 So Ed and Gary and Mary, can you come sit up here? Are you still mic'd? And we have a microphone up front, and this is being videotaped. So we'd love it if you have a question, if you want to step up to the mic. We're a little over time here, but I would hate to prevent you from asking burning questions. I'd love to even hear the panel ask themselves questions. I bet you raise some interesting questions amongst yourselves. Dr. Marcia Stefanik, would you like to lead off? So I have a burning question for Tracy. On the lipolysis experiment, was that thigh fat lipolysis, or where is the lipolysis actually happening? And to take the next part of that question, you're differentiating subcutaneous and visceral. But what about individual subcutaneous deposits? So we have it in our group. We are just starting to actually do lipolysis with isolated cells. And so we can see more lipolysis in the visceral versus the subcutive fat. But we are starting to, we've measured in vivo lipolysis in resistant versus sensitive. So whole body insulin suppression of fatty acid released by fat cells. In cultured adipocytes, we have only looked at subcutaneous and visceral fat cells. But many people have looked at that and shown differences by depot. We are going to move into comparing lipolysis according to race and sex and resistant versus sensitive subgroups. Did I say lipolysis? I meant liposuction. I meant in the lipolysis. Oh, he said lipolysis. I'm sorry, so that's why I was trying to. Yeah, in the liposuction, was it thigh fat or was it abdominal as well as thigh fat? I actually don't know if there was a thigh fat component. I think it was abdominal. But you have subcutaneous abdominal. The reason I'm asking is that you know that the thigh fat is quite different from abdominal subcutaneous fat. So that's what I'm just trying to get at. Right. You know, I will have to see if there was a thigh fat component. I believe it was abdominal. Much shorter answer to that question. Out amongst yourselves, did you raise any questions looking at each other's slides today that you want to share with us? Because we're almost at break time. Very long-winded ones. Somebody almost made a dive for it. Yeah, Randy's going to do it. Thanks, Randy. This is just a real simple question. In terms of the cytomax process, do those cells survive? Because it seems to me that one of the advantages of the fluorescence and traditional cell sorting is that you can do something with the cells after they go through the process. Right. So that's the same question Irv Weissman asked me. And I said, Irv, well, if you could survive passing through a 13,000 degree flame, I'd like to know how. But it's an interesting thing, because you often will show a technology that can do a lot of things, and then people will say, well, here's what it can't do. And not that it's a negative thing. But actually, when Irv asked me that, it kind of bothered me. And so we figured out how to do it. And so Len Hursenberg's original invention was to interrogate the cells with laser. And then to, based on the information you gain at that point in time, sort the cells a little bit later. So information separated from the sort state. So what we figured out how to do was to separate the information from the cell before the cell is sorted. So we have a way of detaching the ions into a parallel stream. The parallel stream of ions is registered according to the cells. That goes into the CyTOF. And then based on the information, the residual, the cell, which is still alive, or at least not destroyed by flame, can then be sorted. So it's a little bit more cumbersome. And it will never compete with flow cytometry at the rate that flow can work. But it can be done. Maya. This is for Dr. McLaughlin. Have you looked at insulin resistant and weight gain? So are the patients who lose weight and are more insulin resistant, more prone to gaining weight afterwards? I mean, do they become resistant when they gain weight or when they regain their weight? Associated with weight gain. So is it more easy for them to gain weight after losing the weight if they're insulin resistant? So the question I believe is, if you're insulin resistant, are you more prone to regain weight that you've lost? We have not found any difference related to their baseline insulin resistance and their ability to regain weight. And there also are a number of prospective studies over 14 years in the San Antonio Heart Study or in Pima Indians, where they looked at baseline level of insulin resistance. And then they just followed people over 14 years to see if the insulin resistant patients gained more weight over time. Because a lot of people believe that because insulin is an anabolic hormone. It promotes fat storage. You would be more prone to gaining weight. And in fact, they did not find that those insulin resistant or hyperinsulinemic individuals gained any more weight. In fact, the most insulin resistant group gained less weight. Or actually, in the most obese subset of the insulin resistant group, they gained less weight over time. So we also don't find any difference in ability to lose weight on a diet compared to their baseline insulin resistance status. So we do not believe that being insulin resistant or hyperinsulinemic promotes weight gain by itself. Neil. Yeah, this question is Dr. Nolan but obviously you're developing these very sophisticated immune signatures from patient samples. And then in the context of this meeting, one of the obvious questions is, have you looked at lean people versus obese to see if there's any difference? Or have you looked at patients who gain weight or lose weight longitudinally to see if there's any alteration in their signature over time? So we haven't directly done that. But with Mark Davis and Gary Fathman, PJ Utz and Bill Robinson, all of whom you probably know in immunology, we've set up what's called the Human Immune Monitoring Core. We actually, I wrote an equipment grant and got another site off to put down there, as well as a number of other analysis tools that are not in pathology yet but are moving out of the laboratory to set up. And so we have twin studies of several hundred individuals for vaccine research largely. And it's set up to basically be a mill for doing many of these analyses time after again. I'm sure amongst the material that we've got and the individuals we've already analyzed will be obese and or non-obese patients followed over time. So I'm sure the data could be re-analysed in the context of the question you just asked, to at least get some hints towards putting together what I'd imagine would be your new nork. Excellent. Anybody else? Well, thanks for this opening session here. We're going to give you 10 or 15 minute break. We're just a little behind. Please don't wander far, but please get up. There's some coffee outside. Can we thank all the panel speakers from this morning? Maybe you can approach them individually. If you didn't feel like stepping up to the mic, some of them can stay and some of them cannot. And we'll return shortly to hear Dr. Gerald Riven give our second keynote. Thank you very much. The preceding program is copyrighted by the Board of Trustees of the Leland Stanford Junior University. Please visit us at med.stanford.edu.