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Published article online:
08 Dec 2006 =
Issue=20 online:
04 Apr 2007

Received for publication: 13 August 2006 = Accepted for=20 publication: 7 September 2006

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International Journal of Experimental = Pathology

Volume 88 Issue 2 Page 85-94, April 2007

To cite this article: Toby Lawrence, Derek W. Gilroy = (2007)=20
Chronic inflammation: a failure of resolution?
International = Journal of=20 Experimental Pathology 88 (2), 85=E2=80=9394. =
doi:10.1111/j.1365-2613.2006.00507.x=20

Next=20 Article

Full Text

REVIEW ARTICLE

Chronic inflammation: a failure of = resolution?

Toby Lawrence**Kennedy Institute = of=20 Rheumatology Division Faculty of Medicine, Imperial College,=20 London and=20
Derek W. GilroyDepartment of Medicine, University College = London,=20 London, UK

*Kennedy Institute of = Rheumatology Division=20 Faculty of Medicine, Imperial College, London, and Department of Medicine, University College = London,=20 London, UK

Dr Toby Lawrence
Kennedy Institute of = Rheumatology Division
Faculty of Medicine
Imperial = College
London W6=20 8LH
UK
Tel: +44(0)20 83834765
Fax: +44(0)20 83834499
E-mail: = t.lawrence@imperial.ac.uk

Summary

Inflammation has evolved as a protective response to = insult or=20 injury, it's a primordial response that eliminates or neutralises = foreign=20 organisms or material, the resolution of inflammation encompasses the = endogenous=20 anti-inflammatory mechanisms that protect us against excessive tissue = injury and=20 promote the restoration of tissue structure and function. In fact, our = well=20 being and survival depends upon its efficiency and carefully-balanced = control.=20 In general, the innate inflammatory response initiates within minutes = and, if=20 all is well, resolves within hours. In contrast, chronic inflammation = persists=20 for weeks, months or even years. Here, we are going to discuss the key=20 endogenous checkpoints necessary for mounting an effective yet limited=20 inflammatory response and the crucial biochemical pathways necessary to = prevent=20 its persistence.

The Inflammatory Response (Celsus = 90 AD)

Acute inflammation is characterized by leucocyte = recruitment from=20 the circulation, classically defined by the initial trafficking of=20 polymorphonuclear granulocytes followed by monocytes which differentiate = locally=20 into macrophages (Majno 1975).=20 Invariably, this response is triggered by tissue mast cells and resident = macrophages, whose degranulation and activation sequentially release a = battery=20 of inflammatory mediators, including bioactive amines (Histamine and = 5-HT),=20 cytokines, chemokines as well as lipid mediators that collectively = recruit and=20 activate inflammatory cells as well as bring about oedema formation. = While this=20 system has an enormous capacity for synergy and redundancy, over the = years it=20 has served as the stable basis for the development of anti-inflammatory = drug=20 discovery, typified by the development of non-steroidal = anti-inflammatory=20 inhibitors of eicosanoid synthesis beginning in the 1960s to more recent = times=20 with the inhibition of the actions of tumour necrosis = factor-=CE=B1=20 (TNF=CE=B1). These early days of inflammation research that = focused on=20 elucidating the nature of soluble pro-inflammatory mediators have now = given way=20 to the view that inflammation is far more complex and sophisticated than = originally appreciated. This is illustrated by the production of both = pro- and=20 anti-inflammatory eicosanoids which have important roles in = orchestrating the=20 inflammatory response (Lawrence=20 et al. 2002). Such clear diversity is not the preserve = of lipid=20 mediators but it extends to cytokines, chemokines and the expression of = both=20 activating receptors and inhibitory receptors by inflammatory cells. On = this=20 theme of biological diversity, recent evidence suggests that alternative = pattern=20 recognition receptors of the scavenger receptor and C-type lectin = families may=20 play equally important roles in the recognition of microbes and the = regulation=20 of the host-inflammatory response. Thus, the C-type lectin, Dectin-1 (Brown & Gordon 2005), was = recently shown=20 to act in concert with the TLR-2 to activate macrophages exposed to=20 =CE=B2-glucans from the yeast candida albicans (Gantner et al. 2003). = A number=20 of these receptors also recognize endogenous inflammatory ligands = including the=20 scavenger receptors SR-A and CD36, both of which have been described to = mediate=20 the phagocytosis of apoptotic cells leading to a downregulation of = macrophage=20 activation (Savill = et al.=20 1990; Ren et al. = 1995; Savill et al. 2003). = Thus, many=20 of the factors that drive inflammation also double up in bringing about = its=20 resolution.

Signalling pathways in inflammation

The inflammatory response is characterized by = coordinated=20 activation of various signalling pathways that regulate expression of = both pro-=20 and anti-inflammatory mediators in resident tissue cells and recruited=20 leucocytes. Currently, most of our knowledge of signalling in = inflammation is=20 gained from studying members of interleukin 1 (IL-1) and TNF receptor = families=20 and the Toll-like microbial pattern recognition receptors (TLRs) which = in fact=20 belong to the IL-1R family. IL-1 and TNF=CE=B1 represent the = archetypal=20 pro-inflammatory cytokines which are rapidly released upon tissue injury = or=20 infection. TLRs recognize microbial molecular patterns; hence, the term = pattern=20 recognition receptor (PRR). Therefore, TLRs represent a germline encoded = non-self recognition system that is hard-wired to trigger inflammation. = However,=20 there is some suggestion that endogenous ligands may trigger TLRs during = tissue=20 injury and certain disease states which may act to promote inflammation = in the=20 absence of infection (Karin=20 et al. 2006). Although structurally different, these = receptors=20 use similar signal transduction mechanisms. Receptor engagement results = in=20 recruitment of adaptor proteins, that possess either Toll-IL-1 receptor = (TIR)=20 domains in the case of TLRs and IL-1R or death domains (DD) in the case = of the=20 TNFR family, linked to the regulation of cell survival (Muppidi et al. 2004). = Once=20 recruited, these adaptors recruit further signalling proteins that = belong to the=20 TRAF family (Arch et al. = 1998;=20 Baud & Karin 2001) and = various protein=20 kinases, including IRAK1 and 4 in the case of TIR signalling (Suzuki et al. 2002) = and RIP=20 kinases in the case of TNFR signalling (Kelliher et al. 1998; = Wertz et al. 2004). = These=20 molecules activate several effector pathways, the most important of = which lead=20 to activation of Mitogen Activated Protein Kinases (MAPK) (Chang & Karin 2001; Kyriakis & Avruch 2001), = including JNK=20 (Karin & Gallagher 2005) = and p38 MAPK=20 (Zarubin & Han 2005), as = well as=20 I=CE=BAB kinases (IKK) (Ghosh & Karin=20 2002). The MAPKs lead to direct and indirect phosphorylation and = activation=20 of various transcription factors, especially those that belong to the = bZIP=20 family: AP-1 (Karin 1995) and = CREB (Park et al. 2005), = which bind to=20 the promoters of pro-inflammatory genes. MAPKs also regulate = pro-inflammatory=20 gene expression through post-transcriptional mechanisms such as mRNA = turnover,=20 mRNA transport and translation (Chen=20 et al. 1998; Dean=20 et al. 2004; Winzen = et al. 2004). The IKKs, which form a complex composed of = two=20 catalytic subunits-IKK=CE=B1 and IKK=CE=B2 and a = regulatory subunit=20 IKK=CE=B3/NEMO, are responsible for activation of the = NF-=CE=BAB=20 transcription factor (Ghosh & = Karin=20 2002), which has emerged as a central regulator of inflammatory and = immune=20 responses (Li & Verma 2002; = Bonizzi & Karin 2004). Target = genes for=20 the IKK and MAPK pathways include IL-1 and TNF=CE=B1, generating = a=20 feed-forward mechanism to amplify the inflammatory response. The=20 pro-inflammatory cytokines IL-6, IL-12 and type I interferons (IFNs), = which are=20 also target genes for IKK and MAPK regulation, signal via receptor = associated=20 tyrosine kinases (RTKs) that belong to the JAK group, whose activation = results=20 in phosphorylation and nuclear translocation of STAT transcription = factors (O'Shea et al. 2002). = Engagement=20 of cytokine receptors as well as TLRs, can also lead to activation of=20 phosphoinositide-3-kinases (PI3K), which in turn activate other proteins = kinases=20 such as AKT (Martin = et al.=20 2003). Collectively, these proteins kinases coordinate the = expression of a=20 large number of pro-inflammatory mediators to initiate and maintain the=20 inflammatory response.

Inhibition of pro-inflammatory signalling

All of the intracellular signalling pathways described above, which=20 contribute to the onset of innate immunity and inflammation are also = subject to=20 negative regulation. PI3K signalling is inhibited by the PTEN = phosphatase that=20 belongs to the Protein Tyrosin Phosphatase (PTP) family; some of its = other=20 members, for instance SHIP, SHP1/2 and CD45, are responsible for = negative=20 regulation of TK signalling (Neel=20 et al. 2003). MAPK kinase phosphatases (MKPs), which = also belong=20 to the PTP family, control the duration of MAPK activation as recently = shown for=20 TNF=CE=B1-mediated JNK activation (Kamata=20 et al. 2005). Inducible suppressors of cytokine = signalling=20 (SOCS), which function as ubiquitin ligases, are responsible for the = negative=20 feedback control of JAK=E2=80=93STAT signalling (Alexander & Hilton 2004). A20 = is another=20 inducible ubiquitin ligase, which functions as a negative feedback = regulator of=20 TLR and TNFR signalling to IKK and NF-=CE=BAB. A20 is also a = direct target=20 gene for the NF-=CE=BAB pathway constituting a negative feedback = loop for=20 NF-=CE=BAB activation (Boone=20 et al. 2004). Recently, a new pathway for negative = regulation of=20 IKK/NF-=CE=BAB was described from observations made in mice that = harbour a=20 variant of IKK=CE=B1, IKK=CE=B1^AA, that cannot = be activated by=20 upstream regulators. Although IKK=CE=B1^AA mice do not = develop=20 =E2=80=98spontaneous=E2=80=99 inflammation, they develop an exaggerated = inflammatory response=20 when challenged with bacteria or fungal cell wall particles (Lawrence et al. 2005). = These=20 studies established that while IKK=CE=B2 catalytic activity is = important for=20 the activation of NF-=CE=BAB through phosphorylation of = endogenous inhibitory=20 (I=CE=BAB) proteins (Maeda=20 et al. 2003), IKK=CE=B1 is required for = termination of=20 NF-=CE=BAB activation through phosphorylation of the = transcription factors=20 RelA (p65) and c-Rel (Lawrence=20 et al. 2005). IKK-mediated phosphorylation results in=20 polyubiquitination of the target protein, leading to its accelerated = degradation=20 via the 26S proteasome. However, while I=CE=BAB degradation is = essential for=20 NF-=CE=BAB activation and nuclear translocation, the accelerated = degradation=20 of nuclear Rel proteins via IKK=CE=B1-mediated phosphorylation, = is important=20 for controlling the duration of NF-=CE=BAB activation. The = evolution of two=20 catalytic sub-units in the IKK complex with opposing, yet complimentary, = activity therefore ensures rapid and transient activation of = NF-=CE=BAB (Figure 1).

As discussed below, pro-inflammatory signalling pathways have the = capacity to=20 induce the parallel expression of anti-inflammatory mediators, such as = IL-10.=20 Recent studies reveal that the signalling pathway used by TLRs to = activate=20 expression of pro- and anti-inflammatory cytokines diverges at the level = of the=20 adaptor proteins TRAF3 and TRAF6, such that TRAF3 is critical for = induction of=20 IL-10 expression and in its absence, expression of the TRAF6-dependent=20 pro-inflammatory cytokines IL-6 and IL-12 is dramatically increased (H=C3=A4cker et al. = 2006). The balance=20 between the TRAF3- and TRAF6-generated signals may therefore play an = important=20 role in controlling the inflammatory response and its perturbation may = interfere=20 with the proper resolution of inflammation.

A deficiency in any one of these negative regulators may = result in=20 either =E2=80=98spontaneous=E2=80=99 chronic inflammation, perhaps = reflecting host cell=20 activation by PAMPs present in endogenous microflora, or an exaggerated=20 inflammatory response to insult or injury that culminates in severe = inflammation=20 and damage to the host. Although all of these negative regulatory = mechanisms=20 affect different signalling pathways, genetic studies in mice have shown = that=20 even the absence of one negative regulator is sufficient to result in = serious=20 inflammatory disorders. Undoubtedly, aberrations in such negative = regulatory=20 pathways will be found to contribute to the development of chronic = inflammatory=20 diseases.

Resolving acute inflammation

The receptors and signalling pathways that initiate and = promote=20 the inflammatory response have become increasingly well characterized; = however,=20 relatively a little is known about how acute inflammation resolves to = prevent=20 chronic inflammatory diseases. We have already discussed the = intracellular=20 checkpoints that limit the activation of inflammatory cells either = directly in=20 response to infection or tissue injury or through paracrine activation = by=20 pro-inflammatory cytokines. If we were to define the fundamental = requirements=20 for the successful resolution of inflammation it would become = increasingly clear=20 that the most simple but absolutely critical determinant for the = inflammatory=20 response to switch off is the neutralization and elimination of the = injurious=20 agents that initiated it in the first place. Failure to achieve this = first step=20 will invariably lead to chronic inflammation with the nature of the = agent in=20 question almost certainly dictating the aetiology of the developing = chronic=20 immune response. For example, chronic granulomatous disease is = characterized by=20 severe, protracted and often fatal infection, which results from a = failure of=20 the phagocytic NADPH oxidase enzyme system to produce superoxide and = kill=20 invading infections leading to a predisposition to recurrent bacterial = and=20 fungal infections and the development of inflammatory granulomas (Goldblatt & Thrasher 2000). = Successfully=20 dispensing with the inciting stimulus will signal a cessation to=20 pro-inflammatory mediator synthesis (eicosanoids, chemokines, cytokines, = cell=20 adhesion molecules, etc.) and lead to their catabolism. This would halt = further=20 leucocyte recruitment and oedema formation. These are probably the very = earliest=20 determinants for the resolution of acute inflammation, the outcome of = which=20 signals the next stage of cell clearance. The clearance phase of = resolution, be=20 it innate [polymorphonuclear leucocyte (PMN) or eosinophil driven] or = adaptive=20 (lymphocyte mediated), also has a number of mutually dependent steps (Figure 2). The clearance routes = available to=20 inflammatory leucocytes include systemic recirculation (Hughes et al. 1997) or = local=20 death of influxed PMNs, eosinophils or lymphocytes followed by their=20 phagocytosis by recruited monocyte-derived macrophages (Heasman et al. 2003). = Once=20 phagocytosis is complete, macrophages can leave the inflamed site by = lymphatic=20 drainage (Bellingan = et al.=20 2002) with evidence that a small population may die locally by = apoptosis (Gilroy et al. 2003). = If all of=20 these pathways are strictly followed then acute inflammation will = resolve=20 without causing excessive tissue damage and give little opportunity for = the=20 development of chronic, non-resolving inflammation. As with the onset = phase of=20 the acute inflammatory response, which is driven by a cohort of = well-described=20 endogenous factors, the resolution phase of the response is also highly=20 coordinated and under the tight control of what may be called = =E2=80=98pro-resolution=E2=80=99=20 factors. In contrast to onset, however, these resolution phase factors = are less=20 well-described.

Early =E2=80=98Stop=E2=80=99 signals

Inflammation is a reaction of the microcirculation that = is=20 characterized by the movement of serum proteins and leucocytes from the = blood to=20 the extravascular tissue with PMNs or eosinophils predominating at the = early=20 onset phase giving way to phagocytosing macrophages leading to = resolution. One=20 well-described event in the transition towards resolution is the = replacement of=20 PMNs or eosinophils by monocytes and phagocytosing macrophages. However, = until=20 recently our understanding of the signals that control this cell profile = switch=20 was unclear. Studies addressing this issue of leucocyte infiltration in=20 peritoneal inflammation have suggested that the interaction between IL-6 = and its=20 soluble receptor, sIL-6R, forms one of the major determinants of this = switch=20 from PMNs to monocytes (Hurst=20 et al. 2001; McLoughlin=20 et al. 2003). It was shown that sIL-6R, produced by the=20 infiltrating PMNs, forms a complex with IL-6 which, in turn, directly = modulates=20 CC and CXC chemokine expression. Thus, CXC chemokine synthesis, induced = by IL-1=20 and TNF=CE=B1, was suppressed, whereas the CC chemokine CCL2 = (MCP-1) was=20 promoted. This chemokine shift suppresses further neutrophil recruitment = in=20 favour of sustained mononuclear cell influx. In addition to chemokines, = the=20 eicosanoids also orchestrate the early transition to resolution in acute = inflammation. Transcellular metabolism of arachidonic acid by=20 lipoxygenase/lipoxygenase interaction pathways gives rise to the lipoxin = (LX)=20 family of eicosanoid metabolites (Serhan=20 2002). LXs display selective actions on leucocytes that include = inhibition=20 of PMN chemotaxis (Levy = et al.=20 2001), PMN adhesion to and transmigration through endothelial cells = (Papayianni et al. = 1996), as well=20 as PMN-mediated increases in vascular leakage (Serhan et al. 1999). = It is=20 unclear at this point whether there is any cross-talk between the LXs = and=20 IL-6/sIL-6R complex signalling in the control of leucocyte profile = switching.=20 Nonetheless, it seems that when acute inflammation needs to resolve the=20 IL-6/sIL-6R, chemokines and LXs representing some of the earliest = signals that=20 control the switch from very early PMNs to = monocyte/macrophage.

The transition to resolution

Once PMNs and eosinophils have done their job and their help is no = longer=20 needed, what happens next? At this juncture, it must be borne in mind = that these=20 are a formidable cell lineage and if left unchecked could do untold = damage to an=20 already inflamed site. After all, these cells are designed to combat = infection=20 by releasing hydrolytic and proteolytic enzymes as well as generating = reactive=20 oxygen species. Therefore, PMNs and eosinophils must be disposed of in a = controlled and effective manner. To oversee this, nature has come up = with an=20 ingenious way of defusing such potentially explosive cells called = programmed=20 cell death or apoptosis. Apoptosis of inflammatory cells is a = physiological=20 process for the non-phlogistic removal of cells. During apoptosis cells = maintain=20 an intact membrane and, therefore, do not release their potentially = histotoxic=20 agents. Necrosis of inflammatory leucocytes, on the other hand, involves = a loss=20 of membrane integrity leading to the release of potentially toxic = intracellular=20 contents (Heasman = et al.=20 2003). Moreover, apoptotic cells express a repertoire of surface = molecules=20 that allow their recognition and phagocytosis by macrophages (Fadok et al. 2001). = Despite=20 stating above that once the injurious agent has been neutralized PMNs = and=20 eosinophils are redundant, in fact, the way in which these cells die = helps the=20 resolution process enormously. Recognition of these apoptotic cells by=20 macrophages does not liberate pro-inflammatory agents from the = macrophages=20 themselves but can release anti-inflammatory signals such as IL-10 and=20 TGF=CE=B2 (Huynh = et al.=20 2002). Thus, not only is apoptosis a non-inflammatory way of = disposing of=20 cells, but this method has the added advantage of conferring upon = macrophages an=20 anti-inflammatory phenotype conducive to resolution. It is important to = note=20 that if not recognized and disposed of apoptotic cells will eventually = undergo=20 secondary necrosis releasing damaging intracellular contents and = amplifying the=20 inflammatory response. Therefore, increasing the rate of apoptosis, as a = potentially anti-inflammatory strategy, must be matched by a mechanism = that=20 upregulates macrophage phagocytic clearance capacity (Ward et al. 1999). = Thus, the=20 removal process might also be susceptible to selective modulation by=20 pharmacological agents for therapeutic gain.

As mentioned above, the strategy of enhancing leucocyte = apoptosis=20 must also be paralleled with enhancing their phagocytosis by macrophages = and=20 other non-professional phagocytes. On this theme, there are an = increasing number=20 of factors that aid the phagocytic clearance of apoptotic granulocytes. = Ligation=20 of the matrix receptor CD44, for instance, results in the rapid and = specific=20 internalization of apoptotic PMN (McCutcheon=20 et al. 1998). Besides, controlling PMN trafficking, LXs = also=20 stimulate monocyte chemotaxis and adherence. Certainly, this may seem = dangerous=20 for inflammation as too many monocyte-derived macrophages can be a bad = thing,=20 but these LX-chemoattracted macrophages accelerate resolution by = enhancing=20 phagocytosis of apoptotic PMNs in a non-phlogistic manner (Godson et al. 2000). = In addition=20 to a role in granulocyte apoptosis, glucocorticoids facilitate the = phagocytic=20 response. It was recently found that exposure of peripheral blood = monocytes to=20 glucocorticoids during the first 24 h of the 5-day culture period = induced a=20 highly phagocytic monocyte-derived macrophage phenotype (Giles et al. 2001). = Functional=20 and morphological homogeneity was matched by cell surface phenotype, = including=20 specific induction of expression of the haemoglobin scavenger receptor, = CD163=20 following glucocorticoid treatment. A potentially pro-resolution role = for CD163=20 was demonstrated recently in both in vitro and in vivo = models of=20 resolving inflammation (Philippidis = et al. 2004). Here, these authors showed that human = peripheral=20 blood monocyte-derived macrophages either in culture medium or in = resolving=20 phase cantharidin-induced skin blisters express CD163. These authors = also found=20 elevated levels of CD163 on circulating monocytes in cardiac surgical = patients=20 during the resolution phase of the systemic inflammatory response to=20 cardiopulmonary bypass surgery. In each case, binding of the=20 hemoglobin=E2=80=93haptoglobin complex to CD163-bearing cells elicited = potent IL-10=20 secretion, which in turn enhanced hemeoxygenase 1, widely shown to have=20 anti-inflammatory and tissue protective properties. Such induction of=20 hemeoxygenase 1 was observed in vivo 24=E2=80=9348 h after = the onset of=20 cardiopulmonary bypass surgery. This is coincident with the observations = of=20 Willis and colleagues who showed that hemeoxygenase 1 was expressed = during and=20 essential for the resolution (24=E2=80=9348 h phase) of a rat = carrageenin-induced=20 pleurisy (Willis et al. = 1996). Thus, apoptosis and the phagocytosis of apoptotic cells are = crucial=20 to the resolution process, failure of which may predispose, as mentioned = earlier, to chronic inflammation and possibly autoimmunity. This has = been=20 proposed in the case of systemic lupus erythematosus; an autoimmune = syndrome=20 that is associated with the presence of autoantibodies to endogenous = antigens=20 exposed on dead or dying cells, which failed to be cleared and disposed = of.=20 Studies in mice, for instance, have established a role for the = complement=20 receptor C1q on macrophages in the development of this disease. C1q was=20 discovered to be important for the phagocytic clearance of apoptotic = cells; in=20 the absence of this receptor mice developed a lupus like syndrome (Botto et al. 1998). The = persistence of apoptotic cells and necrotic bodies led to the = development of an=20 inappropriate immune response to endogenous antigens. Evidence has also = been=20 established in human SLE patients for an association between C1q = deficiency and=20 disease (Walport et al. = 1998). The phagocytosis of apoptotic cells has been suggested to = play an=20 important role in the negative regulation of macrophage activation; = apoptotic=20 leucocytes may well fit into the category of endogenous = anti-inflammatory=20 mediators; therefore, the mechanisms of apoptosis and the clearance of = apoptotic=20 cells may be critical in the development of chronic = inflammation.

Unblocking the drains!

The role of the lymphatic system in the context of the = resolution=20 of acute innate inflammation is shamefully understudied given its = essential=20 function in draining inflammatory mediators and effete leucocyte away = from the=20 inflamed site (Bellingan = et al.=20 1996). We have already discussed the importance of PMN clearance to = the=20 resolution of acute inflammation, but it is equally important that = phagocytosing=20 inflammatory macrophages are cleared away from the inflamed site to = prevent=20 local macrophage-induced tissue damage and potentially granuloma tissue = damage=20 and the development of chronic inflammation. However, despite the need = to=20 understand the endogenous control of macrophage clearance during acute=20 inflammatory resolution, a little is known about this field. There is = increasing=20 evidence that macrophage clearance from an inflamed site is a highly = regulated=20 event. Using an experimental model of acute resolving peritonitis, it = was shown=20 that macrophages adhere specifically to mesothelium overlying draining=20 lymphatics and that their emigration rate is regulated by the state of=20 macrophage activation (Bellingan=20 et al. 1996, 2002) providing the first evidence that = macrophage=20 emigration from the inflamed site is controlled by adhesion molecule = regulation=20 of macrophage=E2=80=93mesothelial interactions. This report highlights = the importance of=20 adhesion molecules controlling clearance of inflammatory macrophages = into the=20 draining lymphatic circulation, thus highlighting new pathways in the = resolution=20 of acute inflammation.

Soluble mediators of resolution: opportunities for drug=20 discovery

Returning to eicosanoids, PGD₂, a metabolite = of the=20 action of hematopoietic prostaglandin D₂ synthase on = COX-derived=20 PGH₂, has emerged recently as an eicosanoid with both pro- as = well as=20 anti-inflammatory properties. PGD₂ undergoes dehydration = in=20 vivo and in vitro to yield biologically active PGs of the=20 J₂ series, including PGJ₂,=20 =CE=94^12,14-PGJ₂ and = 15-deoxy-=CE=94^12,14-PGJ₂=20 (15d-PGJ₂). In addition to being a high-affinity natural = ligand for=20 anti-inflammatory peroxisome proliferators-activated receptor gamma=20 (PPAR=CE=B3), 15d-PGJ₂ also exerts its effects through = PPAR=CE=B3-dependent as well as -independent mechanisms to = suppress=20 pro-inflammatory signalling pathways and the expression of genes that = drive the=20 inflammatory response. 15d-PGJ₂ also preferentially inhibits = monocyte=20 rather than PMN trafficking through the differential regulation of = cell-adhesion=20 molecule and chemokine expression (Gilroy=20 et al. 2004). We have shown that COX 2-derived = PGD₂=20 metabolites contribute to the resolution of acute inflammation = (pleuritis)=20 through the preferential synthesis of PGD₂ and = 15d-PGJ₂=20 (Gilroy et al. = 1999), which,=20 along with the alternative DNA-binding p50=E2=80=93p50 homodimers = complexes of=20 NF-=CE=BAB (Lawrence = et al.=20 2001) bring about resolution by inducing leucocyte apoptosis (Gilroy et al. 2003). = Recently,=20 we extended these studies to examining the role of PGD₂ = metabolites=20 in the resolution of adaptive immunity and lymphocyte function (Proc = Natl Acad=20 Sci USA, in press). Indeed, there is an increasing body of evidence = detailing=20 the differential effects of PGD₂ metabolites on leucocyte = apoptosis=20 as well as the signalling pathways involved (Rossi et al. 2000; Ward et al. 2002). In = addition=20 to the well-known eicosanoids, there is a new generation of lipid = mediators=20 showing real promise as endogenous anti-inflammatories. Resolvins and=20 docosatrienes are fatty acid metabolites of the COX/lipoxygenase = pathways, where=20 the omega-3 fatty-acid constituents of fish oils docosahexaenoic acid = and=20 eicosapentaneoic acid are the substrates and not arachidonic acid. These = resolvins and docosatrienes were identified in inflammatory exudates = during the=20 resolving phase of acute inflammation and shown to be potent inhibitors = of PMN=20 transendothelial migration, microglial-cell cytokine expression and to=20 ameliorate experimental models of dermal inflammation and leucocyte = accumulation=20 in peritonitis at nanogram doses (Serhan=20 2004). These studies on resolvin metabolism are uncovering = surprising new=20 avenues in anti-inflammation research, putting fatty acid metabolites = right at=20 the forefront of potential drug therapy. These studies are also = challenging the=20 existing dogma that not all eicosanoids are detrimental to inflammation = and are=20 putting a balanced view of their role in pathophysiology. To add fuel to = this=20 notion, a recent and very surprising paper has shown that eicosanoids of = the LXs=20 family, described above, are orally active in models of acute = inflammation (Bannenberg et al.=20 2004).

Conclusions

In conclusion, it is clear the inflammatory response has = a number=20 of built-in checkpoint controls that limit the duration and magnitude of = acute=20 inflammation. Defects in these endogenous anti-inflammatory pathways = will=20 undoubtedly predispose to the development of chronic inflammatory = diseases. A=20 further understanding and analysis of these pathways in the pathogenesis = of=20 chronic inflammation is required. This will allow the pursuit of = therapeutic=20 strategies to correct possible defects in these feedback control systems = or=20 manipulate these pathways to suppress inflammation. However, it is = equally clear=20 that the resolution of inflammation is driven by a complex set of = pro-resolution=20 mediators that regulate specific cellular events required to clear = inflammatory=20 cells from the site of injury or infection and restore tissue = homeostasis. These=20 endogenous anti-inflammatory and pro-resolution mechanisms are clearly=20 intimately linked; however, the true goal in the treatment of chronic=20 inflammatory diseases must be to inhibit persistent inflammation and = restore=20 tissue function. To achieve this goal, we must improve our understanding = of the=20 resolution of inflammation and identify possible approaches to promote = this=20 process in combination with anti-inflammatory therapy. Perhaps the, as = yet=20 unidentified, anti-resolution factors that may prevent the proper = resolution of=20 inflammation would represent appropriate targets to achieve this=20 goal.

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url(/templates/jsp/_synergy.2/images/iconFreeAccess.gif); = BACKGROUND-REPEAT: no-repeat } .free_access { BACKGROUND-POSITION: left center; PADDING-LEFT: 20px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/iconFreeAccess.gif); = BACKGROUND-REPEAT: no-repeat } .latest_issue { BACKGROUND-POSITION: left center; PADDING-LEFT: 20px; = BACKGROUND-REPEAT: no-repeat } .favorite_journal { BACKGROUND-POSITION: left center; PADDING-LEFT: 20px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/iconFavorite.gif); = BACKGROUND-REPEAT: no-repeat } .online_early { BACKGROUND-POSITION: left center; PADDING-LEFT: 5px; BACKGROUND-REPEAT: = no-repeat } .online_accepted { BACKGROUND-POSITION: left center; PADDING-LEFT: 5px; BACKGROUND-REPEAT: = no-repeat } .online_open { BACKGROUND-POSITION: left center; PADDING-LEFT: 5px; MIN-HEIGHT: 14px; = BACKGROUND-REPEAT: no-repeat } UL.selection_menu { PADDING-RIGHT: 2px; BACKGROUND-POSITION: left center; BORDER-TOP: #fff = 2px solid; PADDING-LEFT: 22px; PADDING-BOTTOM: 3px; PADDING-TOP: 1px; = BACKGROUND-REPEAT: no-repeat; BACKGROUND-COLOR: #ededed } UL.selection_top { BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/icon_selection_menu_top.gif) } UL.selection_bottom { BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/icon_selection_menu_bot.gif) } UL.selection_menu LI { DISPLAY: inline } UL.selection_menu LI A { Z-INDEX: 4; POSITION: relative } UL#article_authors LI A { Z-INDEX: 4; POSITION: relative } UL.selection_menu LI A:hover { Z-INDEX: 5; BACKGROUND-COLOR: transparent } UL#article_authors LI A:hover { Z-INDEX: 5; BACKGROUND-COLOR: transparent } A.tooltiplink:hover { Z-INDEX: 5; BACKGROUND-COLOR: transparent } A.nameLink:hover { Z-INDEX: 5; BACKGROUND-COLOR: transparent } UL.selection_menu LI A SPAN { DISPLAY: none } UL#article_authors LI A SPAN.tooltip { DISPLAY: none } A.tooltiplink SPAN { DISPLAY: none } A.nameLink SPAN.tooltip { DISPLAY: none } UL.selection_menu LI A:hover SPAN { PADDING-RIGHT: 4px; BACKGROUND-POSITION: left top; DISPLAY: block; = PADDING-LEFT: 4px; LEFT: 0px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/toc_tooltip_bg.gif); = PADDING-BOTTOM: 4px; WIDTH: 189px; PADDING-TOP: 8px; BORDER-BOTTOM: #000 = 1px solid; BACKGROUND-REPEAT: no-repeat; POSITION: absolute; TOP: 18px; = TEXT-DECORATION: none } UL#article_authors LI A:hover SPAN.tooltip { PADDING-RIGHT: 4px; BACKGROUND-POSITION: left top; DISPLAY: block; = PADDING-LEFT: 4px; LEFT: 0px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/toc_tooltip_bg.gif); = PADDING-BOTTOM: 4px; WIDTH: 189px; PADDING-TOP: 8px; BORDER-BOTTOM: #000 = 1px solid; BACKGROUND-REPEAT: no-repeat; POSITION: absolute; TOP: 18px; = TEXT-DECORATION: none } A.nameLink:hover SPAN.tooltip { PADDING-RIGHT: 4px; BACKGROUND-POSITION: left top; DISPLAY: block; = PADDING-LEFT: 4px; LEFT: 0px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/toc_tooltip_bg.gif); = PADDING-BOTTOM: 4px; WIDTH: 189px; PADDING-TOP: 8px; BORDER-BOTTOM: #000 = 1px solid; BACKGROUND-REPEAT: no-repeat; POSITION: absolute; TOP: 18px; = TEXT-DECORATION: none } A:hover SPAN.tooltip .item { MARGIN-TOP: 1em; DISPLAY: block } A:hover SPAN.tooltip .first { MARGIN-TOP: 0px } A#toc_select_all { MARGIN-TOP: 8px; DISPLAY: block; FLOAT: left; WIDTH: 28px; TEXT-ALIGN: = center } DIV.toc_item { MARGIN-LEFT: 30px } DIV.toc_item H3 { PADDING-RIGHT: 6px; MARGIN-TOP: 15px; PADDING-LEFT: 3px; = PADDING-BOTTOM: 2px; PADDING-TOP: 2px; BACKGROUND-COLOR: #a3a3a3 } DIV.toc_item H4 { PADDING-RIGHT: 6px; MARGIN-TOP: 2px; PADDING-LEFT: 3px; PADDING-BOTTOM: = 2px; PADDING-TOP: 2px; BACKGROUND-COLOR: #ededed } DIV.toc_item H5 { MARGIN-TOP: 4px } DIV.toc_item .select_title { CLEAR: both; MARGIN-LEFT: -30px } DIV.toc_item .select_title SPAN.doi_checkbox { DISPLAY: block; FLOAT: left; WIDTH: 30px; TEXT-ALIGN: center } DIV.toc_item .select_title H5 { PADDING-LEFT: 30px } DIV.toc_item P { MARGIN-TOP: 6px } DIV.toc_item P.toc_author { MARGIN-TOP: 4px } DIV.toc_item UL.item_options { MARGIN-TOP: 6px; MARGIN-BOTTOM: 10px } DIV.toc_item UL.bordered { PADDING-BOTTOM: 14px; BORDER-BOTTOM: #ccc 1px solid } DIV.toc_item UL.item_options LI { DISPLAY: inline } #back_to_top { PADDING-RIGHT: 20px; BACKGROUND-POSITION: right center; DISPLAY: block; = PADDING-LEFT: 5px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/top_link_arrow.gif); = PADDING-BOTTOM: 2px; PADDING-TOP: 1px; BACKGROUND-REPEAT: no-repeat; = BACKGROUND-COLOR: #d21c1b; TEXT-ALIGN: right } .synergy_house H2 { PADDING-RIGHT: 6px; PADDING-LEFT: 6px; PADDING-BOTTOM: 2px; MARGIN: 7px = 0px 0px; PADDING-TOP: 2px; BACKGROUND-COLOR: #d21c1b } DIV.subscription_warning { PADDING-RIGHT: 6px; BORDER-TOP: #fff 1px solid; PADDING-LEFT: 3px; = PADDING-BOTTOM: 2px; PADDING-TOP: 2px; BACKGROUND-COLOR: #fae8e8 } .synergy_house TABLE { WIDTH: 100% } .synergy_house TABLE TH { PADDING-RIGHT: 2px; PADDING-LEFT: 2px; PADDING-BOTTOM: 7px; = PADDING-TOP: 7px; BORDER-BOTTOM: #ccc 1px solid; TEXT-ALIGN: left } .synergy_house TABLE TD { PADDING-RIGHT: 2px; PADDING-LEFT: 2px; PADDING-BOTTOM: 7px; = PADDING-TOP: 7px; BORDER-BOTTOM: #ccc 1px solid; TEXT-ALIGN: left } .synergy_house TABLE TH.rh { TEXT-ALIGN: right } .synergy_house TABLE TD.rh { TEXT-ALIGN: right } .synergy_house TABLE TH.remove { PADDING-RIGHT: 10px; BACKGROUND-POSITION: right center; = BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/icon_dn_arrow.gif); = BACKGROUND-REPEAT: no-repeat } .synergy_house UL.links_list { MARGIN: 4px 0px 8px; LIST-STYLE-TYPE: none } .synergy_house UL.links_list LI { PADDING-RIGHT: 0px; PADDING-LEFT: 0px; PADDING-BOTTOM: 3px; = PADDING-TOP: 2px } FORM#institution_select { PADDING-RIGHT: 3px; BORDER-TOP: #fff 5px solid; PADDING-LEFT: 3px; = PADDING-BOTTOM: 1px; PADDING-TOP: 1px; BACKGROUND-COLOR: #e1e1e1 } UL.advice { MARGIN-TOP: 8px; LIST-STYLE-TYPE: none } UL.advice LI { PADDING-RIGHT: 0px; PADDING-LEFT: 0px; PADDING-BOTTOM: 4px; = PADDING-TOP: 2px } OL.advice { MARGIN-TOP: 8px } OL.advice LI { PADDING-RIGHT: 0px; PADDING-LEFT: 0px; PADDING-BOTTOM: 4px; = MARGIN-LEFT: 25px; PADDING-TOP: 2px } UL.bulleted { MARGIN-LEFT: 17px; LIST-STYLE-TYPE: disc } DIV.display_controls { PADDING-RIGHT: 6px; BORDER-TOP: #fff 2px solid; PADDING-LEFT: 6px; = PADDING-BOTTOM: 4px; PADDING-TOP: 2px; BACKGROUND-COLOR: #fae8e8 } DIV.display_controls UL LI { DISPLAY: inline } DIV.display_controls A.rh { FLOAT: right } DIV.search_pagination { PADDING-RIGHT: 0px; PADDING-LEFT: 0px; PADDING-BOTTOM: 3px; = PADDING-TOP: 10px; TEXT-ALIGN: right } DIV.search_pagination H1 { FLOAT: left; MARGIN: 0px } DIV.search_pagination INPUT.go_btn { FLOAT: left; MARGIN-RIGHT: 3px } FORM.main_form H2 { MARGIN-BOTTOM: 10px } FORM.main_form H4 { MARGIN-BOTTOM: 4px } FORM.main_form P { MARGIN-TOP: 0px; MARGIN-BOTTOM: 4px } FORM.main_form DIV.row { CLEAR: both; PADDING-RIGHT: 0px; PADDING-LEFT: 0px; PADDING-BOTTOM: = 8px; PADDING-TOP: 0px } FORM.main_form LABEL { DISPLAY: block; FLOAT: left; WIDTH: 15em; PADDING-TOP: 2px; TEXT-ALIGN: = left } FORM.main_form DIV.form_title { DISPLAY: block; FLOAT: left; WIDTH: 15em; PADDING-TOP: 2px; TEXT-ALIGN: = left } FORM.main_form LABEL.inline { DISPLAY: inline; FLOAT: none; WIDTH: auto } FORM.main_form INPUT.text_field { WIDTH: 21.4em } FORM.main_form SELECT { WIDTH: 32.1em } FORM.main_form SELECT.exempt { WIDTH: auto } FORM.main_form SELECT.searchfield { FONT-WEIGHT: bold; WIDTH: 13em } FORM.main_form SELECT.searchop { WIDTH: 6em } FORM.main_form DIV.search_rh_box SELECT.exempt { WIDTH: 55px } FORM.main_form INPUT.go_btn { MARGIN-TOP: 12px } FORM.main_form DIV.inc_help_text { FLOAT: left; WIDTH: 29em } FORM.main_form DIV.inc_help_text P { PADDING-RIGHT: 2px; PADDING-LEFT: 2px; PADDING-BOTTOM: 3px; = PADDING-TOP: 3px; TEXT-ALIGN: left } FORM.main_form DIV.no_label { PADDING-LEFT: 16em; TEXT-ALIGN: right } DIV#search_area { PADDING-TOP: 8px } DIV#search_area LABEL { WIDTH: 12em } DIV#search_area DIV.form_title { WIDTH: 12em } DIV#search_area DIV.search_rh_box { FLOAT: left; WIDTH: auto } DIV#search_area DIV.search_btn { WIDTH: 76%; TEXT-ALIGN: right } DIV#search_area SELECT.med { MARGIN-BOTTOM: 4px; WIDTH: 23em } DIV#search_area SELECT.journal_indent { MARGIN-BOTTOM: 4px; MARGIN-LEFT: 20px; WIDTH: 20.9em } DIV#search_area SELECT.result_format { WIDTH: 16.4em } DIV#search_area DIV.search_in_indent { PADDING-BOTTOM: 8px; MARGIN-LEFT: 20px } DIV#search_area DIV.search_in_indent LABEL.inline { DISPLAY: inline-block; WIDTH: 9em } TABLE#saved_searches { BORDER-RIGHT: #999 1px solid; BORDER-TOP: #999 1px solid; MARGIN-TOP: = 12px; BORDER-LEFT: #999 1px solid; BORDER-BOTTOM: #999 1px solid; = BACKGROUND-COLOR: #e1e1e1 } TABLE#saved_searches TH { PADDING-RIGHT: 3px; PADDING-LEFT: 3px; PADDING-BOTTOM: 2px; = PADDING-TOP: 2px; BACKGROUND-COLOR: #999 } TABLE#saved_searches TD { PADDING-RIGHT: 3px; BORDER-TOP: #e1e1e1 2px solid; PADDING-LEFT: 3px; = PADDING-BOTTOM: 0px; PADDING-TOP: 0px; BORDER-BOTTOM: #e1e1e1 2px solid; = BACKGROUND-COLOR: #fff } TABLE#saved_searches TD SELECT { WIDTH: 100% } TABLE#saved_searches TD.rh { BACKGROUND-COLOR: #e1e1e1 } DIV.journal_expander_control { PADDING-RIGHT: 3px; MARGIN-TOP: 8px; PADDING-LEFT: 3px; PADDING-BOTTOM: = 2px; PADDING-TOP: 2px; BACKGROUND-COLOR: #e1e1e1 } .alerts DIV.top_border { PADDING-TOP: 6px } DIV.help_block { PADDING-RIGHT: 5px; PADDING-LEFT: 5px; FLOAT: left; PADDING-BOTTOM: = 5px; WIDTH: 48%; PADDING-TOP: 5px } DIV.help_block H4 { BORDER-TOP: #ccc 1px solid; PADDING-BOTTOM: 4px; PADDING-TOP: 4px } DIV.help_block UL { MARGIN-LEFT: 16px } DIV.help_block UL LI { PADDING-BOTTOM: 4px } H1.article_access_warning { BORDER-TOP-STYLE: none } P.article_access_warning { BORDER-TOP: #ccc 1px solid; PADDING-TOP: 4px } .homepage #left_column H3 { BACKGROUND-COLOR: #666 } .homepage #left_column UL LI { BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/left_col_list_icon_alt.gif) } #left_column H3 { PADDING-RIGHT: 6px; PADDING-LEFT: 6px; PADDING-BOTTOM: 2px; = PADDING-TOP: 2px; BACKGROUND-COLOR: #999 } #left_column H3.journal_menu_header { BACKGROUND-COLOR: #666 } #left_column H3.left_col_separator { BORDER-TOP: #fff 5px solid } #left_column DIV { PADDING-RIGHT: 5px; PADDING-LEFT: 5px; PADDING-BOTTOM: 5px; = PADDING-TOP: 3px; BACKGROUND-COLOR: #f8f8f8 } #left_column UL { PADDING-RIGHT: 0px; PADDING-LEFT: 5px; PADDING-BOTTOM: 5px; = PADDING-TOP: 3px; BACKGROUND-COLOR: #f8f8f8 } #left_column DL { PADDING-RIGHT: 0px; PADDING-LEFT: 5px; PADDING-BOTTOM: 5px; = PADDING-TOP: 3px; BACKGROUND-COLOR: #f8f8f8 } #left_column UL LI { BACKGROUND-POSITION: 0px 5px; PADDING-LEFT: 6px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/left_col_list_icon.gif); = MARGIN: 2px 0px; BACKGROUND-REPEAT: no-repeat; LIST-STYLE-TYPE: none } #left_column UL LI.current_location { BACKGROUND-POSITION: 0px 5px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/left_col_list_icon_alt.gif) } #left_column DIV.left_col_image_area { PADDING-RIGHT: 10px; PADDING-LEFT: 10px } #left_column DIV.left_col_image_area A.popup { BACKGROUND-POSITION: left center; PADDING-LEFT: 10px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/left_col_image_link_icon.gif)= ; BACKGROUND-REPEAT: no-repeat } #left_column DIV.left_col_image_area P { MARGIN-TOP: 5px; MARGIN-BOTTOM: 10px } #left_column UL#mini_tools { BORDER-TOP: #ccc 1px solid } #left_column FORM { PADDING-RIGHT: 3px; PADDING-LEFT: 3px; PADDING-BOTTOM: 4px; = PADDING-TOP: 4px; BORDER-BOTTOM: #fff 6px solid; BACKGROUND-COLOR: = #e0e0e0 } #left_column FORM INPUT.text_field { MARGIN: 2px 0px; WIDTH: 97% } #left_column FORM INPUT.go_btn { FLOAT: right; MARGIN-RIGHT: 3px } #right_column { PADDING-BOTTOM: 8px } #right_column H3 { PADDING-RIGHT: 6px; PADDING-LEFT: 6px; PADDING-BOTTOM: 2px; = PADDING-TOP: 2px; BACKGROUND-COLOR: #999 } #right_column P { PADDING-RIGHT: 6px; PADDING-LEFT: 6px; PADDING-BOTTOM: 2px; MARGIN: = 0px; PADDING-TOP: 2px; BORDER-BOTTOM: #fff 2px solid; BACKGROUND-COLOR: = #f8f8f8 } DIV.article_controls { BORDER-BOTTOM: #fff 2px solid; BACKGROUND-COLOR: #f8f8f8 } DIV.article_controls H3 { PADDING-RIGHT: 6px; PADDING-LEFT: 6px; PADDING-BOTTOM: 2px; = PADDING-TOP: 2px; BACKGROUND-COLOR: #999 } DIV.article_controls UL { PADDING-RIGHT: 0px; PADDING-LEFT: 5px; PADDING-BOTTOM: 5px; = PADDING-TOP: 3px } DIV.article_controls UL LI { BACKGROUND-POSITION: left center; PADDING-LEFT: 6px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/left_col_list_icon.gif); = MARGIN: 2px 0px; BACKGROUND-REPEAT: no-repeat; LIST-STYLE-TYPE: none } FORM#frmSearch { BORDER-BOTTOM: #fff 6px solid; BACKGROUND-COLOR: #e0e0e0 } FORM#frmSearch H3 { BACKGROUND-POSITION: left center; PADDING-LEFT: 23px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/icon_quickSearch.gif); = BACKGROUND-REPEAT: no-repeat } FORM#frmSearch FIELDSET { BORDER-TOP-WIDTH: 0px; PADDING-RIGHT: 4px; PADDING-LEFT: 4px; = BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM-WIDTH: 0px; PADDING-BOTTOM: 12px; = PADDING-TOP: 2px; BORDER-RIGHT-WIDTH: 0px } FORM#frmSearch DIV#quick_search_link_block { MARGIN-TOP: 2px; FONT-SIZE: 10px; FLOAT: left } FORM#frmSearch INPUT.go_btn { FONT-SIZE: 10px } FORM#frmSearch DIV#quick_search_link_block A { BACKGROUND-POSITION: left center; DISPLAY: block; PADDING-LEFT: 9px; = BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/icon_alt_search_link.gif); = BACKGROUND-REPEAT: no-repeat } FORM#frmSearch INPUT.go_btn { RIGHT: -19px; POSITION: relative; TOP: 2px } FORM#quick_link { BACKGROUND-COLOR: #e0e0e0 } FORM#quick_link H3 { BACKGROUND-POSITION: left center; PADDING-LEFT: 23px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/icon_quickLink.gif); = BACKGROUND-REPEAT: no-repeat } FORM#quick_link FIELDSET { BORDER-TOP-WIDTH: 0px; PADDING-RIGHT: 4px; PADDING-LEFT: 4px; = BORDER-LEFT-WIDTH: 0px; FONT-SIZE: 10px; BORDER-BOTTOM-WIDTH: 0px; = PADDING-BOTTOM: 14px; PADDING-TOP: 4px; BORDER-RIGHT-WIDTH: 0px } FORM#quick_link FIELDSET SELECT { MARGIN-BOTTOM: 4px; WIDTH: 100% } FORM#quick_link SPAN.sml_field_block { DISPLAY: block; FONT-SIZE: 10px; FLOAT: left; WIDTH: 3.7em } FORM#quick_link SPAN.sml_field_block INPUT { WIDTH: 3.1em } FORM#quick_link INPUT.go_btn { FONT-SIZE: 10px; RIGHT: -11px; POSITION: relative; TOP: 1.2em } FORM#quick_link A { BACKGROUND-POSITION: left center; MARGIN-TOP: 4px; DISPLAY: block; = PADDING-LEFT: 9px; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/icon_alt_search_link.gif); = BACKGROUND-REPEAT: no-repeat } #right_column FORM#full_text_search { PADDING-BOTTOM: 8px; BACKGROUND-COLOR: #e0e0e0 } #right_column FORM#full_text_search FIELDSET { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM-WIDTH: = 0px; PADDING-BOTTOM: 6px; BORDER-RIGHT-WIDTH: 0px } #right_column FORM#full_text_search SPAN.form_legend { PADDING-RIGHT: 6px; BORDER-TOP: #fff 1px solid; DISPLAY: block; = PADDING-LEFT: 6px; FONT-WEIGHT: bold; PADDING-BOTTOM: 2px; PADDING-TOP: = 2px; BORDER-BOTTOM: #fff 1px solid; POSITION: relative; = BACKGROUND-COLOR: #d2d2d2 } #right_column FORM#full_text_search SPAN LEGEND { LEFT: -8px; POSITION: relative } #right_column FORM#full_text_search LEGEND.inline_legend { BORDER-RIGHT: red 1px solid; BORDER-TOP: red 1px solid; DISPLAY: = inline; BORDER-LEFT: red 1px solid; BORDER-BOTTOM: red 1px solid } #right_column FORM#full_text_search SPAN { PADDING-RIGHT: 6px; DISPLAY: block; PADDING-LEFT: 6px; PADDING-BOTTOM: = 2px; PADDING-TOP: 2px } #right_column FORM#full_text_search SPAN.smallcaps { PADDING-RIGHT: 0px; DISPLAY: inline; PADDING-LEFT: 0px; PADDING-BOTTOM: = 0px; PADDING-TOP: 0px } #right_column FORM#full_text_search LABEL { PADDING-LEFT: 3px } #right_column FORM#full_text_search INPUT.text_field { MARGIN-LEFT: 3px; WIDTH: 130px } #right_column FORM#full_text_search SELECT { WIDTH: 11em } #right_column FORM#full_text_search LABEL.legend_label { PADDING-LEFT: 4px } #right_column FORM#full_text_search SPAN.select_bg { PADDING-RIGHT: 0px; DISPLAY: inline; PADDING-LEFT: 0px; PADDING-BOTTOM: = 0px; MARGIN: 0px; PADDING-TOP: 0px } #footer { BORDER-TOP: #fff 8px solid; OVERFLOW: visible; HEIGHT: 6.3em } #footer UL { PADDING-RIGHT: 10px; BACKGROUND-POSITION: right top; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/footer_bg_grad.jpg); = BACKGROUND-REPEAT: repeat-y; HEIGHT: 1.5em; TEXT-ALIGN: right } #footer UL LI { DISPLAY: inline; LIST-STYLE-TYPE: none } #footer P IMG { FLOAT: left } #footer P#copyright_partners { MARGIN-TOP: 3px; FLOAT: left } #footer P#tech_partner { MARGIN-TOP: 3px; FLOAT: right } #main_content IMG.banner { MARGIN-BOTTOM: 6px; WIDTH: 100% } #left_column IMG.banner { BORDER-TOP: #fff 8px solid } #right_column IMG.banner { BORDER-TOP: #fff 8px solid } #left_column { OVERFLOW: hidden } .adPlaceholder1000 { MARGIN-BOTTOM: 0.5em; PADDING-BOTTOM: 0.5em; BORDER-BOTTOM: #666 1px = solid } .otherIssues { MARGIN-TOP: 1em } 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italic } .reference .journal_title { FONT-STYLE: italic } .reference .publication_title { FONT-STYLE: italic } .etal { FONT-STYLE: italic } .docref-title { FONT-STYLE: italic } .issueStyle2 { FONT-WEIGHT: normal } .smallcaps { FONT-VARIANT: small-caps } .toc_item .relatedLink { COLOR: blue } .relatedArticle A { COLOR: blue; TEXT-DECORATION: none } A.virtualArticleLink { COLOR: blue; TEXT-DECORATION: none } A.articleLink:visited { COLOR: purple } DIV.toc_author A:visited { COLOR: purple } DIV.full_text A:visited { COLOR: purple } DIV.searchResult DIV.citation { FONT-WEIGHT: bold } .jCode_apa A.supplementaryIssue .issueStyle1 { COLOR: #6699cc } ------=_NextPart_000_0000_01C82B5D.6748DB40 Content-Type: text/css; charset="iso-8859-1" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.blackwell-synergy.com/templates/jsp/_synergy.2/css/hacks.css .clearfix:unknown { CLEAR: both; DISPLAY: block; VISIBILITY: hidden; HEIGHT: 0px; content: = "." } .clearfix { DISPLAY: inline-block } * HTML .clearfix { HEIGHT: 1% } .clearfix { DISPLAY: block } :unknown UL.selection_menu LI A:hover SPAN { DISPLAY: none } :unknown UL#article_authors LI A:hover SPAN.tooltip { DISPLAY: none } HTML[xmlns] DIV#search_area DIV.search_in_indent LABEL.inline { =09 } UL.accessibility_ie_hack LI { DISPLAY: block } ------=_NextPart_000_0000_01C82B5D.6748DB40 Content-Type: text/css; charset="iso-8859-1" Content-Transfer-Encoding: 7bit Content-Location: http://www.blackwell-synergy.com/templates/jsp/_synergy.2/css/base.css @import url( /templates/jsp/_synergy.2/css/layout.css ); @import url( /templates/jsp/_synergy.2/css/typography.css ); @import url( /templates/jsp/_synergy.2/css/hacks.css ); ------=_NextPart_000_0000_01C82B5D.6748DB40 Content-Type: text/css; charset="iso-8859-1" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.blackwell-synergy.com/templates/jsp/_synergy.2/css/ie_hacks.css BODY { FONT-SIZE: 70% } #header FORM INPUT { FONT-SIZE: 1.05em; WIDTH: 9em; LINE-HEIGHT: 1.07em; HEIGHT: 1.05em } FORM#quick_link SPAN.sml_field_block INPUT { FONT-SIZE: 1.15em; WIDTH: 2.5em; LINE-HEIGHT: 1.1em; HEIGHT: 1.1em } FORM#journal_display_control SELECT { FONT-SIZE: 1.1em; LINE-HEIGHT: 1em } SELECT { FONT-SIZE: 1.1em; LINE-HEIGHT: 1em } #page { =09 } #left_column { WIDTH: 185px } #main_content { PADDING-RIGHT: 192px; PADDING-LEFT: 193px; PADDING-BOTTOM: 0px; = PADDING-TOP: 0px } #right_column { WIDTH: 185px } .homepage #main_content { PADDING-RIGHT: 192px; PADDING-LEFT: 280px; PADDING-BOTTOM: 0px; = PADDING-TOP: 0px } #header FORM LABEL.login_pw { TOP: 0.7em } FORM INPUT.go_btn { HEIGHT: 1.6em! important } FORM#quick_link INPUT.go_btn { RIGHT: -7px } #right_column FORM#full_text_search SPAN { PADDING-RIGHT: 6px; DISPLAY: block; PADDING-LEFT: 6px; PADDING-BOTTOM: = 0px; PADDING-TOP: 0px } #main_content DIV.article_image { MARGIN-TOP: 12px; POSITION: relative; ; HEIGHT: = expression(this.getElementsByTagName("img")[0].height) } #main_content DIV.article_image IMG { POSITION: absolute } SPAN.select_bg { BACKGROUND-POSITION: right top; BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/ie_win_select_dummy.gif); = BACKGROUND-REPEAT: no-repeat } FORM#register INPUT.text_field { WIDTH: 290px } FORM#register DIV.inc_help_text { WIDTH: 290px } FORM#register SELECT { WIDTH: 294px } FORM#register SELECT.multiline { MARGIN-LEFT: 3px } FORM#quick_link { POSITION: relative } DIV#quick_link_select_replacement { BORDER-RIGHT: #999 1px solid; BORDER-TOP: #999 0px solid; DISPLAY: = none; Z-INDEX: 9; LEFT: -413px; BORDER-LEFT: #999 1px solid; WIDTH: = 388px; BORDER-BOTTOM: #999 1px solid; POSITION: absolute; TOP: 0px; = HEIGHT: 187px; BACKGROUND-COLOR: #e0e0e0 } DIV#quick_link_select_replacement DIV#quick_link_heading { BACKGROUND-COLOR: #999; TEXT-ALIGN: right } DIV#quick_link_select_replacement DIV#quick_link_heading H3 { BACKGROUND-POSITION: left center; PADDING-LEFT: 17px; FLOAT: left; = BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/layout/ie_quicklink_icon.gif); = BACKGROUND-REPEAT: no-repeat } DIV#quick_link_select_replacement DIV#quick_link_heading A { FONT-WEIGHT: bold; BACKGROUND-IMAGE: none; COLOR: #fff } DIV#scroll_area { PADDING-RIGHT: 2px; OVERFLOW-Y: scroll; PADDING-LEFT: 4px; = PADDING-BOTTOM: 6px; PADDING-TOP: 6px; HEIGHT: 158px } DIV#scroll_area OL#quick_link_journals { PADDING-RIGHT: 0px; PADDING-LEFT: 0px; PADDING-BOTTOM: 0px; MARGIN: = 0px; PADDING-TOP: 0px; LIST-STYLE-TYPE: none } DIV#scroll_area OL#quick_link_journals LI { FONT-WEIGHT: bold; FONT-SIZE: 1em; PADDING-BOTTOM: 6px; CURSOR: pointer } UL#article_authors { POSITION: relative } UL.accessibility_ie_hack LI { BORDER-RIGHT: #e0e0e0 1px solid; BORDER-TOP: #e0e0e0 1px solid; = BORDER-LEFT: #e0e0e0 1px solid; BORDER-BOTTOM: #e0e0e0 1px solid } DIV#page DIV.help { BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/content/synergy_house/header_help.gi= f); BACKGROUND-REPEAT: no-repeat; HEIGHT: 64px } DIV#page DIV.registration { BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/content/synergy_house/header_registe= r.gif); BACKGROUND-REPEAT: no-repeat; HEIGHT: 64px } DIV#page DIV.mySynergy { BACKGROUND-IMAGE: = url(/templates/jsp/_synergy.2/images/content/synergy_house/header_my_syne= rgy.gif); BACKGROUND-REPEAT: no-repeat; HEIGHT: 64px } ------=_NextPart_000_0000_01C82B5D.6748DB40 Content-Type: text/css; charset="iso-8859-1" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.blackwell-synergy.com/templates/jsp/_synergy.2/css/print.css #page { WIDTH: 640px! important } #main_content { PADDING-RIGHT: 0px; PADDING-LEFT: 17.8em; PADDING-BOTTOM: 0px; = PADDING-TOP: 0px } .homepage #main_content { PADDING-RIGHT: 0px; PADDING-LEFT: 280px; PADDING-BOTTOM: 0px; = PADDING-TOP: 0px } #right_column { POSITION: relative } ------=_NextPart_000_0000_01C82B5D.6748DB40 Content-Type: application/octet-stream Content-Transfer-Encoding: quoted-printable Content-Location: http://www.blackwell-synergy.com/templates/jsp/_synergy.2/scripts/add_load_event.js function addLoadEvent(func) {=0A= var oldonload =3D window.onload;=0A= if (typeof window.onload !=3D 'function') {=0A= window.onload =3D func;=0A= } else {=0A= window.onload =3D function() {=0A= oldonload();=0A= func();=0A= }=0A= }=0A= } ------=_NextPart_000_0000_01C82B5D.6748DB40 Content-Type: application/octet-stream Content-Transfer-Encoding: quoted-printable Content-Location: http://www.blackwell-synergy.com/templates/jsp/_synergy.2/scripts/column_size.js /* =0A= Fix for 3 column layout in the event of left_column or right_column = being longer than main_content=0A= If a page's lh or rh columns are taller than content (so far none = encountered), this script should be included to ensure correct heights.=0A= */=0A= function matchColumns() {=0A= if (! document.getElementById("left_column")) {=0A= return;=0A= }=0A= var h =3D 280; // min height=0A= h =3D Math.max(h, = document.getElementById("left_column").offsetHeight);=0A= h =3D Math.max(h, = document.getElementById("right_column").offsetHeight);=0A= h =3D h + 20; // make main content little longer than side = regions=0A= var m =3D document.getElementById("main_content");=0A= if (m.offsetHeight < h) m.style.height =3D h + "px";=0A= }=0A= // add to the onload queue...=0A= addLoadEvent(matchColumns);=0A= =0A= function fixHeaderHeight() {=0A= var headerHeight =3D 5;=0A= for (var headerhack =3D document.getElementById("headerHack"); = headerhack; headerhack =3D headerhack.offsetParent) headerHeight +=3D = headerhack.offsetTop;=0A= if (headerHeight && (headerHeight > 90 || document.headerHeightSet)) = {=0A= document.getElementById("header").style.height =3D headerHeight = + "px";=0A= document.headerHeightSet =3D true;=0A= }=0A= }=0A= if (window.attachEvent) {=0A= /* for IE */=0A= window.attachEvent("onload", fixHeaderHeight);=0A= window.attachEvent("onresize", fixHeaderHeight);=0A= } else if (window.addEventListener) {=0A= /* for modern browsers */=0A= window.addEventListener("load", fixHeaderHeight, true);=0A= window.addEventListener("resize", fixHeaderHeight, true);=0A= } ------=_NextPart_000_0000_01C82B5D.6748DB40 Content-Type: application/octet-stream Content-Transfer-Encoding: quoted-printable Content-Location: http://www.blackwell-synergy.com/templates/jsp/script.js /* function that will be called from document.onload event=0A= * main event handling, for all pages */=0A= function preload() {=0A= load();=0A= }=0A= function preunload() {=0A= unload();=0A= }=0A= =0A= /* function that will be called from document.onload event=0A= * override this function to do individual onload event */=0A= function load()=0A= {=0A= }=0A= function unload()=0A= {=0A= }=0A= =0A= /**=0A= * Change the forecolor of the element with id eid=0A= * to the color specified by color=0A= */=0A= function changeForegroundColor(eid, color) {=0A= if(document.getElementById && (elem=3Ddocument.getElementById(eid)))=0A= elem.style.color=3Dcolor;=0A= }=0A= =0A= /**=0A= * Shorthand for id'ing elements=0A= */=0A= function $(id) { return document.getElementById(id); }=0A= =0A= /** ccc rights link */=0A= function RightslinkPopUp(aPublisher, aPublication, aTitle, aDate, = aAuthor, aContentId, aCopyright, aVolume, aIssue, aStartPage, aEndPage, = aIssn, aOrderBeanReset, aColor)=0A= {=0A= var location =3D=0A= "?publisherName=3D" + aPublisher=0A= + "&publication=3D" + aPublication=0A= + "&title=3D" + aTitle=0A= + "&publicationDate=3D" + aDate=0A= + "&author=3D" + aAuthor=0A= + "&contentID=3D" + aContentId=0A= + "©right=3D" + aCopyright=0A= + "&startPage=3D" + aStartPage=0A= + "&endPage=3D" + aEndPage;=0A= if (aVolume !=3D null) {=0A= location +=3D "&volumeNum=3D" + aVolume;=0A= }=0A= if (aIssue !=3D null) {=0A= location +=3D "&issueNum=3D" + aIssue;=0A= }=0A= if (aIssn !=3D null) {=0A= location +=3D "&issn=3D" + aIssn;=0A= }=0A= if (aOrderBeanReset !=3D null) {=0A= location +=3D "&orderBeanReset=3D" + aOrderBeanReset;=0A= }=0A= if (aColor !=3D null){=0A= location +=3D "&color=3D" + aColor;=0A= }=0A= =0A= var link =3D "/servlet/linkout?type=3Drightslink&url=3D" + = escape(location);=0A= var winprops =3D = "location=3Dno,toolbar=3Dno,directories=3Dno,status=3Dno,menubar=3Dno,scr= ollbars=3Dyes,resizable=3Dyes,width=3D650,height=3D550";=0A= PopUp =3D window.open(link, 'Rightslink', winprops);=0A= }=0A= =0A= =0A= /* Function to load images.=0A= * note: make this empty method so that=0A= * 1) mininize code changes; 2) for future integration; 3) easier to = take the feature back=0A= */=0A= function MM_preloadImages() {=0A= }=0A= =0A= function MM_swapImgRestore() {=0A= }=0A= =0A= function MM_findObj(n, d) {=0A= }=0A= =0A= function MM_swapImage() {=0A= }=0A= =0A= function menuMouseOver(type, actualType) {=0A= = document.getElementById('MenuItem_'+type).className=3D'MenuItemOver_'+(ty= pe =3D=3D actualType);=0A= }=0A= function menuMouseOut(type, actualType) {=0A= = document.getElementById('MenuItem_'+type).className=3D'MenuItem_'+(type = =3D=3D actualType);=0A= }=0A= function menuClick(type) {=0A= document.getElementById('MenuLink_'+type).click();=0A= }=0A= =0A= // browser detection=0A= function browserCheck() {=0A= this.ns4 =3D (document.layers)? true:false;=0A= this.ie =3D (document.all&&(!window.opera))? true:false;=0A= this.dom =3D (document.getElementById)? true:false;=0A= this.ns6 =3D (window.sidebar)? true:false;=0A= this.moz =3D = (window.sidebar||navigator.userAgent.indexOf('Gecko')!=3D-1)? true:false;=0A= this.opera =3D (window.opera)? true:false;=0A= this.mac =3D (navigator.userAgent.indexOf('Mac')!=3D-1)? true:false;=0A= }=0A= browser =3D new browserCheck();=0A= var Obj;=0A= =0A= // multibrowser get object by id, in NN4 you cannot access all object = (test it first)=0A= function getObjectByName(nameOfObject){=0A= Obj =3D null;=0A= if (browser.ie) Obj =3D document.all[nameOfObject]=0A= else if (browser.dom) Obj =3D findDOMObject(nameOfObject)=0A= else if (browser.ns4) findLayer(window,nameOfObject);=0A= return (!Obj || ( browser.ns4 && Obj =3D=3D window ) ) ? "Object not = found" : Obj;=0A= }=0A= // helper function=0A= function findDOMObject(nameOfObject) {=0A= for (var i =3D 0; i < document.images.length; i++) {=0A= if (document.images[i].name=3D=3DnameOfObject) return = document.images[i]=0A= }=0A= return document.getElementById(nameOfObject)=0A= }=0A= // helper function=0A= function findLayer(node,nameOfObject) {=0A= if ( node.name =3D=3D nameOfObject ) Obj =3D node;=0A= for ( var counter =3D 0; counter < node.document.images.length; = counter++ ) {=0A= if (node.document.images[counter].name=3D=3DnameOfObject) Obj =3D = node.document.images[counter];=0A= }=0A= for ( var i =3D 0; i < node.document.layers.length; i++ ) {=0A= findLayer(node.document.layers[i],nameOfObject);=0A= }=0A= }=0A= =0A= function toggleVisibility(id) {=0A= obj =3D getObjectByName(id);=0A= if (obj) {=0A= v =3D obj.style.display;=0A= obj.style.display =3D (v =3D=3D 'none') ? 'block' : 'none';=0A= i =3D getObjectByName('hiddenImage');=0A= if(i) i.src =3D '/page/imageHack.jsp?object=3D' + id + = '&display=3D' + obj.style.display + '&dummy=3D' + (new Date()).getTime();=0A= }=0A= }=0A= =0A= /** CSS class support */=0A= /** return true if removed, false if not found */=0A= function removeClass(el, className) {=0A= if (!(el && el.className)) return false;=0A= var cls =3D el.className.split(" ");=0A= var ar =3D new Array();=0A= for (var i =3D cls.length; i > 0;) if (cls[--i] !=3D className) = ar[ar.length] =3D cls[i];=0A= el.className =3D ar.join(" ");=0A= return cls.length !=3D ar.length;=0A= }=0A= /** return true if element has that class */=0A= function hasClass(el, className) {=0A= if (!(el && el.className)) return false;=0A= var cls =3D el.className.split(" ");=0A= for (var i =3D cls.length; i > 0;) if (cls[--i] =3D=3D className) = return true;=0A= return false;=0A= }=0A= /** add class to element, if element already had that class - does = nothink */=0A= function addClass(el, className) {=0A= if (!el || hasClass(el, className)) return;=0A= if (el.className) el.className +=3D " " + className;=0A= else el.className =3D className;=0A= }=0A= /** Add CSS rule as last rule in last stylesheet - override all previous = definitions=0A= removing is harder - not implemented, use it with caution */=0A= function addCssRule(selector, rule) {=0A= if (document.styleSheets) {=0A= var css =3D document.styleSheets[document.styleSheets.length-1]; = // get last css=0A= if (css.addRule) css.addRule(selector, rule); // IE=0A= else if (css.insertRule) css.insertRule(selector + "{" + rule + = "}", css.cssRules.length); // W3C=0A= }=0A= }=0A= /** get CSS style of the document */=0A= function getCssText() {=0A= var imports =3D "";=0A= var cssText =3D "\n";=0A= var styleSheets =3D document.styleSheets;=0A= for (var i =3D 0; i < styleSheets.length; i++) {=0A= var css =3D styleSheets.item(i);=0A= var mediaText =3D typeof css.media =3D=3D "string" ? css.media : = css.media.mediaText;=0A= if (!mediaText || mediaText.indexOf("all") !=3D -1 || = mediaText.indexOf("screen") !=3D -1) {=0A= if (css.imports) {=0A= // IE imports=0A= for (var j =3D 0; j < css.imports.length; j++) {=0A= var href =3D css.imports[j].href;=0A= var lastQuote =3D href.lastIndexOf('"');=0A= if (lastQuote !=3D -1) {=0A= // href contains media - "url" media=0A= mediaText =3D href.substr(lastQuote + 1);=0A= if (mediaText.indexOf("all") =3D=3D -1 && = mediaText.indexOf("screen") =3D=3D -1) continue;=0A= href =3D href.substr(1, lastQuote - 1);=0A= }=0A= imports +=3D '@import url("' + href + '");\n';=0A= }=0A= }=0A= if (css.rules) {=0A= // IE rules=0A= for (var j =3D 0; j < css.rules.length; j++) {=0A= // How to filter media rules ???=0A= cssText +=3D css.rules[j].selectorText + " { " + = css.rules[j].style.cssText + " }\n";=0A= }=0A= } else if (css.cssRules) {=0A= // W3C compliant browser=0A= for (var j =3D 0; j < css.cssRules.length; j++) {=0A= var rule =3D css.cssRules.item(j);=0A= if (rule.type =3D=3D rule.IMPORT_RULE || rule.type =3D=3D = rule.MEDIA_RULE) {=0A= mediaText =3D rule.media.mediaText;=0A= if (mediaText && mediaText.indexOf("all") =3D=3D -1 && = mediaText.indexOf("screen") =3D=3D -1) continue;=0A= if (rule.type =3D=3D rule.IMPORT_RULE) imports +=3D = rule.cssText;=0A= else cssText +=3D rule.cssText + "\n";=0A= } else {=0A= cssText +=3D rule.cssText + "\n";=0A= }=0A= }=0A= }=0A= }=0A= }=0A= return imports + cssText;=0A= }=0A= =0A= function loadCss(url, title, media) {=0A= var el =3D document.createElement('link');=0A= el.type =3D 'text/css';=0A= el.rel =3D 'stylesheet';=0A= el.href =3D url;=0A= el.media =3D media || 'screen';=0A= el.title =3D title || 'dynamicLoadedSheet';=0A= document.getElementsByTagName("head")[0].appendChild(el);=0A= }=0A= =0A= function loadJs(url) { =0A= var el =3D document.createElement("script");=0A= el.type =3D "text/javascript";=0A= el.src =3D url;=0A= document.getElementsByTagName("head")[0].appendChild(el);=0A= }=0A= =0A= /** DOM Event support */=0A= /** addEventListener method may already exist, it's not trivial = implement it and not break it, use other mame 'addListener' is simple */=0A= function addListener(el, evname, func) {=0A= if (el.attachEvent) el.attachEvent("on" + evname, func);=0A= else if(el.addEventListener) el.addEventListener(evname, func, true);=0A= }=0A= /** removeEventListener */=0A= function removeListener(el, evname, func) {=0A= if (el.detachEvent) el.detachEvent("on" + evname, func);=0A= else if (el.removeEventListener) el.removeEventListener(evname, func, = true);=0A= }=0A= =0A= /** Server session access */=0A= /** helper method to access session object */=0A= function _getSession() {=0A= return window.session ? window.session : (window.session =3D new = Array());=0A= }=0A= /** send request to server to preserve some value between different = requests, value is accessible using getSessionAttribute */=0A= function setSessionAttribute(name, value) {=0A= /* just to test callback */=0A= function test(doc) {=0A= // alert("Server returned: " + doc.body.innerHTML);=0A= }=0A= = sendServerMsg("/action/sessionAccess?action=3DsetJavaScriptAttribute&name= =3D" + name + "&value=3D" + value, test);=0A= _getSession()[name] =3D value;=0A= }=0A= /** see setSessionAttribute */=0A= function getSessionAttribute(name) {=0A= return _getSession()[name];=0A= }=0A= =0A= /** send request - url - to the server, response is accessible in = document passed to callback function=0A= DO NOT Send anything before page is loaded!=0A= */=0A= function sendServerMsg(url, callBack) {=0A= /* called when frame is loaded */=0A= function _receiveServerResponse(ev) {=0A= var iFrame =3D window.event ? window.event.srcElement : = ev.currentTarget; // IE : W3C=0A= var doc =3D iFrame.contentDocument ? iFrame.contentDocument : = document.frames(iFrame.id).document; // W3C : IE=0A= if (iFrame.callBack) iFrame.callBack(doc);=0A= document.body.removeChild(document.getElementById(iFrame.id));=0A= }=0A= =0A= var iFrame =3D document.createElement('iframe');=0A= addListener(iFrame, "load", _receiveServerResponse);=0A= iFrame.setAttribute("id", "msgFrame" + new Date().getTime()); // = so IE can retrive document=0A= iFrame.setAttribute("src", url);=0A= iFrame.setAttribute("style", "display:none");=0A= if (callBack) iFrame.callBack =3D callBack;=0A= document.body.appendChild(iFrame);=0A= }=0A= =0A= /**=0A= copy innerHTML of src element to innerHTML of target element=0A= */=0A= function copyInnerHtml(src, target) {=0A= var domSupported =3D document.getElementById ? true : false;=0A= var se =3D (domSupported && typeof src =3D=3D "string") ? = document.getElementById(src) : src;=0A= var te =3D (domSupported && typeof target =3D=3D "string") ? = document.getElementById(target) : target;=0A= if (se.innerHTML && te.innerHTML) te.innerHTML =3D se.innerHTML;=0A= }=0A= /**=0A= filter select options, options that do not contain filter text are = removed=0A= in first use, original select options are backed up as attribute = optionsCopy=0A= */=0A= function filterSelect(selectId, value) {=0A= var select;=0A= if (document.getElementById && (select =3D = document.getElementById(selectId)) && select.options) {=0A= if (!select.optionsCopy) {=0A= select.optionsCopy =3D new Array();=0A= select.optionTexts =3D new Array();=0A= for (var i=3D0; i'+document.title+'');=0A= tmp.writeln(el.innerHTML);=0A= tmp.writeln('');=0A= tmp.close();=0A= }=0A= if (anchor) {=0A= var target =3D (tmp.getElementById) ? = tmp.getElementById(anchor) :=0A= (tmp.all) ? tmp.all[anchor] : false;=0A= if (target) {=0A= if (target.scrollIntoView) target.scrollIntoView();=0A= else if (window.scroll && target.offsetTop) = el.popupWindow.scroll(0, target.offsetTop);=0A= }=0A= }=0A= }=0A= }=0A= =0A= /** marks all check box */=0A= function markAllCheckboxes(aForm, aNamePrefix, aChecked)=0A= {=0A= var elmts =3D aForm.elements;=0A= for (var i=3D0; i 0);=0A= if (addElmt)=0A= url +=3D "&" + elmts[i].name + "=3D" + elmts[i].value;=0A= }=0A= window.location =3D url;=0A= }=0A= }=0A= =0A= /**=0A= * @param aAuthorArray array stores all authors=0A= * @param aKeywordArray array stores all keywords=0A= */=0A= function getAuthorsAndKeywords(aForm, aAuthorArray, aKeywordArray, = aForceAdd)=0A= {=0A= setCheckWhenDefine(aForm.sauthusercbx, true);=0A= setCheckWhenDefine(aForm.keyusercbx, true);=0A= =0A= var elements =3D aForm.elements;=0A= var cntAuthor =3D -1;=0A= var cntKeyword =3D -1;=0A= for (var i=3D0; i0) || (aKeywords.length>0))=0A= {=0A= pmurl =3D = "http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?dopt=3DDocSum&cmd=3DSearch= &db=3DPubMed&term=3D";=0A= =0A= for (var i=3D0; i0) && (aKeywords.length>0)) {=0A= pmurl +=3D "+OR+";=0A= }=0A= =0A= for (var i=3D0; i0) || (aKeywords.length>0))=0A= {=0A= adsurl =3D=0A= "http://adsabs.harvard.edu/cgi-bin/nph-abs_connect?db_key=3DAST" +=0A= "&sort=3DSCORE&ttl_syn=3DYES&version=3D1" +=0A= "&txt_syn=3DYES&txt_logic=3DAND" +=0A= "&aut_syn=3DYES&aut_logic=3DAND";=0A= =0A= if (aAuthors.length > 0) {=0A= adsurl +=3D "&author=3D";=0A= for (var i=3D0; i 0) {=0A= adsurl +=3D "&text=3D";=0A= for (var i=3D0; i0) || (aKeywords.length>0))=0A= {=0A= var array =3D [aAuthors, aKeywords];=0A= for (var i=3D0; i]+>/g,"");=0A= }=0A= =0A= // go through page and check for h3 elements within div#main_content=0A= function createJumpers() {=0A= // Browser detect used here to isolate IE Mac - DOM implementation is = too buggy for this script=0A= if (navigator.userAgent.indexOf('MSIE') !=3D -1 && = navigator.userAgent.indexOf('Mac') !=3D -1) return false;=0A= // compatibility tests=0A= if(!document.getElementsByTagName) return false;=0A= if(!document.getElementById("main_content")) return false;=0A= // main function -=0A= // go through the main_content area and get an array of the div tags = present=0A= var divs_arr =3D = document.getElementById("main_content").getElementsByTagName("DIV");=0A= var selected_arr =3D new Array();=0A= var options_arr =3D new Array();=0A= for (var i=3D0; i element=0A= var container_span =3D document.createElement("span");=0A= //container_span.setAttribute("class","select_bg");=0A= container_span.className =3D "select_bg";=0A= // create the