24,424 research outputs found
(CYCLOPENTADIENONE)IRON COMPLEXES IN REACTIONS INVOLVING HYDROGEN TRANSFER
The PhD project focused on the synthesis and catalytic applications of (cyclopentadienone)iron complexes in reactions involving hydrogen transfer. The manuscript is divided into five chapters, and after a rather comprehensive review on the state of the art in chapter 1, the thesis describes, in the remaining four chapters, the original achievements of the PhD candidate. In particular, chapter 2 describes the applications of highly active [bis(hexamethylene)cyclopentadienone]iron tricarbonyl pre-catalyst for the reduction of imine bonds under transfer hydrogenation conditions and for the reductive amination of carbonyl compounds. In chapter 3, the application of the above mentioned pre-catalyst to alcohol amination reactions via a hydrogen borrowing mechanism is discussed. Chapter 4 deals with enantioselective ketone hydrogenations using chiral (cyclopentadienone)iron complexes containing a stereogenic plane (prepared in racemic form and resolved by chiral HPLC), and with the synthesis of chiral macrocyclic (cyclopentadienone)iron complexes, putatively more suited for the transfer of the chiral information from the catalyst to the substrate. Finally, Chapter 5 describes the immobilization of (cyclopentadienone)iron complexes into a solid support, namely Metal Organic Frameworks (MOFs), to realize an active heterogeneous (cyclopentadienone)iron catalyst for catalyst recycling in batch hydrogenation reactions and potential applications in flow processes
Asymptotic properties of eigenmatrices of a large sample covariance matrix
Let where is a matrix
with i.i.d. complex standardized entries having finite fourth moments. Let
in which
and where
is the Mar\v{c}enko--Pastur law with parameter ; which
converges to a positive constant as , and and are unit vectors in ,
having indices and , ranging in a compact subset
of a finite-dimensional Euclidean space. In this paper, we prove that the
sequence converges weakly to a
-dimensional Gaussian process. This result provides further evidence in
support of the conjecture that the distribution of the eigenmatrix of is
asymptotically close to that of a Haar-distributed unitary matrix.Comment: Published in at http://dx.doi.org/10.1214/10-AAP748 the Annals of
Applied Probability (http://www.imstat.org/aap/) by the Institute of
Mathematical Statistics (http://www.imstat.org
An elitism-based multi-objective evolutionary algorithm for min-cost network disintegration
Network disintegration or strengthening is a significant problem, which is widely used in infrastructure construction, social networks, infectious disease prevention and so on. But most studies assume that the cost of attacking anyone node is equal. In this paper, we investigate the robustness of complex networks under a more realistic assumption that costs are functions of degrees of nodes. A multi-objective, elitism-based, evolutionary algorithm (MOEEA) is proposed for the network disintegration problem with heterogeneous costs. By defining a new unit cost influence measure of the target attack node and combining with an elitism strategy, some combination nodes’ information can be retained. Through an ingenious update mechanism, this information is passed on to the next generation to guide the population to move to more promising regions, which can improve the rate of convergence of the proposed algorithm. A series of experiments have been carried out on four benchmark networks and some model networks, the results show that our method performs better than five other state-of-the-art attack strategies. MOEEA can usually find min-cost network disintegration solutions. Simultaneously, through testing different cost functions, we find that the stronger the cost heterogeneity, the better performance of our algorithm
Tick-borne encephalitis virus induces chemokine RANTES expression via activation of IRF-3 pathway.
BACKGROUND: Tick-borne encephalitis virus (TBEV) is one of the most important flaviviruses that targets the central nervous system (CNS) and causes encephalitides in humans. Although neuroinflammatory mechanisms may contribute to brain tissue destruction, the induction pathways and potential roles of specific chemokines in TBEV-mediated neurological disease are poorly understood. METHODS: BALB/c mice were intracerebrally injected with TBEV, followed by evaluation of chemokine and cytokine profiles using protein array analysis. The virus-infected mice were treated with the CC chemokine antagonist Met-RANTES or anti-RANTES mAb to determine the role of RANTES in affecting TBEV-induced neurological disease. The underlying signaling mechanisms were delineated using RANTES promoter luciferase reporter assay, siRNA-mediated knockdown, and pharmacological inhibitors in human brain-derived cell culture models. RESULTS: In a mouse model, pathological features including marked inflammatory cell infiltrates were observed in brain sections, which correlated with a robust up-regulation of RANTES within the brain but not in peripheral tissues and sera. Antagonizing RANTES within CNS extended the survival of mice and reduced accumulation of infiltrating cells in the brain after TBEV infection. Through in vitro studies, we show that virus infection up-regulated RANTES production at both mRNA and protein levels in human brain-derived cell lines and primary progenitor-derived astrocytes. Furthermore, IRF-3 pathway appeared to be essential for TBEV-induced RANTES production. Site mutation of an IRF-3-binding motif abrogated the RANTES promoter activity in virus-infected brain cells. Moreover, IRF-3 was activated upon TBEV infection as evidenced by phosphorylation of TBK1 and IRF-3, while blockade of IRF-3 activation drastically reduced virus-induced RANTES expression. CONCLUSIONS: Our findings together provide insights into the molecular mechanism underlying RANTES production induced by TBEV, highlighting its potential importance in the process of neuroinflammatory responses to TBEV infection
Sizing energy storage on the 11kV distribution network
The cost and limited flexibility of traditional approaches to 11kV network reinforcement threatens to constrain the uptake of low carbon technologies. Ofgem has released £500m of funding for DNOs to trial innovative techniques and share the learning with the rest of the industry. One of the techniques under study is the addition of Energy Storage at key substations to the network to help with peak load lopping. This paper looks in detail at the sizing algorithm for use in the assessment of alternatives to traditional reinforcement and investigates a method of sizing a battery for use on a Network taking into account load growth, capacity fade and battery lifecycle issues. A further complication to the analysis is the method of operation of the battery system and how this affects the Depth of Discharge (DoD). The proposed method is being trialled on an area of 11kV network in Milton Keynes Central area and the simulation results are presented in this paper
Scheduling Manufacturing Systems With Work-in-Process Inventory Control: Single-Part-Type Systems
In this paper, a real-time feedback control algorithm is developed for scheduling single-part-type production lines in which there are three important classes of activities: operations, failures, and starvation or blockage. The scheduling objectives are to keep the actual production as close to the demand as possible, and to keep the level of work-in-process inventory as low as possible. By relating the starvation and blockage to the system capacity, the buffer sizes and the target buffer levels are chosen according to the demands and machine parameters. The processing time for each operation is deterministic. Failure and repair times are random. Whenever a machine fails or is starved or blocked, the scheduling system recalculates short term production rates. To begin with, we study a very simple case, a two machine and one part type system, to get insight into the buffer effects and production control policies. Using the relationship between system capacity and starvation or blockage, we find desirable buffer levels and buffer sizes. The production control policy is determined to meet the system performance requirements concerning low WIP inventory and tardiness. The results from the simple case are extended to N-machine, one-part-type systems
Celecoxib inhibits tumor growth and angiogenesis in an orthotopic implantation tumor model of human colon cancer
Aim: To examine the effect of celecoxib on tumor growth and angiogenesis in an orthotopic implantation tumor model of colon cancer. Methods: Human colorectal adenocarcinoma HT-29 cells were implanted subcutaneously in nude mice. Four groups of animals received different doses of celecoxib after tumor implantation. After 42 days, all animals were evaluated for changes in body weight, the volume and weight of colorectal tumors, and tumor growth inhibition. The content of prostaglandin E2 (PGE2) in the tumor tissue homogenate was estimated by radioimmunoassay (RIA). Cyclooxygenase-2 (COX-2) and CD34 expression in tumor tissue was assessed by immunohistochemistry, and the microvessel density (MVD) of tumor tissue was determined. Apoptosis of the tumor cells was detected by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). The expression of vascular endothelial growth factor (VEGF) mRNA and matrix metalloproteinase-2 (MMP-2) mRNA extracted from the tumor tissue was analyzed by reverse transcriptase polymerase chain reaction (RT-PCR). Results: There was no statistically significant change in the animals’ body weight between the treatment groups. However, with increasing doses of celecoxib, the volume and weight of the tumor decreased. The rates of tumor growth inhibition for the L (low), M (medium) and H (high) groups were 25.30%, 38.80%, and 76.92%, respectively, which were significant compared to the C (control) group. There were significant differences in COX-2 expression in the tumor tissue between all groups, except between the L and M groups. Celecoxib exposure also reduced PGE2 levels in the tumor tissue homogenates. The level of PGE2 correlated to the weight of tumor (r = 0.8814, P < 0.05) and to COX-2 expression (r = 0.8249, P < 0.05). Compared to the control group, the tumor cells from celecoxib-treated mice had a significantly higher apoptotic index. Celecoxib also decreased CD34+ expression in tumors from treated mice. There were significant differences in the MVD between all groups except between groups H and M. Celecoxib significantly reduced the expression of VEGF and MMP-2 mRNA in the group H but not in L and M groups. The MVD in tumor tissue was closely related to the PGE2 levels, as well as the expression of VEGF and MMP-2 mRNA (r = 0.9006, r = 0.8573 and r = 0.6427, respectively; P < 0.05). Conclusions: By inhibiting COX-2, PGE2 synthesis, and VEGF and MMP-2 mRNA expression in tumor tissue, celecoxib enhances tumor cell apoptosis, thereby inhibiting the growth and angiogenesis of orthotopically implanted tumors in a mouse model of human colorectal cancer.Цель: изучить влияние целекоксиба на рост опухоли и ангиогенез в модели ортопической имплантации опухоли толстой кишки
человека. Методы: клетки колоректальной аденокарциномы человека НT-29 подкожно имплантировали бестимусным мышам.
После имплантации опухоли четыре группы животных получали разные дозы целекоксиба. Через 42 дня изучали изменения
веса животных, объем опухолей, эффект ингибирования роста опухоли. С помощью радиоиммунного анализа (RIA) в гомо- RIA) в гомо ) в гомогенате
опухолей определяли содержание простогландина E2
(PGE2
). В опухолевой ткани иммуногистохимическим методом
выявляли экспрессию циклооксигеназы-2 (COX-2) и CD34 и оценивали плотность микрососудов (MVD). Апоптотические
клетки выявляли методом TUNEL. Экспрессия мРНК фактора роста эндотелия сосудов (VEGF) и металлопротеиназы-2
(MMP-2) в опухолях проанализирована методом обратной транскриптазной реакции (RT-PCR). Результаты: статистически
достоверных различий в весе животных между разными группами обнаружено не было. Вто же время, с увеличением
дозы целекоксиба объем и вес опухоли уменьшался. По сравнению с контрольной группой (C), рост опухоли статистически
достоверно ингибировался в L (низкая доза), M (средняя доза) и H (высокая доза) группах животных на 25,30%, 38,80% и
76,92% соответственно. Были обнаружены значительные отличия в экспрессии COX-2 в опухолевых тканях между всеми
группами животных, кроме групп L и M. Было показано целекоксиб-зависимое уменьшение уровня PGE2
в гомогенатах
опухолей. Уровень PGE2
коррелировал с весом опухоли (r = 0,8814, P < 0,05) и экспрессией COX-2 (r = 0,8249, P < 0,05).
По сравнению с контрольной группой опухолевые клетки мышей, получавших целекоксиб, имели значительно более высокий
апоптотический индекс. Целекоксиб также снижал экспрессию CD34+ на поверхности опухолевых клеток. Были обнаружены
статистически достоверные различия в MVD между всеми исследованными группами, кроме H и M. Целекоксиб способствовал
уменьшению экспрессии мРНК VEGF и MMP-2 в группе Н, но не в группах L и M. MVD в опухолевой ткани кореллировал с
уровнем PGE2
, а также с экспрессией мРНК VEGF и MMP-2 (r = 0,9006, r = 0,8573 и r = 0,6427 соответственно; P < 0,05).
Выводы: целекоксиб способствует апоптозу опухолевых клеток, ингибирует рост опухоли и ангиогенез при ортотопической
имплантации мышам колоректальной аденокарциномы человека. Такой эффект целекоксиба связан с угнетением синтеза
COX-2, PGE2 и экспрессии мРНК VEGF и MMP-2 в опухолевой ткани
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