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The A2A adenosine receptor plays a critical and non-redundant role in suppressing inflammation at sites of hypoxia and tissue damage. The tumor microenvironment has high levels of adenosine as a result of hypoxia and ectopic expression of enzymes responsible for the generation of extracellular adenosine. Thus, we sought to determine the ability of A2A receptor null mice to immunologically reject tumors. We observed that mice lacking the A2A adenosine receptor showed significantly delayed growth of lymphoma cells when compared to WT mice. Furthermore, when immunized with a low dose of tumor or with an irradiated GM-CSF–secreting tumor vaccine, A2A receptor null mice showed significantly enhanced protection from a subsequent high-dose challenge from both immunogenic and poorly immunogenic tumor lines. This increase in protection was accompanied by an increase in the number of tumor-antigen-specific CD8 T cells at the vaccine-site draining lymph node. Finally, we found that A2A receptor null mice displayed more robust anti-tumor responses than WT mice when they were treated with a soluble B7-DC/Fc fusion protein designed to antagonize B7-H1-mediated co-inhibition. This combinatorial immunotherapy strategy could also be recapitulated with pharmacological A2A receptor blockade paired with B7-DC/Fc administration. In light of these data, we believe that blockade of the A2A adenosine receptor is an attractive target for tumor immunotherapy that synergizes with other immunomodulatory approaches currently in clinical trials.
Extracellular adenosine is a primordial signaling molecule that serves as a potent regulator of inflammation [1, 2]. This ubiquitous purine nucleoside is normally only found at nanomolar levels in the extracellular environment [3] due to the activity of the enzyme Adenosine Deaminase which rapidly catalyses the generation of inosine. However, the concentration of extracellular adenosine can increase dramatically at sites of trauma, hypoxia and inflammation [4]. Damaged cells with compromised membrane integrity in these environments release into the surrounding interstitial space not only adenosine, but also AMP, ADP, ATP and other purine catabolites [5, 6]. These nucleotides are quickly broken down to form adenosine by the extracellular ectonucleotidase CD39 and CD73 [7, 8]. There are four known adenosine receptors, A1, A2A, A2B and A3, all of which modulate the activity of adenylyl cyclase to influence the generation of intracellular cAMP [9–11]. The A1 and A3 receptors are Gi protein linked and inhibit the generation of cAMP when stimulated, while the A2A and A2B receptors are Gs linked and activate the production of cAMP [12]. These receptors are expressed widely throughout the body, including the heart, brain and lung [13], as well as epithelial cells [14] and lymphocytes [15].
It is becoming clear that this extracellular adenosine is not only the product of inflammation but can profoundly regulate inflammation. Seminal studies by the Sitkovsky group demonstrated the critical role of the adenosine A2A receptor in regulating inflammation [16]. In spite of the fact that there are 4 adenosine receptors, knocking out the A2A receptor led to exaggerated and lethal inflammation in response to normally moderate stimuli. The A2A receptor is found on cells of hematopoietic origin and has been shown to inhibit inflammatory gene expression from activated neutrophils, macrophages, dendritic cells, NK cells and lymphocytes [17–20]. Indeed, acutely, A2A receptor activation is a potent inhibitor of TCR-induced cytokine production [21]. Further, our group has shown that signaling via the A2A adenosine receptor can induce anergy in CD4 T cells despite strong TCR engagement and co-stimulation [22]. In addition, adenosine has been shown to play a pivotal role in regulating the generation and functionality of regulatory CD4 T cells [22, 23] and the expression of inhibitory molecules such as LAG3 on activated T cells [22]. Treatment of mice with agonists to the A2A adenosine receptor has been shown to decrease the severity of several models of autoimmunity, such as Inflammatory Bowel Disease (IBD) [24].
Inasmuch as adenosine is released into the inflammatory milieu, it is thought that signaling via the A2A receptor serves as a negative feedback loop preventing collateral tissue destruction by overzealous immune responses [16]. However, many tumors have subverted the normally beneficial function of this signaling pathway to evade immune destruction [17, 25]. As a result of the highly hypoxic and/or inflammatory conditions, the tumor microenvironment has been shown to have high levels of adenosine which is an ideal situation for A2A receptor activation [2]. In addition to being intrinsically hypoxic due to a high rate of metabolism and insufficient vascular development, many tumors ectopically express the ectonucleotidase responsible for the generation of extracellular adenosine [26, 27].
In this study, we show that mice lacking the A2A adenosine receptor have significantly decreased rates of tumor growth relative to their WT counterparts. Furthermore, A2A receptor null mice show increased responses to both lymphoma and melanoma tumor vaccines, resulting in a greater expansion of tumor-specific CD8 T cells and increased survival of tumor-bearing hosts. Finally, the combination of mitigating A2A receptor signaling and blocking checkpoint-mediated inhibition of anti-tumor immunity with a B7-DC/Fc fusion protein resulted in significantly increased survival in tumor-bearing mice. These results suggest that signaling via the A2A adenosine receptor plays a critical role in regulating tumor growth in vivo and that the inhibition of A2A receptor signaling, when combined with blockade of other inhibitory signals, offers an exciting possibility for enhancing the potency of tumor immunotherapy.
A2A receptor KO and C57Bl/6 WT mice were housed and bred in pathogen-free conditions prior to treatment on the Johns Hopkins School of Medicine East Baltimore campus. All mouse work was done in accordance with the Animal Care and Use Committee guidelines for Johns Hopkins University School of Medicine.
B16 and EL4 cell lines were maintained in RPMI supplemented with 10% fetal bovine serum and 50 μg/mL penicillin, 50 μg/mL streptomycin. Luciferase expressing EL4 cells were generated by retrovirally transfecting EL4 cells with luciferase construct (a generous gift of the Levitsky lab), followed by the enrichment by FACS sorting and purification by limiting dilution.
EL4-luciferase bearing mice were anesthetized by an i.p injection of room temperature ketamine (80 μg/g of mouse) and xylene (17.5 μg/g of mouse). Once unresponsive, the tumor inoculation site was shaved and the mice injected with 1.5 mg of luciferin-potassium salt dissolved in PBS (Caliper LifeSciences). After 15 min to allow complete diffusion of the substrate, mice were imaged using an IVIS system (Caliper LifeSciences).
Superficial inguinal lymph nodes from immunized mice were harvested and passed through a 60um strainer to create a single-cell suspension. Cells were then stained at 21°C with MHC class I OVA tetramer (Beckman Coulter), diluted in FACS buffer (PBS + 10% FBS) followed by surface staining for CD8 (BD). Cells were then analyzed on a FACSCalibur (BD), and post-collection analysis performed using FlowJo (TreeStar).
During initial tumor dose-finding experiments, it was discovered that both WT and A2A receptor KO mice completely rejected a subcutaneously (s.c.) dose of 103 live EL4 cells. In light of these findings, WT and A2A receptor null mice were primed with 103 live EL4 cells and rested for 60 days, whereupon they were challenged with 106 live EL4 cells along with age-matched naïve controls. This high tumor dose was previously determined to be lethal in both WT and A2A KO mice, albeit with a slight delay in the A2A receptor null mice. Tumor growth was monitored by palpation and caliper measurement. Mice were killed once tumor volume exceeded 100 mm3.
WT and A2A receptor KO mice were immunized with 106 irradiated (10,000 rad) GM-CSF–secreting B16 melanoma cells, producing ~300 ng GM-CSF in a 24 h period. After 27 days, immunized mice, along with naive age-matched controls, were injected i.v. via the lateral tail vein with 106 B16 cells. After 15 days, all mice were killed by CO2 inhalation and their lungs harvested, weighed and placed in Fekete's Solution (62% EtOH, 3.3% Formaldehyde, 1.5% Glacial Acetic Acid). After a week of fixation, lungs were removed from solution and visible B16 nodules were counted under a dissecting microscope.
A B7-DC/Fc fusion protein was provided by Amplimmune (Rockville, MD). For experiments using WT and A2A receptor null mice, EL4 tumor-bearing mice were treated with 100 μg B7-DC/Fc or with 100 μg control mouse IgG, by i.p. injection on day 1 post-tumor inoculation and every 3 days following for the duration of the experiment. Pharmacological A2A receptor blockade was achieved by daily i.p. injections of 100 ul of the A2A antagonist ZM-241385 (Tocris) diluted in a 1:1:4 emulsion of DMSO, Cremophor and ddH20 at a concentration of 3 mg/ml. This treatment was supplemented with either 25 μg of control mouse IgG or 25 μg B7-DC/Fc.
Unless otherwise stated error bars were generated using SEM, and P values by a Mann–Whitney t test. Curves were compared using a 2-way ANOVA. All analysis was performed by Prism 5.0c (Graphpad).
Mice lacking the A2A adenosine receptor (A2A KO) have previously been described [28] and show no gross baseline immunologic phenotype compared to WT C57Bl/6 mice. However, in light of the increased severity of inflammation observed in the A2A KO mice in several models of autoimmunity, we decided to determine whether any difference could be detected in their ability to reject a syngeneic tumor challenge. To this end, A2A KO and WT control mice were injected s.c. with 106 luciferase expressing cells from the EL4 thymoma line. Tumor growth was monitored twice weekly by i.p injection of luciferase substrate, followed by whole-body imaging. WT mice showed steady tumor growth, as measured by photon flux, during the 26 day course of the experiment. All mice in the WT group were killed on day 26 due to unacceptably large tumor size. In contrast, mice lacking the A2A adenosine receptor showed a much-reduced rate of tumor growth compared to the WT controls, with several mice showing near complete rejection (Fig. 1a). The difference between the two groups was most evident on day 26 of the experiment, where there was almost a 100-fold difference in the luminescent output (Fig. 1b). However, there was a significant difference in the rate of tumor growth even at early timepoints of the experiment (Fig. 1c) *P < 0.05. These data suggest that absence of the A2A adenosine receptor can increase anti-tumor responses.
During the course of the initial tumor challenge experiments utilizing the non-luciferase expressing EL4 line, several doses of the tumor were used to determine the necessary number of cells required for successful tumor implantation. A dose of 106 live EL4 cells was found to be universally lethal in both WT and A2A receptor null mice, albeit with a slight increase in survival time in the A2A KO mice, while a dose of 105 cells proved lethal to the majority of WT mice but not to A2A receptor KO mice. However, mice from both genotypes easily rejected tumor doses of 104 and 103 cells (data not shown). We wondered whether these low-level tumor doses could act as a tumor vaccine, providing protection against a later high-dose challenge.
WT and A2A KO mice were initially primed with a non-lethal dose of 103 live EL4 cells, which both genotypes easily rejected. Sixty days post-priming, both groups of mice, along with naive controls, were challenged with 106 EL4 cells. Both naive WT and A2A KO mice showed a relatively fast rate of tumor growth, but there was a slightly higher rate of survival in the naive A2A KO group compared to WT controls despite the high tumor dose (Fig. 2a). Both primed WT and A2A KO mice showed greater overall survival compared to their naive counterparts. However, primed A2A KO mice showed the highest rate of overall survival of all experimental groups (P < 0.05) and had a significantly slower rate of tumor volume growth (Fig. 2b). These observations suggested that elimination of the anti-inflammatory A2A adenosine receptor signaling not only enhanced the ability of mice to initially reject tumor but also led to enhanced recall responses.
Given our findings concerning the enhanced rejection of tumor in the A2A receptor knockout mice, we wanted to demonstrate that this was associated with increased anti-tumor T-cell responses. Indeed, our findings concerning the enhanced protection upon rechallenge suggested that A2A receptor null mice would demonstrate robust responses to tumor vaccines. Irradiated GM-CSF–secreting tumor vaccines initiate potent immune responses against a wide range of tumor antigens without the need to immunize with individual, isolated peptides [29]. While this immunization technique is most often used with a single irradiated transformed cell line secreting GM-CSF, it is also possible to induce a bystander response by mixing the irradiated GM-CSF–secreting line with a second, non-cytokine secreting, irradiated target line [30]. To this end, we immunized both WT and A2A KO mice s.c. with a 1:1 mixture of irradiated ovalbumin (OVA) expressing EL4 cells and a GM-CSF-secreting B16 melanoma line. Generation of an OVA-specific CD8 T-cell response was monitored using MHC class I tetramer staining. Flow cytometric analysis of the injection site draining lymph nodes of immunized mice (Fig. 3a) 7 days post-immunization revealed significantly more OVA-specific CD8+ T cells in the A2A KO mice compared to WT mice (Fig. 3b) *P < 0.05. There was no significant increase in the percentage of tetramer-positive CD8 T cell in the draining LN of the immunized A2A receptor null mice compared to their WT counterparts, but the significantly larger size of the A2A KO draining lymph node resulted in the significant increase in the overall number of antigen-specific CD8 T cells. Thus, while both the WT and the A2A receptor null mice demonstrated a robust CD8 +T-cell response, the A2A KO mice were able to generate a markedly increased response to the tumor vaccine.
To further elucidate the potential for tumor vaccine enhancement by the loss the A2A receptor, we decided to again utilize an irradiated GM-CSF–secreting tumor vaccine, this time in the context of a systemic tumor model. To this end, we immunized WT and A2A KO mice with 106 irradiated GM-CSF–secreting B16 cells and rested the mice for 60 days. Immunized mice, along with naive controls, were injected i.v. with 106 B16 melanoma cells. After 17 days, the mice were harvested and the number of lung nodules counted and lungs weighed.
Naive WT mice showed extremely heavy tumor burden at the time of harvest, both in terms of the number of countable metastases and the wet-weight of the lungs. As would be predicted by our previous data, the naive A2A KO mice showed a significantly lower level of tumor growth than the naive WT mice (Fig. 4a, b). Thus, in addition to lymphoma, the A2A receptor null mice demonstrate an increased ability to reject melanoma, even in the absence of vaccine. Lungs from WT mice that were previously immunized with the irradiated GM-CSF–secreting B16 line showed a lower tumor burden than either naive group demonstrating the efficacy of the GM-CSF-secreting tumor vaccine in this model. As we would have predicted, the lungs from previously immunized A2A KO mice showed near complete protection from the growth of the transferred melanoma. Overall these findings demonstrate the ability of A2A receptor null mice to respond more vigorously to GM-CSF-secreting whole cell tumor vaccines than their WT counterparts. The significance of these data is compounded by the fact that the B16 melanoma line is considered poorly immunogenic [31], suggesting that even non-ideal vaccine strategies can be enhanced by elimination of A2A receptor signaling.
Extracellular adenosine is just one of many inhibitory signals that tumors use to evade the immune system. It is clear that tumors have developed mechanisms to activate co-inhibitory receptors on T cells to effectively shut down anti-tumor responses. For example, expression of the inhibitory receptor Programed Death (PD)-1 on activated T cells is a negative feedback signal that under normal conditions serves to limit proliferation and effector function following the resolution of an immune response, but is frequently subverted by tumors to inhibit infiltrating lymphocytes [32]. The canonical ligand for PD1, B7-H1, is normally found on activated antigen presenting cells, including B cells and macrophages [33]. B7-DC is a recently discovered, dendritic cell restricted PD-1 ligand that provides potent co-stimulation to T cells [34]. The exact mechanism by which B7-DC enhances T-cell stimulation is still unknown, but it has been proposed to antagonize the inhibitory PD1/B7-H1 interaction, or interacts with an as-of-yet undiscovered receptor [35]. Many tumors take advantage of the ability of B7-H1 expression to limit the proliferation and cytokine production of PD1 expressing T cells by ectopically expressing the ligand [36]. We wondered whether we could further enhance an anti-tumor immune response by simultaneously mitigating A2A signaling and providing additional co-stimulation signal via B7-DC. To this end, we utilized a B7-DC/Fc fusion protein in the context of an EL4 thymoma challenge in both WT and A2A receptor null mice.
WT and A2A KO mice were injected with 106 EL4 thymoma cells s.c. and treated i.p. with 100 μg of either control IgG or B7-DC/FC on day 1 of the experiment and every 3 days following. IgG-treated WT mice demonstrated steady tumor growth, first showing tumor development by day 8 post-inoculation (Fig. 5a) and reaching the cutoff size for killing by day 37 (Fig. 5b). Also, at this dose of tumor, A2A KO mice showed steady tumor growth during the course of the experiment. A slight increase in overall survival was observed in IgG-treated A2A KO mice compared to similarly treated WT controls, but no difference was observed in the duration of tumor-free survival. WT mice receiving B7-DC/Fc treatment show a marked increase in the duration of tumor-free survival compared to IgG-treated groups (P < 0.001). Interestingly, the B7-DC/Fc-treated A2A KO mice demonstrated a significant increase in the duration of both tumor-free survival and overall survival compared to all other treatment groups, even the B7-DC/Fc-treated WT mice (P = 0.05). In addition, combining pharmacological A2A receptor blockade with B7-DC/Fc treatment resulted in a significant reduction in tumor growth (Fig. 5c). However, this combinatorial effect of pharmacological A2A receptor blockade and B7-DC/Fc administration was only observed during the first week of therapy, after which all groups receiving B7-DC/Fc showed similar reduced tumor growth. These data suggest that combination therapy attacking A2A signaling and co-inhibitory molecules might represent a novel avenue of enhancing tumor immunotherapy.
In this report, we demonstrate the ability of A2A receptor null mice to readily reject syngeneic tumors. In doing so, our data support the findings of Ohta et al. [25] This group, by demonstrating the ability of A2A KO mice to immunologically reject tumors, unequivocally established a role for adenosine in the tumor microenvironment as contributing to the ability of tumors to evade immune responses. Herein we reproduce and additionally extend these findings to demonstrate that mitigating A2A receptor signaling can enhance the efficacy of irradiated GM-CSF–secreting vaccines and additionally can synergize with agents which target co-inhibitory pathways. As such, our findings further support the development of A2A receptor antagonists as a means of enhancing anti-tumor immunity. Interestingly, A2A receptor antagonists have been safely tested in Phase III clinical trials for Parkinson's disease paving the way for the initiation of clinical trials in cancer [37].
Extracellular adenosine is emerging as a potent regulator of inflammation at sites of extensive tissue damage and hypoxia. In cancer, the hypoxic environment of tumors leads to an increase in the local concentrations of extracellular adenosine [2]. In addition, it is becoming clear that tumors upregulate enzymes that lead to the generation of adenosine [26, 27]. For example, it has recently been shown that the ecto-5′-nucleotidase CD73 that catalyzes AMP breakdown to adenosine is upregulated on the cell surface of many tumor cell lines. Indeed, knocking down the expression of CD73 on tumors led to enhanced anti-tumor responses in vivo [27]. This increase in adenosine not only serves to inhibit anti-tumor immunity in terms of T-cell responses but also down modulates the activity of macrophages, neutrophils, dendritic cells and NK cells [17–20]. It is important to keep in mind that the extracellular adenosine found in hypoxic tumor environments can not only influence the host immune response to the tumor, but also the ability of a tumor to proliferate and survive. Several studies have suggested that extracellular adenosine signaling via the A2A adenosine receptor can negatively impact the viability of several tumor lines [56]. These observations highlight the balance a tumor must strike between generating a suppressive microenvironment that can inhibit the ability of the immune system initiate tumor rejection, while still permitting the tumor itself to proliferate.
A2A adenosine receptor exhibits a similar expression pattern and shares some functional redundancy with the A2B adenosine receptor. Recent studies have shown that mice lacking the A2B adenosine receptor show an increased resistance to tumor growth, which is attributable to a decrease in VEGF production by tumor infiltrating lymphocytes [57]. Our current study adds to the numerous previous reports demonstrating a central non-redundant role for the adenosine A2A receptor in mediating the immune-inhibitory effects of adenosine.
While there is a plethora of studies demonstrating the ability of tumor vaccines to both prevent and treat cancer in a wide variety of preclinical models, such findings have yet to be robustly translated in Phase III clinical trials. Of note, however, recently the FDA granted approval to the first therapeutic cancer vaccine. Sipuleucel-T is an autologous dendritic cell vaccine loaded with prostate-specific peptides which has been shown to be efficacious in extending survival in patients with metastatic castration-resistant prostate cancer [38]. Our data suggest that inhibiting A2A receptor signaling has the ability to enhance GM-CSF-secreting whole cell vaccines. Recent Phase III trials using this tumor vaccine strategy failed to demonstrate efficacy in prostate cancer [39]. However, there are a number of other clinical trials demonstrating safety and in some cases hints of efficacy using this vaccine platform [40]. Of note, several studies suggest that the efficacy of irradiated GM-CSF–secreting tumor vaccines can be markedly enhanced when it is combined with agents which block co-inhibition. Specifically, in preclinical models, there is evidence to suggest that blocking PD-1 and CTLA-4 can increase anti-tumor responses in irradiated GM-CSF–secreting tumor vaccines treated mice [41]. Our current studies suggest that blocking A2A receptor signaling represents an additional avenue to enhance vaccine efficacy. Our current data specifically employs GM-CSF-secreting "whole cell" vaccines. Based on these studies, we predict that A2A receptor blockade would also enhance other "whole cell" vaccines such as Sipuleucel-T. Of note, preliminary studies in our laboratory suggest that in addition to "whole cell" vaccines, A2A receptor blockade can also enhance the generation of effector cells in response to viral vaccines (data not shown).
Many tumor-associated antigens have been identified, and indeed various cancer vaccine strategies have been able to induce immunity to these antigens [42, 43]. What is clear, however, is that the tumor microenvironment can inhibit the ability of tumor-specific recognition to lead to immune-mediated tumor destruction. The tumor microenvironment is replete with inhibitory cytokines such as TGF-β, IL-10 and IL-13 [44–46]. Such cytokines not only inhibit anti-tumor Th1-mediated immunity, but also promote the generation of regulatory T cells and monocytic-derived cells [47, 48]. Accumulating data, including our current study, suggest that adenosine in the tumor micro-environment also represents a potent means by which tumors convert anti-tumor recognition by T cells into tumor-antigen-specific tolerance [25].
A2A receptor activation inhibits both CD4+ and CD8+ T-cell proinflammatory cytokine expression [15, 22, 49–51]. Alternatively, A2A receptor signaling does not appear to inhibit anti-inflammatory cytokine expression [50]. In addition, adenosine acting via the A2A receptor has previously been shown to promote T-cell anergy even in the presence of costimulation [22]. Further, A2A signaling has been shown to play a role in not only the generation of Foxp3 and Lag-3+ regulatory cells, but also in mediating their inhibitory effects [22, 23]. Thus, in the setting of infection, adenosine acts as an inhibitory metabokine [52] here preventing self-destruction by effectively down modulating immune responses. In the tumor microenvironment, cancer has usurped the adenosine-induced negative feedback loop to inhibit the anti-tumor immune response.
Co-inhibitory molecules are emerging as potentially potent adjuvants to cancer immunotherapy [53, 54]. Specifically, targeting CTLA-4- and PD-1-mediated negative regulatory pathways has shown promise in a number of clinical trials [55]. Our current data demonstrate that administering B7-DC/FC fusion protein to A2A receptor null mice led to marked enhancement of anti-tumor immunity. In these experiments, mice were challenged with doses of tumor that led to death in the A2A receptor null mice and in the WT mice treated with B7-DC/FC. However, when we treated A2A receptor null mice with B7-DC/FC, there was a significant decrease in mortality. Such data suggest that simultaneously blocking the A2A receptor- and B7-H1-mediated co-inhibition can act additively/synergistically to enhance anti-tumor immune responses. Experiments are underway to determine whether A2A receptor blockade in combination with anti-CTLA4 or anti-PD1 also leads to enhanced responses.
We thank Amplimmune for their generous gift of B7-DC/FC for use in this study, and to Charles Drake and Ivan Borrello for their critical reviews. Funding for this study was provided by the NIH grant R01CA114227.
Conflict of interest Jonathan Powell is a Scientific Founder of Amplimmune, Inc.
Adam T. Waickman, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Angela Alme, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Liana Senaldi, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Paul E. Zarek, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Maureen Horton, Department of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Jonathan D. Powell, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
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And then there were four.
Well, four teams, but only three games left in the NFL postseason. Two of the games are pending this weekend, and then, of course, there's the big one in February in Dallas. The top seeds, however, are gone. No more Tom Brady or Matt Ryan. Ray Rice, Michael Turner and the Law Firm are out as well. And we and the Chicago Bears can't kick the Seattle Seahawks around anymore.
You've got one more shot to change your lineups in ESPN's Gridiron Playoff Challenge, and I'd certainly suggest you look into doing so, even if all nine of your selections are still active heading into conference championship weekend. There are entries with perfect lineups, but I'm guessing you're more like me, having relied on at least one member of the New England Patriots or Atlanta Falcons.
So here we go, one last set of postseason rankings. At this point, you really want to concentrate on players that will be playing two games instead of one. This isn't easy to predict, obviously, especially when so many upsets have littered the schedule the past few weeks and home teams haven't been any more likely to win than road teams.
Full disclosure: I think we'll be seeing a lot of green in Dallas, and not just because Jerry Jones is hosting many of the parties. You're maximizing point potential getting more than one game from your players, and you cannot change rosters next week. Here we go!
1. Aaron Rodgers, Green Bay Packers
2. Mark Sanchez, New York Jets
3. Ben Roethlisberger, Pittsburgh Steelers
4. Jay Cutler, Chicago Bears
Analysis: I know, I know, Cutler produced four touchdowns Sunday and there's no comparing Roethlisberger and Sanchez by pretty much any normal statistical measure. However, I think the Jets will beat the Steelers. That's two games versus one. Plus, I feel like pointing out that Sanchez outscored Roethlisberger this past weekend. Obviously, the Steelers' defense presents a different challenge than the Patriots did, and it's another road tilt, but I'm going with the kid, and in particular, his team's stifling defense. Brady ended up with 299 passing yards, a nice statistical game even though he didn't look nice doing it, but the truth is I like only one of the four remaining quarterbacks this weekend. And I'll set the over/under on Cutler interceptions at three. But the Packers, they are really good.
Running backs
1. James Starks, Packers
2. Matt Forte, Bears
3. LaDainian Tomlinson, Jets
4. Rashard Mendenhall, Steelers
5. Shonn Greene, Jets
6. John Kuhn, Packers
7. Brandon Jackson, Packers
8. Chester Taylor, Bears
9. Mewelde Moore, Steelers
Analysis: Here's where it gets interesting. I think the Packers' defense is at least somewhat susceptible to the running game, though the Eagles and Turner didn't exactly torch them. Starks picked up 25 carries against the Falcons but gained only 66 yards. I expect a better performance against the Bears, with similar touches but more yards. Starks gets the top spot, but I do think Forte is the one Bears player worth risking, win or lose.
In the AFC, Mendenhall seems an obvious choice, and he's easily the most expensive option in the ESPN game. Mendenhall led all running backs with 17 fantasy points this past weekend; I just don't see the Jets allowing him that many. If there was any way to attack the Jets' defense during the regular season, it was definitely through the air, not on the ground. Now I don't think there's a good way. Tomlinson reached double digits in fantasy points this past weekend, one of six running backs to do so. My thinking goes that the Jets would face the Packers, meaning Tomlinson and Greene will get ample work in the big game as well.
Wide receivers
1. Greg Jennings, Packers
2. Santonio Holmes, Jets
3. Braylon Edwards, Jets
4. Mike Wallace, Steelers
5. Hines Ward, Steelers
6. James Jones, Packers
7. Johnny Knox, Bears
8. Donald Driver, Packers
9. Jordy Nelson, Packers
10. Jerricho Cotchery, Jets
11. Emmanuel Sanders, Steelers
12. Earl Bennett, Bears
13. Devin Hester, Bears
14. Brad Smith, Jets
Analysis: Well, I like Jennings a lot, but I also had him ranked first a week ago and he delivered one of the four double-digit fantasy outings from wide receivers. Oddly enough, three of the four were Packers! Rodgers' passing game is so dynamic, even leaving a dome for whatever awaits at Chicago's Soldier Field, four Packers wide receivers rank in the top nine here. I like both Jets starting wide receivers over their opponents for Pittsburgh.
Tight ends
1. Dustin Keller, Jets
2. Greg Olsen, Bears
3. Heath Miller, Steelers
4. Andrew Quarless, Packers
1. Mason Crosby, Packers
2. Nick Folk, Jets
3. Shaun Suisham, Steelers
4. Robbie Gould, Bears
1. Green Bay Packers
2. New York Jets
3. Pittsburgh Steelers
4. Chicago Bears

subset: commoncrawl


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Stuart Lancaster ready for defining period of his England career
Stuart Lancaster accepts the visit of Wales and Australia to Twickenham over the next two weekends will define his stewardship as England's World Cup enters a critical phase.
The magnitude of Saturday's Pool A showdown with Warren Gatland's men was vast even before Lancaster dropped the selection bombshell of demoting George Ford at fly-half in favour of Owen Farrell and picking Sam Burges at inside centre.
But the radical overhaul of England's midfield after Jonathan Joseph was stricken by a chest injury, including the fielding of the 14th centre pairing of Lancaster's reign in Burgess and Brad Barritt, has added a new dimension to a match already billed as the biggest in the old rivals' long history.
Lancaster has been accused of gambling and abandoning his attacking philosophy shaped around the vision of Ford at a decisive moment in his three and a half year reign and while he denies the claims, he is aware his reputation is on the line.
When asked if the evaluation of his tenure hinged on the outcome against Wales, he replied: "It was always going to be the case for this game and the one against Australia.
"Clearly the selection has heightened it. If we win the game it will be judged a success. If we lose the game regardless of what selection I made, I'd be questioned I made in selection in the first place.
"It will come down ultimately to the next two games. I understand the consequences and the stakes because it's the World Cup."


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Barbie: VINTAGE Complete PINK MOONBEAMS Outfit...NR!
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Not mint but great for display. No damage or stains that I noticed. Tagged Barbie ® by Mattel. Slightly wrinkled from storage. The straps and ties on the nightie are limp but intact. Open toe shoes with one marked Japan complete the set .Please email with questions before auction ends . There is no reserve, so high bidder wins!
Now for the fine print:
Import duties, taxes, and charges are NOT included in the item price or shipping cost. These charges are the buyer's responsibility. Please check with your national customs office to determine what these additional costs will be prior to bidding or buying.
Items must be declared for full value and cannot be designated as a "gift". It is a federal offense punishable by fines and/or jail time to falsify customs forms.
Shipping costs are non-negotiable! I ship USPS Priority International Airmail because it is the only option that provides the required online viewable tracking information for PAYPAL seller protection. First class airmail or other methods do not have tracking and I absolutely cannot ship without it! Delays caused by the shipping carrier or customs are beyond my control.
I do not rate anything "mint" unless it is still in the package or I opened it myself. I try to disclose all problems I'


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William Nielsen's Utah Built Crystal Sets
I got interested in radio when my son asked me to build a one tube radio for a school project. I have an old electricity text that had a set that called for a # 30 tube.I knew nothing of how to even find a tube let alone the rest of the parts. Well, after lots of research and 5 years later, I have collected some parts so I decided to build something other than the ones I collected on Ebay.
The circuit for the crystal radio is from the Radio receiver projects book by Homer L. Davidson. The face and bottom are made of 1/2 inch plexyglass. The dial is an original Atwater Kent dial I found in a friends junk pile, With the variable cap still attached. The crystal set is project #4 The permeability-tuned set in the project book. The coil has 2 windings L1= 25 turns #24 enameled and L2= 97 turns same wire.
The crystal detector is completely hand made from the design of the pacient detector. I turned all the brass on a lathe and the round bottom is plexyglass also. I added the diode later and its from an old military receiver also from the junk box.
The small black dial for the grounding cap. was salvaged from an old thermal resistance meter. Lots of great parts on those things. The ground and aerial posts are also original Atwater Kent parts also.
The coil slider coil is wound on a PVC form. I threaded brass rods to hold it together and the contact is made from a cabinet door bullet catch, Most hardware stores have them.
Last of all, The baldy phones were found at a local garage sale, I think brand new. Nathianel Baldwin radio works was located just 5 miles from my house. The building is still standing and is now converted into many small shops.
I think its great to receive a radio signal LOUD, Without batteries. Thanks again,


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Kayda Kanoon Trailer (1993)
10 June 1993 Action, Foreign 150 mins
Former freedom fighter, Sinha, has always believed in the rule of the law over violence. He watches in disapproval as Police Inspector Dawood Durani is arrested, charged with killing his wife, Shehnaz, the daughter of Mirza Lucknowi. He also watches with despair when his pupil, Kishan Kashyap, frequently loses his temper over not getting employed, and when he does get employed as a Police Inspector, shows arrogance and contempt of the law. Sinha's views change dramatically when he watches two women being murdered by a man named Balu. When he reports this matter to Inspector Deshmukh, he is told to check his vision as Balu was somewhere else during this incident. When Sinha persists and decides to approach higher authorities, his lovely daughter, Kavita, the girlfriend of Kishan, is abducted, his Journalist son, Amrit, is killed, and his daughter-in-law, Vimladevi, may well be in league with the killers...
Watch the official Kayda Kanoon 1993 trailer in HD below or find more Kayda Kanoon videos on Vidimovie.


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Watch: New RBW-Associated Girl Group P.O.P Releases MV Teaser For Debut Track Catch You
A new girl group called P.O.P will be debuting very soon!
P.O.P has been trained and produced by MAMAMOOs agency RBW, but it will be managed by DWM Entertainment. The six-member group will be releasing their first mini album Puzzle Of POP on July 26.
You can watch the music video teaser for their debut track Catch You below!
You can also check out the highlight medley of their first mini album below.


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Tag Archives: maine
Maine Recap (and a shout-out to our parents)
Well, we've left the great state of Maine and returned to our quaint little shoe box. Before reality really starts to sink in (work starts for one of us tomorrow), we thought we'd touch on a few more food highlights … Continue reading
Posted in Uncategorized Tagged blueberry pancakes, clam chowder, fore street, francine bistro, lobster rolls, maine, mussels, white barn inn, whitehall inn 4 Comments
So Much Lobster, So Little Time
Hello from Kennebunkport, Maine! After an absolutely fabulous weekend with family and friends, we now get to spend our first days as husband and wife sampling the cuisine of the upper east coast. We've already fallen in love with this … Continue reading
Posted in Uncategorized Tagged clam shack, kennebunkport, lobster, lobster roll, maine, whole belly clams 1 Comment


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7614 Matoaka Road, Sarasota, FL 34243Request info Add to list
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7614 Matoaka Road is an industrial property for lease in Sarasota, FL.
Clean, well maintained 2,500 sq. ft. industrial condominium unit with approximately 750 sq. ft. of office space including reception area, private office, large air-conditioned open work area and two restrooms. Warehouse has 16' ceilings and a 12' x 14' overhead door, plus mezzanine storage above offices. Conveniently located off Tallevast Road, just east of Highway 301.
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Jersey Shore is a borough in Lycoming County, Pennsylvania, United States. It is on the West Branch Susquehanna River, 15 miles (24 km) west by south of Williamsport. It is part of the Williamsport, Pennsylvania Metropolitan Statistical Area. In the past, Jersey Shore held farms, railroad shops, cigar factories, a foundry, and a large silk mill. In 1900, 3,070 people lived here; in 1910, 5,381; and in 1940, 5,432. The population was 4,482 at the 2000 census.
Jersey Shore was incorporated as a borough on March 15, 1826. The history of Jersey Shore begins about 50 years before it was incorporated and on the opposite bank of the West Branch Susquehanna River in what is now Nippenose Township. Colonel John Henry Antes arrived in 1772 and established a homestead along the banks of Antes Creek. Antes also built a gristmill and his fortified home, Fort Antes, provided a safe haven for the early settlers against raids conducted by Loyalist and Indian forces during the American Revolution. Settlers who had sought refuge at Fort Antes and had returned to the right bank of the West Branch to milk their cows were among the first killed when Fort Antes was attacked just prior to the Big Runaway. These pioneers on the north side of the river were counted among the Fair Play Men, a group of squatters who lived outside the jurisdiction of the colonial and revolutionary governments of Pennsylvania. Many of the settlers did not return to the area until after Sullivan's Expedition had forced the Lenape and other Indians allied with the British further west.[3]
Jersey Shore was originally named Waynesburg by the two brothers, Reuben and Jeremiah Manning, who laid out the town circa 1785.[3] Around the time that this was happening, a settlement arose on the eastern side of the West Branch Susquehanna River (Nippenose Township), opposite Waynesburg. A rivalry developed between the two settlements, and those on the eastern shore began referring to the settlement on the western shore as the "Jersey Shore," because the Manning family had relocated from New Jersey. The nickname became so fixed that in 1826 the original name of Waynesburg was officially abandoned and changed to Jersey Shore.[4]
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Meet Our Staff
For trusted and reliable service, hire Mr. Handyman of Greater Cincinnati/NKY
Steve J.
Kyle J.
Operations Manager
Kyle has been working at Mr. Handyman for over 10 years. He has over 15 years of management experience. He enjoys meeting customers in person or speaking to them over the phone. Kyle wants the company to achieve 100% customer satisfaction. He enjoys boating, golfing and spending time with his family.
Joan D.
Office Administrator
Joan has been working for Mr. Handyman part time since 2001, having started in customer service before moving to accounting. She began her time with Mr. Handyman as a mother of three and is now a grandmother of six. When not spending time with her family, Joan enjoys taking fitness classes, reading and crocheting.
Shannon K.
Customer Service Representative
Shannon started with Mr. Handyman in 2017. Shannon has been in the customer service industry most of her career. She will be handling customer calls, insuring customers are truly satisfied with their experience with Mr. Handyman.
Val B.
Customer Service Representative
Val has many years of experience in customer service and is most likely the voice you will hear when calling our office. She takes pride in listening to our customers, ensuring their needs are met and that our customers are truly satisfied and receive the ultimate Mr. Handyman experience. Val enjoys spending her free time with family and friends.
Dan R.
Senior Service Technician
Dan became a Service Technician with Mr. Handyman in 2005. He has over 20 years of construction experience and is a very strong finish carpenter. Dan enjoys making sure every customer is completely satisfied with the service he performs. When Dan isn't working he enjoys camping and vacationing with his wife and son.
George T.
Senior Service Technician
George started with Mr. Handyman in 2013 and has been our lead technician for 2 years. He has a background in kitchen/bathroom remodeling and finish carpentry. He is married with 2 children and enjoys camping on the weekends.
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Senior Service Technician
Glenn has been with Mr. Handyman for over 8 years. He has been in the repair and remodeling industry for several years. Glenn specializes in building relationships with our commercial clients. He is the proud husband to his wife of 20 years. Glenn enjoys riding motorcycles and spending time with friends and family.
Chris D.
Service Technician
Chris started with Mr. Handyman in 2016. He has over 20 years of experience in restoration and remodeling. Chris is very friendly and enjoys meeting new customers. He spends his free time with his family.
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Service Technician
Craig has over 10 years of experience in residential and commercial maintenance and repair. He has a strong background in masonry and carpentry. Craig enjoys being outdoors and spending time with friends and family.
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Service Technician
Earl has over 15 years of maintenance and repair experience. He has a strong background in door repairs and installation. Earl collects baseball cards, is a fan of the Cincinnati Bengals and enjoys spending time with his family.
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Service Technician
Greg has spent over 20 years of carpentry experience. He has held both residential and commercial positions. Greg enjoys meeting new customers and doing something different everyday. When not working at a customers home he enjoys golfing, hunting, fishing and building custom furniture.
Greg H.
Service Technician
Greg has been a Service Tech with Mr. Handyman for over a year. He has 20 plus years of experience in commercial and residential maintenance. Greg enjoys spending time and vacationing with his girlfriend as much as possible. He is looking forward to Alaskan Cruise.
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Service Technician
Jeff has been working as a handyman for over three decades. He has completed all types of residential and commercial repairs and maintenance. Jeff enjoys playing cards, traveling and spending time with his family.
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Justin works as a Service Technician and has over 10 years of experience in the repair and remodeling industry. Justin enjoys boating and spending time with friends and family.
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text: The backsplash is one of the first items that grab your attention when you enter a kitchen, so it requires outstanding planning. It must unify the whole theme of the room. As kitchen backsplash is a piece of decoration that gives your kitchen walls the protection it needs. Backsplashes appear in tremendous variations in both material and color. Here are some backsplash ideas for kitchens. Stone Tiles: Stone tiles will give a natural look to the kitchen. Marble, old rock or limestone tiles are various types of stone tiles. Ceramic Tiles: If you are seeking a great idea for your kitchen backsplash, …Read More »


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We cater specifically for the students and staff of the University of Westminster. Our booksellers liaise closely with lecturers to ensure that the books we stock are the ones you need at the time you need them.
Marylebone bookshop
35 Marylebone Road,
London NW1 5LS
Tel: 020 7911 5049
Fax: 020 7911 5046
Opening Hours
9.30 to 5.00 Monday to Friday


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Welcome to INTERACTIVE DRAMAS, a repository of information, scenarios, critical discussion, and resources related to the scenario-based theatre-style freeform live action roleplaying game and related fields of inquire and performance.
While we've started small here, we hope to eventually have a pretty comprehensive collection of links and the like for introductory information (stored locally and linked from cyberspace) and we'd like to become the major clearing house for publicly available scenarios and games (for use by hobbyists and in the language classroom). By publicly available I do not mean public domain. All rights of original authors apply here. These scenarios are available for folks to use but the authors do not waive their rights or ownership and the like.
These pages are maintained by Brian David Phillips, Ph.D., C.H., an Associate Professor in the English Department at National Chengchi University, Taipei, Taiwan. I am also a Certified Hypnotherapist and Board Certified Hypnosit. Whew! If you want to know more about this rather engaging and interesting person, just click here! And, if you don't want to know anything about this Meiguo Langren Zai Taibei (An American Werewolf in Taipei), don't click here.
I founded the Interactive Dramas Archive webpage in its original incarnation in 1996 as a labor of love. As an educator I have found Interactive Drama activities to be one of the most successful language learning and practice techniques I've ever used in a classroom and have presented numerous academic papers on the subject to various conferences over the past couple of decades and have taught a course on roleplays of this type at the undergraduate level at the university and use interactive dramas in a number of my other courses as learning tools. As a hobbyist, I love the fun of the activities (that's true for both table top Role Playing Games and the Freeform Live Action type). In fact I love the games so much that at one time I was asked to write a regular column about them for a local magazine. The column was published in Chinese for a major gaming magazine in Taiwan. Also, as someone with a heavy "serious" background in drama and literature, I find Interactive Drama to be interesting in terms of how it redefines theatre. I have a B.A. in Speech and Drama from Kansas Wesleyan Univeristy, earned an M.A. in Communication and Theatre from Pittsburg State University, and a Ph.D. in English/Comparative Literature at National Taiwan University where I completed my doctoral dissertation in 1998 specifically on interactive drama: titled Interactive Drama: Critical Perspectives on Freeform Role Plays as Drama (a critical approach to the theatre-style freeform live action roleplaying game as theatrical game form). I founded the Journal of Interactive Drama as part of the major site here in 2005, providing a home to peer-reviewed discourse on live roleplaying within a multi-disciplinary context. Finally, and most importantly, another very major reason for me to put all the work I put into this beastie is . . . simply . . . I love interactive dramas . . . period . . . I just find this sort of thing to be inherently interesting in and of itself.
I'm very interested in this site being the most extensive online repository for interactive drama scenarios. With that in mind I've put up some of my own scenarios as well as those contributed by others.
As I am very interested in the use of roleplay and games in an educational context, particularly the use of interactive dramas as an approach to scenario-based learning, I have also created a special section to house scenarios written by my students - as part of our language learning and practice activities. These pages are showcase pages for student work. Some of the scenarios are HTMLized others are still in text format - eventually they'll all be Webized. Please remember while reading these, they have been written by English as a FOREIGN Language students in Taiwan. Most files have only undergone a small amount of editing so may need major tinkering before play. If you would like to put any of these through a major edit, feel free to email me at email@example.com and I'll most assuredly get back to you as quickly as possible.
These student-written Interactive Drama Freeforms, of a variety of types including fantasy piecies and Murder Mystery Minigame Varieties, were written as part of class assignments in my English Conversation One
(Freshman) and English Composition Two (Junior) English as a Foreign Language classes at National Chengchi University in Taipei, Taiwan. The scenarios here have undergone a bit of cleaning up and editing by me before being posted here but are essentially intact. The scenarios were originally written by students for their classmates to play but may be played by those reading these pages. Feel free to use these as you like as long as the original author and copyright notices are left in place and no fee is charged or monies exchanged when you run the game. All rights are held by the authors.
Each student in my participating classes was asked to use the Freeform Evaluation Form and review three Freeforms (students evaluated their own Freeform and two by their classmates). The authors supplied copies to the members of the class for purposes of review. The reviews were then given to the authors as soon as was possible - but no later than a preset due date. Students then used the feedback to change and modify their games - they also had feedback from their playtesters. It works out very well in terms of allowing students a chance to practice their English conversation skills and it's a lot of fun!
If you are an academic or interactive dramatist interested in formal critique and exploration of scenario-based theatre style interactive drama freeform roleplaying games, you may also wish to explore the Journal of Interactive Drama. If you have graduate-level degree qualifications, feel free to contact me about serving on the editorial board. Otherwise, you may wish to contribute a critical paper or a scenario.
I am also the founding editor of the Journal of Experiential Trance where I have published papers on the use of experiential hypnosis with interactive drama.
This Interactive Dramas archive is open to submissions from anyone as long as the material is original and fits the charter of the archive.
When submitting scenarios to this site, please provide materials in at least one format that directors may edit. Often casting considerations require some slight editing of a piece for gender or player number so it is helpful if the files are in text, rtf, or Word formats that allow editing. Original authors should always receive credit for performance literature.
Brian David Phillips, PhD, CH


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Spurs' depth too much for Thunder's superstars
After five consecutive blowouts in the Western Conference Finals, it kind of felt as though we were due for a Spurs-Thunder game to go down to the wire. On Saturday night, San Antonio and Oklahoma City finally came through, with the Spurs escaping OKC with a 112-107, overtime win to advance to the NBA Finals.
The series' first true officiating controversy nearly became a chief talking point between Game 6 and what would have been Game 7 on Monday, after a missed goaltending call on Serge Ibaka with 44 seconds left in regulation gave the Thunder just enough breathing room to force the extra period. But the Spurs locked down on D in the OT, holding OKC to just 1-of-11 shooting, and put themselves in the Finals in consecutive years for the first time in franchise history.
San Antonio will no doubt have to be better in the Finals than it was at times against Oklahoma City if the Spurs want to avoid a repeat of last year's heartbreaker against the Miami Heat. And the health of Tony Parker, who missed the second half of Saturday's game with an injury, could become a huge obstacle if Parker's injury turns out to be serious (though there is no indication yet that it is).
But this is the Finals matchup many expected and hoped to see from the beginning, and there's no questioning that it will, once again, be the league's two most deserving teams battling it out for league supremacy.
Spurs win 4-2
Takeaway: Given how quickly Gregg Popovich has gone to the hook with his starters in each of the Spurs' other two losses in this series, there was a thought that even the slightest slip-up by San Antonio without Parker in the second half could lead to an early white flag by the Spurs. Instead, San Antonio rallied despite the absence of its achy star and took control of the game with a commanding, 37-20 third quarter that ended with a 9-0 Spurs run over the final 1:20.
The 4-point play Danny Green executed with one second left in the third quarter could very well have been the turning point for the whole second half, but Oklahoma City responded admirably with a strong fourth quarter paced by 24 combined points from Kevin Durant and Russell Westbrook. But Westbrook, once again, tried to do too much in the overtime period, and his 1-of-7 clip in OT may have been what did his team in.
In fairness, Durant also missed all three of his shot attempts in overtime, including two 3-pointers, but he also took just one shot between the 4:11 mark and the 16-second mark in the period, and that's unacceptable for the league MVP in a playoff elimination game. Had Durant played a more active role in OT, it by no means would have been a guarantee that OKC would be playing Game 7 on Monday.
When Durant is taking a backseat to Westbrook at the most critical juncture of the game, Oklahoma City simply isn't putting itself in the best position to win.
But against the Spurs, a team like the Thunder can't afford to be even a hair shy of its best, and when Durant is taking a backseat to Westbrook at the most critical juncture of the game, Oklahoma City simply isn't putting itself in the best position to win.
Star review: Despite his cold snap in the OT, Westbrook did finish Game 6 with a game-high 34 points, with most of his damage coming at the free-throw line, where he hit 17 of 18 attempts. In addition, Westbrook added seven rebounds, eight assists and six steals. But his seven turnovers and his inefficiency when he couldn't get to the line (8-of-23 shooting) both left him culpable in the loss. Like Westbrook, Durant also had trouble keeping the ball in the hands of the guys on the home team, with seven turnovers himself, but KD was much more discerning with his shot selection, and he ran the offense far more deftly than his co-star.
Beyond their stars, the Thunder also didn't get much in the way of assistance from its bench, with Derek Fisher's five points representing all of the bench points while Serge Ibaka (16 points, four rebounds, four blocks) and Reggie Jackson (21 points) accounted for the rest of the OKC scoring. And that, all series, has been one of the main differences between the Thunder and the Spurs, who got 51 points from their reserves in Game 6. That number was largely supported by another great game from Boris Diaw (26 points, 8-of-14 shooting), who made three 3s, and Manu Ginobili (15 points), who was timely despite a poor shooting night overall, knocking down a 3 to give San Antonio a one-point lead with 27 seconds left in regulation.
As for San Antonio's starters, Parker made good use of the 18:52 he did play, adding eight points while hobbling around on an injured left ankle, and Tim Duncan (19 points, 15 rebounds) and Kawhi Leonard (17 points, 11 rebounds) each executed well in the win.
Looking ahead: NBA Finals, Game 1 vs. Miami Heat at San Antonio, Thursday, 9 p.m. ET
What to look for: There's little argument that the Spurs and Heat have been the two most championship-worthy teams throughout the playoffs thus far, but in the end, this rematch of last year's Finals may be decided by the health of Parker's ankle. After Game 6, Popovich played his hand close to the vest – where else? – when asked about Parker, and gave a coy answer about not dealing in hypotheticals when asked if Parker would have played in the second half had it been a Game 7 or a Finals game. But Popovich also intimated that Parker wanted to play in the second half and it was he who decided that it wasn't happening, so with that in mind, you've got to imagine Parker will be just fine for Game 1.
Assuming that's the case, we could be in for another dazzling series, and if it even comes close to living up to the hype of last year's Finals, it'll surely be more interesting than either of these conference finals turned out to be. San Antonio has been the more consistent of the teams for most of the season, and the Spurs have shown an ability to handle superstars, even if that doesn't mean shutting them down. But Miami is well-rested, has championship pedigree and has the most dominant player on Earth, and that alone will make the series worth watching. Miami has gone largely untested in these playoffs, and that should end in these Finals, and when all is said and done, the question of who will win may come down to one not-so-simple answer: Would you rather have the better players or the better team?


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Monday to Friday 8am to 8pm
If you fancy yourself behind the wheel of a brand-new Jaguar XF Saloon this spring, check out our latest stock savings on the Jaguar XF Saloon 2.2d (163) Luxury Auto with reductions of up to £72 a month.
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Brother TN115Y High Yield Yellow Toner CartridgeItem#:� YYD2-TN115YCN �|�Model#:�TN115Y
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RBNo2.1 Font Family
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text:
There are two things most commuters don't realize about Penn: First, there used to be a gorgeous Beaux Arts station that was demolished in the mid-60's. Second: Parts of that old station can still be found today. They've just been buried under the arena that landed on top of them.
On our tour of the Remnants of Penn Station, we'll take you back inside this central transportation hub to discuss the past, present and future plans for the structure. Although Amtrak only acknowledges one remnant remaining, tour participants will learn about station history and discover remnants of the McKim, Mead & White building located in plain sight.
Tours will continue to be supported by photographic presentations of the station by renown photographers Norman McGrath, Peter Moore, and Aaron Rose, along with the work of railroad aficionados Alexander Hatos, an employee of Pennsylvania Railroad and Ron Ziel, a railroad historian.
Tour of the Remnants of Penn Station
- Get a comprehensive history of the past, present and future of Penn Station
- See the various indoor and outdoor old-station remnants hidden in plain sight
- Understand why so much of the current station is actually a remnant of the long forgotten original Beaux-Arts marvel
- Learn insider navigation tips for one of the most cramped and complicated transit hubs in North America
- See never-before-seen old station photos from the collections of three photographers who photo documented Penn's life and demolition
- See overlay photographs of the past Penn Station past with the current one with an augmented reality tool
- Each guest will also receive a framable, reproduction ticket of the first commuter ride into Pennsylvania Station from 1910
Price: $35
What to know: The tour is 1.5 hours long; please consult with the MTA for weekend subway schedules and routing changes.
What to bring: Comfortable walking shoes
ABOUT YOUR TOUR GUIDE: Justin started his career as a New York city middle school English/Language Arts teacher on the Lower East Side dragging his students to historic sites across the city in an effort to bring NYC's lesser known stories to life. That's how he became co-creator of The Wonder City, a graphic novel that re-imagines New York City's entire history currently running as a serial on Untapped Cities. He was also the playwright and producer of The Eternal Space, an off-Broadway play that centered on the demolition of New York City's Pennsylvania Station. It was with this production and one simple tweet that he fell head over heels for Untapped Cities whom he partnered with for his Remnants of Penn Station Tour. Now Justin is a licensed New York City tour guide and continues to develop and lead tours exclusively for Untapped Cities. When he isn't deep in the bowels of NYC he is busy as Founding Director of the Character Connection Initiative, a non-profit organization that connects character education and mindfulness to middle school curricula.
Tour of the Remnants of Penn Station


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Kid's After School Program
After School Program
Monday to Friday
3:00pm to 6:00pm
Ages 3 & Up
$195/Bi Weekly Per Child
The Kids After School Program picks up the kids from school in the Oshawa / Courtice / Bowmanville / Newcastle schools then kids are brought to the Kalsamrit Gym for activities, martial arts and help with homework.
* FREE pick up or drop off from schools in the designated areas
* Home work time
* Marital Arts Uniform (which should be worn daily)
* One hour of Muay Thai/Training daily
Kalsamrit Gym started a martial arts after school program September 2014. Many parents work days do not end at 3:00 when your child is done school, so this is a great program where your children can be safe and have fun. We offer this program for all school kids!
This is not a day care, but a martial arts learning program where your kids can do homework, team build, learn martial arts and build confidence.
Email us to register for September
As space is limited!


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Keeper Stick On Wallet for iPhone 5
• $34.99
• Quirky
With Father's Day just around the corner, tie and wallet manufacturers must be rubbing their hands in anticipation for the impending spike in sales. But if the dad in your life is looking to subtract, rather than add, to the contents of his pockets, consider this leather and plastic 3 card slot wallet designed for the iPhone 5. The easy-to-access flip and clip-close wallet adheres to the back of the iPhone and keeps ID and cards easily accessible. The Keeper can help declutter and simplify his life...a priceless gift, I say!


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text: Chris Young was on Jimmy Kimmel last night...and you would think that being the night girl I could stay up to watch it. Nope, turned the TV to channel 13 and the next thing I knew I had slept through it and woke up to find infomercials on instead of Chris. That's what we have internet for though, right?!


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Sign up to be notified the next time we send names to space!
NASA's OSIRIS-REx mission and The Planetary Society invited you to submit your name for a round-trip ride to asteroid Bennu. Your name will hitch a ride to the asteroid, spend 500 days there, and return in the Sample Return Capsule to Earth in 2023.
Plus your name will be on the spacecraft, which will remain in space long after returning the sample return capsule to Earth.
Like the mission on Facebook for mission updates, plus notifications on just where your name is from launch in 2016 to return to Earth in 2023. Engage the mission on Twitter for late-breaking news.
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Become a member of The Planetary Society and together we will create the future of space exploration.
LightSail 2 will launch aboard the SpaceX Falcon Heavy. Be part of this epic point in space exploration history!


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Ft Bragg (MEN) Yellow-bellied Sapsucker and others continue
Expand Messages
- Hello all. Today my parents and I drove over to the coast, to look for some of the recently reported birds. At Lake Cleone, the adult male WHITE-WINGED SCOTER continues, though we could not find the Common Moorhen. Off Laguna Point were two Red-necked Grebes. Although there was a sizable flock of Surfbirds and Black Turnstones at the Point, the Rock Sandpiper was not amongst them; we didn't find it until about 3:00 (two hours after high tide) on the rocks just north of Virgin Creek Beach. Also at Virgin Creek were two Sanderlings.
At Rose Memorial Park, at the end of Spruce Street in Fort Bragg we easily refound the adult male YELLOW-BELLIED SAPSUCKER in one of the weird, yellow flowered Bottlebrush-like trees. It seemed like most of the trees had Sapsucker wells in them, but we first saw the bird in one of the two shorter trees at the north end of the cemetery that flank a large headstone that reads 'Jordan'. He also frequented several of the pines. He was quite flighty, and I only managed to get some distant record shots, but I think I surprised him when I first found him. Also of note at the cemetery were an Orange-crowned Warbler and an SY male Bullock's Oriole, probably the same one found by Jerry White a few weeks ago. Good birding,
Matt Brady
Potter Valley
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While mental health care has improved by leaps and bounds over the years, it isn't cut and dry with set timelines or a slew of established best practices.
From the very first scene, 'Thor: Ragnarok' emits a strong message about vocation — that is, the roles in which one serves his or her neighbor.
Handwritten words from my loved ones can hit me with the same emotion of past memories as can scents, songs, and pictures.
Marriage is a blessed gift of companionship, love, support, and comfort. It is the base we build our families upon, and thus needs to be kept strong and healthy.
Many mothers struggle with postpartum depression in silence—fearful of judgment, or grappling with shame and doubt. We need to change that.
For the most part, I appreciate the flexibility the American approach to maternity leave affords us parents. To optimize it, you need to plan.
The good news is we professional moms don't have to shuck out a large chunk of our pay just to meet dress code for 40 weeks.
There are indeed many reasons pregnancy is a trial. Yet even amid all of these are certain benefits to this time we spend nurturing and growing our baby.
This holiday takes fatherhood in its entirety, as a grand, amazing vocation and reminds us it is one of honor and might, not just in how it plays in our own personal lives.
Like most holidays, Mother's Day can come loaded with high expectations for us moms. Protect yourself from the inevitable disappointment, because no day is ever perfect.
My generation supports speech policing. In a liberal household, I was taught the opposite.
Politics got you going bananas? Try some of these tips to avoid the election madness.
Thought you'd heard all the rude comments about pregnancy?
For the parents, obviously. And not only after a long day or during a playdate.
Or, in defense of selfies.
Miscarriage is one of the things in life that show we simply aren't meant to know, control, and understand everything that happens.
Some doctors and midwives still recommend wine for pregnant women, while giving craft beer the cold shoulder.
If you have beer sitting in the back of the fridge you can't bring yourself to drink or dump, have I got some ideas for you.
To succeed—or even survive—our children must learn a new set of rules that exist outside the walls of our homes and are based on irrational fears.
The debates and discussions—even the outright screaming matches— of the mommy wars are an opportunity to learn, adjust, and grow.
- 5 Reforms To Gun Laws That Would Actually Make A DifferenceUnlike proposals from the Left that would not have prevcontinue reading >
- 'Glamour 2017 Women of the Year' Awards Completely Ignore Conservative WomenIn all, Glamour honored 10 women at a splashy Brooklyn continue reading >
- Are Red States Tax Takers And Blue States Tax Makers?Against a national average of $1,935 in intergovernmentcontinue reading >


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We meet seniors' needs—for short-term care or around-the-clock home care in the North Seattle, South Seattle and Eastside areas
Our compassionate, professional caregivers enable seniors to live more comfortably and independently in the familiar surroundings of their own home. We also frequently work with clients in senior apartments, assisted living facilities, dementia care units, nursing homes, hospital, hotels and other settings. We're here when you need us—206-686-7440 or 877-281-7111.
We can help with almost any everyday task in home care, including the following:
Personal care
- Bathing, dressing, toileting
- Transfers and wheelchair use
- Medication reminders
- Mobility help and fall prevention
Chores around the house
- Light housekeeping and laundry
- Meal preparation
- Pet care
Activity support
- Medical appointment trips
- Errands and shopping
- Trips to social events
- Physical therapy exercise assistance
Condition-specific care
- Hospice care support
- Home health care support
- Support for those with Alzheimer's, COPD, surgery recovery and most conditions
Nurse delegated care
Specially trained caregivers work under RN guidance to perform:
- Medication administration
- Tube feeding
- Simple wound care
- Blood glucose monitoring


text: Hey everyone, Just wanted to say hi - I never usually worry with introductions but I used this forum a lot when I was deciding which Android device to go for and I am very pleased to be joining the Android community! I had used Windows Mobile for 6 years, when it was the most exciting OS for phones available. But of course that has all changed. I really dislike the iPhone (I won't go into reasons why, I'm sure everyone here has their own ) and finally decided on the Desire. It has changed my life. I am a very, very happy Android user and look forward to getting to know it even better through the forums. Hail Android!


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The Tampa Bay Rays are down 1-0 in their American League Division Series to the Texas Rangers, so obviously that's the organization's primary concern right now. But whether its season ends with an LDS loss or a champagne bath after the World Series, its truly biggest issue is the future of Carl Crawford. Will the Rays bring him back? Can they bring him back?
Rays owner Stuart Sternberg announced going into the season that the payroll would be significantly lower for the 2011 season, hinting that it would drop even below $60 million.
There's a bit of good news. Pat Burrell is already gone (to a fellow playoff team, the San Francisco Giants) and made up $9 million of that Opening Day payroll. Rafael Soriano earned $7.25 million, and nobody really expected to him to be anything more than a one-year pickup in Tampa Bay. Carlos Pena isn't gone yet, but if the Rays bring him back, it'll certainly be at less than his $10 million 2010 salary; he had as good a season as a .196 hitter can have, but a .732 OPS isn't something you pay for at first base.
Once you factor in some raises to players with a few years of service time and the loss of at least $20 million in salary, you might be able to envision a scenario in which the Rays could afford to keep Crawford on a long-term deal.
It might not be that easy, though.


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What I was going to go over tonight was percentages.
There's almost an "optical illusion" in the way percentages transfer to decimals. It's easy enough to see that 0.75 is 75%, and that 23% would be 0.23 as a decimal. (I like to use the "leading zero" in my decimals, your student should check with her teacher, (or employer!) to make sure she keeps up with accepted standards and practices.)
The use of zero is where it starts to get tricky. For example, 20% could be stated as just 0.2 and be correct, without showing its heritage as 0.20. However, this sometimes leads one to think that 7% can be 0.7 instead of 7/100 which is 0.07.
We have to imagine a "leading zero" on single digit percents, as if we were changing something like "07%" to 0.07 decimal. Ask your student about "ghost numbers" we have talked about. This could be added to that list as another example.
Another optical illusion is in our checkbooks these days. Okay, add your own punchline to that, but you and I had been used to getting 3% interest on savings, which would be decimal 0.03 in accordance with what we just said above. However, Annual Percentage Rates (APR) we're getting now are 0.03% which at first blush LOOKS like it should be the same as what we are used to (prior to 2008) but it's really much smaller, and works out as a 'decimated' decimal, that looks like this: 0.0003 so the 'earned' interest that used to buy Mothers' Day Dinner out for four won't even pay a fourth of the tip now.
Another thing about percentages, since you can't calculate with them, it doesn't matter how mixed up they get. 3.75% is the same as 3 3/4 %, it just depends on which way the bank thinks will attract more mortgage re-finance customers. Maybe that seven looks a lot bigger than a three or a four, in print. I have a fraction to decimal practice sheet to familiarize your student with some more examples like that.
Gotta leave something for another blog.


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Offering a most healthy and nutritional range of Food Products under various categories.
About Us
Good Health International is a reliable food supplying firm. We are distinguished exporter and supplier of the market, serving to the demand of numerous food industries with finest range of Vegetable, Amla, Honey, Natural Honey, Bee Natural Honey and Pure Honey. Our products are used in various foods to add flavor and aroma. It is processed by the authorized manufacturers who utilize high grade of ingredients, fertilizers and manures. The range is known for its alluring taste, rich flavor, freshness, purity and high nutritional value.
We preserve our sourced products in spacious warehouse. The storeroom is kept ventilated and cleaned to make sure that stored products are completely free from rodents and moisture. Further, we pack the finished gamut in quality approved packaging material such as plastic sheet, bottles and carton sheet. The proper packing of the gamut helps in its safe transportation to various place.
The vendors of our range are being selected by the competent team of procurement agents. The selection is done by analyzing their marketing credibility on various parameters. In addition to this, we have team of marketing agents who answer to all queries of the customers on time and with reliable solutions. Such effort of our company has taken us to great height of success.
1/844, Iyyappan Nagar, Tiruppalai Post, Near By Petrol Bulk, Madurai - 625014, Tamil Nadu, India
Mr. C. Kasi (Proprietor)
Mobile :+918870511632, +917373473874


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Here are two videos by DisneyHD of the soft-opening of the new version of SSE.
Bear in mind, the attraction is still being tweaked. I'll reserve my own IMHO until I can see it up close and personal, but from what I can see in the video, it does look intriguing.
Part 2:


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Of course, we know that Army officials were forced to reconsider their long-standing policy on 'NO special headgear' by their boss, the Muslim-in-Chief Barack Hussein Obama, who has close ties to CAIR's parent organization, The Muslim Brotherhood.
ORIGINAL STORY HERE: tennessee-junior-rotc-headbag-rule-keeps-muslim-girl-out-of-parade-terrorist-front-group-cair-demands-rule-be-changed
The email address of the Department of Defense is listed below. Please voice your opposition to their bowing to the religious demands of a terrorist front group.
CAIR Welcomes Army Review of JROTC Hijab Policy
CAIR (WASHINGTON, D.C., 11/9/11) — A prominent national Muslim civil rights and advocacy organization today welcomed a U.S. Army decision to review a policy of the Junior Reserve Officers' Training Corps (JROTC) that effectively bars participation by Muslim students who wear an Islamic head scarf, or hijab.
Last month, the Washington-based Council on American-Islamic Relations (CAIR) wrote to Defense Secretary Leon Panetta after a 14-year-old Muslim student at Ravenwood High School in Brentwood, Tenn., was forced to transfer out of a JROTC class when her commanding officers told her she could not wear hijab while marching in the September homecoming parade.
SEE: JROTC's Headscarf Rule Keeps Girl from Parade, Spurs Bias Claim (Tennessean)
VIDEO: Tenn. Muslim Student Not Allowed to Wear Hijab in JROTC (CAIR)
After being contacted by the student's family, CAIR contacted both the school district and the U.S. Department of Defense (DOD) to seek constitutionally-protected religious accommodations for the girl and for future Muslim JROTC participants.
SEE: CAIR Letter to School District
SEE: CAIR Letter to DOD
In a letter sent to CAIR, Deputy Assistant Secretary of the Army Larry Stubblefield wrote:
"I have been asked to provide an interim reply on behalf of the Secretary of Defense to your October 13, 2011 letter concerning Miss Demin Zawity's request to wear a religious head covering (hijab) while participating in an Army Junior Reserve Officer Training Corps (JROTC) event at Ravenwood High School.
"Based on your concerns, the Army is reviewing its policies related to religious accommodation as they apply to JROTC, and we will provide you the results of that review upon completion. Please be assured, that it is not the intent of the JROTC policy to discriminate against any individual or religion."
"We welcome the Army's decision to review its policy that effectively bars Muslim students who are seeking to become better citizens and to acquire leadership skills from participating in JROTC," said CAIR National Communications Director Ibrahim Hooper.
Hooper said CAIR offers a booklet, called "An Educator's Guide to Islamic Religious Practices," designed to help school officials provide a positive learning environment for Muslim students.


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The Scottsdale Arts Festival is coming back to the Phoenix area this month, starting on Friday, March 10, 2017.
There will be several exciting things for guests to see, taste and do during the three-day event, including artworks shown by 175 jury-selected artists, top-notch musical acts, several tasty food vendors and kid-friendly activities for the whole family!
"Foodies will enjoy a moveable feast with more than a dozen of the Valley's gourmet food trucks and eateries serving up savory dishes from around the world, from classic American comfort food to Asian, Latin American and Mediterranean delights," boasts the event's website.
Musical acts include Nikki Hill, Moonlight Magic, Marmalade Skies, Ruca, Carmela y Mas and the Sugar Thieves Duo. Theses musical acts, primarily of the blues and jazz genre, should be big hits with the music and art lovers who attend the festival.
Visit the Scottsdale Arts Festival's website here to find out more about the event and to buy your tickets!
Scottsdale Arts Festival
Scottsdale Center for the Performing Arts
7380 E. Second St.
Scottsdale, AZ
March 10-12, 2017
Fri & Sat: 10 a.m.-6 p.m.
Sun: 10 a.m.-5 p.m.
Single Day Pass: $10
Two Day Pass: $15
Under 12: Free


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Stock Graphic >> Pattern - Vintage Coast Beach Background Paper 68107 by Le Paper Cafe @ CreativeMarket
File Size: 436.08 MB; DPI: 300 DPI; Dimensions: 12 x 12 in.
A vintage inspired set of coastal weathered background papers in a variety of 4 colors, Driftwood Gray, Sand, Lobster & Aqua.
You will receive a total of 20 high resolution background papers.
3600 px x 3600 px (12"x12")
300 dpi
PNG format.
Keywords: beach, vintage, coast, ocean, sand, sea, surf, surfboard, seahorse, background papers, vintage coast, ship wheel, paddles, wood, beach wood, lobster, compass, nautical, le paper cafe, photography.


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How far is Great Ponton from Grantham?
Asked on Jan 31 2010, Transport in Grantham | Report content
Answers (2)
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Depending on transport, 3 or 4 miles.Answered on Feb 7 2010, Report content
Check on a route planner website. We always find the AA Route Planner website a useful tool in these instances.Answered on Feb 1 2012, Report content
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Mary Immaculate College is committed to improving access to higher education for adults and we welcome applications to all our undergraduate programmes from mature applicants. If you are at least 23 years old on the 1st January of the year of entry to College, you are considered as a mature student.
Late applications from Mature Students are currently being accepted to the following programmes: MI001 / MI002 / MI007 / MI009 / MI010 / MI011 & MI012.
Closing date for applications to CAO is 1 May 2017