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The Current Transcript for August 7, 2020

Host: Mark Kelley

STORIES FROM THIS EPISODE

Prologue

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'We had no hospital left': Lebanese doctor recounts aftermath of Beirut explosion

Guests: Sarah Haddad, Mariana Wehbe, Habib Battah

SOUNDCLIP

[Angry demonstrators]

MARK KELLEY: The streets of Beirut were filled with cheers yesterday for French President Emmanuel Macron as he toured the wrecked city. It's been barely four days since those same streets were filled with screams after a deadly explosion at the central port city. The crowds also begged him not to give aid or funds to the Lebanese government, whose corruption many blame for this week's tragedy. Regardless, it's food, shelter and medical services that are in desperate need today. Sarah Haddad is a doctor, a third year neurology resident at the St. George Hospital in Lebanon. She was across the street from the hospital when the explosion hit. Hi, Sarah.

SARAH HADDAD: Hello, Mark.

MK: Take us back to the moments right after that explosion happened. Where were you and what what was happening all around you?

SARAH HADDAD: Actually, first, I would like to thank you for having me, for knowing what happened during that day. All my years of training that was the first time that I would finish before 6:00 in the evening. So I just went home, which is just across the street from the hospital. And we were told that there had been a fire or a possible explosion, which was the first explosion that happened at the port of Beirut. And then the next thing we know, we were just blown away from where we were standing and sitting in the apartment all covered in glass. We heard two consecutive explosions and then everything just shook underneath us. And we weren't- we weren't able to know what had actually happened.

MK: Did you quickly head to the hospital at that point?

SARAH HADDAD: My first instinct was to just step on my white coat and just go to try to see what happened. For me, initially, I was thinking that the hospital is safe. The hospital is safe. People are going to need us there. The biggest shock was to actually see that we had no hospital left. We don't know what's happened to the people inside the hospital or we saw with people just across the street. They died on the floor, some were bleeding heavily, some were already dead. And we were just five people who were readily available at the moment it happened on the floor. So they started calling us to start evacuating people from the building that is just across the hospital, which contains the medical library and some dorm rooms for the nurses who work at the hospital.

MK: Who were who is helping you, Sarah? I can only imagine this was a scene of chaos where you've got so many people being rushed to the hospital and yet you're trying to evacuate the hospital at the same time. So how are you coping with all the injured?

SARAH HADDAD: Everyone who was injured was coming to the hospital because in everybody's mind, the hospital should offer help whereby we were the ones we needed help. Let me tell you, we didn't have any supplies on us. We were just assessing the scene, assessing who was severely injured and who was not severely injured. People were bleeding. We used their own shirt, their own clothes to try to stop the bleed, to put like a tourniquet on the bleed. Luckily, we had people on their motorcycles coming a first aid. The police were not able to reach us because all the roads were blocked. those people were taking people on their motorcycles to nearby hospitals. We made sure to call some of their families to just let them know that they are being transferred to the hospital so that they can go and find their loved ones there. But let me assure you, it was chaotic and we tried to do the best we can with the very minimal supplies that we had because we actually had none. We were not able even to suture people. All we did was just to calm them down, make sure that they were still responding to us, talking to us. Some were heavily, heavily injured; open head wounds, open abdomen wounds. It was just horrific.

MK: I can hear that in your voice, Sarah. And it it must have been so traumatising for you as somebody who is trying to provide care. How are things now and looking forward? I mean, how can you deal with this? We've heard of many hospitals in Beirut that were damaged. How are you coping with all the wounded in Beirut right now?

SARAH HADDAD: All the wounded have been displaced and have been sent to multiple hospitals in Beirut and outside Beirut. The medical teams and the hospitals that were not affected are doing an excellent job. Everyone was taken care of within the first 24 hours. Some surgeries were happening in the same night. No one was left. We were suturing and other hospitals were suturing people just outside the emergency rooms because they were all filled. We are trying to get back up. I can assure you that my hospital, we started cleaning the scene. We are going back to clean the scene to help assess the damages that happened. All the hospitals around us had been as well. Random people are coming and helping.

MK: There's an incredible spirit of the Lebanese people. But I also wonder, is part of you just angry that this happened in the first place?

SARAH HADDAD: Angry would be the least description of what I am feeling and what the Lebanese people are feeling because we were killed. Even those who are living, they are not living. Let me assure you that everyone has died, whether physically or whether on the inside. Angry in the lease. We are furious. We want our answers. We didn't deserve this to happen. No one prepared us for this. Not the people of Beirut. Not the medical team. Not our families. Not anyone. No one. No one prepares you.

MK: I'm so glad, though, to hear how many people volunteered to help you with your job. And I really hope you continue to have that support. I know the international community wants to do whatever we can to support you as well. Sarah, stay strong and hang in there.

SARAH HADDAD: Thank you. Thank you so much, Mark, for having me. Thank you so much for being able to just reflect on the one percent of the of the things that are happening and lead with. I'm very glad to have been with you.

MK: I'm very glad that we could speak today. Sarah Haddad is a neurologist in Beirut. Mariana Wehbe was front and centre while French President Emmanuel Macron was touring the devastation. She's a volunteer with Al-Balad, a soup kitchen in Beirut. She was on the street yesterday handing out sandwiches. Maryanna. Good morning to you. How are you doing?

MARIANA WEHBE: I think, like Sarah said. Well, first, I'm still processing. I'm still processing. We're still processing, getting a lot of flashbacks. I didn't grow up here during the war, so I don't know what it's like. And I walked over dead people to get home. So there's a lot of flashbacks that keep coming out throughout the day. So like Sarah said, we are alive. We don't know how we are alive, but we're actually, we're actually dead. We're shattered, completely shattered.

MK: But I know you're trying to feed people. And food insecurity it's got to be just rampant through the city there. We've heard 300,000 thousand people homeless. Describe for me what you're seeing on the streets as you're going out trying to help feed people. What are you seeing on the streets?

MARIANA WEHBE: Well, we're seeing the community come together. Actually, what we're seeing on the streets is the real Lebanese right now. You're seeing what Lebanon has been about for the past maybe 20 or 30 years. It's all about the community, the private sector, the citizens who kept the country standing. The only reason the country is standing is because of them, because of private initiatives and because of the NGOs. And the government had never, ever, ever supported any of these NGOs. So what you're actually seeing is the youth on the street cleaning. You're seeing men and women going into homes and asking what's needed. And everybody is getting in touch with every NGO that they know in every possible way to just get support to friends, family and people they don't know. This is what's happening on the streets right now.

MK: We heard about that, the those grain silos that that were devastated in the explosion that provided, you know, 85 percent of the grain and the wheat that's needed some basic staple, of course, bread. Where are you getting your food and how are you getting your food? Now, there just must be incredible rush to feed the people.

MARIANA WEHBE: We are - I don't know how - but we are getting calls left, right and centre to donate food. We've just got in today 900 meals for us to distribute because there's also a protest taking on tomorrow, a huge protest in Martyr's Square. And for all of next week, we have donors just coming in and saying, what do you guys need? We're sending you food. How many meals do you need? And we're taking anything we can get. Right now, to be very honest with you. It's complete chaos in our heads. There's so much taking place that we're not able to really sit and think where and how and how much quantity that we still have or anything like that. But for some crazy miracle, we're still getting food right now.

MK: You mentioned that that you've been very independent, working with the private sector or working with people, but not the government. How do you see the government now in Beirut and in Lebanon its role in your future?

MARIANA WEHBE: I don't see that they have any role in our future whatsoever. I see that they have absolutely no role in our future. They need to get out of here. The whole regime needs to fall. We are ready to kill them and hang them with our own hands. We have been going through this for the past 40 years of corruption, greed, sectarianism and everything else you can imagine. So I do not see any role of this government. We have absolutely no trust in them. And we want them out. We need, we need a miracle. We need good people. We need to properly work on the election and on the election now and we need a lot of education to happen very, very, very soon.

MK: You've wanted this. So many Lebanese have wanted this for so long. Do you think that this will be different than the protests have been going on for years? The demands have been going on for years. Will this explosion change your future?

MARIANA WEHBE: As horrific as it is, I don't know why. I have a small, tiny, tiny speck of a mustard seed of hope left. We'll have to implement change in the country. This is our last straw, in my opinion. This is the last straw.

MK: Mariane, I'm so glad that you are safe and you are helping your fellow citizens. I wish you well and I wish you strength.

MARIANA WEHBE: Thank you.

MK: Great to speak to you. Mariana Wehbe lives in Beirut. Tuesday's explosion has intensified the already dire situation in Lebanon. Unprecedented political economic meltdowns have dashed any hope for a smooth recovery from this latest tragedy. Happy Battah is an independent journalist, the founder of Beirut Report. He joins me this morning. Hi, Habib.

HABIB BATTAH: Hi t here.

MK: Is this the moment of change, in your opinion, Habib?

HABIB BATTAH: I mean, we would all hope so, but it's very hard to say. I guess some people have been worse affected than others. This will be written off by many as a negligence. And there's a lot of people to blame. There are many different authorities that are involved, many security [uninteligble], port authorities, customs authorities, ministries. They could pass the blame around to each other. The case has been in Lebanon is that violent and has been how we've gotten here. All the militias that took over during the war were taking over from other powers who they wanted to hang and kill. And so that doesn't, that hasn't really, you know, solved our issue, which is deeply a deep structural problem in this country with the way that the government has run. It's not really a government. It's a band of militias and they're competing over a contract. So what would happened with this case is that the ammonium was stored in this facility for four, six years because of disputes between different government authorities over who would have it and who would possibly sell it and get rid of it. It had come here by accident pretty much because the ship was not able to continue its course and was abandoned at that point if Beirut. So, you know, everyone is trying to help Lebanon in their own way. I guess that's the issue. And for their own objectives. And that's one reason we are here, that these militias should have all died out years ago, but they've been on life support, basically with money and weapons and political support from the same people who claim to be helping Lebanon today.

MK: Well, I heard our own government yesterday were announcing, you know, aid money that was going to head to Lebanon, but our minister was saying we have to find a reliable way or a reliable people to be able to give this money to sort of indicating that, you know, the international community wants to help and we'll help with money. But to your point, we don't know who to give the money to to make sure that it actually gets to the people and it doesn't end up in the pockets of corrupt politicians. I just wonder what this has revealed to what you have known all along is, says the Lebanese people, what is revealed to the rest of the world?

HABIB BATTAH: Well, I mean, the world has been involved in Lebanon for four decades. And I don't think that people don't know where to give money. I mean, I think that people, these decisions on where to give money are very specific. And they're studied and they're done so in a certain way. You know, France gives money to French schools. America gives money to English schools. So, you know, Iran gives money to Hezbollah. You know, the U.S. gives money to Lebanese police. The same police that are, you know, have been abusing and firing tear gas and riot police beating up protesters. So there's a lot of, I think that there's a lot of doublespeak here. Where money should be given, you know, it's very difficult. I mean, I think that Lebanon is also at a constant state of war with its neighbours. And and it's dealing with a lot of burden and the world should be helping with. Lebanon has the biggest refugee crisis in the world per capita. This problem should be shared by the countries who profited from the Syrian war, who sold weapons to the war. And those are the major countries. And Canada itself has also been very heavily involved in the arms trade with Saudi Arabia and others that seek to put a certain agenda in this country to further their interests.

MK: I know there're protests that are already planned. And as you're mentioning, this is a huge structural problem. Just give me an idea, Habib, in the short term, what do you need now?

HABIB BATTAH: We need food. We need- our grain silos, our strategic reserves have been blown apart. I mean, it's an enormous building that is just gone. All of the wheat is floating into the Mediterranean Sea right now. So literally, our economy has become one with the sea, the entire port of the country, which is the bane of the economy, which is so essential at a time of currency collapse, hyperinflation. People have lost 80 percent of their currency value. The port of Beirut is an essential organ to the economy that has been wiped out. Just imagine what it would be like to lose the country's primary port. Any country in the world, especially one that has no manufacturing industry. So we are a trading country, unfortunately, that doesn't produce things. So we're totally reliant on the rest of the world to get there. The damages are 10 to 15 billion dollars. And Lebanon was already asking for 10 billion dollars before the explosion. So Lebanon needs so many billions of dollars. It's unimaginable how to get out of this hole. And the issue is, you know, Lebanon is always rebuilding itself. How many times has this country rebuilt? How many times have these shops that I've seen on television, how have they rebuilt their glass facades? We've had, you know, the war, we've had terrorist attacks all throughout the 90s and the start of 2000 and 2010. So who's going to pay for this? How many times? And the more that we- every time we rebuild, we go into more debt. The recent [unintelligible] today are constantly trying to rebuild a country that's constantly at war. And so you can't really build an economy, bounce back from a war if you don't have peace. And again, this ties back to the fact that not a lot of countries say they want to help, but they're not really truly interested in a peace in Lebanon because they would they wouldn't want to compromise their interests. So, you know, we do need medical supplies. You know, we lost three hospitals at a time of pandemic when there's no ICU beds in the country. So we need urgent medicine. A warehouse containing essential vaccines and PPE was destroyed. And there was already a huge shortage of that in the country. Shelter, two or three thousand people without a home, sleeping with no windows, trying to sleep with friends or different family. And people rely on [unintelliglbe] to survive in this country. They rely on each other, they rely on friends. And they don't rely on the government. But, you know that there are some who do in some ways in terms of patronage and that kind of thing. So, I mean, people need the basics at this time before we try to solve the miracle. We need to get aid to go very fast that are hungry. They have no place to sleep. And our hospitals are overwhelmed. Our hospitals are collapsing even before this, you know, because of the currency devaluation, the Venezuela type situation of Lebanon where the hospitals can't even pay their bills. They can't even afford to buy medicine. That our currency is almost worthless. So I think we need to really shift our focus to support these people have been through so much and no one chose to live this way. You know, over the years, the different powers have blamed people and said, you should do this, you should vote for [unintelligible]r. You know, it's not so easy when you're in a situation of desperation. You try to get help from wherever you can. And that's been the case in Lebanon. It's very easy to say that these parties are terrible and horrible. We should support them. But often people who say that are not those who are hungry, who don't speak foreign languages well, who we don't hear from in Lebanon, it is those who do rely on these parties for their basic needs in their hospitals, schools. They have no choice of their own, because they have no other choice. So and again, these infrastructure networks, these Patrias networks, again, are supported by foreign powers. So I think we have to often ask ourselves, does the world really want to help Lebanon? Are they going to do some soul searching on the parts that they support? Can they put their political interests aside and just help? Because most help, unfortunately, comes with strings attached. And no foreign aid is charity. And I think we should really understand that and ask deeper questions of our own government and what they do in the Middle East and what weapons they fell in the Middle East and where those weapons end up. And they end up often in places like Lebanon.

MK: Habib, I know this is a moment of reflection for so many people in Lebanon. But I also hope this is a moment of change for you all. Change for the better. Hang in there and thank you so much for talking to us.

HABIB BATTAH: Thanks so much. We all hope that. We all hope to see a better a better future. It's a beautiful country and it has so much potential. It just needs to be given a chance. People need a chance.

MK: Yes, I agree with you on that. Thank you. Habib Battah is a former is a founder of the Beirut Report. We were speaking to him in Lebanon today.

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COVID-19 Update

Guest: Andre Picard

[clip] [/clip]

SOUNDCLIP

Sometimes it takes a disaster for society to realise that there's flaws in the system and it needs to be changed.

MK: Henry Tomaszewski isn't the only one calling for change in how we care for our seniors. His mother, Maria, passed away from COVID-19 when an outbreak tore through her long term care home. The number of deaths in these homes has many calling for Canada to develop a better system. Andre Picard is the Global Mail's health columnist. He's been joining us each week during the pandemic. Morning, Andre.

ANDRE PICARD: Good morning.

MK: Andre, for you as a health columnist, what has this pandemic revealed in terms of sort of the ugly truth about the way we care for our seniors in this country?

ANDRE PICARD: I think it's showing a real disdain for our elders. It's shown that ageism is built into our social policy. You know, we have hundreds of thousands of people in institutions and one of the highest rates in the world of institutionalisation of seniors. So that shouldn't give us pause. And then what's happened during this pandemic is, you know, this 80 percent of all our corporate deaths are in these homes. And it just tells us they're not built for people to live. They're built- they're places for people to die. In French, we have a word called 'mouroir', a place you go to die. And that's what these have become, sadly.

MK: You've written about the toll the pandemic has taken on people living with dementia specifically. Tell us about that, just how devastating that's been.

ANDRE PICARD: Well, we go back to these homes and these homes are in large part occupied by people with dementia. You get to a certain point in your care where a candidate just doesn't have adequate home care. And our home care is designed for to take care of people post surgery. So if you're living at home, it becomes almost impossible for family caregivers to care without support. So people end up in these homes. And, you know, if you do the maths, both 80 percent of people in Long-Term Care have dementia. 80 percent of our deaths are in these homes. So it's the vast majority of people in Canada who've died of our pandemic are actually people with dementia. And we don't often think of it in those terms. But again, it's just an example of dementia is something we kind of treat as a death sentence. And it shouldn't be.

MK: Now that that that the pandemic has revealed these uncomfortable truths, what would we do about it as a country? What do we do to address this situation?

ANDRE PICARD: Well, I think that's our big challenge is to say how can we take better care of our elders. And we there are a lot of examples around the world, the one that's always pointed to his Denmark. Denmark has a tremendous respect for its elders. It doesn't have these huge institutions. Some people are institutionalised for their own good. But it's in smaller, homelike settings. It's not in prison like settings. They are integrated into the community. Every effort is made to allow people to stay at home and only as a last resort you go to an institution. And in Canada, we have the opposite. The first, our default is institutionalised. And only if you're fairly wealthy and really [unintelligible] and couldn't sacrifice your career can you keep your parents and your grandparents at home.

MK: I just want to switch gears here, lots to talk to you about this morning. This week, Ottawa signed a deal with two pharma companies, Pfizer and Moderna, for a potential COVID-19 vaccines. I'm seeing this happen in other countries as well where they see everybody seems to be rushing to these pharma companies to sign up. What do you make of what's going on right now?

ANDRE PICARD: Yes, it's a pretty normal people getting procurement contracts or, you know, that something's coming. So you want to get in line and make sure that you're going to get the product. Now, in this instance, it's a bit unusual because we don't have a vaccine yet. So people are kind of hedging their bets. Canada has signed contracts with Pfizer and Moderna hoping, you know, these are going to be groups that get successful vaccines. And what this contract does is guarantee us a certain supply. Now, the problem with the Canadian deal is we have a real lack of detail. We don't know how much money is being spent. We don't know how many doses of vaccines. Other countries have been much more transparent about their purchases.

MK: Are there concerns, Andre, that there just won't be enough? I mean, everybody, as you say, we're rushing to get in line. Just how long is that line? And will we be. Will these companies be able to satisfy everyone in line?

ANDRE PICARD: Well, we you know, we're not going to be able to vaccinate 36 million Canadians, seven billion people around the world all at once. They're going to be waits and we're going to have to figure out how do we do it ethically, who gets it first, et cetera. The other complication is it's not just getting in line. It's figuring out what line to be at. We don't know who the successful vaccine candidate is going to be. There are 200 vaccine projects around the world. Six of them have advanced to the stage of human trials now. And these two that Canada has and most countries have bet on are at that stage. So they're pretty advanced. But we just don't know if they're going to work.

MK: I want to talk to you well, about the back to school programmes that are that are being discussed across the country, provinces now coming out with their plans. There's still I'm hearing a lot of concerns from parents I know here in Ontario, been reading about parents who are worried that they're not reducing class sizes and that this is just an accident waiting to happen. What do you what do you make of our back to school strategies right now? Are we getting it right?

ANDRE PICARD: I think there is a lot of confusion now about what how to do it right. And I think the answer is that there's no right way when we look around the world. The evidence kind of all over the place. There are big infections in some countries. There's nothing in other countries. So I think we just have to. I've been saying this for a few weeks on the show. You have to make a plan and give people something to digest. So what parents want is some certainty. Tell us what's going to happen then we'll make a decision. Do I send my child back or not? So a lot of the debate now is around masking, you know, should kids have to wear masks and. The trend is going towards yes. So that's getting settled in. The big one is how many kids it's safe to have in a class. We have very large class sizes in Canada, 36. I think the what we're learning from other countries is probably no more than fifteen. We'd be safe for or smart. So I think we have to really address that class size issue for the mental health of parents and for the health of children.

MK: Well, on the level of the health of children, I mean, there seems to be this belief out there that the kids don't acquire the virus as much, they don't transmit the virus as much, that they're less of a vote of a concern because of that. Is that a false sense of security?

ANDRE PICARD: That is a false sense of security. That's something that was a belief early on then. It's kind of been withered away. We know that kids get infected at the same rate. They don't die of the same rate. But we can't use mortality as the measure of should kids go back to school. You have to figure out, will they get sick? Will they transmitted to other people who are more at risk, like their grandparents, their parents, their teachers. So it's a complex calculus to be done here. But we have to dispense with this notion that kids don't get sick. It's not true.

MK: Andre, it's always good to talk to you and get your insight. Thanks so much.

ANDRE PICARD: Thanks, Mark.

MK: Andre Picard is a health columnist with the Globe and Mail. He is in Montreal today.

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Episode five of CBC podcast Unlocking Bryson’s Brain

MK: We continue the CBC podcast Unlocking Bryson's Brain with Episode five, Making a Mouse. Today, scientists in Toronto get to work building a mouse with Bryson's precise genetic variant. And the family travels to Atlanta to provide blood samples for a researcher to create DNA based mini brains in his lab. Here's host Anne Bryson's dad, Keith McArthur.

SOUNDCLIP

KEITH MCARTHUR: We're walking down a long corridor in the medical sciences building at the University of Toronto. Room after room is filled with hundreds of small cages, and each cage contains two or three lab mice. Our tour guides are scientists Amy Ramsey and Catherine Ensign. They're studying mice with mutations in their Green One genes, the same gene where my son Bryson also has a life altering mutation. Amy takes my wife, Laura, and I into a cramped room with mouse cages stacked high and deep.

AMY RAMSEY: OK, so we're in the mouse here right now. They have little houses that keep them, keep them with the illusion that they're in their own little den and they use these cotton material to make little nests. In this room, we probably have 20 different strains of mice that have different mutations. The numbers that we want to see are NLX. Those are the mice. Did you find them? OK, so they're over there.

KEITH MCARTHUR: Catherine opens a cage that contains three mice. Two are what researchers refer to as wild type. Their DNA is typical. The other mouse has a mutation in its GRIN1 gene. There's something surreal about seeing this mouse for the first time, because even though it's nothing like Bryson, this mouse and my son, they have a similar change in their DNA. And so I feel a weird bond with this tiny creature.

CATHERINE ENSIGN: So do you see how he has those scabs behind his ears?

KEITH MCARTHUR: The mouse has been scratching himself repeatedly behind his ear. It's abnormal behaviour. And Catherine points out that it's not totally dissimilar from what she's seen in people with GRIN mutations.

CATHERINE ENSIGN: So a human may not necessarily do this, but I've noticed that within a lot of your kids, a lot of them have what we call stereotype behaviours, where they do some kind of repetitive behaviour, either as like a self soothing mechanism or, you know, maybe as a consequence of their seizures. It's not really clear to me. But this guy's repetitive behaviour is scratching himself behind the ears. He's also jumpier. So see how I touch him. And he's a lot jumpier. Whereas if I touch the wild type mouse, you know, like there's not much happening here. He's not bothered by me touching him because he doesn't perceive that as being aggressive.

AMY RAMSEY: Those two are not aren't while type.

CATHERINE ENSIGN: Those two are wild type. And what else can you see here just from looking at them? What how does that one look differently?

LAURA: He's much shorter.

CATHERINE ENSIGN: Much shorter. Yes. Also darker. So within our mice, the change to the NMDA receptor actually changes their colour.

KEITH MCARTHUR: They don't really know why the mouse with the GRIN1 mutation is a different colour. But this is important. It's a reminder that those NMDA receptors that are impaired by presence mutation, they're not only in his brain, they're in other parts of his body, too. Most kids with GRIN1 look typical. They don't have the dysmorphic facial features that are common with some rare diseases. But in these mice, the mutation changes the way they look. And just as most people with GRIN1 have low muscle tone, the mutant mice have similar symptoms. If you take a mouse and hold him upside down at the top of his cage, a typical mouse will wrap his little paws around the wires and hold on for dear life.

AMY RAMSEY: So this is a wild type mouse and you can see that they like to hang onto these. They're reaching for it. And I'm tagging, you know, of course I can pull them off. But. I can feel their resistance. And then this is the mutiny and, yeah, he doesn't, he's not able to hold on as well.

KEITH MCARTHUR: Amy’s team engineered mice with a GRIN1 mutation and a kind of built in on off switch when the mice screw up. They turned off the mutation. And then they performed a bunch of tests on these so-called rescue mice. What they found is that after the mutation is switched off, these mice become much more like wild type mice. They put on weight. They become more social. They get better at solving mazes over time. Even the colour of their fur changes back and their grip their ability to hang upside down from the bars of their cage, that improves, too.

KEITH MCARTHUR: And so with the rescue mice, we would see something in between.

AMY RAMSEY: They actually hang on very well. Did not report that in the in the paper, but we did the tests just like this, you know, not with the stopwatch, but it was very clear that that part was rescued. Yes. Do you want me to- is there more you'd like to- I mean...

KEITH MCARTHUR: Can I hold one.

AMY RAMSEY: Sure. OK. So what you want to do is just grab him by his tail. Right there.

KEITH MCARTHUR: Yes.

AMY RAMSEY: OK. And then put your other hand in. Don't let go of his tail. It'll jump off.

KEITH MCARTHUR: Hi little GRIN1 mouse. [Unintelligible] [laughs].

AMY RAMSEY: [Laughs] They do that.

KEITH MCARTHUR: Amy's mice have a generic mutation. She's manipulated them to lower the expression of the GRIN1 gene. But we're talking with other researchers about using crisper cas9 to create a mouse that has Bryson's exact mutation. This could help us to better understand what's going on in Bryson's brain and potentially use that information to identify a cure.

MIKE SALTER: So I'm just trying to get sort of even closer together.

KEITH MCARTHUR: I don't really like him.

KEITH MCARTHUR: Mike Salter is head of research for the Hospital for Sick Children and Graham Collingridge with the English accent, he's director of the Tense Centre for Research in Neurodegenerative Diseases. They're two of the world's leading experts in NMDA receptors and they're both here in Toronto and NMDA receptors. You might remember our proteins in our brains related to GREN one and six other GREN genes. I'm here with Laura to talk to Mike and Graham about their plans to make what we've come to refer to as a price in mouse. Technically, it's known as a GRIN1 G 620 R mouse bat number 620 refers to the fact that it's the 620th amino acid in Bryson's Green One DNA that isn't typical. That's where the glycine represented by the G has been replaced with R-gene, which is represented by the letter R.

KEITH MCARTHUR: Can I ask one of you to try to just, I guess in layperson's terms, just explain the role of the receptor and why a mutation like the one Bryson has could sort of impact someone? Just generally how it could change how they how they function.

GRAHAM COLLINGRIDGE: So the NMDA receptor is a protein. It's expressed that practically every excitatory sign ups in the brain. So the human brain has about a 100 billion neurones. Each neurone is connected on average 1000 times to other neurones. So we have something in 100 trillion, sorry, 100 trillion synopses. Nearly all of those synopses just have Adam datasets. So it's very, very important in the brain.

KEITH MCARTHUR: You may have heard the saying cells or neurones that fire together wire together. It's a tidy summary of the work done 70 years ago by pioneering Canadian psychologist Donald Hebb. Put simply, the more times we do something, the better we are at remembering how to do it. Think of your computer passwords. You'll easily remember the ones you use every day, but the one you only use every few months. That password is much harder to remember. And NMDA receptors, they play a key role in strengthening neurones. So you remember your passwords or anything else.

GRAHAM COLLINGRIDGE: So if you activate the NMDA receptors in a certain way, the [unintelliglbe] will get stronger if you activate the enemy, etc. in a different way. The sign ups will get weaker and that change could last minutes, hours, days or even lifetimes.

KEITH MCARTHUR: That's what's supposed to happen. But for Bryson and others with grim disorders. The brain chemistry is out of whack.

GRAHAM COLLINGRIDGE: And so if there's a change in that receptor, then it will affect, potentially affect, the ability of the sign ups to undergo this plasticity and hence have impact on the ability to learn and remember in every domain, depending on where the mutation is expressed. So it could affect day to day learning and memory mechanisms, the sort of explicit learning that we are consciously aware of. Or it could be more compressed memories, the memories that motor skills or the ability to sense pain.

KEITH MCARTHUR: This mention of pain is interesting. It raises something we've always wondered about with Bryson, and pain is Mike's speciality when it comes to the NMDA receptor.

KEITH MCARTHUR: One of the things we always notice when Bryson was little, it was that it seemed like when he when he hit his head or something, he didn't seem to react to pain. So it's possible that could be tied to the variance in the gene and the receptor, right?

MIKE SALTER: Yes, it could be. And so I think we're starting to see some evidence for that in some of the animal models we work on where if it's particularly if you have lower NMDA receptor function, some of the animal models will have less pain.

KEITH MCARTHUR: Obviously, our interest is in getting to some kind of cure. And I think, you know, both of your talks gave us some hope that for a number of different reasons that it's possible that there could be something that could change his life quite dramatically. But what do you think that the timing is in terms of if that were possible, how long that might take?

GRAHAM COLLINGRIDGE: That's very hard to answer that. The best hope is that if we see a dramatic change, that we are consistent, a dramatic change, then we can manipulate in the mouse model using an existing available compound.

KEITH MCARTHUR: What he means by that is they're going to test a bunch of different drugs on this mouse and see if any have a positive effect, because if these drugs can rescue a mouse with Bryson's mutation, they may be able to rescue Bryson too. Making a specific mass. Using crisper casts nine technology is usually straightforward, but sometimes it's tricky. Not all mutations take easily. And some make breeding a colony of test mice a challenge. But now that the mouse process is underway, I want to know what other avenues we should pursue to leave no stone unturned in our quest for a cure. Mike mentioned something called induced pluripotent stem cells, or IPSC cells. It's a relatively new technology that allows scientists to take human blood or skin cells and convert them into almost any other kind of tissue using that person's DNA. They can even use these cells to create cerebral organoids, miniature human brains that live inside a petri dish. From a few of Bryson's cells, they could create a mini brain with his exact DNA. This might provide more clues about what's going on in his brain and give us another avenue for testing potential cures. So what would be the next steps then if we wanted to to try to get those stem cells made?

MIKE SALTER: So, I mean, we'd have to trying to think of the logistics because all of these done are done under research protocols. So we'd have to set up a research protocol to do that, get approval from the Research Ethics Board for that protocol, then have that set up in a way that we would.

KEITH MCARTHUR: So, yes, it's complicated. There are hurdles to clear and funding to figure out and probably a long wait to get to the front of the queue and actually get these made. But I ignore all this and focus on the fact that they have a colleague who runs a lab making IPSC cells.

KEITH MCARTHUR: So if we want to I mean, if we want to kind of push to explore as many points as possible, when we reach out directly, there is something more that, you know, depending on where your research goes, you would reach out.

MIKE SALTER: Well, I think it's probably easier for us to do it. And I think my sense would be, let's see what happens with the mice.

KEITH MCARTHUR: So they want me to be patient. But when you have a kid with a rare disease, that's tough. I set aside the idea of getting mini brains made for now and focus on helping Mike and Graham learn as much as they can from the Bryson Mouse.

KEITH MCARTHUR: Is it helpful for you to know sort of the details of the phenotype of the patients? Like, should we do some kind of survey with them to give you kind of their background and whether they have seizures and all those kinds of things?

MIKE SALTER: I think to be extremely useful for some information. Absolutely. And we can work out any common areas and areas where there are differences. We'll be very informative.

KEITH MCARTHUR: So I've got some homework to do.

[Music]

KEITH MCARTHUR: As more and more patients get diagnosed with grim disorders, the number of people we know with Bryson's precise mutation also grows. From to with Olivia to three with one all the way up to seven. Unlike Olivia and Owen, the other four are younger than Bryson, two are in the US. June from Virginia and John from New Jersey. And there are two little girls from Europe, Bethany's in France and coincidentally, another Olivia in Spain. The twins have become septuplets. I put together a survey with input from Graham and Mike and asked the seven sets of parents to fill it out. As I get back the completed surveys, I see that these kids have a lot in common with Bryson. Most startle easily or are bothered by loud sounds. All of them have sweet, loving personalities, though several go through periods of out of control rage. Most have movement disorders involving uncontrolled flapping or beating of arms, legs and feet. And most parents report that their kids seem to feel less pain than typical kids when they hurt themselves. But it's the differences that intrigued me most. How June is much younger than Bryson, but already has dozens of words. How Gwen and Olivia both began walking independently around age five. But none of the other kids can do that yet. Bryson is the oldest of the kids who can't walk. So I start to worry that maybe it's our fault as parents. Have we not done enough to help him? But Laura reminds me how much physiotherapy we've done with Bryson over the years, including sending him to a special school for intensive physiotherapy three days a week over several years. There's also a big difference when it comes to seizures. Bryson has had these seizure like episodes for most of his life, though they've never been recorded on an EEG. Five of the kids don't seem to have seizures, but the 7th has seizures confirmed by EEG. So why so much difference amongst seven kids who all have the same mutation? We don't really know, but there are probably at least two factors that contribute to these differences. The first is environmental, everything from a child's birth experience to a kind of infections they were subjected to as infants, to whether their development has been set back by seizures. But the other factor may be the bigger one is the rest of each child's DNA. For these kids, walking or talking might be a nearly impossible task. Something like you or me running a four minute mile or memorising 60000 digits of pi. Your healthy DNA plays a big role in whether you can do these things. So why wouldn't it be the same for these kids who share one mutant gene but have inherited thousands more from their parents? I can't help feeling disappointed that maybe Bryson is a little behind in this cluster of kids with the G 620 R mutation. Though I'm genuinely so happy for the strides made by these other kids. I've met most of them, and honestly, they're some of my favourite people in the world. And that mass we're building, it's not just a Bryson mouse. It's also an Owen mouse, a June mouse, a June mouse, a Bethanice mouse and an Olivia mouse twice over. And it's a mouse that could help us find a cure for many more kids. Yet to be diagnosed with Bryson's condition.

[Music]

KEITH MCARTHUR: Hi, Laura, I'm downstairs.

LAURA: I'm on my way, give me two seconds.

KEITH MCARTHUR: Thanks so much. Bye.

[Music]

KEITH MCARTHUR: Another day, another mouse lab. Today, Laura and I are at the Centre for Pheno Genomics, the downtown Toronto lab where researchers are using crisper cas9 to make a mouse with Bryson's precise Green One mutation. We're meeting Laurel Nutter, who's the lab's head of science and technology development.

KEITH MCARTHUR: It's great that you're able to come.

LAUREL NUTTER: Yes, I wanted to be here so I get to see what we can learn.

KEITH MCARTHUR: What we should find out if any of the [unintelliglbe] mice took with the mutation.

KEITH MCARTHUR: Hi. Good to meet you.

LAURA: Good to meet you.

KEITH MCARTHUR: This is my wife, Laura.

LAURA: Nice to meeat you, Luarel.

LAUREL NUTTER: So welcome to the Centre for Pheno Genomics. Just to give you a bit of background, we are a jointly owned research infrastructure.

KEITH MCARTHUR: We're here to learn how they make genetically modified mice using crisper cas9. But the biggest thing we want to know is whether Laurel's team has been successful in making the mouse that Michael Graham ordered up. We don't have to wait long to get our answer.

LAUREL NUTTER: And then we also do a lot of bespoke models like this, GRIN1 neat model that we've made, which we have founders' for. By the way, we got the genome typing last week.

KEITH MCARTHUR: So we have the first generation mice.

LAUREL NUTTER: Yes. Yep. Oh, yes we did. I have the sequencing stuff up on my computer. I can show that to you.

KEITH MCARTHUR: In her office. Laurel takes us through the process for making a mouse.

LAUREL NUTTER: The way this works. So the normal DNA sequencing for yours was a G G G. So encodes a glycine here. Right.

KEITH MCARTHUR: So it starts with a careful analysis of the DNA sequence. She's trying to modify.

LAUREL NUTTER: And so where this used to encode a glycine and now encodes an arginine.

KEITH MCARTHUR: Which is a much bigger amino acid.

LAUREL NUTTER: So glycine is very small and flexible and I think it's non polar, whereas arginine is charged and it's bigger and so it's less flexible. So it probably affects how the protein folds in on itself because the charges are now interacting and it's saying, I don't want to be next to you, so get away from me kind of thing.

KEITH MCARTHUR: She studies the letters in the DNA around the mutation to find a suitable 20 letter sequence for crisper cost nine to identify and target. Then she orders this 20 letter sequence from another lab.

LAUREL NUTTER: So we engineered a guide RNA or synthesise a guide RNA that was complementary to this site so that it targets the cas9 here and results in the introduction of a double strand break.

KEITH MCARTHUR: In other words, these crisper cas9 technology to cut out the typical sequence of DNA and replace it with one that mirrors Bryson's. The next step is to get this genetic code into an actual mouse. Laurel takes us to the lab where this gets done before crisper. Building a mouse was a slow and costly process.

LAUREL NUTTER: So you take, you know, on average, what, one to one and a half years to go from an idea to a mouse on the ground.

KEITH MCARTHUR: But with crisper if all goes well, the process can be completed in two or three months.

LAUREL NUTTER: It's like moving at light speed.

KEITH MCARTHUR: They start with a healthy pregnant mouse and remove her embryos, then inject the DNA mixture into each embryos nucleus. Or they can place a bunch of embryos inside the DNA mixture and infuse all of them at once with an electric charge. Then they implant the modified embryos into surrogate moms. The process isn't perfect in Bryson's case. They implanted dozens of modified embryos in the hope that two or three would be viable founders for a colony. It wasn't supposed to be part of the tour, but we asked Laurel if she'll take us to the area where the Bryson mouse is stored.

[Music]

KEITH MCARTHUR: We get in the elevator and go down four stories underground.

KEITH MCARTHUR: And is this all mouse food?

LAUREL NUTTER: Yes.

KEITH MCARTHUR: Okay.

LAUREL NUTTER: So it's all it's all irradiated and sterile because this is what we call it, a specific pathogen free facility.

KEITH MCARTHUR: Laurel asks us to put on lab gowns and takes us through an air shower designed to blow off any particles that might contaminate the mice.

LAUREL NUTTER: So go into this room and the windows start blowing. Basically, just, well, raise your hands. Your hands are turn around to make sure everything gets run off. And then the other side, if you feel uncomfortable or something, there's an emergency button there if you feel claustrophobic or something like that.

KEITH MCARTHUR: Going into the air shower. It's going to be loud.

[Loud noise]

KEITH MCARTHUR: This sterile environment is built a whole 36000 mouse cages, nearly a thousand per room. Much of the process is automated. We see giant robots like you might find in an assembly line in an auto plant filled cages with clean straw so that each mouse house is exactly the same. And other robots that dump out the dirty straw and sanitise the cages.

LAUREL NUTTER: On the other side of this wall is what we call holding A. And that's where only a subset of TCP staff are allowed in there. That's where mice are kept very restricted. So this is all the mice that were first making are on that side to make sure they don't get mixed up with anybody and nobody is not supposed to be using them sees them.

KEITH MCARTHUR: So the 620 green mouse will be over there.

LAUREL NUTTER: Yes. Yes, exactly.

KEITH MCARTHUR: That affection I felt for Amy's mouse, I feel it even more now knowing that the Bryson Mouse is so close. But we're not allowed to see him. The final step is to breed a suitable colony so Mike and Graham can start their experiments.

KEITH MCARTHUR: And how old are they when you start to breed them?

LAUREL NUTTER: The females reach sexual maturity about six months of age and the males about eight weeks. So usually [unintelliglbe].

KEITH MCARTHUR: Mice are pregnant for about three weeks. So the hope is that after that, Mike and Graham will have the start of a colony of Bryce and mice. They can breed for testing. We could have answers within months.

[Music]

KEITH MCARTHUR: But the results from another experiment are already in. Back at the family meet up in Pittsburgh, we signed up to get what's known as a functional analysis done for Bryson's variant. Researchers do the tests by injecting mutated genetic code into frogs' eggs and then applying different chemicals such as glutamate and magnesium. When things are working properly, NMDA receptors function like a system of rivers and dams that open and close to keep brain communication at optimal levels. But in kids with GRIN variance, a chemical imbalance messes with the flow. If there's not enough sodium flowing through the rivers, that's probably a loss of function mutation. The whispering kind. But if the dam doesn't block the flow enough, too much flows through. And that's probably a gain of function. The yelling kind. Finding out which type Bryson has can help us get a better sense of what's going on in his brain and what types of medications might help. But Bryson's results are mixed. There's not enough sodium heading into the rivers. But at the same time, the dams are too small to properly block the flow. So the researchers, they're not sure if this is a gain or loss of function. But other scientists who look at the results think the lack of dams is the biggest factor. Which would make this a gain of function. So after consulting with Bryson's neurologist, we've started giving him magnesium supplements to bolster those damps. We've also put him on a prescription for Memantine. That's a drug that's usually prescribed for Alzheimer's patients, but it's known to slow down the NMDA receptor. But the meds, it's hard to tell if they're working. I'm amazed at how much has come out of our decision to host the GRIN1 family meet up in Toronto. Not just the mice, but building relationships with these researchers as well. I chat regularly with Amy Ramsey. And one day she mentions that a researcher she knows in Atlanta is looking for GRIN patients willing to provide blood samples. He's making [unintellible] cells and many brains. And Amy wants to know if we would consider travelling to Atlanta to be part of his study. Five weeks later, I'm on a plane with Laura, Bryson and his big brother, Connor. I think I mentioned this before, but travelling with Bryson, it's not easy. In the past, we've been able to keep him safe on a plane by buckling him into a car seat. But now Bryson's twelve. And he's outgrown car seats approved by the FAA. So this two and a half hour flight to Atlanta, it's the first time Bryson will be on a plane in a regular seatbelt. He has one big seizure like episode. And another time, Laura, it turns back to see Bryson completely upside down his back on the seat and his legs in the air. But mostly he's pretty calm. So the biggest challenge is that he figures out how to undo his seat belt. Thirty six times he unbuckles and 36 times I buckle back up. I count not because I'm annoyed, but because I'm actually overjoyed at this development.

[Pilot talking to passengers]

KEITH MCARTHUR: Since we're hauling the kids to Atlanta so they can basically get needles, we try to have fun, too. We go to the Georgia Aquarium and all you can eat pie buffet and visit the world of Coca-Cola where the highlight is you get free samples of Coke products from around the world. Connor makes it his mission to sample every single one.

CONNOR: I like Rasberry.

KEITH MCARTHUR: How many of that?

CONNOR: 261.

KEITH MCARTHUR: But the real reason we're here is to give blood samples.

ZHEXING WEN: Hi. Laura?

LAURA: I'm Laura.

ZHEXING WEN: Nice to meet you. Hello, Bryson.

KEITH MCARTHUR: Nice to meet you. How are you?

ZHEXING WEN: Maybe we can go up there. OK.

KEITH MCARTHUR: In order to compare Bryson's DNA researcher, Zhexing Wen also wants samples from me and Laura and Connor volunteers to provide blood as well, in the name of science. Zhexing has made us an appointment at Emory Brain Health Centre. We start with paperwork, signing to confirm that we're giving informed consent to be part of the study.

ZHEXING WEN: So basically, the first page, it just goes everything that this is indeed a study understanding. This study is mainly for dystonia, but we can look at other disorders as well.

KEITH MCARTHUR: And then it's time to draw the blood. Laura, Connor and I are easy. But Bryson. He doesn't want that needle anywhere near his veins. He's strapped into his wheelchair and Laura and I are both trying to hold him still while the technician inserts the needle, but Bryson's thin veins are hard to find at the best of times. The needle pops out and blood shoots onto the floor and the technicians pants, he's had enough. He tells us he has no experience drawing blood from kids like Bryson. And he's too nervous to try again. We scrambled to find someone else who can take Bryson's blood. And after a bit of calling around a paediatric neurologist at Emory arranges for us to get the blood taken at the children's hospital on campus. The nurse there is a pro. She's used to challenging cases and she's successful at getting the blood we need. We head to Zhexing lab to learn about how he makes these organoids.

ZHEXING WEN: So here is the [unintellible] we are growing organoids, and you can see, so you can see the organoid there.

KEITH MCARTHUR: So how big are the organoids.

ZHEXING WEN: So the diameter is about four or five mm.

KEITH MCARTHUR: Four or five mm. So half a centimetre. Well, that's big.

ZHEXING WEN: Yes, yes.

KEITH MCARTHUR: Each of us begins life as a single cell. A fertilised egg that contains DNA instructions to make an entire person. The cell splits, then splits again and again to form stem cells. These stem cells are like a blank canvas that have the capacity to become any cell in the human body. Some become bones. Some become muscle. Some become brain tissue or other organs. Until recently, scientists thought this process couldn't be reversed, that an evolved cell couldn't be turned back into a stem cell. But in 2006, the year Bryson was born. Japanese scientist Shinya Yamanaka figured out a way to turn almost any cell back into a blank canvas.

[Music]

KEITH MCARTHUR: It's kind of like if could take almost any cell in the body and reverse engineer it into something almost like a stem cell.

ZHEXING WEN: Yes, yes. That's called IPS cells. And it was proper than stem cell.

KEITH MCARTHUR: But that's not all. Once they've got the IPS cells, scientists can grow a rough version of a synthetic embryo. And from that, they can cultivate organoids clusters of cell tissue that can roughly approximate the function of human organs such as liver, kidneys or even brains.

ZHEXING WEN: So, first of all, find the IPS cells, we'll make the 3D structure called the embryo body.

KEITH MCARTHUR: From there, Zhexing's gassings team will introduce different chemical compounds that will induce this synthetic embryo to grow into a cluster of cells from a specific part of the brain. Scientists are already using organoids to learn more about diseases of the lung and brain. And they're exploring whether organoids could be used as treatments for specific diseases. For example, Dutch researchers have tried transplanting kidney organoids into mice. The organoids aren't close enough to actual kidneys for this to work yet. But if and when I need another transplant, is it possible that one could be built in a lab for my own cells, one with my exact DNA so there's no risk of rejection. But perhaps the biggest near-term promise for organoids is personalised medicine. These many brains that Dr. Wen is building will contain Bryson's exact DNA. So he can test a bunch of different drugs to see if any have the desired effect on Bryson's NMDA receptor. He's tried a similar approach, using organoids made with stem cells from people with Fragile X and other genetic condition that leads to cognitive impairment. And he's found at least one drug with promise as a potential treatment. He hopes to provide us with some early results within months.

[Music]

KEITH MCARTHUR: A visit to Atlanta also allows us to meet with Steve Traynellis, his team did the functional analysis using Frogs' legs.

STEVE TRAYNELLIS: Hi, Laura.

LAURA: Hi. Steve. Nice to see you.

STEVE TRAYNELLIS: Nice to see you. Is this Bryson? Hi. How are you doing, Bryson? Good to see you, buddy.

KEITH MCARTHUR: Steve has been researching GRIN mutations for years. So I want to get a sense from him about whether I'm tilting at windmills in the search for a cure. Is there really a chance that we could find something that will help Bryson? Or is this all just a father's fantasy? He tells us that until he saw Amy Ramsey's work. He didn't actually think it would be possible for there to be a cure that would help an older child or adult.

STEVE TRAYNELLIS: I think I was always very cautious and was not certain that in an adult or a developed child, that if you simply replace the gene after the brain has undergone its full development, that you'll be able to unwind what had been done. And so I think I think that's, you know, that that was my posture and particularly something like GRIN1, which is, you know, present as early as it can be and involved in all of the connections. And I guess I was surprised that she could turn back many of the phenotype.

KEITH MCARTHUR: So how likely do you think that cure is going to be for at least some people with GRIN disorders? And how long until we might see that?

STEVE TRAYNELLIS: Yes, that's a that's a really challenging question. And, you know, I'd hesitate to put any numbers on that. You know, there's there's a lot of an exciting work going on with gene therapy and other conditions. And, you know, there's a lot of hope for transferring that success to rare diseases, including the GRINs.

KEITH MCARTHUR: Steve tells us there are at least two routes to finding a cure for GRIN disorders. One is using crispier or another form of gene therapy to correct the mutation. Another is using drugs, sometimes called small molecules that can moderate the way the NMDA receptor is working. Drugs that could amplify a loss of function, mutation or quiet a gain of function.

STEVE TRAYNELLIS: There may be situations where a small molecule either repurposed or discovered new just for the GRINs has has value and improves symptoms. And, you know, maybe you couldn't call that a cure, but you might call that the beginning of an effective treatment. And there'll be other times where perhaps a genetic therapy will turn back a lot of the consequences of the variation. Ultimately, we'd like to fix the gene. But once the brain develops, as we were talking about with Amy's work, it's not always clear that that that will simply turn everything back.

KEITH MCARTHUR: The more I speak to these researchers, to Steve and Amy and to Zhexing and Graham and Mike, the more I believe that maybe this isn't just a father's fantasy, that if I keep pushing, maybe I really can help scientists to find a cure. And that's incredible. And something I've always wanted for Bryson. But in the back of my mind, I can't help wondering. Is that what Bryson wants for Bryson? Because cure is a loaded word in disability circles. And there are countless examples of people who have disabilities or rare diseases and are able to communicate, and a cure, they say they don't want one.

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Friday August 7, 2020 Full Transcript

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