Resolvin E1 (RvE1) is an omega-3 eicosapentaenoic acid (EPA)-derived lipid mediator generated during resolution of inflammation and in human vasculature via leukocyte-endothelial cell interactions. RvE1 possesses anti-inflammatory and proresolving actions. Here, we report that RvE1 in human whole blood rapidly regulates leukocyte expression of adhesion molecules. RvE1 in the 10-to 100-nM range stimulated L-selectin shedding, while reducing CD18 expression in both neutrophils and monocytes. When added to whole blood, RvE1 did not stimulate reactive oxygen species by either neutrophils or monocytes, nor did it directly stimulate cytokine/chemokine production in heparinized blood. Intravital microscopy (IVM) demonstrated that RvE1 rapidly reduced leukocyte rolling (ϳ ϳ 40%) in venules of mice. In human platelet-rich plasma (PRP), RvE1 selectively blocked both ADP-stimulated and thromboxane receptor agonist U46619-stimulated platelet aggregation in a concentrationdependent manner. In contrast, ⌬6,14- IntroductionInflammation is now widely recognized as a central component in several of the most prevalent human diseases in the developed world, including rheumatic diseases, asthma, diabetes, Alzheimer disease, and various cardiovascular conditions such as thrombosis, stroke, and atherosclerosis. 1,2 Earlier results from humans and animals suggest that omega-3 polyunsaturated fatty acids (PUFAs) such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have diverse beneficial actions in many inflammatory disorders. [3][4][5] The underlying cellular and molecular mechanisms responsible for their beneficial actions had remained for the most part elusive. Recently, we identified novel families of lipid mediators generated from EPA and DHA named resolvins and protectins, because they possess potent anti-inflammatory and proresolving actions. Collectively, these results emphasize the importance of -3 PUFAs as precursors for novel potent bioactive mediators. [6][7][8] The name resolvin (resolution phase interaction products) was introduced for these endogenous bioactive compounds because they were originally identified in spontaneous self-limited murine inflammatory exudates in vivo. 6,7 Resolvin E1 (RvE1) is also generated by human cell types during, for example, cell-cell interactions from EPA typified by endothelial cell and leukocyte interactions. 6 In vascular endothelial cells, aspirin-acetylated COX-2 converts EPA to 18R-hydro(peroxy)-EPE, which is quickly reduced to 18R-HEPE. 18R-HEPE is then released from endothelium and rapidly transformed by activated human polymorphonuclear leukocyte (PMN) in the proximity to a bioactive trihydroxy-containing product, termed resolvin E1 (RvE1). 6 In addition, RvE1 is also produced in vivo in humans via aspirin-independent routes via mechanisms involving P450 6 and was recently found to be generated from EPA by Candida albicans. 9 RvE1 biosynthesis in C albicans, for example, occurs in the absence of other cellular partners when EPA is present in the milieu and its biosy...
Acute inflammation and its resolution are essential processes for tissue protection and homeostasis. In this context, specialized proresolving mediators derived from polyunsaturated fatty acids are of interest. In this study, we report that resolvin E2 (RvE2) from eicosapentaenoic acid is endogenously produced during self-limited murine peritonitis in both the initiation and resolution phases. RvE2 (1–10 nM) carries potent leukocyte-directed actions that include: 1) regulating chemotaxis of human neutrophils; and 2) enhancing phagocytosis and anti-inflammatory cytokine production. These actions appear to be mediated by leukocyte G-protein–coupled receptors as preparation of labeled RvE2 gave direct evidence for specific binding of radiolabeled RvE2 to neutrophils (Kd 24.7 ± 10.1 nM) and resolvin E1 activation of recombinant G-protein–coupled receptors was assessed. In addition to the murine inflammatory milieu, RvE2 was also identified in plasma from healthy human subjects. RvE2 rapidly downregulated surface expression of human leukocyte integrins in whole blood and dampened responses to platelet-activating factor. Together, these results indicate that RvE2 can stimulate host-protective actions throughout initiation and resolution in the innate inflammatory responses.
Computer guided implant treatment allows implants and associated restorations to be precisely placed during the same procedure directly through the gingiva with reduced postoperative complications and surgical time. When bone height is adequate but very narrow, the virtual guided sleeve is often placed too deeply into the ridge crest interfering with the seating of the surgical template. This case report of a patient exhibiting very narrow residual ridges due to severe resorption describes a new computer guided procedure using a single surgical template maintaining bone height and immediate restoration without a mucoperiosteal flap. The success of this technique is the result of innovative modifications in the software as well as instrumentation. Modifications include planning a different implant length virtually to raise the position of guide sleeves, alteration of drilling sequences, modifications of the start drill, incorporation of osteotomes, and use of an alternative implant seating mount. The combination of these methods allows for deeper site preparation and implant seating beyond the default settings, without any crestal bone reduction. These modifications not only make the guided concept possible for the entire preparation and seating procedures, but also allow for the slight removal of bone that would interfere with the implant seating through the surgical template without a mucoperiosteal flap. This new approach to computer guided surgery maintains prosthetic precision in the fabrication of a provisional restoration prior to implantation with minimal delivery adjustments using prefabricated conical abutments when placing implants at differing levels into the high narrow ridge.
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