 All right, it's 117. Let's go ahead and get started. So first of all, thank you for coming on time. We appreciate you. My name is Janice Guzman. I am a nurse scientist at the Southern Arizona VA Healthcare System. I'm also a trained geriatric nurse practitioner. I am one of your moderators for this panel session. And your other moderator is Alexis Koskan. She is an assistant professor of public health in the College of Health Solutions here in ASU. Did I say that right? Okay, sounds good. And welcome to our session today titled Barriers and Opportunities to Amyloidosis Diagnosis Panel Discussion. I have to preface before I introduce our expert panels that neither I nor Alexis are experts in amyloidosis, but what we are familiar with and have expertise in is in implementation science. So Alexis and I have been working for the past couple of years looking at early diagnosis of cardiac amyloidosis. And so this is an extension of that work that we're doing. I'm going to introduce our expert panels. On my right to your left is Dr. Yasmin Butt, who is an atomic pathologist at the Department of Laboratory Medicine and Pathology at Mayo Clinic here in Arizona. Next to her is Sonia Sibrowski, who is a genetic counselor and instructor in medical genetics at Mayo Clinic. And in the middle we have Dr. Ayushi Chug, a neuromuscular specialist and associate professor of neurology at Barrow's Neurological Institute. And then we have Dr. Brent Goodman, who you've heard before, I think half of our panel you should be familiar with if you were here in the morning. Dr. Brent Goodman is a neurologist and director of autonomic laboratories and autonomic program at Mayo Clinic. And then finally, our last panelist is Dr. Alberta Warner, who started our conference this morning. She is a cardiologist, this is a reminder, she's a cardiologist and the director of cardiac amyloid program at the VA Greater Los Angeles Healthcare System in LA and a professor of medicine at UCLA School of Medicine. Okay, and if you were here last year, you might have noticed that we talked a lot about cardiac amyloid doses and specifically the wild type, TTR wild type. And as Sandesh had mentioned in his welcome speech for this year, we really wanted to go beyond updates and really focus on amyloid doses. And so the focus of this session will be on the hereditary type of amyloid doses, specifically the polyneuropathy clinical phenotype. Another difference in this session is that we want you to be engaged. So we're gonna be asking questions or specifically Alexis will be asking questions to our panelists. What we want you to do is raise your hand if there's something that's, a burning question that popped up as you listen to their responses and discussions. We want this to be interactive, and so while Alexis is asking questions and moving the discussion along, I'll be looking out and seeing if anybody has any questions and I'll bring the microphone to you, okay? I just have a couple of slides to make sure that we're in the same, we have the same understanding, right? So hereditary transthyroidthin mediated amyloid doses or hereditary amyloid doses, also known as ATTR variant is a progressive disease. We've heard that all morning. It leads to misfolded protein aggregation in various organs and tissues and it's really hard to diagnose because there's really, there's some common symptoms but there's really no typical presentation per se, right? There's common symptoms and signs but no one typical symptom. But early diagnosis is important to prevent organ impairments, okay? It's progressive. So the earlier we catch it, the earlier we can prevent morbidity and mortality for our patients. There is also limited guidance on hereditary amyloid doses with polyneuropathy, although it's a common clinical phenotype and when we did the literature review on this before for this session, there's guidelines actually by a Canadian group and then there's another one by a US based clinical consensus by neurologist which is the next slide. But the goal of this session is to describe potential barriers and facilitators of early diagnosis of hereditary amyloid doses with polyneuropathy. So this is, as I was saying earlier, there was actually a clinician consensus guidelines that came out last year. I was published last year by Karam and colleagues and it talks about patients who present with polyneuropathy and how you work them up, right? So they talked about checking for family history and these should be just reminders because a lot of these were covered earlier in the morning. So looking at family history, assessing for comorbidities like autonomic dysfunction, cardiomyopathy, also carpal tunnel syndrome or carpal tunnel symptoms was a big one for them that should raise your suspicion. And then finally, has a patient previously been diagnosed with any progressive neuropathy or unclear origin? So when you have that patients where things have occurred but it's like equivocal findings, what do you do with those? So that should make you more suspicious of potentially amyloid doses. And then they talked about first doing genetic testing, right? And I'm glad we have a genetic counselor because that always comes up and there's always issues around that I'm sure we'll get into. And if it's positive, then they actually recommend for accurate diagnosis either doing and or doing T-shirt biopsy, okay? And or if they have a cardiac phenotype or some symptoms doing the PYP scan or centigraphy. And that's it. So that's currently what's out there. 2023 published, Clinician Census. And next step would be the questions that we're gonna be.