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Five factors that decided the UConn vs. Kentucky national title game
USA TODAY Sports breaks down Monday night's NCAA championship game.
BRACKET HUB:Final Four central
1. Connecticut's harassing backcourt. It was one of the biggest questions heading into the national championship game: Could Kentucky's young guard pairing – the brothers Aaron and Andrew Harrison – handle the Huskies' Shabazz Napier and Ryan Boatright? Through the game's first seven minutes, the Huskies had their way from end to end, stifling the Wildcats' offensive rhythm at the source and dictating a quick-tempo flow from defense to offense. Napier forced Aaron Harrison into a pair of turnovers in the first five minutes, in fact, giving the game's opening stages a decidedly UConn feel. The best moment came via Boatright, who dipped and curved his way past Kentucky guard Dominique Hawkins for a layup at the 13:08 mark, giving the Huskies a 17-8 lead and forcing a timeout.
GAMER:UConn wins fourth national title
2. Julius Randle's quiet start – and strong finish. The Wildcats' biggest weapon – a mauler and a bruiser, an All-American – was missing in action. Blame cramps: Randle shuffled in and out of the lineup during the game's first 30 minutes, playing and sitting in two-minute increments, negating his typically plus-size impact. What is Kentucky without Randle? Think about it: With Randle quiet, the Wildcats needed to run the offense primarily through the backcourt – which had to deal with Napier and Boatright. But he came alive late, scoring four points in the half's final minute and bringing the Wildcats to within four at the break: UConn 35, Kentucky 31.
3. Offenses lose steam. One half was not like the other. If the first half was smooth – with one team making a run, then the other – the second half was anything but, with both teams struggling to convert amid missed shots, botched passes and wasted possessions. But after the Wildcats drew within a field goal, UConn's defense again carried its up-and-down offensive attack. A Niels Giffey three made it 44-39; Ryan Boatright then picked Aaron Harrison's pocket on the next possession and was fouled on a layup, nailing both attempts to make 46-39. Kentucky's next trip down the court ended with Randle throwing a pass into the first row. Napier then made a fallback jumper from the left side to make it 48-39 with 11 minutes left. In a half where points were at a premium, this run stood out.
RYAN BOATRIGHT:Steps out of Shabazz Napier's shadow
4. James Young's dunk. Kentucky's ability to weather any storm, seen clearly during this run through the tournament, belies the five-freshman nature of its starting lineup. In familiar fashion, Kentucky broke back into the mix on pure athleticism: James Young stadium-shaking dunk at the 10:40 mark ended UConn's run and brought the Wildcats storming back into the mix. UK would go on an 8-0 stretch beginning with Young's slam, turning a nine-point UConn advantage into a 48-47 game with 8:13 left. Time and time again, Young would carry Kentucky's offense – and lift its spirits – while Randle struggled to find any rhythm.
HARRISON TWINS:Run out of magic
5. Napier's three propels UConn to the title. This will be a tournament remembered for its parity, underdogs and white-knuckled nail-biters, beginning with the tournament's first full day – four overtime games, a single-day record – and extending through the Final Four. It was one defined by the steady and secure play of Napier, who carried UConn to the finals and then, with Kentucky charging fast, kept the Wildcats at bay and secured the Huskies' fourth national championship. It began with a three: Napier from deep, giving the Huskies at 51-47 lead. Then Giffey nailed a bomb to make it 54-49. Boatright leaned back to make a jumper to lift the lead to 56-50. The capper was his late-in-the-possession dish to teammate Lasan Kromah with 25.1 seconds left; Kromah was fouled on a layup attempt and made both free throws to provide the final margin of victory: UConn 60, Kentucky 54.


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November 8, 2019 @ 10:00 am – 11:00 am America/Los Angeles Timezone
Tushita Kadampa Buddhist Center
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This practice is the heart essence of Kadampa Buddhism. In the first part of the practice, we visualize our Spiritual Guide as Je Tsongkhapa and make prayers and requests to purify negativity, accumulate merit, and receive blessings. This prepares our mind for our meditation on Stages of the Path to Enlightenment. After the meditation, we make prayers to our Dharma Protector, Dorje Shugdän. Through this, we can overcome obstacles to our practice and create favorable conditions so that we can nurture and increase our pure Dharma realizations.

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Palm Project Interview Series: Douglas Nixon
February 8, 2007
About the Palm Project Interviews
TAG has conducted a series of interviews with leading scientists about the underlying pathogenesis of AIDS to gain insights into emerging lines of research and observations about the current research funding environment.
Douglas Nixon, M.D., Ph.D. is a renowned cellular immunologist who has been working in the HIV/AIDS field since the late 1980s. Nixon's first published HIV research paper, which came out in Nature in 1988, involved identifying CD8 T cell responses against the virus. At that time, Nixon was working with Andrew McMichael's immunology group at Oxford in the UK but he subsequently moved to the US, first working at the Aaron Diamond AIDS Research Center before establishing his laboratory at the Gladstone Institute, University of California at San Francisco (UCSF).
Q: What are your research interests at the moment?
We've been working with Dr. Esper G. Kallas in a collaborative manner for the past three years; he's one of the new HIV Vaccine Trials Network sites down in Sao Paolo. That has given us a wonderful opportunity to have an international context on some of the research that we do. The reason we are working with him, apart from the fact that he is an amazing, great scientist and a great guy, is that it gives us the opportunity to study the impact of coinfections on HIV infection in a way that is difficult here.
I'm particularly interested in what happens with MTB coinfection. We have a paper in press in the Journal of Infectious Diseases where we've been studying natural killer T cells. These are not natural killer cells. They're not T cells. But they are a lineage which has lymphoid markers, but a very unique regulatory role. They recognize lipid antigens, presented by the CD1d modules. We found that people with active pulmonary tuberculosis completely lose these cells, they just go. I'm excited about the finding, because there are ways that one could potentially stimulate them. These are early days, but if we find that they are involved in the pathogenesis of the disease, then it gives us another cell type to potentially manipulate in vivo.
We're also looking at coinfection with GBV, we're trying to join that controversy, from a cellular immunological perspective. See whether we can contribute to understanding whether or not the GBV effect (in slowing HIV disease progression) is real. And we're also looking at people who are infected with HTLV-1. That's also reasonably common down in Brazil and the ability to understand how two exogenous retroviruses interact with each other, I think, is unique.
Do NKT cells have the potential to develop into memory cells?
That's actually a very good question. They've been a neglected cell type, partly because they're rare in most people, in peripheral blood. They're common in the liver. And they're about 4% of the human lymphoid population. In the mouse, they're 40%. In humans, NKT cells appear to arrive in the thymus, as you would expect, since they have CD3. And they mature. But there's still debate about their differentiation. They don't appear to have a memory compartment, although we're only now using multicolor flow cytometry to subset these NKT cells into different populations. And it is a good question, because the reason that they're NKT cells is that they have an invariant usage of one of the T cell receptors -- V alpha 24 in humans. And there are V alpha 24 T cells which are not NKT cells. But we don't know whether, for example, if a T cell which has the V alpha 24, which became a memory cell, might, for example, be able to take on characteristics of an NKT cell. So, it's one of those new areas.
But the reason that they're so important is that a small number of NKT cells go a very long way, I like to think, because they are such potent cytokine producers. They produce cytokines probably in minutes; they're much quicker than other cells. And they probably are directing other cells to do things. If you look in mouse models these cells are really important in the NOD mouse diabetic model, for example. And one of the areas I think is really interesting at the moment, and a really dynamic field, is trying to understand regulatory T cell populations, which do not just include the CD25 positive, CD4 positive T cells that we and many, many others are studying, but also these NKT cells. So, there's this sort of family of regulation.
What we're interested in doing is to understand how HIV affects that regulation, or causes dysregulation. Because it's another opportunity to manipulate: if you can manipulate the regulators, you might have a really major effect downstream. Because a lot of us have been working on studying effector T cells, but if you think about it, that's the last stage that they've got to. That's when the differentiation has occurred, the antigen is being recognized, and the cell is either going to do its job or not. But if you can look upstream, and say, well, maybe I can get more of these effector cells going by turning off the regulation…that, from an in vivo manipulation perspective, is something I'm pretty excited about trying.
Any other major areas of interest?
We have a major research interest in work we have not yet published, but we are presenting as one poster and one oral presentation at the Retrovirus conference. This is work in collaboration with the Canadian group of Mario Ostrowski, and, in particular, graduate student Brad Jones in his group, working with Keith Garrison in my group. Brad is giving an oral presentation and Keith is giving a poster presentation. And this is our work on endogenous retroviruses. I think it's the most exciting thing that we're doing at the moment, because it's completely novel and, I think, has some important implications.
What we have found is that HIV does not infect a cell in a retroviral vacuum. We all have endogenous retroviruses as part of our genome; about 8% of our DNA is endogenous retroviruses. Sort of remarkable. These are thought to represent ancestral viral fossils, if you like. The past waves of nasty, infectious diseases. It's like recapitulating, probably, what happened with HIV in a chimp population. I can imagine that if you go back through these primate lineages, that you can see this evidence in the genome for these retroviral sequences which have integrated, and in most cases, lost the ability to have any transcription or translation occurring.
But there are a few members of these families which are probably intact enough that you can get some translation, or transcription and translation, going, in the rather unique developmental circumstances where these endogenous retroviruses have actually been co-opted by the host to do good. And one example is in pregnancy, where the HERV -- human endogenous retrovirus HERV-W sequence, actually -- is lending its envelope to the human body as part of this syncytiotrophoblast that leads to the formation of the placenta. So, humans would not have pregnancy in the way that we know it, unless there was expression of this endogenous retrovirus. But normally, they're not expressed.
I got interested in this when I was back in New York at Aaron Diamond, when I was interested in thinking about endogenous retroviruses in the context of HIV. We did a side project, looking at endogenous retrovirus immunity in people with a past history of seminoma, because these endogenous retroviruses can be expressed in cancer patients with breast cancer, ovarian cancer, or testicular cancer -- germ cell drivers. And so, actually, it was January last year, we finally published our paper looking at T cell responses. So, we could see T cell responses at low levels. But this had got us thinking about, well, what happens with HIV infection? And it's what happens in HIV infection that is absolutely remarkable.
The first thing that we have found is, in cells which are infected with HIV, there is an incredible amount of transcription of endogenous retroviral sequences. So, in an HIV-infected cell, the endogenous retrovirus sequences go wild. And we think that's probably due to a number of mechanisms. The HIV Vif protein has this ability to turn off the natural APOBEC components, which are probably sitting in a cell, turning these endogenous retroviruses off -- that's probably their job. They were there well before HIV came into this. So, we think what is happening is that whatever mechanisms that are keeping endogenous retrovirus sequences untranscribed are released, and you get transcription and translation of endogenous retroviruses.
From a virological perspective, that takes us down one route. But, as immunologists, we were thinking, what would that do? Since we've found translated HERV products that could potentially stimulate an immune response. And in primary HIV-infected people, we see a very strong endogenous retrovirus-specific immune response, and we've gone on to show that that immune response is actually closely related to control of HIV viremia. There's been this controversy about can you tell whether HIV-specific immunity is related to control of viremia. At the moment, we have found that people's viremic level appears to be related to the amount of endogenous retrovirus immunity that they're stimulating. So, that's where we've got to. We're doing tons of experiments in this area.
From a vaccine perspective, we think that this could, potentially, open up a completely new avenue to vaccination. And the rationale is this: if you could stimulate HERV-specific immunity, then those HERV-specific T cells would be able to help in the elimination of HIV by two mechanisms. The first mechanism is that the HERV-specific T cell is only going to recognize an HIV-infected cell, because it's only HIV-infected cells expressing the HERV antigens. The second thing is, we found that there was cross-reactivity between some of the HERV epitopes recognized and some of the HIV epitopes. So, HERV-specific T cells may be able to recognize HIV-presented peptides, in a cross-reactive manner. And so, there are two potential ways of eliminating an HIV-infected cell.
The third thing, which makes me most excited, is that HERVs are invariant. The sequence doesn't change. So, it doesn't matter which HIV has infected the cell -- it bypasses all the potential problems associated with variation in HIV.
Of course, that's our great wishful thinking. We are at an early stage. And we are enthusiastically pursuing research in this, both from a pathogenesis perspective, but also from a vaccine perspective. Clearly, though, a caveat is the many unknowns. And one of the things that people say is, well, might you be stimulating an autoimmune response? And I say, yes, but that's what you want. If you can get an autoimmune response to get rid of your HIV-infected cells, I think that's going to be perfectly acceptable. Because, if you think about autoimmunity, it's really a threshold thing. We've got autoimmune phenomenon going on, and on a daily basis, within us. It's just that it's suppressed in the majority. And then, occasionally, it breaks through. I think that if we can target an endogenous protein that is only expressing HIV-infected cells, then you're going to get rid of the HIV-infected cells, and that would be great. So, that's another thing that we're doing.
Have you conducted research in highly exposed seronegative cohorts?
We have. Another area of interest is, we're looking at NK cells in the exposed seronegatives. There have been a couple of papers, most recently in the Journal of Immunology from a Belgian group, suggesting that there are certain NK cell subpopulations that may be present in exposed seronegatives that are not in control groups. So we are also working with NK cells, and we're very fortunate, in that Lewis Lanier at UCSF, who is one of the world experts on NK cells, likes collaborating with us, and we like collaborating with him. And so we are trying to better understand the role of natural killer cells, and what they may be doing in both helping prevent infection, and also, in the very early stage of infections.
But natural killer cells -- the innate immune response -- people sort of think only in terms of vaccines. So, people think, oh, well, the innate immune response kicks in first, and then you have your adaptive response. But, in the presence of a chronic infectious disease like HIV, it's continuing to replicate in the context of innate immunity. So, it makes a lot of sense to follow up on Mary Carrington's suggestions from the genetics, that there are certain NK cell-related parameters that may be associated with better viral control. And so we're trying to do that here, too.
Do you think that's been overlooked a little?
Well, there was a lot of activity in the 1980s in research on natural killer cells. And then that went quiet. What's happened in the '90s is that people working both in the mouse and in the humans developed new reagents -- new antibodies -- to help better identify different subpopulations of natural killer cells. This is an area that Tony Fauci is pretty good in. He's got a great group working on natural killer cells. They have been helping push this research. But there really aren't all that many people working in this area, compared to the T cell area. And I really do think it's important.
One thing that we found, that we're getting ready for publication, is that the bulk of the interferon gamma that's produced in response to HIV peptides, in our in vitro assays, comes from natural killer cells. And what is happening is that the peptides are presented to T cells, they're stimulated, and they produce cytokines that cause the natural killer cells to release gamma interferon. So, when a cellular immunologist has been thinking that in our PBMC population, all the HIV-specific interferon gamma that we measure is coming from T cells, it's not. Half or more is coming from natural killer cells. So, I think natural killer cells are very important, and also, potentially manipulable in vivo.
I'm not just interested in understanding the mechanisms, which is important and we need to do that. But I'm interested in thinking, well, is this going to be of any use in helping infected people or in the vaccine? So I would like to see more emphasis on natural killer cells.
But one thing that's amusing at the moment is, the people who work on APOBEC, an intrinsic, intracellular defense, are now becoming, if you like, surrogate immunologists. Because they have discovered that the cell itself is defending itself all the time, against, if you like, molecular biological attack. I sort of look upon it like that that, in the sense that, once the cell is infected, then a number of different parts of the cellular machinery are kicked into gear to try and kick those viruses out. So, it's sort of different from the cellular perspective. But they are now talking about the innate immunity of the cell. And when we talk about innate immunity, we're talking about natural killer cells, or natural killer T cells, or regulatory T cells.
I would like to look upon it as a new opportunity for a mix of two different cultures because, normally, virologists and immunologists don't talk all that much to each other. And that's actually one of the problems, I think, in HIV research: we don't have enough virology-immunology crosstalk. But maybe the cellular innate and the intrinsic innate people will be the first to merge. And it will be interesting to see what happens in the next few years on that.
Is that something that has changed over time? Has there been any improvement in immunology-virology collaboration, or is it still an issue?
I would say it's still a bit of an issue. I think, for example, if you just look at the major conferences, the Retrovirus is considered to be a virology/clinical conference, with not so much immunology. And the Keystone conference is considered to be more of an immunology congress, with some virology, and less clinical. So, there really are areas where people don't overlap.
One area I'm real interested in is the intersection of immune responses to drug-resistant mutant virus. But the drug-resistant virology field is a very close knit group who all know each other, and think of things in terms of sequence, and have not really embraced an outside lateral thought about, well, maybe you can pressure the virus in drug-resistant mutant areas with the immune response. And so this is the sort of thing where we do get some good leadership from the NIH, from some of the really good program officers in the Division of AIDS who I'm impressed with. But this is an area where, maybe, they could take more of a proactive role in having the workshops or by saying, well, let's bring the intrinsic and innate immunologists together. Let's bring the drug-resistant virologists and immunologists together. Because I think that's where the next big step is going to come, by mixing these people up. I think there's a role for some continued leadership, and I would like to see the Division of AIDS spearhead that, because they're a neutral territory.
In terms of pathogenesis, do you have particular ideas about where things are with pathogenesis, or where they should be going? There's been a lot of attention on the gut recently, and immune activation, is that part of the territory you cover?
Yes. But, I think when you think about pathogenesis, that all of us are thinking in a global context, so that we have to be looking at activation. We have to be looking at the gut. But you can't study it all. And so, my angle has been to try and understand the impact of coinfections on activation and the gut. And then, also, to look within us, at the viruses within us, these endogenous retroviruses. So, I pay attention to the whole immunopathogenesis picture. But I think it is important to focus in on some areas. And then, one reads, and talks, and collaborates, and communicates with your colleagues, to try and get the bigger picture. But I think the study of the gut is important. And I think there's clear evidence, for a long time, that immune activation is associated with a more rapid decline in CD4 cells. And it's important to understand why, and to understand whether there can be selective suppression of some of that activation. Immune activation is a broad hat, and you don't want to turn some things off.
I think this is where the future of therapeutic immunology is going, in terms of being much more targeted about turning things on and off. And one of the advantages of UCSF is that we have people like Jeff Bluestone around, who, with the immune tolerance network, is helping deliver things. Then I also read the cancer immunology field because they've been doing a lot of immunotherapy work. As we get better tools, I think that immunotherapy will become more targeted, and therefore, potentially, more used.
There's still this immunology and clinician divide, in that clinicians understand viral load measurement, and low is better, and I agree with that. But there's a lot more to it than that. And I think, as with pharmaceutical companies going the route of individualization of treatments, based on genomics, that you can imagine, in some utopian world where there was tons of money, to be able to take an HIV-infected person, and look at their genetics and their viruses, and look at their immune system, and then come up with an algorithm to help that person do best. If someone's HLA B*57, they're probably going to have a low viral load, but you still want to be able to work with that patient, to maximize their chances. Someone who's got a rapid progressing HLA allele, you may want to talk to them individually, and start treatment. And that's just, you know, based on HLA, let alone KIR type, other genetics, virus immune response. I'm not sure we'll ever get there, but it's a nice idea.
Is there anybody working on using immunological analyses in this way? HLA typing is quite expensive, isn't it?
Well, it's, it is quite expensive. It's not a simple test. But I haven't really talked with Steve. One of the wonderful things about working here is the presence of Steve and Rick and other clinicians. But I'm not sure what he would say if I said to him, well, let's start treating patients based on their immunity! Well, it's the sort of thing Steve would do, because he's at the forefront of everything clinical. But it would need to be well thought out.
Switching gears to vaccines, do you think the T cell-based vaccines that are now entering efficacy trials might have some effect?
Well, it depends what you mean by "might have some effect". I am optimistic that they will stimulate T cell immunity in humans. And the question is, is it going to be of sufficient magnitude, and are those going to be T cells with the right multi-potent ability to release cytokines and kill. The multi-killers, I call them. I'm not a part of those trials, so I have not seen the data. That's going to be something I'm going to be very interested in. The caveat is that we have been disappointed in some of the translatability from primate models to humans, in that what appears to have been immunogenic in a primate has not necessarily translated into immunogenicity in humans. And I think that there are some clever people working around that. I'm hopeful that the efforts that are going into learning how to better deliver DNA and to modify the adenovirus or other vectors are going to pay off, and we will be able to stimulate a T cell component of the vaccine. But it still is leaving the neutralizing antibody component, which is as important if not more important. And I think that the variation in HIV is going to be its problem. But I think we'll get the T cell vaccine.
Do you think they might have some effect on the post-infection viral load?
I do. I think it's a pretty exciting time -- well, it's been going on for a while -- in terms of understanding correlates of protective immunity. So, Bruce Walker and Steve Deeks's work, I think, is really going to help look at elite controllers in the terms of what are they producing. And that has to be coupled with studies of looking at people who don't control -- you have to look at the spectrum, so you know what's not working, as well as what is.
I'm curious as to whether we need to better understand the subsets of lymphocytes, in terms of what may be potent in viral control. Because we still have Jay Levy's CAF (CD8 antiviral factor) sitting around uncharacterized. We have the realization that natural killer cells can themselves produce very potent antiviral cytokines. When we subset CD8 or CD4 cells, we can show that certain populations produce more cytokines or kill more than others. So, we're working our way towards a better understanding of what cells we actually need to stimulate, and whether these vaccines stimulate all of them, or maybe they're stimulating some subsets but stimulating a suppressive population at the same time.
What I would like to see in the next two to three years is a better understanding of the cells that are actually producing the best antiviral activity. Someone like Otto Yang is ideally poised to understand which cell types in his viral suppression assay. And then, when he's worked out which cell is the one that's suppressing virus the most, to be looking at these vaccine strategies to see whether they've expanded that population. And, as someone who works on the regulatory T cells, I'm well aware that with any vaccine, you could be stimulating cells that regulate these other cells. And so, maybe you have to work out how to specifically just stimulate those cells that are the most potent. I think that's an area that's also worth putting money into at the moment.
So, there are still some basic questions, you think, about what needs to be switched off, as well as what needs to be switched on?
That's right. But I think that should go in parallel, obviously, with the trials.
Recently, there's been a shift to a sort of big science approach on the vaccine front. Do you think that some of these basic questions may get forgotten in that process?
Well, I think the basic questions are really important. I'm not involved in those big vaccine groups. What I would like to see, of course, is additional money, so that we both have the big vaccine groups, plus additional resources for the investigator-initiated basic research. I think we need more money, more funding.
Has the flat funding of NIH had an impact on your work?
Yes, it has. Although, I must say, the people in the Division of AIDS have been extremely supportive and they are working under difficult circumstances. But when grants are at a 10% or an 8% funding, it means that, as an individual, you're spending, really, most of your time writing grants, and worrying about getting grants, and realizing that some of your colleagues are not getting grants and are moving out of the field, and you wonder about your own grants, and hope for the best.
The hardest thing to see is the demoralization for the younger scientists, who are choosing not to go into HIV research, or to do other things, because the funding is so difficult. And that's a bigger political question, in relation to science education in America and prioritization for funding and career structures for scientists. How to encourage people, while maintaining quality?
When I started, the payline was 22%. And I think, for some people, when they started it was 30%. Nowadays, we're at the stage where good grants -- very good grants -- are not getting funded. Before, you felt that the process was such that grants would be improved, so the good study would get funded. Now, good studies are not getting funded. And HIV continues to be a huge problem.
So, I think it's something which people in the lab really notice. And I feel it's difficult to explain to the younger people how it's going to get better. And that's demoralizing for me. Because I think global infectious diseases -- not just HIV but the others -- this is something that we can really contribute to. We can make vaccines. We just have to put the resources into the right area. So, I think we need more funding.
Are there recommendations that you can think of in terms of trying to support the young investigators?
Well, I believe that UCSF and other institutions are beginning to think about trying to use some of their internal resources to create bridge funding, to get people over this particularly difficult period. You can imagine a situation where a young investigator puts in a grant, and it gets a great score, but is not funded. Now, what do you do with that, as an institution? You've got a potential winner -- someone who is going to do it. But because of the unique circumstances in 2007, funding isn't there. But that's a smart person. That's a person who has been judged by the peers to be good, but they didn't get funded. And so, that sort of person, I would say, from a university perspective, is someone worth giving a $50,000, $100,000 bridge. Cover them over to their next grant resubmission, to answer their critics and to give them some encouragement.
Now, of course, that money has to come from somewhere. And so, maybe the university should be specifically going out to donors and saying, look, in this time we need bridge funding. It's sort of a political issue, but I think that bridge funding would be helpful. But if that bridge funding is used in that way, then maybe it's the pilot studies for established investigators which go. Or something else has to give, somewhere. But I would like to see university sponsored bridge funding for investigators who submitted a really good grant which wasn't funded but was close. And I think that's the only practical immediate thing that could happen that would help lift morale, and also buy people time. And if we can get to 15, 16, 18% funding level, then the young investigators will start to get their grants again. Because -- while I think it's true that you give young investigators a break, on review -- if you're going to fund five grants out of 80, and you have ten senior people who are well established, who all have great grants, all of which you could fund, and then, some young investigators who are clearly very promising but don't have the publication record or the track history, what's the study section going to do?
Are there any other frustrations and obstacles, access to reagents or things that sort, which interfere with the kind of research that you want to do?
For my own research, no. We've had a really good relationship with the NIH AIDS Reagent Program. And I would want to give that a big plug. They've been receptive, responsive, helpful, innovative, really good.
Any other issues that you would like to highlight? Anything else that we could be doing, to help facilitate your work and that of young investigators?
Well, the funding is one. I would say, maybe, co-working with the Division of AIDS, to help identify these areas of collaboration that would bring people together, like the intrinsic and innate immunologists, like the drug resistant virologists and immunologists, like bring a group of clinicians together and say, let's have a -- what did they do at the CDC recently, when they had the flu? -- some sort of mock trial. The idea is to not have a war game, but say, bring clinicians and immunologists, and say to them, OK, we want you to use the immune system to direct your clinical decision makings in this game. And then, you have patients who, you know, you have dummy patients. You've got dummy results. And you say, well, what happened? That sort of think tank. A practical think tank, with an end result, I think, would be very helpful for the advocacy groups to work on.
Glossary & Bibliography
Natural Killer T cells (NKTs): An unsual subset of lymphocytes with properties of both T cells and natural killer cells. http://en.wikipedia.org/wiki/Natural_Killer_T_cell
CD1d Receptor: A receptor expressed by NKT cells. http://en.wikipedia.org/wiki/CD1d_receptor
T cell Receptors (TCRs): TCRs are docking bay-type structures on the T cell surface via which the T cell engages and recognizes pathogens (specifically, small slices of pathogen-derived proteins called epitopes). There are many slightly different shaped TCRs that a T cell can have, so scientists group different TCRs into families. V alpha 24 is the name given to a specific T cell receptor that is found both on normal T cells and the less common subset of natural killer cell/T cell hybrids called natural killer T cells (NKTs, see above). NKT cells possess both the CD1d receptor and the V alpha 24 T cell receptor.
GBV: GB virus C, a virus first identified in 1995 that is genetically related to the hepatitis C virus but does not cause disease. Studies have suggested that infection with GBV may slow HIV disease progression.
CD3: A molecule expressed on all T cells, also called a pan-T cell marker.
Regulatory T cells: T cells that suppress rather than enhance immune responses.
CD25: Receptor for the cytokine interleukin-2, expressed by activated T cells and also used as a marker to identify "regulatory" T cells capable of suppressing immune responses.
HERV: human endogenous retrovirus. HERVs are remnants of ancient retroviruses that infected human germ line cells at some point in history and are now permanent parts of the human genome. HERVs cannot replicate or form infectious viruses.
HTLV-1: human T-cell lymphotropic virus type 1, a retrovirus first discovered in Japan in 1977. http://en.wikipedia.org/wiki/Human_T-lymphotropic_virus
APOBEC: A family of human cellular proteins, some of which have strong antiviral effects. The HIV gene vif is thought to have evolved to suppress APOBEC activity, in order to facilitate HIV replication.
HLA: Human leukocyte antigen system, see HLA genes & immunity article for a brief description: http://www.aegis.com/pubs/iavi/2001/IAVI2001-0707.html
KIR: Killer Immunoglobulin Receptors. Expressed by NK cells, these receptors interact with HLA molecules and facilitate killing of potentially pathogen-infected cells by NK cells. Genes for specific KIRs have been associated with slower progression of HIV infection, suggesting an important role for NK cells in the immune response to HIV.
Multicolor Flow Cytometry: A flow cytometer is a machine that allows labeling and analysis of cells (cyto is Greek for cell). More sophisticated flow cytometers can label multiple different markers on cells with different colors, allowing highly specific sorting of different cell populations.
CAF: CD8 antiviral factor. This is a yet-to-be-identified substance with strong anti-HIV effects, produced by CD8 T cells.
Natural Killer (NK) Cells: Lymphocytes that respond non-specifically to pathogens. NK cells are part of the innate immune system. http://www.immunecentral.com/immune-system/iss9.cfm
NIH: National Institutes of Health, www.nih.gov
>NIAID: National Institute of Allergy & Infectious Diseases, www3.niaid.nih.gov
DIADS: Division of AIDS, www3.niaid.nih.gov/about/organization/daids/
NIH AIDS Research & Reference Reagent Program: Provides important materials (such as virus isolates and peptides that allow analysis of immune responses) to researchers working on HIV infection and AIDS. https://www.aidsreagent.org/Index.cfm
Recent Papers
Ballan WM, Vu BA, Long BR, Loo CP, Michaelsson J, Barbour JD, Lanier LL, Wiznia AA, Abadi J, Fennelly GJ, Rosenberg MG, Nixon DF.
Natural Killer Cells in Perinatally HIV-1-Infected Children Exhibit Less Degranulation Compared to HIV-1-Exposed Uninfected Children and Their Expression of KIR2DL3, NKG2C, and NKp46 Correlates with Disease Severity.
J Immunol. 2007 Sep 1;179(5):3362-70.
Karlsson AC, Chapman JM, Heiken BD, Hoh R, Kallas EG, Martin JN, Hecht FM, Deeks SG, Nixon DF.
Antiretroviral drug therapy alters the profile of human immunodeficiency virus type 1-specific T-cell responses and shifts the immunodominant cytotoxic T-lymphocyte response from gag to pol.
J Virol. 2007 Oct;81(20):11543-8. Epub 2007 Aug 1.
Willberg CB, Pillai SK, Sharp ER, Rosenberg MG, Agudelo JD, Barbour JD, Nixon DF.
Rational peptide selection to detect human immunodeficiency virus type 1-specific T-cell responses under resource-limited conditions.
Clin Vaccine Immunol. 2007 Jun;14(6):785-8. Epub 2007 Apr 4.
Snyder-Cappione JE, Nixon DF, Loo CP, Chapman JM, Meiklejohn DA, Melo FF, Costa PR, Sandberg JK, Rodrigues DS, Kallas EG.
Individuals with pulmonary tuberculosis have lower levels of circulating CD1d-restricted NKT cells.
J Infect Dis. 2007 May 1;195(9):1361-4. Epub 2007 Mar 20.
Northfield JW, Loo CP, Barbour JD, Spotts G, Hecht FM, Klenerman P, Nixon DF, Michaelsson J.
Human immunodeficiency virus type 1 (HIV-1)-specific CD8+ T(EMRA) cells in early infection are linked to control of HIV-1 viremia and predict the subsequent viral load set point.
J Virol. 2007 Jun;81(11):5759-65. Epub 2007 Mar 21.
Karlsson AC, Iversen AK, Chapman JM, de Oliviera T, Spotts G, McMichael AJ, Davenport MP, Hecht FM, Nixon DF.
Sequential broadening of CTL responses in early HIV-1 infection is associated with viral escape.
PLoS ONE. 2007 Feb 21;2(2):e225.
Carr WH, Rosen DB, Arase H, Nixon DF, Michaelsson J, Lanier LL.
Cutting Edge: KIR3DS1, a gene implicated in resistance to progression to AIDS, encodes a DAP12-associated receptor expressed on NK cells that triggers NK cell activation.
J Immunol. 2007 Jan 15;178(2):647-51.
Legrand FA, Nixon DF, Loo CP, Ono E, Chapman JM, Miyamoto M, Diaz RS, Santos AM, Succi RC, Abadi J, Rosenberg MG, de Moraes-Pinto MI, Kallas EG.
Strong HIV-1-specific T cell responses in HIV-1-exposed uninfected infants and neonates revealed after regulatory T cell removal.
PLoS ONE. 2006 Dec 20;1:e102.
Michaelsson J, Mold JE, McCune JM, Nixon DF.
Regulation of T cell responses in the developing human fetus.
J Immunol. 2006 May 15;176(10):5741-8.
Rakoff-Nahoum S, J Kuebler P, Heymann JJ, E Sheehy M, M Ortiz G, S Ogg G, Barbour JD, Lenz J, Steinfeld AD, Nixon DF.
Detection of T lymphocytes specific for human endogenous retrovirus K (HERV-K) in patients with seminoma.
AIDS Res Hum Retroviruses. 2006 Jan;22(1):52-6.


text: Wednesday, December 21, 2011 Foundation Awards Kendall Scholarships, Research Grants The Foundation for Physical Therapy recently awarded Florence P. Kendall Doctoral Scholarships for the 2011-2012 academic year to Ryan Marker, PT, DPT, University of Colorado, Denver; Jennifer Reneker, PT, MSPT, Kent State University; and Bahar Shahidi, PT, DPT, University of Colorado, Denver. The $5,000 Kendall Doctoral Scholarship is awarded annually to outstanding physical therapists as they begin their first year of graduate studies toward a postprofessional doctoral degree. Two physical therapists each have received $40,000 research grants from the Foundation in support of their projects to evaluate the effectiveness of physical therapy interventions. The Magistro Family Foundation Research Grant has been awarded to Kristin Archer, PT, DPT, PhD, an assistant professor at Vanderbilt University Medical Center, for her 2-year project Cognitive-Behavioral-based Physical Therapy: Improving Surgical Spine Outcomes. Jill Heathcock, PT, MPT, PhD, an assistant professor at Ohio State University, is the recipient of the Pittsburgh-Marquette Challenge Research Grant for her 1-year project Transcranial Magnetic Stimulation (TMS) on Children With Hemiparesis.


text:
Kilkenny's Traditional Irish Breakfast.Served all day long. This plate includes two eggs any style, two bangers (Irish sausages), rashers (Irish bacon), a grilled tomato, mushrooms, Irish baked beans, black pudding and Irish soda bread. $12
The Breakfast Boxty. An omelet of rashers, bangers and Irish cheddar inside a boxty topped with Hollandaise sauce. $12
Ballyhale Biscuits and Gravy.Homemade sausage gravy with fresh warm buttery biscuits. Served with two eggs and hashbrowns. $8
Booley's Breakfast Burrito.Fresh diced jalepeño, tomato and Chorizo sausage with pepperjack cheese in a three egg omelette rolled in a fresh flour tortilla. Served with sour cream and Kilkenny's salsa. $10
Gram's Irish Oats.A bowl of steaming rolled oats with your choice of toast, biscuit and gravy or pancakes. Served with raisins, toasted almonds, brown sugar and milk. $6
Traditional Irish Omelette.. Rashers (Irish Bacon), Bangers (Irish Sausage), and Irish cheddar. $10
Garden Omelette. Fresh Julienne cut zucchini, yellow squash, carrots, Portobello mushrooms, red onion and red bell pepper sautéed and topped with Swiss cheese. $8
Florentine Omelette. Sautéed spinach, mushrooms, onions and bacon topped with a Swiss cheese Mornay sauce. $9
Way South O'Blarney.Smokey Chorizo sausage, jalepeno and fresh tomato with spicy pepperjack cheese. $10
Craique Omelette.Sautéed shrimp, lobster and crab topped with Hollandaise. $14
You Name It Omelette.Start with a three egg omelette and get creative. $6
Meats: Bacon, Sausage, Bangers, Rashers, Lobster, Crabmeat, Chorizo, Shrimp, Ham, Chicken $1
Vegetables:: Spinach, Red Bell Pepper, Onion, Tomato, Mushroom, Avocado , Jalapeño $1
Irish Benny.Irish Rashers and poached eggs on grilled Irish muffin halves topped with Hollandaise sauce. $9
Craigue Benny. Cold water lobster, shrimp and crabmeat with poached eggs on grilled Irish muffin halves topped with Hollandaise sauce. $14
Vinesgrove Benny. Julienne cut sautéed vegetables with poached eggs on grilled Irish muffin halves topped with Hollandaise sauce. $7
Florentine Benny.Sauteed spinach, mushrooms, green onions and bacon with poached eggs on grilled Irish muffin halves topped with Swiss cheese Mornay sauce. $9
Kilmacow Benny. Grilled sirloin and poached eggs on grilled Irish muffin halves, topped with Irish whiskey mushroom sauce. $11
Two Egg Breakfast. Two fresh eggs cooked to order and
served with choice of hash browns or fresh sliced tomatoes,
and choice of white, wheat, rye toast, pancakes or biscuit
with gravy. $6
Add American Bacon or Sausage $1
Add Irish Bacon or Sausage $1.50
Add Sirloin Steak $4
Belgian Waffle. A classic waffle. $5
Kilkenny Waffle.Smoked Ham, Chorizo sausage, jalepeño cooked in a Belgian Waffle. $7
Sausage Waffle. Breakfast sausage cooked in a Belgian waffle. $6
Irish French Toast.Traditional French toast made with our famous Irish Brown Bread. $5
Nutty Waffle.Toasted pecans cooked in a Belgian Waffle. Served with peanut butter. $6
Stack O' Cakes. Three fluffy buttermilk pancakes. $4
Mimosa - Sparkling Champagne and fresh Orange juice. $4
Manmosa - A "man sized" Mimosa. $6
Hot Buttered Rum- Just like it sounds. Hot, Buttery and Rumish. $6
Champagne Cocktail- Sparkling wine with a dash of Angostura Bitters and a sugar cube. $6
Irish Coffee - Made the traditional way and topped with our own Bailey's Irish whipped cream. $6
Bloody Mary- Michael's secret recipe. The best in town and possibly the world. $6
Guinness Bloody Mary- Take our Traditional Bloody Mary and add a dash of rich, creamy Guinness. $7
Milk - $2
Make your reservations now!
Call 918-582-8282
Make a Reservation
If there're any questions you have regarding Kilkenny's menu or our accomodations or if you have any complaints please feel free to call us or email us.
© 2019 Kilkennys Irish Pub. ALL RIGHTS RESERVED. WEBSITE DESIGNED BY :PHILLIPS360


text: All In Monday, September 25, 2017 6:30 PM 8:30 PM 18:30 20:30 NEX Atlanta 318 Cherokee Avenue SE, #104 Atlanta, GA, 30312 United States (map) Google Calendar ICS The ALL IN accountability circle meets on the 2nd and 4th Monday's of each month. We tackle the tough stuff about starting, owning,and running a business. This group is facilitated by Yvonne Dodd. You must apply for membership. For more information, go here. Posted in All In, Atlanta Tagged women, support, accountability


text:
outsourcer needed a new logo design and created a contest on 99designs.
A winner was selected from 20 designs submitted by 9 freelance designers.
Gif or Jpeg required to make this site look credible
Quick car insurance quotes
Desired Color Scheme:
Desired Style:
classic - so looks credible
Accepted File Formats:
Standard Web Formats (.jpg, .gif or .png); Vector Formats (.eps, .pdf or .ai)
I need a 794 x 99 image which includes the name of the website:
 and the text: Car Insurance Quotes
 and an image of a car , either a graphic or a photo (UK model car)
 Should fit with colour scheme of site: http://www.phoneus4aquote.co.uk/
Need in a jpeg or a gif and also be supplied with the original vector file
The key is to make this site look trustworthy and credible
Find out how a design contest works or learn more about our logo design services.


text:
Hockeyroos in world media spotlight after Queen photobomb
GLASGOW: Hockeyroos players Jayde Taylor and Brooke Peris have become internet sensations after their selfie was photo-bombed by the Queen.
The picture, retweeted almost 7800 times in the first nine hours, was taken after Australia's 4-0 win over Malaysia in the Commonwealth Games in Glasgow on Thursday.
Hockey Australia officials were bombarded with requests for interviews with the pair from a host of American TV networks, and the photo was splashed across the front pages of most of the British newspaper websites, the frontpage of The Times newspaper the BBC Sport homepage and the Huffington Post.
Taylor admitted the photograph was planned after the Queen met the players on a visit to the Glasgow National Hockey Centre.
"We were warming down on the second pitch after our game and the Queen came out to meet Donny [Madonna Blyth, Australian women's hockey captain]," Taylor said.
"The security guard led us all round and we got to meet her.
"She asked us a bit about the pitch, how we were going and told us to enjoy our time here. She was lovely, really, really lovely.
"Brooke and I planned it so that when she came out the door she would be behind us.
"And then she came out and smiled at the camera. We were in the right spot at the right time."
Other athletes did their best to get their own as the Queen visited other Games venues in Scotland's largest city.
England hurdler Andy Turner uploaded a photo of himself with the Queen in the background and Australian rugby sevens captain Ed Jenkins also boasted of a selfie.
But Australian swimmers dipped out.
Belinda Hocking, Thomas Fraser-Holmes, Matt Abood and Katherine Downie had a moment with the royal.
"We weren't allowed to get any selfies - we asked but they (officials) said no unfortunately," Hocking said.
Queen Elizabeth and the Duke of Edinburgh spent almost an hour at Tollcross Swimming Centre where the swimmers gave her a team badge.
"She was pretty happy and said she would add it to her collection," Abood said.
"It didn't stack up too well with her brooch though - I didn't ask for a swap."
Defending Olympic 100m hurdles champion Sally Pearson didn't selfie either when she met the Queen at lunch.
"It was an honour, very exciting, and we talked about the weather," Pearson said.
"She said that it looks like I brought the sun here."


text:
CAMBRIDGE, Mass. – The America East has announced the 2013-14 women's basketball conference slate, with each team set for a 16-game schedule, a home and away contest versus each of the right other teams in the league, including conference newcomer UMass Lowell.
Following a pair of games at the James Madison Tournament on Dec. 29 and Dec. 30, the Retrievers will open league play on their home court for the fourth time in the last five years, hosting Binghamton on Jan. 4. UMBC travels north to take on Maine on Jan. 8, before returning to the RAC Arena for its next two games, entertaining newbie UMass Lowell (Jan. 11) and New Hampshire (Jan. 15).
The Dawgs get back on the road for back-to-back games, before taking a Thursday off in late-January (Jan. 23). UMBC travels to Vermont on Jan. 18 and heads straight over to take on Stony Brook two days later on Jan. 20.
A UMBC basketball doubleheader at the RAC Arena will kick-off the Retrievers' Hall of Fame Induction Festivities on Saturday, Jan. 25. The black and gold will hop right back on the road for a matchup at the defending America East Champion, Albany on Tuesday, Jan. 28.
February opens inside the RAC Arena, with UMBC hosting Maine on the first of the month. The Retrievers travel back up to New England to battle New Hampshire (Feb. 6) and UMass Lowell (Feb. 8).
UMBC returns to Baltimore for its longest home stretch of the 2013-14 season, when it welcomes Albany (Feb. 11), Vermont (Feb. 15) and Stony Brook (Feb. 19).
The Retrievers wrap up the regular season on the road, with visits to Hartford (Feb. 22) and Binghamton (March 1).
The 2014 America East Men's and Women's Basketball Championship quarterfinal and semifinal rounds will return to Albany's SEFCU Arena for the second-straight year and will take place March 7-9. The 2014 women's championship game will also be played in Albany on Monday, March 10 and will be televised nationally.
Last season, UMBC was picked to finish sixth in the league, but closed out the regular season in a four-way tie (Vermont, New Hampshire and Stony Brook) for fourth place in the conference with a 6-10 league record.
The Retrievers return one starter and four letterwinners from a year ago and welcome nine starters.


text:
Why Romney's White House bid fell short
Throughout the election season, President Obama looked vulnerable. The unemployment rate hung above 8%, the White House and Congress had been unable to resolve the nation's looming fiscal crisis, and the nation seemed weary of big government proposals such as the Obama-backed health care law and stimulus spending.
Mitt Romney seemed to be in good position to capitalize — a successful businessman, a Republican who was elected governor of a Democratic state, a man not tarred by scandal or extreme rhetoric.
And yet, after six years of running for the White House, he fell short.
While books will be written about how the campaign failed to reach the summit, a handful of hurdles stand out.
The economy. The nascent signs of a recovering economy seemed to have given the public just enough confidence in Obama to give him a second term, and deny Romney his chance to try his plan. Several key swing states including Ohio, Virginia, Iowa and Colorado all have seen their unemployment numbers drop below the national average; nationwide, the jobs report released at the beginning of October showed unemployment dropping below 8% for the first time in four years, stealing a key line from Romney's standard stump speech.
STORY:How Obama won re-election
Several Republican governors — such as John Kasich in Ohio, where the unemployment rate has dropped to 7% — argued that the progress was the result of state-level decisons, not presidential action. But ultimately it appears Romney failed to convince enough voters that the recovery was stalled.
Romney's wealth. Romney is not the first multi-millionaire to run for the White House, and his wealth alone may not have been a fatal flaw. After all, it's possible Democratic Sen. John Kerry of Massachusetts is richer than Romney, and his wealth was not a major factor in his defeat by George W. Bush in 2004.
But Romney kept saying things that reinforced a distance from the average American. During an interview with CNN after winning the Florida primary in February, he said he is "not concerned about the very poor. We have a safety net there. If it needs repair, I'll fix it."
A videotape surfaced of Romney saying at a May fundraiser that 47% of Americans were "victims" who paid no taxes, expected government handouts and would vote for Obama regardless.
And he steadfastly refused to release his tax returns for past years, providing only summaries that raised as many questions as they did answers.
The net result is that Romney gave Democrats plenty of material to paint him as an out-of-touch rich guy.
Women. Despite ad campaigns, targeted messages and polls that showed women were warming to Romney in the final days, he still lost the female vote to Obama, 55% to 43%, according to exit polls.
The loss wasn't entirely his fault. Republican Senate candidate Todd Akin in Missouri discussed how women's bodies could prevent pregancies in cases of "legitimate rape," launching a firestorm of protest. A few months later, Indiana Senate candidate Richard Mourdock, for whom Romney had just released an endorsement ad, said he opposed abortion even in cases of rape because God intended those pregnancies.
Romney tried to distance himself from both remarks, but they gave Democrats plenty of ammunition to argue that Republicans just don't like women.
"Etch-a-Sketch." As Romney was closing in on the GOP nomination in March by highlighting his conservative credentials, adviser Eric Fehrnstrom said on CNN that the themes of the general election campaign may be different. "It's almost like an Etch-a-Sketch," Fehrnstrom said. "You can kind of shake it up, and we start all over again."
The remark itself may have had little impact, but it underscored a lingering weakness in Romney that Democrats (and his Republican primary opponents) exploited at every turn — that his positions on such issues as abortion, health care and climate change have shifted over the years. Conservatives ultimately embraced him despite his background as a moderate governor of a New England state, but it may have left doubts among voters about exactly where he stands.
Hispanics. In the nation's fastest growing demographic, Romney was crushed, 69% to 29% the exit polls showed, a performance that was worse than of Sen. John McCain four years earlier. This would seem to pose long-term concerns for Republicans who want to make inroads with Hispanic voters.


text:
Mapmaker: MrBenn
Territory Count: 48 (32 starting)
Bonuses: 5 Regions & 16 Triples
Gameplay: Almost standard, except two/three armies occupy each Shire area.
Size: Large 740px × 760px; Small 565px × 580px
Foundry Stamps:
Version 23/24 - 11 February 2009
- Here is my absolutely final update (I hope)... There are no changes to the small map, but I have made some minor tweaks on the large one... all the army numbers are exactly the same distance (3px) from the territory name. I've redrawn a tiny bit of border by the Ial number, and shifted those names to get it to fit properly.
Here's the XML with the adjusted coordinates: http://www.fileden.com/files/2009/1/9/2 ... XML_05.xml
Here is the small image: http://i275.photobucket.com/albums/jj32 ... les23S.jpg
Here is the large image: http://i275.photobucket.com/albums/jj32 ... les24L.jpg
Here are all the test images:
- Small Map:http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales23S.jpg
Small Map 88 Test: http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales23S-88.jpg
Small Map 888 Test: http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales23S-888.jpg
Large Map:http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales24L.jpg
Large Map 88 Test: http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales24L-88.jpg
Large Map 888 Test: http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales24L-888.jpg
Version 23 - 3rd February 2009
Small Map
Large Map
XML: http://www.fileden.com/files/2009/1/9/2 ... XML_03.xml
- Conquer Club Map Maker
Test XML for Errors
- xml is valid. see test results.
Summary: 0 errors and 0 warnings detected in WalesXML_03.xml (21 continents, 48 territories)
Small Map:http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales23S.jpg
Small Map 88 Test: http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales23S-88.jpg
Small Map 888 Test: http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales23S-888.jpg
Large Map:http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales23L.jpg
Large Map 88 Test: http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales23L-88.jpg
Large Map 888 Test: http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales23L-888.jpg
Version 22 - 9th January 2009
- I have made good use of WM's XML generating spreadsheet, and knocked out the XML; and I've worked out a better way of using the Map Assistant to plot coordinates - and not a single one is out of place after the first attempt... Woohoo!!
The XML lists 21 continents - 16 for the shires, and then 5 for the regions proper.
I've changed the settlement circles on the small map so that the army numbers will centre properly.
The circumflex has been added to the couple of names that needed them - although I now need to update these territory names in the XML
Conquer Club Map Maker
XML: http://www.fileden.com/files/2009/1/9/2 ... XML_02.xml
Test XML for Errors
- xml is valid. see test results.
Summary: 0 errors and 0 warnings detected in WalesXML_02.xml (21 continents, 48 territories)
Small Map:http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales22S.jpg
Small Map 88 Test: http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales22S-88.jpg
Small Map 888 Test: http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales22S-888.jpg
Large Map:http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales22L.jpg
Large Map 88 Test: http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales22L-88.jpg
Large Map 888 Test: http://i275.photobucket.com/albums/jj320/bpawley/Wales/Wales22L-888.jpg
Version 21 - 7th January 2009
Small Map
Large Map
- I have increased the colour saturation of the blobs (official name) on the bonus legend.
The bonus values for the regions have been updated - the total bonus will include +1 for each shire
Hopefully the legend text is now fully comprehensible... the settlement icon has been moved into the first paragraph of instruction and looks a lot more coherent
Version 20 - 29th December 2008
Small Map
Large Map
- I've tweaked some of the background effects - turned them down slightly more on the small map than the large.
On the small map, the labels on the Isle of Anglesey have been moved/shrunk a bit to make it more obvious where the army numbers go
The Settlement image has reappeared on the legend.
Version 19 - 28th December 2008
Small Map
Large Map
- The biggest change is that of the instructive text - hopefully it is now much clearer how bonuses/attacks work
I have also moved the mountain range between green/blue to make the Northern region slightly harder to hold - this is the only thing about the gameplay that bugged me.
Since the addition of the settlements, I have increased the map sizes, and ensured that both versions now fit within the size restrictions.
Version 18 - 12th December 2008
Large Map
- I've added a small space between the two labels in each Shire to aid clarity
Version 17 - 10th December 2008
Large Map
- The map has been cropped a lot more tightly to the Welsh coastline, making the map slightly shorter.
The region bonuses have been moved to the side, and the wording of the explanatory text has been tweaked again.
I've shifted my signature slightly, and the compass has been moved and shrunk in order to accommodate the relocated legend.
I've added in some more mountains between Herefordshire and Shropshire to tidy up the border there, which looked a little odd with the tiny bit of neither county betwixt the two.
The typeface I'm using doesn't have an extended character set, so accented characters will be harder to add than I thought.
Aberffraw and Mon will probably remain the way they are, in order to make the labels best fit the space of the island.
In addition to these significant amendments, there have been a number of tweaks to shades of things, too numerous and petty to mention.
Version 16 - 30th November 2008
Large Map
- This image is at the size I've previously been using as my large, but since I've added the settlements, I'm contemplating using this size as the small...
I have tweaked some of the wording of the explanatory text, and made it slightly larger.
The settlements will all start with 3 neutrals, and can only be attacked by the clans in the same shire...I'm considering making it so they can't attack them back...
Points for discussion - relative merits of 3 territories per shire, and whether the settlements should be able to attack?
Version 15 - 15th November 2008
Large Map
- Here's an attempt at a version with the altered gameplay, as recently suggested. I really like the way it works, and it does give additional options to make a better game...
I have switched to the Welsh labels as suggested by Genghis Khant, and have used the County towns as the settlements. I've been a bit inconsistent with the use of English/Welsh names for the settlements, so will amend them at some point in the future - but at least they're more-or-less in the right place geographically!
My working image is bigger than the small and large images, so the settlement circles will need to be redrawn at the correct size in a future update. It's worth noting here that the settlements will all start neutral, which will negate the need for complex start-positions.
Version 14 - 8th November 2008
Small Map
Large Map
- All I've done is make the Cardiganshire / Montgomeryshire /Merioneth border a bit clearer, and moved some neutrals around.
I had been contemplating starting one of Anglesey neutral anyway - and it has the added bonus of having an equal distribution of players per region.
Second thing... bonuses...
I haven't updated the region bonuses since I've added in the mountains... I've run the numbers in to one of the bonus spreadsheets... (clicky) (The Shire Pairs are taken into consideration in column M)
I think some of the figures are a bit out, as the region size isn't that much of a factor...
Would it be acceptable to set the region bonus at double the number of Shires? ie North+5; SWest+3; Midlands+3;South+2; English+3? That make North a bit too high.... hmmm....
Any and all thoughts welcome
Version 13 - 7th November 2008
Large Map
- Right... here is my first attempt at starting positions... rather than listing them, I've opted to display them using army placement, which is more visually impactive than an XML extract...
In 2 player games, each player will get a complete set of one colour. 6 territories from the unassigned colour will be shared between the two players, with the remaining territories starting neutral. It is possible for each player to receive a maximum of 3 shire pairs from the drop, but nobody will receive a bonus region from the drop. I think I've caluclated that there is 26.5% of dropping at least one shire pair, 7.5% of getting at least 2, and 3.75% of getting 3 pairs... dramatically lower than the list of probabilities I posted above. (I'm deliberately not posting my working out because I expect I've got it hopefully wrong)
In 3 player games, the armies will be divided up so that each player will get a complete set of one colour. Nobody will start with a shire pair or a region bonus.
4+ player games will be distributed totally randomly, and the starting positions will not be taken into consideration.
Version 12 - 23rd October 2008
Small Map
Large Map
- I've added some grunge to the rest of the text on the map
The region names on the English bonus blob been switched so that the Welsh translation is on the top
The bonus blobs for Midlands and South-West have been redone so they look more like the regions on the map.
Version 11 - 22nd October 2008
Small Map
Large Map
- The biggest change is the text - I've gone for Oaktowns poetry, which was marginally superior to mine, although I did have to correct some of the American spellings (neighbor)
I've shifted the colours where the mountains meet... Each mountain is now one colour or the other - I tried an attempt with no colour on them, but it just looked wrong, This version looks tidier than the previous one, which is what I was hoping to achieve.
The text has been mildly grunged, and I've changed the colour to a very dark brown instead of black.
To reiterate how the gameplay is supposed to work; each Shire has two armies. Hold both armies in a Shire for +1. The South-West (red) has 3 Shires, or 6 armies. If you hold this region, you will get (3 x +1) for each Shire, and (1 x +3) for holding the region.
Version 10 - 22nd Sept 2008
Small Map
Large Map
- The burn mark has been the subject of a lot of angst, and has accordingly made a swift departure.
The dark blue blob behind "Gogledd North 3" has been made a bit lighter. It still looks blue enough, but the text should be more visible now (at least that's the hope). I also made the green blob a bit more green.
I have added a Shire suffix to some territory names to help make the interpretation of the poetry a little easier...
Version 9 - 21st Sept 2008
Small Map
Large Map
- I have taken out the 'fold' across the middle as I wasn't really that keen on it.
The colours have been swapped around, and I've made the band of colour thicker to make it easier to distinguish. I think the colours are better placed now, but am tempted to rethink the thickness...
The large image has been made a bit smaller (even if only to appease RJ!)
I've also added a burn-mark. The hole is very slightly off-white, to match the colour of the background on the play-a-game screen.
I have changed the shapes of the region bonuses, picking out a shape from the corresponding region area instead of the previous blobs!
To clarify some of the gameplay issues, there are two territories (clans) in each geographical area(Shire). You get a +1 bonus for holding both territories/clans in each area/shire. The Shires are grouped into regions, which will yield an additional bonus. I have attempted to explain this through the medium of poetry, so some of the finesse may be lost?? In any case, the gameplay will be standard (ie no bombards/one-ways etc), except for the multiple armies per territory...
Version 8
- It's been a little while, but here is my first attempt at a grunged-up version...
I've taken a picture of some scrumpled of paper and added that to the background as a feint texture
There is a bit of 'weathering' to the edges, but I've also sprinkled some over the map at random
I'm not wholly convinced by the fold I've put across the middle, but I'll see what others think.
After much playing around, I have learnt a bit about custom brushes and drawn some mountains I am happy with. I'm using PS6, which doesn't have a 'jitter' feature, but I think they look good regardless.
I haven't swapped the colours around as I flattened the colours layer, and will need to see if I can get an untangled copy from an early version
Version 7
- Unpublished attempts at trying to draw mountains...
Version 6
Large and Small Images
Large Map
Small Map
- I've done a little tweaking, and put together a slightly smaller large image, and a smaller small image...
The sea now has a slight edge to it - there was a suggestion to have a blue tinge, but it didn't look right. I've opted for a slightly murky sea, which seems to fit the style of the map!
I've added the Shire suffix to some of the English territory names where they'll fit, which will hopefully make it slightly more obvious what the poem means when it talks about shires
There are now working small/large images - Gameplay discussion is desperately needed
Version 5
- Unpublished attempts at trying to do something fancy with the sea...
Version 4 (22/08/2008)
- I've added in some pale contour lines to help indicate the reason for the wonky compass. The compass has been faded into the background a bit more so it doesn't jump out so much. I've tried to smooth the dragon outline a little too...
I've updated the 'poetic' text to include the attack rule - how is it for clarity?
The overlapping army numbers have been nudged around a bit, and I've tweaked a border
On the subject of border-tweaking, I've amended the Flint border to get rid of the exclave - purely to assist gameplay.
I've run the region bonusses through a calculator and taken off the amount you'd get for holding the Shire pairs. The English area should really be a +5, but I've upped it to a 6 to add to the confusion in foggy games
Oh, I've also adjusted the Cardigan/Montgomery/Merioneth border to make it clearer.
Version 3
- I've added the Dragon image, and I've drawn in a compass to match.
The font has been updated to one that looks suitably mappy... I like it
The slightly patchy region fills are gone, to be replaced with the edge-effect.
I've added the region names to the bottom of the map, ready to be populated with the region bonuses when they're decided
I've come up with some (cough) poetry (cough), and spent a lot of time playing around with online Welsh translators... If anybody here speaks Welsh, please let me know if it reads OK!
Version 2
- Here's a slightly more 'mappy' version - I've added on some army numbers to give a feel for how the gameplay will work... I thought it would make sense to have a +1 bonus for each county/shire, so have added that too...
Version 1
- Welsh geography is a bit messed up, and there have been several boundary changes to their counties over the past few years, and it looks probable that the administrative areas will continue to be shuffled around indefinitely. There are currently 8 administrative counties/regions in Wales, which is not enough for a CC map (unless you're a Doodle Assassin fan). So instead of using current boundaries, I have opted to use the 13 historic counties of Wales - these are the most consistently defined areas, and apparently have a 'resonance with which Welsh people can identify' (I read that somewhere!). To bump the territory count up, I've included the three English counties on the Wales/England border, some of which have bits which are almost Welsh in any case....
So, 16 counties in total - the bare minimum required for a map. Personally, I think that 16 terrs is still too small, so I had the idea to have two 'territories' per county based on the English/Welsh names for the counties, which makes 32 terrs, and an ideal sized map.


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British & Irish Lions 2013
Lions Watch: Team of the Week
ESPN Staff
September 3, 2012
Fleet-footed Wasps winger Christian Wade lit up Twickenham with a two-try display against Quins on Saturday © PA Photos
With the start of the Aviva Premiership and RaboDirect PRO12 campaigns, the countdown to the eagerly-awaited British & Irish Lions tour to Australia is well and truly on.
As we all tick off the days until the team depart Down Under, ESPNscrum will cast an eye across the action - including the Top 14 battle - and pinpoint those players eligible for the elite tourists who are pushing their selection claims with strong performances.
There is a lot of rugby to be played until the squad board the plane for Hong Kong and plenty of time for hopes to rise and fall with many international stars yet to return to the domestic fray but the excitement is already building.
15. Mike Brown (Harlequins)
The Harlequins fullback scored a second-half brace to secure a thrilling victory over Wasps at Twickenham, coming to their aid as he did so many times last season as they wrapped up a maiden Premiership title.
14. Christian Wade (Wasps)
The flying Wasps winger made a mark on the London Double Header with two superb tries against Harlequins, the second of which conjured memories of the great Jason Robinson's try for the Lions against Australia in 2001. Pushed all the way by a in-form Sarries signing Chris Ashton.
13. Brad Barritt (Saracens)
The England international drops in at outside centre for the purposes of this selection after a typical busy display punctuated with a try as his side swept aside London Irish.
12. Scott Williams (Scarlets)
It will take a big effort for the Scarlets centre to displace Jamie Roberts and Jonathan Davies in the Wales midfield, but he hit the ground running with a try in his region's opening-day hammering of Leinster.
11. Tim Visser (Edinburgh)
Edinburgh came out on the wrong end of the result against Munster at Murrayfield, but their newly-minted Scotland wing kicked-off his season in fine style with a hat-trick of tries.
10. Nicky Robinson (Wasps)
Nick Evans stole the limelight at Twickenham with his second-half heroics, but it was Robinson who lit the touchpaper in the first, with his strong passing game and awareness allowing Wasps to put Wade and Tom Varndell into space out wide.
9. Lee Dickson (Northampton)
The Saints and England scrum-half played a key role in his side's Premiership victory over Gloucester with his quick-thinking and slick hands playing a part in two crucial scores.
1. Tim Payne (Wasps)
The veteran loose-head got in on the scoring act as Wasps rediscovered some form against Quins at Twickenham - could the 33-year-old force his way into the international mix?
2. Dylan Hartley (Northampton)
As far as the Lions go, hooker is one position that is wide open. Hartley made a good start to the season with a try against Gloucester and will hope to prove that he's in the right form and frame of mind to tour come June.
3. Dan Cole (Leicester)
Rock-solid at the set-piece and a devil at the breakdown, Cole was in fine form against London Welsh in the Tigers' opener. Showed his new, rounded game.
4. Joe Launchbury (Wasps)
Just 21, Launchbury should be in with a shout of England selection sooner rather than later. Able to play in the second and back-rows, he was superb in an all-action opening against Harlequins.
5. Geoff Parling (Leicester)
Dominant at the lineout against London Welsh. A real technician in that department and carried very well, taking his try in good style. Has arrived at club level, now to nail down that England spot for good.
6. Aaron Shingler (Scarlets)
Shingler only has two Wales caps to his name but a blistering start to the season in Scarlets colours could soon see that change.
7. Steffon Armitage (Toulon)
Armitage may not be on England's radar at the moment, but he continues to shine in the Top 14 in France where his efforts have helped propel Toulon to the top of the league - most recently with a try in their win against Mont de Marsan at the weekend.
8. Thomas Waldrom (Leicester)
England's Kiwi-born No.8 bagged a brace against Premiership newcomers London Welsh and displayed the kind of dynamic ball-carrying that made his name.
© ESPN Sports Media Ltd.
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DENVER - Denver Broncos tight end Julius Thomas is expected to start in Thursday's season opener against the Baltimore Ravens despite revelations of his arrest last week.
Thomas had been stopped for speeding on Aug. 28 and was then arrested for failing to appear in court for a traffic citation earlier this year, Arapahoe County sheriff's Capt. Glenn Thompson said. A deputy issued a citation to Thomas for allegedly going 57 mph in a 40 mph zone and he was released on $500 bond the same day of his arrest, which was first reported by The Denver Post.
Thomas is scheduled in court on Sept. 12.
Records show that Thomas missed a March 21 court hearing for a citation issued Jan. 25 for failing to yield the right of way to an emergency vehicle.
"We were notified of the issue involving Julius Thomas when it occurred on Aug. 28. It was addressed internally and is being resolved," the Broncos said in a statement.
The arrest of Thomas, a third-year player who earned his starting position during the preseason, is the latest embarrassment for a franchise that has made plenty of off-the-field news this summer.
Executive Vice President John Elway's top two assistants, Matt Russell and Tom Heckert, were suspended following separate arrests for drunken driving. Then, All-Pro linebacker Von Miller was suspended six games for violating the league's drug-abuse policy.
Most Read
Miller's troubles were exacerbated last month when he was arrested at a firearms shop near the Broncos' practice facility on a warrant for failing to appear in court on Dec. 31 for an October traffic stop. He had been charged with careless driving and not having a license or proof of insurance.
Thomas had a terrific training camp to earn a prominent role in Denver's offense. He capitalized on the extra work he got because of injuries to last year's starters at tight end, Jacob Tamme and Joel Dreessen, to build a budding rapport with quarterback Peyton Manning.
Tamme and Dreessen combined for 93 catches, 911 yards and seven touchdowns last season, but it was Thomas, a third-year pro with just one career catch, who stood out this summer.
The 6-foot-5, 255-pound former power forward for Portland State is finally healthy after spending the bulk of his first two seasons in Denver dealing with a bum right ankle.
When Elway remarked recently that he was "truly jealous of the weapons that Peyton gets to throw to," he made sure to mention Julius Thomas along with wide receivers Demaryius Thomas, Eric Decker and Wes Welker.


text: IMG_3147 written by Kenny 24/07/2010 0 comment 0 Facebook Twitter Google + Pinterest Kenny An enthusiast of anything that can be awesome, fun and innovative. Some interests include Japanese classic cars, photo/video, magazines, snowboarding, toys, fitness and many more. An easily amused character that's addicted to anything and everything cool. Leave a Comment Cancel Reply


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Open Government Program
All Resources
Search a listing of Government of Alberta open datasets and publications. Can't find what you are looking for? Suggest a resource.
Views: 58
March 1, 2015
Subdivision and Development Appeal Boards (SDAB) hear appeals from municipal subdivision and development authorities. By hearing appeals and making decisions on land use in Alberta, an SDAB fulfills a vital function in achieving the goals of orderly, beneficial and economic development. Appeal...


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Hostal Po
The Hostal Po was created by a world traveler who wanted to settle in Valparaiso.
The idea was to give life to a place to gather in some way the essence of Valparaiso: art.
The whole building was painted by various local artists who wanted to be part of the project. After several months of work, the building is now open and ready to share with people from all over the world.
The Hostal Po is a new art space that looks cool, mixes music, art and good services at your disposal to make your stay in Valparaiso a joyful, peaceful, loving experience and find good friends.
The site was designed in such a way to show guests a part of Valparaiso in their common areas and also in parts in the rooms.
Located in the heart of Valparaiso, just minutes away from Plaza Anibal Pinto, with supermarkets, restaurants, liquor stores, bars and general trading within the reach of all.
Comfortable beds, shared bathrooms with hot water, kitchen and a comfortable living room to share.
Availability & RatesTo view availability and prices please select dates and click 'Update Dates'
Hostel Facilities & Policies
- Free Breakfast
- Common Room
- Credit Cards Not Accepted
- Free City Maps
- Free WiFi
- Internet Access
- Self-Catering Facilities
- Linen Included
- Security Lockers
- Lock Out
- Luggage Storage
- Tea & Coffee Making Facilities
Cancellation PolicyThis property has a 3 day cancellation policy. Failure to cancel within this time will result in a cancellation charge equal to the first night of your stay.
Must-Read Hostel InfoThis property has specific Terms & Conditions.
Please note:
Cancellation Policy: 3 days before the arrival
Reception from 7Am to 11.30pm
Check In: 2.00 pm
Check Out: 12.00 noon
Method of Payment upon the arrival: Chilean pesos, Cash only!
Breakfast is included.
Taxes are included.
No smoking inside the hostel, but there is a rooftop where you can smoke
Each bed has a locker, you must bring a lock.
Each room has a shared bathroom.
Free use of kitchen, however breakfast is included.
Large living / dining room at your disposal!
DirectionsShow MapHide Map
You can arrive by bus directly from the bus station (take the bus with Aduana signaling).
Then you step into the street and walk up Urriola for two blocks.
In total approximately 15 minutes to get here.
The path is the same whether you go by car from Santiago.
If you plan to walk from the bus terminal, you must take the Avenida Pedro Montt and then walk straight until you reach Calle Urriola, about 30 minutes.
Located Near
We are located in a central street at the intersection with Avenida Prat.
We are right next to the area where you will find banks, between Plaza Anibal Pinto and Plaza Sotomayor.
It is at the bottom of the hill Concepcion, near the tourist area of Valparaiso.


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A Virginia rock climber was indicted on a manslaughter charge, accused of killing a friend with a claw hammer at the Chesapeake & Ohio Canal National Historical Park in Maryland.
David DiPaolo of Bristow was to appear in federal court in Greenbelt on Thursday after being charged with voluntary manslaughter.
He's accused in the death of 68-year-old Geoffrey Farrar at the Carderock Recreation Area. Farrar was found on the trail on Dec. 28 bleeding from the head.
His injuries were consistent with blows from a claw hammer found nearby, police said. The men were seen arguing and DiPaolo was seen running up the trail.
DiPaolo told police they argued and he hit Farrar when Farrar choked him, authorities said. Court records don't list a defense lawyer.


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New Years Resolution BlogHop 2015
So, I missed my chance to update for Christmas, and I thought that was a damn shame. So! Instead, I'm going to be writing up my new years resolutions for you guys! Because I plan on turning 2015 into something AMAZING. <3
Oh, and for those of you who are curious, I had a fantastic christmas! I got a heater, and new knives for my kitchen, and tupperware. And yes, I realize I sound like a horribly old adult for thinking these are amazing gifts, but they really are! ALSO, in a move that absolutely astounded me, my friend Chris Votey gave me a special copy of his book, Terran Psychosis with a special dedication to me inside, and I just about sobbed my heart out. It meant so much to me what he said in there. I won't share it, because it was private between two friends, but let's just say, I've never felt so loved.
So! Here I go, setting goals for 2015.
- Eat two meals a day, every day. NO FORGETTING
- Wash face every day.
- Take a hot, relaxing bath, once a week.
- Save back $50 or more from EVERY CHECK. No exceptions.
- Eat out only ONCE a check. Yes, that includes little meals that only cost $10.
- Read/listen to an hour long of personal finance information each day.
- Publish a book on Amazon by June.
- Publish a blog post every week.
- Write every day.
- Work on Panic-Attack-Helpful-Things
- Start a Garden Outside
So, these are my goals for the year 2015! Join me this year in checking these off the list, and I challenge you to post your own New Years Resolutions on your goal! Make them as extensive or as short as you can! Show me your resolve, and your power! I can't wait to read them, and cheer along with you as we make these goals come true! Consider this the start of a New Years Resolution Bloghop! Post the link to your own post in the comments below, and as I see them, I'll add your link to the Links on this page! <3
BlogHop Participators:
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