排序方式: 共有177条查询结果,搜索用时 16 毫秒
11.
12.
13.
Youhei Tanaka Naohiro Hayashibara Tomoya Enokido Makoto Takizawa 《Cluster computing》2007,10(1):81-93
In this paper, we discuss how to realize fault-tolerant applications on distributed objects. Servers supporting objects can
be fault-tolerant by taking advantage of replication and checkpointing technologies. However, there is no discussion on how
application programs being performed on clients are tolerant of clients faults. For example, servers might block in the two-phase
commitment protocol due to the client fault. We newly discuss how to make application programs fault-tolerant by taking advantage
of mobile agent technologies where a program can move from a computer to another computer in networks. An application program
to be performed on a faulty computer can be performed on another operational computer by moving the program in the mobile
agent model. In this paper, we discuss a transactional agent model where a reliable and efficient application for manipulating objects in multiple computers is realized in the mobile agent
model. In the transactional agent model, only a small part of the application program named routing subagent moves around computers. A routing subagent autonomously finds a computer which to visit next. We discuss a hierarchical navigation
map which computer should be visited price to another computer in a transactional agent. A routing subagent makes a decision
on which computer visit for the hierarchical navigation map. Programs manipulating objects in a computer are loaded to the
computer on arrival of the routing subagent in order to reduce the communication overhead. This part of the transactional
agent is a manipulating subagent. The manipulation subagent still exists on the computer even after the routing subagent leaves the computer in order to hold
objects until the commitment. We assume every computer may stop by fault while networks are reliable. There are kinds of faulty
computers for a transactional agent; current, destination, and sibling computers where a transactional agent now exists, will move, and has visited, respectively. The types of faults are detected
by neighbouring manipulation subagents by communicating with each other. If some of the manipulation subagents are faulty,
the routing subagent has to be aborted. However, the routing subagent is still moving. We discuss how to efficiently deliver
the abort message to the moving routing subagent. We evaluate the transactional agent model in terms of how long it takes
to abort the routing subagent if some computer is faulty.
相似文献
Makoto TakizawaEmail: |
14.
Tagad HD Hamada Y Nguyen JT Hidaka K Hamada T Sohma Y Kimura T Kiso Y 《Bioorganic & medicinal chemistry》2011,19(17):5238-5246
Previously, we reported potent pentapeptidic BACE1 inhibitors with the hydroxymethylcarbonyl isostere as a substrate transition-state mimic. To improve the in vitro potency, we further reported pentapeptidic inhibitors with carboxylic acid bioisosteres at the P(4) and P1' positions. In the current study, we screened new P1' position 1-phenylcycloalkylamine analogs to find non-acidic inhibitors that possess double-digit nanomolar range IC(50) values. An extensive structure-activity relationship study was performed with various amine derivatives at the P1' position. The most potent inhibitor of this pentapeptide series, KMI-1830, possessing 1-phenylcyclopentylamine at the P1' position had an IC(50) value of 11.6 nM against BACE1 in vitro enzymatic assay. 相似文献
15.
16.
Aso Y Okuda K Nagao J Kanemasa Y Thi Bich Phuong N Koga H Shioya K Sashihara T Nakayama J Sonomoto K 《Bioscience, biotechnology, and biochemistry》2005,69(7):1403-1410
Staphylococcus warneri ISK-1 produces a lantibiotic, nukacin ISK-1. The nukacin ISK-1 gene cluster consists of at least six genes, nukA, -M, -T, -F, -E, and -G, and two open reading frames, ORF1 and ORF7 (designated nukH). Sequence comparisons suggested that NukF, -E, -G, and -H contribute to immunity to nukacin ISK-1. We investigated the immunity levels of recombinant Lactococcus lactis expressing nukFEG and nukH against nukacin ISK-1. The co-expression of nukFEG and nukH resulted in a high degree of immunity. The expression of either nukFEG or nukH conferred partial immunity against nukacin ISK-1. These results suggest that NukH contributes cooperatively to self-protection with NukFEG. The nukacin ISK-1 immunity system might function against another lantibiotic, lacticin 481. Western blot analysis showed that NukH expressed in Staphylococcus carnosus was localized in the membrane. Peptide release/bind assays indicated that the recombinant L. lactis expressing nukH interacted with nukacin ISK-1 and lacticin 481 but not with nisin A. These findings suggest that NukH contributes cooperatively to host immunity as a novel type of lantibiotic-binding immunity protein with NukFEG. 相似文献
17.
18.
Youhei Sohma Qing-xin Hua Ming Liu Nelson B. Phillips Shi-Quan Hu Jonathan Whittaker Linda J. Whittaker Aubree Ng Charles T. Roberts Jr Peter Arvan Stephen B. H. Kent Michael A. Weiss 《The Journal of biological chemistry》2010,285(7):5040-5055
Proinsulin exhibits a single structure, whereas insulin-like growth factors refold as two disulfide isomers in equilibrium. Native insulin-related growth factor (IGF)-I has canonical cystines (A6—A11, A7–B7, and A20—B19) maintained by IGF-binding proteins; IGF-swap has alternative pairing (A7–A11, A6—B7, and A20—B19) and impaired activity. Studies of mini-domain models suggest that residue B5 (His in insulin and Thr in IGFs) governs the ambiguity or uniqueness of disulfide pairing. Residue B5, a site of mutation in proinsulin causing neonatal diabetes, is thus of broad biophysical interest. Here, we characterize reciprocal B5 substitutions in the two proteins. In insulin, HisB5 → Thr markedly destabilizes the hormone (ΔΔGu 2.0 ± 0.2 kcal/mol), impairs chain combination, and blocks cellular secretion of proinsulin. The reciprocal IGF-I substitution ThrB5 → His (residue 4) specifies a unique structure with native 1H NMR signature. Chemical shifts and nuclear Overhauser effects are similar to those of native IGF-I. Whereas wild-type IGF-I undergoes thiol-catalyzed disulfide exchange to yield IGF-swap, HisB5-IGF-I retains canonical pairing. Chemical denaturation studies indicate that HisB5 does not significantly enhance thermodynamic stability (ΔΔGu 0.2 ± 0.2 kcal/mol), implying that the substitution favors canonical pairing by destabilizing competing folds. Whereas the activity of ThrB5-insulin is decreased 5-fold, HisB5-IGF-I exhibits 2-fold increased affinity for the IGF receptor and augmented post-receptor signaling. We propose that conservation of ThrB5 in IGF-I, rescued from structural ambiguity by IGF-binding proteins, reflects fine-tuning of signal transduction. In contrast, the conservation of HisB5 in insulin highlights its critical role in insulin biosynthesis. 相似文献
19.
Nakajima Y Kato N Nakayama Y Kim DS Takai H Arai M Saito R Samoto H Shimizu E Ogata Y 《Journal of cellular biochemistry》2006,97(6):1198-1206
20.
Nakayama Y Nakajima Y Kato N Takai H Kim DS Arai M Mezawa M Araki S Sodek J Ogata Y 《Journal of cellular physiology》2006,208(2):326-335