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In this paper, we propose a new method for constructing a bilinear pairing over (hyper)elliptic curves, which we call the R-ate pairing. This pairing is a generalization of the Ate and Ate i pairing, and also improves efficiency of the pairing computation. Using the R-ate pairing, the loop length in Miller's algorithm can be as small as log(r 1/φ(k) ) for some pairing-friendly elliptic curves which have not reached this lower bound. Therefore we obtain from 29% to 69% savings in overall costs compared to the Ate i pairing. On supersingular hyperelliptic curves of genus 2, we show that this approach makes the loop length in Miller's algorithm shorter than that of the Ate pairing.

Acupuncture is frequently used as an alternative therapy for Parkinson's disease (PD), and it attenuates dopaminergic (DA) neurodegeneration in the substantia nigra (SN) in PD animal models. Using proteomic analysis, we investigated whether acupuncture alters protein expression in the SN to favor attenuation of neuronal degeneration. In C57BL/6 mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 30 mg/kg/day), intraperitoneal (i.p.) for 5 days, 2 or 100 Hz electroacupuncture (EA) was applied at the effective and specific acupoint, GB34, once a day for 12 consecutive days from the first MPTP treatment. Both treatments in MPTP mice led to restoration of behavioral impairment and rescued tyrosine hydroxylase (TH)-positive DA neurodegeneration. Using peptide fingerprinting MS, we identified changes in 22 proteins in the SN following MPTP treatment, and nine of these proteins were normalized by EA. They were involved in cell death regulation, inflammation, or restoration from damage. The levels of cyclophilin A (CypA), which is a neuroprotective agent, were unchanged by MPTP treatment but were increased in MPTP-EA mice. These results suggest that acupoint GB34-specific EA changes protein expression profiles in the SN in favor of DA neuronal survival in MPTP-treated mice, and that EA treatment may be an effective therapy for PD patients.

LCB01-0371 is a new oxazolidinone with cyclic amidrazone. In vitro activity of LCB01-0371 against 624 clinical isolates was evaluated and compared with those of linezolid, vancomycin, and other antibiotics. LCB01-0371 showed good activity against Gram-positive pathogens. In vivo activity of LCB01-0371 against systemic infections in mice was also evaluated. LCB01-0371 was more active than linezolid against these systemic infections. LCB01-0371 showed bacteriostatic activity against Staphylococcus aureus.The emergence of multidrug-resistant (MDR) pathogens, such as methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant coagulase-negative staphylococci (MRCNS), penicillin-resistant Streptococcus pneumoniae (PRSP), and vancomycinresistant enterococci (VRE), has generated worldwide concern in the medical community (11). The requirement for effective new antimicrobial agents to treat infections caused by Gram-positive organisms is becoming urgent as resistance to existing agents arises and spreads around the world.The oxazolidinones, a totally synthetic class of novel antibiotics, have strong activity against nearly all Gram-positive organisms, including those resistant to other agents (1, 10). They inhibit protein synthesis by binding to domain V of the 23S rRNA and thereby blocking formation of the initiation complex (6). Linezolid is the first member of the oxazolidinone class approved by the FDA in the United States. The success of linezolid and the occurrence of strains resistant to linezolid in clinical isolates of Enterococcus faecium (4, 5) and S. aureus (12) have inspired further efforts toward developing new oxazolidinones with improved safety and antibacterial activity.LCB01-0371 ( Fig. 1), a novel oxazolidinone with cyclic amidrazone, was synthesized by LegoChem BioSciences Inc. (Daejeon, Republic of Korea). In this study, in vitro activity of LCB01-0371 was compared with those of eight different antibacterial agents against 624 clinical isolates that were collected from several general hospitals in the Republic of Korea. In vivo activity of LCB01-0371 against systemic infections in mice and time-kill studies of LCB01-0371 against S. aureus giorgio (methicillin-susceptible S. aureus [MSSA]) and S. aureus p125 (MRSA) were also investigated.(This study was presented in part at the 49th Annual Interscience Conference on Antimicrobial Agents and Chemotherapy, San Francisco, CA, 2009 [7].)In vitro MICs were determined by the 2-fold agar dilution method as described by the Clinical and Laboratory Standards Institute (CLSI) (3). Mueller-Hinton agar (MHA) medium was used for testing aerobic and facultative organisms. Streptococcus pneumoniae, Streptococcus pyogenes, and Moraxella catarrhalis were grown on Mueller-Hinton agar supplemented with 5% defibrinated sheep blood (Hanil Komed Ltd., Sungnam City, Republic of Korea). Mueller-Hinton agar supplemented with 3% Fildes enrichment (Oxoid Ltd., Basingstoke, Hampshire, England) was used for Haemophilus influenzae. Bacteria (10 4 to 10 5 CFU) were s...

Given its individualized and practical characteristics, KA is expected to make significant contributions to the understanding and the treatment of neurological disorders through basic research and clinical trials.

Acacetin (5,7-dihydroxy-4'-methoxyflavone), a constituent of flavone naturally present in plants, has anti-cancer and anti-inflammatory activities. Neuroinflammation is thought to be one of the major pathological mechanisms responsible for Parkinson's disease (PD), and has been a primary target in the development of treatment for PD. In the present study, we evaluated the neuroprotective effect of acacetin in PD induced by 1-methyl-4-phenylpyridine (MPP+)/or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and examined the related pathways in vitro and in vivo. In primary mesencephalic culture, acacetin protected dopaminergic (DA) cells and inhibited production of inflammatory factors such as nitric oxide, prostaglandin E2, and tumor necrosis factor-α against MPP+-induced toxicity in a dose-dependent manner. Then, we confirmed the effect of acacetin (10 mg/kg/d for 3 d, per os (p.o.)) in a mouse model of PD induced by MPTP (30 mg/kg/d for 5 d, intraperitoneally (i.p.)). In the behavioral test (pole test), the acacetin-treated mice showed decreased time of turning and locomotor activity, which were longer in MPTP-only treated mice. In addition, the acacetin-treated group inhibited degeneration of DA neurons and depletion of dopamine level induced by MPTP toxicity in the substantia nigra and striatum of the brain. Moreover, the acacetin-treated group inhibited microglia activation, accompanied by production of inducible nitric oxide synthases and cyclooxygenase-2. These results suggest that acacetin can protect DA neurons against the neurotoxicity involved in PD via its anti-inflammatory action.

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