And ladies and gentlemen, you're very welcome. My name is Pauline Murphy. Could I ask you before we begin to turn off your mobile phones? I will do it myself. We are very fortunate to have with us today Ivo Dalver, who is chair of the Chicago Council on Global Affairs. I was asking him before the beginning, was this another body beside the Chicago Council on Foreign Relations? And he told me, no, this is the Chicago Council on Foreign Relations. That's what the past how many years? Past 13 years have been changed, yeah. About 80 years we were the Chicago Council on Foreign Affairs. Foreign Relations, yeah. He has an upcoming book called the Empty Throne, which indeed is part of the title of his talk to us, America's Application of Global Leadership. You couldn't have come at a desert time, Ambassador Dalver, to talk to us about this. We, in this institution, indeed public opinion more generally, I think, are very concerned about precisely America's application of global leadership. The implications of this for the international order generally, as a time when not only the United States, but in other countries, forces are militating against precisely this order. So we regard with a particularly serious that this situation should obtain in the United States. Ambassador Dalver has been president of the Chicago Council on Global Affairs since 2013. And prior to that, he served as the US Ambassador to NATO. And I think many of us would have come across his name when he had that responsibility. He has previously been a senior fellow in foreign policy studies at the Brutens Institution, a highly impressive institution, which I think bodies like this one, the Institute for International and European Affairs, try to emulate, but never quite succeed. So Ambassador Dalver, you're very welcome. If you'd like to make a presentation. Terrific. Thank you so much. And thank you so much for the opportunity to come and speak here before the publication of the book, which is actually scheduled to come out in the US on Tuesday. And I should say that it is a book I did not write by myself. I wrote it together with my good long friend, Jim Lindsay, who is the senior vice president and director of research at the Council on Foreign Relations. We're older by about six months than they are. That's what I'd like to remind them. We both have our anniversary in 2022. But Jim and I have been colleagues at Brookings, in fact. We wrote a book on the Bush administration in the early 2000s. And after the shock of the election of Donald Trump, sometime in March of 2017, I called Jim and said, I think we need to do a book on Donald Trump. So that's what we did. The book is actually two things. It's an argument. And I'm going to tell you what that argument is. But it is also meant to be a narrative history of the first 18 months of Donald Trump's foreign policy. And it is written for a public that is perhaps not as engaged in these issues as everybody here is. So it is a basic treatise of what has happened. And actually rereading it once in a while and looking back at it, it's pretty astonishing what's happened over the past 18 months. And we may have many more months if not years to go. So the second edition may be even more interesting. Already thinking about that. The argument that we're making is fundamentally this, that America's global leadership has been the central defining feature of global politics and indeed of American foreign policy for the better part of 70 years. That leadership was born out of the devastation of World War II and World War I and World War II. The fact that the United States was called upon twice within almost a single generation to come to the aid of Europe in order to deal with the reality that Europe could only deal with itself through war rather than peace, unless the United States was involved, led to the assessment in the 1940s, first by Franklin Roosevelt, then by Harry Truman and what were then called the wise men. And unfortunately or fortunately, they were all men to decide that the United States could not do what it did in 1918 and as depart Europe after war, it had to stay. And in fact, it had to stay in the world. That it had the power to do so. It was the largest military power in the world. It was the sole possessor of nuclear weapons in 1945. Its economy was not only intact, but had grown tremendously as a result of the war effort, representing more than 50% of global GDP. It had demonstrated the importance of democracy and human rights and the rule of law in international politics. And it now had to make the decision to remain engaged. And from 1944 to 1950, it used the power that it had to build a new global order, whether you call it the liberal international order or the rules-based order or whatever you want to call it. We call it the rules-based order. It was an order based on three fundamental precepts, one that you needed to create security structures, alliances, to prevent a return to war, and to enable countries in Europe and Asia to focus on rebuilding their economies and their societies in peace. That you needed to create an international economic regime, a trading regime that encouraged prosperity for all and encouraged interdependence of economic activity rather than an autarchy. And that third one had to be in defense, not only defense, but where possible promote democracy and freedom. I remember the Truman-Drock Doctrine in 1947 was a declaration that the United States would defend democracy wherever it was threatened. We saw the declaration of human rights negotiated by the United Nations, pushed by not a president but a First Lady, Eleanor Roosevelt, and the emergence of the rule of law through the UN Charter and other institutions. And so a new order was built, a order that was at its core dependent on American power, and that without American power and without American leadership, it would not be able to survive. It was built on the precepts that the United States should make short-term sacrifices for long-term gain, that you open up your market to others, even if they did not open up their markets to you, because that would build prosperity and therefore a larger consumer base, and therefore the ability for everyone to thrive, that you provided security for others so that they could live in peace rather than have to, you have to come back and fight another world war, that if you promoted democracy among your neighbors, you are more likely to be both free and prosperous. And so the US for 70 years conducted a foreign policy based on the shaping and then maintenance of a global international order that turned out to be the most successful foreign policy conducted by any nation ever in the world, a foreign policy that brought untold security, untold prosperity, and untold freedom to untold numbers of people, and even ended one of the greatest conflicts of the 20th century without firing a shot, that is the Cold War. It was a success that few could have thought was possible when the peace VE occurred in May of 1945 and VJ day in August of that same year. In 1990, the United States emerged from a 40-year-long Cold War as the undisputable global single superpower of the hyperpower that's being called in the world and had to think about how do we use the power that we have to go forward no longer to fight a Cold War and maintain a Western rules-based order but to see what else it could do. And the decision was that the United States could actually do for the world what it had done for the West and to create a more open, more free, more global rules based order. And it was based on two fundamental assumptions that the Clinton and Bush administration, however different administrations they were, shared. One, you might call the Fukuyama, although Frank would dispute it, the Fukuyama hypothesis that we were indeed ending history, that liberal democracy was the final state of development and that the United States now had the power through its attraction with Joe Nye called soft power and through its heart power to enhance liberal democracy throughout the world. America had that power. It could do so by enlarging NATO, which enabled the enlargement of the European Union. And by the way, no country has joined the EU without joining NATO unless it's two former neutral countries, Finland and Sweden. That is, you have to provide the security basis for enlargement before you could provide the economic basis. There was a policy of what one of my call, not only Western enlargement, but Western integration, the ability and attractiveness of bringing in other countries into the Western sphere on the basis that somehow liberal democracy was going to win out no matter where it was pushed. We saw in the 90s and into this first part of the century a commitment to humanitarian intervention where the United States would lead international coalitions to try to bring peace and stability in places that saw neither, first in the Balkans, then in Somalia, onwards in Haiti, and of course later on in other parts of the world, including Iraq and Afghanistan. And then thirdly, there was the belief that somehow freedom was on the march. Remember the second inaugural of George Bush where he said that the United States would support democracy in every nation and every culture and end tyranny in the world. That was the fundamental post-1990 precept of American foreign policy on one leg, that democracy was on the march and could be promoted wherever it was. The second leg of belief was that economic liberalization would inevitably lead to political liberalization, that as you brought countries like Russia and China into the economic order, they would over time liberalize. That's why you wanted Russia to become a member of the WTO. That's why you wanted China to become a member of the WTO if you go back and read Bill Clinton's speech in 1999 where he talks about China having to become a member of the WTO. It is all about the fact that once they economically open up, they will have to change and open up politically. The European Union was based its enlargement proposition on exactly the same principle, that as you brought countries into the single market, you would transform them politically as well. Those two assumptions, the assumption that you could promote and push liberal democracy and that economic liberalization lead to political liberalization, those assumptions turn out to be wrong. History has not been kind to either of them. Turns out that democracy is not necessarily the only way forward as one looks ahead. If you look at what has happened to democracy and the state of democracy in the world, it has been in reverse for the last 11 years. Freedom is not on the march, it is in retreat. Democracy is not on the march, it's in retreat.  But it's not for lack of trying on the part of the Polish people or the Hungarian people or indeed other parts of the world. It's also turned out that force doesn't turn out to be a very effective instrument for changing the internal makeup of other society. That it is much easier to start a war than anthem. It is much easier to insert forces into a country than taking them out. The United States, this with us today is the 11th yesterday, was the, so today, today's the beginning of the 18th year of our war in Afghanistan. The longest war the United States has ever fought in its history, and I've been to Afghanistan many times. I can tell you it is not a thriving democracy. It's many things, but it's not that. And so the extraordinary investment, the billions and billions and billions of dollars that not only the United States, but indeed, at its height, 55 other countries had invested in Afghanistan, sold to their people as a way to bring stability and democracy and freedom to that country has not panned out. And of course, economic liberalization has not led to political liberalization as we see in China, where in some ways the Chinese leadership on the Xi Jinping is more repressive, more dictatorial than at any time since Mao where not only a million Uyghurs and Muslims are held in detention camps, but where the astonishing thing, the head of Interpol can be kidnapped and put on trial after having been promoted as the person who was going to lead the international law enforcement community, but and apparently without any consequence. So the idea that somehow political liberalization and Mao's economic liberalization has been disproven by Vladimir Putin and Xi Jinping, if you wanna put it in those terms, and it hasn't worked. The Obama presidency was predicated on trying to figure out how to do this better and how could the United States use the power to have in order to shape the leadership in the world in a more measured way. With the exception of Libya, which I'm happy to talk about since I was deeply involved in that intervention at the time, it was an administration that did not believe in intervention and certainly did not believe in intervention in order to bring democracy to other countries. It did support democracy, but more from below than from above, so in the Arab Spring the real idea was it had to come from the people and if it didn't come from the people, it wasn't going to work, it didn't work even when it came from the people, if you saw in Egypt. It focused on cooperation with other powers to deal with the big problems of the day, whether it's climate change or nuclear proliferation or even on terrorism. It was a more measured foreign policy that still tried to use the power of the United States to deal with big issues, but it was no longer infused by the hubris and I think it was hubris of the Clinton and Bush administrations on how to use American power in its way and frankly, although I was a part of that administration and I'm a big supporter of the administration, I don't think Obama's foreign policy worked all that well. It didn't, it raised fundamental questions about what is the American role, how are we going to lead in this new world? So in 2015-16, the question was, how is America going to lead globally? And indeed, Donald Trump put on the table whether the United States should lead and it was in part because we had a crisis about how America should lead that Donald Trump was even able to ask the question of whether it should lead. Trump, can you talk about how we got elected? It's like talking about how we got Brexit. Trump was elected and came to power with the fundamental belief that the problem for America wasn't that it was leading in the wrong way, it was that it was leading at all. The rules-based order wasn't working, as he would put it, for the United States. The sacrifices that America had made for 70 years in order to have greater prosperity and more security and more democracy were fine for the people who were the beneficiaries, but they weren't no longer fine for the United States. And that what we needed to do as a country was no longer focus on leading, but focus on winning. And winning is a very different concept than leading. Winning is zero-sum, it's win-lose, it's not win-win. And if you listen to the rhetoric of the president and if you see what he's tried to do ever since, it is about winning. And in winning, you no longer have friends or foes or foes can become friends and friends can become foes. All that matters is that you get a better deal than the other side. It's the real estate's businessmen's approach to international politics. And he has turned that into American foreign policy. Alliances are no longer about building common security but about who pays how much for their defense and contributes to it. And if you don't contribute enough, then maybe we won't be there any longer. But Woodward's book is full of his complaint about having troops in South Korea. We are in South Korea, according to President Trump, to defend South Korea, not because we're defending the United States. NATO is about us defending Europe, not us defending the United States. And as a result, it's a bad deal. If you think you're only doing it for someone else, then by definition it's a bad deal. Trade, same thing. It is all about win-lose. It is defined in very simple terms, which is the trade deficit. And if we export less than we import, then it's bad. And if we import less than we export, then it's good. So we need to export more, import less, and we will have a better economics. That's how we can win. And that's the fundamental way in which Donald Trump has executed his foreign policy. Security alliances are expensive and we should reduce them. Trade has to be balanced in favor of the United States. And all democracy and human rights is for other people, it's not for us. We don't have to spend any time thinking about it. And if you look at his relationship with, say, Vladimir Putin and Kim Jong-un, which is better than it is with his relationship with Justin Trudeau or Angela Merkel, you see the underlying idea that actually working with friends and foes is all about the same thing. It's how can you get the best deal possible? Why does this matter? Well, it matters because the basic nature of international politics has remained unchanged. And if you take American power out of the equation, you go back to the kind of system that existed before 1945. A place in which competition among states is the defining feature of international politics, in which the rules-based system that was created through American leadership no longer smothers that competition, but competition reemerges in full force. And if you read the National Security Strategy of the United States or the National Defense Strategy that Jim Mattis has put out, it is all about the return of great power competition. It's about balancing and deterring powers in that competition. And in the Trumpian world, this is a competition that the United States can win because we are the most powerful country in the world. And if we build up our military strength and we maintain our economic growth, we will have an advantage in a world of global competition. And he's right. The United States will do quite well in a world of great power competition because we are more powerful than everybody else. The question is, will it do better than it does today than it has done over the past 70 years? Whether it will be better to do this alone in the competitive world or together with our allies and friends? And here is where I depart. We depart from Donald Trump, and I think many of us do. If you want to compete in this world, why not compete with people on our side? We have one thing that Russia and China don't have. We have allies. They have clients. Six of the 10 largest defense spenders in the world are allies of the United States. The seventh is the United States. Seven of the 10 top economies in the world are allies of the United States. If you can bring allies back into the fold and believe that in this competitive world, the United States and its allies, together, are much more able to deal with the challenges that we have, whether they are global challenges like terrorism or climate change or nuclear proliferation or indeed the challenge of a competitive world, you're better off doing it with allies than against it. But that's not what Donald Trump has done. Donald, in fact, he has made very clear that he doesn't need allies, and the allies are increasingly saying maybe we have to figure out how to do this without the United States. And so as a final sort of thought experiment, I'm happy to go into this in more detail, which is not in the book, but as an article that Jim and I have just published in Foreign Affairs coming out in the next few days, is how are we going to maintain a rules-based order without American leadership? And our answer is, well, the allies need to step up and start doing it for themselves. And if you look at the large number of allies we have, take the nine largest allies, four big European powers plus the European Union, Canada, South Korea, Australia, and Japan, those powers together represent a third of global GDP. They represent 20% of global military power. They represent 80% of global development assistance and aid of the OECD. And if those nine countries, including the European Union as an actor, were to work together in order to maintain and uphold the rules-based order until such time that the United States decides that it needs to have a president who is also invested in this order, then we are more likely to achieve a world that we've had for the last, to maintain a world that we've had for the last 70 years, where rules matter, where win-win is the outcome that everyone seeks both in security and in economics, and where we are able to achieve the goals that wise leadership in the 1940s set out by the United States for the rest of the world at that time. But without other stepping up, a United States that is increasingly looking only at itself is a United States that will do quite fine for itself, but not for the rest of the world. And if the rest of the world decides that it doesn't want to step up when it needs to, as I think at this moment our countries and our allies should, we're all going to suffer as a consequence. But more importantly, the United States will probably suffer less than most other countries. So that's my basic thesis statement. I have to take this discussion anywhere. I've tried to stay away from the details of Trumpian foreign policy, because we're all very familiar with it, but give you the overarching idea and argument. Thank you.


Thank you for inviting me to participate in this session today. I'd like to first of all congratulate the organisers for a great program. It's not often you get an opportunity to hear from all the players who are affected and involved in assessing fitness to drive. I've been involved in reviewing the guidelines and was also involved in the review in 2003. So my role today is to introduce the new standard which came into effect on the 1st of March to give you a bit of background about it and to provide a very, very quick overview of some of the changes. You might be aware that the first edition of Assessing Fitness to Drive came out in 1998 and that dealt only with private vehicle drivers. The major review in 2003 combined private and commercial vehicle driver standards and we are still in that position and the current standard is similar. So in reviewing the standard this time as in all reviews we really sought to continue to improve the process and continue to improve how we manage health conditions with respect to driving. We've drawn on evidence from many sources, evidence about how health conditions affect driving tasks, evidence about crash risks including coronial inquiries, evidence from consumers in terms of how the standards affect them, from health professionals in terms of how usable the standards are and from driver licensing authorities and the transport industry. So it's been a comprehensive review and involved many people. Ultimately the review is aimed to retain that and maintain that balance between road safety and driver independence which as you can imagine is a tricky one when you all deal in the field. One of the ways of trying to improve the way we manage it is to make it simpler. So a lot of the changes to the standards are structural and hopefully will make them easy to use for you. The 2003 edition had 23 chapters. We've now reduced this to 10, trying to really focus on the conditions that affect fitness to drive. So you'll notice some of these conditions affect acute ability to drive, blackouts, epilepsy, sleep disorders. Others affect functional capacity like muscular skeletal disorders and vision. Perhaps one of the red herrings in there is hearing which there's not a lot of evidence for how hearing effects crashes. It has been retained because the licensing authorities felt there wasn't enough evidence the other way. So the next review will really focus on hearing. So we've also sought in practical terms to improve the guidance for health professionals so that they can undertake this difficult task more easily. There's more information courtesy of the Monash University accident and research centre literature review about how health conditions affect driving and also what the crash risk is associated with various conditions. The new standards emphasize functional capacity rather than diagnosis so in that way it's fairer and easier for health professionals to manage. We've also tried to incorporate more assessment tools and more guidance around how to assess the patient as well as flowcharts to guide the decision making process. Just one example of one of the flowcharts we've incorporated showing the various causes of blackout and guiding you to the different parts of the standard depending on what the cause is. We've also endeavoured to provide greater clarity. A lot of the feedback from health professionals was that the standards were expressed in a rather complicated way. So the review simplifies language. We've also endeavoured to emphasise that in the wording of the standard that it is the driver licensing authority who makes the decision about licensing not the health professional. And I think often that's one of the very difficult things for you as your patients feel that you're taking their licence away. So the wording of the standard is very much around health professionals providing information about whether certain criteria are met. The driver licensing authority then combines that information with a range of other information to make the licensing decision. So just looking very quickly at some of the specific changes you'll be aware that part of the standard there are recommended or minimum non-driving periods for certain conditions designed to help health professionals gauge how long they should keep someone off the road after a health procedure or a condition. As a general piece of guidance obviously it's a minimum requirement called a recipe book approach. But we found these quite helpful but some of them have been impractical and some of them have not represented the risk of the condition. So just some examples with the major changes. With epilepsy for commercial vehicle drivers the seizure free non-driving period has increased from five years to ten years which seems a lot and it is a lot but it is in line with international standards. Some of the non-driving periods have been reduced. So with acute myocardial infarction for commercial vehicle drivers I think it was three months it's been reduced to four weeks. That doesn't mean that every commercial vehicle driver goes back to driving his truck after four weeks but it reflects that we are now able to assess drivers at four weeks as to whether they are capable of going back to driving so that's fairer for them. Also we've introduced non-driving periods for some conditions and a good example is drug and alcohol dependence and that means we can biomedically test people's remissions so that's a fairly feasible non-driving scenario. Periodic review is another way we manage people with health conditions people with conditions like diabetes, progressive conditions like dementia. The periodic review process through VicRoads is designed to help monitor diseases so people can stay on the road for as long as possible and also to pick up any changes in their condition for example like psychiatric conditions. So for some of these periodic review areas we've relaxed the requirements for commercial vehicle drivers where specialist review is required. We've found that that's impractical for common conditions like hypertension and diabetes controlled by drugs such as Metformin so GPs are able to review those patients. We've also increased periodic review for some conditions or introduced periodic review. Dementia now requires reporting to VicRoads for assessment for conditionalised at the time of diagnosis. In the past it was reportable at the time of significant impairment. This aligns with other conditions like diabetes where it's a progressive disorder that needs to be monitored frequently in order to monitor their risk. There have also been a range of changes for in the licensing criteria. I didn't mention earlier some of the chapters that had actually been removed so they're now no longer specific criteria for diseases such as renal failure, liver failure and respiratory failure. By and large the effects of those conditions are on things like cognition which are covered elsewhere in the standard so that's how we've banished to reduce the numbers of chapters. Other conditions that no longer have criteria there's not a cancer chapter because in the end cancer affects various end organs and it didn't make sense to have a chapter on cancer. Some conditions like pregnancy and anesthesia there's no longer specific criteria for that. There's some general guidelines in Part A about temporary conditions like that. For other conditions where the feedback was that the standard was a bit vague and was causing inconsistent decision making we've introduced more specific criteria so monocular vision now has a specific criteria and so does things like subarachnoid There's a document on the Austro's website that summarises all these changes so I urge you to have a look through that. It's about 10 pages which is easier than trying to hunt through the book. One of the areas that may affect you in regional Victoria is access to specialists and this has been quite a controversial issue. In 2003 when we combined the commercial vehicle standards with the private vehicle standards one way of differentiating in terms of risk for commercial vehicle drivers was to require that for conditional licences they needed to be reviewed by a specialist. Access to specialists is obviously a challenge and you can imagine through this review we had a lot of arguments for getting rid of specialist review entirely particularly from Central Queensland and balanced against the very strong view of the medical experts that many of these conditions really couldn't be managed by the GP and they needed that input in order to ensure safety on the road. So we've made as I said earlier for common conditions like hypertension and diabetes control by Metformin a specialist assessment for conditional licences is required initially and then if the specialist and the GP and the DLA agree they can be reviewed by the GP subsequently. If there really is limited access for any other condition so it's not necessarily diabetes or high blood pressure if for any reason access to a specialist is difficult then the DLA will engage in a discussion about what sort of input is required to advise about a conditional licence for a commercial vehicle driver. Also one of the confusions that happened in Queensland in referring commercial vehicle drivers to a specialist they were actually taking them off the road for an assessment like early diabetes which is not the intention of the standard. So a commercial vehicle driver who's applying for a conditional licence doesn't need to stop driving if they've got a condition that's not immediately going to affect their fitness to drive. So in the part A you'll find quite a bit more clarity around how specialists need to be used for those sorts of assessments and we also encourage you to use telemedicine as well that's an option. So in terms of what NTC and Austroids are doing to get the word out I'm told that the books are on their way and I think OTs have received them this week could but the other recipients are all GPs in Australia will get a hard copy. Medical specialists in relation to the relevant areas will get a copy OTs, optometrists and diabetic educators. The book will also be available to be purchased online through Austroids so at $15 a copy and I think bulk orders can be negotiated as well if you have a need locally. So I think in years gone by bureaucracies like the NTC and Austroids felt that once they distributed that was implemented in their mind. So we have chipped away at that over the years and I think we are making some progress but I think implementation really relies on you at a local level to conduct this sort of session to engage you locally in education. So I think we are still very much reliant on that. However we are over the next six months there will be quite a lot of general communication through health professional organisations, through transport organisations, through a variety of groups to alert them to the new standard and through consumer organisations as well. We've produced a very short fact sheet which just talks about responsibilities of the patient in relation to driving. It's quite a handy fact sheet to give to patients when you're talking about fitness to drive but VicRoads and the various consumer organisations also produce some terrific resources. So I urge you to go out and have a look for those and there's I think a lot of them displayed in the room outside today. One of the things we're slowly making progress on and I think is really essential for GP management is to try and integrate some decision making tools into GP practice software, doctor practice software and we're already having some quite useful discussions with the major software provider. So I think that will be if it comes off quite revolutionary in how we can encourage doctors to manage this in a routine way. We'll also be continuing to liaise with major stakeholders. If anything comes out today for example we'd be very keen to hear about it in terms of ideas. NTSC and Austroids now see maintenance and implementation as an ongoing function rather than just turning off their ears and waking up in five years time to think about it. So which is great. And I think also finally you're very fortunate in Victoria to have really great support at VicRoads through the medical review area and through the Victorian Institute of Medicine. Very few states have this level of support where they can actually get sensible advice about individual patients and about the processes. So I encourage you to use them and support them because it's quite a unique service and we have struggled to get other states to take that on. So if you want to find out more about the review and supporting resources the Austroids website is the place to go that it has a review project report which explains all the changes from a medical viewpoint and explains the impact on licensing authorities and consumers and health professionals. And if you really want an interesting read have also a look at the Monash University report. And finally just acknowledging the very many players who have been involved in particular Dr Bruce Hawking who's been the medical advisor on the project. Thank you. Thank you.


All right, it's eight o'clock. We may have some people trickling in, but we'll go ahead and get started. This morning, we're lucky to have Dr. Ying Bing Fu, who's gonna be talking to us about age-related macular degeneration. He's originally from China, but completed his PhD training at Michigan State. And he's been here at the Moran since 2007. So it sounds like he's gonna be talking about a mouse model of age-related macular degeneration and possible implications. His role here at the Moran is he's currently the director for model development at Translational Medicine here at the Moran Center. So thanks, Dr. Fu, for coming and speaking with us this morning. Grand Ramp presentation at Moran. And mostly I work in the research side, but I also feel that deep in my heart, I'm connected to the clinical side. I still remember when I first came here for a job interview. I asked Robert specifically that I wanted my office to be on the clinical side so that at least physically I'm in the territory of the doctors and the residents. Today I'm gonna talk about our research work on age-related macular degeneration. Most of the results I'm gonna present today were published in August. And I also added many new results we obtained very recently. So as all of you know, that AMD is the leading cause of irreversible blinding. So AMD affects the region is the macular, very critical area, responsible for high-acuity vision such as reading and driving. And that's why it's so important. If you zoom in this area, so any damage occurs, all of us AMD can be separated into dry AMD and wet AMD and start to lose this information. So it all comes from majority of AMD and one of the most common early signs of dry AMD is frozen. Yano is deposited between brooks membrane and R. So on the other hand, the wet AMD is very serious for more AMD. And the healthy macular, I just mentioned there's three layers, photoreceptor, the corn photoreceptor, RPEs. And you see the cord vascular is a very nice, nice underneath. But if you look at the wet AMD, what happened is the cord vessels they break the RPE of brooks membrane and invade in the sub-regional space because the vessels tend to be very fragile and then you flew it not and cause serious damage to the mac. So there's a variant of what AMD is so-called polypoidal cord vascular naphthalene, which was first described by Columbia physician, Yano at 1982 as a cause of recurrent hemorrhagic and excessive heat-saving retinal detachment. And there are two key features on indocyanin-green angiography or ICGA. One on that was a branching of normal cord vessels, the other polypoidal vascular dilation. I will come back to this later. In terms of demography to the younger age so currently the pathophysiological mechanism for PCB download. So there are two major regions on the chromosome that can account to the majority of genetic risk for AMD. One is on the chromosome node side, one Q3, there's a well-known company in the factory edge region, a number of labs. Especially Dr. Hickerman's lab has done major contribution in this discovery. On the other region is on chromosome 10, that's centered around two nearby genes when high-temperature requirement effect A1 or HTI1, the other is arms two, no, 387715. So what do we know about the two genes? The HTI1 is highly conserved all the way from human to equinox, even after a family of Hitchcock, seven proteins involved in many functions such as protein quality control, there are growth differentiation and apoptosis. So in humans, we have HTI1234, you can see the 134 are very similar, you'll be quintessely expressed. HTI2 is mainly in mitochondria. One common feature is that they have a system like close domain as a causal type protein inhibitor domain suggesting that enzyme may be self-inhibiting and also has the insulin growth effect of binding domain and they have a signal sequence that are known as proteins to be secreted out of cells. So many functions of HTI1 would be implicated in a number of diseases such as cancer, your muscular disorder or Alzheimer's disease, arthritis and aging. Just reminding you, this is a genetic association studies, HTI1 has been linked to both PC and CMAs and also other types are in contrast to HTI1, very little is known about arms two. Other than that is a primary specific made in old world monkeys with a proposed function in mitochondria but even that is in this field right now. So it's not entirely clear whether it's really equal. Chromosome, one reason pretty much most people agree that the complement factor H is very important role. There's a great deal of controversy surrounding the two competing candidates. There are three major hypotheses. The first one is that increased protein level HTI1 is responsible for increased risk for AMD. The second major hypothesis is that increased level arms two is responsible for the increased risk of AMD. The third one is combination of both. So there's a binary model basically claimed both increase HTI1 and you can always see it's getting the reason for this great deal of controversy is that the two genes are very closely judged on. In other words, all those SNPs are in tight linkage this equilibrium makes genetic association studies very difficult to distinguish. Early studies, the studies on the genetic association studies I should say that that has been replicated in almost all ethnic groups in the world. So the genetic association studies obviously very strong on the contribution of chromosome 10 region to AMD risk. But however, afterwards, a number of labs trying to determine the functional involvement of the chromosome 10 region get a lot of difficulties. For example, the deniesion insertion polymorphism as I mentioned would show the decrease in spread your wonder which one is more important. And there's another polymorphism that's been called an early stop for the R38F associated with a protective or non-risk type was showed by a number of labs that in direct conflict with the idea that increase in labor arms too is associated with increased risk of AMD. And finally, the very recent paper published by Web of Group in Germany the strongest supporter of arms too they concede that currently unimaginably immediate pathogenic effect of the risk associated variance at a chromosome 10 region. So when we come to this project we think okay, the genetic study is quite difficult and we decided to take a functional approach by using animal models. So the idea is quite straightforward. We decided to transgenic spread human FTI1 in mouse RP and we asked a simple question will this transgenic mice exhibit any AMD phenotypes at all? The reason we can do that is that a human and a mouse FTI1 are highly conserved. Both of them have 480, I mean actually it's 91% identical. Even though the domains are almost the same, totally domain, very similar PDG domain, inhibitor domain. So what we predicted is that the human FTI1 when we put it into the mouse or interact with whatever the endogenous interaction partners of the mouse FTI1. So we generate the transgenic mice and we started characterizing them first looking at their expressions. So they looked at the message and ever by real-time RPPCR you can see the FTI1 was specifically expressed in the mouse RP not in the retina, liver, heart or skins. And even the western blood, the proteins we can detect in the transgenic. We're also trying to quantify the expression level of human FTI1 in the mouse RP. So this is by using the purified human recombinant in chemistry, trying to locate the human's consistent with the FTI1 being a protein that may be secreted out of the cells into the actual synonyms matrix. Okay, so now we have generated transgenic mice. Important questions don't as mice have any AMD like phenotypes. So we use a number of techniques. The in vivo imaging is actually exactly the same used by our pharmacists to examine AMD patients. Fluorescent, angiography, ICGA, founders image, OCD, even the machines, the hydra-broke spectrometer thing as used for patients diagnosis. And of course, with the mouse model, the added or the bound disease, we can do a pretty good histology to look at the architectures, okay? This is just a reminder of that. In the human mouse, there are two vascular beds, the cord vessels and inner retina vessels. So the FA is because the emission in the green florescence cannot penetrate the RP. The ICGA is because the infrared emissions, they can penetrate through the RP, you will see, both the retina vessels and the cord vessels, where the OCD, of course, give you in vivo cord sections. With the mouse model, as you can see, we, the machine, the actual analysis to focus from the anterior side to the posterior side. But the bottom line is both the FA and the ICGS are normal as you expected. So then when we started examining the transgenic mice, the FA is pretty normal, I will say. So the, such as the retina vessels, okay. But when we start to look at the ICGS, even starting from the anterior side, they start to see emission, you know. And we're focusing more, more toward posterior side, when we start seeing more emission. So I still remember the student Alex Jones, one of his first Guinness results. He was so excited. He ran out of the vivarium, trying to find me. And I don't know what it is, because with my limited knowledge at that time, or I was thinking AMD is the same way, which is the same region of FA, but a wide FA is normal and ICGS, I saw in these regions. So I called up Paul and Banna and asked them what happened and both of them said that resemble the PCV in human. So this is a composite ICG angiography, which show you almost like a three dimensional structures. You can see the wire types are normal structures, but in transgenic to the wide distribution of emission, they're just, right. So there's a more severe phenotype. Let's also show you another picture, show you really stunning resolution on the vessels, you can see more just reminding you the mouse eye is tiny compared with human eye. So to get this kind of resolution with mouse eye is quite challenging. The student did outstanding job. Okay, so when we started zooming on the bigger nations, if you look carefully, it's not really a bigger nation per se, but it consists of many smaller dots or it looks like really grip, cluster like structure on the branch. So it's very typical for polypoidal nations within the human PCV are patient on ICG. Also, we look at some of the normal porous vessels, branching network, you can see there's no structure of emission in a very similar, in other words, the mouse exactly this phenotype on ICG will fit very well with two key definitions of the human PCV. From that copy, you can see why type is pretty normal on the transgenic mass with all the, they locate actually same location, most of them on ICG emission, suggesting it's probably exudates from the corid vessels that's in the human PCV patients. Okay, so more recently, although with the, or those mice actually say pigment in the background, those on the black six background, very popular background. So with the ICG, you can see the emissions, but here you cannot see very well the vessel structures of the coroid. I mean, most of the vessels in the retina are much more clean on the mouse. So to get around this problem, we decided to take another approach is to bring all those mice into the CD1 is our final background, which will give you much better resolution on the corid vessels. So this one, because we focus on it, we are pretty confident majority of them are actually coroid vessels. And then in the wire type, it shows very normal structure. Okay, so when we start to see the transgenic mass, it's very interesting, we show a couple of them, you can see the way they're much more clear, giving a much better resolution on the black six background. So while still in the process of the anonymized name, also in combination with EMs to see the ultra structures. We also found there's a gradient phenotype variation. Some of the transgenic mouse has very weak phenotype with a few missions. Some of them have a moderate phenotype, some of them have very severe phenotype, you can see there's many missions. We also found there's a gradient variation in terms of phenotype progression. This is a mouse at two months of age. You can see the mission, when we examine three months later, there's not a huge change, I would say, pretty present, but if you look at the other one, it's seven months of age, but three months later, there are far more missions, it's kind of pretty active. And we also found there's a gradient, the influence of genetic backgrounds on the phenotypes. We examined at that time about 114 transgenic mice. Out of them, 67 showed PCV phenotypes with the other 47 denotes, so we call them PCV negative. If we took the PCV positive mice bred with the wild type, Black 6, out of them, majority of them, 78% developed PCV. However, if we took the PCV negative mice and bred with Black 6, majority of them don't have phenotypes. Only 28% developed PCV. So, pretty obvious, a genetic background has an influence on it. In the beginning, I was thinking, maybe the expression level of HTR1 is different in those different mice, but it actually turns out not the case. So you can see in both PCV positive and negative mice have the exact same level, suggesting other factors inside the mouse modulating HTR1 activity. And that's actually pretty interesting when I'm trying to determine what are those factors. So I will come back to this on the internet. The other question is, most of those mice, when we examine them in adulthood, the question is, because the HTR1 transient expression turned down very early on, the question is, do those mice have normal coiled vessels in the beginning? Maybe it's developmental issue. Maybe all those vessels were scrubbed in the very early stage, how do we know? Right, so just to remind you that, for mouse eyes, they don't open their eyes until about two weeks age. So about P14 days. And even that age for mouse, it's kind of difficult to imagine them. So again, we use the image of the mice on our final background, it's much easier. So the P14, wire type, you can say a picture not the best one because the mouse eyes are pretty, pretty smart. Just open their eyes. But we can tell not normal wire type transient mice, we don't see a huge differences with the image in the cup of man. But a few days later, about P19 days, you can see the wire types still normal. But in the transient mice, so based on this, it's such that those mice have normal cord vessels to begin with. But nature with constant accumulation, secretion of X-ray from RPs, they start to have these problems. So we are trying to now, doing EMs on histology, trying to confirm it. We also did all cities, kind of locate the nations, but based on FAs, ICG, we can guess, not just not keeping the cord vessels, but it's in the case. So for physicians that we remind you, so it's probably needed different from one or two of the human or cities. But anyway, so there's ICG, it's mostly located in the beginning. Okay, so with the mouse, we can do systematically look for this histology. And this is transient mice. One thing is actually is really very striking. We always say, two of red blood cells accumulated between the RP and the cord, very rarely seen in the wire type. And we think those were due to leakage from compromised cord vessels. And if we cut ultrasonic plastic sections, about 200 nanometers, you'll see a cluster of very single cord vessels and structure on the cord. There's a cross-section of the artery, you can see. Very nice new wall, very linear, it is doing all the layers of the transient mice, look at the artery, look how thin it is. Okay, so there are also great similarities between the transient mice and the human PCV in terms of histopathology. You can see the single vessel will show you transient mice and the cord vessels and in human PCV patients, you can always see also those very single cord vessels. The other thing is, when you look at retinal vascular journey, this is by Flamon standing with isonectin. So you can see, largely the transient mice are pretty normal vascular on the retinal vessel. This is consistent with the imaging, which I showed you that earlier, the FA is quite normal and also that effect with immunohistochemistry we have shown at TR1 was secreted out from the physical side of RT for the cord. We don't see much of the secretion to the other side, which is to the retinal. So I should say that most of the transient mice, we only have a classical CNV cases because the FA is quite normal but in some of the very old ones, they develop something looks like occult CNV, you can see that on the more than 11 months old on the transient mice, you can see it's speckled hypofluorescence and also this is ICGA. We're also trying to look for whether that's coronation between PCV severities and occult type CNVs. Turns out they don't have really a direct coronation. For example, because some of them have very severe different factors control the development of the two types or subtypes or where type M. Another very prominent feature of the transient mice is the degradation of the nut. Let me show you on the wire. That Brooks member really transient mice very striking that it's a very selective degradation of the quantified the integrity of the EL. Let me just show you that. The definition of the integrity of the EL is that the total length of the EL divided by total length of Brooks member. In other words, if it's 100%, that means no gap whatsoever. So in a wire type, it's pretty good, it's about 95%. The transient mice decrease significantly to about 64% bigger gaps. And the PCV neck is also much better. So this is pretty exciting to us because earlier work by the treatment team shows very nicely that in both early MB and the DMV that decrease thickness and the integrity of the mechanoelastic layer. You can see here compare with the controls. So the idea is that layer is very important or perhaps as a protective barrier to prevent DMV formations. And we think maybe one reason or mechanism for this breakdown of the EL in this region is due to actual activity. So far I have shown you that in the transient mice there are two prominent features. One is the degradation of the correlated vessels. The other is the degradation of the EL of the Brooks membrane. For both of them, a very straightforward explanation is due to the actuality's activity of HTI-1. However, it was not shown before the HTI-1 as inactivity, so we did this in vitro acid. Purified becoming the HTI-1 and then used the resin, quaint resin labeled inactin control with which is the pancreatic inactivity. You can see the HTI-1 indeed has inactivity for 30 times more. By the way, Dr. Hegeman's team also have the same result. We also come back to examine the transient mice because if that's the case, we should see some degraded inactin removal. Which is really the basic building block for the insoluble inactin nature. So you can see that increased degradation in that. Because the basal activity of human HTI-1 is so low, the question is that sufficient to explain the severe phenotype we observed. Just reminding you that HTI-1 is quite complex molecule as quite a few domains. It has been shown previously that both the N-terminal is causal type inhibitor domain and the C-terminal PTZ domain regulates HTI-1 activity. It kind of inhibits their activity. And let me explain why the basal activity of HTI-1 is quite low. And also the removal of inhibitor domain or binding of PTZ domain can activate HTI-1 protease activity by more than three-fourth with a combined effect of nine-fourth, okay. So what we think what happened is that because the basal activity is so low, there must be some other actocentral matrix proteins involved in activating HTI-1 and producing the PTZ phenotypes. That may explain why the variations of phenotypes we observed. We also explained why the Asians has higher prevalence with PTZ while the Caucasians has lower. So in addition to the two main features I just show you, we also observed photoreceptor degeneration and RT atrophies in the transgenic mice you can see in the wire types is the arterial structure very nice of the transgenic mice. On the other hand, with the PCV necromyte, they have a transient but they are pretty normal. When we look in their histology and arterial structure, they also play a very significant role in the progression or in the CME development. So we also explained the VEGF expression in the transgenic mice to see that in both PCV and necromyte, there's increased VEGF levels also by immunocompetible chemistry to show in the RT. Because it's increasing both the PCV past the necromyte, what we think is that increase at chance in the PEP while still trying to determine the mechanism for this. However, we think that VEGF and VEGF itself is more sufficient to induce PCVs. Although it's critical for PCV as in the pathogenesis. I may explain the relatively less effective treatment of anti-VEGF for PCVs in comparison with very effective treatment. So let me summarize what I have talked to you so far. What we conclude is that we show that by increasing the expression level of HGRI in the mouse, it's sufficient to cause PCV phenotype. And because the degradation in the group's membrane and also the inhibition of VEGF is also a significant risk factor for CNVs. So more recently, based on this mechanism and also by the mouse model, we're trying to develop some preventive and treatment strategy for both PCV and CNV by targeting the HGRI molecule. So the idea is to take this very potent peptide inhibitor that was first developed by Michael Hermann's group at Germany. So this is published more recently in 2011. So what they did is they crystallized the catalytic domain of human bacteria one. It's in complex with inhibitors. The challenge is because remember in the mouse model we developed the mouse occurred in the core vessels. The challenge is how to deliver the inhibitor in the posterior side of the core. The way we're trying to figure out this out is to use nanoparticles as a sustained release in the brain and by intervascular injection. So I want to go through all the new features, but quite a few studies to show that by this way you can have the RP take up the nanoparticle pretty nice and you can have sustained release anywhere between weeks to months, okay? So the nanoparticle was prepared by John Rainier at the chemistry department and we did a transmission, you have to look at that much in that complexity. So you can see almost like a hole in the meter, but the average diameter is about 80 nanometer. And then we did intervascular injections. The nanoparticle encapsulating there's a kumarine dye from the resin dye. So we can visualize it as a control. Four days after injection, you can see very nicely they go up to the junction between RP and our segment or the photoreceptor layers. And this is there quite preliminary with this data recently. So we inject of your transgegromite with the PCV phenotype. Before injection with the ICDA, the control is I would inject it with nanoparticles plus the kumarine dye, but the other I would inject it with nanoparticles plus the peptide inhibitors and the kumarine dye. So you can see with the control injection, we don't see much change after 15 days, but with the inhibitors, we can see a decrease of the lesions. So we still need to replicate it with more mice, but it's kind of encouraging, very encouraging to us. Just to remind you currently the treatment for PCV is quite limited. So there's, you can do, I think as far as I know, you can do thermodynamic treatment and also in combination with anti-VAGF, but in most cases that you can reduce the exotations but the lesions most cases they remain very, very resistant. And also in this, I think it's pretty difficult rescue because what we asked is actually in the artificial structure as a severe degeneration on the core of the vessel wars. So not only we have to stop the constant insult by the FTR1, but also we ask the vessels to repair itself. The other way we are currently doing now is that trying to prevent, so that is to inject inhibitors before the mouse develop any PCV phenotypes to see how much we can actually be made on set of phenotypes. So the implication is that maybe by doing so, ways in the future, if people have carried the polymorphism in the concentration region, maybe we can give them inhibitors to prevent this So the implications I just show you that what we think is the analysis activity of FTR1 seems to play a very prominent role in AMD. We also show you a neckly pathological mechanism for PCV development. I also go through that we are trying to develop some preventive and treatment strategies by using the mouse models and to target the FTR1 molecules. We also think that our results may explain why the genetic variance and the chromatin region are preferentially associated with the wet type AMD. And also may explain why the progression of wet AMD is strongly correlated with increase especially in the serum. You can detect that degraded in nothing pretty well. Maybe one factor is due to FTR1. So I will not go through all of them, but this is really time to address the mechanisms. Preventive therapy I already mentioned by the one exciting project that we are doing now is trying to generate a primary models of AMD really based on the success that on the mouse models and this is done in collaboration with a number of net Dr. Hickerman, Paul, and Sandra's lab. The reason is for the simple reason that you cannot really give out a true AMD model with the mouse because they don't have a mechanism. So if we can develop a really primate AMD model in terms of both study the mechanism and treatment it is, I think is a huge step forward. So most of the work was done by very talented student, Alex Jones, post-doc, Sandeep Kumar, and other people in the lab. Robomark's lab has really been instrumental in the EM studies. Bala Nino has been very helpful on the available imaging. Dr. Hickerman, Paul and Sandra are involved in the primate project and Kandah has been involved in the early phase of the project. I don't have time to talk about child care but she provided us the HTI one local device. Thank you, I'll be happy to answer your question. Transcending mice with design is to really express very specific only to the art but the other mouse model we are trying to develop is kind of with systemic expression of HTI one. That's an excellent step. Right, that's an excellent survival read. We don't know what happened. So we want to do this the other ways to get around this with the inducible promoters. So we can get around the developmental stage we can turn it down. Yeah, that's the next one. We have tried a few experiments but the students just get recently so I don't have time to do it but it's very exciting that if we took those mice and put on oxidative stress, so for example, one thing we do is we took those given them very bright light cause night in deals of oxidative stress. And what happened is those PCV-inactin mice quote unquote we saw started to develop PCVs. So pretty clear when you're giving them oxidative stress you make the worse. And then for the treatment, the efficient supplement. So we haven't looked, so we saw on artificial structures we haven't been able to do nothing but if you're, we did, I think we did a lesson to show that we do see increased degradation in lasting in the PCV positive but not in the PCV negative. Maybe not a direct answer. But let's go point the other way where I'm going to do microwave analysis to compare the gene expressions of multiple genes between H1 activity. If that's a case, that means in some cases or maybe we need to make by designing specific factors in H1 activity. The photoreceptor are pretty okay in the PCV negative. Yeah, they are pretty okay. About 80 to 100 nanometers. Oh, no. I think I still show a transmission EM. It's about 80 nanometers. It's reducing some of the injections. So they can always reach to the, I think that other people show that around 100, 150 nanometers. It's a good question. So when we generate transgenic mice it's on a mixed background. It's on the CBA, BlackSix or whatever used by the transgenic core facility. And in the gold standard in the theory you have a back cause with BlackSix for 10 generations. I mean we DNAs, I mean we obviously we're trying to cross them but so all the phenotype we show is in the early stage. One, five, three, four, five generations. So we know it starts from mixed backgrounds and then what we want to know is last month so he's very keen to develop the transgenic mice in a pure background. So the idea that I talk with the transgenic core facility with Susan, he said it's possible either on the pure BlackSix or CD1 backgrounds. It is possible. So it's much easier to inject to a pure background with the pseudo-martyrs than start with 10 generation brilliant ticks forever. Takes very long time. Yeah, that's a good question. But we start from the mixed backgrounds. There's a very little, as far as you can tell there are not many studies to address why the Asians and the Caucasians have different incidents of PCVs. And definitely it's a genetic factor but people don't know. We're trying to do this in the microwave as it's on the mice to say maybe give us some hint. If we find some interesting genes, we can go back to the human genetics. We're trying to develop some S-H-R-N-A's either by Plasmids or use virus. To develop a PCV negative one is more challenging because so far when we put either BlackSix or CD1 background, we're giving it my own pure background, so it's a pure PCV positive set. Oh, we like PCV negative, you know what I'm doing here. Yes, definitely.


We're so proud of you. Thank you. Yes, the machine to me, Penda, and others who live in Kubariki. Thank you. See, it won't be easy. I'm happy. It will be easy. But then I'll be gossiping about what I'm saying. I can say I'm 900K. See, I'm 900K. I'm 100K. It's 1.1 million. 1.1 million? No, it's 1.1 million. No, it's 1.1 million. It's 1.1 million.  It's 1.1 million. Ah, see now. It's 1.1 million. The one I'm talking is Ezra.   Ah, I don't? Yes. I'll sit.  I'll sit on the wall. I'm a neighbor. A neighbor I know. I'm going to sit up in Alitwa. Let's say I'm a vehicle port tally. I'll sit here because I'm a port gari. I'll sit on the wall and I'll sit. But then one of my guys will come and say it's Pema Higarumel and his mom. I'll have a sponsor. That's the mom I know. Well, I don't know what to say.


First, my gratitude to the Catholic Bishop of Abuja, his Eminence, Archbishop Kagama, and also President of Rekor, for the kind invitation to be here today to join you at this opening ceremony of this very important conference. I bring you also the very warm greetings and special felicitations of our president, President Mohammad Buhari, who I also have the privilege of representing here. My Lords, the founding fathers of the economic community of West African states, Echoes, envisioned a West Africa that would be a zone of free-flowing commerce and travel in which people would co-mingle and migrate freely, thereby overcoming the problems that have been associated with colonialism in the past and the barriers that have been created by colonialism in the past. The truth is that since the establishment of Echoes, we have made considerable progress towards establishing the Echoes of our dreams. We have introduced the Echoes passport and we have implemented it. We have protocols that allow us to travel from country to country and to stay for 90 days in each of our countries. We also have the special trade agreements that allow our 15 countries to trade with preferential treatment for various categories of trade. We also have done several protocols. We have signed several protocols that have enabled us more or less to establish the sort of Echoes that we desire. But all our efforts and our greatest efforts to integrate our community have been floated not just by external causes and concerns, especially around sovereignty of our nations. But they've also resulted in a situation where social conflicts in our nations and around our borders have critically affected our capacity to truly integrate in the way that we wish. Internal prices and social conflicts around our borders have created a situation where today our region, we will say, is passing through a season of considerable political and economic and social turmoil. Terrorism and violent conflicts, banditry, affect many of our nations, and especially in the Sahel. In the aftermath of COVID-19, the pandemic, many of our economies have been weakened, while unemployment has escalated and poverty has been deepened. Since 2017, there have been 12 military coups in Africa, and half of them have occurred since 2020. Historically, in times like this, parochial prejudices are heightened, and the fabric of cohesion of society becomes frail as people retreat into ethnic, religious, and other nativist camps. Those that do not speak a language or subscribe to our faith come under great suspicion, and soon they become scapegoats for all our challenges. And ethnic, religious, and separatist conflicts arrive. In all of these, the ideal of an integrated, peaceful, and prosperous subregion then remains and seems almost impossible. Peace cannot reign in our region if it does not first reign in our communities and our countries, which is why I think that the theme of this summit is especially about Fratelli Tutti, a path to build brotherhood and sustainable peace in West Africa. Fratelli Tutti is the powerful notion on which is holiness, the Pope of Francis, and calls his most recent encyclical, titled Fratelli Tutti. And the concept here is a concept of the brotherhood of all humanity, the idea that fraternity and social friendships are the ways to build a better, more just, and peaceful world with the commitment of all peoples and institutions. The encyclical proposes some of the boldest and most radical ideas on securing human unity, peace, and security. In the despair and blickness of the times, these ideas that offer hope and renewal are very much needed. In answer to the challenges that many of our societies face in trying to meld diverse, ethnic, and religious communities under one flag, the encyclical offers, and I quote, if every human being possesses an inalienable dignity, if all people are my brothers and sisters, and if the world truly belongs to everyone, then it matters little whether my neighbor was born in my country or elsewhere, end of quote. Indeed, as people of faith, we look upon the diversity of our people as a gift of providence, not as a cause of conflict. We are gratified that the church has stood out and continues to stand as a powerful voice for ecumenism all over the world and is committed to doing so in our region. By offering concrete prescriptions on building brotherhood and sustainable peace anywhere, the encyclical Fratelli Tutti rightly takes the position that it is not merely the business of governments and political institutions to find means of securing peace. It must also be anchored on our civil societies of which our faith communities are an important constituency. So the role of the church in this enterprise is settled. Indeed, the Catholic Church and the bishop's conferences have established a reputation for speaking truth to power in consonance with the highest prophetic traditions and by continuing its illustrious practice of inspiring social action by the lay faithful. Over the years, the church has modeled profound approaches in challenging the impunity of some state actors and errant power. But my lords, I believe that the times also call for speaking to the growing numbers of non-state actors, violent non-state actors, some propagating genuine causes, but with mindless violence, often leading to the disruption of lives and property. In answer to tendencies that promote violence, force and war in the propagation of even the best ideas, is holding as the pope takes the view and he takes the view, especially quoting Augustine of Hippo. Augustine of Hippo, as you know, is the one who says that there might be justifiable war. He forged the concept of a just war, but he's also the one who says that it's a higher glory still to stay war itself with the word than to stay men with the sword and to procure or maintain peace by peace, not by war. End of quote. This body, this country, this body, this conference can supply a moral and spiritual consensus that underguards the very project of integration. In doing so, I believe that we can also look to the idea of the common good, which is perhaps the cornerstone of the Catholic social teachings. By one definition, this concept of the common good, is said to consist of shared values about which we owe one another as citizens who are bound together in the same society, the norms we voluntary abide by and the ideals we seek to achieve. Again, this finds support in the allusion of Pope Francis in the Encyclical, so the story of the Good Samaritan. And this story is the theological core of the Encyclical, the story that the Lord Jesus Christ told and that story raises sacrifice and concern for the well-being of others over self and it establishes the truth that the love of our neighbor is perhaps the greatest expression of our faith. Concern for our neighbors is the moral foundation of social welfare. It is the moral foundation of social security for the poor and the vulnerable. Schemes that ensure that none is left behind and that no citizen in these blessed West Africa nations needs to go to bed hungry. That we must prioritize universal healthcare while also ensuring free and compulsory basic education. That we must create the environment for millions of young and restless people within our borders to find good paying jobs and live decent lives. For our own part, the government of Nigeria remains committed to collaborating with the church and all well-meaning actors in promoting peace and security. And as you begin this conference, I urge you not only to explore ways of strengthening the bonds of faith between your communities but also building bridges across every divide that threatens to fracture our nations. It's my hope that you will conceptualize the ways of bringing the full weight of the immense moral authority that the church possesses upon our nations and in this sub-region as a whole. It is evident that we cannot create fraternity and harmony in West Africa without our faith communities. On this note, may I then add my voice, the warm welcome that you received already and to say welcome home to all of our West African brothers and sisters who are here. Let me also encourage you to enjoy the ambience and the culinary delights of Abuja. I wish you very fruitful decorations. God bless the federal Republic of Nigeria. God bless all our nations.  Thank you.


The ionosphere is a region of earth's atmosphere that contains charged particles such as electrons and ions. It is affected by the sun's radiation, which causes changes in the density and temperature of the particles. These changes can cause disruptions in radio communication signals, making them difficult or impossible to receive. Researchers have been studying these changes in order to better understand how they affect communications and other aspects of space weather. Two main phenomena in the lower and middle latitudes of the ionosphere are the equatorial ionization anomaly, EIA, and the equatorial plasma fountain, EPF, which involve the removal of plasma from around the equator by the upward E times B drift, resulting in troughs and crests. Additionally, there are regularities in the ionosphere caused by neutral winds and gravity waves. During periods of high solar activity, the EIA is stronger and more pronounced than during periods of low solar activity. This is due to the presence of faster varying prompt penetrating electric fields and equator-word neutral winds. At low solar activity, the EIA is weaker and less pronounced because the slower varying P. This article was authored by Nanon Ballin, Li Bolu, and Huijun Lu. We are article.tv, links in the description below.


Happy Wikipedia Day! So today is the 15th anniversary of the founding of Wikipedia. We've gotten an amazing amount of work done in the last 15 years. Wikipedia now has over 34 million entries in nearly 300 languages. And all around the world today, Wikipedia volunteers are celebrating, thinking about the past but more importantly thinking about the future. With 32 million entries, we've obviously come a long way but there's a huge amount of work to do. Particularly in the languages of the developing world but also even in the really large languages. There's lots of work to do in terms of improving the quality, expanding to more and more obscure topics and just basically trying to have some fun building something that the world is amazed by. I remember in the very early days of Wikipedia I would get up in the middle of the night to check and read all the recent changes just to make sure nobody was vandalizing the site and so forth. It's kind of funny to think about how that was possible back then. Now it's barely even possible to keep up with a moderate size watch list. There's so much going on. So anyway, thank you everyone. Thank you for coming to the celebration. Thank you for all your hard work and looking forward to an amazing next 15 years.


Welcome folks. This is Tom O'Brien of TFNN. We go five days a week. We go 10 hours a day We go 24 hours a day in the internet at TFNN.com Always remember folks, whatever you think about you bring about whatever you focus on grows. Hope everyone's having a great day Safe day. It's a TGIF folks. Let's make it a great one Always do your best take action on your ideas. This is a great card and I do read this a lot on Fridays folks We have a couple days to think about it Doing your best means to take action on your ideas. You're gonna have many great ideas in your head But without action upon an idea. Let me know manifestation no results and no reward Let's take a look at it out here. We have the Dow Industries down 177 Nasdaq are 46 S&P's are five and a half gold gold contract down $3.50 straight and at $14.94 ounce We have silver down a penny $17 59 cents announced light-sweet crew down 26 cents $53 67 cents a barrel copper coppers get a move and we get up four pennies 263 a pound notes and bonds you get the 10 year up for six trade in 130 or 130 year up to at 1608 notes and bonds. They both rejected lower price this week They had light of all you and bottom line that continue to want higher price lower yield and king dollar king dollar finally Went south and we did go south with conviction all week long. You down 325 ticks trade in 97 281 The euros at 111 the yen is at 108 and a half and the pound is at 121 129 to 1 us dollar Our phone number is<PHONE_NUMBER> give us a call folks One that's going on in your world now we're going to go to the world of the pound and the euro Why folks because we're going to be getting a vote on brexit tomorrow And if you go over to the pound first as well as the euro you're going to see they've been running higher all week long We take a look at this pound you get to expect high volatility out here sunday night The pound in the last six days just went from 122 to 129 this baby set up for 133 So I expect by the time that we open on monday morning We are going to see 133 regardless of what happens on the vote by the way because technically this thing is set up Really well it got back inside this higher range once it dipped inside 126 We had two monster bars and these things like to come on threes by the way So I suspect you're going to go right up into this 133 mark. You're at 129 right now We get out and we take a look at the euro euro not as strong as the pound But bottom line you did get some real strength in it if we take a look at the last two weeks The euro is down at 108. We're at 111 right now and we take a look at this one. This thing wants to run to 114 And we put this on a weekly and what you're going to see there We definitely broke the downtrend from only uh, june Okay, it didn't bring the lodges the lodges this both these have been in a downtrend for about three years Uh, bottom line note what the euro also did is get back inside a higher range and that's saying that 114 is game. So I expect we're going to see some good movement there Our own s and p we take a look at our s and p what you're going to see out here today It looks to me like we're going to have a failure on price a failure on volume On the weekly charts right now the uh spies down at 52 cents not not a lot no doubt about that 298 that being said though you start popping these up into The weeklies and I will reset these charts for you Let me see this thing. Let's go right there and There we go Okay, so this back Okay, so we take a look at the spy and what you're looking at is this The high of last week was tune 298.74 We are oh, I love it So this is going to be so cool coming into the close because we're 298 74 right now folks the volume characteristic goes like this Last week 386 million this week 225. That's pretty intense man. Think about that So they'll throw 10 million into this close, but that means there's still 100 million shot 100 million shot. Okay Uh, that would be almost 25 percent shot and you get the higher price bottom line you know none of us would pay up inside a store if there was 100 million less people in the store and the retail Whatever we're buying is saying that they want more money for it. Okay It's not just not how it works, but guess what it's how it works in the market until it doesn't So ndx 100 same setup ndx 100 the benchmark we're looking at coming into this close is 192 dollars and 63 cents Last week we did 143 million and we're going into it with 98 now in both cases folks I am not going into the real benchmark and the real benchmark is the downdraft that was created The first week of august and just let me show you how this works The first week of august we came down on 199 million Versus going up this week with 99 So you're talking about half the amount of volume if I bring you back to the s&p And we take a look at that s&p you're going to see the same type of situation that's set up as that the august first Excuse me timeline and on the august first timeline We came down with 147 million and you're going up with 225. So it is a monster number Gold gold contract bottom line is sideways to slightly higher prices and gold out here today Um This week in general you down three dollars and 40 cents.  We got take a look at the silver market What we have with the silver market out here silver right now is trading at 17 dollars 59 cents you down a penny and we have inside the silver market same type of setup Silver is actually set up a little bit better than gold right now Uh, you know, you kept having you creeping up to a little higher high and we know silver's highly volatile My take is that yes silver as well as gold We're gonna make go make a run for the last highs that were generated out there in Excuse me folks in september and august And why oh good old king dollar? That's the bottom line the king the way king dollar is set up This is a nice fast move down Uh, it's with conviction and the reason I had started with the pound As well as the euro is that they've been down for years folks. Okay bottom line Brexit has been going on for three and a half years Uh, if they basically get this thing done, you know, no matter what is going to happen I suspect we are going to see The the pound as well as the euro get to much higher price Uh, if we take a look at the the dollar in general, uh, I can make the case right now that you know I'm talking about the next step down and the dollar is 95 843 but what you do have on a weekly basis here is that it's broken a trend And it's broken the trend that has been in place since february of 2018 So you can make the case technically that the dollar is going to get out to 88 That'll be quite a move But it totally makes sense when you take a look at our interest rate structure As well as how the golden silver market wants higher price and the golden silver market very well Maybe in a very large abc structure on the way up Stay right there folks come right back down down 159 nazis are 42 s&p's are up four will come right back