Common reed (Fragmites australis), a local invasive grass, was investigated as a possible feedstock for the production of activated carbon. Dried crushed stems were subjected to impregnation with phosphoric acid (30, 40 and 50%) followed by pyrolysis at 400~500℃ with final washing and drying. Obtained carbons were characterized by determining: carbon yield, ash content, slurry pH, textural properties and capacity to remove color bodies from factory-grade sugar liquor. Produced carbons possessed surface area up to 700 m2/g, total pore volumes up to 0.37 cm3/g, and proved to be microporous in nature. Decolorization of hot sugar liquor at 80℃ showed degrees of color removal of 60 up to 77% from initial color of 1100~1300 ICU, at a carbon dose of 1.0 g/100 ml liquor. No correlation seems to hold between synthesis conditions and % R but depends on the degree of microporosity. A commercial activated carbon N showed a comparative better color removal capacity of 91%. Common reed proved to be a viable carbon precursor for production of good adsorbing carbon suitable for decolorization in the sugar industry, as well as in other environmental remediation processes.

We investigated the role of the central MAPK pathways in extra-territorial (referred) pain resulting from inflammation of the temporomandibular joint (TMJ). Experiments were carried out on male Sprague-Dawley rats weighing 220-280 g. Under anesthesia, these animals were injected with 50 μL of complete Freund's adjuvant (CFA) into the TMJ using a Hamilton syringe. In the control group, saline was injected into the TMJ. To identify the extent of inflammation of the TMJ, Evans blue dye (0.1%, 5 mg/kg) was injected intravenously at 1, 3, 6, 9, 12 and 15 days after CFA injection. The concentration of Evans blue dye in the extracted TMJ tissue was found to be significantly higher in the CFA-treated animals than in the saline-treated group. Air-puff thresholds in the vibrissa pad area were evaluated 3 days before and at 3, 6, 9, 12, 15 and 18 days after CFA injection into the TMJ. Referred mechanical allodynia was established at 3 days, remained until 12 days, and recovered to preoperative levels at 18 days after CFA injection. This referred mechanical allodynia was observed in contralateral side area. To investigate the role of central MAPK pathways, MAPK inhibitors (10 μg) were administrated intracisternally 9 days after CFA injection. SB203580, a p38 MAPK inhibitor, significantly attenuated referred mechanical allodynia, as compared with the vehicle group. PD98059, a MEK inhibitor, also reduced CFA-induced referred mechanical allodynia. These results suggest that TMJ inflammation produces extra-territorial mechanical allodynia, and that this is mediated by central MAPK pathways.

The present study investigated the role of ERK in the onset of mechanical and cold allodynia in a rat model of compression of the trigeminal ganglion by examining changes in the air-puff thresholds and number of scratches following the intracisternal injection of PD98059, a MEK inhibitor. Male Sprague Dawley rats weighing between 250 and 260 g were used. Under anesthesia, the rats were mounted onto a stereotaxic frame and received 4% agar (10μℓ) solution to compress the trigeminal ganglion. In the control group, the animals were given a sham operation without the application of agar. Changes in behavior were examined at 3 days before and at 3, 7, 10, 14, 17, 21, 24, 30, and 40 days after surgery. Compression of the trigeminal ganglion significantly decreased the air-puff thresholds. Mechanical allodynia was established within 3 days and persisted over postoperative day 24. To evaluate cold allodynia, nociceptive scratching behavior was monitored after acetone application on the vibrissa pad of the rats. Compression of the trigeminal ganglion was found to produce significant cold allodynia, which persisted for more than 40 days after surgery. On postoperative day 14, the intracisternal administration of 1 μg or 10 μg of PD98059 in the rat model significantly decreased the air-puff thresholds on both the ipsilateral and contralateral side. The intracisternal administration of 10 μg of PD98059 also significantly alleviated the cold allodynia, compared with the vehicle-treated group. These results suggest that central ERK plays an important role in the development of mechanical and cold allodynia in rats with compression of the trigeminal ganglion and that a targeted blockade of this pathway is a potential future treatment strategy for trigeminal neuralgia-like nociception.

The mu opioid receptor (MOR) has been regarded as the main site of interaction with analgesics in major clinical use, particularly morphine. The repressor element-1 silencing transcription factor (REST) functions as a transcriptional repressor of neuronal genes in non-neuronal cells. However, it is expressed in certain mature neurons, suggesting that it may have complex and novel roles. In addition, the interactions between MOR and REST and their functions remain unclear. In this study, we examined the effects of morphine on the expression of REST mRNA and protein in human neuroblastoma NMB cells to investigate the roles of REST induced by MOR activation in neuronal cells. To determine the effects of morphine on REST expression, we performed RT-PCR, real-time quantitative RT-PCR, western blot analysis and radioligand binding assays in NMB cells. By RTPCR and real-time quantitative RT-PCR, the expression of REST was found to be unchanged by either the MOR agonist morphine or the MOR specific antagonist CTOP. By western blot, morphine was shown to significantly inhibit the expression of REST, but this suppression was completely blocked by treatment with CTOP. In the radioligand binding assay, the overexpression of REST led to an increased opioid ligand binding activity of endogenous MOR in the NMB cells. These results together suggest that morphine inhibits the expression of REST in human neuroblastoma cells through a post-transcriptional regulatory mechanism mediated through MOR.

A genome project has been launched and aims to sequence total genome of Cotesia plutellae bracovirus. On this process, several open reading frames (ORFs) have been identified. This study was intended to clone and express protein tyrosine phosphatase genes, PTP1 and PTP6. The ORFs of these two genes consist of 900 and 891 bp, respectively. PTP1 and PTP6 are genes of a group of genes that has been implicated as important regulatory components in cell growth, differentiation and malignant transformation by certain viruses. In this work,we studied the cloning and expression patterns of these genes in Plutella xylostella, a lepidopteran host of C. plutellae. A polymerase chain reaction (PCR) produced the corresponding products of PTP1/6. These PCR products were cloned and expressed using an expression vector pBAD-TOPO, and then over-expressed using an inducer, L-arabinose. Then the purified proteins were confirmed using Western blotting (immunoblotting using V5 antibody) and the apparent molecular weights of both proteins were about 40 kDa. Expression of PTP genes were analyzed in the parasitized P. xylostella by realtime RT-PCR, which indicated late expression pattern of both PTPs during parasitization. We are pursuing to elucidate their physiological function in the parasitized host insect.