Podcasts about intrigued well

Pete and Aaron have a bit of news from Hyundai including a clutch-less manual transmission! Intrigued? Well have a listen now!

In this episode the Histories of the Unexpected team of James Daybell and Sam Willis take on the topic of RABBITS - as an Easter Special! Now, of course, the UNEXPECTED history of loneliness is all about poaching and disputes over land; eighteenth-century England and Mary Toft who allegedly gave birth to rabbits (it was a hoax!); Aborigines and the Stolen Generation in Australia; mapping rabbit warrens in Devon; and bizarrely enough, dead cats soaked in aniseed. Intrigued? Well listen up See acast.com/privacy for privacy and opt-out information.

In this episode the Histories of the Unexpected team of James Daybell and Sam Willis take on the topic of RABBITS - as an Easter Special! Now, of course, the UNEXPECTED history of loneliness is all about poaching and disputes over land; eighteenth-century England and Mary Toft who allegedly gave birth to rabbits (it was a hoax!); Aborigines and the Stolen Generation in Australia; mapping rabbit warrens in Devon; and bizarrely enough, dead cats soaked in aniseed. Intrigued? Well listen up See acast.com/privacy for privacy and opt-out information.

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. Dr Greg Hundley:             And I'm Greg Hundley, associate editor at Circulation and director of the Pauley Heart Center at VCU Health in Richmond, Virginia. Carolyn, have you ever wondered about instead of coding a stent, coding balloons with paclitaxel? Well, the feature article day is going to look at mortality assessments of paclitaxel-coated balloons in a meta-analysis from the ILLUMENATE clinical program, the three-year outcomes. Do you have a paper you want to start us off? Dr Carolyn Lam:                I sure do. First of all, we know that diabetes impairs atherosclerosis regression following cholesterol lowering in both humans and mice. Now in this process of plaque regression, what's the role of functional high density lipoprotein or HDL, which is typically low in patients with diabetes?                                                 Well, this first paper that I chose looks just at that and it's from Dr Fischer from New York University School of Medicine and colleagues, who aimed to test if raising functional HDL levels in diabetic mice prevents monocytosis, reduces the quantity and inflammation of plaque macrophages and enhances atherosclerosis regression following cholesterol lowering. So to do this, the authors used aortic arches containing plaques, which were developed in LDL receptor null mice, and these were transplanted into either wild type or diabetic wild type or diabetic mice transgenic for human APL lipid protein A1, which have elevated functional HDL. Dr Greg Hundley:             So Carolyn, what did they find in this interesting study? Dr Carolyn Lam:                Well, diabetic wild type mice had impaired atherosclerosis regression, which was normalized by raising HDL levels. The benefit was linked to suppressed hyperglycemia-driven myelopoiesis, monocytosis and neutrophilia. Increased HDL improved cholesterol efflux from bone marrow progenitors, suppressing their proliferation and monocyte neutrophil production capacity. ACL also suppressed the general recruitability monocytes to inflammatory sites and promoted plaque macrophage polarization to the M2 phenotype, which is an atherosclerosis resolving state. There was also a decrease in plaque neutrophil extracellular traps or nets, which are atherogenic and increased by diabetes. So raising apolipoprotein AI and functional levels of HDL promoted multiple favorable changes in the production of monocytes and neutrophils and in the inflammatory environment of atherosclerotic plaques in diabetic mice after cholesterol lowering. And this may represent a novel approach to reduce cardiovascular risk in patients with diabetes. Dr Greg Hundley:             Really interesting, Carolyn. Well, I'm going to talk to you a little bit about a large study in patients with valvular heart disease and it's a contemporary presentation and management study and it's from the Euro Observational Research Program Valvular Heart Disease II, Roman numeral two, survey. And the corresponding author is Professor Bernard Iung from Bichat Hospital. So the VHDII survey was designed by the Euro Observational Research Program of the European Society of Cardiology to analyze actual management of valvular heart disease and compare practice with guidelines.                                                 Now in short, patients with severe and native valvular heart disease or previous valvular intervention were enrolled prospectively across 28 countries over a three-month period in 2017. Indications for intervention were considered concordant if the intervention was performed or scheduled in symptomatic patients corresponding to class one recommendation specified in the 2012 ESC and in the 2014 American Heart Association American College of Cardiology valvular heart disease guidelines. Dr Carolyn Lam:                Wow. So what did they find, Greg? Dr Greg Hundley:             Okay, so there's 7,247 patients. 4,483 were hospitalized, and 2,764 were outpatients, and they were included across 222 centers. The median age was 71 years and 1,917 patients were over the age of 80, and 3,400 were women. Now, aortic stenosis was present in 2,000 plus patients, aortic regurgitation in 279, mitral stenosis and 234, mitral regurgitation in 1,114. And multiple left-sided valvular heart disease was present in 1,297, right-sided valvular heart disease in 143, and 2,028 patients had prior vascular intervention.                                                 So the decision for intervention was concordant with class one recommendations in symptomatic patients with severe single left-sided valvular heart disease in 79.4% of those with AS, 77% with aortic regurgitation, 68.5% for mitral stenosis, and 71% for primary MR. Valvular interventions were performed in 2,150 patients during the survey. Of them, 47.8% of the patients with single left-sided native valvular heart disease were in New York Heart Association class three or four, and transcatheter procedures were performed in 38.7% of the patients with AS and 16.7% of those with MR. Dr Carolyn Lam:                Wow, Greg. So what are the take home messages? That was a lot of numbers. Dr Greg Hundley:             Yep. Lots of data there. And so couple things. First, recommendations for interventions in symptomatic patients with severe valve disease are better applied today in this paper than in the previous European survey conducted in 2001, particularly for those individuals with aortic valve disease. Second, multi-modality imaging is now more frequently used, but stress testing remains underused in asymptomatic patients. And finally, transcatheter therapies are now widely used in patients with stenotic valve disease, and we would expect that, particularly for the use in the elderly. Dr Carolyn Lam:                Great, Greg. So what are the clinical implications? Dr Greg Hundley:             Okay, so Carolyn, first, late referral for intervention shows the need for increasing awareness of valvular heart disease by general practitioners and cardiologists. Second, the high burden of elderly patients highlights the need for multidisciplinary heart team approaches to assess the risk benefit ratios of the different modalities of valvular interventions. And finally, number three, echocardiographic quantification of regurgitation should be more accurate and pay more attention to quantitative measurements. Those are the main take homes from this large registry analysis. Dr Carolyn Lam:                Nice. Thanks, Greg. My next paper is the characterization of the first transgenic mouse model of ARVC 5. Now, that is the most aggressive form of arrhythmogenic right ventricular cardiomyopathy caused by a specific mutation in transmembrane protein 43. So this paper's from co-corresponding authors, Dr Lara-Pezzi from CNIC in Madrid and Dr Garcia-Pavia from Hospital Universitario Porto de Hero in Madrid, and with their colleagues, they generated transgenic mice over expressing transmembrane protein 43 in either it's wild type or that specific mutant form in postnatal cardiomyocytes under the control of alpha-myosin heavy chain promoter.                                                 And they found that these transgenic mice expressing the specific mutant in transmembrane protein 43 showed fibro fatty replacement of the myocardium and died at a young age. The model confirmed that transmembrane protein 43 is mostly localized at the nuclear membrane and provides new information regarding the pathophysiological mechanisms underlying ARVC five. One of them is that the GSK3 beta signaling pathway plays an important role in this disease. Dr Greg Hundley:             So that's great, Carolyn. Sounds like we have a new model that's been created by this group and certainly this disease has spread. It's something we definitely worry about. Do you see any therapeutic implications for their work? Dr Carolyn Lam:                Great question, and indeed the authors tested two new therapeutic approaches for ARVC five. In the first they found that targeting fibrosis really had no beneficial effect. But in the second, they found that inhibition of GSK3 beta improved cardiac function and survival, thus opening the way to a new therapeutic approach focused on GSK3 beta inhibition in patients with ARVC five. Dr Greg Hundley:             Very good. So we look forward to seeing what the results of that study will be. How about now we talk about some of the other articles in this issue? Dr Carolyn Lam:                I love that. I think it's a great idea to tell everybody about this amazing issue. So we start with an article from our Global Rounds, and this time from Argentina, so a great status update and future strategies for cardiovascular disease in Argentina. We also have a perspective paper and that's on the new World Symposium on Pulmonary Hypertension guidelines, really questioning some of the cutoffs that we've taken for granted and asking, "Should 21 be the new 25?" Intrigued? Well, you really need to pick this one up and read it.                                                 And then there's a white paper, and this is a report from the 2018 NHLBI workshop that really talks about unlocking the secrets of mitochondria in the cardiovascular system and asking if this may be a path to cure in heart failure. We also have a research letter, and I love these. They're so succinct and really contain an important message. And this one talks about the evolution of Medicare formulary coverage changes for antithrombotic therapy after the guideline update. So very topical subject. Dr Greg Hundley:             Very good, Carolyn. So I've got a couple. There's a Paths to Discovery article that John Rutherford did discussing with Paul Zimmet regarding reflections of the evolving global diabetes epidemic. Second, there is a very nice On My Mind piece from Samuel Tretheway from Birmingham, England who discusses medical misinformation, kind of like medical fake news. And he discusses how this occurs and it depends on the motivation of both authors and publishers, and he reviews responsibilities of all of us, how to avoid generating this type of material. And then finally, a really interesting Cardiology News piece by Bridget Kuehn, who discusses diet and microbes in heart failure, and with that there's a very nice piece of artistry work that would be great for your office. So that's all included in the journal. Dr Carolyn Lam:                Oh, you got us all curious. Finally, I just want to highlight, we have a section called Highlights from Major Meetings, and this time from my part of the world with Dr Aijun Sun and Dr Junbo Ge summarizing the 13th Oriental Congress of Cardiology takeaways. Cool issue, isn't it? Dr Greg Hundley:             Absolutely. So how about onto our feature discussion? Dr Carolyn Lam:                You bet, Greg. Dr Greg Hundley:             Welcome everyone to our feature discussion. And this afternoon or this morning, wherever you may be, we are going to have an opportunity to discuss the utility of paclitaxel-coated balloons in terms of management of patients with peripheral arterial disease. And our article today comes to us from Bill Gray and colleagues from Mainline Health in Philadelphia, Pennsylvania. And we have our own Josh Beckman, associate editor from Vanderbilt, who will be joining us in the discussion. Bill, welcome to Circulation. We really appreciate you sending us this article. Can you tell us a little bit about the background of why you wanted to perform your study and also, what was your study design, study population? Dr William Gray:               The study was really prompted by a prior report by Katsanos et al in JAHA about nine months ago. When we started this study, it was much more fresh. And what we did was we realized we had data from multiple studies using the Stellarex drug-coated balloon that we could use to address some of the issues raised with the Katsanos paper. Just to review that briefly, the Katsanos paper suggested that there was a significant mortality signal in patients who were randomized to drug-coated balloons using paclitaxel versus PTA or patients randomized to drug eluting stent versus PTA or other stents. That signal was seen late at two years and at five years, and so we sought a given the data, the tightly controlled and well-reported data and this experience to see if we could see a signal as well.                                                 The study design really involved taking all the data from the randomized trials, and there were two, which comprised an aggregate of about 600 patients, unequally randomized, about 400 in the drug-coated balloon arm and about 170 or 200 patients in the PTA arm. And then we also looked at all the poolable data, which was controlled data, so we had two randomized control studies I mentioned just a minute ago, as well as three single arm studies in one registry. Now, these had quality oversight and data reporting. And then those data were adjudicated for adverse events, including death, by a blinded third party CEC, and then those data reported out by Kaplan–Meier estimates as well, and then we do a multi-variable analysis looking at predictors of death, and then I can talk about that in a moment. Importantly, the data here has followed out to three years. As I mentioned before, the original paper which incited the concern had reported unequal deaths at two and five years, so we're somewhere splitting that difference. That's the genesis of the study and the study design. Dr Greg Hundley:             So Bill, tell us now about the results. Dr William Gray:               It turns out the baseline characteristics were largely similar between these trials and the patient arms, even though they weren't strictly speaking the same trials, except that the drug-coated balloon arm was a bit younger and smoked more frequently, so they were at a little bit more risk. In the randomized control analysis, which was done first, there was no difference in all-cause mortality between the PTA patients and the patients who received paclitaxel drug-coated balloons. That was true at one year, two years and three years. When we looked at the pooled analysis, which included not only the drug-coated balloon randomized trial patients, but also all the single arm studies and registries, we also found that there was no differences between those treated with drug-coated balloons in those additional studies and the control group of 170 patients in the randomized trial arm of PTA alone.                                                 Interestingly, when we started to look at the multi-variable analyses, we did something that we ordinarily would not do, but because of the pressing issue around paclitaxel mortality, we actually did a standard covariate analysis looking at predictors and then we forced drug and drug dose into the model to see if they would come up positive as a predictor of outcome. As you might expect, not surprisingly, we found that age, congestive heart failure, diabetes and renal insufficiency were the four major predictors of mortality in a group of patients who were largely claudicates with significant peripheral vascular disease. No surprise there. We all know the patients don't die of claudication, they die of cardiovascular disease, and this I think bears that out.                                                 When we force drug into the model, in point of fact, not a dose nor the presence of drug had any impact on death rates in the model, so there was no predictive value there whatsoever. Those are the results. Again, they're out to three years, and I think one of the important things that we have to recognize is that the numbers are relatively small and the follow-up is relatively limited and by itself, although it doesn't show any signal, it probably doesn't stand on its own to refute a larger meta-analysis, but does I think contribute to the dataset that is becoming more evident that the individual analysis do not appear to show mortality effects. Dr Greg Hundley:             Very good. So this is Dr Josh Beckman at Vanderbilt University. Josh, could you talk to us a little bit and put this paper in perspective relative to the prior published literature in terms of how you manage patients with peripheral arterial disease? Dr Joshua Beckman:        I have to say first, I'm really glad that we're able to publish this paper from Bill Gray and his group. We are, and I'm going to put this in really muted terms, in extraordinary times. I have never seen what is going on now happen with any other technology or really even medical therapy in the 20 plus years I've been a practicing physician. I think for the audience, it's really important to understand what is going on right now because if you don't pay attention to this space, you may not realize what's really been happening. Bill did a nice job at telling you why he did the study, which was this Katsanos aggregate level meta-analysis that was published in JAHA back in December.                                                 On the basis of this paper, there has been a rapid development of worry and concern that these devices may be associated with late mortality. This concern has spread to the Food and Drug Administration, which has now put out three letters to healthcare professionals, each of them basically suggesting that you should choose non drug-coated either balloons or stents first, and if you want to use these, you have to have an extended conversation with the patients discussing the risks. And so in response to this aggregate level meta-analysis, which had an extensive number of lost to follow-up patients and didn't account for crossovers and the usual problems with this kind of information, I have been really impressed by the community of people who are interested in this topic and work with these kinds of devices.                                                 And by that, I mean, the response has not just been a series of editorials. The response has really been, "Let's find every single piece of data that we can find to see whether or not this signal holds up," because as evidence-based physicians, we take one piece of data and say that it is one piece of data, and then we have to put it into the context of all of the other pieces of data that were published. And so I know that Dr Gray is old enough to remember 10 years ago when these devices were being used in the coronary arteries with drug eluting stents. And as far as anybody can tell with studies that were two to three times larger or meta analyses two to three times larger than the study published in December, there was no mortality signal.                                                 It should be made clear that in doses that dwarf the doses from these devices, when these medications are given to pregnant women who have breast cancer, not only is the mother fine but the fetus is fine. And so I think paper that we are discussing this morning in particular, but the group of investigators in the space has really stepped forward to publish as much data as possible to fill out our understanding and place the original study in the correct context. And so when you understand what's happening in the community, and there's been a significant reduction in the use of these devices on the basis of that one publication at the expense of patients for whom these devices are really much better at limb outcomes, then you can understand why we were so interested in the paper by Dr Gray.                                                 This is another brick in creating the foundation to really have a fuller and better understanding of any possible relationship between the use of these devices and a nonspecific increase in mortality two to five years later, which as far as I can tell, I've never seen something that may end up being a poison that doesn't have a specific mechanism of causing morbidity or mortality. And so when we got this paper, I was really happy to be able to work with Bill and bring it to the level that it is now so that when it's published in October, it's going to be another really important contribution and I just want to congratulate the authors for doing that work. I will say, and I'd like to get Bill's perspective on how he thinks the information that's now being published is going to help us understand what to do with these devices. Dr William Gray:               Yeah, that's a great question, and I want to emphasize something you brought up, which I did not, which is at the aggregate level data that Katsanos used to publish his analysis was really all he had access to, which means that he had some numerical data from prior published publications but did not have patient level data. And so what Josh is referring to appropriately is the concept that each individual holder of those data, those patient level data, are now coming forward with their own analysis of those data at a patient level, which allows us to look more granularly and more clearly at the causes of death. For example, in this study, the causes of death did not cluster around cancer. They were largely cardiovascular, and they were not dis-equally distributed or unequally distributed between the two groups.                                                 So I think that patient level data, to get back to your original question, Josh, the patient level data will be incredibly important from each of the experiences with the various drug-coated balloons and drug eluting stents on the market because it does allow us to look more closely at the mechanism of death and whether there's any putative cause that might be assigned to paclitaxel. As you mentioned, the pharmacology of this is not understandable. The only type of pharmacology that would work like this was if paclitaxel was radioactive and accumulated a hazard along the way, but we know that's not true.                                                 I think extend your question, it's important to say that both the FDA and other independent groups like VIVA have looked closely at the meta analytic data both from a patient level and aggregate level data set, and they have seen a signal at five years. The problem with that is that data starts to winnow down very quickly at five years. There's not a lot of numbers, so that's the first problem, and the meta-analysis that have followed the publication by Katsanos. The second problem is, as Josh alluded to, there's a lot of missing data. Either patients withdrew or got lost to follow-up, and that didn't happen at an equal distribution between the control and the active arms, so there's some ascertainment bias there.                                                 And lastly, there's a crossover, that is patients who are in the control arm crossed over near as we can tell at a rate of about one in five or one in four to an active arm in the first year alone, which means they need to be reassigned to a risk pool that includes the original assignment of paclitaxel randomization. My sense is that those data will not get any better in the near-term future because the problems I just listed are not going to go away anytime soon. And so we are left with these individual patient level data and other big data, like Medicare analyses of tens of thousands of patients or Optum insurance analyses of again, tens of thousands of patients, which actually show no difference between the treatment with paclitaxel in the real world and patients treated with non-paclitaxel devices. So while we are comfortable and happy to publish these data and we think that are meaningful in terms of contributing to the larger dataset, we recognize the flaws and the limitations in the meta-analysis, which will not be solved soon or quickly. Dr Joshua Beckman:        So, I totally agree with what you just said. I will also say that every time data like this is published, it adds to the picture to make our understanding clearer. And you are responding directly to the Food and Drug Administration, who basically said they are not settled on this question either. It is noted, they are worried about it, and what they've really asked for is for more data to be published. And so when people analyze data like these, I think it is really helpful to the rest of us to create a fuller and more granular picture of the overall state of the field. Dr Greg Hundley:             We want to thank again both Josh for his time and Bill for his time. Hope you have a great week, and both Carolyn and I look forward to sharing with you again next week. Take care everyone. Dr Carolyn Lam:                This program is copyright American Heart Association 2019.  

 Archons of the Crucible,What is that you are holding in your hand? Is this the creature you wish to destroy? In this episode, the knights ponder the way playing KeyForge in the flesh can influence the way we deduce and influence our opponent to gain an advantage in the game. Are these tactics fair game? On that Sir Jake and Sir Dan do not necessarily agree. Intrigued? Well, what are you waiting for? Press play already to hear this meaty discussion and level up as a forger of keys and as an ambassador for this great game.Support Sanctumonius on Patreon: https://www.patreon.com/sanctumoniusJoin the Sanctumonius Discord: https://discord.gg/2YDDRRZNew Sanctumonius Playmats: https://www.inkedgaming.com/pages/search-results-page?q=sanctumonius

After weathering an unexpected attack by A.I.M., your Intrepid Trio is back…although Eric is still handling some repair work in the lower areas of the Lair, so we have Field Agent Bart with us this week. It seems that this is another news filled week, especially in regards to upcoming marvel shows. Intrigued? Well, let’s […]

Welcome to the RMPodcast!   Review: The Predator (@ 1:53)   Relationship Segment (@ 56:45)   Yet again we've got another packed show for you this week. Quite possibly one of the most entertaining pieces of crap this year as well as diving into hopefully #OneDay harnessing the power of pushing one button on your TV remote to get the best picture quality possible for your favorite blockbuster movies at home. And our Relationship segment returns with a very deep, introspective look into loving oneself. Intrigued? Well, listen in and be sure to email us at rmpodcast@redmoonproductions.com   Articles Referenced: Soon-Yi breaks silence on Woody Allen sexual assault and abuse charges Christopher Nolan and Paul Thomas Anderson hate how their films look on TV Infinity War dethrones Titanic in domestic box office run knocking it to number 5

Since leaving Titan last month we’ve been doing a bit of deep space exploration in The Tardigrade. And although space can look a bit… empty, it’s actually as hostile an environment as you’re ever likely to find. Out here we’re totally reliant on some pretty fragile materials and equipment keeping us alive. I’m sure everything will be fine of course, but what if something did go wrong? On this episode we’ll create a simulation that shows a rather unfortunate “virtual Colin” tossed out into deep space wearing only his pants. Intrigued? Well, I wouldn’t be. But whatever floats your space boat I suppose… Things to Learn What would happen to you if you were floating in deep space without a spacesuit? Is it possible to survive in deep space? What's the speed of light? How do scientists talk about the massive numbers we're working with in space.  Why is Earth’s ozone layer so important? Task Send us a tweet @HostileWorldsHQ and let us know where you’d like us to take The Tardigrade next.

Whenever you run into tips on productivity it’s always this earth shaking advice You’re advised to make these monumental changes to improve your business or life. In reality all you need are tiny little tweaks. Important tweaks, but tiny ones. And some of these tweaks are slightly irreverent. Which is what makes these productivity tips even more interesting. You’ll enjoy this episode on productivity—gentle productivity—and here’s a tip. You may end up sleeping a lot more as well! --------------------- In this episode Sean talks about Part 1: How to work with a timer Part 2: The power of sleepPart 3: Why you need to focus on the road, not the destination. Right click here and ‘save as’ to download this episode to your computer. --------------------- I’ve always assumed you needed a nut cracker to open a walnut. Then I learned you could easily use the rear end of a screwdriver. A couple of hard whacks along the ridge, and the nut cracks open easily. To prove the point, I gave my niece Marsha to crack open the nut. She’s just 12 and her gentle taps were driving me crazy until I realised that once again I was assuming erroneously. I found out you don’t need to whack the nut at all. A few Marsha-taps and it opens just as effectively—and without any splatter. We assume we have to do something great and wonderful to get productive. In reality, the changes needed are Marsha-taps. They’re gentle, almost negligible changes that enable us to get a lot done with little or no effort. In fact, one of the biggest productivity tools is to do nothing. Intrigued? Well, follow along. The three points of gentle productivity are: 1) Working with a timer 2) Sleep 3) Focus on the road, not the destination. Part 1: Working with a timer The Psychotactics Article Writing Course is billed as the toughest writing course in the world. And rightly so. In fewer than 12 weeks a participant has to go from a “frozen state” to being able to write an article exceedingly well. When you look at all the components involved in article writing, you run into a mountain of elements to master. A single course covers “topics, sub-topics, outlines, how to start an article, different types of formulas of writing, subheads, objections, examples, summary, sandwiching and yes, the incredibly important task of starting an article.” And in the process of juggling all these components, the participants do something that jeopardises the entire learning process. They will try to write an article that seems to meet their own standard Participants complain about the quality of their article. After they write their articles, they somehow feel something’s missing. So they go back to write and rewrite until they reach some sort of “quality standard. No one starts off wanting to spend three or four hours on an article, but invariably that’s how we go about trying to get our work to a higher “quality”. In reality, all that’s happening is the build up of exhaustion If you spend four hours writing an article today, and four hours writing an article tomorrow, will you be awake on the day after? The chances are you’re just going through the motions as the tiredness seeps into your bones. When you’re tired, you’re not only robotic, but you miss out on very important learning cues. It seems very much like a Catch 22 situation. You can’t create a “great” article unless you work hard at it. And yet, working hard leads to so much exhaustion that the rest of your work suffers. Is there really a way out of this mess? The answer lies in a timer The Article Writing Course runs to a timer. You have a fixed time to do the outlines; a fixed time to do your assignment; and yes, a fixed time to spend your time on the forum looking at the work of others in your group. When your time is up, you’re done. But does this make any sense at all? With a fixed time would the quality not get a lot worse? After all, when you labour over your work, you get time to fix the glitches, tidy the work and make it better. A student that is given just 90 minutes to write an article may well be dissatisfied with their work, but give them 180 minutes and they don’t turn out 200% better work. Their work is probably improved by a mere 5-10%. But their exhaustion level goes sky high when they take more time to do the task. Tasks that have fixed deadlines may not be the best in the world but they’re the key to productivity I draw a daily diary of cartoons in watercolour. I’m fastidious about doing one watercolour every day. Then a big project comes along and I’m suddenly lost. I skip a day, which turns out to be a week. Soon a month has slipped by without any work being completed. What’s worse is that I ache to do that watercolour every day, but hey, a watercolour takes me anywhere between 45 minutes to an hour. Which is why I can’t handle the watercolour when that project rolls along. But what if I only painted for 15 minutes in the day? Instantly I feel the need to rebel. I know it takes 45 minutes so how on earth can I achieve something in 15 minutes? Anyway, I made the rule, so may as well use it, right? And so I did. I did what I could in 15 minutes. Was it as good as the 45 minutes painting. Probably not, but that’s what we found on the Article Writing Course as well. At first, there’s this intense sense of rebellion coursing through the logical part of our brains. Yet, the moment we realise there’s no way out, the creative side seems to take over and we work out how we can achieve the task in a shorter duration. Will it be as awesome as the 45 minute watercolour? Let me be very clear with you. I’ve slaved over a watercolour for 5 hours and it’s not like additional time makes a better painting. Granted there are going to be deficiencies in the final product, but if you keep up the speed every single day, something interesting happens. You manage to put out not average, but some really good work in a fraction of the time. And most importantly, where there was a blank canvas, there’s work. Not only did I do my painting, but I’m proud to have something, instead of nothing. Instead of giving up, I’m moving ahead by putting a restriction on how much time I can allocate to the project. Amazingly this has reflected in the dropout rate of the Article Writing Course When you call a course the “toughest writing course in the world”, it usually lives up to its billing. And at least 20% of the students drop out (most other courses online have a drop out rate of 80-95%). Yet, once we put the timer system in place, we are in Week 7 of the course, and only one student seems to be teetering. Will that student come back? We don’t know for sure, but a lack of exhaustion is the key to productivity. It seems ridiculous to let a timer dictate your output Yet, the timer system works for our courses, for workshops, for our personal productivity and even when Marsha’s doing her school assignments. Given endless time, she fills in the time in some magical way. Put her on a timer and she astounds everyone, including herself. In trying to get more productive we’re looking for that super-big tool that will change our lives. Instead the first of those tools is the humble timer You may go overtime—but you’ll finish your work quickly enough. Will it be amazingly good? No it won’t. But if you don’t use the timer, nothing gets done, which is a lot worse. And that’s the first gentle tool of productivity. So what’s the second tool? You know this one well. It’s called sleep. Sleep? How are you productive when you sleep? Part 2: Sleep enhances productivity—but how? Sleep helps us in many different ways, but we don’t relate garbage disposal to sleep, do we? Lack of sleep affects brain function, reduces learning and impairs performance It also seems to prevent us from transferring short term memory to long term memory. However, researcher, Dr. Maiken Nedergaard has a mind-blowing theory (he submitted a paper to the prestigious journal called Science). His research shows that the brain apparently goes through a garbage clearance when we’re asleep. Nedergaard’s team showed brain cells shrink during sleep. This shrinking of the brain cells opens up the gaps between neurons, which in turn allow fluids to wash the brain clean. The research also suggests that failing to clear away some toxic proteins may play a role in brain disorders like dementia. But let’s put brain disorders aside for a moment, and focus only on the and think of what happens when you don’t sleep. With every sleep deprived hour, more toxins keep building up in our brain, impairing our productivity. We’re more sleep-deprived than ever, and we have the idiots to prove it Everywhere you look, you’ll have the so-called gurus berating you for dreaming about the weekend. Very few people seem to take breaks, let alone weekends. Sleep is associated with laziness, and there’s utter disdain for the afternoon siesta. In many countries, they derogatorily call it the “nana nap”. Yet Nedergaard is pretty clear about the value of sleep and how it affects the clearing of junk from your brain. “You can think of it like having a house party. You can either entertain the guests or clean up the house, but you can’t really do both at the same time.” Productivity is the house party! The more productive we are, the harder we work, the greater the amount of “garbage” we seem to accumulate. And boasting about little sleep is hardly the way to go about getting rid of the garbage. I know this seems ironic seeing that I’m the 4 am guy, but I’m well into counting sheep by 10 pm or earlier. Then there’s a solid hour or even two hours of sleep in the afternoon. This regime of getting more sleep, rather than less is what counts towards productivity. But what if you feel groggy after an afternoon sleep? Many people do. And it’s good to measure how much sleep is restorative and how much makes you groggy. Some people nap in sleep cycles. I’ve found I can sleep in 45 minutes or 90-minute cycles. If I’m woken up in between, I feel groggy. But here’s the really interesting bit. I sleep longer when I’m more rested. On workdays, I’ll sleep for about 45-90 minutes, but on vacation that sleep gets extended to an enormous 3 hours. While no one is asking you to sleep three hours or even 45 minutes, you should try a 20-minute nap at the very least. Instead of trying to create yet another to-do list, your biggest item should be garbage clearance Lauren Hale is an associate professor of preventive medicine at Stony Brook University. She reckons screens of any kind inhibit our sleep. Whether it’s a phone, tablet, computer or TV, it affects our sleep. Getting rid of all those devices at least 30 minutes before you sleep is one way of getting a sounder sleep. Anyway, it stops us from checking e-mail or looking at Facebook, which only increases the churn in our brain instead of letting us sleep well. Sleep may be on everyone’s to-do list and no one’s productivity list We don’t see sleep as important, and yet it’s been amazingly useful when training clients in courses. In the 2008 version of the Article Writing Course, for instance, clients needed to write five articles a week, with no limits on time. And they all turned out decent articles. In the 2016 version of the Article Writing Course, clients are required to write 2-3 articles a week, and there are limits on time. In every instance, the 2016 batch is writing far superior articles in smaller portions of time. And how do I know this to be true? A skill like writing can never be treated like an objective science and it’s always going to be subjective. Yet, I think I could easily slide into a bit of a judging role as I’ve written between 3000-4000 articles in the past 16 years. It includes 52 articles for the Psychotactics Newsletter and between 3-5 articles for 5000bc per week. It doesn’t include several books or reports. And every Article Writing Course generates between 800-1000 articles. Seeing I’ve conducted over ten consecutive courses, that’s about 10,000 articles read over the past ten years. Add it all up and we’re looking at least 14,000 articles over the past 16 years. I know it still makes the skill subjective, but I’d say I have a pretty good handle on good vs. not so great article writing. And the more rested the student, the better the articles. I’d like to say writing more articles per week would make the client a better writer, but it doesn’t. Not in the early stages, at least. Once they’ve got a good handle on the elements of article writing, they write quickly, create less garbage, and they’re able to write every day, if necessary. And yes, without too much of a strain. Even so, sleep helps tremendously which is why weekends and breaks are crucial. This improvement in productivity doesn’t need a team of researchers does it? It’s not just a finding when it comes to article writing. You know from your experience how much you stagger about like a drunk when you’re sleep deprived. You don’t need to get into a lab coat to figure out that sleep does beautiful things for your productivity. Knowing that it helps with removing all that garbage, helps, doesn’t it? Now you can sleep a lot more and contribute to your productivity. This, of course, takes us to our third element: staggering the task. Part 3: Most of us are told to start with the end in mind. The goal. The destination. The dream. And it’s that end point that more often than not, unravels our entire sequence of productivity The end point is why we get involved with any undertaking. We join a cartoon course to learn to draw cartoons. We get into karate class so we can protect ourselves should we find ourselves in a bit of a bother. And yet for most of us, the end point is fuzzy. What would the cartoon you draw in six months from now look like? What kind of moves would you make in karate a year from now? No one can answer that question, no matter how prescient we happen to be. So the end point is important, but in reality it’s just a point in the road. A better way to see an end point is to visualise the drive to your weekend picnic spot. You clearly know your destination, but as you get in the car and get going, what are you looking at? Yes, it’s the road right in front of you. Every turn of the wheels forces you focus not on the endpoint, but the process instead. Michael Phelps is the most decorated Olympian of all time Behind Phelps’ amazing track record is his coach, Bob Bowman. And here’s what Bowman has to say about process. “Champions value the process more than any outcome. Because that’s what controllable and within our ability to deal with”. What he saying is that the journey itself is the benchmark—not the destination or outcome. For example, if we were learning how to write a sales page, we shouldn’t be focused on the end point. We should be more aware of managing the process. On a sales page there are so many elements: headlines, bullets, features and benefits etc. If you’re learning to write headlines, you should be  focusing on the headlines. If you’re writing bullets, they should be your benchmark. You shouldn’t be asking: How is my sales letter doing? That’s the wrong question to ask. Instead, you should say: Am I benchmarking what I learned today? Or this week? The moment we shift our focus on the end point, we’re easily frustrated That’s because every journey has diversions or speed bumps. And if we haven’t accounted for those diversions, we get upset and start to wander away from our destination. And rightly so, because the destination is still a zillion miles away. However, if we focus on the immediate road, things change. Even if you hit diversions, that’s part of the journey. Productivity is often measured by what you do Instead, we also need to measure it by what gets in the way. The moment we’re focused on the end point, we come up with rather silly statements like, “My work isn’t up to the quality I expected”. The reason for this seeming failure is you’re evaluating the entire project, and we’re not there yet. Frustration sets in, and you end up berating yourself, thinking everyone else is better than you. And can you believe being productive when your mental state is in a shambles? The way to approach productivity is to break up your journey into smaller bits When clients write an article, I advise them to first do the outline. Then do nothing for hours on end. After those hours have ticked away, write the First Fifty Words. Again, you can walk away from the article. Bit by bit, mile by mile that article gets built until a day, even two days have passed. But how much time has the client spent on the article? Often it’s just a little less than two hours in all. Yet, how do many writers attack an article? They sit down and try to do what I used to do. I’d be adamant that I wanted to get to the end point, so I’d spend all day on the article. As the hours ticked away, I’d get so lost that many articles never made it to the finish line. Instead, I’d throw yet another article in my article writing graveyard. What seemed like a good idea—the finish line—was, in reality, a terrible mistake. I lost energy, didn’t work with a timer, didn’t have the nerve to take a nap to replenish that energy. And so that article never did make it to the finish line. I was trying to be productive but ended up doing quite the opposite. The end point is just a point. There are points all along the road. No one point is more important than the next. If you managed to get 70% to the end point, it’s better than dropping out. And since productivity is about getting things done, 70% is a lot better than nothing. Next Step: Read or listen to How To Beat Inertia And Why Logic Doesn’t Work http://www.psychotactics.com/beat-inertia/   .

Welcome to the TNS Radio Football Show, episode 27. Normally we're at a football ground, in one of The Venue rooms or on the balcony at Park Hall. However, this week we kick off in Rhyl harbour with Kai Edwards! Intrigued? Well, listen in when all will be revealed! We've also got Graeme Kirkham explaining why Park Hall was jam-packed last Friday evening. Like your soaps and reality TV shows? He also tells you how you can get close to your favourite actors in a forthcoming event we're holding. As always, we've got post-match interviews, this time with Craig Harrison and making his debut on TNS media, Ryan Brobbel.

The death of a Teenage Mutant Ninja Turtle? The Lion King and Palliative Care? Changing the direction a river flows? Intrigued? Well listen on! In this episode Dr Amara Nwosu asks the question "what is culture?" and asks how a society's culture can affect how Palliative Care is considered and delivered. Can we change and create a culture where death and dying are not considered taboo subjects? This is from a UK perspective but hopefully it will be of interest. Topics covered in this podcast: Barbara Gomes - end of life intelligence network - what we know now:http://www.endoflifecare-intelligence.org.uk/resources/publications/what_we_know_now_2013 Andy Couch - Culture Making https://setsnservice.wordpress.com/2008/10/27/a-summary-and-review-of-andy-crouchs-new-book-culture-making-01-05-culture/ Dr Atul Gawande - 2014 BBC Reith Lectures http://www.bbc.co.uk/programmes/articles/6F2X8TpsxrJpnsq82hggHW/dr-atul-gawande-2014-reith-lectures Dr Atul Gawande - Being Mortal http://www.amazon.co.uk/Being-Mortal-Medicine-What-Matters/dp/0805095152 The death of Donatello (Teenage Mutant Ninja Turtles) http://www.techtimes.com/articles/40753/20150321/teenage-mutant-ninja-turtle-44-donatello-gruesomely-killed-in-action.htm Story of the dragonfly http://www.achildofmine.org.uk/The-story-of-the-Dragonfly/I8.htm Copyright Dr Amara Nwosu, KingAmi media 2014. www.amaranwosu.com Music by 'Year of the Fiery Horse' (YOTFH). Soundcloud link: @year-of-the-fiery-horse

He IS The Friend To All Children! This time out on Earth Destruction Directive, everyone's favorite turtle Gamera takes center stage once again! Only this time his Kid Superhero persona is in full effect! And not a moment too soon, as Viras, his spaceship, and a small mountain's worth of stock footage have arrived from deep space! Can Gamera defeat the Space Squid and his bumblebee like fleet? Download and find out! And over in Shogun Warriors #15, things take a turn for the weird as nothing looks or sounds quite right! Intrigued? Well, all is explained and it's not nearly as intriguing as you may think. Plus news, emails, and more on Earth Destruction Directive!Feedback for this show can be sent to: earthdestructiondirective@yahoo.comEarth Destruction Directive can be found on Facebook at https://www.facebook.com/#!/earthdestruction.directive Please rate and review the show on iTunes! You can follow Luke on Twitter at http://twitter.com/ljacone and "add" him on Google+! Two True Freaks! is a proud member of BOTH the Comics Podcast Network (http://www.comicspodcasts.com/) and the League of Comic Book Podcasts (http://www.comicbooknoise.com/league/)!! THANK YOU for listening to Earth Destruction Directive, part of the Two True Freaks Podcast Network... and KEEP 'EM STOMPING!!

He IS The Friend To All Children! This time out on Earth Destruction Directive, everyone's favorite turtle Gamera takes center stage once again! Only this time his Kid Superhero persona is in full effect! And not a moment too soon, as Viras, his spaceship, and a small mountain's worth of stock footage have arrived from deep space! Can Gamera defeat the Space Squid and his bumblebee like fleet? Download and find out! And over in Shogun Warriors #15, things take a turn for the weird as nothing looks or sounds quite right! Intrigued? Well, all is explained and it's not nearly as intriguing as you may think. Plus news, emails, and more on Earth Destruction Directive!Feedback for this show can be sent to: earthdestructiondirective@yahoo.comEarth Destruction Directive can be found on Facebook at https://www.facebook.com/#!/earthdestruction.directive Please rate and review the show on iTunes! You can follow Luke on Twitter at http://twitter.com/ljacone and "add" him on Google+! Two True Freaks! is a proud member of BOTH the Comics Podcast Network (http://www.comicspodcasts.com/) and the League of Comic Book Podcasts (http://www.comicbooknoise.com/league/)!! THANK YOU for listening to Earth Destruction Directive, part of the Two True Freaks Podcast Network... and KEEP 'EM STOMPING!!