The cell adhesion molecule E-cadherin is widely expressed in human atherosclerotic lesions

OBJECTIVE: Various cell adhesion molecules are expressed in atherogenesis and the significance of their involvement in atherosclerotic lesion formation is well appreciated. In the present work, we examined whether the Ca(2+)-dependent cell adhesion molecule E-cadherin is also involved in atherogenesis. METHODS: Specimens of carotid artery and aorta were obtained at operation. Expression of E-cadherin was studied by an immunohistochemical method. The nature of E-cadherin-expressing cells was examined by comparative analysis of consecutive sections and by a double immunostaining procedure. An immunohistochemical approach was also applied to examine how the accumulation of oxidised low density lipoproteins (LDL) by intimal cells is associated with E-cadherin expression. RESULTS: No E-cadherin+ cells were found in normal non-atherosclerotic intima but E-cadherin+ cells were present in 96% of the atherosclerotic lesions. In atherosclerotic intima, E-cadherin was expressed by intimal cells showing varying degrees of transformation into foam cells. These E-cadherin+ cells also contained oxidised LDL in their cytoplasm. Differing numbers of CD68+ foam cells (15% to 60%) expressed E-cadherin but all the CD68+ macrophages without signs of transformation into foam cells were negative for E-cadherin. Neither smooth muscle cells nor foam cells of smooth muscle cell origin (smooth muscle alpha-actin+) were found to be positive for E-cadherin. T-cells (CD3+) and endothelial cells (von Willebrand factor+) were also negative for E-cadherin. Only a few vascular dendritic cells (S-100+) expressed E-cadherin and their expression was weak. We also found that a large proportion (40% to 85%) of E-cadherin+ cells did not stain with any cell-type specific markers. CONCLUSIONS: The finding that E-cadherin is expressed in atherosclerotic lesions expands our knowledge of cell adhesion molecules involved in atherogenesis. That E-cadherin is expressed in intimal cells transforming into foam cells suggests that lipid accumulation might be associated with the alteration and reorganisation of cell-to-cell interactions in atherogenesis. The present observations might assist in understanding the mechanisms associated with intracellular lipid accumulation.     

The effect of exercise on the riboflavin status of adult men

Six sedentary to moderately active men with biochemical signs of riboflavin deficiency were studied under metabolic ward conditions to examine the effects of physical activity on riboflavin status. All participants were subjected to additional exercise (EXER) for an 18 d period between two maintenance (M1 and M2) periods (16 and 13 d respectively) of habitual physical activity. Energy balance and riboflavin intake were maintained throughout the study. Riboflavin status, as judged by a significant reduction in erythrocyte glutathione reductase (EC 1.6.4.2) activation coefficient (EGR-AC), improved on changing from home (1.53 (SD 0.14)) to period M1 (1.36 (SD 0.21)) diets. The exercise period, however, resulted in a significant deterioration in riboflavin status (1.57 (SD 0.31)) which persisted in the subsequent period M2 (1.54 (SD 0.15)). There was a concomitant fall in the urinary excretion of riboflavin only in the EXER period, when results were expressed as a percentage of the dietary intake of riboflavin. These results suggest an increased demand for the vitamin for selective biochemical functions during exercise. However, the energy cost of walking (treadmill 4 km/h), 50 W and 100 W work-loads (bicycle ergometer) as well as delta mechanical efficiency (DME) did not change during the three metabolic periods. The urinary excretion of riboflavin was inversely related to DME (r -0.49; P < 0.05) and directly correlated with haemoglobin levels (r 0.63; P < 0.005). The present study suggests that riboflavin status further deteriorates during a short period of increased physical activity in individuals whose riboflavin status is marginal.     

Chromosome Reconstruction from Physical Maps Using a Cluster of Workstations

Ordering clones from a genomic library into physical maps of whole chromosomes presents a central computational problem in genetics. Chromosome reconstruction via clone ordering is shown to be isomorphic to the classical NP-complete Optimal Linear Arrangement problem. Parallel algorithms for simulated annealing and microcanonical annealing based on Markov chain decomposition are proposed and applied to the problem of chromosome reconstruction via clone ordering. These algorithms are implemented on a cluster of UNIX workstations using the Parallel Virtual Machine (PVM) system. PVM is a software system that permits a heterogeneous collection of networked computers to be viewed by a user's program as a single monolithic parallel computing resource. The parallel algorithms are implemented and tested on clonal data derived from Chromosome IV of the fungus Asperigillus nidulans Perturbation methods and problem-specific annealing heuristics for the parallel simulated annealing and parallel microcanonical annealing algorithms are proposed and described. Convergence, speedup and scalability characteristics of the various parallel algorithms are analyzed and discussed. This revised version was published online in June 2006 with corrections to the Cover Date.     

常态化推进水库标准化管理的对策思考

江西省1万余座水库通过3年标准化管理创建工作,基本达到标准化管理要求.为保持现有成果并逐渐提升工程管理水平,有必要采取针对性的措施来常态化推进水库标准化管理.本文提出了建立标准化管理监管服务平台、培育社会化专业化技术服务市场、加大技术培训力度、健全落实激励机制等4个方面的具体对策措施,具有较强的操作性和实用性,可供各级管理人员参考借鉴.     

电厂热力系统分析方法的研究现状及发展趋势

本文系统介绍了当前国内热力系统热经济性分析方法的研究现状,回顾了国内在该领域的发展过程。根据掌握的文献资料客观地评价了几种目前较典型的热经济性分析方法的优点与不足,最后在总结已分析的基础上提出了对于热力系统分析方法研究趋势的新观点。     

Electric field-induced changes in agonist-stimulated calcium fluxes of human HL-60 leukemia cells

The mechanism of biological effects of extremely-low-frequency electric and magnetic fields may involve induced changes of Ca2+ transport through plasma membrane ion channels. In this study we investigated the effects of externally applied, low-intensity 60 Hz electric (E) fields (0.5 V/m, current density 0.8 A/m2) on the agonist-induced Ca2+ fluxes of HL-60 leukemia cells. The suspensions of HL-60 cells received E-field or sham exposure for 60 min and were simultaneously stimulated either by 1 microM ATP or by 100 microM histamine or were not stimulated at all. After E-field or sham exposure, the responses of the intracellular calcium levels of the cells to different concentrations of ATP (0.2-100 microM) were assessed. Compared with control cells, exposure of ATP-activated cells to an E-field resulted in a 20-30% decrease in the magnitude of [Ca2+]i elevation induced by a low concentration of ATP (<1 microM). In contrast, exposure of histamine-activated HL-60 cells resulted in a 20-40% increase of ATP-induced elevation of [Ca2+]i. E-field exposure had no effect on non-activated cells. Kinetic analysis of concentration-response plots also showed that compared with control cells, exposure to the E-field resulted in increases of the Michaelis constant, Km, value in ATP-treated cells and of the maximal [Ca2+]i peak rise in histamine-treated HL-60 cells. The observed effects were reversible, indicating the absence of permanent structural damages induced by acute 60 min exposure to electric fields. These results demonstrate that low-intensity electric fields can alter calcium distribution in cells, most probably due to the effect on receptor-operated Ca2+ and/or ion channels.     

TCP-DCR: a novel protocol for tolerating wireless channel errors

This paper presents TCP-DCR, a set of simple modifications to the TCP protocol to improve its robustness to channel errors in wireless networks. TCP-DCR is based on the simple idea of allowing the link-level mechanism to recover the packets lost, due to channel errors, thereby limiting the response of the transport protocol to mostly congestion losses. This is done by delaying the triggering of congestion response algorithms for a small bounded period of time /spl tau/ to allow the link-level retransmissions to recover the loss due to channel errors. If at the end of the delay /spl tau/ the packet is not recovered, then it is treated as a packet lost due to congestion. We analyze TCP-DCR to show that the delay in congestion response does not impact the fairness towards the native implementations of TCP that respond to congestion immediately after receiving three dupacks. We evaluate TCP-DCR through simulations to show that it offers significantly better performance when channel errors contribute more towards packet losses in the network with no or minimal impact on the performance when congestion is the primary cause for packet loss. We also present an analysis to show that the number of flows in the network significantly influences protocol evaluation in the wireless networks.