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8 episodes with Saarland University
5 episodes with Saarland University
3 episodes with Saarland University
Sascha Hartel is the Head of Performance at TSG Hoffenheim He is responsible for Performance Diagnostics in the Professional Teams, Youth Teams (Male & Female), also Adler Mannheim (Ice-hockey) and Rhein-Neckar-Löwen (Handball). He also leads the team of S&C coaches as well as sharing responsibility for dat strategy and innovation. He is a consultant within the TSG ResearchLab a non-profit-organisation "bringing Science and Research from Sports to Society”. Ludwig Ruf is a strength and conditioning coach at TSG Hoffenheim academy and research assistant at the TSG ResearchLab. He completed a PhD on monitoring load and fatigue in elite youth soccer at Saarland University, Germany. Prior to this he completed an MSc in Strength and Conditioning at Cardiff Metropolitan University and did an annual internship with Adelaide United, Australia. The main aim of his PhD was to enhance our understanding of applied practice by investigating the usefulness of measurement instruments to assess acute responses to load in elite youth soccer players throughout adolescence. Special consideration is given to growth and biological maturation within the framework of monitoring the youth athlete. In this podcast the pair discuss: What caused Hoffenheim to become interested in monitoring maturation in their players. The methods they were previously using. How they have integrated the BAUSport device into the organisation. The efficacy an influence of the device within Hoffenheim. The effect of the new information on decision making processes. Future research projects taking place within the club . You can follow Ludwig's work via his Instagram page: @rufludwig or via his Researchgate profile here: https://www.researchgate.net/profile/Ludwig-Ruf Follow Sascha's work vis his research gate profile here: https://www.researchgate.net/profile/Sascha-Haertel To learn more about the LTAD Network check out www.ltadnetwork.com or follow on Instagram: @ltadnetwork or Facebook: https://www.facebook.com/ltadnetwork . You can keep up to date with Athletic Evolution via our www.athleticevolution.co.uk , Instagram: @athleticevouk and Twitter: @athleticevouk .
Listen to this interview of Andreas Zeller, faculty at the CISPA Helmholtz Center for Information Security and professor for Software Engineering at Saarland University. We talk about essence — that part of your research left when you've boiled it all down to the meaning. Andreas Zeller : "I think of science as a social process. I think of scientists as social beings — as unsocial as we might sometimes appear to be. Because we scientists are all humans, and so we long for meaning in our daily work, which means too that indirectly, we long for recognition. So, our research is just another form of social activity, and therefore it helps to see science as a social activity where the scientist's job is, ultimately, to enrich the lives of other scientists with ideas that are useful, that give direction." Learn more about your ad choices. Visit megaphone.fm/adchoices
Listen to this interview of Andreas Zeller, faculty at the CISPA Helmholtz Center for Information Security and professor for Software Engineering at Saarland University. We talk about essence — that part of your research left when you've boiled it all down to the meaning. Andreas Zeller : "I think of science as a social process. I think of scientists as social beings — as unsocial as we might sometimes appear to be. Because we scientists are all humans, and so we long for meaning in our daily work, which means too that indirectly, we long for recognition. So, our research is just another form of social activity, and therefore it helps to see science as a social activity where the scientist's job is, ultimately, to enrich the lives of other scientists with ideas that are useful, that give direction." Learn more about your ad choices. Visit podcastchoices.com/adchoices Support our show by becoming a premium member! https://newbooksnetwork.supportingcast.fm/new-books-network
Video Version: https://youtu.be/w9Gs813BxJQTimestamp1:15 — Organizational Change4:51 — Integrated Performance Model7:48 — Book Recommendations10:04 — Circular Model of Action15:06 — Current ProjectsResourcesBook Recommendation #1: Coherence by Dr. Alan WatkinsBook Recommendation #2: The Mental Athlete by Kay PorterAbout Dr. Sebastian BrücknerDr. Sebastian Brückner is an internationally recognized expert in applied sport psychology. Besides working in private practice as mental performance consultant and leadership coach he provides consultancy to ongoing projects funded by the German Federal Institute of Sport Science (BISp) and European Union, and acts as a reviewer for (inter)national sport psychology journals. He has served the Association for Applied Sport Psychology (AASP) in multiple roles: chairing the International Relations Committee, as AASP Newsletter Editor, member of the inaugural Advocacy Committee, and co-editor of the 13 th edition of AASP's Graduate Program Directory.Consultation and interventions he delivers are heavily based on a strong commitment to a scientist-practitioner approach where research informs interventions. His applied work, specifically with the German National Badminton Team, has led to facilitation of elite coaches' education and leadership training programs. Sebastian has established projects with colleagues at Muenster University, Boston University and Kingston University London, where he has been appointed as Honorary Research Fellow.After studying at Saarland University, Texas A&M University and the University of Tennessee, Sebastian worked at Saarbruecken Olympic Training Center from 2008- 2017. There, he worked with (junior) national team and Olympic (caliber) athletes on mental training and dual-career transitions from a holistic, humanistic performance- enhancement perspective. In 2017 Sebastian joined the Department of Sport & Exercise Psychology at the University of Muenster. From 2018-2020, he worked as Executive Manager and Head of Applied/Certification Services for the German Society for Sport Psychology. Since 2021 he has successfully established his private practice. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit noahsachs.substack.com
Video Version: https://youtu.be/SWrMrBQIV7ETimestamp0:54 — Somatic Markers Intervention8:12 — 16 Second Cure15:10 — Applying 16 Second Cure in Golf23:17 — Common Mistakes Athletes/Coaches MakeAbout Dr. Sebastian BrücknerDr. Sebastian Brückner is an internationally recognized expert in applied sport psychology. Besides working in private practice as mental performance consultant and leadership coach he provides consultancy to ongoing projects funded by the German Federal Institute of Sport Science (BISp) and European Union, and acts as a reviewer for (inter)national sport psychology journals. He has served the Association for Applied Sport Psychology (AASP) in multiple roles: chairing the International Relations Committee, as AASP Newsletter Editor, member of the inaugural Advocacy Committee, and co-editor of the 13 th edition of AASP's Graduate Program Directory.Consultation and interventions he delivers are heavily based on a strong commitment to a scientist-practitioner approach where research informs interventions. His applied work, specifically with the German National Badminton Team, has led to facilitation of elite coaches' education and leadership training programs. Sebastian has established projects with colleagues at Muenster University, Boston University and Kingston University London, where he has been appointed as Honorary Research Fellow.After studying at Saarland University, Texas A&M University and the University of Tennessee, Sebastian worked at Saarbruecken Olympic Training Center from 2008- 2017. There, he worked with (junior) national team and Olympic (caliber) athletes on mental training and dual-career transitions from a holistic, humanistic performance- enhancement perspective. In 2017 Sebastian joined the Department of Sport & Exercise Psychology at the University of Muenster. From 2018-2020, he worked as Executive Manager and Head of Applied/Certification Services for the German Society for Sport Psychology. Since 2021 he has successfully established his private practice. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit noahsachs.substack.com
Video Version: https://youtu.be/YENWOhy5GK4Timestamp0:39 — Academic & Professional Background9:11 — Emotional Self-Regulation17:44 — ABC Model26:43 — Golf-Specific Example of ABC ModelResourcesABC Model - https://positivepsychology.com/albert-ellis-abc-model-rebt-cbt/About Dr. Sebastian BrücknerDr. Sebastian Brückner is an internationally recognized expert in applied sport psychology. Besides working in private practice as mental performance consultant and leadership coach he provides consultancy to ongoing projects funded by the German Federal Institute of Sport Science (BISp) and European Union, and acts as a reviewer for (inter)national sport psychology journals. He has served the Association for Applied Sport Psychology (AASP) in multiple roles: chairing the International Relations Committee, as AASP Newsletter Editor, member of the inaugural Advocacy Committee, and co-editor of the 13 th edition of AASP's Graduate Program Directory.Consultation and interventions he delivers are heavily based on a strong commitment to a scientist-practitioner approach where research informs interventions. His applied work, specifically with the German National Badminton Team, has led to facilitation of elite coaches' education and leadership training programs. Sebastian has established projects with colleagues at Muenster University, Boston University and Kingston University London, where he has been appointed as Honorary Research Fellow.After studying at Saarland University, Texas A&M University and the University of Tennessee, Sebastian worked at Saarbruecken Olympic Training Center from 2008- 2017. There, he worked with (junior) national team and Olympic (caliber) athletes on mental training and dual-career transitions from a holistic, humanistic performance- enhancement perspective. In 2017 Sebastian joined the Department of Sport & Exercise Psychology at the University of Muenster. From 2018-2020, he worked as Executive Manager and Head of Applied/Certification Services for the German Society for Sport Psychology. Since 2021 he has successfully established his private practice. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit noahsachs.substack.com
Who needs science fiction when present reality is so spectaculat? That's the question posed by artificial intelligence. AI has been in the new a lot lately thanks to ChatGPT, so we thought it would be good to look at what's going in the area in Europe's largest economy. Is there a German version of the famous chatbot? In what areas does AI have the greatest promise? Can international companies in the field find success if they set up shop in Germany? And why are German researchers so important in teaching AI to have a sense of humor? Azadeh Ghahghaie: Azadeh Ghahghaie is the director at the SAP.iO Berlin, which is part of the global network of equity-free startup accelerators of software giant SAP. There she helps promising startups to integrate with SAP solutions and accelerate their entry into a curated, inclusive ecosystem whose offerings can be easily accessed and deployed. Prof. Antonio Krüger Prof. Antonio Krüger is an internationally renowned expert in human-machine interaction and artificial intelligence. He's the CEO and scientific director and head of the research area "Cognitive Assistance Systems" at the German Research Center for Artificial Intelligence (DFKI). He also holds the Globus Endowed Professorship for Computer Science at Saarland University and is head of the Ubiquitous Media Technology Lab and scientific director of the Innovative Retail Laboratory (IRL) at DFKI. Kian Mirshahi Kian Mirshahi is the founder and CEO of Mayday.ai, a young company devoted to innovative artificial intelligence approaches for disasters and risk intelligence. Mayday has gained recognition and accolades from many UN agencies, as well the European and the German Space Agencies. Mirshahi is an advocate of using the power of AI to manage the impacts of climate change impacts and create resilient communities around the world.
This week, Michael invites Jorgo Chatzimarkakis, CEO of Hydrogen Europe, to debate the importance of hydrogen in powering Europe and the world towards a decarbonized economy. Hydrogen Europe is an industry association of more than 400 members that promotes the role of hydrogen in reaching carbon neutrality in Europe. Chatzimarkakis holds hydrogen to be the miracle molecule of the transition, while Michael's Hydrogen Ladder has a far narrower view of its likely uses on the path to net zero. What follows is a comprehensive, robust – and at moments, fierce - discussion of hydrogen in the transition, covering electrolyzers, fertilizers, freight, transportation and heating, as well as following the “pots of money” behind hydrogen infrastructure and lobbying in Europe. Spark more healthy debate around net zero pathways by liking and sharing the episode, and don't forget to subscribe. Relevant Guest & Topic Links: Learn more about Hydrogen Europe: https://hydrogeneurope.eu/ HE's Hydrogen Act (2021) lays out a roadmap for a ‘European Hydrogen Economy': https://hydrogeneurope.eu/wp-content/uploads/2021/11/2021.04_HE_Hydrogen-Act_Final.pdf HE's Clean Hydrogen Monitor (2022) provides an overview of the European hydrogen market: https://hydrogeneurope.eu/clean-hydrogen-monitor2022/ Explore Michael's Hydrogen Ladder here: https://www.linkedin.com/pulse/clean-hydrogen-ladder-v40-michael-liebreich/ President von der Leyen's speech at the European Parliament Plenary on December 15th 2022: https://ec.europa.eu/commission/presscorner/detail/fi/speech_22_7727 Watch Cleaning Up Episode 111 with Dan Yergin here: https://www.cleaningup.live/ep111-daniel-yergin-the-worlds-most-influential-energy-analyst/ Watch Episode 88 with Patrick Graichen here: https://www.cleaningup.live/ep88-patrick-graichen-germanys-secretary-of-state-for-the-energiewende/ Guest Bio:Chatzimarkakis was a Member of European Parliament from 2004 until 2014 for Germany's Free Democratic Party (FDP), serving on the Committee on Industry, Research and Energy among others. From 1999 to 2004, Chatzimarkakis was Managing Partner at Polit Data Concept, a public affair consultancy, and served as a Science Policy Officer at Germany's Bundestag from 1995 to 1998. Chatzimarkakis holds an MA from the University of Bonn in Political Science. He has held positions as a lecturer at University Duisberg Essen and Saarland University.
In this episode we take you through the experience of building prototypes with SAP BTP in a cooperation of SAP, DFKI and Saarland University and a have fruitful discussion between SAP and Accenture about their long-standing partnership and how they bring value to customers using SAP Process Automation.
This month on Episode 34 of Discover CircRes, host Cynthia St. Hilaire highlights four original research articles featured in the March 4 and March 18th issues of Circulation Research. This episode also features a conversation with Dr Mireille Ouimet and Sabrina Robichaud from the University of Ottawa Heart Institute to discuss their study, Autophagy is Differentially Regulated in Leukocyte and Non-Leukocyte Foam Cells During Atherosclerosis. Article highlights: Pauza, et al. GLP1R in CB Suppress Chemoreflex-Mediated SNA Lim, et al. IL11 in Marfan Syndrome Hohl, et al. Renal Denervation Prevents Atrial Remodeling in CKD Liu, et al. Smooth Muscle Cell YAP Promotes Arterial Stiffness Cindy St. Hilaire: Hi and welcome to Discover CircRes, the podcast of the American Heart Association's journal, Circulation Research. I'm your host, Cindy St. Hilaire from the Vascular Medicine Institute at the University of Pittsburgh, and today I'm going to be highlighting articles from our March issues of Circulation Research. I'm also going to speak with Dr Mireille Ouimet and Sabrina Robichaud from the University of Ottawa Heart Institute, and they're with me to discuss their study, Autophagy is Differentially Regulated in Leukocyte and Non-Leukocyte Foam Cells During Atherosclerosis. The first article I want to share is titled GLP1R Attenuates Sympathetic Response to High Glucose via Carotid Body Inhibition. The first author is Audrys Pauza, and the corresponding authors are Julian Paton and David Murphy at the University of Bristol. Cindy St. Hilaire: Hypertension and diabetes are risk factors for cardiovascular disease. And yet, for many patients with these two conditions, lowering blood pressure and blood sugar is insufficient for eliminating the risk. The carotid body is a cluster of sensory cells in the carotid artery, and it regulates sympathetic nerve activity. Because hypertension and diabetes are linked to increased sympathetic nerve activation, this group investigated the role of the carotid body in these disease states. They performed a transcriptome analysis of crowded body tissue, from rats with and without spontaneous hypertension. And they found among many differentially-expressed genes that the transcript encoding glucagon-like peptide-1 receptor or GLP1R, was considerably less abundant in hypertensive animals. Cindy St. Hilaire: This was of particular interest because the gut hormone GLP-1 promotes insulin secretion and tends to be suppressed in Type 2 diabetes. Moreover, GLP1R agonists are already used as diabetic treatments. This group showed that treating rat carotid body with GLP1R agonist suppresses sympathetic nerve activation and arterial blood pressure, suggesting that these drugs may provide benefits in more than one way. Perhaps the carotid body could be a novel target for lowering cardiovascular disease risk in metabolic syndrome. Cindy St. Hilaire: The second article I want to share is titled Inhibition of IL11 Signaling Reduces Aortic Pathology in Murine Marfan syndrome. The first author is Wei-Wen Lim, and the corresponding author is Stuart Cook and they're from the National Heart Center in Singapore. People with the genetic connective tissue disorder Marfan syndrome, are typically tall and thin with long limbs and are prone to skeletal, eye and cardiovascular problems, including a life-threatening weakening of the aorta. While Marfan syndrome patients commonly take blood pressure-lowering treatments to minimize risk of aortic aneurysm and dissection, there's currently no cure for Marfan syndrome or targeted therapy. Cindy St. Hilaire: The cytokine IL11 is strongly induced in vascular smooth muscle cells upon treatment with the growth factor TGF-beta, which is over activated in Marfan syndrome patients. And TGF-beta is also considered a key feature of the syndrome's molecular pathology. This study found that IL11 is strongly upregulated in the aortas of Marfan syndrome model mouse, and that genetically eliminating IL11 in these animals protected them against aortic dilation, fibrosis, inflammation, elastin degradation and loss of smooth muscle cells. Treating Marfan syndrome mice with anti-IL11 neutralizing antibodies exhibited the same beneficial effects. These results suggest that perhaps inhibiting IL11's activity could be a novel approach for protecting the aortas of Marfan syndrome patients. Cindy St. Hilaire: The next article I want to mention is titled Renal Denervation Prevents Atrial Arrhythmogenic Substrate Development in Chronic Kidney Disease. The first authors are, Mathias Hohl, Simina-Ramona Selejan and Jan Wintrich, and the corresponding authors also Mathias Hohl, and they're from Saarland University. People with chronic kidney disease have a two to three fold higher risk than the general population of developing atrial fibrillation, which is a common form of arrhythmia that can be life-threatening. Chronic kidney disease is associated with activation of the sympathetic nervous system, which can be damaging to the heart. Thus, this group examined myocardial tissues from atrial fibrillation patients with and without chronic kidney disease to see how they differ. They found that atrial fibrosis was more pronounced in patients with both conditions than in patients with atrial fibrillation alone, suggesting that chronic kidney disease perhaps exacerbates or even drives arterial remodeling. Cindy St. Hilaire: Sure enough, induction of chronic kidney disease in rats led to greater atrial fibrosis and incidence of atrial fibrillation than seen in the control animals. Renal denervation is a treatment in which the sympathetic nerves are ablated, and it's a medical procedure that's used for treating uncontrolled hypertension, and it has also been shown in animals to reduce atrial fibrillation. Performing renal denervation in the rats with chronic kidney disease reduced atrial fibrosis and atrial fibrillation susceptibility. This study not only shows that chronic kidney disease induces atrial fibrosis and in turn atrial fibrillation, but also suggests that renal denervation may be used in chronic kidney disease patients to break this pathological link and prevent potentially deadly arrhythmias. Cindy St. Hilaire: The last article I want to highlight is titled YAP Targets the TGFβ Pathway to Mediate High-Fat/High-Sucrose Diet-Induced Arterial Stiffness. First author is Yanan Liu and the corresponding author is Ding Ai from Tianjin Medical University. Metabolic syndrome is characterized as a collection of conditions that increase the risk of cardiovascular diseases, such as obesity, hypertension and diabetes. Among the tissue pathologies associated with metabolic syndrome is arterial stiffness, which itself is a predictor of cardiovascular disease incidence and mortality. To specifically investigate how arterial stiffness develops in metabolic syndrome, this group fed mice a high-fat, high-sugar diet, which is known to induce metabolic syndrome and concomitant arterial stiffness. Cindy St. Hilaire: After two weeks on the diet, the animals' aorta has exhibited significant upregulation of TGF-beta signaling, which is a pathway known for its role in tissue fibrosis, and the aorta has also exhibited increased levels of yes-associated protein, or YAP, which has previously been implicated in vascular remodeling, collagen deposition and inflammation. YAP gain and loss of function experiments in transgenic mice revealed that while knockdown of protein in the animals' smooth muscle cells attenuated arterial stiffness, increased expression exacerbated the condition. Cindy St. Hilaire: The team went on to show that YAP interacted with and prevented the activation of PPM-1 B, which is a phosphatase that normally inhibits TGF-beta signaling and thus fibrosis. Together the results suggest that targeting the YAP, PPM-1 B pathway, could be a strategy for reducing arterial stiffness and associated cardiovascular disease risk in metabolic syndrome. Cindy St. Hilaire: Today, Sabrina Robichaud and Dr Mireille Ouimet from University of Ottawa Heart Institute are with me to discuss their study Autophagy is Differentially Regulated in Leukocyte and Non-Leukocyte Foam Cells During Atherosclerosis, which is in our March 18 issue of Circulation Research. So thank you both for joining me today. Sabrina Robichaud: Thank you so much for having us. It's a pleasure. Mireille Ouimet: Thank you for having us. Cindy St. Hilaire: Yeah, and congrats on the study. So we know that LDL particles contain cholesterol and fats, and these are the initiating factors in atherosclerosis. And it's also really now appreciated that inflammation in the vessel wall is a secondary consequence to this lipid accumulation. Macrophages are an immune cell that, in the context of the plaque, gobble up this cholesterol to the point that they become laden with lipids and exhibit this foamy appearance, which we now call foam cells. And these foam cells can exhibit atheroprotective properties, one of them called reverse cholesterol transport, and that's really one of the focuses of your paper. So before we dig into what your paper is all about, could you give us a little bit of background about what reverse cholesterol transport is in the context of the atherosclerotic plaque? And maybe introduce how it links to this cellular recycling program, autophagy, which is also a big feature of your study. Mireille Ouimet: Yes, so the reverse cholesterol transport pathway is a pathway that's very highly anti-atherogenic. It's linked to HDL function and the HDL protective effects, in that HDL can serve as a cholesterol acceptor for any excess cholesterol from arterial cells or other cells of the body and return this excess cholesterol to the liver for excretion into the feces. There is also trans-intestinal cholesterol efflux that can help eliminate any excess bodily cholesterol. Mireille Ouimet: So reverse cholesterol transport is a way that we can eliminate excess cholesterol from foam cells in the vascular wall, and that's why we're really interested in the process. But the rate-limiting step of cholesterol efflux out of foam cells in plaques is actually, they have to be mobilized in the form of free cholesterol to be pumped out of the cells through the action of the ATP-binding cassette transporters. And so the rate-limiting step of the process is the hydrolysis of the cholesterol esters and the lipid droplets, because that's where the excess cholesterol is stored in foam cells. Mireille Ouimet: And so for years, people investigated the actions of cytosol like lipases in mobilizing free cholesterol from lipid droplets, although the identity of those lipases are not well-known and in macrophage themselves, but our recent work showed a role for autophagy in the catabolism of lipid droplets. And in fact, in macrophage foam cells, 50% of lipid droplet hydrolysis is attributable to autophagy while the other half is mediated by neutral lipases, which makes it really important to investigate the mechanisms of autophagy-mediated lipid droplet catabolism. Cindy St. Hilaire: That is so interesting. I guess I didn't realize it was that significant a component in that kind of rate-limiting step. That's so cool. So really, a lot of the cholesterol efflux studies, and maybe this is just limited to my knowledge of a lot of these cholesterol efflux studies, but to my knowledge, it's been really focused on the foam cell itself, the macrophage foam cell. However, there's been a lot of recent work that has now implicated vascular smooth muscle cells in this process. So could you share some of the research specific to smooth muscle cells and smooth muscle-derived foam cells that led you to want to investigate the contributions of smooth muscle cell-derived foam cells in cholesterol efflux? Mireille Ouimet: Yeah, so you're right in the sense that macrophages have always been the culprit foam cells in the atherosclerotic plaques but pioneering work from several groups, including Edward Fisher and Gordon Francis, they've shown that the smooth muscle cells can actually acquire a macrophage-like phenotype becoming lipid-loaded and foamy. And there's been work specifically looking at the ABC transporters, and their ability to efflux cholesterol from these vascular smooth muscle cell-derived foam cells, because as they trans-differentiate into macrophage-like cells, they acquire the expression of ABCA1, but this is to a lower extent, as compared to their macrophage counterparts. Mireille Ouimet: And the efflux is defective because there's an impairment in liposomal cholesterol processing of the lipoproteins that's really important to activate a like cell, and the expression of the ABC transporters, so vascular smooth muscle cell-derived foam cells are very poor effluxes. Sabrina Robichaud: There's very few studies that look at the vascular smooth muscle cell foam cells, and the very few that did look at it mostly focused on the ABCA1 transporters, and did show that they were poor effluxes. And as we all know, ABC1 is not the only cholesterol transporters that can transport cholesterol out of cells, there's also ABCG1 which is also one of our major findings in our paper. Cindy St. Hilaire: Can you tell us a little bit about the models you chose in the study and why you picked them? And also maybe a step back in terms of, what are the pros and cons of using mouse models in atherosclerotic studies? Sabrina Robichaud: So we chose to use the GFP-LC3 reporter mouse model because it allows us to track in lifestyle the movement of LC3, which is the main component of the autophagosome which is involved in pathology. So by using this reporter model, we could infer whether or not the cells had high autophagy or low autophagy. And to induce atherosclerosis in these mice, instead of backcrossing them to either an LDLR knockout or an ApoE knockout, we chose to do the adeno-associated virus that encode the gain of function PCSK9 instead to kind of minimize the time for breeding. It did have the effect that we needed in terms of raising plasma cholesterol to induce the atherosclerosis. So that was one of the models that we used in our paper. Mireille Ouimet: There's not very many good mouse models to study autophagy flux in vivo and GFP-LC3 is kind of the main one currently. We're working on developing some other tools to track lipophagy in vivo, but these things take time to put in place. So in the future, we hope to have some better tools to track lipophagy in real-time in vivo. Cindy St. Hilaire: How difficult is it to measure autophagy flux in vivo? I know there's certain part like LC3 or P62, a lot of people use a western blot and it's like, oh, it's high, it must be active, but it's a flux. So it's a little bit more... There's more subtleties to that, dynamic than that. So how difficult is it to really measure this flux in in vivo tissues? Mireille Ouimet: Yes, so now there are more recent mouse models that have been developed more recently to replace kind of the GFP-LC3 is the Rosella LC3. So it has both a red and a green tag, and so two LC3, so when autophagosomes are fused to lysosomes and are degraded, then there's preferential quenching of the GFP first, and then you have the red appearance that predominates so we know that then it's kind of like it a live flux measurements. Because we use the GFP-LC3 mouse, Sabrina treated her cells ex vivo. When we dissected out the aortic arches, digested the cells then we divided those into two components and added bafilomycin so that we can inhibit lysosome acidification to see the changes in the flux. And that's really to get the differences in untreated versus bafilomycin-treated. Mireille Ouimet: When we inhibit the lysosome, then we're sure that it is a functional flux or not. But it's kind of an indirect way of measuring it, and it reads very complex when we're talking about P62 and LC3 degradation with or without lysosome inhibition, but you really need that lysosomal inhibition, to show that if you block the degradation of the autophagosomes that fuse in with a lysosome, then you get an increase in the LC3 and the P62, and that's when you know that the flux is you intact. Mireille Ouimet: Because you could get an increase in LC3, that's just related to a defect in the breakdown of the autophagosome. But in our study, we've used phosphorylated ATG16L1, which is a now better marker of active autophagy. And I would recommend researchers to begin to use that rather than the combination of P62 and LC3 together with or without a lysosome inhibitors such as- Cindy St. Hilaire: Oh, interesting. So let's repeat that, phosphorylated ATG- Mireille Ouimet: 16L1, yes. So there's been an antibody that was developed by a colleague at the University of Ottawa, Dr Ryan Russell, and it's commercially available through cell signaling now, and it really has been a great tool to track active autophagy. Cindy St. Hilaire: That's great. I remember my lab was looking at that at one point, and I was trying to explain the flux as... I don't know if people are going to remember this, but there's this amazing, I Love Lucy skit, where her and Ethel are working on a chocolate factory conveyor belt, and it picks up speed. And because she can't get it all done quick, she starts stuffing them in her mouth. And it's like, if you just took a snapshot of that, you would not know whether it's going too fast, or not functioning properly. And so I equate the flux experiments to that. Which are probably aging myself a lot on so. Cindy St. Hilaire: All right, so sticking to kind of the autophagy angle, what were the differences you found in autophagy in early and late atherosclerotic plaques? Because I know you looked at those two time points, but also, importantly, between the macrophage foam cells and the smooth muscle cell-derived foam cells? Sabrina Robichaud: So surprisingly, there weren't that big of a difference between each time point when we were looking at the individual cell type by themselves. Surprisingly, we did find that the macrophages did have a functional autophagy flux, even at the later stages of atherosclerosis, which was kind of interesting in itself. But when we looked at the vascular smooth muscle cell foam cells, though, that was a whole other story, and we found that these were actually defective at a very early stage and stayed defective up until the very late stage of atherosclerosis. Cindy St. Hilaire: And what is the very early stage like? What's that definition with the smooth muscle cell? Sabrina Robichaud: So we did a six-week time points in terms of our atherosclerosis study, and then a 25-week time point. So there are far apart, which shows like the very early, early stage and what would be considered the most effective autophagy at that point with the necrotic core and everything. So surprisingly, the two phenotype were quite similar at early and both late stages for both cell types, but were functional in the macrophages but dysfunctional in the smooth muscle cells. Cindy St. Hilaire: So you mentioned at one point in the discussion that you observed inconsistent lipid loading of the smooth muscle cells, and you mentioned that a lipase, which is excreted from the foam cells can then be internalized by, I assume kind of neighboring or in the vicinity, smooth muscle cells. And so the question I had it's kind of one of those chicken-and-egg question, and it's, is the smooth muscle cell-derived foam cell an independent process? Does it happen alone or de novo as a function of a smooth muscle-mediated process? Or is it really dependent first on this macrophage foam cell providing this lipid that is efflux that is then internalized by a smooth muscle cell that kind of goes on to become a foam cells. It's kind of a question of like the continuum of an atherosclerotic plaque and what do you think is happening, either based on your data or just kind of a hunch? Mireille Ouimet: That's an excellent question. And there's no doubt that macrophages really drive the initiating events of atherosclerosis. So I don't think that without the macrophage there would ever be a vascular smooth muscle cell, or there would be minimal vascular smooth muscle cell-derived foam cells. Definitely the inconsistencies that we observed in our study, were if we added like aggregated LDL on its own to a primary mouse vascular smooth muscle cell, we would get poor lipid loading and a very low percentage of those cells that would become foamy, relative to treating them with cyclodextrin complex cholesterol, for instance. Mireille Ouimet: So free cholesterol, that's cell permeable, will go into the vascular smooth muscle cell, no problem, and generate the foaminess and then allow that cell to acquire the macrophage-like phenotype. But aggregated LDL on its own in our hands, just gave very poor loading. And when we treated the vascular smooth muscle cells with aggregated LDL along with macrophage-derived condition media, we got some improvements, but it was still kind of inconsistent. But then we thought if we treat the vascular smooth muscle cells with aggregated LDL in the presence of conditioned media from macrophage foam cells that were preloaded with the aggregated LDL, would that promote their foaminess to a greater extent? And it did. Mireille Ouimet: So, there have been studies from Gordon Francis's lab that showed that adding recombinant lysosomal acid lipase to vascular smooth muscle cells that contained aggregated LDL, promoted the lysosomal hydrolysis of the aggregated LDL and to generate the foamy macrophages and allow the lysosomal processing. So we know that that vascular smooth muscle cells take up lysosomal acid lipase, and we know that macrophages undergo lysosome exocytosis and they can secrete lysosome acid lipase and acidify the extracellular milieu. Mireille Ouimet: So work from Fred Maxfield group has shown the presence of these cell surface connected compartments that are acidified, containing macrophage-derived lysosomal acid lipase, that even hydrolyze extra cellularly-aggregated LDL for macrophages. So we're not sure whether there's probably a local production of free cholesterol in the plaque by macrophages, this free cholesterol could be taken up by the vascular smooth muscle cell. And also the vascular smooth muscle cells do express some scavenger receptors, whether the expression of these scavenger receptors like LRP or CD36 even goes up when they've taken up a little bit of the free cholesterol. And then that allows the aggregated LDL to come in and then there would be some lysosomal acid lipase secreted by the macrophage foam cells that would promote the lysosomal processing of this aggregated LDL. All of those are very complex questions that will require some addressing in vivo models. Cindy St. Hilaire: You also mentioned in the paper that studies... There's a handful of them now. Studies have shown that between 30% and 70% of the cells that are staining positively for macrophage markers, meaning they're foam cells, are of the smooth muscle cell lineage. And so I believe people have seen that in mouse plaques with lineage tracing, but they've also used newer techniques to really see this also in human atherosclerotic plaques. So we know it's not just from a mouse, we know that smooth muscle cells can turn into a macrophage-like foam cell, and it's 30% to 70%, which is a huge range. Cindy St. Hilaire: So do we know the factors that dictate whether a specific plaque is going to have more or less smooth muscle cell derived foam cells? And I guess more important to what you found in your paper is, how important would it be to know whether a plaque is on the 30% end or on the 70% end in terms of therapeutic strategies? Sabrina Robichaud: Yeah, most of these studies, the range can be attributed to the different time points at which these studies have been collected early on will be a little bit more macrophage understanding would be at a later time point. Now of course in terms of therapeutics, as we saw in our paper, metformin actually will positively increase cholesterol efflux in the vascular smooth muscle cell foam cells, but not in the macrophages. So obviously, being able to know at which point there's a majority of macrophages versus vascular smooth muscle cells, definitely going to determine which therapeutic we're going to be able to use. Sabrina Robichaud: Ideally, we would be able to find a therapeutic that would work in both foam cell, but from what we've seen, the mechanistic behind the autophagy dysfunction between both cell types are so different, that I'm not entirely sure that that would be possible, we would need some sort of combination therapy. But again, we need to be a little bit more targeted depending on the percentage of the foam cells that are comprising the plaque at that particular moment in time. Cindy St. Hilaire: Yeah, so you mentioned there's a function of time there. If you look earlier, there's more macrophage, if you look later, the percent of smooth muscle cell-derived foam cell increases. Is there a point in a very advanced atherosclerotic plaque where it's just mostly smooth muscle cells? Or do those macrophage foam cells stay, and it's just the increasing number of smooth muscle cell-derived foam cells? Do we know? Mireille Ouimet: This is an excellent question, and I was going to bring up the topic of clonal expansion of the vascular smooth muscle cells. So it's a very heterogeneous population and understanding that might be some of the differences that we see in different studies. It could be the model has one type of a smooth muscle cell that's expanding more than another, what are the factors that govern that? Does one clone take over at the later stages versus the earlier stages? We don't know. Mireille Ouimet: But we were surprised in our studies to see that the macrophages that are present at least on the lumen of the plaques were very active in autophagy. They had the highest staining for the phospho-ATG16L1 in that late stage. So we're not sure if it's newly-recruited macrophages that come in, that are more active and in autophagy, and then have good lysosomal capacity that keeps degrading the lipid present in the plaque and tries to ingest it, but also as a consequence keeps releasing some of the degraded cholesterol into the milieu where the smooth muscle cells that are proliferating are internalizing it and becoming more foamy. So these are really great open questions that need to be addressed in the field. Cindy St. Hilaire: So drug-eluting stents are coated with rapamycin or the various chemical compositions that are derived from rapamycin. And rapamycin itself induces autophagy. So while the thought behind using this coating on stents was to prevent smooth muscle cell proliferation, and thus restenosis or ingrowing of the stent, your study suggests that this could also help to promote autophagy in the cells underlying the stent. So has anyone gone in and looked at plaques that have been stented and either failed or not, and investigated the foam cell content or markers for autophagy activity? Mireille Ouimet: Not to my knowledge, and this has been something we've definitely... We think that this is what's happening. Some of the protective effects of these drug-eluting stents that have everolimus or sirolimus or the rapamycin or rapamycin analogs, we do believe that some of their protective effect can be attributed to autophagy activation, but this remains to be demonstrated. We think that autophagy activation locally would promote reverse cholesterol transport and would be one of the processes that prevents restenosis because we can promote the efflux of cholesterol out. Cindy St. Hilaire: Great. So I guess stemming from my question on the stents, what are the other translational implications of the findings of your study? And what would you like to see come out of this? Mireille Ouimet: So one of the things is, as Sabrina mentioned, would be to target both foam cell populations because it seems as though the vascular smooth muscle cell foam cells are very much defective in their autophagy capacity, and they're very poor effluxes, but we could potentially restore autophagy in the cell population to promote reverse cholesterol transport. And looking at prevention of atherosclerosis is a bit different than looking at regression, because regression is at a later stage where the plaques are more advanced. And if they're mostly vascular smooth muscle cell-derived, maybe then those drugs that we're considering that protect against the development of atherosclerosis are effective on the macrophage themselves early on, but might not be mimicking what we would see in the clinic where the patients that present are older. Cindy St. Hilaire: Yeah, it's kind of really reminiscent of like the CANTOS trial and like, where do we want to target the therapy? It's going to be very different if it's an early smaller plaque, versus a late-stage possibly pro close to rupturing type of plaque. Well, Sabrina Robichaud and Dr Ouimet, thank you so much for joining me today. Congratulations again on a wonderful study, and I'm really looking forward to hearing more about this from your group. Sabrina Robichaud: Thank you. Mireille Ouimet: Thank you very much. And we also want to thank all the co-authors on the study, specifically also Adil Rasheed, who is co-first author on the work and Katey Rayner's group for all the support and involvement in this study. Cindy St. Hilaire: That's it for the highlights from the March issues of Circulation Research. Thank you for listening. Please check out the CircRes Facebook page and follow us on Twitter and Instagram with the handle @circres and #DiscoverCircRes. Thank you to our guests, Sabrina Robichaud and Dr Mireille Ouimet Sabrina. This podcast is produced by Ashara Ratnayaka, edited by Melissa Stoner and supported by the editorial team of Circulation Research. Some of the copy text for highlighted articles was provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire and this is Discover CircRes, you're on-the-go source for the most up-to-date and exciting discoveries in basic cardiovascular research. This program is copyright of the American Heart Association 2022, The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more information, visit ahajournals.org.
This week's episode features special Guest Host Mercedes Carnethon, as she interviews author Miriam Cortese-Krott and Associate Editor Charles Lowenstein as they discuss the article "Red Blood Cell and Endothelial eNOS Independently Regulate Circulating Nitric Oxide Metabolites and Blood Pressure." Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast, summary, and backstage pass to the journal and its editors. We're your co-host I'm Dr. Carolyn Lam, associate editor from The National Heart Center in Duke National University of Singapore. Dr. Greg Hundley: And I'm Dr. Greg Hundley, associate editor, director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Dr. Carolyn Lam: Greg, today's feature paper is one of those really, really landmark papers that really advance our understanding of Nitric oxide signaling. And it's about red blood cell and Endothelial eNOS, and how they independently regulate circulating nitric oxide, metabolites, and blood pressure. A real, real must, but let's go on and look at the other papers in this issue first. Greg, you want to go first? Dr. Greg Hundley: You bet, Carolyn. Better grab a cup of coffee. And my first paper is from professor Nathan Mewton from Hôpital Louis Pradel Hospices Civils de Lyon. Carolyn, these authors hypothesized that Colchicine a potent anti-inflammatory agent may reduce infarct size in left ventricular remodeling at the acute phase of STEMI. And so to address this hypothesis, they performed a double-blind multi-center trial and randomly assigned patients admitted for a first episode of STEMI referred for primary PTCA to receive oral Colchicine two-milligram loading dose followed by 0.5 milligrams twice a day, or matching placebo from admission to day five and the primary efficacy outcome was infarct size determined by cardiovascular magnetic resonance imaging at five days. And the relative left ventricular end-diastolic volume change at three months and infarct size at three months was also assessed by cardiac MRI. And these were secondary outcomes. Dr. Carolyn Lam: Nice. Okay. So what were the results? Dr. Greg Hundley: Right, Carolyn. So 192 patients were enrolled. 101 in the Colchicine group and 91 in the controls. And as a result of this trial, the oral administration of high dose Colchicine at the time of Reperfusion. And for five days thereafter did not reduce infarct size assessed by cardiac MRI. And so Carolyn, the clinical implications of these results suggest that other studies exploring the timing, pharma kinetics, and dose-response of Colchicine, as well as other anti-inflammatory agents are needed to identify an effective method to reduce infarct size and limit remodeling in this group of patients. Dr. Carolyn Lam: Wow, it's just such a rich field done with all this about Colchicine. Well, our next paper is a pre-specified sub-analysis of the randomized EAST-AFNET 4 Trial and the sub-analysis assess the effect of systematic early rhythm control therapy that is using Antiarrhythmic drugs or catheter ablation compared to usual care, which means allowing rhythm control therapy to improve symptoms in patients with heart failure. And this was defined in the sub-analysis as the presence of heart failure symptoms of New York Heart Association status two to three or a left ventricular ejection fraction of less than 50%. Dr. Carolyn Lam: Now, the authors led by Dr. Kirchhof at University Heart and Vascular Center UKE in Hamburg, Germany included 798 patients in this sub-analysis of whom 442 had HFpEF, 211 had heart failure with mid-range ejection fraction and 132 had HF-rEF over a median of 5.1 years of follow-up the composite primary outcome of cardiovascular death stroke or hospitalization for worsening heart failure, or for acute coronary syndrome occurred less often in patients randomized to early rhythm control therapy compared with patients randomized to usual care. And this was not altered by heart failure status with an interaction P-value of 0.6. Left ventricular function, symptoms, and quality of life improved equally in both treatment strategies. Dr. Greg Hundley: Wow, Carolyn, a lot of information here. So what can we take away from this? Dr. Carolyn Lam: Well, let's remember that this is a sub-analysis, albeit pre-specified of that randomized trial of the EAST-AFNET 4 Trial, but nonetheless, the data supports a treatment strategy of rhythm control therapy with Antiarrhythmic drugs or ablation within a year of diagnosing atrial fibrillation in patients with signs and symptoms of heart failure to reduce cardiovascular outcomes. Dr. Greg Hundley: Very nice, Carolyn. So, Carolyn, my next paper pertains to Alarmin Interleukin-1 Alpha, and it comes to us from Dr. Thimoteus Speer at Saarland University. So, Carolyn, Alarmin Interleukin-1 Alpha is expressed in a variety of cell types, promoting sterile systemic inflammation. And the aim of the present study was to examine the role of Alarmin Interleukin-1 Alpha in mediating inflammation in the setting of acute myocardial infarction and chronic kidney disease. Dr. Carolyn Lam: Wow, sterile inflammation. It's a really hot topic now. So what did these authors find? Dr. Greg Hundley: Right, Carolyn. So we're going to call Alarmin Interleukin-1 Alpha. Let's just call it IL-1 Alpha and so increased IL-1 Alpha surface expression on monocytes from patients with acute myocardial infarction in patients with chronic kidney disease was found to be associated with cardiovascular events. Next, IL-1 Alphas itself served as an adhesion molecule, mediating leukocyte-endothelial adhesion, and finally, abrogation of IL-1 alpha prevented inflammation after myocardial infarction and ameliorated chronic kidney disease in Vivo. Dr. Carolyn Lam: Wow. So what does this mean clinically? Dr. Greg Hundley: Right, Carolyn, so perhaps targeted therapeutic inhibition of IL-1 Alpha might represent a novel anti-inflammatory treatment strategy in patients with myocardial infarction and in patients with chronic kidney disease. Dr. Carolyn Lam: Amazing. Thanks, Greg. Well, in today's issue, there's also an exchange of letters between doctors Lother and Filippatos on Finerenone and risk of hyperkalemia in CKD and type two diabetes. There's an On My Mind paper by Dr. Sattler on the single-cell immunology and cardiovascular METs in, do we know yet what we don't know? Dr. Greg Hundley: And then Carolyn, from the mailbag, a Research Letter from Professor Wehrens entitled “Atrial Specific LK Beta One Knockdown Represents a Novel Mouse Model of Atrial Cardiomyopathy with Spontaneous Atrial Fibrillation.” Well, Carolyn, how about we turn our attention to those red blood cells and endothelial nitric oxide synthase. Dr. Carolyn Lam: Yeah. Can't wait. Dr. Mercedes Carnethon: Well, welcome to this episode of Circulation on the Run. Our podcasts, where we have an opportunity to speak with authors of important papers that are appearing in the journal of circulation. I'm pleased to introduce myself. My name is Mercedes Carnethon, professor and vice-chair of preventive medicine at the Northwestern University Feinberg School of Medicine. And I'm pleased today to invite our guest author, Miriam Cortese-Krott, who is the faculty of the University of Duesseldorf, and a guest professor at the Karolinska Institute in Stockholm. And we have with us as well the other associate editor who handled the piece for circulation, Dr. Charlie Lowenstein from Johns Hopkins University. So welcome to each of you this morning. Miriam Cortese-krott: Thank you. Dr. Charles Lowenstein : Thanks for having me. Dr. Mercedes Carnethon: Well, thank you. I'm really excited to jump right into this piece, Miriam, can you tell me a little bit about the rationale for carrying out the study, why you pursued it? Professor Miriam Cortese-Krott: The reason is because when I was working as a post-doc, I had to isolate an enzyme from red blood cells, which is a very, very difficult. And if you know, this enzyme is endothelial nitric oxide synthase, which produce nitric oxide, and actually, the red blood cell is full of the worst enemy of nitric oxide, which is hemoglobin. So actually, when I was talking about my project, everybody was asking, "Why are you doing that?" And I was actually able to isolate the enzyme and look at activity and be sure that the enzyme was fine, but the function of this enzyme was absolutely unknown. Professor Miriam Cortese-Krott: And the only way to study proteins in red blood cells is to make modification in the bone marrow of the mice. So in the Erythroid cells, because you can not, of course, if there are cells without nucleus you don't have any chance to modify them in culture, something like that. So the only way was to generate mice with modification specifically in the red blood cells. And I had the chance to create, to generate red cell-specific eNOS knockout mice. And of course, as a control endothelial-specific eNOS knockout mice by using the Cre-loxP technology. And with this technology, I could really understand what's happening to the physiology of the mouse if you remove this protein from the red blood cells. And so this was the whole idea. Dr. Mercedes Carnethon: Thank you so much. It was really exciting for me to read this piece. We are on opposite ends of the scientific inquiry spread as I'm an epidemiologist who does things at the population level, and you're identifying things at the basic science level. I thought the paper was extremely well-written and that encouraged people to dig in, even if you're unfamiliar, and in part that's because you provided such a great explanation of how your findings are used and how they're relevant to the process. Do you mind sharing a little bit about your findings and how you expect that they will be used by our scientific community? Professor Miriam Cortese-Krott: I think the main finding of this paper is that if you remove eNOS from the red blood cells if the mice are hypertensive, have hypertension, and this is completely something that you actually will not expect, as I told you that indeed red cells are full of the enemy of nitric oxide that remove it immediately. So you can ask yourself how it is possible. But I think the key finding here in this paper was that I also generated the opposite model. So I created the model a conditional eNOS Knockout model where you can decide in which tissue you want to have your enzyme. And of course, I applied for red blood cells. And what you see in this model is that you start from a global knockout mouse with hypertension, you reintroduce the eNOS just in the red blood cells, you have normal tension. So this means, this is the main finding. You have a switch in the red blood cells, which is the enzyme eNOS, which it's behaving in a completely different way clearly as compared to the vessel wall eNOS and still regulating blood pressure. Dr. Mercedes Carnethon: Well, thank you so much. I think this is the point at which I like to turn to the associate editor who handled the piece. Charlie, you and I don't get to talk as often given the diversity of work that we each pursue, but Charlie, tell me a little bit about what excited you about this piece? Dr. Charles Lowenstein: Thanks, Mercedes. So I love this piece. I thought Miriam, your article is so great. So a couple of thoughts. One is nitric oxide and nitric oxide synthase are so important in biology and medicine, nitric oxide regulates blood pressure. It regulates neurotransmission. It regulates inflammation. And this is true, not only in the lab, looking at cells in mice, but also in the human. So genetic variance in the endothelial nitric oxide synthase gene or NOS3 are associated with risks for diseases like coronary artery disease. So eNOS is just so important in biology and medicine. And now some ancient history. When I was a cardiology fellow, about a hundred years ago, I worked in the lab that first purified nitric oxide synthase proteins, and we cloned two of the nitric oxide synthase genes that was in the lab of Dr. Solomon Snyder at Johns Hopkins back in the 1700s. Dr. Charles Lowenstein: So when we cloned the nitric oxide synthase genes, when we and others did, we made a huge mistake. We chose the names for these isoforms from the tissue where they were first isolated. So we called the brain nitric oxide synthase nNOS, because it's a neurons, macrophages MCnos we called it MCnos and in endothelial cells, we called it the nitric oxide synthase eNOS or endothelial NOS. But in the last 20 years, lots of investigators have found these isoforms are in other cells, not just the original cells at discovery. And so Miriam's question is just so important, which cells make endothelial NOS also called NOS3. That's the history. Now what Miriam has discovered is just so important. I was so fascinated by her work because as she just said, she made two amazing discoveries. One, red blood cells make endothelial nitric oxide synthase. Dr. Charles Lowenstein: And that's been a controversy for a long time. Some people have said, "Yes." Some, "No." And Miriam made the definitive answer. Yes, red blood cells make eNOS, and secondly, she has discovered so much about the physiology of ENO coming from red blood cells, the nitric oxide that's made inside red blood cells regulates blood pressure. What a magical, interesting, and important finding. That's a little bit about the history. Nitric oxide and NOS are important in medicine. The people who originally cloned and purified the nitric oxide synthase isoforms named them after the tissue in which they discovered. And Miriam has made a major discovery that it's not only endothelial cells that make nitric oxide but also red blood cells. Dr. Mercedes Carnethon: Thank you so much for that summary. And I guess, I would have thought perhaps this was something of an Elixir of youth because if you've been working in this area for 200 plus years and Miriam, you started working on this as part of your dissertation work, you both have a lot of insight and background on where we've been and what the advances are. Miriam, can you tell me a little bit about how you'd like to see these findings used by the scientific community? Professor Miriam Cortese-Krott: I think I would like that the scientific community would use my mice first because I think, as Charles has said, it's not only red cells that express eNOS and it's not only endothelial cells. There are other cells producing eNOS and the function in the other cells is not known even in leukocytes, even when they have iNOS of course, but also have eNOS. So you can use my mice since it's a flux model. You can choose whatever you want, what cell you want, and then knock it in and knock it out. So this is one thing that I think the community could really do. I cannot do everything. So I'm happy to give my mice away. Professor Miriam Cortese-Krott: And the second thing is I would like too that in particular, the clinical community would see this link between Emathology and cardiovascular disease. This is something that was started, of course, there are studies looking at anemia and cardiovascular disease, but these studies have sometimes some issues I of course cannot speak as a basic scientist. I cannot speak about huge clinical trials, but I think this link exists and exists at the molecular level and it can be a target for pharmacological therapy. So I think this is what I would like to transport with this study to the clinical community and the basic science community. Dr. Mercedes Carnethon: Yeah. I think this is the point at which Charlie, I turn it to you because you really stand at the intersection of both of those communities. What questions do you have for Miriam going forward, as you think about spreading the word on this important work? Dr. Charles Lowenstein: So Miriam's discovery is just so important and she now has the tools to help answer really, really important questions. How is nitric oxide made in red blood cells? How is it stored in red blood cells? How is it transported throughout the body in red blood cells? What is the chemistry of nitric oxide, when it is stored, when it combines with oxygen when it forms nitrite and nitrate, how is it released from red blood cells? How is it targeted from a red blood cell to the vasculature? So there're these great basic science questions that Miriam and her colleagues are now poised to answer. So there's the science part of it. Then there's the medicine part of it because Miriam's mice and her great discovery have really huge implications for medicine. And so the question is, how can we use ENO? How can we deliver it? How can we target ENO to human tissues? Dr. Charles Lowenstein: How can we turn on erythrocyte, nitric oxide synthase? How can we turn it off? Because there are all these medical diseases where too much nitric oxide is bad, like in sepsis or inadequate amounts, don't protect the vasculature like atherosclerosis. Then there are all these other interesting questions. When we transfuse red blood cells, sometimes if you transfuse aged red blood cells, it's not good. You can harm people. Maybe we can load up or activate eNOS in stored red blood cells and then help deliver more ENO to patients who need red blood cells. So there are all these fascinating medical questions that we can look at based on Miriam's really important discovery. Dr. Mercedes Carnethon: Well, thank you so much. We're coming to the end of this wonderful and informative podcast. And I guess, I'd just ask Miriam, do you have anything else you'd like our listeners to know about your work and about the findings from this study? Professor Miriam Cortese-Krott: I would like people know that hard work help a lot, and that you have to believe in what you are doing and the quality of your science at the end would bring their true discoveries. So I think it's important specifically, for the young women in science that having this message too. So the science per se must be excellent and to proceed, you need a lot of work, but then the work goes to a good end. Dr. Mercedes Carnethon: Miriam, thank you so much for that inspirational note. The hard work that scientists need, the persistence across one's career and building from earlier discoveries, and bringing those forward through one's career are always critically important. And so I hope everyone has really enjoyed this episode and this opportunity to hear from Dr. Cortese-Krott. Miriam, you've done such wonderful work, and thank you as well, Charlie, for your insights about the intersection of this work with clinical care and basic science. Professor Miriam Cortese-Krott: Thank you. Dr. Charles Lowenstein: Thank you. Dr. Mercedes Carnethon: Thank you all very much for joining us today in this episode of Circulation on the Run. Dr. Greg Hundley: This program is copyright of the American Heart Association, 2021. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, visit ahajournals.org.
In this episode, we chat to David Adelani, a computer scientist, PhD candidate at Saarland University in Germany, and active member of Masakhane. Masakhane is a grassroots organisation whose mission is to strengthen and support natural language processing research in African languages. There are over 2000 African languages, so David and the Masakhane team have their work cut out for them. We also discuss how to build technology with few resources and the challenges and joys of participatory research.
In this episode, I converse with Prof. Ratnesh Jain, an Assistant Professor in the Department of Chemical Engineering, and Prof. Prajakta Dandekar, Assistant Professor in the Department of Pharmaceutical Sciences at the Institute of Chemical Technology. Ratnesh and Prajakta completed their graduate studies at ICT and went on to complete a Postdoctoral Fellowship at Saarland University in Germany before joining the faculty at their alma mater. Ratnesh and Prajakta direct the Nanomedicine Research Group at ICT and their interests straddle drug delivery systems, tissue engineering, and nanomedicine. We indulge in a fascinating conversation on their incredible journey in science; terrific mentors who have guided them; taking rejections in their strides; the joys and perils of doing science in India and together as a duo; the contours of industry-academia scientific collaboration; academics challenges plaguing the Indian university system at large; and many more things!!
Abstract of the talk… ENG: Cloud&Heat has always focused on providing energy-efficient data centers. In the last 8 years, we have developed an innovative water cooling technology for servers, converting waste heat into a valuable asset. By doing so, we have already greatly improved the energy efficiency of individual data centers. However, this isn't enough. To globally maximize the efficiency of distributed data center infrastructures, this talk presents Krake. Krake is an orchestration software for compute-intensive jobs. It improves the global cost and energy efficiency of infrastructures by balancing the load between data centers. Krake evaluates and selects the most efficient site to run jobs based on certain metrics, such as energy availability, heat demand, and latency. It also reacts to changes in the system by migrating jobs. In other words, it ensures a job is run in the most energy- and/or cost-efficient way at any given time. ESP: Cloud & Heat siempre se ha centrado en proporcionar centros de datos energéticamente eficientes. En los últimos 8 años, hemos desarrollado una innovadora tecnología de refrigeración por agua para servidores, que convierte el calor residual en un activo valioso. Al hacerlo, ya hemos mejorado enormemente la eficiencia energética de los centros de datos individuales. Sin embargo, esto no es suficiente. Para maximizar globalmente la eficiencia de las infraestructuras de centros de datos distribuidos, en esta charla presentaremos Krake. Krake es un software de orquestación para trabajos intensivos en computación. Mejora el costo global y la eficiencia energética de las infraestructuras al equilibrar la carga entre los centros de datos. Krake evalúa y selecciona el sitio más eficiente para ejecutar trabajos según ciertas métricas, como la disponibilidad de energía, la demanda de calor y la latencia. También reacciona a los cambios en el sistema mediante la migración de trabajos. En otras palabras, asegura que un trabajo se ejecute de la manera más eficiente en términos de energía y costo en un momento dado. Bio… ES: Juan A. Fraire es investigador asistente en CONICET en Argentina, profesor asociado en la Universidad de Saarland en Alemania y arquitecto de soluciones cloud en Cloud&Heat en Alemania. Su principal interés gira en torno a las aplicaciones en red y distribuidas habilitadas por técnicas informáticas de vanguardia. Además de aplicar esto al dominio del cloud computing en tierra, Juan lidera un esfuerzo internacional para llevar la visión al dominio del espacio. De hecho, Juan es el fundador y presidente del STINT Workshop desde 2014, ha sido coautor de más de 55 artículos publicados en revistas internacionales y conferencias líderes, y ha construído una visión novedosa de redes en su libro “Delay-Tolerant Satellite Network ” en coautoría con colegas de la NASA. EN: Juan A. Fraire is an assistant researcher at CONICET in Argentina, an associate professor at Saarland University in Germany, and cloud solutions architect at Cloud&Heat in Germany. His main interest revolves around networking and distributed applications enabled by state-of-the-art informatics techniques. Besides applying this to the cloud domain on ground, Juan leads an international effort in pushing the vision into the space domain. Indeed, Juan is the founder and chair of the annual Space-Terrestrial Internetworking Workshop (STINT) since 2014, has co-authored more than 55 papers published in international journals and leading conferences, and has imprinted a novel networking vision in his “Delay-Tolerant Satellite Network” book co-authored with colleagues from NASA.
In this episode, Fulbright Austria alumna Astrid M. Fellner and EUR Diversity Coordinator Susanne Hamscha talk about European and US borderlands, the symbolic power of borders, and borders in times of Covid-19.Astrid M. Fellner is professor for North American Literary and Cultural Studies at Saarland University, Germany. She received a Fulbright grant to study at the University of Texas at Austin (1991-92). Astrid's research focuses on Border Studies and U.S. Latino/a literature.
2020 has been a historic year in energy markets, with a dramatic price crash caused by a collapse in economic activity resulting from the pandemic. In recent weeks, major oil and gas companies around the world have been reporting their worst quarterly results in history and seem to be positioning themselves for prolonged pain still to come. Yet we have also seen several companies reaffirm commitments to a net-zero carbon future by 2050, and we continue to have rising concern and evidence of the tangible impacts of climate change around the world. This all raises the question of whether the pandemic will be an accelerator or decelerator of the energy transition, and how leading oil and gas companies are responding to today’s uncertain and challenging environment. In this edition of Columbia Energy Exchange, host Jason Bordoff is joined by Mario Mehren, who leads the largest independent oil and gas company in Europe. Mario Mehren is the Chief Executive Officer and Chairman of the Board of Wintershall Dea. He was previously responsible for the company’s activities in Exploration and Production in Russia, North Africa and South Africa. Before joining Wintershall, Mario worked as a specialist adviser in the BASF Group’s Corporate Finance Department before becoming the Head of Finance and Accounting at BASF Schwarzheide and later its Managing Director of Finance and Administration. Mario studied business administration at Saarland University in Saarbrüken.
"If you always go for something your manager agrees to, then you're likely not bold enough. The magic is turning a no into a yes." Benno Dorer is the CEO & Chairman of The Clorox Company - a post he’s held since 2014. Benno started at Clorox in 2005 rising through executive roles across Laundry, Home Care, International businesses, and Corporate Strategy. Prior to joining Clorox, Benno spent 14+ years at P&G - in senior marketing positions around the world, including the Glad Products joint venture. He has been the highest-rated US CEO on Glassdoor, among the Bay Area's Most Admired CEOs by the San Francisco Business Times, and was awarded Out & Equal’s CEO of the Year. Benno has a degree in Economics from University of Freiberg, graduate degree in business administration from Saarland University and as a multilingual leader - has worked in Germany, Sweden, Belgium, Ohio, and California. In this candid conversation, Benno shares his philosophies on creating a culture of transparency, ownership and empowerment - as well as his thoughts on the importance of finding joy and meaning in the workplace,
Our entire show is based on the idea that we might say something interesting enough that it might get you to perk up your ears, figuratively speaking. Or, as a team at Saarland University has found, maybe not so figuratively speaking. Plus: a sculpture garden in Dublin, Ohio pays tribute to ears of a different kind. Our animal inheritance: Humans perk up their ears, too, when they hear interesting sounds (Science Daily) Field of Giant Corn Cobs (Roadside America) Keep backing Cool Weird Awesome on Patreon and we'll keep giving you great shows to hear --- Send in a voice message: https://anchor.fm/coolweirdawesome/message
Voice your comments, suggestions, feedback, etc, in our awesome forum: http://robbtv.com/forum Welcome to Music In Film with Luana. All you need to know about music in film, summarized across different topics that range from composing music for film to sync licensing and more. Taught by Luana, a professional musician, singer-songwriter and actress who studied at the Saarland University of Music (Hochschule für Musik Saar) in Saarbrücken, Saarland, Germany. Pay attention to every detail. You will learn a lot. All aspiring musicians and composers are welcome to join. ----more---- ROBB TV (RTV) is an on-demand IPN (Internet Programming Network™). In other words; we produce and distribute episodic content for the awesome internet. Say hello to the new broadcast/cable network. ROBB ENTERTAINMENT is a New York-based Media and Entertainment company that specializes in the production, marketing, and distribution of short and long-form entertainment, across multiple platforms. The company was established in 2008 by ROMANE ORLANDO ROBB, and is owned by SIMPLEROBB, INC. - A ROBB CORPORATION COMPANY. For more information, please visit us at http://robbent.com. __ FOLLOW US:__ WEBSITE: https://robbtv.com INSTAGRAM: https://instagram.robbent.com FACEBOOK: https://facebook.robbent.com TWITTER: https://twitter.robbent.com ROBB ENTERTAINMENT: https://robbent.com __ #robb #creative #marketing #showman #musicvideo #commercials #viral #videos #socialmedia #major #music #filmmakers #filmmaking #love #lyrics #fun #entertainment #knowledge #power #laugh #engage #inspiration #work #learn #romane #orlando #ceo #chairman #boss #finance #corporation #holding #wallstreet #money #food #beverage #fashion #retail #logistics #netflix #tv #studios #productions #theatre #plays #amaznon #yahoo #google #instagram #youtube #robbtv #robbentertainment
Voice your comments, suggestions, feedback, etc, in our awesome forum: http://robbtv.com/forum Welcome to Music In Film with Luana. All you need to know about music in film, summarized across different topics that range from composing music for film to sync licensing and more. Taught by Luana, a professional musician, singer-songwriter and actress who studied at the Saarland University of Music (Hochschule für Musik Saar) in Saarbrücken, Saarland, Germany. Pay attention to every detail. You will learn a lot. All aspiring musicians and composers are welcome to join. ----more---- ROBB TV (RTV) is an on-demand IPN (Internet Programming Network™). In other words; we produce and distribute episodic content for the awesome internet. Say hello to the new broadcast/cable network. ROBB ENTERTAINMENT is a New York-based Media and Entertainment company that specializes in the production, marketing, and distribution of short and long-form entertainment, across multiple platforms. The company was established in 2008 by ROMANE ORLANDO ROBB, and is owned by SIMPLEROBB, INC. - A ROBB CORPORATION COMPANY. For more information, please visit us at http://robbent.com. __ FOLLOW US:__ WEBSITE: https://robbtv.com INSTAGRAM: https://instagram.robbent.com FACEBOOK: https://facebook.robbent.com TWITTER: https://twitter.robbent.com ROBB ENTERTAINMENT: https://robbent.com __ #robb #creative #marketing #showman #musicvideo #commercials #viral #videos #socialmedia #major #music #filmmakers #filmmaking #love #lyrics #fun #entertainment #knowledge #power #laugh #engage #inspiration #work #learn #romane #orlando #ceo #chairman #boss #finance #corporation #holding #wallstreet #money #food #beverage #fashion #retail #logistics #netflix #tv #studios #productions #theatre #plays #amaznon #yahoo #google #instagram #youtube #robbtv #robbentertainment
Voice your comments, suggestions, feedback, etc, in our awesome forum: http://robbtv.com/forum Welcome to Music In Film with Luana. All you need to know about music in film, summarized across different topics that range from composing music for film to sync licensing and more. Taught by Luana, a professional musician, singer-songwriter and actress who studied at the Saarland University of Music (Hochschule für Musik Saar) in Saarbrücken, Saarland, Germany. Pay attention to every detail. You will learn a lot. All aspiring musicians and composers are welcome to join. ----more---- ROBB TV (RTV) is an on-demand IPN (Internet Programming Network™). In other words; we produce and distribute episodic content for the awesome internet. Say hello to the new broadcast/cable network. ROBB ENTERTAINMENT is a New York-based Media and Entertainment company that specializes in the production, marketing, and distribution of short and long-form entertainment, across multiple platforms. The company was established in 2008 by ROMANE ORLANDO ROBB, and is owned by SIMPLEROBB, INC. - A ROBB CORPORATION COMPANY. For more information, please visit us at http://robbent.com. __ FOLLOW US:__ WEBSITE: https://robbtv.com INSTAGRAM: https://instagram.robbent.com FACEBOOK: https://facebook.robbent.com TWITTER: https://twitter.robbent.com ROBB ENTERTAINMENT: https://robbent.com __ #robb #creative #marketing #showman #musicvideo #commercials #viral #videos #socialmedia #major #music #filmmakers #filmmaking #love #lyrics #fun #entertainment #knowledge #power #laugh #engage #inspiration #work #learn #romane #orlando #ceo #chairman #boss #finance #corporation #holding #wallstreet #money #food #beverage #fashion #retail #logistics #netflix #tv #studios #productions #theatre #plays #amaznon #yahoo #google #instagram #youtube #robbtv #robbentertainment
Voice your comments, suggestions, feedback, etc, in our awesome forum: http://robbtv.com/forum Welcome to Music In Film with Luana. All you need to know about music in film, summarized across different topics that range from composing music for film to sync licensing and more. Taught by Luana, a professional musician, singer-songwriter and actress who studied at the Saarland University of Music (Hochschule für Musik Saar) in Saarbrücken, Saarland, Germany. Pay attention to every detail. You will learn a lot. All aspiring musicians and composers are welcome to join. ----more---- ROBB TV (RTV) is an on-demand IPN (Internet Programming Network™). In other words; we produce and distribute episodic content for the awesome internet. Say hello to the new broadcast/cable network. ROBB ENTERTAINMENT is a New York-based Media and Entertainment company that specializes in the production, marketing, and distribution of short and long-form entertainment, across multiple platforms. The company was established in 2008 by ROMANE ORLANDO ROBB, and is owned by SIMPLEROBB, INC. - A ROBB CORPORATION COMPANY. For more information, please visit us at http://robbent.com. __ FOLLOW US:__ WEBSITE: https://robbtv.com INSTAGRAM: https://instagram.robbent.com FACEBOOK: https://facebook.robbent.com TWITTER: https://twitter.robbent.com ROBB ENTERTAINMENT: https://robbent.com __ #robb #creative #marketing #showman #musicvideo #commercials #viral #videos #socialmedia #major #music #filmmakers #filmmaking #love #lyrics #fun #entertainment #knowledge #power #laugh #engage #inspiration #work #learn #romane #orlando #ceo #chairman #boss #finance #corporation #holding #wallstreet #money #food #beverage #fashion #retail #logistics #netflix #tv #studios #productions #theatre #plays #amaznon #yahoo #google #instagram #youtube #robbtv #robbentertainment
Voice your comments, suggestions, feedback, etc, in our awesome forum: http://robbtv.com/forum Welcome to Music In Film with Luana. All you need to know about music in film, summarized across different topics that range from composing music for film to sync licensing and more. Taught by Luana, a professional musician, singer-songwriter and actress who studied at the Saarland University of Music (Hochschule für Musik Saar) in Saarbrücken, Saarland, Germany. Pay attention to every detail. You will learn a lot. All aspiring musicians and composers are welcome to join. ----more---- ROBB TV (RTV) is an on-demand IPN (Internet Programming Network™). In other words; we produce and distribute episodic content for the awesome internet. Say hello to the new broadcast/cable network. ROBB ENTERTAINMENT is a New York-based Media and Entertainment company that specializes in the production, marketing, and distribution of short and long-form entertainment, across multiple platforms. The company was established in 2008 by ROMANE ORLANDO ROBB, and is owned by SIMPLEROBB, INC. - A ROBB CORPORATION COMPANY. For more information, please visit us at http://robbent.com. __ FOLLOW US:__ WEBSITE: https://robbtv.com INSTAGRAM: https://instagram.robbent.com FACEBOOK: https://facebook.robbent.com TWITTER: https://twitter.robbent.com ROBB ENTERTAINMENT: https://robbent.com __ #robb #creative #marketing #showman #musicvideo #commercials #viral #videos #socialmedia #major #music #filmmakers #filmmaking #love #lyrics #fun #entertainment #knowledge #power #laugh #engage #inspiration #work #learn #romane #orlando #ceo #chairman #boss #finance #corporation #holding #wallstreet #money #food #beverage #fashion #retail #logistics #netflix #tv #studios #productions #theatre #plays #amaznon #yahoo #google #instagram #youtube #robbtv #robbentertainment
Voice your comments, suggestions, feedback, etc, in our awesome forum: http://robbtv.com/forum Welcome to Music In Film with Luana. All you need to know about music in film, summarized across different topics that range from composing music for film to sync licensing and more. Taught by Luana, a professional musician, singer-songwriter and actress who studied at the Saarland University of Music (Hochschule für Musik Saar) in Saarbrücken, Saarland, Germany. Pay attention to every detail. You will learn a lot. All aspiring musicians and composers are welcome to join. ----more---- ROBB TV (RTV) is an on-demand IPN (Internet Programming Network™). In other words; we produce and distribute episodic content for the awesome internet. Say hello to the new broadcast/cable network. ROBB ENTERTAINMENT is a New York-based Media and Entertainment company that specializes in the production, marketing, and distribution of short and long-form entertainment, across multiple platforms. The company was established in 2008 by ROMANE ORLANDO ROBB, and is owned by SIMPLEROBB, INC. - A ROBB CORPORATION COMPANY. For more information, please visit us at http://robbent.com. __ FOLLOW US:__ WEBSITE: https://robbtv.com INSTAGRAM: https://instagram.robbent.com FACEBOOK: https://facebook.robbent.com TWITTER: https://twitter.robbent.com ROBB ENTERTAINMENT: https://robbent.com __ #robb #creative #marketing #showman #musicvideo #commercials #viral #videos #socialmedia #major #music #filmmakers #filmmaking #love #lyrics #fun #entertainment #knowledge #power #laugh #engage #inspiration #work #learn #romane #orlando #ceo #chairman #boss #finance #corporation #holding #wallstreet #money #food #beverage #fashion #retail #logistics #netflix #tv #studios #productions #theatre #plays #amaznon #yahoo #google #instagram #youtube #robbtv #robbentertainment
Voice your comments, suggestions, feedback, etc, in our awesome forum: http://robbtv.com/forum Welcome to Music In Film with Luana. All you need to know about music in film, summarized across different topics that range from composing music for film to sync licensing and more. Taught by Luana, a professional musician, singer-songwriter and actress who studied at the Saarland University of Music (Hochschule für Musik Saar) in Saarbrücken, Saarland, Germany. Pay attention to every detail. You will learn a lot. All aspiring musicians and composers are welcome to join. ----more---- ROBB TV (RTV) is an on-demand IPN (Internet Programming Network™). In other words; we produce and distribute episodic content for the awesome internet. Say hello to the new broadcast/cable network. ROBB ENTERTAINMENT is a New York-based Media and Entertainment company that specializes in the production, marketing, and distribution of short and long-form entertainment, across multiple platforms. The company was established in 2008 by ROMANE ORLANDO ROBB, and is owned by SIMPLEROBB, INC. - A ROBB CORPORATION COMPANY. For more information, please visit us at http://robbent.com. __ FOLLOW US:__ WEBSITE: https://robbtv.com INSTAGRAM: https://instagram.robbent.com FACEBOOK: https://facebook.robbent.com TWITTER: https://twitter.robbent.com ROBB ENTERTAINMENT: https://robbent.com __ #robb #creative #marketing #showman #musicvideo #commercials #viral #videos #socialmedia #major #music #filmmakers #filmmaking #love #lyrics #fun #entertainment #knowledge #power #laugh #engage #inspiration #work #learn #romane #orlando #ceo #chairman #boss #finance #corporation #holding #wallstreet #money #food #beverage #fashion #retail #logistics #netflix #tv #studios #productions #theatre #plays #amaznon #yahoo #google #instagram #youtube #robbtv #robbentertainment
Voice your comments, suggestions, feedback, etc, in our awesome forum: http://robbtv.com/forum Welcome to Music In Film with Luana. All you need to know about music in film, summarized across different topics that range from composing music for film to sync licensing and more. Taught by Luana, a professional musician, singer-songwriter and actress who studied at the Saarland University of Music (Hochschule für Musik Saar) in Saarbrücken, Saarland, Germany. Pay attention to every detail. You will learn a lot. All aspiring musicians and composers are welcome to join. ----more---- ROBB TV (RTV) is an on-demand IPN (Internet Programming Network™). In other words; we produce and distribute episodic content for the awesome internet. Say hello to the new broadcast/cable network. ROBB ENTERTAINMENT is a New York-based Media and Entertainment company that specializes in the production, marketing, and distribution of short and long-form entertainment, across multiple platforms. The company was established in 2008 by ROMANE ORLANDO ROBB, and is owned by SIMPLEROBB, INC. - A ROBB CORPORATION COMPANY. For more information, please visit us at http://robbent.com. __ FOLLOW US:__ WEBSITE: https://robbtv.com INSTAGRAM: https://instagram.robbent.com FACEBOOK: https://facebook.robbent.com TWITTER: https://twitter.robbent.com ROBB ENTERTAINMENT: https://robbent.com __ #robb #creative #marketing #showman #musicvideo #commercials #viral #videos #socialmedia #major #music #filmmakers #filmmaking #love #lyrics #fun #entertainment #knowledge #power #laugh #engage #inspiration #work #learn #romane #orlando #ceo #chairman #boss #finance #corporation #holding #wallstreet #money #food #beverage #fashion #retail #logistics #netflix #tv #studios #productions #theatre #plays #amaznon #yahoo #google #instagram #youtube #robbtv #robbentertainment
Prof. Dr. Henning Madry, an MD, tenured professor, and Director of the Center of Experimental Orthopaedics at Saarland University in Germany, describes the new OARSI-affiliated journal Osteoarthritis and Cartilage Open and how his background in both basic science research and as a clinician prepared him to serve as the journal’s editor. More information about Prof. Madry’s research can be found at www.uks.eu/ieo and about the journal (including contact information) at www.journals.elsevier.com/osteoarthritis-and-cartilage-open.
In this episode of the podcast, Iryna speaks with Susanne-Marie Kirsch, a research student in Department of Materials Science and Engineering, Faculty of Natural Sciences and Technology at Saarland University about elastocalorics and the promising technology to replace existing vapor-compression refrigeration systems. Also, they discuss alternative shape memory materials, cooling/heating efficiency, environmental impact and other topics.
Heike is back with Roger for a more detailed look into gender studies. They are discussing what this particular field of social sciences is about, who does and who maybe should study it, and what aspects there are in terms of research topics and interdisciplinary facets. The UdS Gender Studies Certificate If you want to read up on Saarland University's gender study course, follow this link for more information.
The Ripple credit network has emerged as the payment backbone withindisputable advantages for financial institutions and the remittanceindustry. Ripple's market capitalization is currently third only toBitcoin and Ethereum. Its path-based IOweYou (IOU) settlements acrossdifferent currencies conceptually distinguishes the Ripple blockchainfrom the cryptocurrencies (such as Bitcoin) and makes it highly suitableto an orthogonal yet vast set of applications in the remittance worldand beyond. In this talk, I present our recent study of the structure and evolutionof the Ripple network since its inception, and our research resultsregarding its vulnerability to attacks that harm the IOU credit of itswallets. We find that about 13M USD are at risk in the current Ripplenetwork due to inappropriate configuration of the rippling flag oncredit links that paves the way to undesired redistribution of creditacross those links. Although the Ripple network has grown around a fewhighly connected hub (gateway) wallets that make the core of the networkand provide high liquidity to users, such credit link distributionresults in a user base of around 112,000 wallets that can be financiallyalienated by as few as 10 highly connected gateway wallets. Indeed,today about 4.9M USD cannot be withdrawn by their owners from the Ripplenetwork due to PayRoutes, a gateway tagged as faulty by the Ripplecommunity. Finally, we observe that stale exchange offers pose a realproblem, and exchanges (market makers) have not always been vigilantabout periodically updating their exchange offers according to currentreal-world exchange rates. For example, stale offers were used by 84Ripple wallets to gain more than 4.5M USD from mid-July to mid-August2017. Our findings should prompt the Ripple community to improve thehealth of the network by educating its users on increasing theirconnectivity, and by appropriately maintaining the credit limits,rippling flags, and exchange offers on their IOU credit links. About the speaker: Pedro Moreno-Sanchez is a PhD student in the Department of ComputerScience at Purdue University. His advisor is Prof. Aniket Kate. Hiscurrent research focuses on the areas of security, privacy andreliability of credit network based systems such as Ripple. Previously,he also worked on network access control in distributed scenarios suchas eduroam. Before moving to Purdue University in August 2015, he started his PhDstudies at Saarland University in 2013 under the supervision of Prof.Aniket Kate. Previously, he was an intern researcher at IBM Research -Zurich (Switzerland) in 2017 under the supervision of Christian Cachin;at Ripple (USA) in 2016 under the supervision of Stefan Thomas; and atPhilips Research Europe (The Netherlands) under the supervision of OscarGarcia-Morchon and Rafael Marin-Lopez. He received his bachelors andmasters from University of Murcia (Spain) in 2011 and 2013 respectively.
Hugh Fullagar joins me on the podcast after a recent career move from the Oakland Raiders, as their Assistant Strength & Conditioning Coach, to UTS as a Lecturer in Sport & Exercise Science. Hugh has a PhD from Saarland University in Germany looking at sleep related issues facing professional footballers. It was anabsolute pleasure to chat with Hugh and chat about his experiences in Germany working at the FIFA medical and more recently with the University of Oregon and the Oakland Raiders. In this episode, you will learn - Who is Hugh Fullagar (background, education and current role) Realities of working in the NFL Demands of the game Recovery protocols The big rocks The ‘real’ opportunities Integration of Sports Science/medical research into practice in the NFL Advantages and disadvantages of working in overseas environments 2 most influential books The Power of Choice: You Can Do It - Yes, You Can! Driven: How Human Nature Shapes our Choices Driven to Lead: Good, Bad & Misguided Leadership Hugh can be found on Twitter @HughFullagar This episode of the Pacey Performance Podcast is sponsored by Vald Performance, the team behind the NordBord and the new Groinbar, a hip and groin strength measuring solution. They can be found at valdperformance.com and you can get more information on the groin bar at groinbar.com and on Twitter @groinbar. This episode is sponsored by Fatigue Science. Fatigue Science combine wearable technology with biomathematical science developed by the US Army to offer fantastic insights into sleep and cognitive fatigue. This episode is also sponsored by Forcedecks. If you want to know more about ForceDecks, listen to episode #139 of the Pacey Performance Podcast with co-founder, Dr. Daniel Cohen. Keep up to date with everything that is going on with the podcast by following on Twitter @strengthofsci or visiting strengthofscience.com. Enjoy PP
Anjana is fascinated by languages, both human and machine, and the connections between the two. She recently completed a MS in computational linguistics at Saarland University in Germany, where she studied speech technology, machine learning, and computer-assisted language learning. Her spontaneous talk "Learning Functional Programming with JavaScript" has been viewed over a half-million times on YouTube. She talks to Scott about her thoughts on languages and her strategies for learning.
Join the interview in progress featuring Ben Stock, post-doc researcher at CISPA, Saarland University as he discusses the highlights of his research regarding vulnerability notification. Ben and his colleague Christian Rossow, Professor of IT Security at CISPA, Saarland University will be presenting, “Hey, You Have a Problem: On the Feasibility of Large-Scale Web Vulnerability Notification,” on Tuesday, June 13th at 11:45-12:15.
Differential privacy aims at learning information about the population as a whole, while protecting the privacy of each individual. With its quantifiable privacy and utility guarantees, differential privacy is becoming standard in the field of privacy-preserving data analysis. On the other hand, most cryptographic systems for their privacy properties rely on a stronger notion of indistinguishability, where an adversary should not be able to (non-negligibly) distinguish between two scenarios. Nevertheless, there exists some cryptographic system scenarios for which the notion of indistinguishability is known to be impossible to achieve. It is natural to ask if one can define differential privacy-motivated privacy notions to accurately quantify the privacy loss in those scenarios. In this talk, we will study two such scenarios.Our first scenario will consider (non-)uniform randomness employed in cryptographic primitives. It is well-known that indistinguishability-based definitions of cryptographic primitives are impossible to realize in systems where parties only have access to non-extractable sources of randomness. I will demonstrate that it is, nevertheless, possible to quantify this secrecy (or privacy) loss due to some non-extractable sources (such as the Santha-Vazirani sources) using a generalization of indistinguishability inspired by differential privacy.Our second scenario will capture privacy properties of anonymous communication networks (e.g., Tor). In particular, I will present our AnoA framework that relies on a novel relaxation of differential privacy to enables a unified quantitative analysis of properties such as sender anonymity, sender unlinkability, and relationship anonymity. About the speaker: Prof. Aniket Kate is an assistant Professor in the the computer science department at Purdue university. Before joining Purdue in 2015, Prof. Kate was a junior faculty member and an independent research group leader at Saarland University in Germany, where he was heading the Cryptographic Systems Research Group. He was a postdoctoral researcher at Max Planck Institute for Software Systems (MPI-SWS), Germany for 2010 until 2012, and he received his PhD from the University of Waterloo, Canada in 2010.Prof. Kate designs, implements, and analyzes transparency and privacy enhancing technologies. His research integrates applied cryptography and distributed systems.
Over the last seven years we have been observing a tremendous growth of crypto-currencies such as Bitcoin and IOU credit networks such as Ripple. Their decentralized and pseudonymous nature, ability to perform transactions across the globe in a matter of seconds, and potential to monetize everything regardless of jurisdiction have been pivotal to their success so far. Despite some major hiccups, their market capitalization is increasing steadily over the years. It is now believed that, in the form of the blockchain technology and the internet of value, these concepts are here to stay.In this talk, I will first present some of our recent and ongoing efforts to improve the privacy of these inherently distributed systems. I will define the concept of peer-to-peer mixing, present an efficient P2P mixing protocol, and instantiate it in Bitcoin and Ripple. In the latter half of the talk, I will present an innovation application for these payment systems. In particular, I will present a novel Bitcoin-based smart contact for non-disclosure agreement (NDA) among mutually distrusting partners that monetarily penalizes malicious disclosures of the confidential documents. About the speaker: Prof. Aniket Kate is an assistant Professor in the the computer science department at Purdue university. Before joining Purdue in 2015, Prof. Kate was a junior faculty member and an independent research group leader at Saarland University in Germany, where he was heading the Cryptographic Systems Research Group. He was a postdoctoral researcher at Max Planck Institute for Software Systems (MPI-SWS), Germany for 2010 until 2012, and he received his PhD from the University of Waterloo, Canada in 2010. Prof. Kate designs, implements, and analyzes transparency and privacy enhancing technologies. His research integrates cryptography, distributed systems, and hardware-assisted security.
A credit network models trust between agents in a distributed environment and enables payments between arbitrary pairs of agents. With their flexible design and robustness against intrusion, credit networks form the basis of several Sybil-tolerant social networks, spam-resistant communication protocols, and payment systems.In the first half of the talk, we introduce the concept of credit network and its application in the currently deployed Ripple payment system. We further characterize the privacy issues in Ripple as the result of clustering heuristics to group wallets based on observations on the publicly available Ripple network graph. In the second half of the talk, we show PrivPay, the first provably secure privacy-preserving payment protocol for credit networks. The distinguishing feature of PrivPay is the computation of the maximal credit between two agents without revealing any information about the credit network, the transaction or the agents themselves. Finally, we present our results on privacy-preserving payments on a distributed credit network, where each agent locally stores its own financial information. About the speaker: Pedro Moreno-Sanchez is a PhD student in the Department of Computer Science at Purdue University. His advisor is Prof. Aniket Kate. His current research focuses on the areas of security, privacy and reliability of credit network based systems such as Ripple. Previously, he also worked on network access control in distributed scenarios such as eduroam.Before moving to Purdue University in August 2015, he started his PhD studies at Saarland University in 2013 under the supervision of Prof. Aniket Kate. Previously, he was an intern researcher at Philips Research Europe (The Netherlands) under the supervision of Dr. Oscar Garcia-Morchon and Dr. Rafael Marin-Lopez. He received his bachelors and masters from University of Murcia (Spain) in 2011 and 2013 respectively.
Making conflicting statements to others, or equivocation, is a simple yet remarkably powerful tool of malicious participants in distributed systems of all kinds. In distributed computing protocols, equivocation leads to Byzantine faults and fairness issues. In this talk, I will cover my recent work towards preventing or penalizing equivocations in decentralized Systems.In the first half of the talk, we study how the resilience of asynchronous distributed computing tasks such as Byzantine agreement and multiparty computation can be improved using an increment-only counter that implements non-equivocation, a mechanism to restrict a corrupted party from making conflicting statements to different (honest) parties. In the second half of the talk, we show how equivocation can be monetarily disincentivized by the use of crypto-currencies such as Bitcoin. To this end, we have designed completely decentralized non-equivocation (smart) contracts, which make it possible to penalize an equivocating party by the loss of its money. About the speaker: Prof. Aniket Kate is an assistant Professor in the the computer science department at Purdue university. He is an applied cryptographer and a privacy researcher. His research projects aim at bridging the large gap between cryptographic research, and systems security and privacy research.Before joining Purdue in 2015, Prof. Kate was a junior faculty member and an independent research group leader at Saarland University in Germany, where he was heading the Cryptographic Systems Research Group. He was a postdoctoral researcher at Max Planck Institute for Software Systems (MPI-SWS), Germany for 2010 until 2012, and he received his PhD from the University of Waterloo, Canada in 2010.
Research has found that prayer is good for you even on a scientific level. A study was done by German psychologists at Saarland University on the effects more »
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