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Play Episode Listen Later Jun 13, 2022 27:32

This week, please join author Christan Mueller, editorialist Christopher deFilippi, and Associate Editor Torbjørn Omland as they discuss the research article "Skeletal Muscle Disorders: A Non-cardiac Source of Cardiac Troponin T" and the editorial "Skeletal Muscle Disorders: A Non-cardiac Source of Cardiac Troponin T." Dr. Greg Hundley: Welcome, listeners, to this June 14, 2022, version of Circulation on the Run. I am Dr. Greg Hundley, associate editor and director of Poly Heart Center at VCU Health in Richmond, Virginia. This week I don't have my good friend Carolyn with me, but we will grab a cup of coffee and work through several of the articles in the issue. Dr. Greg Hundley: Well, first, I want to tell you about the feature discussion today, and we're going to interview with Christian Mueller and talk about the utility of cardiac troponin T and its association with an elevation in those individuals with skeletal muscle disorders, but, before we get to that, let's go through some of the other articles in this issue. Dr. Greg Hundley: Listeners, the first study comes to us from Professor Haidong Kan from Fudan university. These investigators conducted a time stratified, case crossover study among 1,292,000 acute coronary syndrome patients from 2,239 hospitals across 318 Chinese cities between January 1 of 2015 and September 30 of 2020 to determine the associations between sub-daily or hourly levels of criteria air pollutants with the onset of an acute coronary syndrome. Dr. Greg Hundley: Now, hourly concentrations of fine particulate matter, coarse particular matter, nitrogen dioxide, sulfur dioxide, carbon monoxide and ozone were collected, and the hourly onset data of acute coronary syndrome and its subtypes including ST segment elevation myocardial infarction, non-ST segment elevation myocardial infarction and unstable angina were obtained. Dr. Greg Hundley: Listeners, what did the investigators find? Well, their results indicated that transient exposure to the air pollutants of fine particulate matter, nitrogen dioxide, sulfur dioxide, and carbon monoxide, but not coarse particular matter or ozone may trigger the onset of acute coronary syndrome even at concentrations below the World Health Organization Air Quality Guidelines. Now, greater magnitude of associations were observed among patients that were older than 65 years in age or those without a history of smoking or chronic cardiorespiratory diseases and those in the cold seasons. Dr. Greg Hundley: Listeners, next, we're going to move from the study of air pollution to the world of preclinical science. Listeners, this study comes to us from Dr. Ming-Hui Zou from Georgia State University. Indoleamine 2,3-dioxygenase 1 or IDO1 is the rate limiting enzyme for tryptophan metabolism. IDO1 malfunction is involved in the pathogenesis of atherosclerosis, and vascular smooth muscle cells with an osteogenic phenotype promote calcification and features of plaque instability, but it remains unclear whether aberrant IDO1-regulated tryptophan metabolism causes vascular smooth muscle cell osteogenic reprogramming and arterial calcification. Dr. Greg Hundley: Listeners, what did this study find? Well, this investigative team and their results revealed the previously unrecognized protective role of IDO1 in arterial calcification in that vascular smooth muscle cells defective of IDO1 result in enhanced runt-related transcription factor 2 and ectopic calcium deposition in plaques. In contrast, administration of kynurenine via intraperitoneal injection markedly delayed the progression of intimal calcification in parallel with decreased RUNX2 expression. Dr. Greg Hundley: Also, listeners, the authors found that patients with coronary artery calcification have abnormal tryptophan metabolism, and serum IDO1 activity was inversely associated with calcification development in clinical settings, so, listeners, what are the clinical implications here? Well, this work reveals a protective role for IDO1 in mitigating arterial intimal calcification through kynurenine production and then, secondly, developing interventions toward the IDO1 kynurenine RUNX2 access may prevent the pathogenesis of arteriosclerotic complications. Dr. Greg Hundley: Well, listeners, a really interesting article, and now let's turn our attention to some of the other articles in the issue. Well, first, there's a Research Letter from Professor Modarai entitled “A Higher Incidence of Chromosomal Aberrations in Operators Performing a Large Volume of Endovascular Procedures,” and then, also, there is an AHA Update from our exiting AHA president who addresses “What Does the American Heart Association Do (and How Can You Help)?” Well, now, listeners, let's turn now to our feature related to a discussion of the utility of troponin T as well as troponin I in those with skeletal muscle disorders that may also present with acute coronary syndromes. Dr. Greg Hundley: Welcome, listeners, to this June 14 issue, and we're very excited today. We have with us Dr. Christian Mueller from the University Heart Center at Basel, Switzerland, Dr. Torbjorn Omland from the University of Oslo in Oslo, Norway, and Dr. Chris deFilippi from Inova Heart and Vascular Institute in Falls Church, Virginia. Dr. Greg Hundley: Welcome, gentlemen, and, Christian, we'll start with you. Could you describe for us some of the background information that went into your study, and what was the hypothesis that you wanted to address? Dr. Christian Mueller: Thank you very much for giving me the opportunity in this podcast to discuss our study with you and together with Torbjorn and Chris, who both contributed so enormously to the field with their own research. It's about cardiac troponin, cardiac troponin, an essential pillar in our early diagnosis of myocardial infarction. In this specific study, we tried to address possible non-cardiac causes of cardiac troponin T. In our clinical practice, we use and guidelines recommend both cardiac troponin T and I more or less as equivalent in providing identical information and, when going back from the clinical practice to biology, we have learned that, the troponin complex, that it is composed of three isoforms, T, I, and C. Dr. Christian Mueller: While they are very similar in their function, they are distinct regarding amino acid sequence in configuration in cardiac and skeletal muscle. As the cardiac form, of course, is the one that we are interested in, cardiac-specific assays have been developed both for cardiac troponin T and cardiac troponin I. As with any other tests in medicine, they are very good, but they may have limitations, and the specific questions that we had set for this study is whether skeletal muscle disease might be non-cardiac source for cardiac troponin T as measured in blood, therefore, with the possible harm of having false positive increases that could lead to a misdiagnosis of acute myocardial infarction. Dr. Greg Hundley: Very nice. We're trying to understand the utility of cardiac troponin T measures in those individuals that may have concomitant skeletal muscle disorders. Christian, what was your study population, and describe for us your study design? Dr. Christian Mueller: Our study had two components, a clinical component and a translational component. The clinical component included 211 consecutive patients that presented with active and chronic muscle symptoms to a workup either with a rheumatologist or a neurologist or internal medicine specialist, so more or less elective workup for muscle, skeletal muscle symptoms, to have a population that is broad and reflects all possible skeletal muscle disorders, their possible impact on cardiac troponin T concentration. Dr. Christian Mueller: In this population, we quantified cardiac involvement as this is common in some of these musculoskeletal disorders to be either major, minor or are not. They're according to patient history, according to … ECG and cardiac imaging, and we did the measurement of high sensitivity cardiac troponin using the high sensitivity cardiac troponin T assays used all over the world and three high sensitivity cardiac troponin I assays to look for mismatches, the percentage of patients that might have elevated T concentration, but not I as a possible sign that the T might be from the muscle, not the heart, particularly in those patients that didn't have any imaging evidence of cardiac involvement, and then we correlated the amount of high sensitivity cardiac troponin T with the amount of muscle injury as quantified by CK. Dr. Christian Mueller: In the translational part, those patients who have received a skeletal muscle biopsy with quantified by differential gene expression, the MRNA of the cardiac isoform of cardiac troponin T as well as of I in those patients who had the biopsy and matched it and compared it to controls to see whether the cardiac isoform would be upregulated in those with the cases of skeletal muscle disease. Dr. Greg Hundley: Very nice, and so, Christian, was this one single measurement at one point in time or did you have a series of measures over time? Dr. Christian Mueller: In fact, this is a large, ongoing project where patients will receive followup appointments. The current study reports the first phase versus single measurement at a single time point was performed. Dr. Greg Hundley: Very good. Christian, what did you find? Dr. Christian Mueller: We first found that even in those patients with active skeletal muscle disease, cardiac troponin T still reflected the presence of cardiac disease. Those patients with severe cardiac disease did have significantly higher concentration than those patients with mild or with no cardiac disease. That was the good thing. However, the more challenging one for this biomarker in this setting is that high sensitivity cardiac troponin T was significantly higher in these patients as compared to controls. We had the chance to have a couple of thousand controls from another study that presented with non-cardiac chest and no skeletal muscle disease and, while high sensitivity troponin I concentrations were similar, cardiac troponin T was elevated, resulting in a much higher prevalence of elevated T concentration versus elevated I concentration and corresponding mismatches in these patients. Dr. Christian Mueller: In the second part, we were able to show that there was a significant correlation between high sensitively cardiac troponin T with CK quantifying somehow muscle damage while this was not seen in the correlation with high sensitivity I, and that signaled that some of the systemic cardiac troponin T concentration seems to be derived from the muscle. It was confirmed in the translational part of the study in which the differential gene expression showed an eightfold over-expression of cardiac troponin T in skeletal muscle biopsies of those patients with disease, so with active skeletal muscle disease. This … expression correlated with disease activity, a pathological score that quantifies the extent of damage in the skeletal muscle history and correlated with the high sensitivity cardiac troponin T plasma concentration measured with the immunoassay. Dr. Greg Hundley: Very nice. Listeners, it sounds as if, in patients with skeletal muscle disorders, Christian's team observed an elevation in cardiac troponin T, but not necessarily cardiac troponin I, and you've got mechanistic understanding from the biopsies where you see this cardiac troponin T expression in the damaged skeletal muscles. Well, Torbjorn, you have many papers come across your desk. What attracted you to this particular paper? Torbjorn Omland: Thank you, Greg. I think, in general, when I receive papers from circulation, there are three main criteria I consider. The first is whether this is an interesting research question and then, second, whether the study is well-designed and the third is whether they're in themselves are novel, robust and interesting with potential clinical implications. Torbjorn Omland: For this specific papers, I must say it seemed to me to fulfill all these criteria and that it would be able to bring this field forward. The study of re-expression of troponin T in skeletal muscle is not entirely novel because it has been done in small samples, but mainly with rare and neuromuscular diseases previously, but this study broadened that or generalized that to a much more clinically relevant population. The clinical implications also seemed to be much greater than what has been reported by previous papers. Dr. Greg Hundley: Very nice. Listeners, we have in addition to Dr. Omland, we have another expert with us today, Dr. Chris deFilippi, really in the area of biomarkers particularly as they pertain to cardiac injury. Dr. Greg Hundley: Chris, now turning to you, how do we put the context of the results today really with the broader scope of what we have learned about cardiac troponin I and cardiac troponin T and then their use in diagnosing acute ischemic syndromes or even forecasting future cardiovascular events down the road? Dr. Christopher deFilippi: Thank you, Greg, and thank you Circulation for inviting me to participate in this podcast and to write this editorial. First, Christian, this was a terrific paper and one that was probably great to review during the pandemic because, as I spent a good Sunday peeling back layers of the onion and reiterating what Torbjorn said, this paper makes a tremendous contribution where there already was some knowledge to maybe the expression of the cardiac specific troponin T and skeletal muscle, but there's something there for everyone just to get the takeaway message, but for those who really want to delve in, there are supplemental tables that contribute a huge amount of nuance and detail that I think will help guide researchers in the future in maybe how to optimally use cardiac troponin T and troponin I both in the evaluation for acute myocardial infarction and then in a variety of chronic conditions, so first putting this in context of how you would evaluate patients with acute myocardial infarction, and that's the predominant indication for measuring a high sensitivity troponin T or troponin I. Dr. Christopher deFilippi: As Christian in an earlier study has shown and others have shown, actually, the correlation between a high sensitive troponin I by a variety of commercial assays. Troponin T is really pretty good. I think in one study from Christian's group, it was measured at 0.89. Now, the issue that's relevant is more around the edges. People who come in with just a low elevation and, as Christian pointed out and colleagues pointed out in the paper, using the ESC algorithm, a number of those patients would have qualified for myocardial infarction with the skeletal myopathies particularly the myositis or the non-inflammatory myopathy. If there is an index of suspicion for these disorders I think particularly around the cutoff for troponin T, one has to be cautious. Whether one can actually look at serial changes and try to differentiate that way I think is an open question. It may be. Dr. Christopher deFilippi: I think the other thing that gets quite interesting for me in an area that we've delved in over the past decade is the use of high sensitive troponin T or troponin I as a measure of chronic injury that's been codified in the fourth universal definition of MI published four years ago to identify individuals at risk. These can be individuals who are living in the community without known cardiovascular disease or actually without, perhaps, a lot of other comorbidities other than advanced age, for example, who an elevated troponin I or troponin I can be indicative of an increased risk for incident heart failure over the next five to 10 years. It can be patients with other chronic comorbidities. Dr. Christopher deFilippi: Actually, what drew me to this paper and thinking along these lines was a paper that Torbjorn had published back in 2013 where, using the key study which are individuals who have chronic ischemic heart disease without heart failure, he measured both troponin I and troponin T and found there was quite a discordance. There, we're looking at … value of about 0.4 and found that troponin I was a great predictor for the risk of coronary heart disease event and an acute myocardial infarction in the future, but T was not, but both T and I were good predictors of incident heart failure in the future. Dr. Christopher deFilippi: Other investigators, the … investigators, investigators from Scotland have also found this discordance between I and T in chronic ambulatory populations with or without comorbidities, and so it opens an interesting question in individuals with maybe conditions of pre-frailty or frailty or some element of sarcopenia, subclinical skeletal muscle disease. Does this cause this discordance? Ultimately, we know particularly with heart failure, with preserved ejection fraction, it is a systemic disorder, and measures of skeletal muscle disease may be relevant in ultimately determining who's going to have symptomatic heart failure. Dr. Christopher deFilippi: I think it really opens things wide open potentially to further investigation. Is this modifiable? Is it through intervention simply like physical activity? Could you see changes in cardiac troponin T that may be reflecting cardiovascular changes and skeletal muscle changes, but maybe not so much with I, and does this have relevant prognostic implications? I think I was really excited about it based on the defined pragmatic findings with respect to evaluating patients for myocardial infarction who have these underlying skeletal muscle diseases, but also implications, what this might mean in chronic disease populations as well. Dr. Greg Hundley: Very nice. Well, Chris, you've led us really to our next series of questions, and maybe we'll circle back with each of you, first, Christian. What do you see, Christian, as the next study to be performed in this space? Dr. Christian Mueller: I think the next study should address two aspects. The first one is I think we already, with the current population have found that skeletal muscle disease includes various pathologies, and as indicated by Torbjorn, the cardiac troponin T re-expression seems to be at least of our current understanding limited to the two groups of myositis and the muscular dystrophies, whereas the other skeletal muscular disorders at least in those that we have currently investigated did not seem affected. However, we were limited by the number of patients in this subgroup, and so for sure need a larger population to cover all aspects or all classifications of skeletal muscle disease in more detail. Dr. Christian Mueller: The second point that I'd like to highlight is the followup and to look for cardiac events and to look for cardiac changes, functional or anatomical changes in cardiac imaging, because it still may be that some of the T that is more commonly seen in this patient, that the majority of this is derived from the heart, so it's not a black and white, it's only from the muscle or only from the heart. It's still possible that some of the higher concentration of T found in these patients, as in many of the skeletal muscle systemic disorders, they have cardiac involvement which may not be identifiable by current imaging techniques at the first visit. This may become apparent during followup, and so these studies will help us to get a better quantitative understanding, so ideally to understand is it just a tiny amount, I don't know, 10, 20% of the systemic T concentration that is derived from the muscle? Then it would have a very different clinical implication as compared to if, I don't know, more than 50% of the systemic concentration would be derived from the skeletal muscle rather than the heart. Dr. Greg Hundley: Very nice. Torbjorn, I would like to turn to you. What do you see as the next study to be performed in this space? Torbjorn Omland: Oh, I agree with Christian that the serial assessment of changes of disease activity versus troponin changes would be very interesting to study in more detail and also correlate that to changes, for instance, by cardiac MRI if you can see whether there are actually correlations there. Long-term prognostic implications of skeletal muscle derived cardio troponin is another subject, and then, finally, I think that we do need to know even more accurately what is the impact of these alterations on the diagnostic workup in the acute coronary syndrome setting. Is it really a clinically important confounder? I think studies that could address that will be important. Dr. Greg Hundley: Very nice, and then finally Chris, and, Chris, I want to add just another question. Just from my listening to this, if I'm trying to identify someone with an acute ischemic syndrome and then they may also have an underlying skeletal muscle disorder, both Christian was talking about inflammation, but you brought in frailty and things of that nature. Should we really then turn clinically to measuring cardiac troponin I in this setting when we're trying to rule out, for example, acute myocardial infarction? Dr. Christopher deFilippi: Yeah. I don't want to overstate that. I mean, Christian's work and others have shown actually a high sensitive troponin T and a variety of different high sensitive troponin Is in a very heterogeneous chest pain population have been equivalent, looking at receiver operator curves area under the curbs, and so they're probably our people at the margins where this will make a difference, but it should be. Listeners should be reassured at this point because troponin T is a very common assay that it's still quite efficacious and accurate for the diagnosis of acute myocardial infarction from what we know, and a lot of Christian's work has identified this. Dr. Christopher deFilippi: Again, moving into the more chronic disease population outside the evaluation of acute myocardial infarction, maybe where we can use it as a differentiator, it could be helpful in some instances to look at interventions. Earlier work has shown in just small numbers of patients have been published, but patients with hypothyroidism, patients with statin-induced skeletal myopathies, the treatment of these has actually led to a decrease in high sensitive troponin I corresponding with decreases in CK, so there may be opportunities for lifestyle interventions like physical activity, and you could see that response and whether that has prognostic implications. This could be of interest for future research. Dr. Greg Hundley: Very nice. Well, listeners, what an incredible discussion today. We want to thank Dr. Christian Mueller from University Heart Center in Basel, Switzerland, Dr. Torbjorn Omland from the University of Oslo in Oslo, Norway, and also Dr. Chris deFilippi from the Inova Heart and Vascular Institute in Falls Church, Virginia, for really helping us understand that in patients... from this research, that in patients with active chronic skeletal muscle disorders, elevations in cardiac troponin T are common and may not be related to cardiac disease. These elevations were not observed in those with assessment of cardiac troponin I and, coming back to in the case of cardiac troponin T based on this wonderful biopsy work, the elevations of the troponin T appear related to re-expression of troponin T and skeletal muscle. Dr. Greg Hundley: Well, listeners, on behalf of Carolyn and myself, we want to wish you a great week, and we will catch you next week on the run. Dr. Greg Hundley: 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, please visit aha journals.org.

Patch Notes 3.5 - Intersectional Torbjorn

No Cartridge Audio

Play Episode Listen Later Jun 3, 2022 56:28 Very Popular

Trev and Jon are here again with The News of the Day (The Day meaning Late May).Support this podcast at — https://redcircle.com/no-cartridge-audio/donationsAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy

Digital transformation of developing countries

The Standards Show

Play Episode Listen Later Apr 19, 2022 39:55

In this episode Matthew and Cindy look at how standards support the digital transformation of developing countries.Cindy speaks to Torbjörn Fredriksson of the UN Conference on Trade and Development (UNCTAD) and Nick Williams of the African Development Bank (AfDB). Torbjorn and Nick share the story about a new partnership between BSI, UNCTAD and AfDB forged through the eTrade for all initiative. The initiative is focused on leveraging the value of international standards to address the barriers to digital transformation. They also discuss a new standards-based digitalization toolkit - a key recommendation of a recent BSI Whitepaper on digital transformation - and UNCTAD's upcoming ecommerce week. unctad.org/eweek2022In this episode there's also news of a new series – Standards in 10 Minutes.@standardsshow@thestandardsshow education@bsigroup.com

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Episode 266: Versatilist with Torbjorn Netland

The Versatilist

Play Episode Listen Later Feb 7, 2022 31:55

In this episode of the Versatilist, I speak with Torbjorn Netland about his work "Teaching in Virtual Reality: Experiences from a Lean Masterclass." For more information about Torbjorn's work, check out www.factoryvr.ch, including all their papers on the subject and the YouTube video they made for Reimagine Education https://youtu.be/3mUghoxnWLU.

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Go Dj | Episode 90 | The No Structure Podcast

No Structure Podcast

Play Episode Listen Later Oct 25, 2021 74:27

You are now tuned into Episode 90 of the No Structure Podcast titled “Go DJ” with a guest appearance from our engineer Torbjorn. Tor joins us to talk music creation, going on tour, edm vs hip hop crowds, going on tour and MORE. Don't forget to subscribe/rate/review/share … thanks for tuning in.

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The Geologic Podcast Episode #732

Geologic Podcast

Play Episode Listen Later Sep 24, 2021 48:05

The Show Notes Movies vs. Novels and “Once Upon a Time In Hollywood”IntroFantastic FungiRupert McClannahan's Indestructible Bastard - Angela HernandezReligious Moron of the Week - Hossam Metwally from Steve HarrisLewd Sounding Cities in Every State: Part IAsk George - Genesis? from Torbjorn in NorwayMinoishe Interroberg's To Make With The Good English - Pair of Pants?Damian Handzy's Facts That'll Fuck Y'up - Quickfire EditionSeven Songs: Ep. 30, Friday 9/24: ANIMALS Show close Mentioned in the Show VODACAST ................................... SUBSCRIBE! You can sign up at the Geologic Podcast page or at Subscriber.GeorgeHrab.com where you can learn more about the perks of being a Geologist or a Geographer. If you've already subscribed, stop by Subscriber.GeorgeHrab.com to check out the archived content which we at the Geologic Universe are rolling out in phases. As always, thank you so much for your support! You make the ship go. ................................... Sign up for the mailing list: Write to Geo! A reminder that the portal to the Geologic Universe is at GeorgeHrab.com. Thanks to Joseph Kolasinski, our webmaster. Check out Geo's wiki page thanks to Tim Farley. Have a comment on the show, a Religious Moron tip, or a question for Ask George? Drop George a line and write to Geo's Mom, too!

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[Torbjorn on Singing on Your Own Beats]

The Human Music Podcast

Play Episode Listen Later May 11, 2021 72:06

Ep. 055 - [Torbjorn on Singing on Your Own Beats] This week we interview Producer, DJ and vocalist Torbjorn. He hails from the Northwest of the US and has extensive experience as both a musician and a music educator. Catch him every Monday night on his Twitch live stream “Bass of the Mondays.” We dive into the history of Dubstep, transitioning from band life to producer life, his favorite sound design and EQ techniques, singing on his own beats and his latest tune “Tell Me” and the remix EP that just dropped for it (links below!). Sponsors: The Weekly Download: Learn from ill.Gates in his private weekly group lessons and get access to over 220 more episodes in the archive for only $20 per month! https://www.thehumanmusicpodcast.com/producerdojo Guest Practices: Learn from Seth Drake at the Approach Institute, the BEST engineer we know. First class is free! https://www.thehumanmusicpodcast.com/theapproach Gvngaroo Records Music Distribution: Unlimited Uploads for Under $10 https://www.thehumanmusicpodcast.com/gvngaroo-records Follow Torbjorn: https://www.beatsbytor.com/ https://www.instagram.com/beatsbytor https://twitter.com/beatsbytor https://www.facebook.com/BeatsByTor/ Stream Torbjorn: https://www.twitch.tv/beatsbytor https://soundcloud.com/beatsbytor https://audius.co/beatsbytor https://open.spotify.com/artist/32CiCEHhLH5VsWrn70chVA?si=fL2Z-H3sQJ6NvO3V8qNQeA ‘Tell Me' Song & Remix EP Song: https://open.spotify.com/track/0CIv3wgnb7kuIb2OfsQEwM?si=fb1c87c675c34a2b Remix EP: https://hypeddit.com/link/i52vu8

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A Chat with Torbjorn Zetterlund: Cloud Strategy and Digital Innovation at Greenpeace

The Inquisitive Analyst

Play Episode Listen Later Apr 29, 2021 20:33

T.I.A (Ep 29). Torbjorn Zetterlund talks about being a Digital Innovation Manager at Greenpeace. He also brings to light crucial elements necessary for project success; how PMs can be efficient and effective; how PMs can optimize cloud strategies and services; and a bit about business delivery process. YouTube: https://www.youtube.com/watch?v=2I6tGudQPA4 Torbjorn Zetterlund: LinkedIn: https://www.linkedin.com/in/torbjornz/ Sponsored by The Lewis Institute: Website - https://lewisinstituteinc.com/; Project Leader Courses (60% discount) - https://lewisinstitute.kartra.com/page/Wif255 Business Agility Institute: Emergence Journal - https://businessagility.institute/emergence; promo code "analyst" (for 10% discount on annual subscription)

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Circulation December 1, 2020 Issue

Bleav in Overwatch League

Play Episode Listen Later Nov 30, 2020 25:06

This week's episode features author Torbjørn Omland and Senior Guest Editor Vera Bittner as they discuss the artile "Growth Differentiation Factor-15 Provides Prognostic Information Superior to Established Cardiovascular and Inflammatory Biomarkers in Unselected Patients Hospitalized with COVID-19." TRANSCRIPT BELOW: Dr. Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary, and backstage pass to the journal and its editors. We are your co-hosts, I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: I'm Dr. Greg Hundley, Director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Well, Carolyn our feature this week gets into inflammatory biomarkers in patients that have been hospitalized with COVID-19, but before we get to that, how about we grab a cup of coffee and work through some of the papers in the issue. Would you like to go first? Dr. Carolyn Lam: Absolutely. With both the coffee and the papers. So great, for this first paper, have you thought about concentric versus eccentric cardiac hypertrophy? We traditionally associate them with pressure versus volume overload respectively in cardiovascular disease, both though conferring an increased risk of heart failure. These contrasting forms of hypertrophy are characterized by asymmetric growth of the cardiac myocytes in mainly width or length respectively. However, the molecular mechanisms determining myocyte preferential growth in width versus length remain poorly understood. Dr. Carolyn Lam: That is until today's paper, and it is from Dr. Kapiloff from Stanford University, and Dr. Rosenfeld from UCSD, School of Medicine and their colleagues, and what they did was used primary adult rat ventricular myocytes, as well as Adeno associated virus mediated gene delivery in mice, to define a regulatory pathway controlling pathological myocyte hypertrophy, and they found that asymmetric cardiac myocyte hypertrophy is modulated by serum response factor phosphorylation, constituting an epigenomic switch balancing the growth in width versus length of adult ventricular myocytes In vitro, and In vivo. Dr. Carolyn Lam: Serum response factor phosphorylation was bi-directionally regulated at signalosomes organized by the scaffold protein muscle, A kinase anchoring protein beta. This newly identified molecular switch controlled a transcriptional program responsible for modulating changes in cardiomyocyte morphology that occurs secondary to pathological stressors. Dr. Greg Hundley: Very nice, Carolyn. So switches controlling this transcriptional program. Tell us a little bit, and bring us back to the clinical relevance of this and starting with that concentric versus eccentric hypertrophy? Dr. Carolyn Lam: I thought you may ask. The identification of a molecular mechanism regulating that asymmetric cardiomyocyte growth, really provides a new target for the inhibition of pathological cardiac hypertrophy. Studies in mice using these Adeno associated virus based gene therapies to modulate that signalosome, really provided proof of concept for translational potential in the treatment of pathological cardiac remodeling and prevention of heart failure. Dr. Greg Hundley: Oh, wow. Very nice, Carolyn. Well, my first paper comes to us from Professor Dirk Westermann from Hamburg, and focuses on cardiogenic shock patients, and veno-arterial ECMO, the results from the international multicenter cohort study. So Carolyn this study evaluated data from 686 consecutive patients with cardiogenic shock treated with VA ECMO with or without left ventricular unloading using an Impella, and they conducted this at 16 tertiary care centers across four countries. They examined the association between left ventricular unloading and 30 day mortality. Dr. Carolyn Lam: Huh, so what did they find? Dr. Greg Hundley: Okay. Carolyn. Well, left ventricular unloading was used in 337 of the 686 patients enrolled, and after propensity matching 255 patients with left ventricular unloading were compared with the 255 patients without left ventricular unloading. In the match cohort, left ventricular unloading was associated with lower 30 day mortality without differences in the various subgroups. However, complications occurred more frequently in patients with left ventricular unloading, like severe bleeding, which happened in 38.4% versus only 17.9% in those without unloading. There was also access-related ischemia and renal replacement therapy. Dr. Greg Hundley: So Carolyn, the take-home message from this International multi-center cohort study, is that left ventricular unloading is associated with lower mortality, and cardiogenic shock patients treated with VA ECMO, despite higher complication rates. In the absence of randomized trial data these findings support the use of left ventricular unloading and cardiogenic shock patients treated with VA ECMO, and call for further validation, ideally in a randomized controlled trial. Dr. Carolyn Lam: Very nice. Well for my next paper, Greg, it's all about desmin. Now we know that mutations in the human desmin gene caused myopathies and cardiomyopathies. Well, today's authors, Dr. Hermann and Schroeder from University Hospital Erlangen in Germany and Dr. Lilienbaum from University of Paris and France and their colleagues, report an adolescent patient who underwent cardiac transplantation, due to restrictive cardiomyopathy caused by a heterozygous R406W desmin mutation. Sections of the explanted heart were analyzed with antibodies specific to 406W-desmin, and to intercalated disc proteins. Effects of this mutation on the molecular properties of desmin were then addressed by cell transfection and In vitro assembly experiments. They further generated these desmin mutation knock-in mice haboring the orthologous form of the human, R406W-desmin. Dr. Greg Hundley: So Carolyn, what did they find? Dr. Carolyn Lam: Well, they demonstrated a novel pathomechanism in which cardiotoxic R406W-desmin, could adapt dual functional status with the abilities to integrate into the indogenous intermediate filament network, and to cause formation a protein aggregates. This R406W-desmin modified the extra sarcomeric cytoskeleton, such that desmin filaments were not anchored to desmosomes anymore. Thereby destroying the structural, and functional integrity of intercalated discs. Dr. Greg Hundley: What are the clinical implications? Dr. Carolyn Lam: Well, since these cardiotoxic desmin mutations could affect the integrity of intercalated discs, thereby inducing conduction defects and malignant arrhythmias, they suggest early implantation of pacemaker, or cardioverter defibrillator devices, may be considered to prevent certain cardiac death in patients with these mutations. Furthermore, state-of-the-art basic molecular risk stratification of desmin mutations may encompass a multidisciplinary experimental approach as exemplified by the approach taken here, which comprises assessment of the tissue pathology in conjunction with genome analysis and desmin assembly studies as well as patient mimicking cell and animal models for the In vivo validation of these mutations. Dr. Greg Hundley: Well, fantastic, Carolyn. Well, my next paper comes to us from Dr. Ravi Shah from the Massachusetts General Hospital. This study evaluated 2,330 white and black young adults, average age of 32 years, in the Coronary Artery Risk Development in Young Adults, or the cardiac study, to identify metabolite profiles associated with an adverse cardiovascular disease phenom that included, myocardial structure and function, fitness, vascular calcification, and then also mechanisms, and other cardiovascular outcomes that would occur over the next two decades. Statistical learning methods, including elastic nets and principal component analysis, and Cox regression generated parsimonious metabolite based risk scores, validated in over 1800 individuals in the Framingham Heart Study. Dr. Carolyn Lam: Wow. What did they show, Greg? Wow, that's a lot of work. Dr. Greg Hundley: Yeah. So Carolyn, the authors found two multiparametric metabolite-based scores linked independently to vascular, and myocardial health. With metabolites included in each score specifying microbial metabolism, hepatic steatosis, oxidative stress, nitric oxide modulation, and finally collagen metabolism. Over nearly 25 year median follow-up, and cardia, this metabolite based vascular score, and the myocardial score, and the third and fourth decade of life were associated with clinical cardiovascular disease. Importantly, the authors replicated these findings in 1,898 individuals in the Framingham Heart Study followed over two decades, such that young adults with poor metabolite based health scores had higher hazard ratios of future cardiovascular disease related events. Dr. Carolyn Lam: Oh wow. Greg, what an elegant study with both development and validation cohort evaluating the metabolome. Dr. Greg Hundley: Yes. Carolyn. So metabolic signatures of myocardial, and vascular health in young adulthood specify known novel pathways of metabolic dysfunction, relevant to cardiovascular disease associated with outcomes in two independent cohorts. So these data suggests that efforts to include precision measures of metabolic health in risk stratification to interrupt cardiovascular disease at an early at stage, are warranted. Dr. Carolyn Lam: Wow. So interesting. Other very interesting articles in today's issue, there's an In Depth article by Dr. Angiolillo entitled, “The Antithrombotic Therapy for Atherosclerotic Cardiovascular Disease Risk Mitigation in Patients with Coronary Artery Disease and Diabetes.” There's also Research Letters, one by Dr. Sultan on, “The Longterm Outcomes of Primary Cardiac Lymphoma” and one by Dr. Wang on, “Loss of Phosphatase and Tensin Homolog Promotes Cardiomyocyte Proliferation and Cardiac Repair Following Myocardial Infarction.” Dr. Greg Hundley: Great, Carolyn. Well, I've got a couple other articles in this issue as well. One is by Professor Ganesan Karthikeyan who has an On My Mind piece entitled an “Alternative Hypothesis to explain Disease Progression in Rheumatic Heart Disease.” Dr. Stuart Chen has an ECG challenge entitled, “Alternating QRS Duration and a Normal T-waves. What is the mechanism?” Then finally, Carolyn, a series of Letters to the Editor, one by Dr. Peterzan and the other by Dr. Mehmood regarding the prior published article, entitled “Cardiac Energetics in Patients with Aortic Stenosis and Preserved Ejection Fraction.” Well, Carolyn, how about we get onto that feature article and learn more about inflammatory biomarkers in hospitalized patients with COVID-19? Dr. Carolyn Lam: Yes. Let's go. Greg. Biomarkers are really playing an increasingly important role in cardiovascular disease, and even in the current COVID 19 pandemic, there's been a lot of news about how biomarkers such as traponin may be prognostic, and in fact, we're all wondering about maybe even newer biomarkers. In fact, today's feature discussion does bring to light one of the newest, and in fact, this is the first publication on the role of Growth Differentiation Factor 15 or GDF-15 in COVID-19. We're so pleased to be discussing this with the corresponding author, Dr. Torbjørn Omland from University of Oslo, in Norway, as well as our senior guest editor, Dr. Vera Bittner from University of Alabama at Birmingham. So welcome both. Tobjorn, could you tell us a little bit about GDF-15 and what made you look at it, and what did you find? Dr. Torbjørn Omland: Yeah, so GDF-15, that's a very interesting biomarker. It's considered a biomarker of biological aging cellular stress, and perhaps also the inflammation, and tests being studied within the cardiovascular field for some years now, and it has been shown to be a strong prognostic indicator across the cardiovascular spectrum, actually. So it is a new biomarker in one sense, but there are some data already in the cardiovascular field. Dr. Carolyn Lam: Not in COVID. So this is the first study to really look at its prognostic value in COVID 19. So congratulations Torbjorn, and if I may also to the first author, Dr. Peter Meer, a good friend as well, but please, could you tell us about your study and what you found? Dr. Torbjørn Omland: Yes. So when the COVID pandemic hit Norway in the spring, we thought that we should plan a prospective biomarker study. So we had to really fast track approval by the IRB and so forth, and we're able to actually cover most of the patients that were hospitalized in our hospital, Akershus University hospital, which is right outside of Oslo, and it's a pretty large hospital by Norwegian standards. It covers about 11% of the Norwegian population. Dr. Torbjørn Omland: So in that period, when we were including, we had 136 patients hospitalized with confirmed COVID 19, and we have biobank bank samples from 123 of these, and then there have been reports from retrospective studies, first from China, that seemed to suggest that markers like cardiac troponin, Anti-Troponin T, and Ferritin were associated with outcome, but those studies were prone to selection bias in that the measurements were performed in the most sick patients. So in this study we included all patients and then we thought we should examine a broad panel of biomarkers, and that included Interleukin 6, CRP, Procalcitonin, Ferritin, and the D-dimer Cardiac troponin, and N-terminal pro B, and GDF-15. Dr. Carolyn Lam: Wow. Thank you, Torbjorn. Even before you carry on with the results, can I just say having visited your hospital in pre-COVID days, I can only imagine what a work of love this was to do it prospectively. Any particular experiences to talk about, to get a fast-track even in the midst of to perform a well done prospective study, that must have taken a lot. Dr. Torbjørn Omland: Yes. But it's also interesting in that the whole sort of ablation on Norway was very much into this from the highest political level. Also, the decision that the older research on COVID should be prepared to retire, then the IRB had an eight hour and deadline for them to approve or not approve the study. So that's went surprisingly smoothly, I must say. Dr. Carolyn Lam: Wow, that's great. So what did you find? Dr. Torbjørn Omland: Yeah, so we found that among these biomarkers, several seem to predict outcome, and the primary end point of this study was to combined end-point of the hospitalization in the ICU, or death. We found that also markers like cardio traponin, BNP, ferritin, and the D-dimer and so forth, in univariable analysis, were very associated with outcome, but when we perform a more comprehensive, mostly variable modeling, then the prognostic value of some of these markers disappeared. In contrast, for GDF-15, it seemed to perform very strongly, both on the baseline sample, and interestingly also it increased in those reaching the primary end-point during the hospitalization. So it provided a very strong and independent information also when we adjusted for clinical risk scores, like the NEWS score. So that was a very pleasant surprise to see that there was one marker that's actually performed so well. The other marker that's also performed well was Ferritin. Dr. Carolyn Lam: Very interesting, and so the new score being the National Early Warning Score. Thank you. Verra, I really love to bring in your thoughts. I mean, could you take us behind the scenes with the editors? What did you think when you saw this paper? Dr. Vera Bittner: As you know, I mean, a lot of journals have been inundated by COVID papers, and so this one stuck out to us, because it's the first time that we had seen that anybody linked GDF-15 to a COVID population, even though it has been out in the literature for ACS, and in my prognostication, and in a healthy populations, and in chronic coronary disease populations, heart failure, and so on. So this is the first time that we've seen it applied there. Dr. Vera Bittner: Then I would echo some of the things that Torbjorn said, that we were also impressed, that it was prospective, because when you look at some of the other biomarker studies, what was prognostic in one with then not shake out the other one, because either different variables were included in the models, because the population's differed. So to have something that was representative of the population that was actually admitted to this, Norwegian Academic Hospital, stood out to us. So we're excited to get this paper basically for circulation, and hope that it also will be impetus for future research. Dr. Carolyn Lam: Thank you so much for sharing that end for helping us publish such a beautiful paper. Did you have some questions for two of your own? Dr. Vera Bittner: Yeah. So what stuck out to me is that you had this a whole crew of biomarkers, and then when you looked ultimately at the final model, there were two that were standing out, that was ferritin, and it was the GDF-15, and then when I looked at your graph, it looks like not only did these biomarkers measure different contrasts, but their time-course also seemed to be different, and so I was just wondering whether you had thought about, maybe using these to joint the model outcome, and whether we might even be able to get more information that way. Dr. Torbjørn Omland: I think that's an excellent suggestion, and as you correctly pointed out, they do have different sort of profiles and ferritin being an acute phase reactant, having various sort of dramatic early rise whereas we see that GDF-15 increased progressively during the course of hospitalization in the most severe patients. I think when combining them, is actually a great IMT that we should look further into. Dr. Carolyn Lam: Very nice. Torbjorn, if I could, I've got a couple of questions too. So 123 patients, 35 of whom had the primary outcome, right? So that may be sort of seen as, is this too small? and they're all hospitalized patients. So could I ask, what do you predict maybe seen in a larger population or outside of Norway or in a non-hospitalized population? Dr. Torbjørn Omland: So as you say, we were early with this report, but since it was submitted, there has been a couple of smaller studies that seemed to confirm our results. So that is reassuring, but of course we would like to have studied this in logical patients. We are in touch with the other biobank samples that could possibly confirm the data. So that's one obvious step. Then it's very interesting, as you say, could we sort of expand this to also apply to non-hospitalized patients? I think that it would be a very interesting hypothesis to test, and I think there's still a pretty good rationale for this. Dr. Torbjørn Omland: It's interesting that the insoluble group actually showed a correlation that when the soluble ST2 concentrations and GDF-15. So there might be that those with more susceptibility to COVID infections, actually, I thought that, that is actually reflected by GDF-15 concentrations, but the challenge is how to sort of get a representative non-hospitalized population, but interestingly, I was approached by some of the hospital staff that actually are in contact with general practitioners, and wanted sort of implement this test also for this group. Dr. Carolyn Lam: So Verra, we're really grateful that Allan Jaffe was working with you in managing this beautiful paper, and if you don't mind me cheekily paraphrasing that you said you might channel him, if you could, what would the channeled Allan Jaffe perhaps say about what's needed in this whole biomarkers fear in COVID-19? Dr. Vera Bittner: Hopefully, many. A channeling element is obviously difficult, because he is such an incredible expert on biomarkers that I can't even pretend to be able to see, that you might be thinking, but it seems to me that one thing that we could all agree on is that it would be really exciting if something like the: get with the guidelines COVID registry, could decide to measure this marker perspectively in the participating hospitals, for example. Dr. Vera Bittner: Then be able to look at this in a much, much larger population. I mean, especially with different ethnic backgrounds as well. I mean, I noticed actually to my surprise that, this Norwegian study how to fairly high proportion of Asians in the sample, but that may not be the ethnic distribution that we might see in different regions of the US, or different regions of the world. So it would be really nice to incorporate the measurement of this biomarker in much larger datasets. So things can be explored a bit further. Dr. Carolyn Lam: That's excellent, and Torbjorn, if you could channel Allan. What would you say? Dr. Torbjørn Omland: That's a difficult path, but absolutely just to me what Verra said. Then I think the importance of prospective studies in the COVID biomarker field, I think is our at most importance. Dr. Carolyn Lam: I think on behalf of both Torbjorn and I, and in fact everyone in circulation. Thank you, Verra for the amazing work that you and your team do for circulation as well. Thank you so much for making the time to share your thoughts today and thank you for that beautiful, beautiful paper both of you. Thank you. (singing). Listeners you've been listening to Circulation on the Run. Thank you for joining us from Greg and I. Don't forget to tune in again next week. Dr. Greg Hundley: This program is copyright, the American Heart Association 2020.

S2E37 - Torbjorn Musk

Play Episode Listen Later Oct 22, 2020 68:58

Welcome to the off-season everyone! Join us this week as we take a look at how Elon Musk got Torbjorn's turrets changed, the new Tracer comic, and all the changes already happening to the League's rosters.

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S2E2Night Of The Tapes!!! Featuring: Thomas Holm and Torbjorn Jorgensen

Cover Decoder

Play Episode Listen Later Oct 15, 2020 54:28

The Cover Decoder horror trilogy has begun! In this first terrifying Halloween installment, Tapes crawls from the cauldron with the terrifying VHS covers of Pumpkinhead and chases you screaming like a falsetto banshee into King Diamonds haunted gallery. Beware of murder! Betrayal! and Adult Gordes! Covers await and they are hungry!!

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HMPR Torbjorn Ekelund

Hispanic Marketing and Public Relations

Play Episode Listen Later Oct 5, 2020 60:12

Brought to you by HispanicMPR.com

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TPT #270: The Midgard Campaign Setting & Torbjorn

Total Party Thrill: RPG Advice From Our Table to Yours

Play Episode Listen Later Oct 1, 2020 56:33

Hosts I-Hsien and Shane wander into the Margreve as they discuss the Midgard Campaign Setting. In the Gates of Mourning campaign, the party uncovers new horrors, and Torbjorn kicks off Overwatch-tober with a bang (of his hammer) in the Character Creation Forge. (56m) Sponsors: Kobold Press: The Scarlet Citadel Kickstarter is live! Important Links: Skyjacks […]

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BRS Golf & Torbjorn Johansson GCTUK 028

Golf Club Talk UK

Play Episode Listen Later Sep 9, 2020 70:39

Episode 28 features our new sponsor "BRS Golf". Leighton talks to Bob and Peter from BRS about how COVID has affected rounds played as well as membership but they also talk through some of the great innovation that BRS are producing to help clubs. From membership management to member finance they are building the complete package for golf clubs. Leighton then talks to Torbjorn "Toby" Johanssen, Director of Education with CMAE. CMAE are moving towards more online education platforms and Toby explains. He also touches on such things as Golf in Sweden and Scandinavia. BRS Golf - BRS Golf – Online Golf Tee Time Booking Reservation System Software – BRS Golf – Ireland, UK, England, Scotland, Wales CMAE Europe - https://www.cmaeurope.org/home

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EPISODE 7 - Where Is She?

arcturus sharn khalida torbjorn

Play Episode Listen Later Jul 29, 2020 61:43

In this Episode: With one mysterious assailant down, and the other making off with Khalida, the party is left shocked and devastated in the sewers of Sharn. Their only lead is the defeated dwarf at their mercy, and they will make him talk - one way or another. Lord Nirro still doesn't know what his staff does, but he threatens to use it nonetheless. Arcturus uses his paladin powers to brutal ends. Torbjorn begins breaking fingers, and that's only the beginning. At the end of it all, Jimena receives a vision from her enigmatic patron telling them one thing: they must reach the ruins of Dorasharn, and the forgotten forge therein. Does our party learn anything? Will Khalida's disappearance change the direction of their mission? Stay tuned to find out: this is Quarantine Quest.

EPISODE 6 - There's Something In Your Eye

arcturus khalida torbjorn

Play Episode Listen Later Jul 8, 2020 67:37

Just when they think they're out of the water, the party awakes to find themselves in even deeper shit. (Get it? Because they're in the sewers?) Khalida and Arcturus are down for the count. Jimena fights strange shadows that steal her strength. Torbjorn gets knocked out by a letter, then comes back up swinging. Lord Nirro does some Earthbending. And once the fight is done, the real trouble begins. Who is after the party now, and why? Is their quest for the schema worth the trouble? And will the party be down another member? Stay tuned to find out: this is Quarantine Quest.

EPISODE 3 - The Bloody Bridge

Play Episode Listen Later Jun 10, 2020 84:35

It's a good old fashioned penthouse party for your favorite fancy bois. Lord Nirro hits the open bar for Baby's First Drink. Torbjorn makes friends with Bofi the Barkeep. An uncomfortable Niko gets incessant praise and an offer of patronage from Baron Merrix d'Cannith. An even more uncomfortable Jimena finds solace in the brief company of Matron Ulara from House Jorasco. Khalida and Edmund are... nowhere to be found? All those party vibes disappear as the group stumbles upon murder most foul, and fight off the mysterious Warforged perpetrators before calling it a night. What is the truth behind the murder of Bonal Geldem? Stay tuned to find out on Quarantine Quest.

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EPISODE 2 - Dragonmark Row

Push The Point: Overwatch League Storylines and News

Play Episode Listen Later Jun 3, 2020 101:25

The party seeks patronage from a variety of Dragonmarked houses, Greek row rush-style. Niko starts a fight, and Torbjorn finishes it. Jimena surprises some good-willed Halflings. Edmund has a member of House Lyrandar hot on his tail. Nirro meets his new favorite teacher. Khalida schmoozes politicians and helps people kick her brother's ass. Everyone ends up being invited to the same penthouse party. What's up with Baron Merrix d'Cannith? Stay tuned to find out on Quarantine Quest.

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#55: OWL Online Week 9

Play Episode Listen Later Apr 7, 2020 61:02

We're covering Week 9's #OWL2020 action including the return of a strong San Francisco Shock, Torbjorn's big splash in the meta, and all of this week's biggest news stories! Check it out!

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S2E9 - COWL Fans: The Unexpected Consequence of Mei's Absence

Casual OWL Fans

Play Episode Listen Later Apr 7, 2020 46:56

Aluramore and Howleir are back, and they're late, after an adjusted weekend schedule of #OWL2020. Torbjorn meta wasn't on our "BINGO!" cards, but regional metas are as fun as we'd hoped! The impact of Hero Pools is stronger than we thought, and the schedule is still in flux as North America based teams of Korean players move around.Follow COWL Fans on Socials! Twitter Facebook InstagramFollow us on Twitter: Popped Off! Aluramore HowleirVisit our website

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EHF EURO 2020 - 22 January: Torbjorn Bergerud a happy chap in Norway's goal, experts galore and a live audience

(Un)informed Handball Hour

Play Episode Listen Later Jan 22, 2020 45:25

EHF EURO journalists Courtney Gahan and Adrian Costeiu join the crew, and a live audience of 1, to look forward to the final day of main round matches. We caught up with Norway keeper Torbjorn Bergerud and Alex unleashes his shooting percentage quiz.

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327 - Bigs Backyard Ultra - Torbjorn Gyllebring

Pursuit of the Perfect Race

Play Episode Listen Later Nov 13, 2019 94:32

Tobbe went to Big's for the opportunity to explore his limits in the lastman standing backyard ultra format really. He found what he was searching for and it left him confused and determined to get back to do it all over again.-Photo’s provided by: @irun4ultra-Weather that day: 5072Water Temperature: Age Group: Human. (There's no age or gender division at Bigs)Height: 5'10"Weight: 154Calories per hour: Nutrition Company used: GU & Tailwind-Follow Tobbe,Instagram: @drunkcod-Follow Coach Terry:Instagram: @PerfectRacePodcast

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327 - Bigs Backyard Ultra - Torbjorn Gyllebring

Pursuit of the Perfect Race

Play Episode Listen Later Nov 13, 2019 94:32

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165 - Omnic Lab: Torbjorn 2.0 with Fuey500 & Chro (Going Deep)

Omnic Weekly - An Overwatch podcast

Play Episode Listen Later Sep 17, 2019 84:34

This week, Andres & Rob are joined by top 500 Grandmaster and well known Torbjorn connoisseur, Fuey500l! In addition, another streamer joins us to help us out with the one and only Chro! Join us for this deep dive with Fuey of one of the most misunderstood heroes in the roster! GAME NIGHT: September 27th WEBSITE: http://www.omniclab.com/links PATREON: http://www.patreon.com/omniclab DISCORD INVITE: https://discord.gg/vZ26JX4 SPOTIFY: https://open.spotify.com/show/4PNaj8fM0j5pdIaGEDrPPJ Shownotes: https://docs.google.com/document/d/1LxIDkOhOuUH-3ThXh8aqI5baeJkIqtsH62LDL4X1EEo/edit?usp=sharing PARTNERS: Humble Bundle Monthly Affiliate: https://www.humblebundle.com/monthly?partner=omniclab Patreon: REF1RE, Shazear, Shepherd, Crimsonfail, Brenden D, Chrisdaplaya, TragicZac, Darren WRob: twitter.com/notrob, twitch.tv/notrobmay Andres: twitter.com/iplaigames Fuey500: https://twitter.com/Fuey500, https://www.twitch.tv/fuey500, https://www.youtube.com/user/Fuey500, Chro: https://www.twitch.tv/prolikechro, https://www.youtube.com/channel/UCkw6l3jIjVtrXom_xqftSMA

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The Omnic Weekly: Episode 68 - Hanzo's Beachbody

Play Episode Listen Later Jul 21, 2019 78:20

Blizzard surprises us by releasing the summer games. The community is divided into team Torbjorn and Team Hanzo. Role queue got confirmed and is on PTR right now and hero 31 was leaked! We talk about the playoffs of stage 3 and LP is back with a brand new el pipi. Listen now! -------------------------------------------------------------------------------------------- Music by Tom Bleys @ Audio Ninjas Editing & Mastering by Tom Bleys @ Audio Ninjas

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Behind the Roll | Campaign 1 | Episode 4

Behind the Roll

Play Episode Listen Later Jun 27, 2019 64:03

Welcome to Behind the Roll where we go in depth into our most recent session of Saved by the Roll. In this episode we learn a bit about Torbjorn's past, a little more about the Vistanti along with our most epic battle to date, here's a hint at least one of our characters go down Support on social platforms: Facebook: https://www.facebook.com/Level2GamersSTL/ Twitch: https://www.twitch.tv/level2gamersstl Discord: https://discord.gg/0wUzRi9GdnHu8Qir Twitter: https://twitter.com/Level2GamersSTL Instagram: https://www.instagram.com/level2gamersstl/ Companies we're partnered with: Gamefly: https://goo.gl/VA6FgX Tubebuddy: https://www.tubebuddy.com/L2G Microsoft: https://afflnk.microsoft.com/c/1264386/433017/7593 Support us in other ways: Patreon: https://www.patreon.com/level2gamersstl Merch: https://shop.spreadshirt.com/Level2gamersstl/ People who make cool shit: Intro music courtesy of Tripbuk: https://www.youtube.com/channel/UCN0P6mJt3XqgQck8GtSYvhg Animation by Eric White: http://erictheanimator.com --- Support this podcast: https://anchor.fm/savedbytheroll/support

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16.juni 2019 - Torbjorn Tande - Lev med Gud i hverdagen

Betania Stathelle Taler

Play Episode Listen Later Jun 16, 2019 26:17

Barnepastor Torbjørn Tande taler på avskjedsfesten før deres utreise til Portugal.

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40 Years of Clay | Torbjørn Kvasbø | Episode 524

The Potters Cast | Pottery | Ceramics | Art | Craft

Play Episode Listen Later May 16, 2019 47:07

Torbjørn Kvasbø lives and works in Venabygd, Norway. When Torbjørn was a child, his father said, "For God's sake, never get a regular job. With those words to encourage him, Torbjørn has pursued his own ambitions and intentions without hesitation. Clay has been the pursuit that Torbjørn has worked with instead of getting that "regular job". Even Torbjørn's work with clay has been far from "regular". He approaches clay punches, massage, kneading, rolling, throwing, pressing, stretching, and stamping all the while trying to get clay to become the vision that dances in Torbjørn's own mind.

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Episode 167- Tiredness = Sickness: How to Stay Healthy

Touching the Trail Podcast

Play Episode Listen Later Mar 13, 2019 30:19

When your body becomes run down you are more likely to get sick. That simple truth is clearly apparent when you are fatigued and stressed because often those are the times when you become sick. The science backs this up, with many studies corroborating the fact that fatigue can weaken your immune system, leading to an increased risk of infection. As I am just overcoming a recent cold I have been thinking a lot about the best practices that one can employ to prevent fatigue and therefore prevent sickness. The key is to listen to your body. During times of tiredness and stress your body sends clear signals that you need to slow down and rest. Often, when you don’t listen to those warning signs, you become sick. The more that you can return to center and stay focused on keeping your body healthy the less likely it will be that you will get sick. Join me today as I explore a few key practices to stay energized and prevent sickness from day to day.AUM,Jarod Contrerastouchingthetrail.com/writings/2019/2/2/why-you-should-wake-up-earlytouchingthetrail.com/resources/#meditationSources:mayoclinic.org/diseases-conditions/insomnia/expert-answers/lack-of-sleep/faq-20057757webmd.com/sleep-disorders/features/immune-system-lack-of-sleep#1sciencedaily.com/releases/2015/06/150629110803.htmJanssen, N., et al. "Fatigue as a predictor of sickness absence: results from the Maastricht cohort study on fatigue at work." Occupational and environmental medicine 60.suppl 1 (2003): i71-i76.Akerstedt, Torbjorn, et al. "Predicting long‐term sickness absence from sleep and fatigue." Journal of sleep research 16.4 (2007): 341-345.Support Touching the Trail:touchingthetrail.com/donatetargetreleaserecovery.comFind Touching the Trail:touchingthetrail.comTouching the Trail Weekly: touchingthetrail.com/signupInstagram: @touchingthetrail instagram.com/touchingthetrailTwitter: @touchthetrail twitter.com/touchthetrailFacebook: Touching the Trail facebook.com/touchingthetrail

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OVERBYTE Ep. 20

10x Ambassadors Experience

Play Episode Listen Later Jan 29, 2019 77:55

In episode 20, the lads discuss their disappointment with the Lunar New Year Event. Go over the brief PrOverwatch notes then give their hot takes on the power rankings for season 2!

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10x Ambassador: Torbjorn Bergstrom | ep. 6

Play Episode Listen Later Jan 25, 2019 47:35

10x Ambassador: Torbjorn Bergstrom Success from the 10x Ambassador group: The people I’ve met in the group have been amazing. The real value in any event like growth con is the networking, and the ability to network with the people who have been active in this group gives me an advantage when I walk in the door at growth con. But even better I was able to join the team at pickamentor.com, where we’ve come together to share from our experiences and help people select a mentor who will help them.

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OVERBYTE Ep. 19

Play Episode Listen Later Jan 22, 2019 52:40

In episode 19, the lads discuss the small amount of PrOverwatch news. The Katsuwatch short and the lead-in the the Lunar New Year event.

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OVERBYTE Ep. 18

Play Episode Listen Later Jan 15, 2019 41:41

In episode 18, the lads discuss the small PrOverwatch news and their confusion with the power rankings people have been putting out.

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OVERBYTE Ep. 17

Play Episode Listen Later Jan 8, 2019 43:49

In episode 17, the lads discuss the recent PTR changes and what they mean for the game.

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OVERBYTE Ep. 16

Play Episode Listen Later Jan 4, 2019 55:17

In episode 16, the lads discuss the recent OWL bans, Dafran (in a good way) and what to do about GOATS

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OVERBYTE Holiday Special 2018

Play Episode Listen Later Dec 26, 2018 25:46

Happy Holidays from the OverByte podcast!In this episode, the lads play a game of comp and give you the play by play of how the Mei on our team ruined it!

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OVERBYTE Ep. 13

Play Episode Listen Later Dec 17, 2018 55:09

We're back!Sorry for the big delay on releasing this episode.To be clear this was recorded a week after episode 12.In this episode, the lads discuss PrOverwatch and the upcoming holiday event.

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OVERBYTE Ep. 11

Play Episode Listen Later Nov 21, 2018 58:36

In episode 11, Mikey and Erik discuss more PrOverwatch, the massive PTR patch and the current state of OW competitive.

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123 - Omnic Lab: Lore & Speculation

Convert to Raid Presents: The podcast for World of Warcraft and other Blizzard Games!

Play Episode Listen Later Oct 23, 2018 81:47

This week Andres and Rob talk about some lore around Talon, Blackwatch, and a whole lot of speculation for what we think could be soon around the corner for us in the game! ANNOUNCEMENTS: GAME NIGHT: 10/26 SPONSOR: Top Score Solutions Ben aka “INeedPeeling” is offering free business consulting in the eSports field. If you are aspiring to coach, starting a team, developing an app or service, trying to boost your subscriber base, or just want to work in eSports, you can visit his website at topscoresolutions.com, get him on Twitter @topscoreEsports, or join his Discord server. Ben has a Masters in Sport Management, Finance and Data Analytics as well as experience in sales, marketing, and company development. His services are free, and they will stay that way as long as demand allows it. Omnic Meta: (Homepage) Humble Bundle Monthy Affiliate! Our Affiliate Link: https://www.humblebundle.com/monthly?partner=omniclab Con Before the Storm - Overwatch Panel Nov. 1, 10:00-11:00pm (4th Floor, Anaheim Hilton) Discussion Points: Overwatch Lore 2017-2018 The start of the story: “Over thirty years ago, without warning or explanation, a decommissioned set of automated megafactories re-activated themselves and launched a worldwide military campaign against all humanity dubbed the Omnic Crisis. Despite deploying new technologies including powered armour and super-soldier programs, no nation alone could stand against the growing omnic army.” The UN formed OW For 20yrs OW served as a global peacekeeping force & overall world & space betterment Controversy struck their missions & forced disgraceful retirements through failed missions and allegations plus the uncovering of Blackwatch’s covert operations surfaced The UN investigated and the OW Swiss headquarters was destroyed and Jack & Gabriel were reported dead during the investigations. The UN still decided to shut down OW & BW even with the destruction ruled as an “accident” The Petras Act declared all OW activity illegal & could be prosecuted Since then: Vishkar Corp. destroyed Calado Tower to control Rio de Janeiro Side note: Lucio’s Father worked on design & creator for sonic tech for Vishkar Lucio also is a known enemy & freedom fighter to force them out of Rio de Janeiro Satya Vaswani (Symmetra) was a high rank hard-light architect & trade agent for Vishkar Symmetra was the key in destroying Caldo Tower with Sanjay Korpal (Vishkar agent & Talon leader) who helped assist after they couldn’t negotiate a contract with the Mayor of Rio de Janeiro. Hyde Global hired 2 international criminals Junkrat & Roadhog to swindle insurance Heroes Introduced since launch: Talon: Sombra (Origin Story) Animated Short Doomfist (Origin Story) “Conflict & War is the Crucible by which we evolve.” Doomfist Smashed the airport in Numbani & OR-15 models Moira (Origin Story) Blackwatch Associations: Genji McCree Moira Overwatch & Misc: Ana - Fareeha’s (Pharah’s) Mother Lore Origin Story OW Sniper with original Overwatch Faked her death just like Jack Morrison (76) & Gabriel (Reaper) Brigitte - Torbjorn’s Daughter, Reinhardt is the Godfather Lore Origin Story Orisa (Origin Story) OR-15 modified by Effie Odele to an OR15A Wrecking Ball (Origin Story) Connected to Horizon Lunar Colony & Dr. Winston Name: Hammond -- Connections with winning a Junkertown Arena Animated Shorts: “The Last Bastion” - Bastion The only animated short with zero dialogue Shows that Bastion was abandoned in a forest in Sweden after the Omnic Crisis Ganymede somehow activated Bastion (the bird) The Omnic has PTSD from the battles in the crisis Finds some abandoned B73 models destroyed in a field & uses his repair tech to get a memory note on what happened Remembers what it’s supposed to attack in the city, but takes the bird to help understand it is in the past Apparently, Bastion met Torbjorn after this and took him under it wing & upgraded it “Infiltration” - Sombra with Widowmaker & Reaper (Guest Zarya) Talon assassination mission in Volskaya Industries (RUS) Chairman Katya Volskaya? (defender against the omnics) Sombra Blackmails her with knowledge of the Chairman using tech from Omnic technicians. (Chairman also shows her daughter) Mechs being built use Particle Beams that Zarya utilizes & Shield Arms like her barriers Zarya arrives at the end “Junkertown: The Plan” - Junkrat & Roadhog (Teaser for The Queen?) Mostly Map & World building, Character fun “Rise and Shine” - Mei & Snowball Mei & companions in Antarctica ran low on resources. Cryo-froze themselves to power down the base. Only Mei woke up from Cryo-sleep Atmospheric predictions were far worse than expected. Comms lost & they slept through the OW/Blackwatch controversy Asleep for 9 years resulting in the companions’ tanks to malfunction. On the plus side, the 9 years the base while they slept. Companions died to the Cryonics “Malfunctioning” Opara (Cryonics) - from Numbani, Africa Arrhenius (Climatologist) - from Sweden Torres (Cryonics) - from Spain Macready (Engineering) - from USA Adams (Researcher) from USA Mei sets out with the data and some snow gear to get back to Overwatch from Antarctica “Honor and Glory” - Reinhardt & Brigitte (OR-14 Orisa Model & Bastion models) Rein & Brigitte talking to avoid going back to OW Reinhardt’s young crusader days “Live with Honor, Die with Glory” Shows his arrogance and aggression while not protecting his men An OR-14 Unit gets deployed and cuts Reinhardt’s Eye open with a blade. Reinhardt’s senior officer gets a mortal wound from the same unit to rescue him Fun fact: One of the crusaders helping while Reinhardt is on his rampage is a female crusader! This means that there could be more of his unit that were female or even omnics! Reinhardt’s superior rests in Eichenwalde (or at least the armor does) Speculations? Omnics vs humans, thoughts? Lots of story retrospection, but how will they move forward? Talon, how do they come into play? Will Sanjay Korpal, Talon leadership show up? He’s also Vishkar’s CEO This guy was in the Symmetra comic (A Better World) & Masquerade Comic as well as the Moira Origin Story & sat with Moira & Maximillien when Doomfist returned. More Overwatch heroes? “Sound Quake” from the original trailer has STILL gone unmade “has chest missiles” according to punch kid Special Thanks to Diamond Sponsors & New Patrons: Ben K, Britmus, Chrisdaplaya, DurandaL, JanJinkle, Lisome, Mr. Marz, Roger B, Shazear, Solo PS4, Terry F, Top Score Solutions, TragicZac Omnic Lab Links: Omnic Lab is now a Twitch Affiliate! Sub now with Twitch/Amazon Prime!Twitter, Facebook, PatreonTwitch, Youtube, MERCHDiscord: discord.me/omniclabEmail: omniclabpodcast@gmail.com Website: http://www.omniclab.com iTunes, Google Play Music, RSS-->Full Extended Show Notes

live father strategy deep masters fun team finance ptsd character mayors heroes sweden daughter discord controversy rio esports floor janeiro competitive antarctica speculation lore lab overwatch comp remembers composition crucible data analytics asleep companions google play music comms bastion atmospheric lucio reinhardt ow sport management marz finds mechs cryo doomfist black watch twitch affiliate zarya symmetra torbjorn pharah con before roger b durandal omnic omnic lab numbani more overwatch eichenwalde

BNN #98 - Convert to Raid presents: Spooky Stuff!

Play Episode Listen Later Oct 10, 2018 84:16

For videos, audios, and all things CtR, join us online at http://converttoraid.com Pat Krane, Thorn and Thyst (Lagging Balls) join the crew this week to talk about WoW and more! 5:15 - Talking DPS in WoW (casual) 13:55 - Mike Morhaime stepping down, J. Allen Brack the new President of Blizz 19:00 - BLIZZCON HYPE 33:00 - WoW: LFR Wing 3 (w/ run through) 41:30 - Other stuff this week. Is the Call to Arms working as intended? 46:45 - Getting Caught Up in WoW 1:02:30 - Overwatch: Junkenstein, New skins, Torbjorn changes 1:17:40 - Outro Follow us on Twitter at http://twitter.com/converttoraid or individually: Pat Krane - http://twitter.com/PatKrane Thyst - http://twitter.com/Thyst03 Thorn - http://twitter.com/Thornbrow

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⚙

The Art Of Struggle.

Play Episode Listen Later Oct 8, 2018 6:24

⛏

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Episode 1: Into the Fray

Ready Set Pwn - A Vancouver Titans Overwatch League Podcast

Play Episode Listen Later Oct 7, 2018 22:12

Episode Notes Hosted by Chris (@lyteforce), the first episode of the Ready Set Pwn podcast has finally hit the internet.Outline 0:48 min - Introduction to the podcast It's the first episode, hear me out! 2:15 min - The Payload Chris outlines everything we know about the Vancouver Overwatch League franchise, hereby known as VanOWL, and also outlines what it is we still don't (source). Jesse Wilson's (@jp3ilson) Canadian Team Concepts can be found on Behance 9:49 min - The Fray News and updates from around OWL California Cup and Gilded Gala events Overwatch news, such as a Road Hog minor rework and thoughts on the major Torbjorn rework. 15:49 min - Wrap-up Where can you find us? Website, Twitter, Facebook Got some feedback? Shoot an email to feedback at readysetpwn dot com. And think you have some podcasting chops? Chris is looking for someone to join him - shoot him a note if you're interested. And a huge shout-out to Burn7 on Soundcloud for the awesome track, Heroes Never Die Music used under a Creative Commons licenceThis podcast is powered by Pinecast. Try Pinecast for free, forever, no credit card required. If you decide to upgrade, use coupon code r-d07915 for 40% off for 4 months, and support Ready Set Pwn - A Vancouver Titans Overwatch League Podcast.

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010 - Tinker, Tailor, Soldier, Torb

Heroes Needed

Play Episode Listen Later Oct 1, 2018 47:19

In this episode, Dave and Richard discuss the UK vs France Overwatch World Cup matchup (spoilers for the result within) and how the big plays compare to the Overwatch League.They also cover the upcoming Torbjorn rework in detail (MOLTEN CORE!!!), the No Limits Arcade game mode and the Tank hero class (including its different applications in a team composition). Hosted on Acast. See acast.com/privacy for more information.

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Episode 63 - Touching Torbjorn

Watchpoint Radio – Overwatch News, Discussion, and Community

Play Episode Listen Later Sep 26, 2018 67:36

This week we're joined by long-time fan "Jazz" (aka Jeff) for discussions about the latest Dev Update including all the changes being made to Torbjorn, Pharah, McCree, and so many more. Lots of great discussion this week.

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#127: Buff Daddy

Play Episode Listen Later Sep 26, 2018 103:29

The long awaited Torbjorn rework changes are here!... Almost. The new Torb is on the PTR along with another round of character balance. Additionaly, we dive into the Pursuit and Visor bans put in place by the Overwatch team.

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OVERVIEW Ep. 3

Play Episode Listen Later Sep 25, 2018 47:05

In the third installment of OVERVIEW. The lads talk OWWC (again) the Torb rework, future events and some major OWL roster moves.

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119 - Omnic Lab: PTR & Torb Rework!

Omnic Weekly - An Overwatch podcast

Play Episode Listen Later Sep 24, 2018 70:15

This week Andres & Rob revisit a more fireside chat style and just talk about news, PTR changes, and especially the new Torbjorn rework coming soon. ANNOUNCEMENTS: GAME NIGHT: 9/28 Report! SPONSOR: Top Score Solutions Ben aka “INeedPeeling” is offering free business consulting in the eSports field. If you are aspiring to coach, starting a team, developing an app or service, trying to boost your subscriber base, or just want to work in eSports, you can visit his website at topscoresolutions.com, get him on Twitter @topscoreEsports, or join his Discord server. Ben has a Masters in Sport Management, Finance and Data Analytics as well as experience in sales, marketing, and company development. His services are free, and they will stay that way as long as demand allows it. Omnic Meta: (Homepage) Player Stats: Link Omnic Lab Episode Spreadsheet Humble Bundle Affiliate PTR Updates Pharah Brigitte McCree Soldier 76 Orisa Mei visual Patch Notes: Sept 11th Roadhog Added Torb Rework New Kit New Ultimate Special Thanks to Diamond Sponsors & New Patrons: Ben K, Britmus, Chrisdaplaya, DurandaL, JanJinkle, Lisome, Mr.Marz, Roger B., RickyTicky, Shazear, Terry F, Tim W, Top Score Solutions, TragicZac. Omnic Lab Links: Omnic Lab is now a Twitch Affiliate! Sub now with Twitch/Amazon Prime!Twitter,Facebook, Patreon Twitch,Youtube,MERCH Discord:discord.me/omniclab Email: omniclabpodcast@gmail.com Website:http://www.omniclab.com iTunes,Google Play Music, RSS -->Full Extended Show Notes

The Omnic Weekly: Episode 34 - Torb Juice

Play Episode Listen Later Sep 23, 2018 76:17

In this week's episode the gang talks about the new Torbjorn, all the buffs and nerfs in patch 1.29, upcoming skins for the Halloween event, the World cup and other esports news. Listen now! -------------------------------------------------------------------------------------------- Music, Editing & Mastering by Tom Bleys

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Episode 179 - Raiding Gets Confusing

Geeks of Azeroth - A Podcast for Blizzard Gamers

Play Episode Listen Later Sep 22, 2018 64:09

In this weeks episode, we talk all about patch 8.1 including the new confusing raid. We also touch up on the new HotS event and the Torbjorn rework

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Torbjorn Johansson, CMAE - PCR 142

Private Club Radio

Play Episode Listen Later Sep 17, 2018 22:43

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Episode 62 - Stop Touching Me

Omnic Weekly - An Overwatch podcast

Play Episode Listen Later Aug 26, 2018 53:12

Blizzard! Why dost thou messeth with our heroes? Torbjorn changes? Really? Plus our guesses at what's going to be unveiled at GamesCom 2018, tips for playing Hammond, and endorsements making better players!

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Episode 23 - APB Reloaded, MapleStory 2, Torbjorn Noises

The Weekly Cooldown

Play Episode Listen Later May 13, 2018 62:01

Kamijace brings on most of the Stuffington Press family (Paul, Tricky/Wes, and Markayam) to talk about APB Reloaded and GamersFirst being bought out, MapleStory 2 closed beta, Egress, a new Dark Souls styled RPG-Battle Royale game, and the E3 press conference lineup. Check out this fun, mess of an episode now! You can find the Stuffington Press dudes on their twitch channel: https://www.twitch.tv/stuffingtonpress Find Markayam on the Stuffing Press Twitch Stream...whenever. And also on Tumblr: https://markayam.tumblr.com/ Find Wes on the Stuffington Press Twitch Stream on Saturdays! Find the mono-induced Biggs on Twitch Streams on Sunday! Find Paul on twitter @paulsrockintwit and on Twitch Streams on Tuesdays! Website: wkcooldown.com Patreon: Patreon.com/Weeklycooldown Twitter: @Kamijacegaming / @WkCooldown Facebook: https://www.facebook.com/TheWklyCldwn/ Intro music by Captive Portal/Zach Brider Music by audionautix.com --- Send in a voice message: https://anchor.fm/wkcooldown/message

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The Omnic Weekly: Episode 12 - Talon World

Play Episode Listen Later Apr 2, 2018 79:34

In this week's episode D. is joined by Hana, LP and Bane to discuss the new Uprising event, the Torbjorn buff, Moira changes, who runs Blizzard World and this weeks eSports news/drama! At the end there is an other Overwatch Quiz, with game master LP! Listen now! -------------------------------------------------------------------------------------------- Music by Tom Bleys Editing & Mastering by Myles Morgan

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Overwatch Lore - Brigitte, Torbjorn, and Reinhardt

Lore Boys

Play Episode Listen Later Mar 28, 2018 57:25

Would you be okay with your war veteran friend, at age 60, taking your 18 year-old daughter on a tour of Europe for months at a time? Something to consider while we dive into another chunk of Overwatch lore! We're talking about Brigitte and her two daddies -- that is, her father and godfather.Talking points include: swivel chairs from Ikea; the fact that Reinhardt's tall and that's good; mobile big buildings made to build big buildings; and Reinhardt on all fours in front of some Dragons. So grab your earbuds and hop in to learn all about Overwatch's newest hero.For anyone looking to help out the show make sure to follow us and leave a review on iTunes and across all our social media, Facebook, Twitter, and Instagram. Also check us out on twitch if you’ve ever wanted to see us play the games we talk about.Also to Eric Skiff as thanks for the use of their song as our shows theme, we'll let you take our daughters across Europe any time you want. See acast.com/privacy for privacy and opt-out information.

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Power Pals 089: The Death Of Toys R Us, The Gang Gets Emotionally Real About Brigitte in Overwatch, Bruce The Spruce, and Andrew's Daughter Is Introduced To Batman The Animated Series

Power Pals Podcast

Play Episode Listen Later Mar 26, 2018 63:37

The Gang is back in the studio. Avery hosts after a rough week with hilarious results, lament the death of Toys R Us, get way too real about Brigitte and Torbjorn, and talk about introducing Andrew's daughter to Batman: The Animated Series. a2exyj2y Theme Music: Video Dungeon Boss Kevin MacLeod (incompetech.com) Licensed under Creative Commons: By Attribution 3.0 License creativecommons.org/licenses/by/3.0/ Video Game Read more at http://powerpals.libsyn.com/#LQcuxdEew4H08ZH4.99

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Circulation March 20, 2018 Issue

Geeks Under Grace Podcast

Play Episode Listen Later Mar 20, 2018 21:45

Dr Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr. Carolyn Lam, Associate Editor from the National Heart Centre and Duke National University of Singapore. How common is perioperative myocardial injury after non-cardiac surgery, and what is its significance? A very important question and a very important feature discussion coming right up after these summaries. Our first original paper this week tells us that risk assessment using only non-laboratory based risk factors may be a useful alternative in the absence of informational lipids, in predicting adolescents at risk of developing pre-clinical atherosclerosis. First and corresponding author, Dr. Koskinen from University of Turku Finland and colleagues, studied almost 2,900 participants, age 12-18 years, from four longitudinal cohort studies from the United States, Australia, and Finland, and followed these adolescents into adulthood. When carotid intima media thickness was measured, a mean followup of 23 years later. Non-laboratory based risk factors such as age, blood pressure, body mass index, and lipids measured in adolescence, independently predicted high carotid intima media thickness in young adulthood. The addition of lipid measurements to these traditional clinic based risk factor assessments provided a statistically significant but clinically modest improvement on adolescent prediction of high carotid intima media thickness in adulthood. The next study demonstrates the feasibility of large scale aptamer multiplexing at a level that has not previously been reported and with sample proof that greatly exceeds other existing proteomic methods. Now, like antibodies, DNA aptamers can be generated as affinity reagents for proteins. Emerging data suggests that they can be used to measure blood protein levels in clinical cohorts. However, the technology has, to date, remained in its infancy. In today's study, co-first authors, Dr. Jacob and Dr. Ngo, co-corresponding authors, Dr. Jennings and Gerszten, from Beth Israel Deaconess Medical Center in Boston, tested the scalability of a highly multiplexed expended proteomic technique that uses single stranded DNA aptamers to assay human proteins with a markedly expended platform containing approximately 5,000 aptamers targeting a far broader range of analytes than previously examined using this technology. They applied the platform to a cohort of individuals undergoing septal alcohol ablation for hypertrophic cardiomyopathy, using this as a human model of planned myocardial injury. Now, in addition to confirming findings from prior studies, they identified nearly 150 additional putative markers of myocardial injury. Thus, these findings suggest that the expanded aptamer based proteomic platform may provide a unique opportunity for biomarker and pathway discovery following myocardial injury. The next study addresses the potential long-term effects of low LDL cholesterol on neurocognitive impairment and decline. This has been a concern with pharmacologic PCSK9 inhibition. The first author, Dr. Mefford, corresponding author, Dr. Levitan from University of Alabama at Birmingham, investigated the association between PCSK9 loss of function variants and neurocognitive impairment and decline in the regards study. In this general population sample of African American adults, they found no association between PCSK9 loss of function variants and neurocognitive impairment or longitudinal neurocognitive decline. There was also no association between lower LDL cholesterol levels and neurocognitive impairment or decline during follow-up. The study, therefore, provides evidence in a contemporary population that PCSK9 loss of function variants and resulting lifelong exposure to low LDL cholesterol levels are not associated neurocognitive impairment or decline. The final study explores long-term outcomes in patients with Type 2 myocardial infarction and injury. First and corresponding author, Dr. Chapman from University of Edinburgh and his colleagues identified more than 2,000 consecutive patients with elevated cardiac troponin I concentrations at a tertiary cardiac center. All diagnoses were adjudicated as per the universal definition of myocardial infarction. They found that at five years, all cause death rates were higher in those with type 2 myocardial infarction or injury compared with type 1. Although the majority of excess deaths with type 2 myocardial infarction or injury were due to non-cardiovascular causes, the observed crude major at-risk cardiovascular events are MACE rates were similar between groups. Coronary heart disease wan an independent predictor of MACE in those with type 2 myocardial infarction or injury. Thus, despite an excess in non-cardiovascular death, patients with type 2 myocardial infarction or injury have a similar crude rate of major at-risk cardiovascular events to those with type 1 myocardial infarction. Identifying underlying coronary heart disease in this vulnerable population may help target therapies that could modify future risks. That wraps it up for our summaries. Now, for our feature discussion. So, I'm gonna go back to my first question on this podcast. How common is perioperative myocardial injury after non-cardiac surgery and what is its significance? Well, to give us an answer, I am delighted to have the first and corresponding author of today's feature paper, Dr. Christian Mueller from University of Basel in Switzerland, and we also have Dr. Torbjorn Omland, and he is associate editor form University of Oslo in Norway. Now, in case you're having deja vu, you are right. I have had these gentlemen on this podcast before and they were so successful, I had to call them back. So, welcome, welcome Torbjorn and Christian. Thank you for coming back again. Christian, congratulations on another beautiful paper. Could you tell us the highlights of what you did and what you found, but this time in particular tell us the novel aspects in view of the previously published vision study that was just published last year. Maybe you could just point out some of the differences. Dr Christian Mueller: The topic is about an interdisciplinary topic and something, I think that is so important for us as cardiologists to get involved in with much more detail in the future. So, we are aware of acute myocardial infarction, sustained myocardial infarction event that we have studied extensively for decades and for which I think we have a fuller understanding of its cardiophysiology and we have excellent treatments. Completely novel entity is perioperative myocardial injury, so cardiomyocytes that die in the context of non-cardiac surgery. It's something that we as cardiologists should be really focused on because its likely the most important contributor to death in the perioperative period. So, the death rate among non-cardiac surgery is despite improvements in anesthesia and surgery remains remarkably high, between 1 and 4% within 30 days, depending on patient characteristics and surgical directives. And, it seems from our current understanding that the heart really plays a major role, rather high percentage of these deaths. So, what is new in our study? Overall, our study took advantage of insight gained in the first phase of the vision study in that its has been documented that this perioperative myocardial injury fairly commonly occur without the patient or we as physicians getting aware of it. Either because the patient is still having anesthesia or because he may have symptoms that are atypical. So, we can only reliably detect this event if we screen an appropriate population, and that's what we have done. So, I think the criteria where a patient that's at higher risk of cardiovascular complication is defined at an age of 65 or higher or having pre-existing cardiovascular disease. So, this is the first major difference in which also much younger patients were enrolled. That's the most important differentiate as we had an open label screening. So, the screening was part of clinical routine and it was fine tuned to patients of whom we thought may have a reasonable high risk of developing this complication. Dr Carolyn Lam: And, your main findings, because they were striking. Dr Christian Mueller: As our most important finding, we were able to report the incidence of how many patients actually have a relevant amount of cardiomyocytes dying during the operation, and it was one out of seven patients entering our study. So, an incredible high incidence of this complication and that this complication not only is a very good end point that you shouldn't care too much was highlighted again and in full agreement, the suspicious is that if patients develop this complication of perioperative myocardial injury, their risk factor of whether they have any symptoms or atypical ischemic symptoms, and again, only a small minority had the risk of dying both within 30 days as well as in one year, was substantially increased. Dr Carolyn Lam: Christian, before you go on, could you just please clarify, how did you define perioperative myocardial injury in this case, and was it the same as the definition used in Vision? Dr Christian Mueller: The perioperative myocardial injury concept initially in Vision it was defined as detecting an elevated troponin just after a non-cardiac surgery, and why this was a perhaps an appropriate definition at the time when we were still using very poorly sensitive troponin assays inevitably is no longer appropriate nowadays because its obvious that particularly elderly patients may have chronic elevations and high sensitive troponin usually. Mild elevations due to a variety of disorders and [inaudible 00:11:51] important studies for us to understand that it is mild elevations troponin is quite common in patients with heart failure, with coronary artery disease or hypertensive heart disease, whatever. So, if we could detect or start detecting likely elevated troponin only after operation, we would never know whether this is something related to the operation itself or whether it's perhaps had already been around for months and weeks and represents the chronic condition. So, the novel concept is that we have to identify an acute rise in troponin, a dynamic genetics or just like that requested for the universal definition of myocardial infarction also of course [inaudible 00:12:32] So, we requested in this study, an increase from the concentration prior to surgery of at least 14 ng/l of high sensitivity cardiac troponin. Dr Carolyn Lam: Right. Wow. What a great study. So systematic. So, all patients, basically had readings before and after surgery. You know, I've got so many questions, but I really, since you mentioned Torbjorn, I would really like to ask his perspective on what you think was the most striking parts of it and any questions you may have on Christian. Dr Torbjorn Omland: First, I would like to say that this is a very impressive study with some very important results in a neglected area of medicine, really. So, there are several very strong points with this study, and I think that if we're able to, in such a large population, both have pre-operative and post-operative and was able to calculate the delta, and the importance of that was a very strong part of the study, because it showed that, as Christian alluded to, the baseline level did carry some information but there was also important additional information from the serial measurements. So, that's maybe one of the most important findings, I think. Then, we addressed the question, how should we use these data? So, my question to Christian is actually, how will screening for exceptional myocardial injury affect clinical practice? Will it lead to clinical deficiency interventions that will improve outcome or will it just result in unnecessary testing? Dr Christian Mueller: Very good important point, Torbjorn. I think you are absolutely right in indicating that I think we are just beginning to understand all of the part of physiology behind the event that we can now capture, detect really, rather simple and precisely with troponin screening. So, I think it's important that we highlight that the part of physiology behind this event differs from patient to patient. So, there are some patients who clearly have a type 1 myocardial infarction as the cause of myocardial injury. Very likely, they are the minority in this setting. Likely, the majority to have a kind of a type 2 myocardial infarction have a physiology with imbalance between supply and demand, and again, in these patients, of course, the management needs to be to identify the trigger and to correct the trigger as rapidly as possible. And it can be that detecting myocardial injury by the rise in troponin, is the first indication that there is a problem ongoing. Now the patient can have a physiological rearrangement might have already been aware to the physicians if it's a type 1 myocardial infarction, then obviously very likely the same therapy will be beneficial to this patient as we would apply in spontaneous myocardial infarction. A very important, and I'm glad you alluded to that the different ways of, a rather wide variety of patient settings that are summarized of the term perioperative myocardial injury. And the consequences, likely will have to be individualized to really ensure that we do something good for the patient. And if I may, I would like to ask you and Carolyn for your thoughts about the most appropriate wording. So, the current wording that we used, of course, has to be in any scientific precaution, a very conservative one, perioperative myocardial injury. And it's important that, in fact, there are some entities where likely injury is derived from the patients who have the injury related to serious sepsis or related to a stroke, or pulmonary embolism. However, it's very likely that the vast majority of patients, the term perioperative myocardial infarction would be appropriate. And, I think it's so important to be aware of the implication that this, perhaps, on first slight small difference might have. As long as we keep using the term "injury", cardiologists will not really feel the same need to be involved, the same need to really take care of this patient as compared to the use of "myocardial infarction". So, I think it's a balance between scientific accuracy, but also the need to create awareness. So, I feel that if cautiously applied, we'll do more good if would more liberally use "myocardial infarction" within this context. So, would you agree with this perchance? Dr Carolyn Lam: I think "injury" is at least better than what we used to say, "a leak'. You know, we used to say, "Oh, it's just a troponin leak". So, at least we're saying injury, recognizing that there is damage done. I just wanna highlight that in your paper, something that really struck me was that these patients with perioperative myocardial injury or infarction, indeed did as badly as those who did or did not fulfill myocardial infarction criteria. So, that kind of supports what you are suggesting. I did get that right, right? In your paper? Dr Christian Mueller: Absolutely. I think for spontaneous myocardial infarctions, so clearly that the criteria defined in the universal definition are mandatory. There's nothing to discuss about, but we cannot criticize a patient who is undergoing general anesthesia that he doesn't feel chest pain, and therefore, we deny him the appropriate word of the events. I think is just important that we clearly highlight that it really can be the same event in the chest without symptoms. But, not due to anything else but because he is undergoing anesthesia. Dr Carolyn Lam: Very good point. You know, I would really like, though, to go back to Torbjorn's point, because I think that skeptics are gonna say we've created a problem that we don't know how to solve, or that we don't know how to treat. Do you know what I mean? So we're detecting all these things, because now we have all these assays. Patients are asymptomatic, and then we really don't know whether it's modifiable. We don't know what to do to improve outcome. So, could I ask both your expert thoughts on what the future should hold? What is next step? Because, I see a gap. Dr Torbjorn Omland: Yes, that's of course, a key question. So, I think we need to be innovative and patient, because what we really need is clinical trials, perhaps and more clinical trials looking into different strategies. But, of course, that's also challenging because as Christian told us, the path of physiology among this group of patients with perioperative myocardial injury differs. So, what's going to be appropriate for one patient, may not be the appropriate therapy for the next patient. So, I think his suggestion of an individualized approach is the best thing we can say at this moment, while we are awaiting data from future clinical trials. Dr Christian Mueller: I fully agree with Torbjorn [inaudible 00:19:53] what you said, you will criticize some people will argue to that it's irrelevant. Why do you measure this and you don't want to hear it? You don't want to see it. But, I think it's important to remember the starting point for us as cardiologists is to get involved is death. If death is within 30 days after non-cardiac surgery in a patient who was fit, relatively fit otherwise, who underwent a surgery that was not a very high risk surgery from which he would expect a certain percentage of patients to die. So, that's the starting point. Again, of course perioperative myocardial infarction is not the only contributor to perioperative death. But, it seems, in addition to severe sepsis, to be the second commonest and most important. So, I think it's really, really important to first, as a really as a first important thing to increase the awareness of this problem and to encourage our colleagues to start bringing their research efforts, so that we get smarter in identifying the underlying part of physiology in these infarcts or injuries. Because, only once we understand, or have a reasonable understanding what is the mechanism, we will be smart enough to select the most important priority for any intervention study. Dr Carolyn Lam: Wow. What a wonderful note to end this podcast on. Words of wisdom, as always from both of you, Christian and Torjorn. See, listeners. Didn't I tell you this was gonna be a great podcast? Don't forget to tune in again next week.

Episode 4 | Overwatch: Part 4

Game Science the Podcast

Play Episode Listen Later Mar 7, 2018 78:08

Torbjorn, ready to work! We're back with you again, this week we get through all of the defense heroes and onto one of the tanks! things are moving a bit quicker now! Enjoy your two favorite gamers as they pretend to know what they are talking about, and let's play some video games! Have something you want to ask us about a game? Something to say? Questions? Comments? Let us know on social media! Email: GameSciencePodcast@gmail.com Facebook: www.facebook.com/gamesciencepodcast/ Twitter: twitter.com/gamesciencepod Our theme song is Gumption and Guts by Bella Ruse. Check it out here: www.youtube.com/watch?v=cZAacJPTN-E Our logo is by Keely Wright-Ogren: https://twitter.com/keelywog Thanks for listening, Game On!

overwatch guts game on gumption torbjorn bella ruse

Episode 119: Faith Shines in Hollywood

Play Episode Listen Later Feb 28, 2018 88:47

This week we have some very special news. Faith shines in Hollywood this week as some notable stars step out in their faith; always something we enjoy talking about. Torbjorn's daughter rumored to be new Overwatch character https://www.gamespot.com/articles/following-overwatch-tease-blizzard-shares-somethin/1100-6456984/ Death Stranding cast pulls voice talent from The Last of Us and Days Gone https://www.gamespot.com/articles/death-stranding-cast-adds-the-last-of-us-and-days-/1100-6456934/ Nuaghty Dog Director hopes a Last of Us movie will never happen https://screenrant.com/naughty-dog-last-of-us-movie-neil-druckmann/ Also praises Uncharted movie's origin concept https://screenrant.com/naughty-dog-uncharted-origin-movie-neil-druckman/ Black Panther Actress Chooses Jesus (What a link…) Letitia Wright Princess Shuri https://ijr.com/the-declaration/2018/02/1069827-black-panther-star-chooses-faith/?_hsenc=p2ANqtz-_hOMINNG8SOYkWkPc14BvJrXUf588Fj8H0Nm1ZitIhJPiEon-priURYBFI6mA5VbYi8ctZcCww_Fjex6oY0ptshuz6Mw&_hsmi=60917149&utm_campaign=Conser vative+Daily&utm_content=60917149&utm_medium=email&utm_source=hs_email Death of Superman First Image https://screenrant.com/death-superman-movie-first-look-image/ Mark Hamill Wants To Join Guardians 3 https://screenrant.com/mark-hamill-guardians-galaxy-3-james-gunn/ Kevin Smith Recovering From Heart Attack https://screenrant.com/kevin-smith-heart-attack-recovery/ http://comicbook.com/marvel/2018/02/26/kevin-smith-heart-attack-chris-pratt-james-gunn/ First Look At Krypton's Brainiac https://screenrant.com/syfy-krypton-tv-series-brainiac-first-look/ Netflix Reboot Reboot https://screenrant.com/netflix-reboot-guardian-code-trailer/ If you'd like to donate to our Pledge drive: www.youcaring.com/2018pledgedrive Represent the Podcast with the official shirt! www.geeksundergrace.com/shop For more Geeks Under Grace: http://www.geeksundergrace.com http://www.youtube.com/geeksundergrace http://www.twitter.com/geeksundergrace http://www.twitch.tv/geeksundergrace https://www.patreon.com/GeeksUnderGrace For more Cody Armour: http://twitter.com/CodyArmour https://www.youtube.com/ArmourCody For more Joe Morgan: http://twitter.com/JoeKnowsGames http://www.twitch.tv/righteousfurygaming http://twitter.com/righteousfuryg http://www.hitbox.tv/righteousfurygaming https://gaming.youtube.com/channel/UCvbAv8jROBkaDw3GfpnDEhg/live For more Shelley Waltar: http://twitter.com/theshellshock24 http://www.twitch.tv/shellshock24 If you'd like to contact our producer: Lj.Lowery@geeksundergrace.com https://twitter.com/WarHeroLJ

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Circulation January 30, 2018 Issue

Pinsemenigheten Betania Stathelle

Play Episode Listen Later Jan 29, 2018 20:47

Dr. Carolyn Lam: Welcome to Circulation On The Run. Your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. In just a moment, we are going to be discussing the diagnostic conundrum of elevated high sensitivity cardiac troponin levels in a patient with renal disease, but also suspected of acute coronary syndrome. Aha! I bet I caught your attention. A very, very familiar diagnostic dilemma. So stay tuned right after these summaries. Cardiac allograft vasculopathy is the leading cause of death in patients more than five years post cardiac transplantation. It has been hypothesized that cardiac allograft vasculopathy results from interrupted lymphatic drainage post surgery. Since the donor lymphatic vessels are not inesthimozed to that of the recipient during transplantation, thus the lymphatic system may play a crucial role in the alloimmune response. Well, these hypothesis are addressed in the first paper in today's journal from first author Dr. Edwards, corresponding author Dr. Wong and colleagues from Kings College, London. These authors use spect CT lymphoscintigraphy in a pre-clinical model. And therefore provided objective quantification of lymphatic flow following transplantation and showed that this correlated to cardiac allograft vasculopathy. They demonstrated that cardiac lymphatic remodeling and lymphatic transport dysfunction post transplant was associated with cardiac allograft vasculopathy and transplant rejection. They further showed that lymphatic flow was increased during chronic rejection. This in turn may have resulted in enhanced trafficking of antigen presenting cells to the local draining lymph nodes in an augmented alloimmune response. Now although the cause and effect of this phenomenon could not be fully established, these data provided the impetus for the investigation of lymphangiogenesis inhibition as a means to dampen chronic rejection. The absorb bioresorbable vascular scaffold is known to completely resolve within three years after coronary artery implantation. However, what is the safety and effectiveness of these bioresorbable scaffolds during this critical three year period. First author Dr. Ali, corresponding author Dr. Stone and colleagues from Columbia University Medical Center performed an individual patient level meta analysis of the four randomized absorb trial and demonstrated that compared with metallic everolimus eluting stents, the bioresorbable vascular scaffold had higher rates of target lesion failure and device thrombosis cumulatively to three years and between one and three years. Multi-variable analysis identified the number of treated lesions, current tobacco use and previous cardiac interventions as independent predictors of three year target lesion failure. Whereas diabetes was predictive of three year device thrombosis in bioresorbable vascular scaffold treated patients. The next paper reported the three year follow up of the FAME 2 trial, which compared PCI guided bi-fractional flow reserve with best medical therapy in patients with stable coronary artery disease to assess clinical outcomes and cost effectiveness. First and corresponding author Dr. Fearon and colleagues from Stanford cardiovascular institute showed that major adverse cardiac events at three years were significantly lower in the PCI group, compared with the medical treatment group. This difference was primarily as a result of a lower rate of urgent revascularization. Mean initial costs were higher in the PCI group, but by three years, were similar between the two groups. The incremental cost effectiveness ratio for PCI compared to medical therapy was more than $17,000 per quality adjusted life year at two years and $1,600 per quality adjusted life year at three years. Thus the authors concluded that percutaneous coronary intervention in patients with stable coronary artery disease and at normal fractional flow reserve may be advantages compared to with medical therapy alone, because it results in improved clinical outcomes and quality of life at no increased cost by the end of three years follow up. The next study shows for the first time, that pioglitazone may prevent stroke as a single stand-alone outcome. Today's paper by first author Dr. Yaghi, corresponding author Dr. Kernan from Yale School of Medicine and colleagues was a secondary analysis of the iris trial, which showed that pioglitazone reduced the risk for a composite outcome of stroke on myocardial infarction among non-diabetic patients with insulin resistant and a recent stroke or transient ischemic attack. Now, the current planned secondary analysis used updated American Heart Association 2013 consensus criteria for ischemic stroke to examine the effect of pioglitazone on stroke outcomes. The study found that pioglitazone reduced the risk by 25% by five years, with absolute rates of 8% with pioglitazone versus 10.7% with placebo. Pioglitazone reduced the risk for ischemic strokes, but had no effect on the risk of hemorrhagic events. These findings add to the evidence that pioglitazone may be a potent therapy for vascular disease risk reduction and may help inform shared decision making by providers and patients for the use of pioglitazone after ischemic stroke or transient ischemic attack. Well, that ends it for our summaries. Now for a feature discussion. The cardiac troponins have really revolutionized cardiology. We use them in of course the diagnosis of myocardial infarction and in fact the recent European Society of Cardiology recommendations say that the rapid zero and one hour triage algorithm for rule in or rule out of non STEMI should use high sensitivity troponins and interestingly irrespective of renal function. Now this latter point has caused some confusion, some questions, since we all know that patients with chronic kidney disease frequently have higher or increased levels of cardiac troponins, especially since we now can detect them with the high sensitivity essays. And this is even in the absence of an acute coronary syndrome. Well, this week's journal contains two papers that address this topic so well. And I am delighted to have with us the corresponding author of the first paper, Dr. Christian Mueller from University Hospital Basel in Switzerland and the author of the second paper, Dr. Nicholas Mills from University of Edinburgh in Scotland. For the more, we have Dr. Torbjorn Omland, associate editor from University of Oslo in Norway. Lot's to talk about. Christian, could I start with you? Could you say in your own words the rationale for looking at this vulnerable population and then perhaps describe what you did in your study? Dr. Christian Mueller: I'm very thankful that Circulation shed a lot of light on the population of patients with renal dysfunction, because both as a clinician and as a researcher, I'm definitely convinced that they merit a lot of our attention for several reasons. So first, it's important to be aware that the incidents of acute myocardial infarction among patients presenting with acute chest pain is much higher in patients with renal dysfunction, as compared to patients with normal renal function. And second, atypical clinical presentations also are more frequent in patients with renal dysfunction. Then possibly third, the ECG of course also a mandatory tool in our assessment is more often showing unspecific signs that may mimic or obscure the presence of myocardial infarctions and most of them are related to left ventricular hypertrophy. And in addition, patients with renal dysfunction are more prone to adverse events, both related to cardiovascular medication. For example, anticoagulation as well as our cardiovascular procedures, including PCI. Now again, as both papers have a strong focus on troponin, also cardiac troponin is a bit more difficult to interpret in patients with renal dysfunction related to exactly as you mentioned chronic elevations of cardiac troponin, TNI related to chronic cardiovascular disease. And I think that's so important to stress, any troponin signal in a patient with renal dysfunction is real and should not be incorrectly attributed to just a problem of impaired secretion by the kidneys. Dr. Carolyn Lam: So definitely an even greater need to diagnose myocardial infarction accurately in this very high risk population. So tell us what you did. Dr. Christian Mueller: We assessed this challenging sub group within the APACE study. So APACE is a large international prospective diagnostic study that is run in five countries with 12 centers. And we actually enroll consecutive patients presenting with suspected myocardial infarction. And then all patients get a very detailed workup and then adjudicated final diagnosis. And the adjudicated file diagnosis is done by two independent cardiologists and is based on two enormous extensive sets of data. The clinical data set that has been obtained at the local site and of course includes cardiac imaging and standard troponin testing, ECG data. In the second set of data that includes the study specific data sets, including serial measurements with high sensitivity carry troponin essay and a lot of details characterization of patients and patient follow up. So this is the reference standard against which the one hour algorithm the European Society of Cardiology evaluated. And the one hour algorithm has been derived and previously validated in overall population. Mainly patients with normal renal function. And so we tried to evaluate the performance of this predefined algorithm specifically in patients with renal dysfunctions. So among a bit more than 3,000 patients, the prevalence of patients with renal dysfunction was 15%. So we had about 500 patients with renal dysfunction. And the interesting finding from our work is that first the prevalence of N-STEMI was nearly threefold in patients with renal dysfunction as compared to patients with normal renal function. And, fortunately the rule out part of the algorithm regarding sensitivity still works very well. It is, however, the efficacy of rule out that is lower in patients with renal dysfunction, simply because fewer patients really have very low troponin concentration and are therefore ineligible for rule out. However, as a clinician, the main concern with troponin and renal dysfunction is the rule in part, and specificity. And as you would think, specificity of the one hour algorithm was in fact significantly lower in patients with renal dysfunction. It was still appropriate for therapeutic consequences, but it was lower as compared to patients with normal renal function, so the specificity was 89% in patients with renal dysfunction, as compared to 96.5% in normal renal function. So the overall efficacy of the algorithm was lower in patients with renal dysfunction, however then when trying to create and derive optimized cut off levels, so all cut off levels optimized for use in renal dysfunction, we didn't really find alternative cut offs that would do a much better job than the official cut off levels recommended in the guidelines. So our conclusion is that in patients with renal dysfunction, the safety of the one hour algorithm still is very high, however the specificity of rule in and overall efficacy are decreased. Dr. Carolyn Lam: Right. That's beautifully summarized. And also that different cut offs didn't really help to increase the efficacy of this algorithm. And just to clarify to our listeners, I believe you defined renal dysfunction as an estimated GFR of less than 60, which is so beautiful because it's perfectly consistent with the second paper. Nick, could you please tell us about your study and your take home messages as well. Dr. Nicholas Mills: So high stakes is our clinical trial that we're conducting across hospitals in Scotland to evaluate the best way to use high levels of cardiac troponin in clinical practice. One of the areas of uncertainty is whether these assets really add any additional value for patients with chronic kidney disease, where troponin concentrations tend to be higher. And the premise of a high sensitive test is that we can measure lower concentrations and improve the sensitivity. But is this just going to create uncertainty for clinicians? So we evaluated 5,000 consecutive patients for performance of high sensitivity cardiac to put in testing. And those with and without renal impairment. And based upon what Christian, we identified that patients with renal impairment are less likely to have very low concentrations, but that you can rule out myocardial infarction safely in patients with renal impairment. And similarly that those with renal impairment are more likely to have an abnormal troponin concentration at presentation. Around about 40% of all patients have troponins above the upper reference limit. And whilst the specificity for myocardial infarction is lower, type one myocardial infarction or myocardial infarction due to plaque rupture or cardiac thrombosis remains the most common diagnosis in this group. Finally we looked at one year outcomes. And this is really critical. Because we found that patients with renal impairment were two to threefold more likely to die from cardiovascular disease one year following their presentation than those without renal impairment. And I think that my general experience during these tests in clinical practice is that troponin elevations in patients with kidney disease are often ignored and there's a concern about what they mean, and therefore these patients don't get access to the fantastic treatments we have for coronary heart disease. So our take home message is that high sets of troponin testing in patients with renal disease does have value, it's useful for identifying low risk patients although there are fewer of them, and it performs well as a diagnostic test, highlighting in particular a group of patients that really have poor clinical outcomes. As a cardiological community, we need to do better. Dr. Carolyn Lam: What I really love about both or your papers is the consistency in the messages. Torbjorn, I want to bring you in on this. You managed both papers. Such a lovely pair of papers that we're so proud to be publishing and you had also invited an editorial by Dr. deFilippi and Seliger. Would you like to comment on your perspective and perhaps the clinical take home message to our audience? Dr. Torbjørn Omland: Yes, I think this has been pointed very well out by both Christian and Nick. And I think it's worth recapitulating that renal dysfunction is a major problem that clinicians often try to explain by just lack of renal filtration. But that the closest probably are increased production and underlying cardiac disease. So in the editorial Dr. deFilippi Filippi and Dr. Seliger points also out in these things. Moreover they try to look forward and have made comments to recent studies that showed that in patients with renal dysfunction have different troponin fragments than patients with acute myocardial infarctions. Dr. Carolyn Lam: I find that so fascinating. And it really, really relates to the field of heart failure and what we are also talking and thinking about with natriuretic peptides and their different fragments and the possible different meanings. And how different essays maybe non specific for different fragments. Christian, you think a lot about these things. I'm curious, what are your thoughts on this and areas of future work that are very urgent? Dr. Christian Mueller: I think Torbjorn very nicely addressed this. So the current high sensitivity essays for T and I that we use in clinical practice, they are designed kind of to detect everything in blood that looks like troponin, either T or I, including various fragments. And I think it's a fantastic new avenue of research, trying to find out that the biochemical signatures can be further differentiated and exactly that perhaps different troponin fragments or tricordinate products more prominent in patients having ischemic injuries like treat myocardial infarction, as compared to for example other modes of injuries. So I think that's very nice hypothesis and some early data. But at least from my perspectives and to the best of my knowledge until now, the diagnostic algorithms that we have other ways to approach this in clinical practice. And so it's the higher the blood concentration in patients with acute chest pain, the more likely it's acute myocardial infarction. It's not any chronic disease and again the higher the change from presentation to one hour or two hours, the more likely it's acute as a dynamic disorder resulting in an acute increase in cardiac troponin, as compared to the chronic release patterns typically seen in patients with renal dysfunction. Dr. Carolyn Lam: Yeah. That's just so fascinating. Nick, we sadly are running out of time, but I do want to give you the last word. The clinical take home message, once again. What do you think listeners should take home that may change their practice, after listening to this podcast? Dr. Nicholas Mills: I think the key message for clinicians, is that in a patient with suspected acute coronary syndrome and has renal impairment and elevated troponin concentration, serial testing is mandatory to differentiate between those that have chronic myocardial injury due to subclinical heart disease and those that are having acute myocardial injury as a consequence of a presumed acute coronary syndrome. Field testing is critical to inform which treatment path and what investigations we recommend for our patients. Dr. Carolyn Lam: Wonderful. And to take any elevations seriously, because this is a high risk population. Well, audience you heard it right here on Circulation On The Run. I'm sure you've enjoyed this. I certainly have. Don't forget to tune in again next week.

2018 02 04 - Torbjorn Tande

Play Episode Listen Later Jan 21, 2018 38:57

Bibelen er vaart speil

bibelen torbjorn

2018 02 04 - Torbjorn Tande

Pinsemenigheten Betania Stathelle

Play Episode Listen Later Jan 21, 2018 38:57

Bibelen er vaart speil

bibelen torbjorn

The Big Interview Quality V Cost With Torbjorn A. Pettersson From Telia Carrier

ROCCO RADIO

Play Episode Listen Later Dec 7, 2017 32:27

In all aspects of Telecoms we come to the question is it better to offer a service which is economical or that is focussed on high quality. Mostly we settle in the middle somewhere, but clearly the options are cultural and differ from one country to the next. Recently I had the great pleasure to talk to one of industries quality gurus, Torbjorn Pettersson from Telia Carrier. His insights and scope of knowledge is rare in our industry and we had a great discussion. Most people will know Torbjorn from his work in the GSMA but his history in telecoms is really extensive. A rare and interesting interview.

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Torbjorn (PLVL 1.16)

Prepare to Attack: Learn Overwatch and it's Characters

Play Episode Listen Later Nov 9, 2017

One of Torb's favorite sayings is "they always underestimate the engineer." In this episode you'll discover the best ways to use Torbjorn's abilities effectively, and be as efficient as possible with everyone's favorite engineer.

torbjorn torb

Torbjorn (PLVL 1.16)

Prepare to Attack: Learn Overwatch and it's Characters

Play Episode Listen Later Nov 9, 2017 63:33

torbjorn torb

74 - Omnic Lab: Going Deep: Zenyatta

Play Episode Listen Later Oct 15, 2017 86:53

In the Lab this week Andres & Rob sit down with another Top500 player, RossianSpy, to talk about Zenyatta on yet another transcendent edition in the going deep series. We’ll bring some yin and yang your way to hopefully experience tranquillity as you look to master this hero with us this week! Correction from Last week: Last week i misspoke about Sombra doing 50% bonus dmg to hacked targets. This is 100% incorrect. I should have said you can see targets at 50% health through walls with Opportunist like Widow Ult or Hanzo Sonic Arrow. Going Deep: Zenyatta What roles does Zen fill or what is his job in a game? What are the fundamentals of the hero (maybe for Low Tier play as well)? Let’s talk about using Discord Orb effective use. Vancity: how/who do you prioritize (target selection) when you are not in an organized group (solo queue) OmegaMan: how long do you keep discord on targets? How do you know when to switch? Let’s talk about using Harmony Orb effective use. How to do we get the most out of Charging up Orbs of Destruction? Choosing Primary or Volley? Transcendence breakdown When to use, where to be, who to prioritize How many kills is enough//Zoning Pressure Combo ult with what? Charging tips Can we chat about positioning and how to use your cover & team to maximize damage and pressure? Raynorwilky: how do you gauge distance from the front line during games? Are you usually far away or does the threat of flankers put you closer than you would like? Where's the sweet spot as between you & the front line? Switch: Are there times where it is okay to play aggressive vs conservative in positioning Now let’s work on proper engagement and disengages. Switch: How important is it for Zen to act as the shotcaller in soloq/comp environment? Matchups: Synergistic hero picks for team building with Zen. Heroes that give you trouble. Winston_Smith: any tips for dealing with a Tracer 1v1? Switch: There has been talk in the Overwatch community about new D.Va posing a particular problem for Zen (D.Va can dive and new missiles are high DPS vs. low mobility Zen). Your thoughts? News & Blue Posts: Omnic Meta: (Homepage) PC Meta Oct. 9, 2017 - Holy Mercy Mains Batman! Halloween Terror 2017 is out! Oct. 10 to Nov. 1 Skins: Symmetra, McCree, Ana, Torbjorn, Reaper, Mei, Zenyatta, Zarya Update regarding Gravestone availability in loot boxes Console Genji Bug: “Be aware that the Henji slash bug has made it to live on both consoles. This means that Henji can perform an extra slash during his ult activation animation, resulting in a very quick kill if he ults near an enemy. There appears to be a host of patch problems (queue errors, Zenyatta new skin voice lines not added) that have affected console only. Expect a follow up patch soon, and perhaps stay away from ranked if you fear the extra lethal Genji.” Special Thanks to Diamond Sponsors & New Patrons: Chrisdaplaya, Good Apollo, Lisome, Magic, Michael Crits, NotMuaddib, RcCrispy, RickyTicky, Silverback, Sketchy Nonsense Podcast, TragicZac, & Trinium. Omnic Lab Links: Twitter, Facebook, Patreon Twitch, Youtube, MERCH Discord: discord.me/omniclab Email: omniclabpodcast@gmail.com Website: http://www.omniclab.com iTunes, Google Play Music, RSS Full Extended Show Notes Rob: Twitter, Twitch, Velen's Chosen Podcast, Concept Craft Podcast Andres: Twitter, audioblender.studio, soundcloud RossianSpy: Twitter, Twitch, Youtube ConBeforetheStorm: Website, Bob’s Tweet “Don’t be a lab rat, be a scientist!"

strategy magic deep team twitch heroes va zen competitive correction lab overwatch comp charging composition reaper sombra google play music going deep orbs dps tracer opportunists omega man gravestones genji silverback mccree winston smith vancity switch how zenyatta torbjorn halloween terror top500 omnic low tier tweet don omnic lab switch there

63 - Omnic Lab: When Doomfist Comes Punching In

Play Episode Listen Later Jul 30, 2017 80:03

In the Lab this week we have the release of Doomfist to live with all the crazy updates to ranked and a big surprise for us for Attackers having an advantage in Overtime! Last we want to make sure we highlight the big rollout for the reporting toxic players feature. News & Blue Posts: Omnic Meta: (Homepage) Console Meta Report S5 W8 Possible Junkrat changes to PTR (Source) PVPTwitch Thoughts Video Possible Roadhog change coming to PTR (Source) OWL Signings & Salaries (Source) OW World Cup LA Tickets on sale $14.99-$39.99 (Source) LIVE: Reporting & Penalty System Improved (Blue Post) LIVE: Attackers’ Advantage//Defender Respawn adjusted (Blue Post) Patch Notes: 1.13.02 - General Doomfist is now playable. Lootbox Update!Credits instead of duplicates or more credits for when you do get duplicates New Highlight Options Top 5 Highlights available for 24 hrs or until the next patch Players can generate highlights 12s in the past from a button press command Adjusted Respawn timers as mentioned before. Custom Games & Browse User Interface CUSTOM RETICLES Options > Controls > Reticle > Advanced Valkia Reticle Tutorial Guide Video TIE GAMES NO LONGER INCLUDED FOR WIN PERCENTAGE CALC. Patch Notes: 1.13.02 - Heroes & Bugs D.Va Defense Matrix & Genji Deflect - New sounds & VO for eating ultimates McCree - Flashbang - Stunned targets slowed more heavily (mentioned before) Reaper - Shadow Step - Sound & VO distance reduced 50% (mentioned before) Reinhardt - Rocket Hammer - Swing Speed up 10% Zarya - Graviton Surge - Now disables mobility abilities on all affected targets Bugs: Could cause UI to incorrectly indicate enemies being hit when colliding with them. Projectilesthat could pass through shields sometimes passed through other surfaces. Sometimes losing audio during matches. Sombra took damage sometimes on using Translocator. Roadhog sometimes could hook Orisa Ult Rein’s Bloodhardt, Blackhardt, & Wujing skins now have sounds that sound like Axes! Rein’s Rocket Hammer had lots of hit registration bugs, all fixed. Lucio sometimes didn’t get full speed boost when wall-riding backwards. Torbjorn sometimes could not build/upgrade the turret. Special Thanks to Diamond Sponsors & New Patrons: Awestruct, Ben W, IceWeasel, HannibalSnowden, Lisome, Magic, Michael Crits, RcCrispy, Sketchy Nonsense Podcast, Spektr, TragicZac, Trinium, & Zampano. New Patrons this week (2 NEW): Kevin S & Chris C Omnic Lab Links: Twitter, Facebook, Patreon Discord: discord.me/omniclab Email: omniclabpodcast@gmail.com Website: http://www.omniclab.com iTunes, Google Play Music, Youtube Twitch, RSS, MERCH Full Extended Show Notes Rob: Twitter, Twitch, Hearthstone Podcast: Velen’s Chosen Andres: Twitter, audioblender.studio

strategy magic deep team twitch heroes players competitive lab overwatch comp overtime ui credits rein composition punching vo sombra google play music attackers lucio axes patch notes doomfist torbjorn roadhog omnic omnic lab translocator

Episode 37 - Doomfist and Torbjorn at IHOP

Play Episode Listen Later Jul 14, 2017 65:18

Doomfist now on the PTR! What about a Netflix original series? The stuff we talked about in the last show is on the PTR Kotaku dive methodology changing with Reaper Bungie.net profiles can now be linked to Blizzard authenticator. Closing Where to find us on social media @voiceofthebigjb, youtube.com/thebigjb, twitch.tv/streamthebigjb @DavidKidney1, All of this is on the homepage of our site Email: uberviewshow@gmail.com Website- UberViewshow.com Best ratings get read out on the show Thanks to everyone and bye

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57 - Omnic Lab: Going Deep: Torbjörn with DesRow

Play Episode Listen Later Jun 18, 2017 82:16

In the Lab this week we have our second defense hero in a row, Torbjorn for the next going deep! We have a top GM torb player DesRowFighting here with us to help strategize about the hero! Additionally, we got some cool news to cover with you all! News & Blue Posts: Destiny 2 PC Release day announced for Oct. 24th. $60/$90/$100 Price points 2 Planned Expansion Omnic Meta: S5 W2 Console Meta Torb Community Questions: MrStealYoBeef - What would you consider is the sneakiest torb turret you've ever used on an enemy team? How effective was it? SonicShadow - What made you pick Torb in the current meta where people disagree with Torb? What separates a good Torb from a bad one? How does someone use Torb on Attack? L chris L - When do you decide to throw down a lvl 1 turret asap or to strategically go for lvl 2? Bioshrimp - How do you deal with haters? InfiniteNo1 - Are there any skins that give you or turret any camo/visual advantage? Reef - How does dive comp effect your torb play? Egwollz - Are there any specific "pro" strategies regarding utilizing and deploying armor packs for yourself and your teammates? Switchfox - Any particular heroes that give Torb trouble in 1v1s? How much does keeping turret up 100% of the time matter? What is a good hero to duo-queue with if I want to climb as Torb? VirtualDJ - Is it worthwhile to put a turret near enemy spawn at start of match on certain maps versus having the protected turret toward the back line from the start? Tyserian - When should you treat your turret as: An Extra DPS source: putting it behind a shield (Classic Dorado First Engagement). A Back-Line Defender: placement in a protected spot that can only shoot people after they've reached a point (Numbani Point A Small Room). Flanker’s Protection: placement where it fires warning shots and slows down common flanking routes (Volskaya Point A High Ground). Special Thanks to Diamond Sponsors & New Patrons: Ben W, IceWeasel, HannibalSnowden, Jason A, Lisome, Magic, Michael Crits, RcCrispy, RoadtoSwole, Sketchy Nonsense Podcast, Svornair, TragicZac, Trinium, & Zampano. Omnic Lab Links: Twitter, Facebook, Patreon Discord: discord.me/omniclab Email: omniclabpodcast@gmail.com Website: http://www.omniclab.com iTunes, Google Play Music, Youtube Twitch, RSS, MERCH Full Extended Show Notes Rob: Twitter, Twitch, Hearthstone Podcast: Velen’s Chosen Andres: Twitter, audioblender.studio DesRowFighting: Twitter, Twitch, YouTube

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Circulation April 25, 2017 Issue

The League of Ridiculous Conversations Podcast

Play Episode Listen Later Apr 24, 2017 19:29

Dr Carolyn Lam: Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore. Our feature paper this week really adds to our understanding of the cause/effect relationship between obesity and heart failure, this time by comparing the effects of gastric bypass surgery versus intensive lifetime treatment on heart failure risk. Before we talk about that, though, let me give you your summary of this week's journal. The first paper brings us one step closer to understanding cardiac recovery in response to mechanical unloading by left ventricular assist devices and it does this by showing that this process may involve the transverse tubular system, which is a micro structural feature of ventricular cardiomyocytes important for contractility and consisting of tubular invaginations of the sarcolemma predominantly located at the Z-lines of sarcomeres. This transverse tubular system is crucial for efficient excitation contraction coupling by bringing L-type calcium channels in the sarcolemma in proximity to clusters of ryanodine receptors in the sarcoplasmic reticulum. In the current study by co-corresponding authors, Dr. Seidel and Drakos and Sachse from University of Utah, the authors studied left ventricular biopsies obtained from five donors and 26 patients with chronic heart failure undergoing implantation of left ventricular assist devices or LVAD's. They used three dimensional confocal microscopy and computational image analysis to assess the transverse tubular system's structure, density, and distance of ryanodine receptor clusters to the sarcolemma. They found that the majority of heart failure myocytes showed remarkable transverse tubular system remodeling, particular sheet-like invaginations of the sarcolemma, which is previously unknown phenotype. This sheet-like transverse tubular system remodeling led to increased distances of ryanodine receptors to the sarcolemma causing heterogeneous intracellular calcium release and consequently inefficient excitation contraction coupling. High degrees of transverse tubular remodeling at the time of LVAD implantation was associated with absence of functional cardiac recovery during mechanical unloading, whereas preserved transverse tubular systems structure was associated with recovery. In summary, cardiac recovery during unloading may require an intact transverse tubular system at the time of LVAD implantation. And characterizing this system may help to identify patients with a high probability of functional cardiac recovery in response to mechanical unloading. There have been a proliferation of algorithms based in high sensitivity assays for cardiac troponins for the diagnosis or exclusion of myocardial infarction. All these algorithms have the potential to overwhelm clinicians with options. Well, there is help in this week's issue with two observational studies directly comparing the diagnostic performances of multiple high-sensitivity troponin testing strategies. Now, before I describe these two studies in detail, here are some important reminders. Remember that as of early 2017, although high-sensitivity troponin assays are routinely used in many regions of the world, they are not available in the United States. Thus, the specific algorithms discussed here are not applicable with the contemporary sensitive assays that are presently used in the United States. Next, let's remind ourselves that both the United States and European professional guidelines recommend serial measurement of cardiac troponins at presentation or zero hours and three to six hours later with additional testing beyond six hours in patients who have electrocardiographic changes, or intermediate or high clinical risk features. The 2015 European Society of Cardiology Guidelines also included an alternative strategy reducing the sampling interval to one hour when using a high sensitivity troponin assay with a validated zero and one hour algorithm based on the 99 percentile cutoff of these high sensitivity troponin assays. Now to the two studies in the current issue, which tie together the expanding evidence with direct comparisons of several of the strategies using the same high sensitivity cardiac troponin assay by Abbott. Dr. Chapman and colleagues from the royal infirmary of Edinburgh, United Kingdom, compared the standard ECS zero and three hour strategy based on the 99th percentile upper reference limit at both time points with the high sensitivity troponin in the evaluation of patients with acute coronary syndrome, or high stakes algorithm, and that would be a zero, three, and six hour algorithm that incorporates a zero hour criteria and at a very low cutoff of five nanogram per liter and a three hour criterion that directs patients with either a rising concentration or with an absolute concentration above the upper reference limit to additional testing. Among 1,218 patients with suspected myocardial infarction, the high stakes algorithm delivered both a higher proportion ruled out for myocardial infarction at zero hours and a higher negative predictive value of 99.5% versus 97.9%. The ESC pathway missed 18 index and two recurrent myocardial infarction events, whereas the high stakes pathway missed two index and two recurrent myocardial infarction events. These findings demonstrate the value of adding a very low zero hour cutoff to facilitate earlier rule out as well as the value of a delta criterion to exclude increasing values among patients that progress to three hour sampling. In the next study, first author, Dr. Boeddinghaus, corresponding author Dr. Mueller and colleagues from University Hospital of Basel, Switzerland compared the ESC alternative zero and one hour strategy with three other approaches using either a single cutoff at zero hours, or the one hour strategy. Among 2,828 patients with symptoms suspicious for myocardial infarction and no ST elevation, each of these four approaches delivered a negative predicted value above 99% comparing favorably to the ESC zero and three hour algorithm that had a negative predictive value of 98.4%. Now, although each of the strategies performed similarly among patients presenting more than two hours after symptom onset, among the early presenters, the negative predictive value and sensitivity were diminished using the single zero hour cutoff of five nanograms per liter. The authors concluded that the single cutoff strategy, the one hour algorithm, and the zero and one hour algorithm, allow the triage towards rule out of myocardial infarction in more than half of consecutive patients presenting with suspected MI to the emergency department. However, the single cutoff strategy should not be used in patients presenting early after chest pain onset. These papers are discussed in an excellent editorial, which also puts everything in perspective by Dr. David Morrow from Brigham and Women's Hospital in Boston, Massachusetts. I particularity want to refer all of you to the figure that's found in its editorial which really helps you to understand the different strategies involved. The final study tells us about potential death averted and serious adverse events occurred from the adoption of the SPRINT intensive blood pressure regimen in the United States. As a reminder, the systolic blood pressure intervention trial, or SPRINT demonstrated a 27% reduction in all caused mortality with a systolic blood pressure goal of less than 120 versus less than 140 mm Hg among American adults at high cardiovascular risk, but without diabetes, stroke, or heart failure. In the current study, Dr. Bress and colleagues from the University of Utah School of Medicine applied the SPRINT eligibility criteria to the 1999 to 2006 National Health and Nutrition Examination Survey or NHANES and linked this with the national death index through December, 2011. They found that if fully implemented in eligible US adults, intensive blood pressure treatment was projected to prevent about 107,500 deaths and 46,100 of heart failure per year. But, you also give rise to about 56,100 episodes of hypertension. 34,400 episodes of syncope, 43,400 serious electrolyte disorders, and 88,700 of acute kidney injury per year compared to standard blood pressure treatment. Thus, they take home message is careful patients selection and implementation are important because intensive treatment while preventing deaths is associated with increased risks of hypertension, syncope, electrolyte abnormalities and acute kidney injury. Well, that brings us to a close for the summaries, now for our feature discussion. We are discussing obesity and heart failure. Now, we've heard of the obesity paradox, but we also know that obesity may be a risk factor for heart failure and the study today really puts perspective on this and is really one of the largest most convincing studies I've read on this topic. I am so pleased to have the person corresponding author, Dr. Johan Sundstrom from Uppsala University Hospital in Sweden. Welcome, Johan. Dr Johan Sundstrom: Thank you, lovely to talk to you. Dr Carolyn Lam: And especially pleased to have back on the show again, Dr. Torbjorn Omland from University of Oslo, Norway. Hi, welcome back, Torbjorn. Dr Torbjorn Omland: Thank you very much. It's a great pleasure being here. Dr Carolyn Lam: Johan, you know what? Could you just start by telling us about your study? Dr Johan Sundstrom: So, we were fortunate enough to have two great databases here in Sweden. One was the obesity surgery registry called SOREG in which all people have a gastric bypass surgery, for people who are registered. And we also have a company called Itrim who provide intensive lifestyle program, which takes people down on average about 11 kilos, and they have a very structured database as well. So, we were able to pull this data in order to try and understand the effects of intentional weight loss to two different levels of weight loss, what that does to the heart failure incidence. This is a bit of a comparative effectiveness study, so it's of course necessary to make the examples as similar as possible to apply exclusion criteria. We took away everyone who had a body mass index of less than 30 and above 50 and then we applied propensity scores to those two data sets and we had to trim the data sets a little bit further in order to get so called region of common support, which means that we were left with two samples who could have either had surgery or a lifestyle intervention. And then we applied an inverse probability weighting scheme to that. It's statistically complicated but what that does, is it's a matching, but it's not as complicated as matching. With matching, you just give people a weight of 1 or 0, but this gives people other weights as well. So, we end up with characteristics that were very similar at baseline. So, we tried to mimic as close as possible what a randomized clinical trial looks like, but of course we did it posthoc and it's observational. So, we get our table one, sort of, in this paper that shows very similar characteristics of the two groups. So, what we did then is we noted what happened to the people in these two groups in terms of heart failure incidence and we followed them in our national inpatient registry. So, all the Swedish citizens get a personal identification number so we can use that to follow people in our patient registry. So, we know exactly what drugs people will collect from pharmacies, and we know what they died from, and we know all of their hospitalizations. And we previously validated their heart failure diagnosis in the Swedish Inpatient Registry and we noted that you were in a pretty good position if you were hospitalized with heart failure as the main cause of hospitalization and we noted that people who had agreed to do surgery, had about half the incidence of heart failure than people who were in the intensive lifestyle program. We also noted, if you looked at the achieved weight loss one year after baseline, we noted that a ten kilo weight loss after one year was related to about a 23% lower risk of heart failure. So we noted a litany of association between the achieved weight loss and heart failure incidence. It should said, though, that heart failure in this age group, they are only 41 on average, 41 years old. Heart failure's still very unusual at this age, even in many of these people. We only had 73 cases of heart failure. So, the exact numbers need to be taken with a pinch of salt and have wide confidence intervals around them. Dr Carolyn Lam: Johan, this is exactly why I'm so impressed with your data. First you showed a dose response relationship between the weight loss and risk of heart failure. You also show that it's not an event that occurs very often and so, it would be very difficult to imagine doing a randomized controlled trial for example in this setting and having to wait very long for these events. So, it really goes to show your observational data are extremely important. And I really like the way you took the pains to describe how you tried to overcome the differences that exist between the groups and try to make it as much resembling a randomized trial setting as you could. So, maybe I could turn it over to you, Torbjorn. Could you tell us what you think the implications of this paper are? Dr Torbjorn Omland: First, I will say that that this paper has all the characteristics of a very high quality study. It's a very timely topic that interests a lot of people. The paper's very well written. It's a large sample size as you said and it was very clinically meaningful difference between the groups and that translated into very clear and robust answers. So, I think that this has every mark of high quality paper. But, of course, the very important question is how will this translate into actions? How can we use this information to prevent problems? We know heart failure is a very prevalent disease, especially in the elderly and although the incidence was lower here, I think my question for Johan at least is what would be the next step? What changes can we implement to reduce heart failure among the obese? Dr Johan Sundstrom: That's a great question. I think in this study puts a little piece of the puzzle on the table and that's trying to add a little more evidence towards a causal association between obesity and heart failure. I'm not sure about what we can offer these patients and what will be the translation to lower heart failure incidence in the long run. Of course, we need to follow this sample for longer to have more heart failure cases, because I don't think we've seen the full impact of weight loss in these two samples. We might need to follow them into older age where they would have a higher heart failure incidence. But, how to tackle obesity, I think we'll need accommodate population strategies and high risk strategies. I think if the general consensus in the scientific community after reading this and other important papers, is that there's causal link between obesity and heart failure, then we might need to understand that people who are obese and who have shortness of breath and perhaps swelling or what not, may not just be having low fitness, they might actually behaving signs of heart failure. So, I think as a sort of increased diligence on heart failure, these people might be one thing. But, we didn't really study that. So, I wouldn't draw conclusion. But, otherwise I think it's more of a causal inference piece of the puzzle that we've laid rather than a clinical care piece of the puzzle. Dr Torbjorn Omland: No, I agree, and here you won't to make any recommendations in regards to what interventions you should recommend particularly based on this particular study. Dr Johan Sundstrom: No, because I think there are so many other things that need to be taken into account when it comes to treatment of obesity. Heart failure is actually one of the uncommon outcomes in this age group. We're looking at other outcomes after they present. Myocardial infarction, ventral fibrillation and mortality are actually much more common. So, I think a lot of other data should go into decisions on how to treat patients, not just for heart failure, which is still fairly uncommon at this age. Dr Carolyn Lam: Going back to the other question that Torbjorn asked, do you think that this question still needs to be answered in any way? You've got the Mendelian randomization data. Now, you've got your data. Do you think it's still a question of whether obesity is a risk factor for heart failure? And just in case there's any confusion out there, would you put that together with the so called obesity paradox in heart failure? Dr Johan Sundstrom: To answer the first one, I think we're not going to have any randomized evidence. Treatment of heart failure with intensive programs and prevention of heart failure ... It needs for huge samples that I don't think we're going to have any much better observational evidence anytime soon either. So, we can probably set that question aside a little bit. But, when it comes to the obesity paradox, first of all that's not what we studied here. We didn't have anyone with heart failure in this sample. We included all those people. We can only speculate. I'm a clinical epidemiologist myself, but I'm envious of people who have animal and other models because I think there's a lot more work to do in terms of ppars and and lipid metabolism in obesity and in heart failure. So, I think there'll be more interesting experimental research to come that can help us answer the obesity paradox. Dr Carolyn Lam: Please don't forget to tell your friends about this podcast, and tune in again next week.

Super League of Ridiculous Hammer Bros Part 2

Play Episode Listen Later Apr 21, 2017 93:10

Welcome to PART 2 of this Overwatch lovefest! Did you miss Part 1? Then go check out our buddies at (on iTunes and social media) to hear Jordan aka JordanIsABear and Anthony aka KillSpookyKill join GrizGeek to hear where this all began. In Part 1 we talked about our Mains, our hated enemies, and the Lore, in Part 2 we get into our favorite stages, some tips for our favorite characters, and more mechanics of the game. #AnaBanana Follow, Friend, and Like Us on / / Subscribe to us on / Email us at lorcpodcast@gmail.com

Episode 28 - An Upstanding Uprising

Watchpoint Radio – Overwatch News, Discussion, and Community

Play Episode Listen Later Apr 17, 2017 41:19

The latest event is incredible! And not necessarily focused on a particular season. JB and Brandon sing their praises and also talk about how much they'd be willing to pay for skins they want instead of loot boxes. Especially the fan-created Betrayer skin for Reaper.

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#36: Keep it in Your Pants, Torbjorn.

Play Episode Listen Later Dec 20, 2016 79:36

Tracers gay, Torbjorn can't keep it in his pants, we hope you like Tanks, and there is still hope for Sombra.

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Old School (Reinhardt & Torbjorn Overwatch Lore) – KTLO 05

Know The Lore: Overwatch

Play Episode Listen Later Aug 4, 2016 13:00

In this episode of Know the Lore we continue to figure out info on the mysterious Sombra based on information from San Diego Comic Con, and then talk about a couple old favorites, Reinhardt and Torbjorn! Facebook: http://facebook.com/nerdsloth Twitter: https://twitter.com/nerdsloth Website: http://NerdSloth.com/category/podcast/ktlo/

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Episode 50 interview with Keith Silverstein

Popanimecomics Lounge

Play Episode Listen Later Jul 16, 2016 51:08

Episode 50 Interview with Keith Silverstein What we talk about : How he first got into voice acting His first role His early days in voice acting Many of his anime/ cartoon roles including Timber Wolf, Naruto, Sailor Moon Other roles : Bleach, Eureka Seven, Honey and Clover Monster as Johan Liebert and how this role was different from other roles His role in Rozen Maiden as Laplace and Dective Kun-Kun His role in Gundam Unicorn as Full Frontal and in Gundam : the Origin as Char His role in Iron Blood Orphans and Hunter X Hunter And finally with his anime roles we talk about Glitter Force We also talk about his video game roles of being the character Hunk, Vector the Crocodile and as Torbjorn from Overwatch and as always we pick his brain for advice for people who want to become voice actors

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Avsnitt 71 - Torbjorn Persson

MAXstyrka Radio

Play Episode Listen Later Jul 8, 2016 51:29

I avsnitt 71 av MAXstyrka Radio bjuder vi in Torbjörn Persson in i studion. Torbjörn pratar om sin deformerade arm, berättar hur man kan underlätta gripperträning och hur man breder smörgåsar med vänsterhanden. 00:01 – Intervju med Torbjörn Persson 47:30 – Intervjun är slut 51:28 – Slut

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Episode 79 - Cobblers and Totems

Geeks of Azeroth - A Podcast for Blizzard Gamers

Play Episode Listen Later Jun 28, 2016 66:43

Starcraft 2 ladder changes: https://twinfinite.net/2016/06/starcraft-ii-ladder-revamp/ Overwatch Ranked mode hits PTR: https://playoverwatch.com/en-us/blog/20157263 Overwatch to nerf overpowered Torbjorn (on consoles): http://www.gamespot.com/articles/overwatchs-torbjorn-is-being-nerfed-heres-how-and-/1100-6441259/ Quitters Never Win: Leave mid-game in Overwatch too often and you could be banned for a season: http://www.digitaltrends.com/gaming/overwatch-penalizing-for-leaving-mid-game/ Professions Q&A: http://www.wowhead.com/news=253765/6-23-weekly-legion-developer-q-a-professions-with-senior-game-designer-paul-kubi ____________________________________________________ Thank you very much for listening. Our show, as always, is available in iTunes, Stitcher, Youtube, and Twitch You can also catch us on Twitter: @GeeksofAzeroth Tarley - @Tarley_pawz Britzza - @Britzza_EG Big Voodoo - @b1gv00d00 Icarus - at Wendys You can contact the show with your messages, questions, and shout outs via geeksofazerotheg@gmail.com And remember to check us out on www.epicgeeks.co.uk for more shows. We’ll be back same time, same place next week - until then have a great week in Azeroth.

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Overtime – Ep 5 – EdgeReaper

Overtime: An Overwatch Podcast

Play Episode Listen Later Jun 28, 2016

In this weeks episode we cover -Torbjorn console nerfs -Competitive mode is introduced -We discuss Zenyattas role in competative -Dive into how to play Reaper All this and more on this episode of Overtime! Follow Overtime on Twitter at https://twitter.com/OW_Overtime and email questions to owovertime@gmail.com

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Overwatch: Defense (MOLTEN COOOORE) EP 94

NNZ (The Numbaz)

Play Episode Listen Later Jun 25, 2016 60:00

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Episode 36: Overwatch Is Fun As Hell

Kotaku Splitscreen

Play Episode Listen Later Jun 23, 2016 72:24

In the wake of E3, the only big news Kirk and Jason really want to see is a Torbjorn nerf. Today we're talking E3 recovery, Zelda, the power of Overwatch, and some of the other games we're playing these days. Plus some bonus Game of Thrones talk!

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11 - Omnic Lab: Offense & Pressure

Play Episode Listen Later Jun 18, 2016 88:56

In the Lab today we have TONS to chat about. We’re going to talk about the newest patch notes, balance changes, a big Blue Post from O Captain, My Captain Jeff Kaplan, and the main strategies for playing offense and putting on pressure! What We’re Testing: *Rob: finally found a main character! MERCY BOYZ. Testing: Mercy, Pharah, Torbjorn, & Junkrat on defense for damage boosts. Also testing: Mercy, DVa, Genji, Widowmaker/Soldier 76, Bastion/Pharah, Roadhog/Zarya (Comp we ran at the LAN) *Andres: Testing out the new McCree changes & alternating to soldier 76...Practicing a lot of Genji! News & Patch Notes: *10 Million Players in Overwatch! (June 14) https://twitter.com/PlayOverwatch/status/742761244159942656 *Patch Notes: --McCree Fan the Hammer - 45 dmg (was 70)//0.3s (was 0.75s) --Widowmaker Ultimate charge 10% longer to charge//scope animation must finish before rescoping//base damage - 12 (was 15) (MAX 120 - was 150)//headshot ratio increased to 2.5x (was 2.0x) --Misc. Bug fixes: *Cynical Nerds’ Max opinions on the Blue Post: https://youtu.be/sRTxcij0-Mw *MEGA Blue Post by Kaplan: http://us.battle.net/forums/en/overwatch/topic/20745285677#post-12 Picking a balanced Offensive Team: 1. Area Control/Soakers 2. Frontline Damage 3. Main Support 4. Long Range Cover 5. Flanker 6. Utility/Flex The 4 Steps of Attack: Recon, Prep, Execute, Recoop *Reconnaissance: Scout Enemy heroes and positions. Take out out of place heroes and clear starting area. Send out flanker to scout and dispose of appropriate threats. *Preparation: Build up ultimates. Define an attack route and position the team. Define key Target(s). Neutralize key defenses and look for an OPENING. *Execution: Once the call has been made move to be point as a team. Focus key targets quick. Commit! Move as a team, die as a team. Continuous pressure is key! *Recuperation: Regroup after wiping, resist the urge to go solo. Reassess: what caused the wipe? Team Composition. Team positioning. Sloppy execution. Poor teamwork. Simply Outplayed. Back to preparation! Special Thanks: Scientist Level Patrons: Brian K and Blackbyrd thanks again for your generous pledges for the Scientist Level of support, when your payment clears we’ll get started on your perks! *Also thanks to our brand new Patrons this week: LA Instrumental,Toby H, & Eric S (New Scientist Level Patron!) *Also thanks to our iTunes reviews from: Totemlydrunk, Wickedella, HugeFan18, Tautsu, Jposty, PvP Necro, Maxx Hubris, Jbport, BaileyMatt6102, Dij4, & Goose792! Links for the Week: *Overwatch Myths Vol.4: https://youtu.be/FxdmvNEz7e0 (reaper teleport myth may have changed this patch) *Getting Better at Overwatch Parody: https://youtu.be/A2oSItJ-hBg *The Deep Japanese Culture behind Hanzo & Genji:https://www.youtube.com/watch?v=3Xth8OsQaDo *Funny Kaplan Response to UI Request:http://us.battle.net/forums/en/overwatch/topic/20745255910?page=2#post-22 You can find the Omnic Lab on: *Twitter: https://twitter.com/OmnicLab *Facebook:https://www.facebook.com/omniclab *Discord: discord.me/omniclab *Email: omniclabpodcast@gmail.com *iTunes: https://itunes.apple.com/us/podcast/omnic-lab-podcast/id1102068116 *Google Play Music: https://goo.gl/app/playmusic?ibi=com.google.PlayMusic&isi=691797987&ius=googleplaymusic&link=https://play.google.com/music/m/I4y3phepidybxbkdmdvccdcr44m?t%3DOmnic_Lab:_A_Strategic_Overwatch_Podcast *Patreon: https://www.patreon.com/omniclab *Youtube: https://www.youtube.com/channel/UCZsJLxSSdwXqvh0M5BzpvbA *Twitch: https://www.twitch.tv/omniclab *Website: http://www.omniclab.com *RSS: http://feeds.feedburner.com/omniclab *Full Extended Show Notes:https://docs.google.com/document/d/1CNuwFR5G_ulAGBONM1DzYTvV-DteXRLpGMpDSpf2BqE/edit?usp=sharing Rob here: *Twitter: https://twitter.com/notrob *Facebook: https://www.facebook.com/notrobmedia *Twitch: http://www.twitch.tv/notrobmay *Hearthstone Podcast: www.velenschosen.com And Andres here: *Twitter: https://twitter.com/IplaiGames *Twitch: https://www.twitch.tv/iplaigamez *Hearthstone Podcast: www.coinconcede.com

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09 - Omnic Lab: Defense & Setting Up

Play Episode Listen Later Jun 3, 2016 80:43

In the Lab today we break into strategizing about defense! We’re going to talk about compositions, rough positioning, and concepts for how to set-up a team strategy for defense. We’ll even cover map-specifics to the best of our ability for the audio-only listeners! News & Patch Notes: *Overwatch Tweaks coming for D.Va, Reaper, and McCree: http://www.ign.com/articles/2016/06/01/overwatch-tweaks-coming-for-mccree-dva-and-reaper *Blizzard drops the Ban Hammer again on cheaters: http://kotaku.com/thousands-of-overwatch-players-have-already-been-banned-1780109893 What We’re Testing: *Rob: Practicing a lot of Soldier 76, Symmetra, Mercy, Zarya, and McCree. **Cool Team Composition: Soldier 76, Tracer, McCree, Reinhardt, Mercy/Lucio, Flex Spot. *Andres: Finally started a competitive team! Practicing as Support/Flex (Lucio, Symmetra, Winston, McCree) **Composition we are practicing as Team: Reinhardt, Mercy, Lucio, McCree, Widowmaker, Flex (Zarya, McCree, Winston, Torbjorn) Playing Defense in Overwatch: Playing defense in Overwatch can be one of the most challenging modes, specially if going against an organized team. Poor communication and organization can lead to a quick demise and not a great feeling! A solid defense on the other hand can be demoralizing for the enemy team. 1. The objective is everything: **From the start of the game the objective and map layout will dictate everything. Ask yourself these questions: a) Is it a payload, point capture or both? b) What roles need to be filled? (map specific, not team specific). 2. Establish a choke-point. 3. Protecting access routes (parts of the map that go around the main routes). 4. Look-out after each other. 5. Have a contingency measure (Planned Panic Button) 6. Learn when to retreat! Special thanks to our first Patreon supporter Lance K. Also thanks to the amazing folks giving us itunes reviews: Blackbyrd3, DanBeforeTime, Nick1742, Bobsta14, & Anthony! Ya'll are the best! Links for the Week: *AskJoshy: Map Call Outs: King’s Row Video:https://www.youtube.com/watch?v=sLfqDmBACrM *AskJoshy: Map Call Outs: Hollywood Video: https://www.youtube.com/watch?v=Ypk7dy_Ki7s *AskJoshy: Map Call Outs: Dorado Video: https://www.youtube.com/watch?v=VR4Wgf2Jg9A *Overwatch Myths Vol.1: https://www.youtube.com/watch?v=WG53pICIGIo *Overwatch Myths Vol.2: https://www.youtube.com/watch?v=5WbSRlRyEE0 *Hang in League of Overwatchers Discord with all other content creators: https://discordapp.com/invite/0hXPcX6IxHepRXAj You can find the Omnic Lab on: *Twitter: https://twitter.com/OmnicLab *Facebook:https://www.facebook.com/omniclab *Email: omniclabpodcast@gmail.com *iTunes: https://itunes.apple.com/us/podcast/omnic-lab-podcast/id1102068116 *Patreon: https://www.patreon.com/omniclab *Youtube: https://www.youtube.com/channel/UCZsJLxSSdwXqvh0M5BzpvbA *Twitch: https://www.twitch.tv/omniclab *Website: http://www.omniclab.com *RSS: http://feeds.feedburner.com/omniclab *Full Extended Show Notes: https://docs.google.com/document/d/1X7AIGw4HXgiiCfxKXWHy8HSTtpYmATEMIkj0GTZ1vyw/edit?usp=sharing Rob here: *Twitter: https://twitter.com/notrob *Facebook: https://www.facebook.com/notrobmedia *Twitch: http://www.twitch.tv/notrobmay *Hearthstone Podcast: www.velenschosen.com And Andres here: *Twitter: https://twitter.com/IplaiGames *Twitch: https://www.twitch.tv/iplaigamez *Music Work: In the works...soon ™ *Hearthstone Podcast: www.coinconcede.com

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Born in the Eighties 216: #Gandalfvapelife

Born in the Eighties

Play Episode Listen Later May 16, 2016 91:48

The Gandalfs of the future will all be piping sick ass e-liquids. Jon leads his space-foxes to prosperity throughout the galaxy in Stellaris. Matt wants to get a new GTX 1080 video card, which would make Overwatch run that much better. Adam, the honorary Vape King, returns from an assignment at the theater, and promises are made about Jon's diary next week. Don't be a serial vapist, download this episode! #gandalfvapelife,e-liquid,civil war,marvel,captain america,iron man,Stellaris,space fox,monk,gandalf,vape tricks,wizard khalifa,overwatch beta,reaper,torbjorn,d.va,tracer

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05 - Omnic Lab: Basics: Defensive Heroes