Can you guys see the Neuromatch conference? I saw a bit of it. I saw your talk, actually, that was good. I thought it worked really well. I was impressed also by the platform and the organization and the software, yeah. It's just 200,000 people came. This sort of seems extraordinary to me. Yeah, it's crazy. They're doing a couple of them. Yeah. And I also saw that CNS is now going fully online. Oh, really? The Nuclear Science Society, yeah. Oh, yeah, yeah, yeah, yeah. Oh, okay. Yeah, that's cool. I feel like it's gonna have a big effect in the long term. There's people who will realize it's possible and will realize that they don't need to travel hover around the world. Yeah. I don't know whether it'll totally kill all, like, will conference as well. I think it'll certainly make an impact. Yeah. I think it seems like there've been more and more conferences popping up. It might just force people to refocus a little bit in which ones are actually worth traveling for. Yeah, exactly. Tim, we have 75 attendees online and we're live on YouTube. So over to you. Ah. I'm gonna start right now. Is that right? Please do, yeah. Hi. So welcome to our open research webinar, Eli's open research webinar. So what we're trying to do here is give early career researchers a platform to distribute their work during the time when a lot of conferences have been canceled and when it's difficult to get jobs, et cetera. And so this is an E-Life program and there are a number of E-Life programs trying to help people in these situations. So I'm Tim Barron. So I'm a Deputy Editor at E-Life. So I'm also a neuroscientist. And today we're gonna hear from, come over to the next slide, yeah, from Catherine Voet, post-doc at Harvard, talking about internal state configures or factory behavior and early sensory processing and Drosophila larvae. And Megan Creed, who's an assistant professor at WashU, who's gonna talk about ventral palatal neurons, modulate a cumble activity to amplify reward value. And Ilke Spak, who's a Vaini research fellow at Donders in Holland, who's gonna talk about the hippocampal and prefrontal theta band mechanisms underpin implicit spatial context learning. Great, so after each 10 minute talk, we have five minutes for questions for the speaker and then we'll move on to the next talk. And so if you wanna ask a question, you can type it into the chat on Zoom or directly into the Google document linked here. You can see that and the link is also in the chat. And we're also joined by Miranda, Anya, and Naomi from Elife, who are working in the background to support you.  So if you're able to, I'll invite you by name to ask your question and the team will then unmute you so you can do that. Otherwise, I can read your question out loud and include your name where possible. So the open notes document is also a place for you to contribute shared public notes. I mean, welcome to that. And so if you've got chats or discussion about something that's unclear in the talk, you think the other people can help with. And you can list yourself as a contributor on the list above for today's webinar. Okay, finally, I'd just like to let you know we're recording this webinar and also live streaming it on YouTube. And so I'm just gonna ask you to be respectful, honest, inclusive, accommodating, appreciative, and open to learning. Don't attack, demean, disrupt, harass, or threaten others or encourage such behavior. And if you feel uncomfortable or unwelcome on any of these webinars, please contact by Elife by email to eventsatelifesciences.org. And so this inbox is being watched by Miranda and Anya Elife. And lastly, the Elife organizers reserve the right to ask anyone to leave or deny access to a subsequent webinar on Zoom. Cool, thanks very much indeed. So first up, we'll hear from Catherine. Over to you, Catherine. Thanks. I'll share my screen. Thank you all for coming and thank you for the opportunity to present my work here. Start this. Okay, does it work? Yeah, I think that's great. So yeah, thank you. And I'm a postdoc in Harvard and I'm working with Christopher LaLarva and how internal state effects are factory processing. And as a neuroscientist, I'm interested in how the brain works, how the brain integrates information and comes up with the best behavior in the end. So you might imagine a situation where there's a sensory queue where it's really good to have a fast and a flexible behavior. But you also might think that you don't even really need a brain for such a stereotype behavior. However, there's other situations, for example, when you go shopping in the supermarket, where there's a sensory queue that can elicit several behaviors. And it really depends on context, on your experience and also on your internal state, how you respond to the sensory queues, for example, what to buy in the supermarket. And I think you really need your brain for that. And especially internal state is really important and I think all of you know this example where you normally wanna do and go shopping something like this, but in the end, you end up with a cart like this because you're hungry. So I think this is really interesting because we're exposed to the same stimuli, but our behavior changes due to some change in internal processing of the sensory queue. And I'm interested in how this works in the brain and what is the underlying neural circuit. And so this is really hard to look at this in humans. So I turn to the fly larvae and we don't send the fly larvae to the supermarket, but we can ask them about their olfactory preference. So we put them in this little petri dish and on the right side, you see a little order well where we have an order and we ask them if they approach or avoid the order. And we can use fed larvae fresh from the food or we can food deprived them in border for a few hours and then test them in the setup. And we found this order journal acetate where in the fed state, the larvae do not approach the order well. You can see that they accumulated the opposite side of the petri dish. Whereas in the food deprived state, they actually go and approach the order and check it out. So there's a drastic change in behavior due to internal state. They go from avoidance to the order to attraction to the order. So indeed they showed us, I think sophisticated behavior. And now in the drosophila, we can go and we can use the broad range of genetic tools to manipulate single cell types and cell components, especially in the larvae, we can do functional imaging and intact animal because they are transparent. So we can look at the activity of the neurons and we already know very well the anatomy of the neural circuits because there is EM reconstruction of almost the whole brain available. Okay, so now if we test larvae that have non-functional sensory or factory neurons, they do not respond to the order. So we think it's something is happening in the processing of the olfactory information.  So the order is received by olfactory receptor neurons, the orange. And then projected to the brain, to the antenna lobe, which in mammals would be the olfactory bulb, where it's sent to glomeruli. And then from these glomeruli projection neurons bring the information to the higher brain in the fly, it's to the lateral horn for innate behavior to the much from body for learning in memory. And so I'm asking, so where in this processing system, where is this food deprivation come in and change the processing? So first we wanted to look at the activity of these neurons and we are using this functional imaging setup where we build a microfluidics chip where we can immobilize the fly larva and we can present olfactory stimuli. So on the bottom left, you see the tubes that come into the chip that bring the olfactory sensory stimuli. On the right, you can see the little larva squeezed in this channel with its nose stuck to out of the channel to proceed olfactory stimulus. And in the larva, we can see, for example, something like this. So here you can see the olfactory sensory neurons and one of them highlighted in green. And you can see that they're sit at the nose of the larva on the top, where there's the dendrites and the cell bodies and then further down in the body of the larva as the brain and we can see the antenna lobe. And all the imaging I'm doing is done in this, in this antenna lobe in the first olfactory processing center. So if we now look at the response of the orange to the order, here you see orange or AB2A. You can see that they strongly respond to the order but there is really no difference whether they're fed or food deprived. So we don't see any modulation at this stage. However, if we look a step further down in the olfactory projection neurons, we can actually see that one of them, the uniglomerular projection neurons shown increase in activity upon order. And then based on the M data, we also know that there is a second type of projection neurons, the so-called multi-glomerular projection neurons that project to a different part of the brain. And if we look in one of these neurons, we can actually see that we see a decrease in activity upon food. And then we were also interested if these neurons actually play a role for behavior. So we silenced these neurons. And if we do this for the uniglomerular projections, we can see that they do not switch anymore from avoidance to attraction, but they always show avoidance to the order. So the food deprived behavior is impaired. However, if we look at the multi-glomerular projection neurons, actually the avoidance behavior is impaired and they already show attraction in the fat state. So the modulation has to come in in the antenna lobe. And what's happening upon food deprivation is that the avoidance pathway is inhibited and the attraction pathway is excited. But we were wondering, how does it actually work in the antenna lobe? So first we let's look at the inhibition of the multi-glomerular projection neurons. So we noted glutamate is actually inhibitory in the fly antenna lobe because it activates the glutamate-gated chloride channel. So we were wondering what happens if we take out this chloride channel using RNAi, is there still this inhibition going on? And actually we do not see this inhibition anymore. So we think this is mediated via glutamate and we also see the phenotype in the behavior. So if we take out this glutamate-gated chloride channel from this multi-glomerular projection neurons, they do not change their behavior to attraction anymore. So this was really interesting. But we also know, I don't have time to show the data, but we noted this glutamate is coming from local inhibitory neurons. So we don't think that this is actually the source of the food deprivation signal. So we actually also looked at this uniglomerular projection neurons which show the increase in activity. If you look at those, it has been shown that they express excitatory serotonergic receptor, the 5-HT7 receptor. So we used a novel cell-specific CRISPR-Cas9 knockout tool to actually get rid of this receptor in these uniglomerular projection neurons. And if we do this, yeah, we don't see the increase anymore. So we think this is actually mediated via serotonergic signaling. And the same in behavior. If we block this receptor and use neurons and we test the larvae for behavior, they do not switch to the attraction behavior. And so the source of serotonin we know is the serotonergic CSD neuron which is very prominent in the olfactory system of the fly larvae. On the bottom, you see the antenna lobes. On the top, you see that it has a lot of projections in the higher brain. It's actually input regions. So it receives a lot of input in the higher brain and projects down to the antenna. If you look at the activity of this neuron, you can also see that it has increased response into food deprived state. If we silence this neuron, you can see that it's also required for the attraction. So what we see is happening. And then we were wondering if there's actually connections between the CSD neuron and the uniclomerular projection neuron because they seem to have a big influence on each other. But actually we do not see any synapses in the wiring diagram in the EM data. So what we think is happening that upon increased activation of the serotonergic neuron, we get a synaptic overspell or non-synaptic release of serotonin that only then the serotonin is able to modulate the uniclomerular projection neurons. So since the CSD is a feedback neuron from the higher brain, we were wondering if this serotonergic signaling is actually sufficient to induce the food deprived behavior and also modulates the avoidance path failure at the MPNs. So what we did is we actually artificially activated the CSD neuron to see if we can do a normally fat larvae would avoid the order. And we want to see if we activate this neuron in a fat larva, if we can mimic the food deprived behavior which would be attraction to the order. And indeed that's what we see. If we activate the CSD neuron, the larvae are already attracted to the order and mimic the food deprived behavior. So we think that CSD is actually the food deprivation signal that's feeding back from the higher brain to the internal. And to bring all this data together, we also built a very simple computational dynamical systems model where we put in information from the connectome about connection connectivity and the connection weights based on number of synapses. And we also integrated information about the neural activity from experiments about the non-synaptic neural modulation but also about the signs of connections which is the either excitatory inhibitory. And this model actually works and we can also perform manipulations in this model and we see also the same results as we see in the experiments. Okay, so to sum this up, I hope I could show you that actually the early, the first early olfactory processing centers much more complicated thought. If you wanna read more about this, there is a preprint available in bioarchive about this study. And shortly I just wanna highlight that we found a new projection neuron pathway that's going to a different region in the higher brain which is also required for innate avoidance behavior. So it's not just these uniglomerular projection neurons as we thought before. And also I could show that there is certain energetic feedback from the higher brain which brings information into the antenna lobe about internal state and which severely modulates the processing in the antenna lobe. And I think this could be a general mechanism how internal state could affect different sensory processing regions, also in other animals. I hope I could convince you that drosophila is a really great model organism. We can all use all these tools, genetic tool here, cost imaging, EM reconstruction, modeling to actually really learn a lot about the brain. And if you wanna read more about functional connectomics in drosophila, feel free to look at a little perspective that I wrote which is on Journal of Neurogenetics. And yeah, then I end and thanks to the lab and all the collaborators and the funding and thank you all for listening. Cool, okay. So hang on a second. So, sorry, I guess there are loads of questions and I'm new to this too. So I'm just figuring out how I get the question. So superb talk by the way, lots of round of applause. So Naomi, should I invite Peter Ape up to give this first question here? Now we've posted you a first question in the chat, I'll post it again. How do I look at the chat? Do I have to stop? So Naomi's posting to me in the chat and I'm supposed to be the clever one. Oh, so this question here that I'm supposed to ask is apparently from, okay, so could you refer the circuit function just based on the conectomics data? I guess the answer to that is no, but you should answer that question. Yeah, no, I mean, our initial hypothesis was based on the conectomics data because we saw that there might stay dependent activity because we found a cascade of inhibitory neurons. So there might be two states in one state, one of the inhibitory neuron is active in another state. The downstream inhibitory neuron would be active. So the conectomic data already suggested that there's like a two-state system, but we really know what's going on and how it works and how it switches. And yeah, and as you could see, we also found some connection which was not synaptic and which was not predicted by the EM. So yeah, I think it's really hard. I think we can get a lot of hypotheses and ideas from the conectome, but in the end, we really have to look at details and neurotransmitters and receptors to really see what's going on. Cool, excellent. Good, Miranda, who shall I call up now? Who, what shall I be doing now? Sorry. Hi, Tim, don't worry. There's Dana Galleli on the line who's got a good question here in the chat. Okay. If you're ready, we can unmute you. I'm just coming to you now. It's a very long list of attendees. It's amazing. All right, Dana, you're allowed to talk if you'd like to share your question. Hello, my question is, do you think other PN channels are also affected by feeding state or is this channel unique? So we already found two channels that are affected. It's this type of uniglomerular projection neurons where there's 21 and they're all very similar. And then we found this multi-glomerular projection neuron, which is one out of 14. So there's 13 other multi-glomerular projection neurons that all have different projection patterns and input patterns. And I guess they might also be affected, but we don't really know what's their function. And for most of them, we don't have driver lines so we can't really look at them right now. So I'm happy we found this one line for this MPM that I showed you. But yeah, I think there is much more stuff happening, yeah. And next we have Karen Chang. You've also got an interesting question. I've allowed you to talk if you'd like to unmute yourself. Hi, great talk. I was just wondering what is known about CSD neurons modulate? What do you think internal state modulation in adults also might be mediated through them? But there is a lot of studies in the adult fly and also it's in moth and in other insects. But so far it's not really known what's the function of this neuron. We know that it affects the antenna lobe in similar ways. Also in the adult, there's different types of serotonin receptors expressed in different neurons in the antenna lobe and they're affected by the CSD at least most of them. But what's the actual function? We don't know yet, yeah. Okay, so it looks like that was a fantastic talk. So we sure have another, I don't know how rounder applause works on Zoom but we should all have another flap. And then we're gonna move on to Megan now talking about ventral palatal neurons and I'll leave it up to you. Fantastic, thanks Catherine. Okay, so thank you very much for the opportunity to speak to you today. I want to tell you about new work from my lab looking at different populations of ventral palatal neurons and how they modulate reward seeking and processing. So for those of you who don't know, the Vettral balladum is a critical node in the basal ganglia. According to classical models of the basal ganglia, you have the nucleus accumbens which integrates excitatory inputs from a variety of brain structures and sends inhibitory projections downstream to the ventral paladum. And one of the more consistent findings in behavioral reward neuroscience is that during reward consumption, you have an inhibition of the nucleus accumbens which disinhibits or releases these downstream structures which is involved in the seeking or processing of reward. And I say this is a consistent finding in neuroscience. This is a recent meta analysis looking across a variety of behavioral paradigms and looking at the proportion of inhibitory responses recorded in the nucleus accumbens during reward consumption. However, there's a lot of heterogeneity in these tasks so different reinforcers are used. There's different operant contingencies or metabolic states. So the first thing I wanna show you is that we can replicate this in our own hands. And the way we did this was to do in vivo recordings of the nucleus accumbens shell in freely moving mice. These were sated mice so there was no metabolic need and there was no operant contingency. So these are just mice that are freely able to like a highly palatable reward in a free access manner during a one hour session. And this is the licking behavior shown here just aligned to a optical locometer. And even these conditions who are able to replicate this result, here's a single unit example in the nucleus accumbens showing a pronounced decrease of accumbal firing. The average of all are significantly modulated units. And consistent with prior literature we did find that even in the absence of any instrumental responding or contingencies we still saw this robust inhibition of the nucleus accumbens shell during reward consumption. We did a further experiment to show that this was in fact causal to reward consumption by using an inhibitory opsin injected into the nucleus accumbens shell to specifically inhibit these neurons in a closed loop way during reward consumption. So that's what you're seeing here. So the closed loop stimulation is being driven by the reward consumption. So we're further inhibiting these neurons during this reward consumption state trying to mimic this endogenous pattern or amplify this endogenous pattern. And we see that in our GFP control mice we don't see any effective stimulation but in our channel rhodopsin mice, sorry, our archaeodopsin mice when we inhibit the neurons we're able to further drive reward consumption by amplifying this inhibition. So nothing too controversial here. We've repeated this finding from the literature that nucleus accumbens shell inhibition is causally related to reward consumption. But what we don't know is what the neural substrate of this nucleus accumbens inhibition is. And turning back to our very classic simplified model of the ventral basal ganglia where we have the nucleus accumbens shell inhibiting the ventral pallidum. We know that the ventral pallidum also plays a really active role in reward processing. So firing rates within the VP encode the expected and actual value of reward. They also encode the bigger or motivation to go seek reward. And critically, a recent work out of Patricia Genek's lab has shown that if you record in both the accumbens and the ventral pallidum simultaneously that these value signals are more widely represented in the VP and they actually occur earlier in the ventral pallidum relative to the nucleus accumbens. So we started looking at old anatomical papers where they've reported this thin palatal fugal projections back to the nucleus accumbens. And we're referring to these for the purposes of this talk as the ventral archipaladol neurons after the pathway that's been described in the dorsal basal ganglia from the globus pallidus back to stritum. And our hypothesis was that this thin projection of neurons from the ventral pallidum back to the accumbens is actually an important source of inhibition that drives this pause in accumbal firing. So rather than just being a passive output of the nucleus accumbens this VP is actively orchestrating accumbal responses as well. And to test this whether the VP is a source of inhibition we first need to tell you that the nucleus accumbens a heterogeneous. So it contains different classes of projection neurons that come in two types based on their expression of the dopamine receptor either D1 spiny projection neurons or D2 spiny projection neurons. It also has different classes of interneurons. Here we're focusing on the cholinergic interneurons or chats and the part-validine neurons or the PV cells. So we first tried to answer this question by injecting a channel radopsin into the ventral paladum. And then we took slices of the accumbens and we used different transgenic lines that expressed a fluorescent reporter in each of these cell types to record from identified nucleus accumbens neurons. This is showing you what that looks like under the patch microscope. So we're going in and targeting identified cells and this is a labeled fibers from the ventral paladum expressing channel radopsin in close opposition. And we patched over a hundred cells of each cell type. So about 420 cells total. And this is showing you the location of those cells within the accumbens here. This is the commissure and the locations of recorded neurons around the accumbens shell. And what's readily apparent is that there's really high rates of connectivity. So this is quantified here looking at the spiny projection neurons where we see over 75% of the neurons that we recorded had this input from the ventral paladum. And a smaller but still significant proportion of interneurons were also innervated. So about 28 to 30% of the cholinergic and parvalbumin interneurons. And I don't have time to show you any of the data, but pharmacologically and biophysically we determined that these connections are all inhibitory. So they release GABA and they're monosynaptic. So we say they're monosynaptic, but we know that the nucleus accumbens has a lot of recurrent local connectivity. And so when we take slices we might be missing a lot of the important network dynamics. And so stimulation of the ventral paladum might have complex effects on the structure. So we've repeated this experiment but instead of cutting slices we performed in vivo recordings. So we have the same channeled-opsin injection into the ventral paladum, but instead of taking slices we're now in planting an electrode array into the nucleus accumbenshell that's coupled to an optic fiber to stimulate in vivo. And we recorded from the accumbenshell and we used electrophysiological properties to isolate putative medium spiny neurons. These are the projection neurons and putative interneurons. We also had a fair number of multiunits where we couldn't distinguish what cell type were determined that they only came from one unit. And consistent with our sliced data what we saw is when we illuminated the terminals in the ventral paladum those cells in the nucleus accumbens showed this robust inhibition in vivo. So these are all single unit examples that you're seeing here. This is the firing of a putative medium spiny neuron when we shine the light we see this robust and immediate inhibition that lasts for the duration of the light pulse. And this is the average data shown here. So very robust consistent response regardless of the post-synaptic cell type. So what we've confirmed is that in vivo and ex vivo the ventral paladum does send a projection back to the accumbenshell and can inhibit those neurons. This is the summary data shown here showing the inhibition. But we haven't shown. So if we know that is that the, or we haven't asked rather is are these ventral paladal neurons active during reward consumption? So if we know the nucleus accumbens is inhibited during reward consumption that these cells inhibit the nucleus accumbens in vivo we predict that they would in fact be active during reward consumption. And we answered this question using fiber photometry in vivo to measure bulk calcium signal. We injected first a retrograde Cree virus into the nucleus accumbenshell and then a Cree dependent calcium indicator G-Camp6 into the ventral paladum. This is going to allow us to express that option only in these NAC projecting VP neurons. So selectively targeting the subpopulation. And we just measure bulk calcium signal in vivo as the mouse is doing the same pre access reward consumption task. If we look at the calcium signal aligned to the onset of these lickbouts we see that yes, consistent with our hypothesis we do see an increase in the G-Camp signal immediately after reward consumption onset. We don't see this in our GFP controls which is reassuring. And we took this analysis one step further so for each subject we took the top quartile trials so the quartile where the mice showed the highest G-Camp response and the quartile where they showed the lowest G-Camp response at the onset of lickbout. So all the mice are included in this analysis and then we asked how does the behavior or does the behavior differ between these two classes of trials? We found that in the mice, in the trials that were preceded by the highest G-Camp signal had significantly longer lickbouts. So even 10 seconds after that G-Camp peak we see that mice are, there's a 50% chance that the mice are being, are so engaging in this lickbout whereas if we look at the behavior on those low G-Camp trials immediately after the mice have initiated the lickbout they've dropped to a 50% probability of continuing. So we do see a really robust change in behavior that's predicted by this initial difference in the G-Camp signal immediately after reward consumption onset. And we wanted to test this relationship in a more causal way. So this is correlating the endogenous activity with the behavior. But our next question was whether this ventral palatal arc whether this archipalatal activity can actually promote reward consumption. And we did this by turning back to our optogenetic stimulation. So here we're injecting we're still sticking with that same free access task. We're injecting channel redoxin into the ventral palatum and we're stimulating fibers over the nucleus accumbens to selectively target those ventral palatal projections innervating the nucleus accumbens shell. And we stimulated in two ways. The first was using that same closed loop stimulation. So whenever the mice approach the rewards this triggers the onset of the light stimulation in a closed loop way. And then it almost as a control experiment we did an open loop stimulation. So we took back the same pattern of light but played it in a random way scrambled for the trial to ask if the stimulation on its own would drive reward approach. And this is showing the histology here showing our infection site in the ventral palatum and the terminal fields in the accumbens shell with the optic fiber implanted over the accumbens shell to activate those terminals. So what we found is that relative to the unstimulated condition when we applied stimulation in the open loop way so randomly throughout the trial we didn't see any effect on behavior. But if we stimulated in a closed loop way we saw this twofold increase in the amount of time that the mice spent drinking or consuming this highly palatable reward. And this was driven by an increase in the mean bout length. So the mice are spending longer time at each reward bout. And it wasn't driven by the number of reward approaches or the number of like about. So we're not changing how many times the mouse is approaching the reward we're just extending those ongoing like abouts. And this is significant because this shift in the microstructure of the looking towards longer lookouts is one index of palatability or hedonic value of reward. And we hypothesize that the ventral pallidum is encoding a value signal. And we tested this a little bit more explicitly in two different ways. The first was by filming mice at 140 frames per second and scoring these oral facial reactivity reactions to the consumed reward. Something that has been done for decades in the behavioral pharmacology literature. And we did in practice see that relative to unstimulated trials when the mouse were consuming rewards they did show more of these hedonic facial reactions which represent the effective response independent of motivation. And we also ran the mice in a two bottle choice task. So this was a choice where the mouse had the choice between two different bottles of reward that were exactly identical. Except one of the bottles was paired with reward with the stimulation, sorry. And the other bottle was unstimulated. And despite the fact that these two bottles were identical the majority of mice developed a preference for the bottle that was paired with the stimulation of this ventral archipelago pathway which was an effect that was not evident in the control mice that just received light stimulation without the active oxen being expressed. And as a final control, we did an operant task where the mouse were allowed to just nose poke and receive stimulation directly independently of reward. And in fact, we didn't see any preference so the mice were not willing to work or we're not willing to work to receive stimulation of the ventral archipelago pathway in the absence of the reward. So suggesting that stimulation of this pathway itself is not reinforcing, but when paired with another reward it promotes or enhances the value of that reward. So in summary, what I've shown you is that the Nucleus Cummins inhibition is in fact necessary for reward consumption that these ventral palatal neurons inhibit the nackshell both in vivo and ex vivo. That the endogenous activity of the ventral archipelago pathway predicts subsequent reward consumption and that these ventral palatal neurons amplify reward value to drive further consumption. With that, I'll thank lab members, specifically Jessica Tuley and Ivan Baches who did a lot of the work on this project and take any questions. Hey, so thanks for really very much indeed, Megan. I think I'm a bit more in control this time so I know what I'm doing, but unfortunately the chat's been closed so we have to wait for questions by email. So in the meantime, yeah, so I'm sorry about that. In the meantime, so it's really, really interesting stuff and so it seemed to me that at the end of the day you think that these palatal neurons are encoding value and feeding that value back to the accumbens and I feel like that would do two things. One, it would make them drink longer and the second thing it would do would make them find the stimulus more rewarding next time they were going to, so they would learn something from that value, right? In a sort of classic reward prediction or reinforcement learning style way. And I wonder if you could dissociate that, those two effects, is it just like a physical mechanism for making them continue to drink or is it something about the value? By making them, by figuring out do they actually return more often to that thing or is it just that they stay there longer when they're there? Yeah, so that's a good question whether it's specifically for meal termination or whether it is actually the value. So I think that the two things, the first is that this oral facial reactivity for what it's worth, that's all post-ingestive behavior in response to the reward. So that's one sort of piece of evidence that it's not just a meal termination response. But the other thing is when we look at the two-bottle choice task where we had the two identical rewards, this was one in an overnight session, so they had two identical rewards, one shared with the stimulation, the other wasn't. If you look at the time course of that behavior, it does emerge as a learning signal. So we didn't do a progress afterwards to see if we condition like left, but it's right-bottle doesn't. I noticed that graph was a percentage of total time or something at the reward. It wasn't like how often they would choose that one versus the other one, is that correct? Right, okay, so that was the volume, the total volume that they drank out of the assumed rewards. But if we look at the learning throughout the nighttime session, if we take the last half of the night, then we see that the mice are returning to that bottle more and they're spending more time with that bottle. So we don't see that at the beginning of the session, although whether that's really learning because they're still getting the stimulation even though they're going back there more, it's harder. But there is a learning component to it if it's changing. Yes. It is, but we haven't done the experiment where we put them back in the next day and ask, now that we've removed the stimulation, we haven't done a probe test to see if we really have conditioned that response over the course of the night, which would be interesting to do. And do you have a feeling for where the VP is getting these signals from or how it's computing these signals itself? That's a pretty, that's a very loaded question. We know that the VP gets input from, well, it gets a lot of the input from the accumbens. We also know that it, I mean, I know that there are lots of people working actively on this problem, whether they're our brainstem or early signals that, or polemic signals that are coming in that are maybe a little bit more immediate than ones that have gone through this accumbul loop and come back to the VP. It can't be accumbul stuff because it's because accumbul stuff is being, it's silent, it's that input in order to get an input from somewhere else. Right. So now we have a question from, so can we unmute, Marie? Is it Labus, Labus? I'll try, Marie, I'm gonna try and find you right now. Or I could just ask this question from Marie. Marie is able to unmute. Yes, can you hear me? Yes, we can. Well, actually my question was the question that Tim just, what the input might be. I was wondering whether dopamine neurons arrive in the VP and might promote activity of archipelago neurons. I don't know that's, obviously that's not what you've been studying, but I was just curious. Yeah, so we do know that the VP expresses D1, D2 and D3 dopamine receptors. And recording studies from about 20 years ago showed that if you do recordings of these cells while infusing dopamine agonists, the cells are responsive. They show very mixed patterns of activity in response to dopamine agonist infusion. So they do get dopamine innovation. It's functional in the VP, but we haven't started to tease out that heterogeneity or where these signals are coming from. And then we've got one more question, I think a clarification question that maybe, A McDonald, I'm not sure what it is. I think that's Alison. So Alison, if you're able to unmute, you can ask that question now. Go ahead, Tim, go and ask it. Thank you. So Alison's just asking a clarification question. I may have missed it, but do ventral archipelodal neurons make up a large percentage of VP neurons? No, so they make about 20%. When we've done, we had a lot of data that we obviously didn't show in the 10 minutes, but we've done retrobe tracing and dual retrobe tracing, looking at classical projection targets. So seeding in the ventral tegmental area, which is one of the classical output targets of VP and looking at the proportion of overlap. We don't see much overlap. So it seems like they're a distinct population in these classical projection ventral patterns, but they make up slightly under 20% by our rough calculation, given the imperfect nature of these retrograde dual tracing techniques. What a fabulous talk and a great set of questions. Thanks very much indeed, everybody. Fantastic. Yeah, thank you. I'm just going to hop in here. Hi, I'm Naomi, and I'm running in the background. I just want to thank everybody for their patience while we deal with some trolls and especially Megan and Ketchum who had to do their talks with some interference on the chat while they were talking. You've done an excellent job, and those questions that just came in were really good. We think we've probably managed to kick off the one or two people that were coming in with different usernames. So we're just going to proceed as normal and just thank you. Unfortunately, these things happened, but it's really great to see how many genuine attendees we have here. And these are great talks. Thanks for sharing as well, Tim. No problem at all. And welcome Ilka to give our next talk. Who's going to be talking about Hippocampal Theta? I don't have the title in front of me now, but I probably could, here we go. Yeah, Hippocampal and Refrontal Theta. So kick over to you, Ilka. Thank you very much. I'll just share my screen here. There we go. All right, yeah, so a bit of a gear change from Drosophila to rodents to humans and more of a cognitive study here. So yeah, Hippocampal, Refrontal Theta mechanisms underpin spatial context learning. But before I go into the details of this particular study, just a little bit of background of the research I'm interested in general. So I'm interested in the relationship between predictive processing in the brain and conscious visual perception. And of course, I'm not the first one to come up with the idea that there might be a relationship between the two. It's actually quite a popular topic. These last a few decades, perception as a result of an inference process with 21st century authors associated with this idea, like the ones I'm listing here. And usually when you read papers about this idea, perception as a result of an inference process, they trace the idea back to Helmholtz in the 19th century. But I just thought I'd take the opportunity in a talk like this is a point out that actually you can trace this back at least to the 11th century Arab scholar, Al-Hazan, which I thought was quite interesting. It's not my scholarly discovery, I have to say. It's something that I write in actual scholarly papers and it might, with a bit of goodwill, you can even trace it back to Ptolemy's optics from the second century. So this is a very old idea that there is this relationship between perception as a result of an inference process and conscious visual perception. So that's kind of the background of my research interest. But of course, this is still too vague for an actual experiment. So for the study I'm going to present to you today, I've narrowed down to these research questions. So how does the brain learn and exploit spatial contextual information or spatial contextual priors, if you will? And does this process require conscious awareness of what is being learned? So a little bit of a motivating example if I present to you this image of a messy desk which apparently according to science is a sign of genius. And I ask you to locate the computer mouse. You're able to do this quite well. That's where it is. And that's because the mouse is usually located next to the computer keyboard and below the computer monitor. So there are these spatial contextual associations that humans are very good at exploiting in order to navigate through a visual scene, if you will, in order to locate relevant objects. Now in the experiment I did, I did not use a messy desk but I used a very classical visual search task where human observers were presented with this search array and where they had to search for this oriented T amongst L-shaped distractors. And then once they found it, they needed to push a button left or right to indicate the orientation of the T. Now what the participants did not know is that some of these search arrays, in fact, half of them were repeated over and over again throughout the course of this experiment. So in a schema ties, you can see it like this. So if this is the first trial, then the next trial would be a new trial because it's completely different from the first one. But then later on there will be also an old trial because the configuration of the displays identical to the first one. No, they were identical. I'm talking about the location and the orientation of all the distractors and the location of the target but not the orientation of the target. So participants could not learn the correct response given the spatial context where they could learn associations between the spatial context and the location of the target. This is quite a classical study. It's known as the contextual queuing task. And what I recorded while people were doing this task is a magnetoencephalography. So MEG data to look at the brain responses while people were doing this. But first the behavioral data. So I was able to reproduce this very classical contextual queuing effect where people get faster for all trials compared to new ones and also more accurate. And this was a very clear effect during the second half of the experiment. But like I said, this is not new. This has been shown before. But what I noticed when I looked at these reaction time curves over the course of the experiment is that it appears like there's no effect in the beginning of the experiment. And then all of a sudden there is an effect that appears to remain constant throughout the rest of the experiment. And I wanted to quantify whether that is indeed the case or whether that is an artifact. So what I did was I fitted several models to this effect curve. So first of all, I computed the effect curve which was just all the minus new, basically the reaction time benefit that participants are having. And I compared that to different models. So one was a no effect model, a constant effect model or indeed a switch point or what you might intuitively expect linear effect models. And what I found was that the switch point model was clearly the best one. So it appears indeed that there is no behavioral benefit in the beginning of the experiment. Then there's a sudden switch and after participants have learned that there are these repeats in the experiment, then there is a constant reaction time benefit. So far for the behavioral results, as I mentioned, I recorded MEG while people were doing this and I was mainly interested in the neural oscillatory mechanisms during this experiment and particularly how all trials might be processed differently from the new trials. So when I look at that contrast, I'm plugging that here, what I see is this clear effect in the theta band frequency range. In the first, let's say 500 milliseconds of stimulus processing with a somewhat diffuse sensitive photography which fortunately becomes quite clear after I do source reconstruction on this effect. And then I found that this effect is stemming from two clear clusters, one in the right hippocampus and one in the bilateral, mainly left superior prefrontal cortex. What I can then do is zoom into these clusters to see how this effect evolves over the time course of the experiment. And that's what I'm plotting here for the hippocampus. So blue is all trials again, red is new trials and you can see that all trials have elevated hippocampal theta power, mainly in the beginning of the experiment but no effect anymore in the later part of the experiment whereas the prefrontal cortex behaves very differently. So there's no effect in the very beginning and after which there is a sustained effect for old versus new throughout the rest of the experiment. I can take that effect and plot those on the same axis to compare them directly. Now I'm just computing again a different score old versus new. That's what I'm showing here for the hippocampus. So you can see the exact same. It ramps up and then down again to no effect levels. And now I plot the reaction time data also old versus new on the same axis. You can actually see that as this hippocampus effect ramps up and then down again only as it's ramping down. Do you see the reaction time effect ramping up? And interestingly the prefrontal cortex does something very different to the hippocampus and actually mirrors this reaction time effect quite closely. So it seems that beginning of the experiment people have not learned anything but are still trying to pick up on what's going on. That's what's involving the hippocampal theta rhythm. After hippocampal theta ramps down again you see a behavioral effect which is mirrored by a theta band effect in the prefrontal cortex. So on to the next question, what about awareness? So after people did 22 blocks of this search task I asked them a subjective question. Did you have the feeling that some displays occurred multiple times over the course of this experiment? And they gave a simple yes no answer. And after they gave an answer to this question they had to do one block of an objective recognition task. So instead of having to search for this T people were just asked, have you seen this display before? Yes or no. And that allowed me to assess the explicit memory that people might have formed about these search displays. So remember they've seen these old displays 22 times already over the course of the experiment. Now what's a classical finding in these contextual queuing tasks, this is not novel, is that people if you analyze the whole behavioral sample people are actually at chance level in recognizing displays as old. So that's usually taken as evidence that this is an implicit effect, but that's heavily debated. In my experiment ensemble I was able to replicate that. So I also see that the sample as a whole is at chance level. But I see quite a lot of variance here in this recognition accuracy. But now because I also had this subjective question, did you have the feeling that there were a PTS no? I could do a split, about half of the people answered yes, about half answered no, fortunately for me. And I see that, excuse me, the people who had no feeling that there were repeats are indeed at chance level. But the people who did have the feeling that there were repeats indeed also have objectively speaking explicit memory about the repeats in the experiment. And now the crucial question, of course, is how does this relate to the search task benefit that people form during the search task? How does this relate to the contextual queuing effect? And what I found was completely opposite to what I had expected. I see that both these groups, the people with and without feeling of recognition, have a significant contextual queuing effect. But the people who did not form any explicit knowledge have a considerably greater contextual queuing effect than the people who did form explicit knowledge. So remember, this is the split based on the subjective feeling. So I just asked them, did you have the feeling that there were repeats? Yes, no. But I also have this objective metric of accuracy. And when I then correlate that across the participants to how much contextual queuing they show during the search task, I actually see an inverse relationship here. So wrapping up, people learn spatial contextual associations, or in other words, prior expectations about spatial relationships rapidly and implicitly. And in fact, what's more is that the less conscious they are and the less explicit knowledge they have about these repeats, the greater the behavior benefit, which is quite in contrast to my expectations. The learning phase in this task transiently involves the hippocampal theta rhythm. And after that, there's not really a gradual change, but there is an abrupt switch to an exploitation phase in the behavior, which is dominated by theta rhythm in the prefrontal cortex. So taking together these findings shed light on how the brain continuously adapts its model of the world to optimally structure perception and guide behavior. And what I think is quite an interesting corollary here is that high level cortical structures like the hippocampus and the prefrontal cortex are not necessarily linked to awareness of stuff that's being learned. So I'll end by thanking you all. Also thanks, of course, to everyone in the Langer Lab. I didn't put any names, but nonetheless, thank you very much. And I'll point you to this paper in case you're interested, which is about exactly what I just presented. It was published a few months ago. So thanks, and I'll take questions. Hey, brilliant, excellent talk. Very, very clear, beautiful data. Again, we're going to wait for some questions. And I'll ask you a couple of my own in the meantime. I think now I should announce that we're going to go back to asking questions on this chat. OK, so cool. So I think that you're saying that the people who have the biggest effects are doing it subconsciously. And so does that hippocampal theta, which is like a subconscious recognition memory style effect, does that also show a cross-subject correlation? Then it should do if that's the right argument. So actually, I'm glad that you asked this, because I have a slide about this. So actually, the hippocampal theta effect does not correlate directly with the behavioral performance. But the prefrontal effect does. So this is what I'm showing here. So I'll just show them all. So I'm showing here hippocampal theta power on the x-axis for a prefrontal cortex in the right and hippocampal in the left, separately for the old trials in the top and the new trials in the bottom. And what I see is only the theta power on the old trial in the prefrontal cortex correlates across the participants with the contextual curing effect. So like you said, I completely expected also the hippocampus to correlate, but that's not the case. Only see this effect for the prefrontal cortex, yeah. I thought you were arguing that that frontal one was like in a hormone contrast. I understand what's going on. And the, but OK, I may have missed this. No, so I think what's going on is that the, I think both these effects are reflective of the implicit, both these neural effects are reflecting the implicit behavioral benefit. And I didn't find anything related to the explicit. Sorry, I misunderstood. OK, cool. I'm going to move on to a great question. So hang on, from Daniel Whitblitt. So maybe I probably pronounced that wrong, but maybe we can invite him onto the chat to... He's got a microphone. Would you be able to read out his question, please? Sure, I can. Thanks, Naomi, for handling everything. So would you be able to explain exactly how you define theta power is the question? Yes, I can explain that. So I'll try to go back to the slide with the time frequency. So this is so I computed power in many frequency bands and across many different time points. And here theta, I take to understand oscillatory power between the three and nine hertz frequency band. Does that answer the question? Three and nine hertz. Yeah, that seems to answer the question to me. Cool. And we have a second question from Wu. I think it is... Yeah, I'm just going to see if he can talk or she can talk. They can talk. Hi. Sorry. I think I missed some information about the minutes of the figure of the blue activities and the newer sort of old contracts across the blocks, with also hippocampus fronto and also the reaction time. I think it was another strike. Yeah, not this one. This one? Yeah, I think this one. Because I think there's a lot, so many information in these figures. So I'm like, what does... Like what does this mean? I mean, for example, why the prefrontal cortex, the significant box as from like five to 10 blocks and also in the end of the experiment, I think. Mm-hmm. Yeah, so this is showing the evolution over the time course of the full experiment. So I'm not sure I'm fully understanding your question, but maybe if I take one step back, so in this slide, this is more the raw data, the raw power that I'm showing for the old trials, so the ones that were repeated over and over in blue. And then for the new trials, so the ones that were randomly generated every trial in red. And then I see here for hippocampus, you see this effect early on, where all trials have more theta power than new trials. And frontal cortex have more theta power for all trials only later on in the experiment. So then when I can just basically subtract blue minus red to just get one curve, which allows me to explore it a bit in more detail. And that's what I'm plotting here. So yeah, what I'm thinking is going on is that hippocampus is picking up the association. So hippocampus is doing the learning in the theta band. And then later on, once this knowledge needs to be exploited, which we can see in the reaction time, that's when the prefrontal theta rhythm kind of takes over after this switch. Does that answer your question? Oh, yeah, thank you. Okay. Okay, so I think I've... Naomi, can we ask some more questions here? Yeah, I feel like there's some good ones coming in. Is that okay? The round, we've got a couple of things to do before we end on the hour, but we would like to keep people on if they've got a few more minutes to stay. We'd love to support that. So let's try and do that then. So there are two or three interesting-looking questions that maybe can be asked in about two minutes' time. Perfect, thank you. So what do I... So is there something that I should be reading out now, Naomi, or is it a movie? I can do it if you like. That's okay. What we'd like to do, we'd like to see how we can make these talks more engaging. Obviously, we have to have mechanisms to deal with trolls, but that's okay, that's on us. So we would like to actually ask a few questions of the audience right now. We've actually just got the one question that I'm gonna launch right now and attendees should be seeing this question. So it's basically, if we changed anything about this format, which two things do you think we should prioritize? And it may be nothing and that's okay as well. You can't post things in the chat, I recognize, sorry. We're just gonna give them 30 seconds. And actually, so Tim, what we discussed up front, we'd like to keep this, we think we've got the trolls out now. We'd like to keep this Zoom open for 10 minutes or so just to help those questions be answered and for people to chat with the speakers. Are you comfortable with that? I can hang around for 10, 15 minutes, yeah. I have to go and sort the kids out quite soon, but I've got 10, 15 minutes. Sure, thank you. We can also wrangle that. Okay, cool, and if everyone else is up for that. Yeah, if attendees want to stay on, no one's answering this question right now. So if you can answer the question, that would be great. Can you see it? I can see a question, yes. So there were several questions. I can't see a question. All right, okay. If people can't see it, okay. So I'm just gonna end it, we'll move on. Sorry. No, here it is. I see it suddenly arrived on my screen. Oh, it's just appeared. Thank you, Tom. Oh, yes, now I can see this as well. Yes, great. We'll just give you 10 more seconds if you could click away. Oh, actually, I can't vote. Oh, yeah, sorry, it tells me that. They are not allowed to vote. You don't have the powers. Oh, yeah. And then we've just got some thank you slides, Tim, with an advert for the next one. And it's on page 11 of your doc. Good, look at me just wheeling out things. Okay. That's okay, everyone gets to see how this works. Okay, I'm gonna end the poll now. Well, I'll give you five seconds. Okay, cool. Thank you so much, everyone. So thanks very much to Catherine, Megan, and Ilka for sharing their work with us today and to you all for listening and asking great questions. So our online research talks continues on, actually, this says Thursday, but it's not Thursday. The next one is Tuesday, is it? Next week. Yeah, Tuesday, sorry. Yeah, so it should be Tuesday. And I think it's 9 a.m., not 5 p.m. as well. So my script is wrong. And that's, is that also neuroscience or is that a? No, it's not. And it's chaired by Anna, not you. Sorry. Yeah, right. And then, when's the next, let us know when the next neuroscience one is for this audience, please. So is that in order? This is the end of Neuroscience Week. There are other neuroscience talks to come along. If you carry on with the next bit, I'm gonna find out when. Okay, cool. So, yeah. So for updates about the series, if you just follow Eli Community on Twitter and you can find the schedule and registration information there, cool. So today we're gonna keep the Zoom open for another 15, 20 minutes to give you a chance to chat directly with the speakers. And the speakers are staying on with us. So if you'd like to stay, please do. And we're gonna stop the live stream, but the Zoom is gonna carry on. Yeah, for Neuroscientists, the next one's April the 14th, which is a Tuesday. So that's 9 a.m. in British summertime. 9 a.m. Tuesday 14th is the next Neuroscience one. Neuroscience talks in that one, yeah. Brilliant. Five.


As we mentioned previously, DHIS2 is an application-based platform. The University of Oslo develops, again, about 30 core applications that we consider to be the minimal functionality that countries need to have DHIS2 serve as a national health management information system. All of the applications that the University of Oslo make are publicly available for ETOs. The University of Oslo also develops what we call an app platform. This app platform is a library of components, resources, and tools that are generic and can be layered to produce our applications that we have in the core, but as well as third-party applications.  The 30 core applications that the University of Oslo produce are not always suitable to every context. Many countries require specialized tools for different projects, different kinds of clinical services, different types of end users. And using the app platform, these third-party developers are able to produce their custom applications and they're able to reuse that library of components, resources, and tools that we use in our core applications for their own applications as well. And so what that means is it becomes easier to maintain those apps over time for those third-party developers. The third-party applications are not always published. They could just be for one country. But we do see an increasingly number of third-party applications being made generic that could be used in any DHIS2 database and published on our app hub. They are also not always free to use. Different organizations have different approaches to sustaining these applications. Some of these applications could have a freemium model where they are free to use the base functionality but any additional new functionality or services are at cost. Some of them may have additional add-on services that have costs as well, for example, hosting. So while the core of DHIS2, those 30 generic applications, are publicly available, free to use for anyone, are maintained over time, the third-party applications may not be. Many are, but some are not, and they have different ways in which they secure funding and resources to maintain the apps over time. One final note about the applications is, again, all of the applications are available on our app hub. Not just the third-party applications, but also the core applications that the University of Oslo developed. They're all available here on our app hub, and you can access the app hub through our website as well through any DHIS2 instance. A key component of the DHIS2 interoperability is its well-documented Rest Application Programming Interface, or API. Essentially, the API enables clear pathways of communication between DHIS2 and other external software or platforms. There are many examples of where DHIS2 is interoperating or communicating with third-party platforms. For example, national population registries, HR systems, as well as other specialized data capture tools, for example, ComCare, OpenMRS, and ODK. Many of these larger platforms, for example, ComCare, OpenMRS, and ODK, have fairly straightforward connections between DHIS2 via the Rest API, because many of the projects that are using ComCare or ODK are also using DHIS2, or there is a requirement to communicate to DHIS2. One key point to make is integrations with DHIS2, situations at which software needs to be brought into DHIS2, must adapt the DHIS2 metadata configuration. And we do have some support for this, but the maintenance of the integration over time has to include the metadata updates that we are continuously making to DHIS2. We recommend for interoperability that users or projects looking to form some kind of connection between DHIS2 and another platform. Consider using a middleware system, for example, OpenHIM. Instead of hard coding bespoke integrations or interoperability, we see that many projects and countries struggle to maintain interoperability over time. And by using these middleware systems, you put off some of the maintenance of that interoperability to another platform, as opposed to having to maintain it internally over time. You can find more information about the ongoing work on integration and interoperability on our website, dhis2.org backslash interoperability. DHIS2 is also a platform for innovation and collaboration. And here we wanna make the point that many countries are doing very innovative things with DHIS2. They are producing their own applications. They are putting DHIS2 into domains and use cases that are unique and novel. And in those situations, what we strive to do is to bring back those innovations, those insights that people are already pioneering around the world with DHIS2 back to the core. And when we say core, what we mean is the University of Oslo supported applications, our resources, our guidance, our training, so that insights that are made in one place can be shared globally. And that everyone can benefit from everyone else's innovation and experience. We have two examples of that here on the screen. Starting on the left, we see a application that was developed in Sri Lanka to do contact tracing for COVID-19. So in this, you see that each pink dot represents a person who has deposited for COVID. And the arrows are representing the contacts that that person has. This kind of what we call a network graph really makes it very easy to do contact tracing and mapping. This application was developed in Sri Lanka, but they developed it in such a way that it was generic and could be used for any country that needed to do contact tracing, initially for COVID, but for really now any disease. We on the core are also studying this use case and application to see how can we bring this type of network graph into the core analytics applications that we maintain. On the right side of the screen, we see a dashboard developed in Uganda for testing and contact tracing. This dashboard is a custom dashboard that is used in their operations and rapid response division in the Ministry of Health. This dashboard introduced a lot of new functionality, new types of analytics that have not been available in the core dashboard application that the University of Oslo maintains. So Hisp, Uganda, the developers of this dashboard made this dashboard app in such a way that it is generic and can be used in any country. And we at the University of Oslo have also been studying this dashboard and bringing in some of the functionalities that introduced into our core dashboard app as well. A quick summary of this presentation. First, on the left, let's start with the HMIS characteristics. Again, an HMIS is a health management information system. It is used for routine health data for decision making. It needs to include data from many programs and sources. Again, this should include supply chain data, HR data, infrastructure data, as well as all of the health data, clinical service delivery data, disease surveillance data, anything coming from health facilities. It can contain both aggregate and individual data, as well as event data. And data is entered and used at multiple levels. So data can be entered at the lowest level, community health worker or village level. Data can be entered for individual patients in a village or a household. Data can be entered in aggregate at health facilities and on up to hierarchy. And data is used at all of those levels as well for decision making. And the use is extremely important, especially at the lowest levels to help guide interventions, to help guide outreach campaigns and workflows for those who are actually on the ground, interacting with patients, conducting health programs. Shifting now to the right side of our screen, we see that DHIS-2 primary use case is that of an HMIS. DHIS-2 is a platform, again, is highly generic and flexible and used in many other domains, such as education, agriculture, land use, organizational management. But the principal use case of DHIS-2 has been and will remain as a national health management information system. And DHIS-2 is the world's largest platform serving as an HMIS. DHIS-2 is able to capture various different data types, aggregate, tracker and event data. And DHIS-2 is able to capture that data as well as produce analytics from that data both on web and mobile. DHIS-2 is highly extensible, meaning that DHIS-2 has the ability to be innovated on top of new apps produced for different use cases that require more custom functionality and services. And DHIS-2 is highly interoperable via the REST API, connecting DHIS-2 to other platforms and software. We consider DHIS-2 to be a global innovation platform, a place at which various countries can produce new innovations, new insights. And then they are able to share those innovations and insights around the world so that everyone using DHIS-2 can benefit from everyone else who is doing new and novel things with DHIS-2.


Welcome to Stand on the Energy Band. I'm Stand on the Energy Band and I'm currently retired on my third try, I'm getting better at it every time. I'm glad to be here at Think Tech Hawaii at Pioneer Plaza and trying to bring some good energy news to you. Last week when we had Ryan Woven's on the show, we talked a little bit about having the courage to be an early adopter and having the fortitude to go out and just be the change. You just go out and do it instead of waiting for the government to tell you or waiting for somebody to make an incentive, like put it on the sale or give me any kind of incentive.  We talked about it, but it's a lot harder to do when you don't have the experience to do energy things. This week's guest is Russ Kohler and he's the president of the Hawaii chapter of the Association of Energy Engineers and he's going to talk to us a little bit about the folks that are out there in the world, in the community, that can help you make good decisions on energy choices, particularly if you're on a larger scale, but even if you have a smaller project, they'll help narrow down the search for a good engineer and good folks that can help you out. So thanks for being on the show today. It's my pleasure, Stand. So give us a little bit of background on yourself and then we'll start talking about your organization. Well, I'm originally from New Jersey. I went to a Merchant Marine Academy. This is where I started learning all about energy and really the study was about cogeneration. I've always felt that a ship was the best form of cogeneration that we know of. I graduated with an engineering degree. Immediately came out to California to work with my dad, who had started an energy management company, California American Energy Savings. So that's when I really started cutting my teeth on energy management. That was way back in 1976. So I've been involved with energy for quite some time. We're going to talk a lot about the Association of Energy Engineers and how it kind of overlaps my experience. AEE was actually founded in 1977. Oh, so you predate AEE. I predated AEE as an incorporated association. I actually joined with my brother in 1980. I've been a member for quite a few years. I got my certified energy manager certification in about mid-early 90s. I became a life member in around 1999. When you started, you talked about going to the Merchant Marine Academy. I had a show a couple months ago where we talked about maritime fuel cells. Some of the technology out there, and there's a company out there now, shoot, I can't remember the name of it, and they specialize in cogeneration. And they have a technology that uses low grade waste heat to generate power. And they claim that on a ship, they can produce 20% of the ships. This is a cruise ship, so they've got a lot of power requirements. 20% of the cruise ship's energy off the waste heat from the engine. That's probably true, Stan. And that's probably an organic rink and cycle system. I've been involved with a couple of organic rink and cycles. You mentioned fuel cells. I've worked a lot with fuel cell energy out of Connecticut. They actually produce a cogeneration style of fuel cell using natural gases to fuel, breaking up the methane from the O2 and the water and just using the hydrogen. And it becomes a cogeneration system. I almost put a 11 megawatt system into our pharmaceutical company in California so that we could eliminate boiler load, at least 2,700 horsepower boilers, producing steam with the fuel cell, and certainly being almost near zero emission, no combustion. Orc cycle is definitely a good way to use waste heat. Fuel cell energy built a 15 megawatt plant, or I can't remember the name of the utility in Connecticut, that did not have any use for the waste heat. So they put the organic rink and cycle on the far end, took all the waste heat from the fuel cell, produced another megawatt of electricity that went directly into the grid. That's great, because I know that when we talk about building systems, energy efficient systems, sustainable systems, one of the first things you do is go for efficiency. Absolutely.  Exactly. You make it more efficient, you'd have to put less PV into the house. Let's talk a little bit about your organization and some of the criteria that the qualifications you have to have to be a member of the organization, what is that like? So one qualification is obviously schooling, an engineering degree of some sort, whether it be civil, electrical, mechanical, what have you. Otherwise, you can have enough experience within your lifetime within the field that will qualify you to be able to sit for a certification. The prime certification from Association of Energy Engineers is the Certified Energy Manager, CEM. There are 23 different certifications. And really what AEE is about is teaching. They bring this teaching not just to the state or nationally, but it's an international organization. We're in 100 different countries. And my favorite thing to do annually is to go to their world conference. This year happens to be in Washington, D.C. Gives me two benefits. My son is actually at Georgetown grad school. Oh, me. I get to spend some time with him, but also spend a time with some great people and a lot of people that are focused on the same areas that I am and certainly you are. Last year, 2018, I was honored by being inducted into the Association of Energy Engineers Energy Manager Hall of Fame. Oh, well, congratulations. Thank you very much. Out of the, you know, 18,000 plus members of the Association, there's only 64 that have been inducted to a year. In fact, I nominated a person from Hawaii this year, George Benda. You might know George. He's been in the energy field for many, many, many years. Founded the Chelsea Group here in Hawaii, has since retired. He didn't make the nomination this year, but the induction, but I'm going to nominate him again next year. He's plugging away. Absolutely. Plug away. He was our Vice President of Malachi, Lanai. In his previous years. So you get a background either before my education in engineering or, you said or by experience, because you give us an example of the kind of experience that would allow you to get us, get certified. Sure. In fact, I'm trying to help a person at the base, the military base that I work at. He's got a lot of HVAC experience. He's got a lot of energy management system control experience. Those are two of the primary areas of experience you need for a certified energy manager or many of these certified energy auditing. So when I say experience, I'm talking probably 10, 15 to 20 years experience. And how many people belong to the Hawaii chapter? About 130 on all islands that belong to the chapter at this point. And how would people go about contacting these folks or why would they contact them? Would people be seeking out members of the AEE to get expertise or are they consultants? They are. They're all walks of life out here from HECO, from NAVFAC, Johnson Control, Zamoresco. Any one of the major companies out here, even a Chelsea group that I mentioned, which has now become part of Amoresco, they all have folks that have a CEM certification. We offer classes. In fact, I have two classes right now that we're working on. One is in December, December 8th, which is open to the public for certification of energy management. It's going to take place here in Honolulu at a HECO site. And I just arranged another one for NAVFAC that's going to take place October 21st. It's a one day class. It's a four day class. And the half a day, fifth day is the exam. So you have to pass an exam and I would say study hard. Lots of math. Door and a week. There's enough math to give people a scare. But Vicky, who you met not too long ago, she's actually a CEM and a CEA. So she's quite a good secretary for me. She's secretary of the YA chapter, that's correct. She's from the Big Island. I plan to be working with her. She wanted me to introduce her to the Blue Planet Research folks. I connected her up with Paul Ponti over there and I'm hoping that works out well because I think she struck me as being a really sharp individual and Paul's a really bright, he's actually an architect. She is a very sharp individual. Before she got her CEM, she actually is a PhD in a different subject. She mentioned to me an event at Blue Planet at the end of the month, August 30th. I don't know exactly what's going on, but there's going to be an exhibit there showing all the different wares, including the hydrogen barbecue. She's asked me if I wanted to come out and I would take her up on it. I'm going to go ahead and take her up on it. In fact, if you ever get invited to go out to see Blue Planet Research's laboratory and what they do, I would take that opportunity right away. I want to. The Hawaii chapter covers a lot of folks that are employed in the industry to deal with energy. It's really more like a certification that kind of piggybacks on or adds to your actual job. Absolutely. Some of the qualifications for a lot of the positions these days at the, anyone on the military bases, they call resource efficiency managers. I'm a senior energy engineer. All of those positions required to have a CEM. What I'm noticing, even throughout NAFAC, even the energy manager I mentioned earlier at my base, these guys come into these positions and are required that within two years they get their CEM certification. I've seen it now nationwide where it's actually a qualification on the position. You either have it or you guarantee to get it within a certain amount of time. Right now, Hawaii has an energy portfolio standard that requires us to be 100% renewable on the grid by 2045. To me, that's a really tall order. I don't know that most people think much about what that really means in practical terms, in terms of the grid architecture and things like that. What are your thoughts on trying to meet that 2045 goal and where we're at now getting there? I've spent a lot of time thinking about that. In fact, I spent a lot of time thinking about that before I even came to Hawaii. I didn't mention, but I've only been in Hawaii full-time since summer of 2017. My wife was born and raised there. She's a local. She went to high school. We got married out here in 1985, but I only transitioned out here in the last couple of years. I've spent a lot of time thinking about Hawaii and that 2045 goal, which it's a very tough goal for Hawaii to achieve. What makes it so tough? I think I understand why, but a lot of people out there I don't think appreciate the complexity. Could you give us an idea of some of the complexity? One of the complexities is that Hawaii Electric that supplies all of our electricity is still running on fuel oil. For them to transition to what they claim to be biofuel, in my mind, it's still a combustion fuel. It's still carbon-based. It's still carbon-based. It's still going to put out an emission. For me, that doesn't make that qualification. That right there tells me there's no way you're going to meet that 2045 goal. I have looked at many different things and just to talk story, the AES coal plant is going to go away. What's the thinking on how are we going to replace that 180 megawatts of load? I know what I've been thinking about with firm power. I think we should be replacing it with fuel cells. How would we do that? How would we generate or produce all that hydrogen to do that? To me, it's a two-way thing. You've got a pipeline going right through there that's got natural gas from Hawaii gas. You could start out with natural gas fuel cells, for a lot of that load, and you could back that up with hydrogen fuel cells. Right now, fuel cell energy has a model fuel cell that will produce hydrogen. It'll produce electricity and hydrogen. It could be used both ways. Take another step. You've got the 90 megawatt incineration plant. I'll call it an incinerator. H-power. H-power, thank you. H-power is an incinerator. That's emitting worse emissions than even HECO is with the fuel cell. In particulates and everything you can think of that's bad. Why don't we take that municipal solid waste and convert it into hydrogen? You've got all that municipal solid waste coming from Oahu that could easily be introduced, put into gasification systems. Gasification systems are going to create syngas, turn the syngas into hydrogen, and there you go. This way you're doing two things. You're eliminating what's going to the landfill, just like what they're doing with the incineration, but you're doing it now with near zero emission. If not zero emission, you might have a tiny bit of emission coming from the gasification system, but even that's supposed to be zero percent oxygen. I tell you what, we're going to take a quick break here and we'll be back in 60 seconds and talk some more about some of the details that get into 2045 in clean energy. Hi, I'm Rusty Komori, host of Beyond the Lines. I was the head coach for the Punahou Boys varsity tennis team for 22 years and we're fortunate to win 22 consecutive state championship. This show is based on my book which is also titled Beyond the Lines and it's about leadership, creating a superior culture of excellence, achieving and sustaining success, and finding greatness. If you're a student, parent, sports or business person, and want to improve your life and the lives of people around you, tune in and join me on Mondays at 11 a.m. as we go Beyond the Lines on Think Tech Hawaii. Aloha. Aloha. My name is Wendy Lowe and I want you to join me as we take our health back. On my show, all we do is talk about things in everyday life in Hawaii or abroad. I have guests on board that will just talk about different aspects of health in every way, whether it's medical health, nutritional health, diabetic health. You name it, we'll talk about it. Even financial health will even have some of the Miss Hawaii's on board and all the different topics that I feel will make your health and your lifestyle a lot better. So come join me. I welcome you to take your health back. Mahalo. Hey, welcome back to Stand to Energy, man. We just started launching into Mission Impossible, that is trying to get Hawaii off of fossil fuels by 2045, at least on the grid. We just started rolling before the break, so we're going to get right back to that. Russ, we were talking about some of the options, but another thing that makes the hydrogen piece kind of interesting to me on our grid is that if we're going to keep using solar and wind, those are intermittent renewables. Unlike the coal, unlike the H-power, those are intermittent and that gives HECO fits in terms of balancing their grid, stabilizing their grid. That's correct. So when you have that kind of instability, one of the perfect things to do to help stabilize your grid is throw electrolyzers out there. So when you're producing too much solar or too much wind, you dump it into those electrolyzers and make hydrogen to make energy for later in the day or at night when you need it. So is that one of the possible solutions, maybe doing hydrogen in combination? Absolutely, it is. Let's take a base. A base that I'm familiar with has a landfill. It has a wastewater treatment plant and it has lots of land. We could take that wastewater treatment plant and we could take all that sludge material, put it into the same thing, gasification system, turn it into sin gas, renewable natural gas the way Hawaii gas is doing out at the Huli-Huli. On the Huli-Huli. On the Huli-Huli wastewater treatment plant, making renewable natural gas. In our case, we could turn it into hydrogen. On a base that I'm particularly familiar with, I want to make that wastewater treatment plant, it's on microgrid. Perfect.  Oh yeah. You know, the heart of the system. Well that's what we know when we talk about one of the other challenges with our grid is that if you have a natural disaster and you lose power, now all of a sudden your sewage systems and your freshwater systems and your hospitals and other things that require energy or require pumping to move things around are dead in the water. Whereas if you build the system correctly, your wastewater treatment plant becomes self-sustaining. You fix whatever little minor things might be happening from the storm itself and then it's taking care of itself. You don't have to wait for the grid to come up or you don't have to find diesel fuel someplace to get a generator in there. That's exactly the point. Everything that we deal with now at a base has to do with being resilient. Department of Defense is requiring every base up with a plan to be resilient for a minimum of 14 days. And that's what you said, natural disaster. It actually is for a natural disaster or a man-made disaster. It could be an attack. I was recently, well recently a couple months ago, I was at the Joint Base Pearl Harbor Industry Day because they're looking at putting a resilient plant in. And the number one thing they opened the entire conference up to was we've got threats. We've got threats from China. We've got to deal with this. We need power. All of your forward bases for any sort of a response is right here. This is it.  Those are the forward bases for anything that happens. That struck me very seriously because it told me that you need this power like tomorrow and they need 100 to 150 megawatts of resilient power. I didn't quite agree with how they wanted to do it, but that's okay. I already have my strategy for the base that I work with and that we have a hydrogen fuel station. Just like you have down at Hickam, yours is much bigger than ours. I would like to expand our hydrogen fuel station so that we can have enough hydrogen for firm power, not just transportation power. And then use our landfill to create as much storage for hydrogen as we can. As we've talked about wastewater treatment plant, microgrid that plant by itself and use the resources that we have. We need to bring in more hydrogen. Fine, we bring in more hydrogen, but that needs to be a self-sustaining operation within the base. I've carved out a section of this base for wind turbines. I've carved out other areas for larger solar farms along with battery storage and hydrogen energy storage and potential for geothermal. So currently though, I'm familiar with at least the Air Force side. The critical facilities, facilities you need to have up and running, maybe your clinic and your commissary or, you know, for food storage and things like that, you have diesel generator backup systems or communications networks and things like that. But I point out to the DOD, I used to do that, we're on an island. If our ports are impacted, damaged, and can't receive cargo, or our airports are closed out and can't receive aircraft, we only have seven or so days worth of fuel that, at that point, now the hospitals and everybody else are going to be all wanting that same fuel for priority reasons. And the DOD becomes competition for those assets. And the DOD should probably be more self-sufficient. Couldn't agree with you more. It sort of weighs into a segment that I mentioned during that Joint Base Pearl Harbor victim conference. I questioned the lead civilian for Pearl Harbor. I said, do you consider fuel oil to be a resilient fuel? And he looked at me and I said, I don't. That has to come over here by ships. You're talking about war. You're talking about tsunamis, hurricanes, and potential for war. That to me is not a resilient fuel if it has to come over here by ship. What fuel can you produce here in Hawaii? Not natural gas, and it's not fuel oil, it's hydrogen. You know better than I that hydrogen being the most abundant substance in the universe is something Hawaii could take advantage of. Every one of the states can take advantage of it. Everything I mentioned about doing it at the base translates to eco. Translates to the rest of the island and the rest of the state. And that's where I tell my board with AEE, this is what I'm doing here at the base, but this is all stuff that I want to translate out to the island of Hawaii. This is what we should be doing. We need to be talking about more than just transportation, we need to be talking about firm power. And the discussion has literally come full circle now because you think of Kojen, you think of using waste heat, and you think of the big island as not only a big beautiful island but has some of the hottest territory right under the skin that could be generating electricity like nobody's business. And we could be importing that energy to Oahu in the form of ammonia or hydrogen or some hydrogen rich liquid fuel or gaseous fuel and providing that base load power or eco to be able to carry on in their new micro rated system. Absolutely. Eco could be doing the same thing that we're talking about. On the statewide scale. On the statewide scale. I didn't mention but years ago when I was now running the energy company that my father built and founded, we were representatives of two co-generation systems. Eco-jen, which is a small 454 Hulman and Moody engine co-generation package, but then capstone turbines. Capstone turbines were used in buses and all sorts of different scenarios but there's a lot of mainland, in fact Maui has a hotel with several capstone turbines running for their waste heat using all the waste heat in the co-gen. I tried to give a capstone turbine to Eco back in the early, back in the 90s and didn't want it. I just wanted to send it to him, let him test it. Well I hope that we can convince Eco to broaden her aperture a little bit, work with folks like you and the folks at the EE to really get us to that goal because it's pretty ambitious, it's a lot more complicated than people think, but I think we'll get there. Believe it or not, we've hit 30 minutes already Russ. I told you I'd go by quick, but I want to thank you really for being on the show today. You're very welcome. My pleasure. It was fun. Well we'll have let you a little more time over at Kanoi and maybe if you can get the military to let you talk about specific things over there while having back on the show and talk about some of the issues that you're working with. That would be fantastic. Well thanks again and until next week Friday, we'll see you here on Stand Energy Man of ThinkTech Hawaii. Aloha.


Hi guys, welcome back to my YouTube channel. This is Daniel Rossell here. Today's sound comparison video I'm going to be comparing the wired using this microphone wired. This microphone is the Shure PGA48. I think it's an excellent XLR microphone for its price point about 50 bucks thereabouts in the US and then comparing this same microphone with the Lakato MKMW1, I'm sorry wireless lavalier system. It's a wireless lav system that doesn't require power. As you can probably hear, it's quite windy out today. We're shooting this in a public park so we're also going to get a bit of a sense for wind protection on this microphone without a dead cat and also how it works wirelessly. It's going to be probably about the same wind on both goes. What I'm going to do is read a excerpt from this book, Impact by Sir Ronald Cohen. I'm going to read it with both microphones So you guys can hopefully hear the difference. Nearly 20 years ago I gave a speech at an event to celebrate the 30th anniversary of APAC's partners, the venture capital and private equity firm I co-founded and led for so many years. I warned then that if we did not tackle the needs of those left behind more effectively, a curtain of fire would soon separate the rich from the poor in our cities, countries and continents. Okay, now I swapped over to the wireless system. It's the Lakato MWM and the same microphone is before the Shure PJ48, so I'm about probably only 1.5 meters from the camera So not very very far at all, but nevertheless, I'm going to do a range test as well after this same wind conditions, a little bit of a breeze going on here I'm going to read the intro again to the book. Nearly 20 years ago I gave a speech to celebrate the 30th anniversary of APAC's partners, the venture capital and private equity firm I co-founded and led for so many years. I warned then that if we did not tackle the needs of those left behind more effectively, a curtain of fire would soon separate the rich from the poor in our cities, countries and continents. So that's the testing guys. Obviously, it's a lot more enjoyable to have the wireless benefit of wireless and this is a pretty cheap XLR wireless system but I was actually I did a little bit of testing myself and I thought it was fairly decent. Let's go now and do a range test to see how it holds up over the distance. Okay. Now for the all-important range test on the Lakado MW1 XLR wireless system. What can I say about this? It's a great wireless system because it plugs straight into the camcorder, which is so much fun We're probably about seven meters now and where that wall is behind me. I reckon it's about a good 20 meters So 10 meters now should I regale you with the story? A little bit of wind here and I'm going all the way back probably now approaching 15 meters I always think at this point it doesn't really matter because when I'm using a wireless system for interviews Typically you're going to be probably max 10 meters in the camera. I'm walking back towards the camera now So the range is decreasing Continuing to talk about the beautiful olive trees here. Lovely little public park here in Jerusalem one of many and this is the Shure PGA XLR microphone doesn't require phantom power going into the Transmitting wirelessly over the Lakado MW1 system going into the Canon XA40 and that is how it sounds So thank you for watching this comparison. Let me know in the comments If you thought there was a real difference between the wired and the wireless I've done this test myself and I think it's pretty good the wireless transmission So thanks for watching if you want to get more videos from me, please subscribe to this YouTube channel


Let's talk about how that works. Okay, so the way how I think about it, and this isn't the only diagram in a step that could change, we'll evolve as we go, but there's typically the person that you're talking to, and they have a conclusion, and between the person and the conclusion there's a through line that I call the method, it's the reasoning that they're using to reach their conclusion. In reality, my mind, the way how I see this relationship is a lot more like this, and that's because people tend to personally invest a lot into themselves as well as their conclusions. You'll hear that when they say, I'm a Christian, I'm a Baptist, I'm an atheist, I'm a Vols fan, or go yellow jackets. Anyway, so the thing is when you try to address questions towards the conclusion, particularly as an atheist to a theist, it doesn't work out as well because as far as the theist is concerned, or the person who holds that conclusion is concerned, they're one and the same, and they'll treat that as a personal attack on them. They'll think, he's talking about my faith, he's talking about me, and you'll get responses that are very similar to as if you had just called them, or and questioned them. What's better is to question the method, and what Essie's best geared towards is asking questions about the method because there's a lot less ego invested there. And by attacking the method, or by challenging the method, by targeting the method with your questioning, you can allow the person to avoid like these pratfalls of where they invested their personal ego into, and allow them to have an open, thoughtful conversation about how they reached their conclusions. One of two things will happen within Essie. One, they'll either replace the method that they have with a better method, and as a theist I think we should be absolutely open to that, we should be looking for better methods to believe what we believe. So that's a great improvement. Otherwise, the other alternative is that they can't find a method to get to their conclusion.  And they end up being a person that's still open for finding better methods for better conclusions, or more reliable conclusions with better methods. And that's the basis of how Essie works.