Abstract-Aging is associated with dysfunction of endothelial progenitor cells (EPCs), and shear stress has a beneficial impact on EPC function; however, the effects of aging and shear stress on the endothelial repair capacity of EPCs after arterial injury have not been reported. Here we investigated the influence of aging and shear stress on the reendothelialization capacity of human EPCs and the related molecular mechanism. Compared with EPCs isolated from young subjects, EPCs from the elderly displayed an impaired migration and adhesion in vitro and demonstrated a significantly reduced reendothelialization capacity in vivo after transplantation into nude mice with carotid artery denudation injury. Shear stress pretreatment enhances the migration, adhesion, and reendothelialization capacity in both young and elderly EPCs; however, it was to a greater extent in EPCs from the elderly. Although basal CXC chemokine receptor 4 (CXCR4) expression was similar in EPCs from the 2 age groups, the stromal cell derived factor 1-induced CXCR4 and Janus kinase 2 phosphorylations were much lower in the elderly than in young EPCs. Shear stress treatment upregulated CXCR4 expression and phosphorylation and, importantly, restored the stromal cell-derived factor 1/CXCR4-dependent Janus kinase 2 phosphorylation in the elderly EPCs. Furthermore, short hairpin RNA-mediated knockdown of CXCR4 expression or pretreatment with Janus kinase 2 inhibitor diminished the enhancement in the migration, adhesion, and reendothelialization capacity of the elderly EPCs from shear stress treatments. Thus, our study demonstrates that upregulation of the CXCR4/Janus kinase 2 pathway by shear stress contributes to the enhanced reendothelialization capacity of EPCs from elderly men. A ging is a well-recognized risk factor for cardiovascular disease. 1,2 The impact of aging, a traditional detrimental factor, for the increased development of cardiovascular disease is initiated by abnormalities in structure and function of the vascular endothelium.3-5 Thus, it is of particular importance to maintain the integrity of the vascular endothelium after arterial injury with aging.Accelerated reendothelialization is an important therapeutic means for repair of injured artery. Accumulating evidence indicates that circulating endothelial progenitor cells (EPCs) provide an endogenous repair mechanism to counteract ongoing risk factor-induced endothelial injury and to replace dysfunctional endothelium, 6-10 thus suggesting an important role of circulating EPCs for restoration of the integrity of the vascular endothelium with aging. Previous studies showed that aging leads to a reduction in the number of circulating EPCs, and aging is associated with dysfunctional EPCs in both healthy persons and patients with cardiovascular disease, [11][12][13][14][15][16] which is, at least in part, responsible for the development of age-related endothelial injury in humans. [17][18][19] However, the mechanism underlying age-related EPC dysfunction is not fully understood. It is, t...

Abstract-CD4 T cells, through the release of cytokines as well as direct effector functions, have been implicated in promoting inflammation of the atherosclerotic plaque. Plaque-infiltrating CD4 T cells include a specialized subset of CD4 ϩ CD28 Ϫ T cells that express a unique profile of regulatory receptors and are responsive to novel microenvironmental cues. Here we report that CD4 ϩ CD28 Ϫ T cells, either isolated from the plaque tissue or from the blood of patients with acute coronary syndrome (ACS), spontaneously express interleukin (IL)-12 receptors, even in the absence of antigenic stimulation. CD4 ϩ CD28 Ϫ IL-12R ϩ cells responded to IL-12 stimulation with the upregulation of the chemokine receptor CCR5 and the C-type lectin receptor CD161, both implicated in regulating tissue homing of effector T cells. IL-12 treatment of CD4 ϩ CD28 Ϫ T cells enhanced their chemotaxis and transendothelial migration toward the chemokine CCL5. In vivo relevance for the role of IL-12 in regulating the recruitment of CD4 ϩ CD28 Ϫ T cells into the atheroma was examined in human atheroma-SCID mouse chimeras. Exposure of nonstimulated CD4 ϩ CD28 Ϫ T cells to IL-12 was sufficient to amplify T-cell accumulation within the inflamed plaque, and coadministration of anti-CCR5 antibodies blocked T-cell recruitment into the plaque. Thus, CD4ϩ CD28 Ϫ T cells functionally resemble NK cells, which have proinflammatory activity even in the unprimed state and respond to any IL-12-inducing host infection with a shift in tissue trafficking and accrual in inflammatory lesions. (Circ Res. 2006;98:524-531.) Key Words: inflammation Ⅲ interleukins Ⅲ cytokines Ⅲ T lymphocyte Ⅲ vascular inflammation T he cellular and biological events causing acute coronary syndrome (ACS) have been linked to the process of plaque rupture and superimposed thrombosis, leading to vessel occlusion and ischemia. 1 Tissue disruption in the atheroma has multiple underlying causes; yet the presence of plaque inflammation is an excellent predictor of vulnerability. 2 Plaque-infiltrating cells are composed of macrophages, dendritic cells (DC), and T cells, all of which contribute to the ultimate outcome of tissue injury. T cells mediate inflammatory damage through 2 pathways: either by regulating the functional activity of macrophages, 3 endothelial cells, and vascular smooth muscle cells or via direct cytotoxicity. 4 Little is known about signals that regulate T-cell recruitment to and retention in the plaque and their functional activity in the nonlymphoid microenvironment of the vessel wall.Plaque-infiltrating T cells are enriched for a particular subset, CD4 ϩ CD28 Ϫ T cells. 5 Such CD4 ϩ CD28 Ϫ T cells are proinflammatory lymphocytes, which produce high amounts of interferon (IFN)-␥ 6 and tumor necrosis factor (TNF)-␣. 7 They also are efficient killer cells, expressing perforin and granzyme B, and lyse endothelial target cells. 8 CD4 ϩ CD28 Ϫ T cells have an unusual chemokine receptor profile, including expression of CX 3 CR1, a receptor typically expressed by NK cells ...

Figure 1. Examples created by Text-to-Viz. (a)-(d) are generated from the statement: "More than 20% of smartphone users are social network users." (e) and (f) are generated from the statement: "40 percent of USA freshwater is for agriculture." (g) and (h) are generated from the statement: "3 in 5 Chinese people live in rural areas." (i) and (j) are generated from the statement: "65% of coffee is consumed at breakfast." (k)-(m) are generated from the statement: "Among all students, 49% like football, 32% like basketball, and 21% like baseball." (n) and (o) are generated from the statement: "Humans made 51.5% of online traffic, while good bots made 19.5% and bad bots made 29%."Abstract-Combining data content with visual embellishments, infographics can effectively deliver messages in an engaging and memorable manner. Various authoring tools have been proposed to facilitate the creation of infographics. However, creating a professional infographic with these authoring tools is still not an easy task, requiring much time and design expertise. Therefore, these tools are generally not attractive to casual users, who are either unwilling to take time to learn the tools or lacking in proper design expertise to create a professional infographic. In this paper, we explore an alternative approach: to automatically generate infographics from natural language statements. We first conducted a preliminary study to explore the design space of infographics. Based on the preliminary study, we built a proof-of-concept system that automatically converts statements about simple proportionrelated statistics to a set of infographics with pre-designed styles. Finally, we demonstrated the usability and usefulness of the system through sample results, exhibits, and expert reviews.