF2α pathway, as well as the apoptotic pathways of the UPR such as CHOP and caspase-4. Knockdown of PERK enhances Aβ neurotoxicity through reducing the activation of eIF2α and Grp8/Bip in neurons. Salubrinal, an activator of the eIF2α pathway, significantly increased the Grp78/Bip ER chaperone resulted in attenuating caspase-4 dependent apoptosis in Aβ treated neurons. These results indicate that PERK-eIF2α pathway is a potential target for therapeutic applications in neurodegenerative diseases including AD.

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To determine the apoptotic signaling pathway which tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/ Apo2L) induced, we investigated the contribution of reactive oxygen species (ROS), p38 mitogen-activated protein (MAP) kinase and caspases in human adenocarcinoma HeLa cells. Here we show that upon TRAIL/Apo2L exposure there was pronounced ROS accumulation and activation of p38 MAP kinase, and that activation of caspases and apoptosis followed. Pretreatment with antioxidants such as glutathione or estrogen attenuated TRAIL/Apo2L-induced apoptosis through a reduction of ROS generation and diminished p38 MAP kinase and caspase activation. The p38 MAP kinase inhibitor SB203580 prevented apoptosis through a blockage of caspase activation, although ROS generation was not attenuated. Furthermore, the pan-caspase inhibitor Z-Val-Ala-DL-Asp-fluoromethyl ketone fully prevented apoptosis, while neither ROS accumulation nor p38 MAP kinase activation were affected. Therefore, our results suggest that TRAIL/Apo2L-induced apoptosis is mediated by ROS-activated p38 MAP kinase followed by caspase activation in HeLa cells. ß 2002 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.

Ni supported on calcined ceria nitrate catalyst is highly active and stable for low-temperature CO 2 methanation reaction (CO 2 conversion: 70% at 180 °C, 0.05 bar, and gas hourly space velocity (GHSV) of 14 400 L kg −1 h −1 ). We investigated CO 2 adsorption and CO 2 + H 2 reaction on the surface of Ni/CeO 2 and Ni/CeO 2−x catalysts to examine the structure and strength of adsorbed species using diffuse reflection infrared Fourier transform spectroscopy (DRIFTS). At temperature of 180 °C, weakly adsorbed bridged carbonate was generated on the surface of CeO 2−x support by new active sites of oxygen vacancies created by addition of H 2 . High reducibility of Ni/CeO 2−x catalyst played an important role in increasing low-temperature CO 2 methanation catalytic activity.

Objective Tissue factor (TF), the major activator of the extrinsic pathway of coagulation, is abundant in the placenta and decidua. The aim of this study was to determine the maternal plasma concentrations of TF and its primary inhibitor, tissue factor pathway inhibitor (TFPI), in women who delivered small for gestational age (SGA) neonates, and in preeclampsia. Study Design A cross-sectional study included the following groups: 1) women with normal pregnancies (n=86); 2) patients who delivered SGA neonates (n=61); and 3) women with preeclampsia (n=133). Maternal plasma concentrations of TF and TFPI were measured by a sensitive immunoassay. Non-parametric statistics were used for analysis. Results 1)Women with preeclampsia had a significantly higher median plasma concentration of TF than patients with a normal pregnancy (median: 1187 pg/ml; range: 69–11675 vs. median: 291.5 pg/ml; range: 6.3–2662.2; p<0.0001, respectively); 2) Similarly, TFPI concentrations were higher in preeclampsia than in normal pregnancy (median: 87.5ng/ml; range 25.4–165.1 vs. median: 66.1 ng/ml; range: 14.3–86.5; p<0.0001, respectively); 3) Surprisingly, mothers with SGA neonates had a lower median maternal plasma concentration of TF (median: 112.2 pg/ml; range: 25.6–1225.3) than women with a normal pregnancy (p<0.0001). Conclusion 1) Maternal plasma concentrations of TF in patients with preeclampsia, but not in those who delivered an SGA neonate, were higher than in women with normal pregnancies; 2) While the role of immunoreactive plasma TF in coagulation remains controversial, our observations suggest that changes are present in the context of complications of pregnancy.

In this paper, we implement the intelligent neural network controller hardware with a field programmable gate array (FPGA)-based general purpose chip and a digital signal processing (DSP) board to solve nonlinear system control problems. The designed intelligent control hardware can perform real-time control of the backpropagation learning algorithm of a neural network. The basic proportional-integral-derivative (PID) control algorithms are implemented in an FPGA chip and a neural network controller is implemented in a DSP board. By using a high capacity of an FPGA chip, the additional hardware such as an encoder counter and a pulsewidth modulation (PWM) generator is implemented in a single FPGA chip. As a result, the controller becomes cost effective. It was tested for controlling nonlinear systems such as a robot finger and an inverted pendulum on a moving cart to show performance of the controller.Index Terms-Digital signal processing (DSP), field programmable gate array (FPGA), inverted pendulum, neural network controller, proportional-integral-derivative (PID) controller, robot finger.

Identification of the factors associated with improved facial nerve function after treatment of Bell palsy is important to provide patients with early and effective treatment. OBJECTIVE To identify factors that are associated with improved treatment outcomes in patients with Bell palsy.