From: Subject: Progress on Antiangiogenic Therapy for Patients with Malignant Glioma Date: Wed, 5 May 2010 23:41:27 +0200 MIME-Version: 1.0 Content-Type: multipart/related; type="text/html"; boundary="----=_NextPart_000_0000_01CAECAC.7B17FC60" X-MimeOLE: Produced By Microsoft MimeOLE V6.00.2900.5579 This is a multi-part message in MIME format. ------=_NextPart_000_0000_01CAECAC.7B17FC60 Content-Type: text/html; charset="utf-8" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2850510/?tool=pubmed =EF=BB=BF Progress on = Antiangiogenic Therapy for Patients with Malignant Glioma
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J Oncol. 2010; 2010: 689018.=20
Published online 2010 = April 6.=20 doi:=20 10.1155/2010/689018.
PMCID:=20 = PMC2850510
Copyright=20 =C2=A9 2010 M. S. Ahluwalia and C. L. Gladson.
Progress on Antiangiogenic Therapy for = Patients with=20 Malignant Glioma
Manmeet S. Ahluwalia1, = 2 and Candece L. Gladson1,=20 3*
1Brain Tumor Neuro-Oncology = Center,=20 Neurological Institute, Cleveland Clinic, Cleveland, Ohio 44195, = USA
2Department of Solid Tumor = Oncology, Taussig=20 Cancer Institute, Cleveland Clinic, Cleveland, Ohio 44195, = USA
3Department of Cancer Biology, = Lerner=20 Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, = USA
*Candece L. Gladson: Email:=20 gladsoc/at/ccf.org
Academic Editor: = Arkadiusz=20 Dudek
Received November 21, 2009; Revised = January 25,=20 2010; Accepted February 11, 2010.
This is an open access article = distributed under=20 the Creative Commons Attribution License, which permits = unrestricted use,=20 distribution, and reproduction in any medium, provided the = original work=20 is properly cited.
Abstract
Glioblastoma (GBM) = is the most=20 common primary brain tumor occurring in America. Despite recent = advances=20 in therapeutics, the prognosis for patients with newly diagnosed = GBM=20 remains dismal. As these tumors characteristically show evidence = of=20 angiogenesis (neovascularization) there has been great interest in = developing anti-angiogenic therapeutic strategies for the = treatment of=20 patients with this disease and some anti-angiogenic agents have = now been=20 used for the treatment of patients with malignant glioma tumors. = Although=20 the results of these clinical trials are promising in that they = indicate=20 an initial therapeutic response, the anti-angiogenic therapies = tested to=20 date have not changed the overall survival of patients with = malignant=20 glioma tumors. This is due, in large part, to the development of=20 resistance to these therapies. Ongoing research into key features = of the=20 neovasculature in malignant glioma tumors, as well as the general=20 angiogenesis process, is suggesting additional molecules that may = be=20 targeted and an improved response when both the neovasculature and = the=20 tumor cells are targeted. Prevention of the development of = resistance may=20 require the development of anti-angiogenic strategies that induce=20 apoptosis or cell death of the neovasculature, as well as an = improved=20 understanding of the potential roles of circulating endothelial = progenitor=20 cells and vascular co-option by tumor cells, in the development of = resistance.
Malignant gliomas = include WHO=20 grade IV gliomas, also known as glioblastomas (GBM), and WHO grade = III=20 gliomas referred to as anaplastic gliomas (AG) (anaplastic = astrocytoma,=20 anaplastic oligodendroglioma, and anaplastic oligoastrocytoma). = GBM is the=20 most common primary brain tumor occurring in the United States of = America;=20 approximately 10,000 new cases are diagnosed each year [1, 2]. In this review, we will focus on the status of=20 antiangiogenic therapy for GBM, as these tumors characteristically = show=20 evidence of angiogenesis (neovascularization) on histologic = examination.=20 Despite recent advances in therapeutics, the prognosis for = patients with=20 newly diagnosed GBM remains dismal; the median survival is 15 = months when=20 treated with the current standard of therapy, which is a = combination of=20 maximal surgical resection followed by concurrent chemoradiation = and six=20 months of adjuvant temozolomide [3]. Most patients with GBM develop tumor recurrence = after the=20 above therapy, and many centers are now treating these patients = with=20 bevacizumab (a monoclonal antibody to vascular endothelial growth = factor=20 (VEGF) that was recently approved by the FDA). Although clearly of = benefit=20 to some patients, the majority die within 6-9 months after = initiation of=20 anti-VEGF therapy [4=E2=80=936]. Other antiangiogenic agents also have been = examined in=20 phase I or II clinical trials for patients with GBM, and promising = results=20 have emerged; however, a statistically significant increase in = overall=20 survival has not been reported to date. It is now becoming = apparent that=20 tumors also can act to enhance their vasculature through other = mechanisms=20 such as =E2=80=9Cco-option=E2=80=9D of the existing vasculature. = The contribution of these=20 processes to tumor vascularization and their potential effects on=20 anti-angiogenic therapies is an emerging field of great=20 interest.
GBMs are among the = most=20 vascular tumors known and hence the tumor-associated vasculature = is an=20 attractive therapeutic target [7]. It is now well established that tumors can = promote the=20 formation of new vessels through the process of angiogenesis. It = is=20 thought that when a tumor reaches a certain size, the requirements = for=20 oxygen and nutrients lead to the growth of new blood vessels [8, 9]. The neovasculature that is formed in GBM never = completely=20 matures; however, this leads to an atypical vasculature that is = constantly=20 undergoing remodeling. There also is evidence to suggest that = prior to the=20 triggering of the process of formation of new vessels, tumor cells = can=20 obtain the necessary nutrients and oxygen by = =E2=80=9Cco-opting=E2=80=9D existing blood=20 vessels [10]. This process appears to occur in very small = tumors and=20 appears to be dependent on the microenvironment in the specific = organ and=20 perhaps on the tumor type. In transplanted C6 rat gliomas in the = rat brain=20 co-option of existing blood vessels by tumor cells occurred = initially when=20 the tumors were several mm in diameter, and this was followed by = vascular=20 regression and ultimately by the development of a neovasculature = [10]. Moreover, the process of vasculogenic mimicry = [11], in which tumor cells function as blood vessel = lining=20 cells, may contribute to the blood supply in malignant tumors. = Most of the=20 research concerning tumor vasculature has focused on the = mechanisms that=20 promote the formation of new blood vessels through the process of=20 angiogenesis and it is these mechanisms that have been targeted in = the=20 development of antiangiogenic therapies. Currently, relatively = little is=20 known concerning the mechanisms underlying co-option of blood = vessels and=20 vasculogenic mimicry, the effects of anti-angiogenic therapies on = these=20 processes, or the role of these processes in the activity of, or=20 resistance to, the anti-angiogenic therapies that have been = developed.=20
2.1. Angiogenic Growth Factors: = Their=20 Receptors and Function
The signaling of VEGF, a = proangiogenic growth factor, is important for GBM angiogenesis and = involves paracrine interactions between the glioma cells, and the=20 inflammatory cells that secrete VEGF, and the tumor-associated = endothelial=20 cells (EC) that express receptors for VEGF (VEGFR) [9]. The VEGF gene family is composed of five = members: VEGF-A,=20 VEGF-B, VEGF-C, VEGF-D, and the placental-derived growth factor = (PlGF) [10=E2=80=9312]. Of these, family members VEGF-A, VEGF-B, and = PlGF are=20 involved in vascular angiogenesis, whereas VEGF-C and -D regulate=20 lymphatic angiogenesis [9]. VEGF-A was originally discovered as a factor = that induces=20 vascular permeability, and has since been shown to be an important = EC=20 mitogen [13, 14]. It belongs to the platelet-derived growth = factor (PDGF)=20 superfamily and is located on chromosome 6 [15]. Once secreted by the tumor cells, stromal = cells or ECs,=20 VEGF can be tethered in the extracellular matrix (ECM) due to an=20 association with proteoglycans or glycosaminoglycans [16, 17].
The main receptors for VEGF-A are = VEGFR1 and=20 VEGFR2 [15]. These receptors are upregulated on the ECs in = GBM as=20 compared to the ECs of normal brain [18]. VEGFR-2 is a major mediator of the mitogenic = and=20 angiogenic effects of VEGF through its activation of the = phosphatidyl=20 inositol 3-kinase (PI3K)/protein kinase B (AKT) and RAF-MAPK = kinase-(MEK-)=20 extracellular signal-regulated (ERK) MAP kinase pathways [15].
Basic fibroblast growth factor = (bFGF) is=20 another proangiogenic growth factor that is upregulated in GBM, in = which=20 it is expressed focally by tumor cells and also is expressed by = the=20 vasculature [19, 20]. The receptors for bFGF include FGFR1, FGFR2, = and FGFR4.=20 FGFR1 is upregulated in GBM and is expressed by both the tumor = cells and=20 the tumor ECs. FGFR4 is expressed only by the tumor cells, and = FGFR2 is=20 not expressed in the tumors but it is expressed in the normal = brain [21, 22]. As is the case for VEGF, once secreted by the = tumor=20 cells, stromal cells or ECs, bFGF can be tethered in the ECM due = to an=20 association with proteoglycans or glycosaminoglycans [16, 17]. Binding of bFGF to its receptor results in = activation=20 of the protein kinase C=CE=B1 (PKC=CE=B1) = pathway [23, 24] and the ERK pathway [23, 25].
In addition to VEGF and bFGF, = several other=20 proangiogenic molecules have been implicated in the initiation or=20 amplification of angiogenesis in GBM including stem cell factor = (SCF) and=20 interleukin-8 (IL-8), hepatocyte growth factor and urokinase [26=E2=80=9330]. SCF mediates its signals through activation = of the=20 c-KIT receptor and may be of particular interest in GBM as its=20 overexpression is associated with a shorter survival in patients = with=20 malignant glioma [31]. IL-8 is a chemokine that is synthesized by = macrophages,=20 ECs (where it is stored in the Weibel-Palade bodies), and other = cell types=20 (such as epithelial cells) [32, 33]. IL-8 is released from macrophages as a result = of a host=20 inflammatory response and activates ECs through the chemokine-1 = and 2=20 receptors (CXCR1 and CXCR2) [34].
Finally, in normal blood = vessels,=20 angiopoietin-1 (Ang-1) is expressed by pericytes, binds the Tie2 = tyrosine=20 kinase receptor expressed on the associated EC and signals for = survival=20 and stabilization of the blood vessel [35, 36]. In GBM there is increased expression of both = Ang-1 and=20 its antagonist angiopoietin-2 (Ang-2); Ang-2 is expressed by the = ECs,=20 whereas Ang-1 is expressed by the tumor cells and is not expressed = by the=20 tumor blood vessels [37]. This has led investigators to speculate that = Ang-2 may=20 have a proangiogenic function in the neovasculature of tumors. Of = note,=20 Ang-2 expression has been implicated in the co-option process as = described=20 below [10].
2.2. Proteolytic Degradation of = the=20 Basement Membrane, Endothelial Cell Sprouting, and Tube = Formation
Proteolytic degradation = of the EC=20 basement membrane by matrix metalloproteinases (MMPs) exposes the = ECs to=20 ECM proteins that can regulate angiogenesis and promote EC = movement or=20 sprouting [11, 28, 31]. These cell-ECM interactions occur through = specific=20 receptors and binding partners expressed on the EC surface, such = as=20 integrin cell adhesion receptors that recognize specific ECM = molecules [9, 28, 34, 38, 39]. In addition, integrin receptors cooperate, = collaborate,=20 or cross-talk with growth factor receptors in a specific manner to = enhance=20 the signaling of both the integrin and the growth factor receptor. = For=20 example, in the chick chorioallantoic membrane model of = angiogenesis,=20 integrins =CE=B1v=CE=B25 and = =CE=B1v=CE=B23, which are=20 expressed on the EC, bind ligands in the chorioallantoic membrane = and=20 promote EC survival, proliferation, and sprouting (migration) by=20 cooperating with VEGFR2 and FGFR, respectively [39]. At the same time, activation of the = platelet-derived=20 growth factor (PDGF) receptor signaling pathway recruits pericytes = to the=20 new EC tube, where they deposit ECM proteins that aid in the = formation of=20 a new EC basement membrane, inducing the expression of fibronectin = and=20 nidogen-1 by the ECs [40=E2=80=9343]. Pericyte recruitment to the EC tube also = promotes the=20 upregulation of certain integrin receptors = (=CE=B16=CE=B21,=20 =CE=B13=CE=B21, = =CE=B11=CE=B21, and=20 =CE=B15=CE=B21) on the ECs that mediate the = interaction of the EC=20 with fibronectin, nidogen-1, and laminin in the new basement = membrane [42, 43].
Pericytes are necessary for = stabilization of=20 the new EC tube. The finding that EC tubes lacking pericyte = coverage=20 become dilated [42] suggests that pericyte coverage of the EC tube = is=20 necessary for maintaining the appropriate vessel diameter. This = concept is=20 consistent with the dilated and tortuous blood vessels that are = observed=20 on histologic examination of many GBM tumors and suggests that = this may be=20 associated with the reduced pericyte coverage of blood vessels = observed in=20 these tumors [36, 44].
Endothelial progenitor = cells (EPCs)=20 from the bone marrow may also contribute to the neovasculature. = EPCs are=20 mobilized from the bone marrow by the cytokine stromal-derived=20 factor-1=CE=B1 (SDF-1=CE=B1) [45] that is expressed by angiogenic vessels in = GBM,=20 SDF1=CE=B1 binds to the G protein-coupled chemokine 4 = receptor (CXCR4)=20 expressed on circulating EPCs and also on tumor vessels [46]. A role for the SDF1=CE=B1/CXCR4 = signaling pathway=20 in the development or maintenance of the GBM neovasculature is = suggested=20 by a report that demonstrated that the administration of a CXCR4=20 antagonist to an orthotopic xenograft mouse model of GBM inhibited = tumor=20 growth [47].
2.3. Abnormalities in the = Neovasculature=20 of GBM and Hypoxia
The failure of the GBM=20 neovasculature to mature completely results in an atypical = neovasculature=20 that demonstrates excessive leakiness and lacks a normal blood = brain=20 barrier (BBB). Electron microscopic examination of the = neovasculature in=20 GBM has revealed that the tight junctions and adherens junctions=20 (important contributors to the BBB) are abnormal and that the = actin=20 filaments associated with the junctions are disorganized [48]. These changes likely decrease the osmotic = gradient=20 between the vasculature and interstitium, elevating the = interstitial fluid=20 pressure in the tumor [49]. This has certain important clinical = implications.=20 First, the elevated interstitial fluid pressure can compromise = drug=20 delivery to the GBM. Second, the abnormalities in the = neovasculature may=20 enhance tumor cell access to the vasculature and aid in tumor cell = migration and invasion along the EC basement membrane to = previously=20 uninvolved brain tissue.
In addition, the = neovasculature in=20 GBM demonstrates prominent thrombosis, promoting local hypoxia = within the=20 tumor. This local hypoxia is exacerbated by the rapid growth of = these=20 tumors, which frequently results in an extensive necrotic core = that=20 further accentuates the hypoxic microenvironment. Hypoxia can = promote=20 tumor angiogenesis through activation of the transcription factor=20 hypoxia-inducible factor -1=CE=B1 (HIF-1=CE=B1) = which, in turn,=20 enhances production of proangiogenic growth factors. Normally, the = von=20 Hippel-Lindau (VHL) molecule inhibits the function of = HIF-1=CE=B1 but=20 hypoxia destabilizes VHL causing it to dissociate from = HIF-1=CE=B1.=20 This results in HIF-1=CE=B1 binding to the hypoxia = response element=20 (HRE) in the promoter of several proangiogenic factors (i.e., VEGF = and=20 SDF-1=CE=B1) thereby initiating their transcription [45, 50]. A second HIF family member, = HIF-2=CE=B1, is also=20 activated by hypoxia and likely plays a role in promoting tumor=20 angiogenesis in GBM [51]. Li and colleagues [51] have recently demonstrated that = HIF-2=CE=B1 is=20 preferentially expressed in glioma stem cells, in comparison to = nonstem=20 tumor cells and normal neural progenitors. Their work showed that=20 HIF2=CE=B1, not HIF1=CE=B1, is selectively = activated in glioma=20 stem cells by hypoxia, inducing the expression of VEGF. In tumor=20 specimens, HIF2=CE=B1 colocalized with markers of cancer = stem cells.=20 Furthermore, targeting HIF in glioma stem cells inhibited = self-renewal,=20 proliferation, and survival in vitro, and attenuated the tumor = initiation=20 potential of glioma stem cells in mouse xenografts. Therefore,=20 HIF2=CE=B1 likely represents a promising new therapeutic = target in=20 patients with GBM [51].
2.4. Role of Cancer Stem Cells = in Tumor=20 Angiogenesis
In recent years, a = minor=20 population of cells has been identified in GBM and other malignant = tumors=20 that has characteristics of tumor-initiating cells. These cells = have been=20 referred to as cancer stem cells (CSCs) and in the case of GBM are = referred to as glioma stem cells [52=E2=80=9354]. There is still some debate regarding the = appropriate=20 definition of CSCs, but an emerging consensus holds that these = cells are=20 capable of self-renewal, sustained proliferation, and initiating = tumor=20 formation when injected in very low numbers into an = immunocompromised=20 mouse host [55]. Of particular relevance to this review, a = small but=20 growing number of papers have suggested that CSCs promote = angiogenesis in=20 tumors. For example, Bao and colleagues (2006) demonstrated that=20 conditioned media from glioma stem cells significantly promoted EC = migration, proliferation, and tube formation as compared to = conditioned=20 media from nonstem glioma cells [56]. Consistent with this observation, Calabrese = and=20 colleagues (2007) showed that ECs interact closely with brain = tumor stem=20 cells in the perivascular location (this has been termed a = vascular niche)=20 and secrete factors that maintain these cells in a stem cell-like = state=20 [57]. Investigators have speculated that this = vascular niche=20 is an important target for therapeutic intervention, as disruption = of the=20 niche microenvironment can ablate the growth of CSCs and arrest = tumor=20 growth [57, 58]. It should therefore be borne in mind that = this is a=20 potential mechanism by which anti-angiogenic drugs could inhibit = brain=20 tumor growth [57]. Most recently, Folkins and colleagues (2009) = compared=20 the angiogenesis in tumor xenografts from C6 glioma cells = containing=20 either a low or a high fraction of CSCs, and found that CSC-high = xenograft=20 tumors demonstrated an increased microvessel density and blood = perfusion,=20 as well as inducing greater mobilization and recruitment of bone=20 marrow-derived EPCs to the tumors [59]. Also, the CSC-high C6 cultures and xenograft = tumors=20 expressed higher levels of VEGF and SDF1, and blocking of these=20 proangiogenic factors resulted in a reduction in the growth of the = tumors=20 compared to that observed with CSC low C6 cells [59]. These data suggest that CSCs do contribute to = tumor=20 angiogenesis by promoting both local EC activity and systemic = angiogenic=20 processes that involve the recruitment of bone marrow-derived EPC = in a=20 VEGF-and SDF1-dependent manner [59].
2.5. Role of Bone = Marrow-Derived=20 Progenitor Cells in Tumor Angiogenesis
There is evidence that = the adult=20 bone marrow plays a significant role in endothelial and lymphatic=20 neovessel formation that supports tumor growth and invasion [60, 61]. As the brain lacks a lymphatic system, = lymphatic=20 neovessel formation is not relevant for GBM. The nonhematopoietic=20 (CD45=E2=88=92) bone marrow-derived = population of=20 cells that likely contribute to tumor angiogenesis, bone = marrow-derived=20 EPCs, may directly contribute to the EC layer by merging with the = wall of=20 a growing blood vessel and differentiating into ECs, thereby = providing an=20 alternative source of ECs [62]. The circulating EPCs originally reported by = Asahara et=20 al. (1997) (defined as CD34+/ VEGFR2+) were = shown to=20 be capable of differentiating into an EC phenotype that expressed = EC=20 markers in vitro, and to be capable of incorporating into = neovessels at=20 sites of ischemia [62]. Shaked and colleagues (2006) showed that = administration=20 of a vascular disrupting agent, such as combretastatin, or=20 chemotherapeutic drugs, such as Paclitaxel or 5-fluorouracil, to a = mouse=20 model of cancer resulted in the recruitment of bone marrow-derived = EPCs to=20 the tumor as well as severe tumor necrosis [63]. Other studies have suggested that circulating = EPCs may=20 contribute to tumor neovascularization in mouse models of cancer = [64].
It should be noted that the = contribution of=20 circulating EPCs to neoangiogenesis has been questioned and the = markers=20 that identify bone marrow-derived EPCs have been debated = vigorously [65, 66]. The reported level of incorporation of = circulating EPCs=20 into new blood vessels varies considerably and ranges in different = studies=20 from 5% to 50% [53, 63, 65, 67]. In addition, technical challenges exist in = identifying=20 vessel-incorporated bone marrow-derived EPCs. Most recently, Rafat = and=20 colleagues (2009) suggested that in 12 patients with GBM higher = numbers of=20 circulating EPCs appeared to correlate with a significantly higher = tumor=20 vessel density, as compared to patients with lower numbers of = circulating=20 EPCs [68]; however, this observation needs to be = validated in a=20 larger study.
Bone marrow-derived = hematopoietic=20 cells have also been reported to contribute to tumor angiogenesis = and=20 invasion. Unlike the circulating EPCs discussed above, these cells = are=20 CD45+, and they include myeloid progenitor cells = identified as=20 GR1+CD11b+ in the mouse (in the human=20 CD3+, CD14+, CD19+, = CD57+ and=20 HLA-DR negative) [69], CD11b+F4/80+ = tumor-associated=20 macrophages (TAMs) [70], Tie2-expressing monocytes [71], CXCR4+VEGFR1+ = hemangiocytes [72], bone marrow-derived circulating cells that = comprise a=20 heterogeneous population of myeloid cells identified as=20 CD45+CD11b+ in the mouse and human [73], platelet-derived growth factor receptor=20 (PDGFR)+ pericyte progenitors [74], and vascular endothelial-(VE-) = cadherin+=20 CD45+ leukocytes [75]. Supporting their potential importance in the = response=20 of the tumor to therapy, Shojaei and Ferrara reported that the = recruitment=20 of bone marrow-derived GR1+ myeloid cells resulted in a = tumor=20 that was refractory to treatment with inhibitors of VEGF [76]. In general, the above CD45+ bone=20 marrow-derived cells are not thought to incorporate into the EC = layer of=20 the new vasculature; rather, some of the above cells are thought = to=20 incorporate into the tumor neovasculature as perivascular cells = where they=20 function to promote angiogenesis through paracrine mechanisms, = such as=20 local secretion of VEGF [73].
2.6. Co-Option of Existing = Blood Vessels=20 Occurs in Very Small Tumors
As discussed above, = there is=20 evidence to suggest that in small tumors, in which the = neovasculature has=20 not developed, the tumor cells obtain the necessary nutrients and = oxygen=20 needed for growth by co-opting existing blood vessels [10]. Of note, in transplanted C6 rat gliomas in = the rat=20 brain co-option of existing blood vessels by tumor cells occurred=20 initially when the tumors were several mm in diameter, and this = was=20 followed by vascular regression and ultimately by the development = of a=20 neovasculature [10]. The same study also showed co-option of = existing blood=20 vessels with the propagation of rat mammary cancer cells in the = rat brain=20 and with the metastasis of Lewis lung cancer cells to the lung = after=20 intravenous injection. In each of these models, Ang-2 expression = was=20 upregulated at the co-opted blood vessels, suggesting a role for = Ang-2=20 signaling in the co-option process [10]. Vessel co-option has been observed in several = other=20 tumors, including melanoma, ovarian carcinoma, and Kaposi sarcoma=20 (reviewed in [11]).
Another mechanism = contributing to the=20 blood supply in malignant tumors is vasculogenic mimicry [11]. In vasculogenic mimicry, tumor cells function = as blood=20 vessel lining cells and this has been described in several types = of=20 malignant tumors, including melanoma [11].
3.1. VEGF Inhibitors
Bevacizumab is = a monoclonal=20 antibody directed toward VEGF that has become the prototype of=20 anti-angiogenic agents in clinical use for treatment of GBM (see = = Table 1). In a = phase II=20 clinical trial, 68 patients with recurrent malignant glioma = (33AG and 353D"GBM) were treated with bevacizumab and irinotecan in = two cohorts=20 (see = Table 2). The = combination=20 therapy produced an impressive initial radiographic response rate = of 57%=20 for GBM and 61% for AG [5, 77]. This compared favorably with the benchmark = response=20 rate for temozolomide therapy at the first tumor recurrence, 5% = for=20 patients with recurrent GBM and 35% for patients with recurrent AG = [78=E2=80=9380]. With the combination of bevacizumab and = irinotecan the=20 progression-free survival at six months (PFS-6) was 43% for = recurrent GBM=20 patients and 59% for AG patients, and this was an improvement over = the=20 accepted PFS-6 standard of 15% for GBM patients and 31% for AG = patients=20 treated with temozolomide [79, 80]. Therapy with bevacizumab and irinotecan also = resulted=20 in neurological improvement and a reduction or discontinuation in = the use=20 of corticosteroid treatment in 31% of patients. The regimen was = well=20 tolerated; only one CNS hemorrhage was reported in 68 patients = treated,=20 eight patients were taken off of the study for thrombotic = complications=20 (four patients with pulmonary embolism (PE), two with deep vein=20 thrombosis, one with thrombotic thrombocytopenic purpura, and one = with=20 thrombotic stroke), and two patients died (one with PE and one = with a=20 thrombotic stroke). Other side effects reported included, = proteinuria,=20 fatigue, and gastro-intestinal toxicity; these have been described = with=20 bevacizumab therapy for other types of cancer. Other prospective = and=20 retrospective studies have demonstrated initial radiographic = response=20 rates of between 35% and 50% with the combination of bevacizumab = and=20 cytotoxic chemotherapy [4, 81=E2=80=9383].
=
3D"Table<= /DIV>
= Table=20 1
Examples = of=20 antiangiogenic agents in clinical trial for patients with = high grade=20 glioma.
As irinotecan has limited activity = as a single=20 agent, a phase II randomized clinical trial was performed to = evaluate the=20 benefit of the addition of irinotecan to bevacizumab. In this = clinical=20 trial 167 patients with recurrent GBM received either bevacizumab = alone or=20 bevacizumab in combination with irinotecan; there was no = statistically=20 significant difference in the median overall survival (OS) for = bevacizumab=20 therapy alone (9.2 months) when compared to the combination = bevacizumab=20 and irinotecan therapy (8.7 months) [6]. A recent study evaluated the approach of = bevacizumab=20 monotherapy in patients with recurrent GBM followed by irinotecan = combined=20 with bevacizumab [84]. In this study, 17/48 patients (35%) achieved = an initial=20 radiographic response and the PFS-6 was reported to be 29%. = Addition of=20 irinotecan to patients who progress on bevacizumab monotherapy = failed to=20 produce an objective radiographic response in any of the 19 = patients [84]. Bevacizumab is presently being evaluated in = the upfront=20 setting with temozolomide and radiation in two randomized phase = III trials=20 sponsored by the Radiation Therapy Oncology Group and Hoffmann-La = Roche=20 [85, 86].
Other VEGF/VEGFR-targeted = inhibitors=20 include, Aflibercept, a soluble VEGF decoy or hybrid = receptor=20 that consists of portions of VEGFR-1 and -2 fused to an = immunoglobulin G1=20 Fc region [87=E2=80=9389] and Cediranib (AZD2171), a pan-VEGFR = tyrosine=20 kinase inhibitor with activity against PDGFR and c-KIT [90] (see = Table=20 1).
4. Multikinase Receptors Inhibitors (MTKI)
A number of MTKIs = have been=20 studied in GBM patients (see Tables = 1 and = 2) including,=20 Imatinib [95=E2=80=9399], Sorafenib [100=E2=80=93102], Sunitinib [103], Vandetanib (ZD6474) [104=E2=80=93107], Vatalanib (PTK787) [91, 108=E2=80=93114], and XL184 [92, 115=E2=80=93117].
5. Other Anti-Angiogenic Agents
Other = anti-angiogenic agents=20 evaluated in GBM (see Tables = 1 and = 2) include,=20 Thalidomide [93, 118=E2=80=93123], Lenalidomide [124, 125], Tamoxifen [126=E2=80=93129], Enzastaurin (LY317615) [130, 131], and the integrin inhibitor = Cilengitide [94, 132, 133].
The Macdonald Criteria = have been=20 used since 1990 to define response or progression in clinical = trials of=20 malignant glioma [134]. The Macdonald Criteria, based on WHO = Criteria,=20 utilizes measurement of the largest cross-sectional area of tumor = on=20 contrast-enhanced CT or MRI scan. Malignant gliomas can be = irregular in=20 shape, include large necrotic cavities, or be partially or = completely=20 nonenhancing, creating difficulty in accurately measuring the = largest=20 cross-sectional area on contrast-enhanced CT or MRI scan. In = addition, the=20 interpreter needs to take into account concurrent corticosteroid = use and=20 changes in neurological function. Thus, response evaluation based = on=20 finding a difference in the largest cross-sectional area of tumor = on=20 contrast-enhanced CT or MRI is even more difficult with = anti-angiogenic=20 therapy.
Clinical trials with = drugs that=20 modify signal transduction through the VEGF signaling pathway = (e.g.,=20 bevacizumab, and cediranib) can produce a rapid decrease in = enhancement=20 after initiation of therapy [5, 135], resulting in an apparent high response = rate. Some of=20 the changes observed on contrast-enhanced CT or MRI scan result = from a=20 rapid normalization of abnormally permeable blood vessels and are = not due=20 to an antitumor effect. Anti-angiogenic therapy likely decreases = vascular=20 permeability and restores at least in part the integrity of the = BBB, this=20 leads to less contrast leakage from the vasculature. There is = evidence=20 that VEGF pathway-targeted anti-angiogenic drugs likely alter the = image=20 characteristics of enhancing tumor more effectively than of = nonenhancing=20 tumor. Hence the extent of reduction in contrast enhancement may = not=20 reflect true antitumor activity of the anti-angiogenic agent. Not=20 infrequently, the radiographic image observed after = anti-angiogenic=20 therapy suggests a radiographic response that is more impressive = than the=20 clinical benefit derived from the therapy. The term = =E2=80=9Cpseudoresponse=E2=80=9D has=20 been used to define the situation wherein the contrast-enhanced = MRI=20 suggests an antitumor effect that does not correlate with a true = clinical=20 benefit [136]. Therefore, treatment response based on = radiographic=20 images is probably not an optimal end point for clinical trials = evaluating=20 anti-angiogenic agents. The international Response Assessment in=20 Neuro-Oncology (RANO) Working Group has developed new criteria for = evaluating tumor response in malignant gliomas that take into = account both=20 enhancing and nonenhancing tumor (best visualized on T2 and=20 fluid-attenuated inversion recovery (FLAIR) MRI sequences) images = [136]. This working group proposes that increased = T2-FLAIR=20 signal likely reflects growing tumor, such as when it appears = outside of=20 the radiation field, it produces mass effect, or it involves the = cortical=20 ribbon, and when it occurs in the absence of other potential=20 explanation.
Although the = anti-angiogenic therapy=20 of patients with malignant glioma has resulted in a small increase = in the=20 PFS-6, in general these agents have failed to produce a sustained = clinical=20 response. For example, patients with malignant glioma treated with = a VEGF=20 inhibitor have shown temporary improvements, seen as reduced edema = on=20 imaging or tumor stabilization on imaging; however, the tumors = ultimately=20 progress after a brief response. In patients with tumor = progression during=20 treatment with bevacizumab, the downhill clinical course is often = rapid,=20 and may be fueled by discontinuing the agent. In a retrospective = analysis,=20 patients with malignant glioma who were treated with a second line = regimen=20 containing bevacizumab after failure of treatment with an initial = therapy=20 combination of bevacizumab and a cytotoxic agent had a median PFS = of only=20 37.5 days [137]. Shaked and colleagues showed that treatment = withdrawal of a vascular disrupting agent, such as combrestatin, = to a=20 mouse model of cancer resulted in the development of an aggressive = and=20 angiogenic tumor [63]. Supporting the concept that malignant tumors = ultimately=20 develop resistance to therapy with a VEGF inhibitor, two recent = studies=20 (one of which included a xenograft mouse model of GBM) suggested = that=20 treatment with a VEGF inhibitor alters the natural history of the = tumor=20 and promotes a highly invasive and metastatic phenotype [138, 139].
The anti-angiogenic therapy = failures described=20 above are thought to be due to the development of resistance to=20 anti-angiogenic therapy. Resistance to anti-angiogenic therapy has = been=20 broadly classified as either adaptive or intrinsic [140]. Animal models of malignant glioma and of = other=20 malignant tumors have shown that tumors adapt to treatment with=20 angiogenesis inhibitors by upregulating, or acquiring, an = alternate=20 mechanism(s) to sustain tumor growth, which has been termed = =E2=80=9Cadaptive=20 evasive resistance=E2=80=9D. This can occur even when the specific = target of the=20 anti-angiogenic agent remains successfully inhibited. Adaptive = resistance=20 along with intrinsic resistance is thought to be the reason for = the=20 progression of malignant tumors treated with anti-angiogenic = therapy. In=20 tumors that show an initial response to anti-angiogenic therapy, = adaptive=20 evasive resistance is thought to be the main mechanism for the = development=20 of resistance, that is, blockade of one proangiogenic growth = factor can=20 lead to upregulation of an alternate proangiogenic growth factor = [141]. For example, in a study of GBM patients = treated with=20 the pan-VEGFR inhibitor cediranib (AZD 2171), blood levels of the=20 proangiogenic factors bFGF and SDF1=CE=B1 were noted to = be higher in=20 patients at the time of tumor progression or relapse as compared = to the=20 levels observed during the phase in which the patients showed a = response=20 to cediranib therapy [142].
Recruitment of vascular progenitor = cells from=20 the bone marrow may aid in the process of adaptive evasive = resistance.=20 Certain anti-angiogenic therapies can cause regression of tumor = vessels=20 resulting in hypoxia and lead to the recruitment of various bone=20 marrow-derived progenitor cells. Bone marrow-derived progenitor = cells=20 (including both vascular progenitor cells and vascular modulatory = cells)=20 can be recruited through hypoxia-induced HIF1=CE=B1 = activation=20 resulting in the expression of the downstream effector = SDF1=CE=B1 [45, 143=E2=80=93146]. GBM tumors with low HIF1=CE=B1 = levels contain=20 fewer bone marrow-derived cells and exhibit lower levels of = angiogenesis=20 and tumor growth, as compared to GBM tumors with high = HIF1=CE=B1=20 levels [146]. This suggests that the recruitment of bone=20 marrow-derived progenitor cells may constitute a mechanism for the = development of adaptive evasive resistance to anti-angiogenic = therapy.=20
One reason for the initial = response to=20 bevacizumab therapy reported for some patients with GBM may be = that the=20 GBM neovasculature typically contains a reduced density of = pericyte=20 coverage [36]. Pericytes are important constituents of blood = vessels=20 in general and of tumor blood vessels, they provide prosurvival = signals to=20 ECs. ECs are thought to induce pericyte recruitment, thereby = promoting=20 their own survival. Two of the best characterized prosurvival = signals for=20 ECs are VEGF and the signals derived from pericyte association = with ECs=20 [36]. Tumor vessels lacking adequate pericyte = coverage are=20 more vulnerable to VEGF inhibition as they lack the pro-survival = signal=20 from pericytes [147]. Blood vessels covered with the normal = density of=20 pericytes probably survive therapy with a VEGF inhibitor as the = pericytes=20 can signal for EC survival or quiescence [148, 149].
Finally, the possibility of the = development of=20 an alternative mechanism, such as co-option, for tumor cells to = acquire=20 oxygen and nutrients must be considered in terms of resistance. = Notably,=20 in an orthotopic mouse model of GBM treated with a VEGFR selective = kinase=20 inhibitor or with a multitarget VEGFR kinase inhibitor, tumor = progression=20 (growth) ultimately occurred that was highly invasive. = Perivascular tumor=20 invasion similar to tumor co-option of blood vessels was observed = at=20 autopsy. Moreover, two other recent studies have suggested that = tumor=20 co-option of pre-existing blood vessels can support a more = invasive tumor=20 cell phenotype and tumor growth after VEGF- or VEGFR2-targeted = therapy [150, 151]. As Ang-2 signaling has been implicated in = mediating=20 blood vessel co-option in the untreated early C6 rat glioma model = of=20 malignant glioma [10], human GBM tumors were immunostained for Ang-1 = and Ang-2=20 and it was reported that Ang-2 expression was upregulated at tumor = co-opted blood vessels. Whether the co-opted blood vessels that = were=20 observed post anti-angiogenic therapy also showed upregulation of = Ang-2=20 remains to be determined.
The second mechanism of = resistance to=20 anti-angiogenic therapy that has been suggested is an intrinsic or = inherent resistance [140]. This concept stems from the observation = that a=20 minority of patients do not appear to respond to anti-angiogenic = therapy.=20 It has been suggested that this may be due to the pre-existing = activation=20 of multiple proangiogenic signaling pathways or a pre-existing=20 inflammatory cell infiltrate that provides a source of tumor VEGF=20 resulting in vascular protection [140].
Drug concentrations = within the=20 central nervous system are dependent on multiple factors that = include, the=20 permeability of the agent across the BBB, the extent to which it = is=20 actively transported out of the brain, and the volume of = distribution in=20 the brain parenchyma [152]. The BBB is an anatomic- physiologic barrier = that is=20 formed by multiple components, including tight junctions between=20 endothelial cells, pericytes, and the astrocytic foot processes. = This=20 barrier selectively allows entry of some substances, such as = glucose,=20 lipid-soluble molecules, and oxygen, while preventing entry of = other=20 substances. It is important to understand that although the BBB = may be=20 disrupted in some areas of a GBM, a substantial proportion of = glioma cells=20 can be located in areas with an intact BBB. The magnitude of tumor = vascular permeability varies within these tumors, with the = greatest=20 permeability being found in the tumor core and a relatively intact = BBB at=20 the proliferating tumor edge. The presence of an intact BBB in = some areas=20 of the tumor and the presence of a partially functional BBB in = other areas=20 of the tumor can prevent the effective delivery of active = therapeutic=20 compounds.
The BBB expresses high = levels of drug=20 efflux pumps such as P-glycoprotein (P-gp), breast = cancer-resistance=20 protein (BCRP), and other multiple drug resistance proteins (MRPs) = that=20 actively remove chemotherapeutic drugs from the brain [153]. Efflux transport systems such as by P-gp = and the MRPs=20 at the brain capillary ECs may play a role in limiting the passage = of=20 therapeutic agents across the BBB [154]. For example, the brain distribution of the = tyrosine=20 kinase inhibitor imatinib is reduced by active efflux via the=20 P-glycoprotein [155]. The BCRP drug efflux transport pump is = expressed in a=20 number of normal tissues, in addition to the BBB [156]. Modulation of drug transporters represents = a new=20 potential strategy to improve efficacy of targeted agents. = Anti-angiogenic=20 agents such bevacizumab that mainly target the EC on the luminal = side of=20 the vessel may not depend on the ability to cross the BBB; = however, this=20 remains a concern for tyrosine kinase inhibitors like=20 imatinib.
Currently, there are no = validated=20 biomarkers to monitor the progress or response to anti-angiogenic = therapy=20 in patients with malignant glioma or other cancers [157]. Two promising biomarkers for assessment of=20 angiogenesis in malignant tumors are the number of circulating = endothelial=20 cells (CECs) and the number of circulating endothelial progenitor = cells=20 (EPCs). A growing body of literature suggests that the number of = CECs and=20 circulating EPCs is significantly elevated in patients with = different=20 types of cancer [65]. Furthermore, in a small number of preclinical = animal=20 studies successful antitumor response to anti-angiogenic therapy = was=20 correlated with changes in the number of CECs and circulating EPCs = [158]. Rafat and colleagues have evaluated the = number of=20 circulating EPCs in the blood of patients with malignant glioma, = and=20 reported that they were higher in patients with GBM as compared to = healthy=20 volunteers [68]. Higher tumor blood vessel densities were = noted in the=20 patients with GBM having higher numbers of circulating EPCs as = compared to=20 those patients with lower numbers of circulating EPCs [68]. This supports the further evaluation of = circulating=20 EPCs as a novel biomarker for the assessment of angiogenesis and = for the=20 assessment of the response to anti-angiogenic therapy in patients = with=20 GBM.
Measurement of VEGF = plasma levels may=20 not be a generally useful biomarker of tumor angiogenesis. For = example,=20 baseline plasma VEGF levels are not correlated with survival = outcome for=20 patients with metastatic colorectal cancer or for patients with = metastatic=20 nonsmall cell lung cancer [159, 160]. As expected, the plasma level of VEGF in = patients=20 with GBM and brain metastases is elevated as compared to normal = healthy=20 volunteers. In patients with metastatic breast cancer higher = plasma levels=20 of VEGF were associated with shorter time of progression [161]. Thus, additional studies need to be = performed to=20 determine whether the measurement of plasma VEGF levels is useful = in=20 monitoring the response to anti-angiogenic therapy in general and = to VEGF=20 inhibitor therapy. As previously noted, blood levels of bFGF and=20 SDF1=CE=B1 were noted to be higher in patients at the = time of relapse=20 as compared to levels observed in the response phase in patients = with=20 recurrent GBM treated with cediranib [142].
Despite the remarkable = progress in=20 our understanding of the process of angiogenesis and the potential = promise=20 of targeting these processes for the treatment of GBM, several = critical=20 questions need to be addressed. These include questions regarding = the=20 fundamental processes involved in GBM vascularization and their = role in=20 the failure of therapy. Pressing questions in this category are: = (1) are=20 the GBM tumors in patients that have failed bevacizumab or other=20 anti-angiogenic therapy avascular, or are the tumors co-opting the = existing blood vessels to obtain the oxygen and nutrients needed?, = (2) is=20 the angiopoietin signaling pathway driving a blood vessel = co-option=20 process in human GBM that have failed therapy with a VEGF = inhibitor or=20 other anti-angiogenic agent?, and (3) do cancer stem cells (or = glioma stem=20 cells) promote angiogenesis in malignant gliomas and could we = target them=20 specifically with novel therapy?
There also is an urgent = need to=20 improve the ability to assess the effects of the anti-angiogenic = therapies=20 on angiogenesis (rather than tumor growth). Questions in this = category=20 include: (1) does the number of CECs and circulating EPCs in = patients with=20 tumors correlate with the tumor grade, and could their number be = used to=20 monitor anti-angiogenic therapy? (Phenotyping circulating EPCs = with a=20 comprehensive set of endothelial, progenitor, and hematopoietic = markers=20 should be performed to address the issue of what are the = appropriate=20 markers to be used to identify circulating EPCs in patients [65]), (2) what is the contribution of circulating = EPCs to=20 angiogenesis in untreated virgin tumors?, and (3) could a = biomarker be=20 identified that would aid in identifying adaptive evasive = resistance=20 (escape pathways) that should be targeted when a patient's tumor = develops=20 resistance to anti-angiogenic therapy?
Anti-angiogenic = therapy appears=20 to be a promising and novel approach for the treatment of = malignant brain=20 tumors. Clinical trials have shown improvement in the short-term=20 progression-free survival. The response of patients with GBM to = therapy=20 with a VEGF inhibitor likely depends, at least in part, on whether = the=20 tumor neovasculature contains a normal density of pericytes, how = capable=20 the tumor is in co-opting pre-existing blood vessels, and whether=20 previously co-opted blood vessels exist in the tumor. A better=20 understanding of the mechanisms of resistance to anti-angiogenic = therapy=20 is needed such that we can improve our treatment strategies for = these=20 patients. The development and optimization of biomarkers to = measure=20 angiogenesis in tumors, such as quantitation of the numbers of = CECs and=20 circulating EPCs, will potentially help us identify patients that = are=20 responding to, or failing, anti-angiogenic therapy. Theoretically, = these=20 markers could also be used to identify the subset of patients that = would=20 benefit from anti-angiogenic therapy and thereby individualizing = therapy=20 for patients with malignant tumors, such as GBM. In addition, new=20 anti-angiogenic therapies that induce apoptosis of the ECs in the=20 neovasculature are needed, as this type of anti-angiogenic therapy = may be=20 less likely to induce therapeutic resistance.
Acknowledgments
We thank Drs. Gene Barnett, Derek = Raghavan,=20 and Fiona Hunter for critical review of this manuscript. This work = was=20 supported by grants CA 109748 and CA 127620 from the National = Institutes=20 of Health-National Cancer Institute to = CLG.
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161. Burstein HJ, Chen Y-H, Parker LM, = et al.=20 VEGF as a marker for outcome among advanced breast cancer patients = receiving anti-VEGF therapy with bevacizumab and vinorelbine = chemotherapy.=20 Clinical Cancer Research. = 2008;14(23):7871=E2=80=937877. [PubMed]
Articles from Journal of=20 Oncology are provided here courtesy of
Hindawi Publishing=20 Corporation
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Selected = clinical=20 trials in patients with recurrent high grade = glioma.

PubMed articles by these = authors

  • Ahluwalia,=20 M.
  • Gladson,=20 C.

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.x-btn-click .x-btn-center { BACKGROUND-POSITION: 0px -126px } .x-panel-btns-ct .x-btn-click .x-btn-right { BACKGROUND-POSITION: 0px -84px } .x-panel-btns-ct .x-btn-click .x-btn-left { BACKGROUND-POSITION: 0px -63px } ------=_NextPart_000_0000_01CAECAC.7B17FC60 Content-Type: text/css; charset="iso-8859-1" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.ncbi.nlm.nih.gov/core/ext.ncbi/1/css/themes/xtheme-oldentrez.css .x-panel { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-STYLE: solid; BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-STYLE: = solid; BORDER-LEFT-STYLE: solid; BORDER-RIGHT-COLOR: #d0d0d0; = BORDER-BOTTOM-STYLE: solid } .x-panel-header { BORDER-RIGHT: #d0d0d0 1px solid; BORDER-TOP: #d0d0d0 1px solid; = BACKGROUND-IMAGE: url(../../img/oldentrez/panel/white-top-bottom.gif); = BORDER-LEFT: #d0d0d0 1px solid; COLOR: #333; BORDER-BOTTOM: #d0d0d0 1px = solid } .x-panel-body { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-bbar .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-tbar .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-tbar-noheader .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-mc .x-panel-tbar .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-body-noheader { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-mc .x-panel-body { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-tl .x-panel-header { COLOR: #333 } .x-panel-tc { BACKGROUND-IMAGE: url(../../img/oldentrez/panel/top-bottom.gif) } .x-panel-tl { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND-IMAGE: = url(../../img/oldentrez/panel/corners-sprite.gif); BORDER-BOTTOM-COLOR: = #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-tr { BACKGROUND-IMAGE: url(../../img/oldentrez/panel/corners-sprite.gif) } .x-panel-bc { BACKGROUND-IMAGE: url(../../img/oldentrez/panel/top-bottom.gif) } .x-panel-bl { BACKGROUND-IMAGE: url(../../img/oldentrez/panel/corners-sprite.gif) } .x-panel-br { BACKGROUND-IMAGE: url(../../img/oldentrez/panel/corners-sprite.gif) } .x-panel-mc { BACKGROUND: #f1f1f1 } .x-panel-mc .x-panel-body { BORDER-RIGHT: 0px; BORDER-TOP: 0px; BACKGROUND: none transparent scroll = repeat 0% 0%; BORDER-LEFT: 0px; BORDER-BOTTOM: 0px } .x-panel-ml { BACKGROUND-IMAGE: url(../../img/oldentrez/panel/left-right.gif) } .x-panel-mr { BACKGROUND-IMAGE: url(../../img/oldentrez/panel/left-right.gif) } .x-tool { BACKGROUND-IMAGE: url(../../img/oldentrez/panel/tool-sprites.gif) } .x-panel-ghost { BACKGROUND: #e0e0e0 } .x-panel-ghost UL { BORDER-LEFT-COLOR: #b0b0b0; BORDER-BOTTOM-COLOR: #b0b0b0; = BORDER-TOP-COLOR: #b0b0b0; BORDER-RIGHT-COLOR: #b0b0b0 } .x-grid-panel .x-panel-mc .x-panel-body { BORDER-RIGHT: #d0d0d0 1px solid; BORDER-TOP: #d0d0d0 1px solid; = BORDER-LEFT: #d0d0d0 1px solid; BORDER-BOTTOM: #d0d0d0 1px solid } .x-btn-left { BACKGROUND-IMAGE: url(../../img/oldentrez/button/btn-sprite.gif) } .x-btn-right { BACKGROUND-IMAGE: url(../../img/oldentrez/button/btn-sprite.gif) } .x-btn-center { BACKGROUND-IMAGE: url(../../img/oldentrez/button/btn-sprite.gif) } .x-border-layout-ct { BACKGROUND: #f0f0f0 } .x-accordion-hd { BACKGROUND-IMAGE: url(../../img/oldentrez/panel/light-hd.gif) } .x-layout-collapsed { BORDER-LEFT-COLOR: #e0e0e0; BORDER-BOTTOM-COLOR: #e0e0e0; = BORDER-TOP-COLOR: #e0e0e0; BACKGROUND-COLOR: #eee; BORDER-RIGHT-COLOR: = #e0e0e0 } .x-layout-collapsed-over { BACKGROUND-COLOR: #fbfbfb } .x-tip .x-tip-top { BACKGROUND-IMAGE: url(../../img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-top-left { BACKGROUND-IMAGE: url(../../img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-top-right { BACKGROUND-IMAGE: url(../../img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-ft { BACKGROUND-IMAGE: url(../../img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-ft-left { BACKGROUND-IMAGE: url(../../img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-ft-right { BACKGROUND-IMAGE: url(../../img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-bd-left { BACKGROUND-IMAGE: url(../../img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-bd-right { BACKGROUND-IMAGE: url(../../img/oldentrez/qtip/tip-sprite.gif) } .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND: = url(../../img/oldentrez/toolbar/bg.gif) #f0f4f5 repeat-x left top; = BORDER-BOTTOM-COLOR: #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; = BORDER-RIGHT-COLOR: #d0d0d0 } .x-toolbar BUTTON { COLOR: #444 } .x-toolbar .x-btn-menu-arrow-wrap .x-btn-center BUTTON { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/btn-arrow.gif) } .x-toolbar .x-btn-text-icon .x-btn-menu-arrow-wrap .x-btn-center BUTTON = { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/btn-arrow.gif) } .x-toolbar .x-btn-over .x-btn-left { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-over .x-btn-right { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-over .x-btn-center { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-over BUTTON { COLOR: #111 } .x-toolbar .x-btn-click .x-btn-left { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-pressed .x-btn-left { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-menu-active .x-btn-left { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-click .x-btn-right { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-pressed .x-btn-right { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-menu-active .x-btn-right { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-click .x-btn-center { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-pressed .x-btn-center { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-menu-active .x-btn-center { BACKGROUND-IMAGE: url(../../img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .ytb-sep { BACKGROUND-IMAGE: url(../images/default/grid/grid-split.gif) } .x-tab-panel-header { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND: #eaeaea; BORDER-BOTTOM-COLOR: = #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-panel-footer { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND: #eaeaea; BORDER-BOTTOM-COLOR: = #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-panel-header { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-panel-footer { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } UL.x-tab-strip-top { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND: = url(../../img/oldentrez/tabs/tab-strip-bg.gif) #dbdbdb repeat-x left = top; BORDER-BOTTOM-COLOR: #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; = PADDING-TOP: 2px; BORDER-RIGHT-COLOR: #d0d0d0 } UL.x-tab-strip-bottom { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND-IMAGE: = url(../../img/oldentrez/tabs/tab-strip-btm-bg.gif); BORDER-BOTTOM-COLOR: = #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-strip SPAN.x-tab-strip-text { COLOR: #333 } .x-tab-strip-over SPAN.x-tab-strip-text { COLOR: #111 } .x-tab-strip-active SPAN.x-tab-strip-text { COLOR: #333 } .x-tab-strip-disabled .x-tabs-text { COLOR: #aaaaaa } .x-tab-strip-top .x-tab-right { BACKGROUND-IMAGE: url(../../img/oldentrez/tabs/tabs-sprite.gif) } .x-tab-strip-top .x-tab-left { BACKGROUND-IMAGE: url(../../img/oldentrez/tabs/tabs-sprite.gif) } .x-tab-strip-top .x-tab-strip-inner { BACKGROUND-IMAGE: url(../../img/oldentrez/tabs/tabs-sprite.gif) } .x-tab-strip-bottom .x-tab-right { BACKGROUND-IMAGE: = url(../../img/oldentrez/tabs/tab-btm-inactive-right-bg.gif) } .x-tab-strip-bottom .x-tab-left { BACKGROUND-IMAGE: = url(../../img/oldentrez/tabs/tab-btm-inactive-left-bg.gif) } .x-tab-strip-bottom .x-tab-strip-active .x-tab-right { BACKGROUND-IMAGE: url(../../img/oldentrez/tabs/tab-btm-right-bg.gif) } .x-tab-strip-bottom .x-tab-strip-active .x-tab-left { BACKGROUND-IMAGE: url(../../img/oldentrez/tabs/tab-btm-left-bg.gif) } .x-tab-strip .x-tab-strip-closable A.x-tab-strip-close { BACKGROUND-IMAGE: url(../../img/oldentrez/tabs/tab-close.gif) } .x-tab-strip .x-tab-strip-closable A.x-tab-strip-close:hover { BACKGROUND-IMAGE: url(../../img/oldentrez/tabs/tab-close.gif) } .x-tab-panel-body { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND: #fff; BORDER-BOTTOM-COLOR: = #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-panel-bbar .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-panel-tbar .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-panel-header-plain .x-tab-strip-spacer { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND: #eaeaea; BORDER-BOTTOM-COLOR: = #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-scroller-left { BORDER-LEFT-COLOR: #aeaeae; BACKGROUND-IMAGE: = url(../../img/oldentrez/tabs/scroll-left.gif); BORDER-BOTTOM-COLOR: = #aeaeae; BORDER-TOP-COLOR: #aeaeae; BORDER-RIGHT-COLOR: #aeaeae } .x-tab-scroller-right { BORDER-LEFT-COLOR: #aeaeae; BACKGROUND-IMAGE: = url(../../img/oldentrez/tabs/scroll-right.gif); BORDER-BOTTOM-COLOR: = #aeaeae; BORDER-TOP-COLOR: #aeaeae; BORDER-RIGHT-COLOR: #aeaeae } .x-window-proxy { BORDER-LEFT-COLOR: #b0b0b0; BACKGROUND: #e0e0e0; BORDER-BOTTOM-COLOR: = #b0b0b0; BORDER-TOP-COLOR: #b0b0b0; BORDER-RIGHT-COLOR: #b0b0b0 } .x-window-tl .x-window-header { COLOR: #555 } .x-window-tc { BACKGROUND-IMAGE: url(../../img/oldentrez/window/top-bottom.png) } .x-window-tl { BACKGROUND-IMAGE: url(../../img/oldentrez/window/left-corners.png) } .x-window-tr { BACKGROUND-IMAGE: url(../../img/oldentrez/window/right-corners.png) } .x-window-bc { BACKGROUND-IMAGE: url(../../img/oldentrez/window/top-bottom.png) } .x-window-bl { BACKGROUND-IMAGE: url(../../img/oldentrez/window/left-corners.png) } .x-window-br { BACKGROUND-IMAGE: url(../../img/oldentrez/window/right-corners.png) } .x-window-mc { BORDER-RIGHT: #d0d0d0 1px solid; BORDER-TOP: #d0d0d0 1px solid; = BACKGROUND: #e8e8e8; BORDER-LEFT: #d0d0d0 1px solid; BORDER-BOTTOM: = #d0d0d0 1px solid } .x-window-ml { BACKGROUND-IMAGE: url(../../img/oldentrez/window/left-right.png) } .x-window-mr { BACKGROUND-IMAGE: url(../../img/oldentrez/window/left-right.png) } .x-panel-ghost .x-window-tl { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-collapsed .x-window-tl { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-window-plain .x-window-mc { BORDER-RIGHT: #eee 1px solid; BORDER-TOP: #d0d0d0 1px solid; = BACKGROUND: #e8e8e8; BORDER-LEFT: #d0d0d0 1px solid; BORDER-BOTTOM: #eee = 1px solid } .x-window-plain .x-window-body { BORDER-RIGHT: #d0d0d0 1px solid; BORDER-TOP: #eee 1px solid; = BACKGROUND: none transparent scroll repeat 0% 0%; BORDER-LEFT: #eee 1px = solid; BORDER-BOTTOM: #d0d0d0 1px solid } BODY.x-body-masked .x-window-mc { BACKGROUND-COLOR: #e4e4e4 } BODY.x-body-masked .x-window-plain .x-window-mc { BACKGROUND-COLOR: #e4e4e4 } .x-html-editor-wrap { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-noborder .x-panel-body-noborder { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM-WIDTH: = 0px; BORDER-RIGHT-WIDTH: 0px } .x-panel-noborder .x-panel-header-noborder { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM: #d0d0d0 = 1px solid; BORDER-RIGHT-WIDTH: 0px } .x-panel-noborder .x-panel-tbar-noborder .x-toolbar { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM: #d0d0d0 = 1px solid; BORDER-RIGHT-WIDTH: 0px } .x-panel-noborder .x-panel-bbar-noborder .x-toolbar { BORDER-TOP: #d0d0d0 1px solid; BORDER-LEFT-WIDTH: 0px; = BORDER-BOTTOM-WIDTH: 0px; BORDER-RIGHT-WIDTH: 0px } .x-window-noborder .x-window-mc { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM-WIDTH: = 0px; BORDER-RIGHT-WIDTH: 0px } .x-window-plain .x-window-body-noborder { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM-WIDTH: = 0px; BORDER-RIGHT-WIDTH: 0px } .x-tab-panel-noborder .x-tab-panel-body-noborder { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM-WIDTH: = 0px; BORDER-RIGHT-WIDTH: 0px } .x-tab-panel-noborder .x-tab-panel-header-noborder { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-RIGHT-WIDTH: 0px } .x-tab-panel-noborder .x-tab-panel-footer-noborder { BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM-WIDTH: 0px; BORDER-RIGHT-WIDTH: = 0px } .x-tab-panel-bbar-noborder .x-toolbar { BORDER-TOP: #d0d0d0 1px solid; BORDER-LEFT-WIDTH: 0px; = BORDER-BOTTOM-WIDTH: 0px; BORDER-RIGHT-WIDTH: 0px } .x-tab-panel-tbar-noborder .x-toolbar { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM: #d0d0d0 = 1px solid; BORDER-RIGHT-WIDTH: 0px } .x-panel-header { FONT-SIZE: 90%; FONT-FAMILY: Arial, Verdana, Sans-Serif; = BACKGROUND-COLOR: #e3e3e3; xbackground: none } ------=_NextPart_000_0000_01CAECAC.7B17FC60 Content-Type: text/css; charset="iso-8859-1" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.ncbi.nlm.nih.gov/portal/portalrc.fcgi/40468/css/40126/37583.css .footer { CLEAR: both } .dynamic_footer { FONT-SIZE: 62.5% } #footer { LINE-HEIGHT: 1.8em; FONT-FAMILY: "Helvetica Neue", GillSans, helvetica, = "lucida sans", arial, sans-serif } #NCBIFooter_dynamic { LINE-HEIGHT: 1.8em; FONT-FAMILY: "Helvetica Neue", GillSans, helvetica, = "lucida sans", arial, sans-serif } #footer H3 { FONT-SIZE: 1.1em; COLOR: #505050 } .foot_list H3 { FONT-SIZE: 1.1em } #footer { FONT-SIZE: 1.1em } #NCBIFooter_dynamic { CLEAR: both; FONT-SIZE: 1.1em; Z-INDEX: 10; COLOR: #505050; POSITION: = relative; TOP: 2.5em; _top: -1.5em } .breadcrumbs { LEFT: 1.6em; POSITION: absolute; TOP: 1.1em } .help_desk { RIGHT: 1em; POSITION: absolute; TOP: 1.1em } #NCBIFooter_dynamic A { COLOR: #14376c; TEXT-DECORATION: none } #footer A { COLOR: #14376c; TEXT-DECORATION: none } #NCBIFooter_dynamic A:hover { TEXT-DECORATION: underline; BORDER-BOTTOM-STYLE: none } #footer A:hover 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BACKGROUND-POSITION: 0px -84px } .x-panel-btns-ct .x-btn-over .x-btn-center { BACKGROUND-POSITION: 0px -105px } .x-panel-btns-ct .x-btn-click .x-btn-center { BACKGROUND-POSITION: 0px -126px } .x-panel-btns-ct .x-btn-click .x-btn-right { BACKGROUND-POSITION: 0px -84px } .x-panel-btns-ct .x-btn-click .x-btn-left { BACKGROUND-POSITION: 0px -63px } .x-btn-menu-wrap { WIDTH: 0px! important } .x-menu { BACKGROUND: #f0f0f0 0px 0px } .x-menu-list-item IMG { DISPLAY: none } .x-menu-list-item A.x-menu-item { PADDING-LEFT: 8px } .port H1.x-panel-header-text { PADDING-RIGHT: 0px; PADDING-LEFT: 0px; FONT-SIZE: 100%; PADDING-BOTTOM: = 0px; MARGIN: 0px; PADDING-TOP: 0px } .port H2.x-panel-header-text { PADDING-RIGHT: 0px; PADDING-LEFT: 0px; FONT-SIZE: 100%; PADDING-BOTTOM: = 0px; MARGIN: 0px; PADDING-TOP: 0px } .port H3.x-panel-header-text { PADDING-RIGHT: 0px; PADDING-LEFT: 0px; FONT-SIZE: 100%; PADDING-BOTTOM: = 0px; MARGIN: 0px; PADDING-TOP: 0px } .port H4.x-panel-header-text { PADDING-RIGHT: 0px; PADDING-LEFT: 0px; FONT-SIZE: 100%; PADDING-BOTTOM: = 0px; MARGIN: 0px; PADDING-TOP: 0px } .port H5.x-panel-header-text { PADDING-RIGHT: 0px; PADDING-LEFT: 0px; FONT-SIZE: 100%; PADDING-BOTTOM: = 0px; MARGIN: 0px; PADDING-TOP: 0px } .port H6.x-panel-header-text { PADDING-RIGHT: 0px; PADDING-LEFT: 0px; FONT-SIZE: 100%; PADDING-BOTTOM: = 0px; MARGIN: 0px; PADDING-TOP: 0px } DIV.x-panel-body { PADDING-RIGHT: 5px; PADDING-LEFT: 5px; PADDING-BOTTOM: 5px; = PADDING-TOP: 5px } .port .x-panel-header { PADDING-RIGHT: 3px; PADDING-LEFT: 5px; PADDING-BOTTOM: 4px; = PADDING-TOP: 5px } .x-panel { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-STYLE: solid; BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-STYLE: = solid; BORDER-LEFT-STYLE: solid; BORDER-RIGHT-COLOR: #d0d0d0; = BORDER-BOTTOM-STYLE: solid } .x-panel-header { BORDER-RIGHT: #d0d0d0 1px solid; BORDER-TOP: #d0d0d0 1px solid; = BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/panel/white-top-bottom.gif); = BORDER-LEFT: #d0d0d0 1px solid; COLOR: #333; BORDER-BOTTOM: #d0d0d0 1px = solid } .x-panel-body { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-bbar .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-tbar .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-tbar-noheader .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-mc .x-panel-tbar .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-body-noheader { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-mc .x-panel-body { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-tl .x-panel-header { COLOR: #333 } .x-panel-tc { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/panel/top-bottom.gif) } .x-panel-tl { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/panel/corners-sprite.gif); = BORDER-BOTTOM-COLOR: #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; = BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-tr { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/panel/corners-sprite.gif) } .x-panel-bc { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/panel/top-bottom.gif) } .x-panel-bl { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/panel/corners-sprite.gif) } .x-panel-br { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/panel/corners-sprite.gif) } .x-panel-mc { BACKGROUND: #f1f1f1 } .x-panel-mc .x-panel-body { BORDER-RIGHT: 0px; BORDER-TOP: 0px; BACKGROUND: none transparent scroll = repeat 0% 0%; BORDER-LEFT: 0px; BORDER-BOTTOM: 0px } .x-panel-ml { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/panel/left-right.gif) } .x-panel-mr { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/panel/left-right.gif) } .x-tool { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/panel/tool-sprites.gif) } .x-panel-ghost { BACKGROUND: #e0e0e0 } .x-panel-ghost UL { BORDER-LEFT-COLOR: #b0b0b0; BORDER-BOTTOM-COLOR: #b0b0b0; = BORDER-TOP-COLOR: #b0b0b0; BORDER-RIGHT-COLOR: #b0b0b0 } .x-grid-panel .x-panel-mc .x-panel-body { BORDER-RIGHT: #d0d0d0 1px solid; BORDER-TOP: #d0d0d0 1px solid; = BORDER-LEFT: #d0d0d0 1px solid; BORDER-BOTTOM: #d0d0d0 1px solid } .x-btn-left { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/button/btn-sprite.gif) } .x-btn-right { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/button/btn-sprite.gif) } .x-btn-center { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/button/btn-sprite.gif) } .x-border-layout-ct { BACKGROUND: #f0f0f0 } .x-accordion-hd { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/panel/light-hd.gif) } .x-layout-collapsed { BORDER-LEFT-COLOR: #e0e0e0; BORDER-BOTTOM-COLOR: #e0e0e0; = BORDER-TOP-COLOR: #e0e0e0; BACKGROUND-COLOR: #eee; BORDER-RIGHT-COLOR: = #e0e0e0 } .x-layout-collapsed-over { BACKGROUND-COLOR: #fbfbfb } .x-tip .x-tip-top { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-top-left { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-top-right { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-ft { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-ft-left { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-ft-right { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-bd-left { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/qtip/tip-sprite.gif) } .x-tip .x-tip-bd-right { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/qtip/tip-sprite.gif) } .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/bg.gif) #f0f4f5 repeat-x left = top; BORDER-BOTTOM-COLOR: #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; = BORDER-RIGHT-COLOR: #d0d0d0 } .x-toolbar BUTTON { COLOR: #444 } .x-toolbar .x-btn-menu-arrow-wrap .x-btn-center BUTTON { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/btn-arrow.gif) } .x-toolbar .x-btn-text-icon .x-btn-menu-arrow-wrap .x-btn-center BUTTON = { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/btn-arrow.gif) } .x-toolbar .x-btn-over .x-btn-left { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-over .x-btn-right { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-over .x-btn-center { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-over BUTTON { COLOR: #111 } .x-toolbar .x-btn-click .x-btn-left { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-pressed .x-btn-left { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-menu-active .x-btn-left { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-click .x-btn-right { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-pressed .x-btn-right { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-menu-active .x-btn-right { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-click .x-btn-center { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-pressed .x-btn-center { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .x-btn-menu-active .x-btn-center { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/toolbar/tb-btn-sprite.gif) } .x-toolbar .ytb-sep { BACKGROUND-IMAGE: = url(/core/extjs/ext-2.1/resources/images/default/grid/grid-split.gif) } .x-tab-panel-header { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND: #eaeaea; BORDER-BOTTOM-COLOR: = #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-panel-footer { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND: #eaeaea; BORDER-BOTTOM-COLOR: = #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-panel-header { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-panel-footer { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } UL.x-tab-strip-top { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND: = url(/core/ext.ncbi/1/img/oldentrez/tabs/tab-strip-bg.gif) #dbdbdb = repeat-x left top; BORDER-BOTTOM-COLOR: #d0d0d0; BORDER-TOP-COLOR: = #d0d0d0; PADDING-TOP: 2px; BORDER-RIGHT-COLOR: #d0d0d0 } UL.x-tab-strip-bottom { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/tabs/tab-strip-btm-bg.gif); = BORDER-BOTTOM-COLOR: #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; = BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-strip SPAN.x-tab-strip-text { COLOR: #333 } .x-tab-strip-over SPAN.x-tab-strip-text { COLOR: #111 } .x-tab-strip-active SPAN.x-tab-strip-text { COLOR: #333 } .x-tab-strip-disabled .x-tabs-text { COLOR: #aaaaaa } .x-tab-strip-top .x-tab-right { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/tabs/tabs-sprite.gif) } .x-tab-strip-top .x-tab-left { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/tabs/tabs-sprite.gif) } .x-tab-strip-top .x-tab-strip-inner { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/tabs/tabs-sprite.gif) } .x-tab-strip-bottom .x-tab-right { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/tabs/tab-btm-inactive-right-bg.gif) } .x-tab-strip-bottom .x-tab-left { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/tabs/tab-btm-inactive-left-bg.gif) } .x-tab-strip-bottom .x-tab-strip-active .x-tab-right { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/tabs/tab-btm-right-bg.gif) } .x-tab-strip-bottom .x-tab-strip-active .x-tab-left { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/tabs/tab-btm-left-bg.gif) } .x-tab-strip .x-tab-strip-closable A.x-tab-strip-close { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/tabs/tab-close.gif) } .x-tab-strip .x-tab-strip-closable A.x-tab-strip-close:hover { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/tabs/tab-close.gif) } .x-tab-panel-body { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND: #fff; BORDER-BOTTOM-COLOR: = #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-panel-bbar .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-panel-tbar .x-toolbar { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-panel-header-plain .x-tab-strip-spacer { BORDER-LEFT-COLOR: #d0d0d0; BACKGROUND: #eaeaea; BORDER-BOTTOM-COLOR: = #d0d0d0; BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-tab-scroller-left { BORDER-LEFT-COLOR: #aeaeae; BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/tabs/scroll-left.gif); = BORDER-BOTTOM-COLOR: #aeaeae; BORDER-TOP-COLOR: #aeaeae; = BORDER-RIGHT-COLOR: #aeaeae } .x-tab-scroller-right { BORDER-LEFT-COLOR: #aeaeae; BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/tabs/scroll-right.gif); = BORDER-BOTTOM-COLOR: #aeaeae; BORDER-TOP-COLOR: #aeaeae; = BORDER-RIGHT-COLOR: #aeaeae } .x-window-proxy { BORDER-LEFT-COLOR: #b0b0b0; BACKGROUND: #e0e0e0; BORDER-BOTTOM-COLOR: = #b0b0b0; BORDER-TOP-COLOR: #b0b0b0; BORDER-RIGHT-COLOR: #b0b0b0 } .x-window-tl .x-window-header { COLOR: #555 } .x-window-tc { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/window/top-bottom.png) } .x-window-tl { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/window/left-corners.png) } .x-window-tr { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/window/right-corners.png) } .x-window-bc { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/window/top-bottom.png) } .x-window-bl { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/window/left-corners.png) } .x-window-br { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/window/right-corners.png) } .x-window-mc { BORDER-RIGHT: #d0d0d0 1px solid; BORDER-TOP: #d0d0d0 1px solid; = BACKGROUND: #e8e8e8; BORDER-LEFT: #d0d0d0 1px solid; BORDER-BOTTOM: = #d0d0d0 1px solid } .x-window-ml { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/window/left-right.png) } .x-window-mr { BACKGROUND-IMAGE: = url(/core/ext.ncbi/1/img/oldentrez/window/left-right.png) } .x-panel-ghost .x-window-tl { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-collapsed .x-window-tl { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-window-plain .x-window-mc { BORDER-RIGHT: #eee 1px solid; BORDER-TOP: #d0d0d0 1px solid; = BACKGROUND: #e8e8e8; BORDER-LEFT: #d0d0d0 1px solid; BORDER-BOTTOM: #eee = 1px solid } .x-window-plain .x-window-body { BORDER-RIGHT: #d0d0d0 1px solid; BORDER-TOP: #eee 1px solid; = BACKGROUND: none transparent scroll repeat 0% 0%; BORDER-LEFT: #eee 1px = solid; BORDER-BOTTOM: #d0d0d0 1px solid } BODY.x-body-masked .x-window-mc { BACKGROUND-COLOR: #e4e4e4 } BODY.x-body-masked .x-window-plain .x-window-mc { BACKGROUND-COLOR: #e4e4e4 } .x-html-editor-wrap { BORDER-LEFT-COLOR: #d0d0d0; BORDER-BOTTOM-COLOR: #d0d0d0; = BORDER-TOP-COLOR: #d0d0d0; BORDER-RIGHT-COLOR: #d0d0d0 } .x-panel-noborder .x-panel-body-noborder { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM-WIDTH: = 0px; BORDER-RIGHT-WIDTH: 0px } .x-panel-noborder .x-panel-header-noborder { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM: #d0d0d0 = 1px solid; BORDER-RIGHT-WIDTH: 0px } .x-panel-noborder .x-panel-tbar-noborder .x-toolbar { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM: #d0d0d0 = 1px solid; BORDER-RIGHT-WIDTH: 0px } .x-panel-noborder .x-panel-bbar-noborder .x-toolbar { BORDER-TOP: #d0d0d0 1px solid; BORDER-LEFT-WIDTH: 0px; = BORDER-BOTTOM-WIDTH: 0px; BORDER-RIGHT-WIDTH: 0px } .x-window-noborder .x-window-mc { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM-WIDTH: = 0px; BORDER-RIGHT-WIDTH: 0px } .x-window-plain .x-window-body-noborder { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM-WIDTH: = 0px; BORDER-RIGHT-WIDTH: 0px } .x-tab-panel-noborder .x-tab-panel-body-noborder { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM-WIDTH: = 0px; BORDER-RIGHT-WIDTH: 0px } .x-tab-panel-noborder .x-tab-panel-header-noborder { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-RIGHT-WIDTH: 0px } .x-tab-panel-noborder .x-tab-panel-footer-noborder { BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM-WIDTH: 0px; BORDER-RIGHT-WIDTH: = 0px } .x-tab-panel-bbar-noborder .x-toolbar { BORDER-TOP: #d0d0d0 1px solid; BORDER-LEFT-WIDTH: 0px; = BORDER-BOTTOM-WIDTH: 0px; BORDER-RIGHT-WIDTH: 0px } .x-tab-panel-tbar-noborder .x-toolbar { BORDER-TOP-WIDTH: 0px; BORDER-LEFT-WIDTH: 0px; BORDER-BOTTOM: #d0d0d0 = 1px solid; BORDER-RIGHT-WIDTH: 0px } .x-panel-header { FONT-SIZE: 90%; FONT-FAMILY: Arial, Verdana, Sans-Serif; = BACKGROUND-COLOR: #e3e3e3; xbackground: none } DIV.section.port { MARGIN-TOP: 0.5em; PADDING-TOP: 0.5em; FONT-FAMILY: = Arial,Helvetica,Sans-Serif } 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elmnts.length; i < len; i++)=0A= {=0A= if (elmnts.item(i).className.indexOf(className, " ") = !=3D -1)=0A= {=0A= elmnts.item(i).innerHTML =3D innerHTML;=0A= unObscuredEmails[className] =3D true=0A= =0A= }=0A= }=0A= }=0A= }=0A= catch(e){=0A= }=0A= }=0A= =0A= //=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D=3D=3D=3D=3D=0A= function pubMedDbLinkSubmit(control) {=0A= try{=0A= if (control.pubmedOption)=0A= control =3D control.pubmedOption=0A= if (control.options)=0A= location.href =3D = control.options[control.options.selectedIndex].value;=0A= }=0A= catch(e){}=0A= return false;=0A= }=0A= =0A= //=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D=3D=3D=3D=3D=0A= // elements "a", "area" with "ref" attribute report to redirect utility = before dereferencing link=0A= //=0A= function initRedirectClicks(report_url) {=0A= =0A= if (report_url && typeof jQuery !=3D 'undefined')=0A= jQuery(document).click(function(e) {=0A= =0A= //=0A= if (!e) return true;=0A= //=0A= if (e.shiftKey || e.altKey || e.ctrlKey) return true;=0A= //=0A= var target =3D jQuery(e.target).closest("a[ref], area[ref]");=0A= if (!target || target.length =3D=3D 0) return true;=0A= //=0A= var ref =3D target.attr("ref");=0A= var href =3D target.attr("href")=0A= =0A= // special processing of href element for pubmed's authors=0A= if (typeof (href) !=3D 'undefined' && = href.indexOf('sites/entrez') && href.indexOf('%5Bauth%5D'))=0A= {=0A= var newHref =3D replacePubMedUnsupportedChars(href);=0A= if (newHref !=3D href)=0A= target.attr("href", newHref)=0A= }=0A= =0A= // append ref with value of href if 'redirect-to-url' is = missing in ref.=0A= if (typeof (ref) !=3D 'undefined' && = ref.indexOf('redirect-to-url') =3D=3D -1)=0A= {=0A= ref =3D ref + '&redirect-to-url=3D' + = encodeURIComponent(href)=0A= //=0A= jQuery.ajax({=0A= type: "HEAD",=0A= url: report_url + '?' + ref,=0A= timeout: 1000,=0A= async: false=0A= });=0A= }=0A= =0A= return true;=0A= });=0A= };=0A= =0A= // function to replace unsupported charachters in author names to be = searchable in PubMed database.=0A= function replacePubMedUnsupportedChars (str)=0A= {=0A= // replace low 128 chars automatically=0A= str =3D str.replace(/%26%23(x000[0-7][0-9a-f])%3b/ig,=0A= function($0, $1){=0A= return (String.fromCharCode('0' + $1))=0A= }=0A= )=0A= // replace others based on map and if it is not in the map replace = with empty string.=0A= str =3D = str.replace(/%26%23(x[0-9a-f][0-9a-f][0-9a-f][0-9a-f][0-9a-f])%3b/ig,=0A= function($0, $1){=0A= return (pubmedUnsupportedCharMap[$1] ? = pubmedUnsupportedCharMap[$1] : '')=0A= }=0A= )=0A= return str;=0A= }=0A= //=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D=3D=3D=3D=3D=0A= // Based on script written by Dean Edwards, 2005=0A= // http://dean.edwards.name/=0A= =0A= var pmc_script =3D {=0A= addEvent: function(element, type, handler) {=0A= // assign each event handler a unique ID=0A= if (!handler.$$guid) handler.$$guid =3D this.addEvent_guid++;=0A= // create a hash table of event types for the element=0A= if (!element.events) element.events =3D {};=0A= // create a hash table of event handlers for each element/event pair=0A= var handlers =3D element.events[type];=0A= if (!handlers) {=0A= handlers =3D element.events[type] =3D {};=0A= // store the existing event handler (if there is one)=0A= if (element["on" + type]) {=0A= handlers[0] =3D element["on" + type];=0A= }=0A= }=0A= // store the event handler in the hash table=0A= handlers[handler.$$guid] =3D handler;=0A= // assign a global event handler to do all the work=0A= element["on" + type] =3D handleEvent;=0A= =0A= =0A= function handleEvent(event) {=0A= var returnValue =3D true;=0A= // grab the event object (IE uses a global event object)=0A= event =3D event || fixEvent(window.event);=0A= // get a reference to the hash table of event handlers=0A= var handlers =3D this.events[event.type];=0A= // execute each event handler=0A= for (var i in handlers) {=0A= this.$$handleEvent =3D handlers[i];=0A= if (this.$$handleEvent(event) =3D=3D=3D false) {=0A= returnValue =3D false;=0A= }=0A= }=0A= return returnValue;=0A= };=0A= =0A= function fixEvent(event) {=0A= // add W3C standard event methods=0A= event.preventDefault =3D fixEvent.preventDefault;=0A= event.stopPropagation =3D fixEvent.stopPropagation;=0A= return event;=0A= };=0A= =0A= fixEvent.preventDefault =3D function() {=0A= this.returnValue =3D false;=0A= };=0A= =0A= fixEvent.stopPropagation =3D function() {=0A= this.cancelBubble =3D true;=0A= };=0A= },=0A= =0A= // a counter used to create unique IDs=0A= addEvent_guid: 1,=0A= =0A= removeEvent: function(element, type, handler) {=0A= // delete the event handler from the hash table=0A= if (element.events && element.events[type]) {=0A= delete element.events[type][handler.$$guid];=0A= }=0A= }=0A= }=0A= =0A= =0A= // = *************************************************************************= ***=0A= // implementation of figure's popup using jQuery and = jQuery.fn.hoverIntent lib=0A= // it set appropriate handlers for all "a" elements with "figpopup" = class name.=0A= // = *************************************************************************= ***=0A= if (typeof jQuery !=3D 'undefined' && typeof jQuery.fn.hoverIntent !=3D = 'undefined') {=0A= (function($j) {=0A= // = =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D hoverHandlers = 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= 'undefined' && hires !=3D this.src)=0A= ? hires : this.src=0A= }=0A= )=0A= =0A= // make arrangement of canvas in the view port = nearby parent element.=0A= var cnvsRltvToPrnt =3D = this._x_arrange_canvas(canvas.coords, prnt.coords, win.coords)=0A= =0A= // visualize the canvas with images.=0A= canvas.css('top', cnvsRltvToPrnt.top + 'px')=0A= canvas.css('left', cnvsRltvToPrnt.left + 'px')=0A= canvas.css('display', 'block')=0A= } // canvas=0A= }, // over=0A= //=0A= out: function (el) {=0A= var canvas =3D $j('.large-thumb-canvas', el)=0A= canvas.css('display', 'none')=0A= },=0A= //=0A= _x_offset: function(el, elname) {=0A= var c =3D {}=0A= if (el[0] =3D=3D window )=0A= c =3D this._x_scroll(el, elname)=0A= else=0A= c =3D el.offset()=0A= //console.info('%s.offset {top,left} =3D {%s, %s}', = elname, c.top, c.left)=0A= return c=0A= },=0A= _x_scroll: function(el, elname) {=0A= var c =3D {top: el.scrollTop(), left: = el.scrollLeft()}=0A= //console.info('%s.scroll {top,left} =3D {%s, %s}', = elname, c.top, c.left)=0A= return c=0A= },=0A= _x_width: function(el, elname) {=0A= var w =3D el.outerWidth() || el.width()=0A= //console.info('%s.width =3D %s; outerWidth =3D = %s; width =3D %s', elname, w, el.outerWidth(), el.width())=0A= //IE: alert(elname + '.width =3D ' + w + '; = outerWidth =3D ' + el.outerWidth() + 'width =3D ' + el.width())=0A= return w=0A= },=0A= _x_height: function(el, elname) {=0A= var h =3D el.outerHeight() || el.height()=0A= // console.info('%s.height =3D %s', elname, h)=0A= return h=0A= },=0A= _x_coords: function(el, elname) {=0A= var size =3D { width: this._x_width (el, elname), = height: this._x_height(el, elname)}=0A= var coords =3D {=0A= scroll: this._x_scroll(el, elname),=0A= width: size.width,=0A= height: size.height,=0A= offset: this._x_offset(el, elname),=0A= size: size=0A= }=0A= return coords=0A= },=0A= _x_get_rltv_coord: function(trgtObj, baseObj, = label) {=0A= var c =3D {top: trgtObj.top - baseObj.top, left: = trgtObj.left - baseObj.left}=0A= //console.info("%s {top: %s, left: %s}", label, = c.top, c.left)=0A= return c=0A= },=0A= //=0A= _x_get_empty_space: function(objCoords, = objSize, viewPortCoords, viewPortSize, label) {=0A= var objRelToViewPort =3D = this._x_get_rltv_coord(objCoords, viewPortCoords, '_x_get_empty_space: = for ' + label);=0A= var c =3D {above: objRelToViewPort.top,=0A= below: viewPortSize.height - = (objRelToViewPort.top + objSize.height),=0A= left: objRelToViewPort.left,=0A= right: viewPortSize.width - = (objRelToViewPort.left + objSize.width)}=0A= $j.each(c, function(k, v){c[k] =3D (v < 0 ? 0 : v)})=0A= //console.info("%s {above: %s, below: %s, left: %s, = right: %s}", label, c.above, c.below, c.left, c.right)=0A= return c=0A= },=0A= //=0A= _x_get_bigest_space_area_name: function(spaces, label) {=0A= var sArr =3D [];=0A= for (k in spaces){ sArr[sArr.length] =3D {k: k, v: = spaces[k]} }=0A= // sort in reverse order=0A= sArr.sort (function(a,b){return ( a.v < b.v ? 1 : ( = a.v > b.v ? - 1 : 0 ) )})=0A= // console.info('%s: %s', label, sArr[0].k)=0A= return sArr[0].k=0A= },=0A= //=0A= _x_get_space_ratios: function(spaces, = viewPortSize, label) {=0A= var ratios =3D {above: 0, left: 0}=0A= if (viewPortSize.height > 0)=0A= ratios.above =3D spaces.above / = viewPortSize.height=0A= if (viewPortSize.width > 0)=0A= ratios.left =3D spaces.left / viewPortSize.width=0A= // console.info('ratio: %s {above: %s, left: %s}', = label, ratios.above, ratios.left)=0A= return ratios=0A= },=0A= _x_arrange_canvas: function(c_c, prnt_c, = viewp_c) {=0A= // then calculate empty space areas around parent = element of the canvas, which is ususally an anchor ("a" element)=0A= var emptySpacesArndPrntInViewPort =3D = this._x_get_empty_space (prnt_c.offset, prnt_c.size, viewp_c.offset, = viewp_c.size, 'emptySpacesArndPrntInWinPort')=0A= =0A= // get the area name, where the most linear space = avaiable=0A= var areaName =3D = this._x_get_bigest_space_area_name(emptySpacesArndPrntInViewPort, = viewp_c.size, 'spacios areaName')=0A= =0A= // calculate the proportions of area to be taken by = canvas in empty space area=0A= // relativly to the parent element.=0A= var ratios =3D = this._x_get_space_ratios(emptySpacesArndPrntInViewPort, viewp_c.size, = 'ratios')=0A= =0A= // calculate parent's coordinates relative to view = port=0A= var prntRltvToViewPort =3D = this._x_get_rltv_coord(prnt_c.offset, viewp_c.offset, = 'prntRltvToViewPort')=0A= =0A= // declare canvas relative coordinates=0A= var cnvsRltvToPrnt =3D {top: 0, left: 0}=0A= =0A= // choose appropriate location for placing canvas.=0A= // and choose the 1st element of an array as the one = with the biggest area around parent of canvas.=0A= // console.info ('place it at the %s', = bigestEmptySpaceAreaName)=0A= // calculations are relative to the left corner of = the parent element of canvas. (it has to have the css property = position:relative)=0A= switch (areaName)=0A= {=0A= case 'above':=0A= cnvsRltvToPrnt.top =3D - c_c.height=0A= cnvsRltvToPrnt.left =3D prnt_c.width * 0.5 - = c_c.width * ratios.left=0A= break;=0A= case 'below':=0A= cnvsRltvToPrnt.top =3D prnt_c.height=0A= cnvsRltvToPrnt.left =3D prnt_c.width * 0.5 - = c_c.width * ratios.left=0A= break;=0A= case 'left':=0A= cnvsRltvToPrnt.left =3D - c_c.width=0A= cnvsRltvToPrnt.top =3D prnt_c.height * 0.5 = - c_c.height * ratios.above=0A= break;=0A= case 'right':=0A= cnvsRltvToPrnt.left =3D prnt_c.width=0A= cnvsRltvToPrnt.top =3D prnt_c.height * 0.5 = - c_c.height * ratios.above=0A= break;=0A= }=0A= =0A= // recalculate canvas' coordinates relative to = parent into coordinates relative to view port.=0A= var cnvsRltvToViewPort =3D {=0A= top: prntRltvToViewPort.top + = cnvsRltvToPrnt.top,=0A= left: prntRltvToViewPort.left + = cnvsRltvToPrnt.left=0A= }=0A= //console.info("cnvsRltvToPrnt {top:%s, left: %s}", = cnvsRltvToPrnt.top, cnvsRltvToPrnt.left)=0A= //console.info("cnvsRltvToViewPort {top:%s, left: = %s}", cnvsRltvToViewPort.top, cnvsRltvToViewPort.left)=0A= =0A= // adjust relative position of canvas to the window = if calculated values=0A= // are forcing canvas go out of view port=0A= // next order should be preserved to keep left top = corner visible always=0A= =0A= // adjust right side and move a bit to the left=0A= if (cnvsRltvToViewPort.left + c_c.width > = viewp_c.width)=0A= {=0A= var horAdj =3D c_c.width - (viewp_c.width - = cnvsRltvToViewPort.left)=0A= cnvsRltvToPrnt.left -=3D horAdj=0A= cnvsRltvToViewPort.left -=3D horAdj=0A= //console.log('adjust right side and move to = the left %spx', horizontalAdjustment)=0A= }=0A= =0A= // adjust below side and move to the top=0A= if (cnvsRltvToViewPort.top + c_c.height > = viewp_c.height)=0A= {=0A= var vertAdj =3D c_c.height - (viewp_c.height - = cnvsRltvToViewPort.top)=0A= cnvsRltvToPrnt.top -=3D vertAdj=0A= cnvsRltvToViewPort.top -=3D vertAdj=0A= // console.log('adjust below side and move to = the top %spx', verticalAdjustment)=0A= }=0A= =0A= // adjust left side and move to the right=0A= if (cnvsRltvToViewPort.left < 0)=0A= {=0A= // console.log('adjust left side and move to the = right %spx', -(cnvsLeftRelativeToWindowPort))=0A= cnvsRltvToPrnt.left -=3D = cnvsRltvToViewPort.left=0A= cnvsRltvToViewPort.left =3D 0=0A= }=0A= // adjust above side and move to the bottom=0A= if (cnvsRltvToViewPort.top < 0)=0A= {=0A= // console.log('adjust above side and move to = the bottom %spx', -(cnvsTopRelativeToWindowPort))=0A= cnvsRltvToPrnt.top -=3D = cnvsRltvToViewPort.top=0A= cnvsRltvToViewPort.top =3D 0=0A= }=0A= // console.info("cnvsRltvToPrnt adjusted {top: %s, = left: %s}", cnvsRltvToPrnt.top, cnvsRltvToPrnt.left)=0A= // console.info("cnvsRltvToViewPort adjusted {top: = %s, left: %s}", cnvsRltvToViewPort.top, cnvsRltvToViewPort.left)=0A= return cnvsRltvToPrnt=0A= }=0A= })=0A= // = =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D end of hoverHandlers = =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=0A= =0A= =0A= // = =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D $j.fn.figPopup = =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D=3D=3D=3D=3D=0A= function hoverOverHandler () {=0A= var h =3D new hoverHandlers();=0A= h.over(this)=0A= }=0A= =0A= function hoverOutHandler () {=0A= var h =3D new hoverHandlers();=0A= h.out(this)=0A= }=0A= =0A= $j.fn.figPopup =3D function(opts){=0A= var config =3D {=0A= interval: 500,=0A= timeout: 0,=0A= over: hoverOverHandler, // handler onMouseOver=0A= out: hoverOutHandler // handler onMouseOut=0A= }=0A= $j.extend(config, opts)=0A= return config=0A= }=0A= =0A= // = =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D= =3D end of $j.fn.figPopup = =3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=3D=0A= =0A= }) (jQuery) // end of extention of jQuery with figPopup=0A= =0A= =0A= =0A= jQuery(document).ready( function () {=0A= var fp_cfg =3D new jQuery.fn.figPopup()=0A= jQuery('a.figpopup').hoverIntent(fp_cfg)=0A= });=0A= }=0A= =0A= // end of hoverIntent routines for figures' popups=0A= // = *************************************************************************= ***=0A= // implementation of ....=0A= // = *************************************************************************= ***=0A= ------=_NextPart_000_0000_01CAECAC.7B17FC60 Content-Type: application/octet-stream Content-Transfer-Encoding: quoted-printable Content-Location: http://www.ncbi.nlm.nih.gov/corehtml/pmc/js/noext.menu.js if (typeof(noext) =3D=3D=3D 'undefined') { noext =3D {};=20 } if (typeof jQuery =3D=3D=3D 'undefined') { throw new Error('noext.Menu: jQuery must be present'); } // Constructor noext.Menu =3D function (n, subMenuStyle) { this.n =3D n; this.subMenuStyle =3D (subMenuStyle =3D=3D=3D 'ext') ? 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