Hello everybody, E here welcome back to another Stephen King book review today. We are talking about hearts in Atlantis This is a great book right off the bat if you're sitting there wondering hasn't he already reviewed this? No, I have not I have a written review on Goodreads, but I've never done a video Review of it. What you're probably thinking about is my series Thursday theorist Where I connect all of Stephen King's books to the Dark Tower and the Stephen King universe in general This one has a film adaptation of only the first Novella, I guess you'd call it we're gonna talk about that in just a second how this book is structured It's with Anthony Hopkins I can't remember any of the other actors and I liked it all right But it's not one of the more memorable ones at least not for me And they had to change so much about it because it ties into the Dark Tower So so drastically it's still a good. It's still a good movie I would probably give it three three and a half stars Anthony Hopkins is of course as great as he usually is but back to the book There is some discussion about whether or not this book is a collection of stories Or if it is a mosaic novel I am on the side of mosaic novel because there is that for one simple reason This is the only Stephen King collection Without a table of contents In fact because of that I have problems remembering the titles of each and every story So if I'm glancing at the book, I apologize But the the first novella in fact Wikipedia says that it is a Collection of two novellas and three short stories I think they get progressively shorter over time if I remember correctly the last time I read this was in audiobook format, so I Still not a hundred percent sure on you know what stories are what lengths But the first one low men in yellow coats. I hope I'm getting that right If you're a Dark Tower fan, you already recognize the low men But the first novella is about Ted Brodigan who pops up a lot in the later Dark Tower books Well, not a lot, but he pops up. He has a pretty significant role in I believe it's the final one I don't want to get into spoiler territory, but I think that's spoiler enough just saying that he pops up in the series It's very interesting how King worked him in but the story pretty much revolves around Bobby Garfield who is a little boy at the time that he meets Ted and this is a recurring theme or scenario in Stephen King's books where a young person will meet a older person and Someone is basically grandfather grandmother age and be and comes to friend them. You have mr. Harrigan's phone. You have apt pupil You there's so many like this and I'm wondering who that person was for King When he was growing up I've don't think I've ever heard him talk about it So if you guys can share any interviews or anything where he might talk about it It just seems odd that it's such a recurring thing for him to have not had An an older figure in his life Him also growing up without his father, you know Who who was that person that he latched on to that was an older adult when he was a young boy Was there one at all? I don't know The rest of the story revolves around the I believe the before during and after of the Vietnam War And it's a mosaic novel in the sense that each and every story is from a different main character's point of view But it also includes the main character from the previous stories My favorite story in here is the first one. That's probably why I remember it so well The other ones are let's see here. You got hearts in Atlantis is a second one I remember that it's not even mentioned in in this one, but it's a group it revolves around a group of college kids playing hearts In college that one. I don't I don't remember a whole much a whole lot about that one It's and in fact the rest of the story is pretty forgettable for me I went back and read my review on Goodreads and that would probably the complete opposite of what I'm saying now But the one that really sticks with me is the opening one And that's probably because I've done so much reading and research into the Dark Tower series that I'm more Fascinated with the Ted Brodigan character than I am anything else I'm not gonna go through the other stories because like I said I don't have that great of a memory of them, but I do Recommend this book if for nothing else for the opening novella King really shines when he's writing about young people and older people Right right there in the middle. He has some great middle-aged characters But I think where he he really shows off his talents is when he's writing about well young Young people of a certain era kind of deal new newer Kids he he does struggle with sometimes. I think it's because he doesn't have too many People around him that are that age and if your only view of the world The world of young Adults is something like Twitter or the internet then you're just not seeing all of it And I think that's part of where some of the awkwardness And the cliched young characters for nowadays comes from I don't know I could be way off the mark But I know there was a lot of talk about how the kids in the Institute Didn't act like kids. I thought they did they they were all hyper-intelligent children and smart kids tend to talk like that and smart kids tend to be very cringy and awkward and Not very or too self-aware. Maybe is that and they they realized their faults But yeah, so that's that's my two cents on King writing kids But this one I do remember there's I believe there's one of the stories revolves around a vet who's homeless now this could be bandela effect I don't know and it of course wasn't in the movie because they only did the first The first one the first novella But I remember enjoying that one I really do need to reread this book and give it a proper review But if you're looking for more of an in-depth review, I'll leave a link down to my Goodreads review down there in the doobly-doo But I'm giving this one off the top of my head four stars Simply because of the first novella and my question for you today is how do you look at this collection? Do you look at it as a collection or do you look at it as an as a novel as a mosaic novel? Like I said, I have I'm on the side of the fence that it is a mosaic novel But I'd love to hear from you guys Also, whether or not you like the book leave all that down there in the doobly-doo, but until next time I have any you've been you this has been another Stephen King review. I'll talk to you guys later. Bye. Bye


Code is everywhere. It comes from beautiful minds. Hey, my name is Sebastian Lin. My name is Mike Israel. My name is Isang Idio Jr. My name is Don Huang. And with the wonder of open source, there are always new worlds to explore. A monitoring tool where you can live monitor your Linux server. Using the negative selection algorithm to identify anomalies in Linux systems. The world with unpiling is how to make it running on IBM's machines. When it's done, how the mapping of commands and works to enable better solutions. It's not about finding the next big thing, but having the freedom to see how many next big things you can find. I've been contributing a few open source projects since the first day in college. And I absolutely love doing it. It's simply the future. So let's get to it. Let's code the future. It's great to be here today. That video also reminded me of what I felt like when I was an undergrad just getting my feet wet with open source and using Linux. I was hooked from the moment it started. I was hooked on the speed. I was hooked on the ability to get things done. And I was hooked on the ability to contribute back and share with others what I was able to do. When I joined IBM, nothing changed except it actually got more dramatic. I was able to be on software teams, use more open source and lead teams and contribute that much more back to the community. And now, today, I have Linux in my title at IBM. So how cool is that? Linux 1, if you're not familiar with it, is a family of highly engineered systems that combine the best of open and Linux with the best of enterprise computing. I'm going to talk to you a little bit about what we've been up to around Linux 1 today and then have Sean come up and tell an awesome story about how he's helping to change the world. I don't have to tell you all about the importance of open source, but I also do think it's helpful every once in a while to engage in a little thought experiment. What would the world be like without open source? To me, we'd probably end up with a handful of very large tech companies, IBM, producing maybe mediocre software and not a lot of innovation, not a lot of motivation to innovate. We'd be, in short, decades behind where we are today. But where we are today is very different. We have countless open source projects that many of you all are involved in that are tackling and going after great opportunities, but also at the same time tackling some of the most vexing challenges that we face. Developers are collaborating in their code, and code is the engine that's going to drive us forward. Open source plays a critical role in how fast we can innovate, but also how fast we can deploy new technologies once they are made available. And IBM's been a very active participant in open source for years. We were an original funder of the OSDL, a precursor to the Linux Foundation. We've created dozens of projects and all told we have over tens of thousands of employees that contribute to open source on a regular basis. Up here are a few recent projects that we've been very active in. I'll touch a little bit on Hyperledger because we're convinced of its power to drive new innovative business models and transform industries. A year and a half ago it was created, the Hyperledger project with 19 general members. Now there are over 130. It's one of the fastest, if not the fastest project in the Linux Foundation history. If you haven't started to play around with Hyperledger, you can get started today. We have plenty of SMEs that can help you get engaged and get you plugged in and going. And at IBM, we're delivering a premier blockchain solution. It's fully integrated. It's ready to go. It allows you to develop, govern and operate a blockchain network across multiple entities, be it companies, be it partners, be it others in the industry. It was built on over 400 engagements that we've had with clients and partners. It's flexible software as a service, but it's built on open source. It's delivered through IBM Cloud and it's powered and secured by Linux One. That's right. When you go to IBM.com and IBM Cloud and provision a blockchain service, it's actually running on a Linux One server in our cloud data centers. There are many companies and partners that we're working with to create very innovative solutions, and I'm showing a few up here. IntellectEU is integrating new blockchain business processes with core legacy systems. Everledger is trying to take fraud and abuse out of the supply chain for high value goods, and SecureKey is doing nothing short of trying to create the next generation of identity and authentication solutions for the modern world. And as we like to say, you to the power of IBM. You worry about your code. You worry about delivering that next new innovation, that thing that's going to change the world, and you let us worry about delivering systems that will deliver performance at scale, availability at scale, and security at scale. And just on this point, I know Joseph was just up here and the story around HitRecord is awesome from a collaboration perspective, but I wanted to make another tie-in to Edward Snowden and his work in that portrayal. What Edward Snowden did, you may have your opinion on it, regardless of what that opinion is, what he laid bare was the fact that there is a tremendous amount of opportunity out there and threats from both the outside of your company but also within your company. Those internal threats can have access to compromise credentials or elevated credentials that can give them a wide range of access to critical data. Not many days go by without a data breach. That data is a company's data, but really it's your data, right? Every day we see something in the news about how our data about our personal lives is being compromised and put in the hands of others. And with Linux One, we've created unique security infrastructure to help protect against internal and external threats. It's known as secure service containers. This is a firmware-based secure Linux environment that offers tamper resistance and pervasive encryption of the entire stack of software and the data that is running in the container. If an administrator wanted to or was asked to provide the contents of what's running in that container, they'd not be able to do this. This underpins our blockchain offering, and it's up until now really only been available through that blockchain offering. What we are announcing today is that we are announcing a beta as we start to open up this technology and make it more broadly applicable and available. Additionally, as I mentioned at the start, two years ago we introduced the Linux One family to the world. We did it at LinuxCon. At the time, we introduced two systems. The Emperor, the bigger one, and the Rockhopper, a smaller one. And today we are announcing another family member, the Emperor 2. We've continued to innovate across the entire stack that we provide. That goes all the way down to the microprocessor where we've delivered new capabilities for symmetric multithreading, SIMD, we've increased the amount of silicon we've devoted to encryption by 4x. You move up a layer into the system design, we deliver an overall balanced system design that allows you to scale up and support data serving and cloud services in a secure manner. What this allows you to do again is to not worry about things like scalability, security, performance, and again, get back to you and focus on delivering capabilities that are going to help you achieve your goals. We have three clients that I'm showing here, just to give you a sense of what they're doing with the technology. Huawei Express is a transportation provider in China that is enabling the purchase of mobile tickets for buses and trains from their mobile phone to the Chinese population, not a small population. Sinfonia RX provides medical therapy management treatment programs for one out of seven U.S. citizens. And Cognition Foundry is building out secure premium services that allow startups to get going really fast and deliver technology and their solutions in a secure way and at scale. And now I'd like to invite Sean Frankson up to tell his story. Sean's the co-founder of Plastic Bank, and I hope you're going to be interested in how he's changed in the world. Sean? Hello, hello. My name is Sean Frankson. I'm the co-founder of a company called the Plastic Bank. And at the Plastic Bank, we are on a mission to use code to stop ocean plastic. And this is so important.  This is like filling this entire room with plastic. Every couple of minutes, just dumping it into the seas. And, you know, it's so important that we look at the grand challenges we face in the world and not get upset, but just see the opportunities of solving these problems with code. And honestly, the more messed up that I see the world getting, the more optimistic I am that code will be the script that saves this planet. And, you know, I'm inspired with how can we solve these grand challenges with code. So I'd like to show what we're doing to use code and technology to stop ocean plastic while reducing global poverty at the same time. And for us, it starts with the riddle. If you walked into the kitchen and the sink was overflowing, and you have water pouring onto the floor and just piling up, and all you have is a bucket and a mop, what do you do first? And the answer is simply you turn off the tap. As important as it is to take the plastic out of the ocean, the real step one root cause is how can we use technology to turn off the tap and stop the flow of ocean plastic? So we discovered that 80% of ocean plastic actually starts on land in developing countries where they have almost no waste management systems. It's actually common practice in these regions to just throw the plastic into the rivers, the canals, and the ocean bound waterways. And they do it because they see plastic of waste.  So the difference between garbage and value is simply perception. So we look at ways to use technology to reveal the value in plastic to make plastic too valuable to enter the ocean. So we set up recycling ecosystems around the world. We make it possible for someone to just go out, collect plastic, and earn a living. All the plastic we collect is called social plastic. And we create these reward and incentive systems to bring in social plastic, have it sorted, recycled, and then we sell it to some of the world's largest companies to turn it into products so that these companies can say that this product helps stop ocean plastic while improving people's lives. And we have just had an amazing response. We've had millions of people on social media ask corporations to use social plastic. We've had thousands of people come to us and we get calls daily of asking how can we bring the plastic bank to my country. And it was just huge demand and self-proof and social proof that has really just brought the need to scale overnight. We need to go from nothing to exponential. We need to develop and deploy. We needed safety, security, trust. Honestly, we needed help. And the beautiful thing is when you create a movement and an awareness of what you're trying to do, you attract the right people who can genuinely help do what you're trying to do. So we had cognition foundry come to us. So Ron Argent heard what we're doing. Kind of had an idea of where we're trying to go. And when he painted the picture of the tools and technology that could get us there, it was just an amazing fit. Because my business partner and I, we're technology entrepreneurs, but we have no idea how to scale the technology globally. But when we can have the partners working with us, putting the right minds together, the right tools together, literally everything became possible. So for us, the foundation of what we do is blockchain and hyperledger fabric on Linux 1.  The front end system is Apache Cordova, Angular 2. And what this does is it creates an entire ecosystem where all parts of the recycling chain can be united. So the app-based platform that we have at its core starts with a digital wallet where we have an asset-backed token where when we're in the world's most vulnerable economies where you can't have a bank account or it's dangerous to have cash, we can actually replace these entire recycling ecosystems and allow someone who doesn't qualify for a bank account to safely save through recycling. And we start building these ecosystems where the app goes beyond a basic user and has it where anyone can operate a plastic exchange system in any country in the world where they can become eligible to receive the plastic bank digital rewards and slowly have an entire economy where outside of recycling even anyone can operate a storefront with the real vision that anyone in the world can operate a convenience store for the world's poor where they can afford everything through recycling which provides complete financial inclusion. And again, this is entirely done because some of the world's largest corporations are buying the plastic to use in products and very much like fair trade, we're able to pass on that value to the collector who needs it. But at the same time when products are made, we have blockchain-authenticated supply chains. We have blockchain-authenticated social and environmental impacts. And this is when we can really bring trust back to the world of technology and back to the world of doing good. I mean, one of the hardest challenges is how do you deliver on the promise of doing good and have the world trust it? And for us, it's all about those trust stamps. Blockchain is a trust stamp. Linux 1 is a trust stamp. And honestly, for us, IBM is a trust stamp when it comes to our investors, our partners. When people ask, you know, as a startup, how do you plan on scaling around the planet? It's these trust stamps that really make everything possible. And, you know, for us, it's been an amazing lesson because one of the challenges is how do you develop technology for the world's bottom billion? But at the same time, I just get so inspired because code is universal. Code speaks all languages and code crosses all borders, which encourage all of you in any of the applications you build. If you can have a way that it doesn't exclude the bottom billion, there's a huge opportunity because we've been through the slums of the world, we work in multiple countries, and almost every single person, even in the worst conditions nowadays, have a cell phone. And more often, the world's bottom billion has a smartphone that has applications, which means any of the code we're building, any of the platforms we're building, can literally be used by the world. And when we have that mentality of how can we include the bottom billion, that is the next billion users, the next billion customers. And again, the reason that I get inspired and optimistic about the future of this planet is that when we have open source codes and we can build on things and have one solution make another one possible, this is really when I think the script to save this planet will be written in code. And I thank all of you for playing your part. So thank you. Thank you, Sean. And for the work you're doing at Plastic Bank and Foundry, it's really awesome, great to see. We've been inspired by it at IBM and so while we're here, we're going to try to do something different. We are going to take, for every bottle you all bring to the IBM booth, we will work with Plastic Bank to keep 500 bottles out of the ocean. We have a couple thousand people here. You each bring a bottle. We all today, in the next couple of days, could keep a million bottles out of the ocean and help fight poverty. So with that in closing, again, I invite you to come talk to an IBMer. Come to the booth. Take a selfie with the Linux 1 box that's there. As soon as you walk in, if you keep walking straight, you'll hit it. You can sign up for Unchain the Frame, which is a hackathon with $50,000 worth of prizes. And if you want to get your hands on the technology, you can sign up through the IBM Linux 1 Community Cloud and get access. So again, thank you very much and thanks again, Sean. Thank you.


Okay, did I get. Welcome to the Jenkins platform special interest group meeting it's the 7th of May 2021 reminder that we abide by the Jenkins contributor code of conduct. So, thanks very much for being here. Topics that I had on the list open action items, securing the Jenkins delivery pipeline, Java 11 as default in all our images. Those docker changes. Security scanning status. Anything else that we should add to the agenda Alex or Gareth anything that you have that needs to be included. Nothing for me. Okay, all right. So, so on the action items topic then I've still got this one, the jet process really is becoming easier and easier intentionally so this is there's no excuse I just need to get it done. We've got a proposal on the second action item proposed to include to provide plugin installation manager docs as part of the Jenkins on Kubernetes documentation project and you can see it's RV. Sudakar is working on it. With the doc sig. So glad to glad to see that it's I think second or third. See the see the proposed outline in the docs mailing list. So, some questions are happening there and one of the one of the items is that that exact topic of plugin installation manager let's document how to use it well inside of our docker images and thus inside Kubernetes. So, the finalization and multi arch is is arm 64 as 390 still interesting not yet happened. And I have opened the PR for changes from the contributor summit so at least one item is done on this list. The next piece was securing the Jenkins delivery pipeline. So, Gareth and I have worked on a elastic access plug in has switched to use semantic version automatic semantic versioning with continuous delivery. Gareth, I saw a comment from Jesse Glick expressing concern about the technique. Have you got any insights on on Jesse's Jesse's concerns or is it something I should take up with him separately. Actually, I thought his concern was on the other versioning scheme. Oh, oh, it was, it was hard to read because it's a slack thread, but it's difficult to read but I took it as, when I put the example is a 27 dots and random char. I think his concern was with that is that's going to work with me from versioning semantics. All right, so to, so I just need to let me take the action I'm to discuss with him to confirm that the the technique we're using an elastic access is not going to be a problem for Maven because as far as I understood what we did there looks exactly like semantic versioning right it's exactly three components and applies the semantics of okay patches increment the right most component features increment the middle and breaking changes increment the left. So that that versioning tool to Jack's release version is used throughout Jack's and most of the libraries that it creates so it has no problems being no deciding the version of component that's used as an dependency somewhere. That should be fine. Okay, super. All right, so that for me was was the experience is great. I haven't yet released off of a branch. So there's still some work to be done there on elastic access to be sure that it works but it felt good when when Gareth and I did it it just seemed to work. We've also released the tech on client plugin today with the same approach. So that switched over to use the, we're already releasing with the jet 229 but we had we were kind of munging a version together. Because we didn't want to go with the one dot zero zero yet, but today we switched to the one dot zero zero and now it's using the same approach as elastic access. Cool. Okay, so so now we've got two reference implementations that we can use to decide. This is this is a test great. Where do I look for the, what's needed to implement that is that here let's let me like to do that on token macro. Yeah, has token macro already switched to use continuous delivery. Yes, the other way. Yes, I'm not sure you want to go. I haven't released anything yet. Oh you haven't. Okay, all right well so then, then let me put a link here. GitHub.com. Yeah, report version dot channel. No, actually, I think it's workflow GitHub action so let's, and maybe. I've just popped, popped one in the chat, which should be pretty much identical to what you have. Perfect. All right, so this one. This is the tech on client one good. All right, so I'm just put that link here. And then the elastic access one I can put because the same thing should work for elastic access right that same path. There it is. It does. Okay. All right, cool. Yeah, so at least, at least it's a I think it's worth. Yeah, the report version pipeline we added as a sort of a method of debugging what Jax release version was going to determine as the next version. Gotcha. Okay, because because it can be run on workflow dispatch you can select a branch to run it against so it's just it's just a useful debug tool, it's prints out to see what the version is quite handy. So and truly this has been a fun experiment so when I click deploy, let's see was it deploy. Yeah, this will now tell me the next version number it would use. Oops, no I have to click it correctly don't I report version I say run workflow on master. Yeah. And now I get the output will tell me what version number it would have done the increment to good. Okay. All right. So token macro. All right, now I'm still, I'm still not fully personally through the transition yet to using some using can what oh there it's conventional commits is is still a learning curve for me right I haven't yet train myself to always use a conventional kind of text marker text and and that's just needs practice. Anything else on securing the Jenkins delivery pipeline. I mean, as something in the future that you could do. You could determine the next version number base on the release draft a conflict. It's almost the release after conflict but with the release draft a content. If we say it's a major release or breaking change we would use that to bump the next version. So it would be a case of getting hold of the doing the API call to get the release stuff and then analyzing the text in the same way that the interesting check does. I mean, looking basically at the contents of this next thing. Yeah, so you're so you're like if you have a new features and improvements for instance, that would be that's a feature. You know that's a minor release there. If it comes up as major changes then we know to bump it from that. So if you, if you don't want to use the conventional commits as a as a process or as a way of determining this stuff that may be an easy way of doing it. Right. But and there it would need either extensions to JX release version or something other than JX release version to decide the version number is that how that would work. I think other than JX release version, but I think I mean you could. It wouldn't be too difficult to do because I think the difficulty would be like, if you have to make a multiple get had calls, have API calls to be able to determine that then it's going to be difficult. And you probably need to write something to be able to do that handle that. You should be able to do it. You've got there's already the logic there in the, in the current deal have action to get that content and pull it back. So, and you've got the logic to interpret that they're ready for you so it shouldn't be too bad to make that decision about. Oh, right. Because we're already exactly as you said we're already reading the contents of this thing inside the action. Yeah. Right. Good. Okay, thank you. Right. Good. So you read that read, use and use the release drafter content. It's really use the release drafter content we're already reading to decide the level to increment. Right patch. Minor or major. Yeah, that could be an alternative to conventional commits if that's something that people don't want to use for instance. Right, right. Good, good insight that is that is an alternative. Thanks. Okay. Anything else on securing the delivery pipeline. Okay, next topic then was Java 11 as default in all our images so the conversations. We have moved between. Drop Java eight. The most aggressive maintain Java eight for a limited period. And yeah, that I think was the two comments. Anything the two of you want to guide there in terms of where we should go with that I think I'm prone to this maintain Java eight for a limited period. I think we should go with that because, because it's, we don't have enough Java 11 adoption yet in the in the Jenkins install base that I can see. Yeah, I think we probably have to maintain Java eight for a period of time. Based on the feedback that was on the main list about Java 11, and that was just for that wasn't even for the Docker images necessarily that was just in general for updating the source level to 11. But it seems like there's still a lot of people use Java eight so we can't really just drop it. Right. Okay, although for Docker containers, to me it seems kind of weird that we don't deliver that much. Oh, I see you know what I mean is, we could, we could could drop Java eight from Docker containers that's not stopping the project from using Java eight, but just don't deliver any more Java eight in the Docker containers. So the platforms that we deliver Docker containers for support Java 11, and even better, actually then Java eight on like S390 X and so forth. Right. So, yeah, that's, that's my take. Okay, thank you so I'll, I'll bring that comment to the to the discussion and I think Oleg had noted time to submit a gap. Right. So let me put one action item for me that that I need to submit a gap for Mark open a gap for Java 11 as the default as the standard Docker image basis. Okay, good. Right now. Back up. Okay, so anything else on Java 11. Okay, Docker changes. So multi arch builds, no progress. Alex you had noted arm 64 improvements, anything you want to report there or still still sort of holding. I'm still holding right now. I do want to get back to this but I just haven't a chance yet. No problem. That's great. Yeah, and, and this one, more and more people are using plugin install manager. I think this one is a is a good one to do as we publish the documentation for plugin install manager that's when we merge that and declare. Hey, we've changed to use this new way of doing it. The question is, should we ask Sudakar to sequence documentation of plugin installation manager first, so that we can use it sooner. Comments more docs is always good. Okay, yeah, so that's great. All right. So user on agent Docker images. I'm not sure I think that's not yet been merged so or or Gareth is this one that the to change was made it's definitely not been merged is this one that the change was made in the infra images so that the infra images are not using root. So we've worked around it in infra that we're actually not executing as rude anymore. Yeah, possibly. So it's only on the it's only on the agent side. Right. I think this was because this was all part of that. It's quite a large change change set that they mean was looking at. And I think what he wanted to do was look at a much better or more efficient way of building these images. I think that was the, the idea. So he's looking at the change the pipeline library to support multiple different Docker builds and that kind of stuff from a single repo. Got it. Investigating back at the safe, you can have almost like better inheritance. It's not an American's in the container but at least in the logic that we use so we don't have to duplicate it everywhere. All right, thank you. And announcing those changes we're not ready to merge them nothing to announce yet security scanning so Oleg is has made further progress with Linux foundation security and sneak, and is is actively doing a co-working thing with them to help adapt sneak to better understand or adapt what we need in sneak so that it will better understand Jenkins use of Maven, and not incorrectly flag things as a dependency that are that are included as a dependency and by the Maven HP bar our HPI process. There's, there's work going on there. So, very glad for the progress always making he regularly reports on that and the governance meeting and elsewhere. Code QL scanning. I'm, I think this is where we're now in discussions of how do we deploy it more broadly and hosting requests so, oops. So, Alex in terms of hosting requests I assume it's still being used there. Is that correct. The code QL. Yes. Yeah, it's not like a. Yeah, it's still just a local copy it's not a. Oh, right so this is not a systematic review. This is okay. So, so as you are stepping away from hosting requests, and we're getting more people added to the hosting team will they likely use this local as well, or is there something different. That's a Daniel says we he and Oleg and I, we got on that meeting yesterday. No one else showed up so just kind of chatted about some things. And that was one of the things he said was he was happy to give people access that we're doing the hosting requests processing so. Okay, good. I don't know if he's going to do like a blanket everybody who you know starts doing it right away, but I think, you know, at some, you know, as people are vetted or whatever it will be access will be given. Right, and that makes sense. Very good. Any other topics we should discuss today. Okay, Alex, Gareth, thank you very much. I'll post the recording after probably later today or within a few days. Awesome. Thanks, Mark. Thanks.


University of Pikeville head women's basketball coach Brandon Bias out his first ever summer camp as a head coach. With a quality turnout and plenty of knowledge to share, these girls are going to have plenty of valuable experience to take away from this camp and put towards their basketball careers. It's pretty awesome. I'm happy with the turnout and it's something that we want to definitely expand in the next couple summers and offer more camps than the two that we offer. A lot about this camp is a lot of fundamentals and working on just shooting and ball handling and rebounding. A lot of things that these young kids kind of need to learn and get better at. It's a lot more challenging. You see a lot more movement and just basic skill for yourself instead of as a team. You get more individual out of it. I come last season and it really helped me throughout the season so I look forward to next season getting to be able to bring this into season and see what I can do for myself. With Coach Bias, he teaches like the fundamentals and like the importance of basketball. They're going to have a lot of drills that they can now do on their own at their house for the whole entire summer that maybe they didn't know about before. Learn a lot more here and it's like the fundamentals here. I think it's awesome because it can help you be a starter on 18 middle school and then when you get in college that will help you a lot. I would recommend this camp for girls in the summer because it's valuable knowledge to keep on the court. Yes, I'd love for this crowd to grow every year and get a little bit bigger in that way. They can just get to know us a little bit more and get to learn a lot of fundamentals here at this camp. It's really great for young kids. It's like to personally thank each parent that supported these 41 kids coming and hopefully it's something we're going to grow on and looking forward to many more years of summer camps. Reporting in Pikeville for EKB News, I'm Mikaela Colley.


All right, thanks very much, and I'm glad to have the chance to try and fill in some of the gaps, pardon the pun there, from yesterday. And what I want to do is two things this morning. First tell you a little bit about some of the work that we have done in our research program that led to some of these insights that contributed to the debate on incidental findings, and then in the second part tell you a little bit about the incidental findings report itself. So predictive medicine is an interesting business to explore. And it's interesting because it's difficult and it's challenging, and it's something that a lot of people are happy to talk about in the general, but when you start actually talking specifics and making predictions, people get really uncomfortable. And I've learned a lot about our field in doing this, and it has been an interesting journey. So what we learned from is this project we call ClinSeq, which we started back in 2006 before we could even do clinical sequencing practically, and we at that time predicted that we would be coming to this juncture, although to be honest with you we weren't predicting it would come as fast as it did. So we went ahead and started to build a cohort of people that we consented for full genomic interrogation and began to gather them, and we started by focusing on atherosclerosis, and worthwhile phenotype because it's known genetic complexity, and it was basically a positive control for some phenotypes that we wanted to study. And we phenotyped the patients very lightly for that disorder, but then recognized that what we needed to be able to do, and this was critical to the study, is iteratively phenotyped the patients. So that is after we go in and dig into their genomic findings, we take the genomic findings and use that to drive the phenotyping. And that has been something that has led us to some surprising findings and conclusions, and I think it is one of the ways that we'll need to go forward, and also it models how I think medicine can be practiced in a different way. And so we were piloting incidental findings and predictive medicine through this study and began to dig in since we're focused on atherosclerosis initially, then we did not ascertain these patients for other phenotypes, and they can be regarded as an unbiased, ascertained population for other traits. And so what we started with was cancer susceptibility. So we went through the literature, catalogued every known heritable cancer syndrome we could find, and asked the question, how many of our participants have variants in genes known to cause these traits? And the number was pretty surprising, which includes, in fact, more than one percent of our population has a known pathogenic variant in a gene known to cause inherited cancer susceptibility, most of which is heritable breast and ovarian cancer susceptibility, and the variants are listed there. And I will remind you of following on Bruce Korf's comment yesterday, these variants are not in the category of variants that one would wonder whether they cause cancer susceptibility or not. These are very well-established pathogenic variants, and so there isn't really any debate in the field amongst experts who study these genes as to whether these variants are pathogenic or not. And arguably, our threshold is too high, and that we are bypassing variants that are potentially pathogenic because we're trying to set our positive predictive value to be high so that we're not chasing ghosts and finding things that are real when we find them in the patient. So Dan. Clearly pathogenic, are they 100% penetrant? Almost no variant in cancer susceptibility is 100% penetrant, so that is not a realistic metric to target for. The breast and ovarian, the high penetrant ones run in the 80 to 90% range. The Dell 185 AG, I think, is about 60%. No, those are high. Those are high. They're not 100. Yeah. And so, yeah, the relative risk is high for females for those. It's stupendously high for BRCA2 for males. Actually, the relative risk of cancer is higher for men than it is for women with these mutations for breast cancer. There are a lot of other traits we have begun to explore. We have a paper in press now on malignant hypothermia, an important gene environment trait that predisposes people to have a catastrophic reaction to certain anesthetics. Prevalence is stupendously hard to nail down. The estimates are all over the map, and people argue about it incessantly, and one of the reasons is because the ascertainment is so erratic and difficult. But what we can do with genomics is now begin to get a clearer picture of what the actual prevalence is, and we went through our participants and found a known pathogenic variant. Interestingly enough, there's, you talk about standards and guidelines for things like ClinVar. This is sort of a wonderful gold standard for this trait. There are actually two societies, the American Malignant Hyperthermia Society and the European Malignant Hyperthermia Society, and they have developed consensus mutations for variants that they believe are unambiguously pathogenic for this trait. And it turns out that this particular variant that we identified in our participant is present on both groups' lists, and they agree that this is a pathogenic variant. And interestingly enough, we go back and look at this gentleman's family history. He does not have a personal or family history of malignant hypothermia, but he's been exposed three times to anesthetics that could cause such reaction. When you study families who have malignant hypothermia susceptibility, this is what you see. Many of them, they just pop up out of the blue, and it is not with every exposure that the reaction develops. And so this is, we would regard as a great catch of an individual who has the susceptibility, and there are relatively straightforward steps that one can take to minimize his risk going forward, test his family for segregation of this, et cetera. Cardiomyopathies and dysrhythmias are another challenge. These are extremely heterogeneous traits. They are harder. And they're harder because a lot of the variants that cause these traits are missense variants. They're extreme genetic heterogeneity and allelic heterogeneity. And some of the reports are very thin on actual data, and it can be very difficult to make determinations of causality. But the iterative phenotyping really helps here because these are traits that you can get some phenotypic traction on. So we found three variants in the cardiomyopathy category that we were intrigued by, and then went back and either did additional studies or dug out clinical data on these patients, and we found confirmation of the traits in all three of these participants. So the first one has a fascinating disorder called non-compaction cardiomyopathy. The variant predicted that. And it turns out this gentleman had had a previous MRI done for other reasons, and pursuant to the incidental findings discussion, interestingly enough, the radiologist missed the finding of non-compaction cardiomyopathy on his MRI. We went back and pulled it up, and with a focused look at that MRI data, the finding is there. So he absolutely does have this trait that predisposes to congestive heart failure and dysrhythmias and is a manageable disorder. The next two are more straightforward cardiomyopathies, and both of these participants did have evidence of abnormal echofindings consistent with cardiomyopathy. And what's interesting about all three of these families is that they all had a positive family history of sudden unexplained cardiac death. And so they had enrolled in a study on atherosclerosis thinking that they had sudden MIs, or sudden cardiac death, presumably MIs, because that's the attribution that is most commonly made. And we don't think that that's actually what's going on in these families. They've been misdiagnosed, and this trait is what they have. Lester, did you do the targeted phenotyping on the cancer mutations that you found? Because you said you found all those, but you didn't report on whether there was a family history or anything of cancers in those patients.  So for the breast and ovarian cancer susceptibility, we implemented screening for those individuals per the standard recommendations for those traits. But when we look at those patients- Was there a family history? Was there a family history? Half of them, yes. Half of them, no. And that is actually what the oncologists will tell you they generally find when they do genetic testing in the cancer clinic, when patients have disease, when they order testing, half of the ones that are mutation positive, half have a family history and half don't. When we look at our family histories, what do we see in the ones that have a negative family history? Turns out that most of them are either from families with very small, sipship sizes, i.e. there's not a lot of people in the family, or in the breast and ovarian cancer susceptibility families, they're loaded with males. And the penetrance for males being much lower than females has masked the segregation of the trait in those families, but it's there. And several of the participants have female offspring who are at risk, and we've identified them before the disease has manifested. And it's a very interesting phenomenon, too, because we have this paradigm for cancer genetics, which is you go to an oncologist because of either a family or a personal history of this disorder, and you're screened and evaluated to determine if you meet the criteria that would justify the test. Which basically what we're saying to people is, no, no, no, we're not testing you until people have suffered or died from the disease. That's our standard today. And so we're very comfortable with that. There's good reasons for that related to the resources and the positive predictive value and the false positives. But it is actually kind of a funny place to be in.  And so how do you do it? But that's prediction, and it is challenging to do. We're also exploring the sort of the wider space of variants. And there was a wonderful paper by the Thousand Genomes Project where they categorized all null variants in thousand genomes. Really interesting how many there are. And what we set out to do is ask the question, okay, how many null variants are there in our thousand patients, and do they actually have a phenotype? And that's one of the strengths of our approach and one of the Achilles' heels of thousand genomes is you can find a null variant in a patient in thousand genomes. But what does it mean? And there's actually a striking, there is a lack of phenotypic data there of necessity. It was appropriately done, but you just can't go back and ask the question. We can go back and ask the question. Yes, sir. Nonsense, missense, canonical splice, plus one, plus two, minus one, minus two, or deletion of the entire gene. So that's what we consider to be a null variant. And we have to be careful, too. I will tell you also we have null variants in genes that cause nearly 100% penetrant malformation syndromes in patients in their sixth decade who absolutely, positively don't have those traits. Not all null variants are truly nulls, and you have to be very careful about how you interpret those. And we have criteria for how we filter those to make sure that they're in regions of genes that are pathogenic, et cetera. We are looking at heterozygotes. It's very, we have some experience looking for bililic mutations. Mathematically, that's just much harder to do in a population, a cohort of only a thousand people. You're just not going to find that many. We found a patient who had an undiagnosed familial partial lipodystrophy and a PPA or gamma mutation. I was stunned. We found a patient with a hox mutation. Hox mutations cause congenital anomalies, and we thought, sure, this is a false positive, right? And we call up this gentleman and we start saying, well, actually, sir, we have some questions about your hands and feet that cause limb anomalies. He says, what do you mean? You mean the fact that I can't wear flip-flop sandals? I said, what do you mean? Well, he says, there's no space between any of my toes. He has phenotype. We didn't phenotype his feet because we're studying atherosclerosis. If you go back and ask the pointed question, there is the trait. It's not a medically actionable disorder to be sure, but there's an example of a developmental anomaly in a person in their 60s undiagnosed. And we have identified a patient with Burd-Hawk-DeBase syndrome, undiagnosed, negative family history, brought them into the clinic.  And we actually had a dermatologist carefully examine the patient, had some suspicious lesions, biopsied, he has the lesions. So finding of this disorder in a person with no personal or family history. We have explored a copy number. I have a question. I'm sorry. What is the specificity of these findings? In other words, do you have subjects that have these null variants that didn't have any phenotype? Absolutely. So we have, I studied years ago, a disorder called Gregg's cephalopolysyndactyline syndrome, which is a disorder that causes polydactyline of all four limbs and craniofacial abnormalities caused by loss of function mutations in Glee 3. And we found a patient who had a nonsense mutation. I think it was in codon 15 of Glee 3, so way five prime. We were stunned. We go back. The patient has absolutely no phenotype. I think what that's telling us is that that is not an obligate exon in that gene, even though we thought it was, because we know what the phenotype is and it sort of unambiguously does not have it. So there are examples of that. And I could enumerate those. I just don't have time to go through them this morning. So you absolutely have to be careful. And that's why we think the iterative phenotyping is essential. You don't just take the variant at face value. The analytic validity of the findings we don't think is our challenge. What's the challenge is coupling it to the phenotype. And that is the core activity we think of this process, which is a clinical researcher or a clinician taking these raw data from the genome and integrating it into the phenotype and asking the question, does this make sense? What's the specificity of the phenotype? Does the patient have or not have the phenotype? And that's what we think is going to have to be done. And that's the core activity that we're going to need to learn how to do. But for a national ability standpoint, I think the specificity of the finding is quite important for sort of point of care or at least preventive measures or other interventions. You couldn't agree more and that for sure when you have a non-refutable phenotype, such as a cancer susceptibility syndrome, then you're in a tough spot and then you're relying more on the actual positive predictive value of the finding itself. We had some variant patients who had a variant in a gene that has been reported to cause gastric cancer. It's really a tough phenotype to deal with. It's very difficult to manage that. We had two patients in our cohort and actually we went so far as to actually contact the research group that published the finding and come to learn that they have since become skeptical of that variant. It was too frequent in databases, honestly, to cause that trait. And they have, in their own minds, downgraded that from pathogenic to benign, but they never published that finding. And so that's an example of how you have to sort of chase things down in the weaknesses in our databases. That's a big challenge. Yes, sir. So you're dealing, in terms of phenotyping, you're dealing, how do you do, one problem you have is age of onset, obviously. Yeah. And also most susceptibility genes are the major contribution to probably most medical problems in terms of numbers, comments. So how do you, you're just looking at things that are specifically causal, is that right? Or how do you handle any susceptibility? So you're talking about lower penetrance and lower relative risk. Yes. So what we're doing is basically taking this data set and starting from what we think is the top end of penetrance and relative risk. And going through those and working our way down the list. And one of the things I think that we will do in the process of doing this is, two of the things we'll do, is figure out sort of where, how that's, what the shape of that curve really looks like by studying these patients and these phenotypes. And the other thing I think we will learn is where the fatigue point is in the participants. Right? We can't keep finding, because each one of them has thousands of variants. We can't keep going back to patients forever and saying, oh, isn't this interesting? We'd like to look at this. They're going to start telling us, you know what, this isn't sufficiently important to bother me with. Would you please leave me alone? That's an important finding. We need to know where that is, because we need to know how far to push this predictive model. And we don't have good data on that. It's a great question. Oh, we have explored CNVs. It's hard to do CNV calling from exome data, as many of you will know. But from whole genome sequence data, one of our participants, and two exomes, we were able to identify a CNV, which is a known pathogenic CNV and a gene called PMP22, peripheral myelin protein 22, which causes patients to have hereditary liability to nerve and pressure palsies. And it turned out when we interviewed these patients that in fact they had these symptoms and they were in all three cases undiagnosed. Interestingly enough, the prevalence of this disorder is supposed to be one in 50,000 people. And we have it in three out of 1,000 people, which is startling. I'm, of course, biasing you because I'm only telling you of our positive findings, not of our negative findings, right? So just get to be careful with that math. But when we explored this with the participants, one of them had actually been misdiagnosed with a lumbar disc radiculopathy and was booked for surgery on his spine because his orthopedic surgeon was convinced that his neuropathy was from his MRI finding, which showed a mildly herniated disc. He canceled that surgery, went to physical therapy and is doing fine. And I think it's a good example of how a correct diagnosis can keep you out of the operating room, save expenses, and save healthcare costs. So what we've shown, I think, is that you can extract clinically meaningful results from exome and genome sequences. Genomic analytic validity to us is not the major challenge. It's integrating the variant findings with the phenotype, which is why we think that the main action is in the clinic room with a clinician who understands both the genomic data and the phenotypic data, understands family history, understands genetics, understands how to integrate all these different data to make a sensible clinical conclusion about a provocative genomic finding. We have become rather enamored with our notion of what we're calling hypothesis-generating research, using the genomic data to tell us what to phenotype and not trying to phenotype patients a priori. And I will tell you that counseling these patients is challenging because in our prior genetic model, what we do, again, is we have patients come to us who have a family history or personal history of a disorder. They have a lot of experience with that disorder. They know what it's about. They know how it's affected them. They've done a lot of the emotional hard work of adapting to that trait, and we take the next step in that process. When you take a patient effectively off the street, sequence them, and say, oh, by the way, you have a disease that you have no experience in our understanding with, it's more startling. There are more challenges, and it takes more time to get those patients adapted to the finding and get them to do what needs to be done to manage that trait. Okay, so I don't want to minimize the challenges here. Predictions are very difficult, and as the gentleman in the background said, they are beyond the domain of exact prediction, not because of lack of order in nature, but because of the variety of factors in operation. Of course, he's talking about particle physics. We're talking about genomics, but the exact same principle applies. We need to understand clearly what the boundaries of the precision of our predictions are so that we can apply them thoughtfully and sensibly to improve the patient's health care. So Rumsfeld was quoted yesterday, I think, by the Admiral. Sort of paraphrase him here. There are things we know are problems and things we know we don't know, and we have to anticipate all of these. It's absolutely clear that clinicians are not ready for this. It's fascinating to return results to these patients' doctors. Some of them do actually kind of wig out when you tell them because this doesn't fit their paradigm. They're used to taking care of patients because they're sick, and we're telling them, no, you need to start taking care of this patient because of a genomic finding, and that is challenging. Databases are an enormous problem. We talked about that yesterday. And what we know from this kind of work is that we don't actually understand the full phenotypic spectrum of most of the traits that we've studied because we've only studied the highly loaded, dominant, recessive, clearly inherited families in the past. And so these kinds of research projects are an opportunity to actually ascertain patients in a less biased way and understand the full spectrum of genotype-phenotype correlation, which will again allow us to make better predictions. Not to say that we can't make predictions today, and that's a false argument. We can make predictions today for a subset of variants and a subset of situations, and we have to know which or which. We do have to address the sensitivity problem. I told you that we're trying to set our threshold very high for the calls that we make. That leads us then to make a different error, which is that when we don't return a result to a patient, they may still have a risk for some of these diseases. And we do worry about patients misinterpreting the absence of a finding as a clean bill of genetic health and making incorrect medical decisions on that basis. And we work hard with our participants to do that, and I think as a field, we're going to have to struggle with that so that we say, yes, this is an extremely powerful technology when we find something, and when we don't find something, it's not a strong negative predictor of risk, and that's a hard message to get across. Changing the paradigm which we're doing causes discomfort, and I talked to you a little bit about how it causes discomfort amongst our colleagues also causes discomfort amongst ourselves, and I think it's within our own field. We have a lot of challenges, and that leads me to the college statements. The college has taken these sorts of scenarios and data into account and made recommendations for how incidental findings should begin to be approached. The statements actually comprise four documents that need to be viewed as a whole, and I would encourage you to look at all of those. I can circulate these if anybody needs them. The college comprised a working group of about 14 or 15 of us co-chaired by Robert Green and myself to actually ask questions about how we should approach the problem. The charge from the college was whether or not the college should have a policy and or a list of incidental findings that should be sought in the process of doing exome and genome sequencing clinically, only in the clinical realm. And if so, what that list should look like and what it should include as far as genes and phenotypes. What we settled on as a working group was that, yes, we should go forward with such a recommendation and we set some general parameters for what the traits ought to comprise high penetrance and or clinical confirmatory testing that would allow the prediction to be affirmed to be true. Long asymptomatic period meaning that there was opportunity for misdiagnoses that the sequencing could correct. Some kind of efficacious treatment screening avoidance process, et cetera, that would markedly increase the patient's health or survival disorders not detected by newborn screening. We focused on newborn screening as a separate realm. And then we focused only on a subset of highly pathogenic variants and agreed for a lot of reasons that this list was going to have to be updated constantly over time going forward. So what we set out was a minimum list of medically relevant or you could use the word actionable conditions and that the variants and the genes that we specified should be returned to clinicians and this is the key thing. The recommendation is that the variants should be returned to the ordering clinician is what we say and then the clinician has to contextualize that and determine when and how that result is returned to the patient. We controversially did say that the variants should be returned regardless of the age of the patient which seemed to some to contradict prior guidance on this topic. I'll get to that in a minute. And we estimate from some of the work that we and others have done that in the order of about one percent of people who undergo clinical exome or genome sequencing would get a result from the list that we generated. Now it is absolutely clear that these recommendations diverge from current clinical genetics practice. No doubt about that and I think that's because the change in the technology mandates that we change how we handle the patients. What's interesting though is most of the recommendations actually converge with practice in other disciplines of medicine and I'll talk about that more in a minute. Controversies, preferences. We, this recommendations clearly require informed consent and that's a big part of the recommendations. What they don't include is preference setting by patients. We did not settle on a notion that patients would get this pick and choose amongst the disorders to decide which of them that they want and that overturns a long held practice in genetic medicine which is the patient decides which tests they undergo. What we reasoned is that the incidental findings are an inextricable part of the clinical assay i.e. the genome or exome sequencing and it is a package just like radiology is a package where you get the indicated finding and the incidental findings whether you wish to have them or not. So again this overturned the precedence in genetics. And the pediatric recommendation is based on the transient nature of where we are in the field right now which is that genome and exome sequencing is not widely available. It is commonly done in a setting of sequencing a trio of individuals where usually it's the child who sequenced for a pediatric onset disorder and the parents are sampled for segregation or genoval status, etc. And since parents don't have already access to genome or exome sequencing today we reasoned that finding a variant in a child even though it's not actionable in childhood but it's clear medical implications for one or the other of their parents in almost all circumstances and until genome or exome sequencing is widely available we felt that because of that reason if you find an adult onset disease variant in a child it should be reported back to the parents because of its potential action ability in the parents. Again this is controversial. Physician thank you very much Pearl. Yeah you are, I appreciate that. Again so consent is a big part of this. There's been some unjustified criticisms that we don't endorse consent. This is exactly what the documents say. I don't think you could have a more robust consent policy and in fact it exceeds the consent policy that we have in all other areas of medicine for all other incidental findings. So arguably I think our consent policy is too strong when you compare us to the rest of the medicine. Other clear controversial element is the level of evidence and it is absolutely clear that there isn't sufficient evidence on an objective randomized controlled trial basis of how you could do these studies to justify everything that we recommend. These recommendations are based on expert opinion of a process that I would argue is very thorough. This process took about 14 months of committee calls. A lot of input from membership of the society and the board of directors including an open forum on the column. And Robert Green pointed out this statement to me. The U.S. Preventive Services Task Forces sometimes use it as a cudgel to abuse people who don't have robust evidence but I thought it was really interesting he found this quote from Preventive Services Task Forces. Even though the evidence is insufficient the clinician must still provide advice. Patients must make choices and policy makers must establish policies. This is not a reason not to have evidence. We all want more evidence but we also have to acknowledge that we live in a real world where this technology is being ordered. Thousands of genome and exome sequences have been already performed clinically and we felt that it was appropriate to use the best knowledge that we have today and make a sensible statement, acknowledge that the data are imperfect, that it will evolve over time and that we will improve these practices and avoid the chaos. So making these recommendations has been a really good learning exercise and some of you might recognize this is a device called a Rorschach block and I think these recommendations are somewhat of a Rorschach block for our field and they're telling us a lot about how people view medical genetics, medical genomics and predictive medicine and in some cases, I don't want to get too psychoanalytic on you here, I think they're actually telling us more about the people who are criticizing these recommendations than they are telling us about the recommendations themselves and what people bring to this debate are a lot of long held and cherished assumptions that seem to my mind not to recognize the fact that the technological landscape has changed underneath us. John Maynard Keynes said in a rebuttal to a criticism he once got, he said, well sir, when my information changes, I change my conclusions. What sir, do you do? And the truth is some people don't change their conclusions when the facts change and I think that's sort of where we are in this debate and we're learning a lot about that. Some of these concerns that have been raised are absolutely valid and I think in some ways we as a field are afraid of ourselves and our shadow, if you will, is a legacy where we have this terrible history of things like eugenics, we have a long history of diagnosing disorders for which there is no effective medical treatment. We also have a long history. The most established part of genetic practice is in fact in prenatal diagnosis where we have no business making recommendations to patients about what they should or shouldn't do with those data. So those events have conspired to make us be extremely reticent as a field to use a piece of genomic data and tell a patient you should do this. But now again, the landscape has changed and we have to recognize there are some situations we shouldn't always be afraid of our legacy and our shadow and we should actually become comfortable with saying to patients, here is what the deal is, you need to do this to keep yourself alive and healthy and we have to change that culture and I think the challenge is more in ourselves sometimes than our colleagues. So I'll stop there. I've certainly enjoyed being part of this process. We have been the target of a fair amount of criticism but I think that is a good thing for our field that shows that this process is really important not only to us but to the entire field of medicine and we're changing the terms of the debate and moving genomics into medicine and we all have to acknowledge that's going to be hard and we're going to get a lot of criticism when we try and do that but it's worth it nonetheless. I'll stop there. Take any questions. Thanks. So we're running late but I think we'll take a couple of questions. Yes. Deborah? I think it's very interesting in your ClinSeq program you did the phenotyping yet the ACMG recommendation is that you return this result to the clinician. When do we start being the clinicians who are specialists in what the genomic information means because this result is going to go back to primary care physicians who don't necessarily know what to do with this information and I think we should be stepping up to the plate to work with patients directly to have them understand what this means and then refer them to a specialist. I mean when you send someone to an oncologist they don't send the diagnosis back to the primary care physician and say so you give the chemotherapy and I think we have to start thinking about ourselves differently. So I think when we're in the realm of highly penetrant disorders that are Mendelian or nearly so I think the medical geneticist is a person who has a lot of expertise in these kinds of questions and it is the case in all realms of medicine that it is a dicey proposition when a clinician orders a test when that clinician doesn't understand how to interpret and use the data. Now that's not to say that they can't order because we all know they do but the recommendations are quite clear in the guidelines promoted by the college and Bruce you might want to comment on this are quite clear that the person ordering the test should have the expertise to interpret the test and there is a good reason for that. So did you define who should order? That's so much genome sequencing because I think that's a very good question. It is a good question. My personal view is that the college has a slightly different policy than my own personal view so I'll give you mine first and then I would ask Bruce to comment. My view is that I wouldn't say that it has to be ordered by a board-certified medical geneticist nor would I say that the counseling that is also recommended to be part of this process has to be provided by a board-certified genetic counselor. I think that's a little too narrow and unrealistic of a scope. I think what we should strive for is that the person ordering the test and talking to the patient understands the core of what the test is about what the implications are for the patient so they understand it and then upon receipt of the return of the results can manage them and put them in the correct context for the patient and get them to the right person when they have a result because the clinical geneticist should not be implementing the colonoscopies for the MSH2, right? That's silly and they need to have a network of providers and that's how all of medicine works is we have to understand what our boundaries are go as far as we are capable and comfortable going and not go farther and who that person is neurologists are going to order a lot of exams. They can learn how to do this. I'm absolutely convinced they can. Bruce, do you want to comment on that? So I don't think this is that different from a lot of areas of medicine. I'm licensed to perform surgery I think probably somewhere along the way but I don't think it would be very wise for me to do that and I think there are many examples, the example of not pushing chemotherapy if you're not trained in that is another such example and there's no law that says you can't. It's just that you know that you're likely to get into trouble. So part of what we have to accomplish here I think is to educate the community about what the power can be and where things are applicable in daily practice and where it is highly advisable to seek the assistance of people whose training is such that they would be better qualified to do this and I think this is an example where that is the case. Now the college in its points to consider does make a strong statement about the need for a person who is trained in genetics and genetic counseling to provide both the pre-test counseling and the post-test counseling and doesn't go to the extent of saying it has to be a board-certified medical geneticist although it does recognize that there are such individuals and as far as I'm concerned this is why there are such individuals just there's a reason why there are oncologists who are specially trained and so it seems peculiar to me to talk about creating new specialties or repurposing specialties when there is a specialty that is qualified to do this and has the experience. Now you could argue there aren't enough of them but that's because this is a changing field and until recently probably the potential of applying this on a very wide population scale didn't exist. So it may create a pipeline problem and I can tell you the college is actually working now to try to overcome that but that's not an argument not to do it. It's an argument why a new paradigm exists and there's a lot of opportunity for people to enter an exciting field. So I just think this is very much like other areas of medicine. It's an easy box to check perhaps but it is not an easy thing to do and requires some special skills and training. I think we've really got to move on because we're running quite late but this is clearly a topic that there will be a great deal of additional discussion about. So I think next, well then maybe you can use that as a starting point to expand this discussion then for a little bit of time.


Hi everybody, Joe for jaskiescasebrakes.com. Happy Wednesday, Humpty coming out to you with 2021 Panini Flawless Baseball, a one brief case random team break number one with a March madness spot being given away at the end. We'll do that randomized at the end along with any other randomizer that may or may not be. Big thanks to this group for making it happen. Thanks to the people who bought spots straight up and congrats again to the people who won spots in those quick pitch packs. All 30 teams are in. Let's roll it and randomize it. Two and a one, three times. One, two and three, easy. We got David on the pole, pole position and Steven in the 30 spot. Two and a one, three times for the teams. One, two and three. After three we got the Cleveland Guardians down to the Chicago Cubs who signed that Japanese player, Seya Suzuki. All right, David with Cleveland, Martin with Baltimore, Michael with the Astros and the Rockies. Rocky's picking up Chris Bryant for seven years. Danny with the Pirates, Nick with the Braves, Martin with the Giants, Matt with the Red Sox, Steven with the Marlins, Michael with the A's, David with the Brew Crew, Pete with the Padres, Matt with the Nats, Rex with the Reds, Nicholas with the Royals, Michael with the Mets, Matt with the Mariners, Brian with the White Sox, David with the Diamondbacks, Danny with my Dodgers, Martin with the Blue Jays, Gregory with the Twins, David with the Angels, Steve with the Tigers, Ed with the Yankees, Martin with the Cardinals, Danny with the Phillies, Rangers and Reyes and Steven Flatt with the Chicago Cubs. Sort by team, alphabetically by team. Rex has the Reds up for trade while you're considering trades. And before we pause the video, we're gonna pop open this fresh case right here. We're gonna see which briefcase we're gonna do. Yeah, Rex looking for a Rangers. Danny's got the Rangers. Danny should be in the chat. All right, we're gonna select one die out of here. We'll use that nice Dodger Blue die. We'll go one, two, three for the top briefcase, four, five, six for the bottom. And it's the bottom one, one, two, three, four, five, six. So that's the one we're gonna break and the next box will mark one box random team two so we know they're from the same case. And this is already up on jaskyscasebreaks.com right now. But this is the only one with the March Madness promo attached to it. All right, let's flip back over here. We're gonna pause the video, see if there's any trades that get made. And when we come back, we'll do the break as well. Stick around, be right back. All right, welcome back everybody. There were a little bit of trade chatter, but in the end, no deals were done. But there's a list hot off the presses. Thanks everybody for getting in on the action. Let's see what we have in here, ladies and gentlemen. All right, there's usually two encased cards. Sometimes you'll get a third. Let me just cover up the other encased cards first. No, we don't get a third here. We've got an autograph on the right side. I didn't see who it was and a gem on the left side. I did not see who it was. And the small print says that the gems are naturally mine, not lab grown. And use another blank card to slow play the hits right there. There's that stack you can see on the top camera as well. Good luck, everybody. We got Nolan Aronado, two out of five Nolan Aronado, the train whistles to start the action. I think you can see a little bit of, I wanna say there's like a little bit of infield dirt right here, that which is really cool. Cardinals, train whistle for Martin who won that spot in one of our fillers. Got randomized the Cardinals, gets a train whistle to open things up. All aboard the Big Hit Express. Woo-hoo! We got three out of 20.  Washington Senators, and that version of the Senators turned into the Twins. Glad I had that checklist open. So Minnesota will get that one. That'll be for Gregory with the Twins. The old burlap jerseys from back in the day. Next up is Alejandro Kirk. It's a cool patch there. 15 out of 25 for Toronto. Blue Jays, Martin with the blue birds. Not the Jays with the spot he bought straight up. Next is Alec Baum for the Phillies. 12 out of 20. Rookie, jersey, and autograph for Danny and the Fightin' Fills. Next up, Star Swatch Signatures. Seven out of 20. Tyler Stevenson, that's a cool path right there. Part of the letter. Part of Reds, or his name. That goes to the Red Legs. Rex with the Reds, try to trade. Couldn't trade Mojo. Nice one, Rex. Next one is for the Rangers. Rookie, patch, signatures. Kohei Arihara, four out of 15. That's for Danny and the Rangers. Next up is Estevan Floreal, 14 out of 15 for the Yankees. Yankees makin' some trades, re-signing Anthony Rizzo, and Aaron's with the Bronx Bombers. All right, final auto down here is gonna be one out of three, premium ink Tom Glavin for the World Champion Braves. Nicholas L with the ATL. It's the out of three, Glavin, their top loader here. And out of five and under, get the train whistle. Nicholas, all aboard the Big Hit Express. Woo-hoo! Now the two in case hits. Good luck. Remember, we have another random team in the store right now. First one here should be the Gem. Nine out of 10. MVP? MVP's Cody Bellinger for my Dodgers. I feel like he's gonna have a nice bounce back season. Now that that shoulder should be healed up. Danny with my Dodgers. There you go, Danny. The autograph. Good luck. Is gonna be, is gonna be Fernando Datis Jr. Two out of 10 autograph. The motorcyclist going to Pete and the Padre. He's me out a few months because apparently he fell off a motorcycle multiple times and hurt his wrist. Still nice. I'm sure he'll still end up with like 30 home runs by the end of the season. All right, case is closed on Flawless. Let's see who wins that March Madness spot. So let's go back to the list. Let's gather everybody's names from David Yang down to Matt Buckler and everybody in between a new dice, new list. Name on top is in the March Madness promo. Details on jaskiescasewrakes.com. Five and a one, six times. Good luck. One, two, three, four, five, and a one. Six and final time. Good luck, everybody. Name on top. Drum roll, drum roll, drum roll. Post-Nicolas, no cigar, but a cigar for Michael. There you go, Michael, with a spot that you won in one of those filler breaks. After six times, your name is on top and you're in that March Madness promo. I'm Joe for jaskiescasewrakes.com. I'll see you next time for the next one. Bye-bye.