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Hypothermia is an effective neuroprotective treatment for brain injury caused by intracerebral hemorrhage (ICH). It is reported to reduce brain edema and neuronal cell death. Thrombin, a coagulation protease released from blood clots, is critical in brain edema formation following ICH. Protease activated receptor-1 (PAR-1), matrix metalloproteinase-9 (MMP-9) and aquaporin 4 (AQP4) are edema-associated mediators that have been implicated in ICH pathology. In the present study, thrombin was used to induce brain edema in adult male Sprague-Dawley rats. Differences between a focal mild hypothermic group (33±0.5 °C) and a normothermic group (37 °C) were investigated. Following hypothermia, brain water content and blood-brain barrier (BBB) disruption was assessed at 6, 24 and 48 h and subsequently at 3, 5 and 7 days. At the same time, the mRNA and protein expression of PAR-1, MMP-9 and AQP4 were also determined. It was identified that brain water content and BBB disruption increased at 6 h and reached a maximal level at 24 h in the normothermic group. The mRNA and protein expression levels of PAR-1, MMP-9 and AQP4 started to increase at 24 h and reached a maximal level at 48 h. Focal mild hypothermia tended to significantly reduce brain water content, BBB disruption and PAR-1, MMP-9 and AQP expression at 24 and 48 h. The present data suggest that focal mild hypothermia is an effective treatment for edema formation through moderation of the mRNA and protein expression of PAR-1, MMP-9 and AQP4. [ABSTRACT FROM AUTHOR]

Background: The receptor for advanced glycation end products (RAGE) and its proinflammatory ligand, S100-calgranulins, are critically implicated in the pathological progression of multiple sclerosis (MS). A functional polymorphism within the V-type immunoglobulin domain of RAGE gene, p.82G>S (c.557G>A), has been shown to affect ligand binding affinity and thus may affect susceptibility to MS.Methods: The RAGE p.82G>S polymorphism was genotyped in 144 MS patients and 156 healthy controls using polymerase chain reaction – restriction fragment length polymorphism. A replication study was performed on a second cohort comprising 138 patients and 150 controls. The relationship between the RAGE p.82G>S polymorphism and circulating levels of soluble RAGE (sRAGE), a secreted decoy receptor against RAGE signaling, was also investigated.Results: In both initial and replication cohorts, an increased MS risk was detected in RAGE p.82G>S variant allele carriers (odds ratio [OR] = 1.786, p = 0.0134 and OR = 1.732, p = 0.0210, respectively). This association signal persisted in subgroups of women and patients with relapsing–remitting MS. Moreover, compared with the wild-type 82GG carriers, carriers of the variant allele presented a faster progression of disability and a reduced serum sRAGE level.Conclusions: The present study provides preliminary evidence that the gain-of-function p.82G>S polymorphism in the RAGE gene is associated with an increased risk of MS in the Chinese population. [ABSTRACT FROM AUTHOR]

The receptor for advanced glycation end products (RAGE) is associated with several pathological states including Alzheimer’s disease (AD) pathology, while its soluble form (sRAGE) acts as a decoy receptor. We have tested for association of AD with a functional single-nucleotide polymorphism (SNP) in the RAGE gene (G82S; rs2070600), a SNP associated with increased ligand affinity of RAGE. Analysis of a Chinese cohort (276 cases; 254 controls) showed a higher prevalence of the RAGE 82S allele and GS + SS genotype in the patients [82S vs. 82G: P = 0.017, odds ratio (OR) = 1.431; GS + SS vs. GG: P = 0.025, OR = 1.490]. Further stratification analysis revealed that the association of the RAGE G82S polymorphism with AD was significant in early onset AD stratum. Moreover, plasma sRAGE levels were lower in AD than in normal elderly controls, and the presence of the risk allele was associated with further plasma sRAGE reduction and a fast cognitive deterioration. The present study provides preliminary evidence that the RAGE G82S variant is involved in genetic susceptibility to AD. [ABSTRACT FROM AUTHOR]

Background/Aim: Interleukin-8 (IL-8), a potent chemoattractant for neutrophils, has been implicated in the pathogenesis of Alzheimer’s disease (AD). The ability of individuals to produce high levels of IL-8 is partially determined by the IL-8 –251 T/A polymorphism. Therefore, we investigated the association between this polymorphism and AD in a Chinese population. Additionally, in light of the stimulatory effect of homocysteine on the production of IL-8, we also sought to determine whether the methylenetetrahydrofolate reductase (MTHFR) gene 677 C/T variant, a genetic modifier of the serum homocysteine level, may interact with the IL-8 –251 polymorphism in determining the AD risk. Methods: Genotyping of 198 AD patients and 240 matched controls was performed by PCR-RFLP. Results: The presence of the MTHFR 677 C/T and 677 T/T genotypes conferred a marginally significant increase in the risk for AD (OR = 1.666, 95% CI = 1.022–2.715, and OR = 1.892, 95% CI = 1.124–3.187) and the presence of the IL-8 –251 polymorphism was not associated with AD. However, the OR for AD associated with joint occurrence of the MTHFR 677 T/T and the IL-8 –251 A/A genotypes was 2.512 (95% CI = 1.151–5.483). Conclusion: Our data suggest a critical role for IL-8/MTHFR interactions in the development of AD. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

In this paper, we propose a practical parallel algorithm for computing a mod c. The algorithm is based on RNS representatins of integers. In particular, a technique is introduced for avoiding overflow. The algorithm is easy to be implemented on hardware and achieves linear speedup. [ABSTRACT FROM AUTHOR]

The contract net protocol has developed to specify problem solving communication for nodes in a distributed problem solving. Task distribution is affected by a negotiation process, a discussion carried on between nodes with tasks to be executed and nodes that may be able to execute those tasks. In contract net protocol, once negotiation successes, the task execution is assumed to success. However, in real world, even though a task is awarded to successfully bidding nodes, it may be delayed. Such delay may badly propagate in whole system. Here, we introduce real-time constraints into contract net protocol to manage task execution for avoiding the task's delay, or even though being delayed, the failure cannot propagate to whole system. In this paper, we first present a real-time contract net protocol which is an extension of contract net protocol with real-time constraints for distributed computing. Our proposition extends the basic negotiation protocol to negotiation and controlling execution of task. The controlling process is based on task deadline time we also present an extension of the internode language of contract net protocol specification with real-time constraints [ABSTRACT FROM AUTHOR]