Podcasts about S0

The Oscars were…horrible, actually. They had the right ideas, I know, I did an award show a week ago and they used many; I did no clips, instead, people talking about movies; I let winners speak their truth, so did they. But someone the Dorians made it, while the Oscar's didn't. Why? Because it's organic for one and not for the other to be diverse. Can you force diversity, inclusion? Or is that the problem with America today? We want our institutions to change, update, modernize, but they can't really, because they simply aren't modern, updated or inclusive? Listen where you get your podcasts watch at reallykarel.com subscribe at youtube.com/reallykarel and support at patreon.com/karel

In this podcast, we celebrate one of you. S0 many of you who join us week after week are actually doing the work and changing not just your lives, but the lives around you. We want to celebrate so many of you in a time when Muslim women are not as recognized for all the good that they do. Meet Zainab, a university student from the UK who will share her secrets to feeling and living better. We celebrate her and the important accomplishments that she has made and continues to make. + To reach me, message me on IG @Mindfulmuslimah. + The registration to our exclusive global community, Thrive Muslimah, is closing in @2 weeks! To get in apply here: https://mindful-muslimah.com/thrive-muslimah-apply/ * We will be speaking at Why Islam this Saturday 7pm EST. https://www.youtube.com/user/877whyislam We will be speaking at ICNA Houston on Sunday - no registration needed - just join us on Sunday at 4pm EST here: http://www.icna.org/dawah --- Send in a voice message: https://anchor.fm/mindfulmuslimah/message Support this podcast: https://anchor.fm/mindfulmuslimah/support

Description This week we discuss beers, define FOMO for James, Darin embraces a shift, James claims he’s not useless and spits beer through his nose, all while executing a retro on the inaugural season (S0) and solving some issues around a potential second season (S1).Show Notes 00:00:00 - Pre ShowIPAs, Microbrews, Snicklefritz and all the other things.00:02:46 - Show Start00:03:01 - Season 0 (ie. season 1) - Live Retro “30” ish minutesOpening Tangent - Office move out adventuresThe AgendaSet the stage Gather Data (starts/stops, lacks/wants, keep/kills)BrainStorming (grouping/discussing/taking issues)Solutions (IDS live)Conclusion00:18:18 - Set the Stage - lets kick this retro offMEPS (meeps, mips) - how are we all feeling?Shift Move - bringing Darin back above the bar2 Versions of James (spoiler alert: neither include empathy)FOMO - one of us had no clue what it means and when it peaked in societyOpening Segue - How we start every meeting (reminder of CV’s, Commitments)00:19:28 - Gather Data (AKA: Podcast Audio Gold)Three Each Person on:What went well? What didn’t go well? What we learned?Where did we fall short of expectations?What Went Well:Drum Beats, Sharing, and more…What Didn’t Go Well: (This segment interrupted by “James spits his beer out”)What We Learned:Why this podcast is the Meta, Meta discussion and “gosh darnit, people like us”Where we fell short:Great leaders set clear(ly) low expectations00:43:01 - BrainStorm (AKA: More Audio Podcast Gold) Fun and TearsTweed JacketsNice “Clusters”Oh...and 9 actual issues to a potential second season (S1)00:57:56 - Solutions (James pulls rank on a podcast of “seemingly” peers?)Are we going to do a second season?Oysters and Pearls?“The Show Must Go On”We take away 4 Todos (follow up on ToDos next week)Making up new acronyms (CSC?)01:20:08 - Conclusion -  Wrapping up our retro and the show in just under “30” ish minutes (total edit fail)Quick ReflectionOverall Rating (1-5) on the Inaugural season of Only Way To FailThe CreditsHosts, Garret Richardson, Tyler Samples, Darin Kelkhoff, and James MaesShow Notes by Garret RichardsonProofing and Title by Darin KelkhoffEditing, Mixing, and Mastering by Brenton Wainscott

We explore Church Militant article's Catholic Politicians like Joe Biden , Nancy Pelosi, and the late Ted Kennedy and many others love Free political manoeuvres articles like the seamless garment Focus on many social Justice issues but bury abortion under topics like The environment immigration Joblessness Poverty: LGBTQ rights: today abortion is Constitutional right for Democrats so its not issue. S0 what do we as Catholics do ? --- Send in a voice message: https://anchor.fm/ned-jabbar/message

Der Porgcast ist wieder zurück. Es melden sich C3-Bernie-O, Niko der Nikto, der Tolgalorianer, Mari-2-S0 und Franco Fett aus der Quarantäne. Heute analysieren wir Rogue One - A Star Wars Story. Danke an Manni für die Nachricht und vielen Dank an Star Wars Union für die Unterstützung. Möge die Macht mit euch sein...immer! Blog: https://porgcast.eu/ Spotify: https://spoti.fi/2Uotitn iTunes: https://apple.co/2UottF3 YouTube: https://bit.ly/2Ysm7Cg Facebook: https://www.facebook.com/porgcast/ Instagram: https://www.instagram.com/der_porgcast/ Twitter: https://twitter.com/derporgcast E-Mail: mail@porgcast.eu

３月２５日（水）に開催した ZENKEI AI FORUM ライブストリーミングの模様をポッドキャストにしました。パート３は引き続き、ゲストのあらんさんの講演「人工知能の歴史・3次ブームを超えて...(なんちて)」の後半です。ZENKEI AI ポッドキャスト、これまでのあらんさんの出演回： S01E02 人工知能の歴史・3次ブームを超えて（あらんさん）前半 S01E03 人工知能の歴史・3次ブームを超えて（あらんさん）後半 S01E05 （おまけ）金沢のAIパン屋さん S0..

A Homily for Lent II March 8, 2020 All Saints Anglican Church, Prescott, AZ   Text: Matthew 5:27-37   Let the words of my mouth and the meditation of our hearts be always acceptable in thy sight, O Lord our strength and our redeemer. Amen.               Every Lent I set up for myself these incredibly high standards – “this Lent, I think to myself, I’m going to do a million things and become super awesome,” and on the surface I tell myself that it is for the sake of my soul, for the stripping away of all that is not of God. But I think deep down inside I want to be what St. Paul calls a super-apostle. A mocking term for those who added to the gospel of Jesus Christ at the church in Corinth.             This year was really no different And with some of my Lenten disciplines – I lasted 48 hours.             Then I had a revelation – for me – this year – I think Lent is as much about mortification of the flesh through abstaining from certain pleasures, especially those which lead me into sin – as it is of learning the habitual act of repentance. Relearning repentance as a central part of the Christian life – learning to recognize when we’ve sinned, learning to flee from that sin when it comes at us, but not simply to flee from it, but flee into the arms of a loving God, flee into the grace of Christ who died on the cross for all our sins. For each of us – Lent ends up being different – some must abstain from something – others must add a new discipline, while others may simply need to relearn the old habit of repenting regularly.             I recently stumbled across an article on Biblical manhood. The author lamented that one of the things that we tend to do as the church is tell people, men in particularly what not to do – and these admonitions are good – but we rarely tell them what to do. One of his exhortations was that men of God do “not merely avoids habitual sin, but cultivates habitual repentance.”             Lent is a season of habitual repentance, habitually turning away from our sin, and turning back to God. Daily dying to ourselves and daily coming alive in Christ. It is our opportunity to recapture that calling to habitual repentance.             This morning’s lesson is hard – I would be lying if when I read it on Monday as I started to prepare, that I thought “good! I get to preach on lust, adultery, divorce, and lying!”             Perhaps my attitude was not as good as it should have been because we are privileged to have a lectionary that guides and directs us so that ultimately, we submit ourselves to the whole teaching of Christ, submit ourselves even to those parts that make us uncomfortable and this is an uncomfortable subject because chances are – lust – divorce – or a lack of truthfulness has affect each and every one of us – if not all three, at least one or two, for we are sinners who are broken, who struggle to allow God to fill every inch of our hearts and chase after every fleeting thing – and so, by the grace of God, we must wade through difficult passages such as these. For it is ultimately our calling to fill our hearts with the grace that we find in Christ. We are called to be endued with the spirit, to the glory of God in all things.             Before we go any further – I want to say these two things – first – I speak as one who has a log in my eye – I do not presume to preach to you as one who is morally perfect – but as one like all of us has sinned, has fallen short of the glory of God, who has missed the mark. I have struggled with all kinds of sins, and seen my own darkness in my heart. So, do not hear me as one who is mightier than you – but as one who has sinned, who has repented, who is saved not by my own works but by the grace of God found in Christ Jesus. Hear one who finds Christ’s strength in his own weakness.               Secondly – you may very well feel yourself being uncomfortable with this subject matter, your conscience might arise within you and tell you – “repent!” If this is the case, the Holy Spirit is calling you, drawing you back to Christ, this is God calling you back to flee from whatever sin you struggle with. In that – I pray you would be reminded of what the Anglican Puritan Richard Sibbes said “there is more mercy in Christ than sin in us.”             While our sin may very well drive us to our knees, may very well make us feel broken and devastated inside – it is in our brokenness and while we are on our knees that Christ finds us. If we feel this sense of sinfulness, if we feel this sense of brokenness – may we also be reminded to flee back to Christ, may that sense also remind us of His incredible mercy, His incredible goodness, may we not despair but turn back to Christ and ask for our brothers and sisters in Christ help in running the race that lies before us.             Now – you might be wondering – why even bother talking about this? Or perhaps, you are thinking “man, this is uncomfortable, I don’t want our young unmarried, celibate priest to talk about sexuality.” But think about this – the average American over the age of 15 spent two hours and forty six minutes a day watching TV.             This number nearly doubles for retirees over the age of 65 – to four hours fourteen minutes a day! Now, perhaps these are edifying shows – but a lot of what we consume on television tells us the antithesis of the gospel of hope – tells us the antithesis of a message of purity. It tells us that we should get what we want, and we should get it now, it tells us that the hook up culture that is so pervasive in our culture is okay and normal, it tells us that self-centeredness and selfishness is a good way to live. It portrays sexual immorality as good and right.             Meanwhile, we might spend an hour and a half or two hours in corporate worship a week, and another two or three hours in fellowship. S0 we spend 21 or more hours a week being catechized by the culture and at most five hours being catechized by the church and perhaps a couple more if we are disciplined in our devotional life. If we do not live with a critical mind, if we are not diligent about how we fill our time and our minds – which is more likely to have an effect on how we think? Which is most likely to form our minds and souls? Which is more likely to shape our worldview?             My friends – we must be on guard to what is forming our minds – and aware of how we think through things and what affects us out mind, body, and soul. And let us not be formed by the secular culture – but let us be formed by the word of God – be formed by His truth, by His church, and let us fully submit ourselves to it that our lives may be good and glorify God.             Now, let us tackle the first uncomfortable thing – Christ says: “everyone who looks at a woman with lustful intent has already committed adultery with her in his heart.” How we view the other effects how we think of them – upon seeing an attractive person do we seek after that person for our own gratification, do we try to have them for our own pleasure, in reality or in our mind?             Let’s take this a step deeper – I mentioned a minute ago the statistics on the consumption of television because we live in a time and culture that has been classified as “pornified” by not just concerned Christians but secular commentators as well. In younger generations – pornographic consumption is normalized – and shows on TV that would have been considered objectionable twenty or thirty years ago for their objectification of women are so normal that we don’t even blink. If we pause a moment and really think critically about this – we know it to be true. I could share here statistics on rates of consumption, and annual budgets on pornography, as they are readily available – but I suspect that we do not need further evidence of this and I do not wish to dwell in this dark place for too long.             But let be aware that the sexualization of our culture is everywhere – and it has corrupted the heart of our present age.             But perhaps you’re wondering – why does this even matter? What I do in the privacy of my own house is my business, or perhaps, what happens between two consenting adults is their business! How we view people is fundamental to our worldview – are people there to fill our wants and needs? Are human beings there to fulfill our want for pleasure? Are we using the other to give our heart some place to rest, instead of letting our hearts rest in God?             One thing I’ve noticed in talking with people who struggle with lust and sexual immorality is that they often don’t feel worthy of love – we live in an isolating culture and these people typically feel completely alone, feel too broken for community and sexual sin provides a brief reprieve from these feelings, it provides a brief, all be it artificial connection. But my friends although sin, whatever it may be, feels dark and dreadful – and it may seem as though it is a bleak and painful spiral that never ends. Let me also tell you that there is healing in repentance – there is healing in Christ. Perhaps my favorite St. Augustine quote is “our hearts are restless until they rest in thee O Lord.” Until we learn to allow our hearts to rest in the Lord – we will look for other things to fill them – it may not be lust, or sexual sin, it may be gluttony, greed, gossip, or something else but each of these will leave us empty. Instead, let us learn to root out these sins, and let us learn to let our hearts truly rest in the Lord.             And so what do we do to root these sins out? How do we live in such a time? Christ’s instructions are stark “If your right eye causes you to sin, tear it out, and throw it away. For it is better that you lose one of your members than that your whole body be thrown into hell.”             Now – let us not make the mistake of Origen, who took this a bit too literally – who in fact removed a part of his body because he felt it caused him to sin and he became hopeless. With the exception of Origen no church father took this commandment literally – but rather as a sharp hyperbole to give no room for sin. In a culture that looks at sexuality as a fluid and throw away thing – we are called to live a life of purity, we are called to give sin no place in our life. If there is something causing you to stumble – prayerfully root it out!             This does not mean we will live a perfect life – and this certainly doesn’t mean that we will live in constant perfection – this is not promised in Holy Scripture – it does however mean that we would prefer they way of the Lord over the way of the flesh and the world.             Now, I hope we have thoroughly established that lust and sexual sin is bad – and that it should be rooted out. I want to suggest a better way – there are many practical steps we can take but I want to suggest one this morning and that is instead of seeing someone else as an object to be consumed or a place to find our happiness – we recapture the other as the image bearer of God. In a collection of liturgical poems and prayers written by an Anglican Priest – called “Every Moment Holy” there is a prayer called “Upon Seeing a Beautiful Person” and it captures this heart which we are trying to cultivate perfectly and goes as follows: “Lord I praise you for divine beauty, reflected in the form of this person. Now train my heart so that my response to their beauty would not be twisted downward into envy or desire, but would instead be directed upward in worship of you, their Creator – as was your intention for all such beauty before the breaking of the world.”             Let us learn to praise God for the beauty that we see, the goodness that we experience, all that is true and wonderful in the world – not to desire to have dominance over it, not to make it our own but let us learn to give thanks to God for all He has done.             No, my friends – the other – the brilliant, the beautiful, the funny, the fantastic, the ugly, the utterly destructive, the clown, and the klutz – every single person we will ever experience – each and every one of them are created in the image of God. Let us be mindful of this – and let us not grow to desire to have them for our own but rather learn to love God all the more for the wonders He has made for each and every one of us is fearfully and wonderfully made!               Here, before we tackle divorce – I want to make one more note as we read and meditate upon the Sermon on the Mount, Christ does something – he flips the cultural standard on the head – it’s fine to appear good – but Christ is more concerned with what is going on inside the heart.  For the Christian purity comes from casting aside the sins of the mind  and the heart. It comes from not simply from avoiding the bad thing or looking good to the world, but with the prayer that God will give us a pure heart. It is tempting to focus only on outward appearance – but let us be more concerned with God’s healing of our own hearts.               And now divorce – I pray that I approach this with care – I know that divorce has touched several in our midst– I know that many of you have experienced divorce or someone you love has gone through it for one reason or another. If this is you – as we explore this difficult question I encourage each of us to remember the words we started with from Richard Sibbes - “there is more mercy in Christ than sin in us.”             First – let us be very clear – divorce is bad. Period – divorce is not the way it was supposed to be and our hearts should break when it happens.             Christ makes clear that there is one reason for divorce – sexual immorality – the word is fairly all encompassing – this can include an affair – this can include habitual, unrepentant use pornography – basically anything that violates the sanctity of the marriage bed.  Again – we see a high view of sexual purity being portrayed by Christ.             Most theologians, though not all, agree that there is two other Biblical reason for divorce and the first is spousal abuse. I agree with this – abuse – like sexual immorality fundamentally shatters the covenant of marriage, and as such we should give no quarter to it. Likewise – when a spouse is abandoned by the other – this is a reasonable cause for divorce as well.             In all three of these cases we should take deep and careful care, and bear love for the victim or victims, and have sharp and strong calls to repentance for the perpetrator.             Beyond this – scripture gives no room for divorce.               For some – this may be hard to hear – and for some this may be a comfort affirmation of what is in the past – but in all of this, let us be mindful that there is grace found in the deep love of Christ.             Next – let us take a moment to talk about why divorce is so bad – God created the union of marriage to bring two people together – to bind two in flesh into one – for His glory and our sanctification. It is a reflection of God’s love for his people. To fall into divorce is to break these bonds, it is to shatter the covenant, and to kill something good.             I think what is best here – is if you find these words to be a struggle, or that they hit too close to home – let us talk, let us dive deep into repentance and into the grace of God. For God can heal all wounds – and can draw you away from your past pains and sin and into a deeper and more beautiful relationship with Him. My friends – no matter how dark your past is – please be assured that God loves you – you are forgiven – and there is hope for a brighter future. Much can be said about the painful nature of divorce  – but let us turn now and focus on how we can move forward – how we can create better relationships, and have better health, for we all come to the table with our own brokenness, we all come with past hurts from people who we thought we could trust, we all come with our own foibles and fears. Our culture tells us – that the foundation of intimacy is sexuality – what if instead of that as Christians we start the simplest of things – we realize that intimacy is not magically found but that it is built. Think for a moment about your walk with God. If you never come to church, never crack your bible, never pray – what will your relationship with God be like? It will not exist. If you only pray when you come to church on Sunday, and that is the only time you hear the word of God – your relationship might be a little bit better – but if you find yourself in constant prayer, in the word, devouring it day in and out, spending time in fellowship, being encouraged and encouraging – then your relationship with God will be deep and intimate. Why do we expect human relationships to be any different? They take work. To quote a theologian I know and respect: “great relationships are not simply ‘discovered’; they are slowly and skillfully built.” As a community in a microwave world – let us be committed to building relationships that last – not just marriage but friendships as well – the same theologian spells out the three following ingredients they are important for genuine friendships and for intimate marriages.             Now, let me again be honest – I do not teach this as someone who has relationships all figured out – but as someone who knows relational brokenness too well, as someone who has hurt and been hurt. But – I believe if we focus on building good relationships within the body of Christ – if we focus on building intimate friendships and solid marriages the world will be blessed by us, we will grow in Christ, and we will continue to find healing from all the past pains – whether it be divorce, familial betrayal, or other darkness from our past.             At the foundation of good relationships comes – emotional intimacy – sharing with one another our burdens, our hurts, and our past sorrows and even our sins. For as we share with God all our hurts and failures – we learn trust when we become vulnerable with one another.             Likewise – relational intimacy – committing to time together – letting our yes be our yes and our no a no, learning not only to bear with each other’s burdens and delight in each other’s joys, but to walk through the sorrows of our souls. In this commitment to one another it builds those good bonds that draw us deeper and deeper.             And finally – appropriate touch – as you all know my least favorite – but this continues the deeper bonds of intimacy. In a culture that is profoundly touched starved – we have an opportunity to model healthy touch, touch that portrays not lust but love – and it is even in touch that Jesus heals – and at times to show deep affection with those whom he loves. Think of John at the last supper where he is reclining upon Jesus.             It is out of these basic elements – that good – strong friendships and marriages come. The sexual union that is the mark of marriage, and comes after these elements not before – so when we wrongly order how we build our relationships – it is no wonder that there is so much dysfunction. True intimacy comes from knowing the other – and loving them deeply and self-sacrificially – not from desiring having them for your own. So much could be said upon both of these topics – but I hope that these words have encouraged you – have helped you to turn to a hope-filled future – helped you turn away from fleeting worldly pleasures, and not beat you down but shown you the richest love that Christ has poured out for us.             Finally – we must note that Christ tells us to let our yes be yes and no a no. Much ink has been split on this – what does it mean? Should Christians make vows? Should we swear when we are called into court? These are worthy questions – but for now simply know that at the heart of it is this call – it is to be honest. If you say you’re going to do something – do it. If you can’t do it for some reason or if you aren’t going to do it – say no. Say yes when you mean yes, and no when you mean no.             We have covered some hard topics and I didn’t spend nearly as much time as I would have liked on any of them – and I do not want to weigh you too heavily. Let us seek the holiness God has called us to and remember that for all our foibles and failings there is grace. I stumbled across a good quote the other day that I want to end with: “Having a Christian worldview means being utterly convinced that biblical principles are not only true but also work better in the grit and grime of the real world.”             Having now started to establish a Biblically principled view of sexuality – let us repent from any past sins, turn away from our old way, and stand firm in the way of Christ, not because we are better than others but because we are thoroughly convinced that they are good – because in the nitty gritty of life they work – because life is better when we live in them and most importantly because when we live in Christ’s holiness our lives glorify God.             In the name of the Father and the Son and the Holy Ghost. Amen.

Interview with Jeremy Mcmanus, General Manager of Commercial and Investor Relations for Neometals (ASX:NMT)Mining Intelligence is phrase we like. Mining Derivatives is another. Why? Because there are some companies that can give you exposure to mining investment but without the risks and a lot of upside.Take a look at NeoMetals. They made their money with Lithium mining project, Mt Marion in Australia, and timed their exit beautifully. They pocketed c.AUD$140M, not only that they have returned c. AUD$45M to shareholders. And they have retained an option on the Lithium spodumene. A smart piece of negotiations. And that typifies their approach to business.Neometals has three projects, the most exciting of which is their battery recycling business. So while a lot of companies are telling us how the EV revolution because of what they will be putting in to batteries, NeoMetals is telling us what they are going to take out of batteries through their recovery process for spent or dead batteries.McManus views Neometals as a "project development business." Neometals has a variety of assets with differing commodities, but the battery thematic is the key driver. There are 3 core projects with Neometals' focus: the Barrambie Titanium Vanadium Iron Project in Western Australia, a Lithium Refinery Project and of course it most advanced project, the battery recycling businessNeometals Ltd has a market cap of AU$111M. It started the year with a share price of AUD$0.24, reached a peak of AUD$0.26 in May, fell to a low in September of S0.17, before re-stabilising at today's price of $0.20AUD.Having identified the growing demand to recycle lithium batteries as a focal point, the company is working towards commercialisation of its proprietary process for recovering cobalt, nickel, lithium and other valuable materials from spent lithium batteries. Neometals' pilot process has generated a high purity (+99%) cobalt sulphate product at a high recovery rate (+98%).Neometals' management has created an ecosystem of experts in their field with the ability to solve complex problems currently related to lithium, titanium and vanadium.Neometals hydro-metallurgical recycling method is unique. And with strategic partnerships, supply lines and MOU's already in the bag, the ecosystem seems to be close to delivering on its ability to move the pilot in to commercial reality at scale in Europe. We follow this story with great interest.What did you make of Jeremy Mcmanus? Is Neometals the answer to our waste-related problems? Are they a better bet than a conventional junior mining company?Company page: https://www.neometals.com.au/Make smarter investment decisions, subscribe here: https://www.cruxinvestor.comFor FREE unbiased investment information, follow us on Twitter, LinkedIn and Facebook:https://twitter.com/cruxinvestorhttps://www.linkedin.com/company/crux-investor/https://www.facebook.com/cruxinvestorTake advantage, hear it here first: https://www.youtube.com/CRUXinvestor

How times change? Ten years ago it was a struggle to speak to people wanting repeatable accuracy better than 10 microns. Nowadays, low figure micron and sub-micron tolerances appear to be the norm for tolerancing workpieces. Another major change is the physical sizes of features that are now required on workpieces. This does not mean that the workpieces are very small but features such as a wall thickness has a tight tolerance, drilled holes have a smaller diameter, threads are getting smaller and materials are either getting softer or much harder. What is industry doing today? As a micro-machining person, Arthur Turner takes a closer look at what is achievable. Forty years ago, I worked at an aircraft manufacturing company and was tasked with drilling holes at 0.010” inch (0.25 mm) diameter in cobalt chrome - a monumental task given my knowledge and the machines and tool coatings of the era. Today, I have no concerns over providing tools more than ten times smaller to customers. Armed with the right information, holes can be successfully drilled. One customer recently ordered 0.010, 0.015 and 0.020mm (0.0004, 0.0006 and 0.0008 inch) diameter drills, which I know he will have used correctly. A key factor in micro-machining is having tool concentricity correct. On a machining centre, tool run-out is easily controlled, either by buying a machining centre with nearly zero spindle run-out or using a tool holder where the tool can be independently controlled away from the shank. These holders are readily available from stock from numerous suppliers. A second key factor is getting feeds and speeds correct. Micro machining requires a different set of rules, especially when drilling. An important fact is not to run the spindle too quickly, as the tool needs a chance to cut - and you don’t want to create too much friction at the web which is in constant contact with the workpiece, unlike an end mill where a tooth will be in continuous ‘short-term’ contact. When discussing tooling as small as 0.010mm diameter, customers are very surprised that these tools can actually be manufactured. Yet there are numerous manufacturers that can produce drills and end mills at these dimensions that can give machining depths up to 6xD and 10xD. Similar size end mills generally have shorter cutting lengths. This is testament to the really well produced tool grinding machines that pay remarkable attention to workholding, wheel measurement and positioning. They are well assisted by the oil coolant suppliers and importantly the raw carbide suppliers who are developing systems to provide carbide grains small enough to be bonded together, yet still be machined to micron tolerances. These tool manufacturers can also offer CBN, diamond, PCD and HSS products. Drilling into the challenges of micro-drilling When customers drill they are taking some of the uncertainty out of machining because like a piece of chalk, the strength is in its longitudinal axis and not across its width. Therefore using small diameter drills creates fewer issues than small end mills. Parameters are influenced by the material, the forms to be cut, surface finish and the type of tool. This results in the tool needing to be very resilient to wear. Consideration also needs to be given to whether coolant is required and if so, is it water based, oil mist or pure oil? I cannot easily supply an answer, as each job is a different challenge and due consideration has to be applied to each individual question asked. One manufacturer had a long machining cycle but improved the quality of the job by 75%, just by changing from a water based coolant to oil mist (MQL). When the end mill diameter is small, the geometry options are reduced. In macro tooling, ball nose, corner radius and square end mills are the norm, but as we get to micro, the ability to grind a corner or ball nose forms becomes more difficult. With polymer machining, carbide end mills generally only have a single flute when going below 0.1mm diameter, the tool cutting edges will vary in length with 2xD, 4xD and 6xD readily available. If you want a CBN tool, they are generally only supplied in 1xD length, reducing form depths - again it must be stressed that tool concentricity is critical. A common thread in micro-machining For threads, our watchmaking friends show how small parts really should be made; not only with the turned screws but also with threaded holes in plates. A good example is an S0.30 thread whirling tool with an OD of just 0.21mm. This tool only has one tooth but if more teeth are required why not try a multi-fluted S0.8 thread tool with an outside diameter of just 0.6mm. Having discussed threading, how about putting threads in sintered tungsten carbide? I can hear people saying ‘not possible’, but it is. And with all machining, if you have spindle concentricity, the correct feed and speed - it’s easily achievable. Threads from M2 to M8 can be machined with depths from 4 to 24mm. Firstly, a hole in tungsten carbide is required - again I can hear people thinking about EDM, but no, let’s just drill a hole. Drills are available from 0.4mm diameter and require 20,000rpm, but once the diameter increases to 0.5mm, the spindle speed drops rapidly to 15,000rpm, so it is in the range of most high-quality machining centres. Additionally, surfaces of tungsten carbide can be milled and tooling is available from 0.2mm to 6.0mm diameter in either ball nose or corner radius tool design that is capable of surface finishes as good as Ra0.010µm. Answering the questions around achieving micron precision Machining small features on a workpiece invariably raises the question of accuracy, is it positioned where the feature is required and within the agreed tolerance? Is the measuring machine accurate enough to measure to the required dimensions? Is the machining centre toleranced to position the feature within the target area? There are many machines being offered that refer to a national standard that may have been set a number of years ago. Does that standard include an allowance for reversal error? What is the tolerance for circular interpolation in both clockwise and anti-clockwise directions? There are lots more questions that can be asked but suffice to say there are manufacturers specifying the accuracy of the machine by what it will produce on your workpiece, which is the information that you really need to know. With all customers, I ask the question “is the tool running true?” and this phrase can be read a number of times in the previous paragraphs, but its importance cannot be stressed enough. Spindle speeds and feeds can be varied for a tool on different machines, but tool concentricity is what ensures the workpiece is correct. Each element of small feature or tight tolerance machining will raise questions as to how all the elements fit together. There are now more companies thinking they can achieve their goal, but not achieving it. This is because they haven’t addressed issues mentioned here. Surface finish, size and tolerances are all achievable, we just need to tackle the problems correctly - and not just assume that particular parameters are acceptable.

I chat with Dr Niraj Rai from The Birbal Sahni Institute of Palaeosciences about the latest paper published in www.cell.com. Dr Rai is one of the co-authors of this paper. You can read the paper here https://www.cell.com/cell/fulltext/S0... You can follow Dr Rai on Twitter @NirajRai3 You can follow me on Twitter @kushal_mehra

Foundations of Amateur Radio The other week I participated in a contest. This particular contest was on the 80m band, around 3.5 MHz. The contest itself, while worthy of a mention, the Harry Angel Memorial Sprint, runs for 106 minutes and commemorates every year of Harry's life, at the time, the oldest radio amateur in Australia. I made two contacts. Count 'm and weep. Two. So, you could do the thing that I might have done in a previous contest, smiled, thought, "Wow, that's not very many contacts." and got on with life. You're free to do that, but I wouldn't be talking about this today if I shared your view. In fact I'm sure that in my activities as a radio amateur I've managed to learn, and in some ways unlearn some things along the way. In a previous contest I might have operated a club station, made contacts a plenty, added to the overall club score, added new countries and multipliers, had some good natured ribbing to go along with it and walked away with nothing to show for it on my own log. The truth is that for many of my on-air contest activities I made contacts for other callsigns, those of fellow amateurs, clubs, special events, you name it, I made contacts. Don't get me wrong, there's absolutely nothing wrong with that, nor was it a waste of time. I learnt loads from those experiences, but my own callsign log rarely, if ever, got an outing in such activities. So, this contest was for me. For my callsign, using my radio, my antenna, my location, my patience and my skills. I did the contest because I wanted to, for me. As you know, I'm a fan of operating QRP, that is, low power, so this contest I used 5 Watts, a Yaesu FT857d, a multi-tap vertical antenna, screwed onto a mount on the back of my car, parked next to a river with water to the East of me, so I could benefit from any gain that water nearby might offer me. As an aside, I'll talk more about water and gain at some other time, because it appears that not is all as my handed-down in hush-hush terms from mentor to me, would have me believe. I don't yet know enough to point at anything, but there's more than apparently meets the eye. Watch this space. Anyway, two contacts. Not even that far from me, about 230km South and 20km North East. Both with SSB. I heard about 20 stations, some up to 3,500km away, but they were dealing with S7 noise where I had none. That's right, no noise, S0, in the middle of the city. In addition to a heart stopping moment when the lights came on in the car park where I had set-up, my biggest fear being noisy lights, which turned out to be unfounded, my other take-aways were that I really should bring spare batteries for my LED lamp, and that I called it an LCD lamp last week. Not sure what I was thinking. I logged using pen and paper, in doing so I was upholding a fine tradition of radio amateurs everywhere, pen and paper is by far the most popular method of logging and with two contacts made, that's not surprising. I'm still on the lookout for sensible logging on a phone, but so-far that's eluded me. Perhaps I should write one and sell it, become rich and famous, retire, become loved in the community, kiss babies ... who am I kidding? Seriously though. What would the ideal phone based logging app look like to you? As for the baby-kissing famous one, let me know when you meet them, I'll stay away. I'm Onno VK6FLAB

Dr. Paul Wang:           Welcome to the monthly podcast On the Beat for Circulation Arrhythmia and Electrophysiology. I'm Dr Paul Wang, editor-in-chief, with some of the key highlights for this month's issue. We'll also hear from Dr. Suraj Kapa reporting on new research from the latest journal articles in the field.                                                 In our first article, Barry Maron associates report on the long term clinical course of hypertrophic cardiomyopathy patients following ICD therapy for ventricular arrhythmias. They studied a cohort of 486 high-risk hypertrophic cardiomyopathy patients with ICDs from eight international centers. Of these 486 patients over 6.4 years, 94 patients or 19% experienced appropriate ICD interventions, terminating VT or VF. Of the 94 patients receiving appropriate ICD therapy, 87 were asymptomatic or only mildly symptomatic at the time of appropriate ICD interventions. Of these 87 patients, 74 or 85% remained in classes one or two without significant change in clinical status of the subsequent 5.9 years up to 22 years. Among the 94 patients, there was one sudden death in three patients who died from non arrhythmic hypertrophic cardiomyopathy related processes. Post ICD intervention, freedom from hypertrophic cardiomyopathy, mortality was 100% at one year, 97% at five years, and 92% at 10 years, distinctly lower than the risk of ischemic or non ischemic cardiomyopathy in ICD trials.                                                 Hypertrophic cardiomyopathy patients with ICDs interventions reported the heightened anxiety and expectation of future shocks. However, they did not affect general psychological well-being or quality of life. The authors concluded that in hypertrophic cardiomyopathy, unlike ischemic heart disease, prevention of sudden death with ICD therapies unassociated with a significant increase in cardiovascular morbidity and mortality, nor transformation into heart failure deterioration, ICD therapy does not substantially impair overall psychological and physical well-being. In our next article, Abdulla Damluji and associates examined the cost of hospitalizations for cardiac arrest using the US nationwide inpatient sample from 2003 to 2012. Using the log transformation of inflation adjusted costs the authors examined 1,387,396 patients who were hospitalized after cardiac arrest. They had a mean age of 66 years. Inpatient procedures included coronary angiography in 15%, PCI in 7%, intra-aortic balloon pump in 4.4%, therapeutic hypothermia in 1.1%, and mechanical circulatory support in 0.1% of patients.                                                 Notably the rates of therapeutic hypothermia increased from 0 in 2003 to 2.7 in 2012, p less than 0.001. Both hospital charges inflation adjusted costs linear increased over time. In a multi-variant analysis predictors of inflation adjusted costs included large hospitals size, urban teaching hospital, and length of stay. Among co-morbidities, atrial fibrillation or fluid and electrolytes imbalance were the most common associated with cost. The authors found that during the period between 2003 and 2012 post cardiac arrest, hospitalizations had a steady rise and associated healthcare costs likely related to increase length of stay, medical procedures and systems of care.                                                 In our next paper, Peter Huntjens and associates examined intrinsic interventricular dyssynchrony as a predictor of human dynamic response to cardiac resynchronization. The authors use a cardiovascular computational model CircAdapt to characterize the isolated effect of intrinsic interventricular or intraventricular activation on resynchronization therapy response that is the change in LV dP/dt max. The simulated change in LV dP to dt max had a range of 1.3 to 26.5% increased considerably with increasing inter ventricular dyssynchrony. In contrast, the isolated effect of intra ventricular dyssynchrony was limited with the change in the LV dP/dt max range and the left ventricle from 12.3 to 18.3% in the right ventricle from 14 to 15.7%.                                                 Secondly, electrocardiographic imaging derived activation characteristics of 51 CRT candidates were used to create individual models of ventricular activation in CircAdapt. The model predicted change in LV dP/dt max was close to the actual value in left bundle branch block patients with 2.7% difference between measured and simulated when only intrinsic interventricular dyssynchrony was personalized. Among non left bundle branch block patients a change in LV dP/dt max was systematically over predicted by CircAdapt with a 9.2% difference between measured and simulated. Adding intra ventricular activation to the model did not improve the accuracy of response prediction. The authors found that computer revealed intrinsic interventricular dyssynchrony is the dominant component of the electrical substrate driving the response to CRT.                                                 In the next paper Kenji Kuroki and associates examined the use of voltage limit adjustment of substrate mapping and fast Fourier transform analysis of local ventricular bipolar electrograms during sinus rhythm to predict VT isthmuses. They performed these studies and nine post infarction patients who underwent catheter ablation for total of 13 monomorphic ventricular tachycardias. Relatively higher voltage areas on electroanatomical map or defined as high voltage channels, which were further classified as full or partial if the entire or more than 30% of the high voltage channel was detectable. 12 full high voltage channels were identified in seven of nine patients. Relatively higher fast Fourier transform areas were defined as high frequency channels, which were located on seven of 12 full high voltage channels. Five VT isthmuses or 71% were included in the seven full high voltage channels positive in high frequency channel positive sites.                                                 While no VT isthmuses were found in five full high voltage channel positive but high frequency channel negative sites, high frequency channels were identical to 9 out of 16 partial high voltage channels. Eight VT isthmuses or 89% were included in nine partial high voltage channel positive in high frequency channel positive sites, whereas no VTs isthmuses were found in the seven partial high voltage channel positive and high frequency channel negative sites.                                                 All high voltage channel positive in high-frequency channel positive sites predicted VT isthmus with a sensitivity of 100% and specificity of 80%. The authors concluded that based on this small series that combined use of voltage, limited adjustment and fast Fourier transform analysis may be useful method to detect VT isthmuses.                                                 In the next study, John Whitaker and associates examined the use of lesion index, LSI index, a proprietary algorithm combining contact force, radio-frequency application duration, and RF current. Cardiac CT was used to assess atrial tissue thickness. Ablation lines two to three per animal were created in the right atrium in seven mini pigs with point lesions using 25 watts of energy. Two weeks after the ablation, serial sections of targeted atrial tissue or examine histologically to identify gaps and transmural ablation. LSI guidelines had a lower incidence of histological gaps. Four gaps in the 69 catheter moved or 5.8% compared to ablation using LSI plus two millimeter lines in which there is seven gaps in 33 catheter moves or 21.2% and using LSI plus four millimeter lines in which there are 15 gaps in 23 moves or 65.2% p less than 0.0. The change in LSI was calculated retrospectively is a distance between two adjacent lesions above the mean LSI of the two lesions. Changing LSI values of 1.5 or less were associated with no gaps in transmural ablation.                                                 The authors concluded that in this mod of chronic atrial ablation delivery of uninterrupted transmural linear lesions may be facilitated using LSI to guide catheter movement. When change in LSI between adjacent legions is 1.5 millimeters or lower, no gaps in atrial linear lesions should be expected.                                                 In our next paper, Matthew Bennett and associate examined whether their response to antitachycardia pacing in patients with ICD could further discriminate ventricular from super ventricular arrhythmias in patients receiving ATP in the RAFT trial. The RAFT trial randomized 1,798 patients with New York Heart Association class two or three heart failure, left ventricular ejection fraction less than or equal to 30%, in QRS duration 120 millisecond or greater, to an ICD plus or a minus cardiac resynchronization. Beginning with 10,916 ATP attempts for 8,150 tachycardia episodes in 924 patients, the author's excluded tachycardias where ATP terminated the episode or were the specific etiology tachycardia was uncertain. In this study, they analyzed 3,676 ATP attempts delivered to 2,046 tachycardia episodes in 541 patients. The authors found that a shorter difference between the post pacing interval is PPI minus TCL, was more likely to be associated with VT than SVT, mean of 138.1 milliseconds for VT and 277.4 milliseconds for SVT p, less than 0.001. A PPI minus TCL value of less than or equal to 300 milliseconds had a sensitivity in 97.4% and a specificity of 28.3% for VT.                                                 The authors concluded that specifically the PPI minus TCL following antitachycardia pacing may help distinguish ventricular from supraventricular arrhythmias.                                                 In the next study, Shailee Shah and Amr Barakat and associates examined the outcomes after repeat AF ablation. The authors examined 137 patients out of a total of 10,378 patients undergoing Afib ablation who had had initial long-term success defined from recurrent arrhythmias for greater than 36 months off anti-arrhythmic drugs in subsequent underwent repeat ablation for recurrent atrial fibrillation. The median arrhythmia free period that define long-term success was 52 months. In redo-ablations reconnection of at least one of the pulmonary veins was found in 111 or 81% of patients. Additional non PV ablations were performed in 127 or 92.7% of patients. After a mean follow-up of 17 months, 103 patients or 75% were arrhythmia-free, 79 off anti-arrhythmics, and 24 on arrhythmics. The authors found that repeat ablations with re-isolation to the point of veins and modifying the atrial substrate had a good success rate.                                                 In the next article Qiongling Wang and associates hypothesized that genetic inhibition of CaMKII oxidation in a mouse model of Duchenne muscular dystrophy can alleviate abnormal calcium homeostasis thus preventing ventricular arrhythmias. The authors tested whether the selective loss of oxidation of the CaMKII effects ventricular arrhythmias in the mouse model of Duchenne muscular dystrophy. Genetic inhibition of ox-CaM kinase II by knocking replacement of the regulatory domain methionines with valines, which we'll call MMVV, prevented ventricular tachycardia in the mdx mice. Confocal calcium imaging of ventricular myocytes, isolated from the mdx MMVV mice revealed normalization of intra-calcium release events compared to myocytes from the mdx mice. Abnormal action potentials as assessed by optical mapping mdx were also alleviated by genetic inhibition of ox-CaMK II. Knockout of the NADPH oxidase regulatory sub-unit P 47 Fox normalized elevated ox-CaMK II, repaired intracellular calcium hemostasis and rescued inducible ventricular arrhythmias in the mdx mice. The authors concluded that inhibition of ROS or ox-CaMK II protects against pro-arrhythmic intracellular calcium handling, preventing ventricular arrhythmias in a mouse model of Duchenne muscular dystrophy.                                                 In the next article, Kyohei Marume and Teruo Noguchi and associates examined whether the combination of QRS duration of 120 milliseconds or greater in late gadolinium enhancement is a precise prognostic indicator for the primary endpoint of all cause death and a composite of sudden cardiac death or aborted sudden cardiac death in 531 patients with dilated cardiomyopathy. They also analyzed the association between the combination of late gadolinium enhancement and increased QRS duration in these end points among patients with a class one indication for implantable defibrillator. The author's divided study patients in three groups according to late gadolinium enhancement in QRS duration. Two negative indices that is late gadolinium enhancement negative and narrow QRS, one positive index with either late gadolinium enhancement positive or wide QRS or two positive indices late gadolinium positive and wide QRS and followed them for 3.8 years. Multiple variable Cox regression analysis identified to positive indices as significant predictors of all cause death. A hazard ratio of 4.29 p equals 0.026. Among the 317 patients with a class one indication for ICD, the five year event rate of sudden cardiac death or aborted sudden cardiac death was lowest in the two negative indices groups, 1.4%. With propensity score matching cohorts the two negative indices group had a significant lower event rate of sudden cardiac death or aborted sudden cardiac death than to two other groups hazard ratio 0.2, p equals 0.046.                                                 The authors concluded that the combination of late gadolinium enhancement in wide QRS provides additional prognostic stratification compared to late gadolinium enhancement status alone.                                                 In the next study, Matthew Sulkin and associates examined whether a novel local impedance measurement on an ablation catheter identifies catheter tissue coupling and is predictive of lesion formation. The author's first studied explanted hearts, 10 swine, and then in vivo 10 swine, using an investigational electro anatomical mapping system that measures impedance from an ablation catheter with mini electrodes incorporated into the distal electrode. Rhythmia and Intellanav, Boston Scientific.                                                 Explanted tissue was placed in a warmed 37 degree celsius saline bath mounted on a scale, and the local impedance was measured 15 millimeters away from the tissue to five millimeters of catheter tissue compression at multiple catheter angles. Lesions were created for 31 and 50 watts from 5 to 45 seconds for an N of 70. During in vivo valuation of the local impedance measurements of the myocardium 90 and blood pool 30 were guided by intracardiac ultrasound while operators were blinded to the local impedance data. Lesions were created with 31 and 50 watts for 45 seconds in the ventricle with an n of 72. The local impedance of myocardium, which was 119.7 ohms, was significantly greater than in blood pool 67.6 ohms the p of less than 0.01. Models that incorporate local impedance drop to predict lesion size had better performance that models incorporate force time integral r squared of 0.75 versus r squared of 0.54 and generator impedance drop r squared of 0.2 versus r squared of 0.58. Steam pops displayed a significantly higher starting local impedance and a larger change in local impedance compared to successful RF applications, p less than 0.01.                                                 The authors concluded that local impedance recorded for miniature electrodes provides a valuable measure of catheter tissue coupling and the change in local impedance is predictive of lesion formation during RF ablation.                                                 In the next paper, Boaz Avitall and associates found that the rising impedance recorded from a ring electrode placed two millimeters from the cryoballoon signifies ice formation covering the balloon surface and indicates ice expansion. The authors studied 12 canines in a total of 57 pulmonary veins, which were targeted for isolation. Two cryoapplications were delivered per vein with a minimum of 90 and a maximum 180 second duration. Cryoapplications was terminated upon reaching a 500 ohm change from baseline. Animals recovered 38 plus or minus six days post procedure, and the veins were assessed electrically for isolation. Heart tissue was histological examined. Extra cardiac structures were examined for damage. Pulmonary vein isolation was achieved in 100% of veins if the impedance reached 500 ohms in 90 to 180 seconds. When the final impedance was between 200 and 500 ohms within 180 seconds of freeze time, pulmonary vein isolation was achieved in 86.8%. For impedance of less than 200 ohms pulmonary vein isolation was achieved in 14%. No extra cardiac damage was recorded. The authors found that impedance rise of 500 ohms at less than 90 seconds with a freeze time of 90 seconds resulted in 100% pulmonary vein isolation.                                                 In our final papers Sally-Ann Clur and associates examined left ventricular isovolumetric relaxation time as the potential diagnostic marker for fetal Long QT Syndrome. Left ventricular isovolumetric contraction time, ejection time, left ventricular isovolumetric relaxation time, cycle length, and fetal heart rate were measured using pulse doppler wave forms in fetuses. Time intervals were expressed as percentage of cycle length, and the left ventricular myocardium performance index was calculated. Single measurements were stratified and compared between Long QT Syndrome fetuses and controls. Receiver operator curves were reformed for fetal heart rate in normalized left ventricular isovolumetric relaxation time. A linear mixed effect model including multiple measurements was used to analyze fetal heart rate, the left ventricular iso volume metric relaxation time, and the left ventricular myocardial performance index. There were 33 Long QT fetuses in 469 controls. In Long QT fetuses the left ventricular isovolumetric relaxation time was prolonged in all groups, p less than 0.001, as was the left ventricular isovolumetric relaxation time.                                                 The best cutoff to diagnose Long QT syndrome was the normalized left ventricular isovolumetric relaxation time greater than equal to 11.3 at less than or equal to 20 weeks, giving a sensitivity in 92% and a specificity of 70%. Simultaneous analysis of the normalized left ventricular isovolumetric relaxation time and fetal heart rate improved the sensitivity and specificity of Long QT Syndrome, AUC of 0.96. The normalized left ventricular isovolumetric relaxation time, the left ventricular myocardial performance index, and fetal heart rate trends differed significantly between Long QT Syndrome fetuses and controls throughout gestation.                                                 The authors concluded that left ventricular volumetric relaxation time is Prolonged QT fetuses. Findings of a prolonged normalize left ventricular isovolumetric relaxation time, and sinus bradycardia can improve the prenatal detection of fetal Long QT Syndrome.                                                 That's it for this month, but keep listening. Suraj Kapa will be surveying all journals for the latest topics of interest in our field. Remember to download the podcasts On the Beat. Take it away Suraj. Suraj Kapa:                          Thank you, Paul and welcome back to On the Beat were we will be summarizing hard-hitting articles across the entire electrophysiologic literature. Today we'll be starting within the realm of atrial fibrillation where we're review an article within the realm of anticoagulation and stroke prevention. Quon et al. published in last month's issue of JACC cardiac electrophysiology on anticoagulant use and risk of ischemic stroke and bleeding in patients with secondary atrial fibrillation. It is well known that use of anticoagulation in atrial fibrillation can reduce overall thromboembolic outcomes. However, its role in secondary atrial fibrillation is unclear. Thus, the authors sought to evaluate the effects anticoagulant use on stroke and bleeding risk. Amongst those where atrial fibrillation occurred in the setting of acute coronary syndrome, pulmonary disease, or sepsis. Amongst around 2300 patients evaluated retrospectively there was no evidence of a lower incidence of ischemic stroke among those treated with anticoagulants compared to those who are not.                                                 However, anticoagulation was associated with a higher risk of bleeding in those with new onset AF associated with acute pulmonary disease. The authors suggest as a result that there is unclear overall benefit for long-term anticoagulation in patients with presumed secondary atrial fibrillation. The difficulty in assessing this is how to define secondary atrial fibrillation. However, in many studies patients who developed in the setting of acute illness still had a high risk of developing quote unquote clinically significant AF in long-term follow-up. However, this was not necessarily absolute as many patients not necessarily develop AF that could be considered clinically significant. Thus, the clinical question that arises is: how long should we treat a patient with anticoagulation when they have presumed secondary atrial fibrillation. These data seem to suggest that there may be no net overall benefits. In other words, all-comers with secondary atrial fibrillation should not necessarily be forever treated with anti-coagulation. However, this slightly requires clinical trials to evaluate further.                                                 Next we delve into the realm of cardiac mapping and ablation where we view an article by Gaita et al. entitled 'Very long-term outcome following transcatheter ablation of atrial fibrillation. Are results maintained after 10 years of follow-up?', published in Europace last month. While pulmonary vein isolation is a widely accepted approach for treatment of atrial fibrillation, most reported studies review outcomes in terms of freedom of AF over a relatively short time period, generally two to five years. However longer term follow up is inconsistently reported. Gaita et al. sought to review 10 year outcomes amongst 255 patients undergoing ablation in a single center. They noted 52% remainder arrhythmia-free amongst a mixed cohort of both paroxysmal and persistent patients while 10% progressed to permanent atrial fiBrillation. They found that absence of increases in blood pressure, BMI, and fasting glucose was protective against an arrhythmia recurrence.                                                 These findings suggest that in a relatively small cohort of patients limited to a single center that even long-term outcomes after pulmonary vein isolation are generally quite good, exceeding 50%. However, future freedom from atrial fibrillation is heavily tied to control of other risk factors. In other words, if a patient is going to have poor control of diabetes, blood pressure, or gain weight, the benefit of their pulmonary vein isolation over long-term follow-up is likely less. These data thus highlight both the potential long-term benefit of PVI, but also the importance of counseling patients regarding the need for continued management and control of future and existing risk factors.                                                 Staying within the realm of atrial fibrillation we next review an article by Weng et al. entitled 'Genetic Predisposition, Clinical Risk Factor Burden, and Lifetime Risk of Atrial Fibrillation' published in last month's issue of circulation. The probability of detecting atrial fibrillation in patients based on clinical factors and genetic risk is unknown. Weng et al. sought to clarify whether a combination of clinical and polygenic risk scores could be used to predict risk of developing atrial fibrillation over long-term followup in the Framingham Heart Study. Amongst 4,600 individuals, 580 developed incident atrial fibrillation and had an overall lifetime risk of developing atrial fibrillation of 37%. Those are the lowest risk tertile based on clinical risk factor burden and genetic predisposition had a lifetime risk of 22% versus 48% in the highest. Furthermore, a lower clinical risk factor burden was associated with delayed atrial fibrillation onset. In order to identify patients with atrial fibrillation, before negative sequelae such as stroke occur, patient and physician understanding of risk and monitoring needs is necessary. The fact is that it will be great to identify every single patient who has atrial fibrillation before they have a negative sequela of that atrial fibrillation such as ischemic stroke.                                                 However, performing continuous monitoring of all patients with potential negative sequelae of atrial fibrillation is extraordinarily difficult. The reason is it's excessively costly. We cannot monitor the entire population irrespective of whatever the risk factors are. However, if we're able to identify the highest risk cohorts early on before the atrial fibrillation onsets, this may offer opportunities for use of newer cheaper monitors. The work by Weng et al. suggests one such possible approach combines clinical and polygenic risk scores. Actionability of these data, however, remains to be seen and further validation other cohorts is necessary to clarify generalized ability.                                                 The next article we review is published in last month's issue of the Journal of American College of Cardiology by Lopes at al. entitled 'Digoxin and Mortality in Patients With Atrial Fibrillation. Lopes et al. sought to evaluate the impact of the Digoxin on mortality in patients with atrial fibrillation and the association with the Digoxin serum concentration and heart failure status. They value this association in over 17,000 patients. At baseline 32% were receiving Digoxin. Baseline Digoxin use did not associate with risk of death, but even in these patients a serum concentration of greater than 1.2 nanograms per milliliter was associated with a 56% increase in mortality risk. For each .5 nanogram per milliliter increase in oxygen concentration the hazard ratio increased by 19% for overall mortality. This was irrespective of heart failure status. Furthermore, in patients who are newly started in Digoxin over the follow-up period, the risk and death and sudden death was higher. These data suggests a significant risk associated with Digoxin use for management of atrial fibrillation irrespective of heart failure status. Furthermore, serum valleys above 1.2 require close consideration of dose de-escalation. Whether there is any optimal dose, however, from the study is unclear. These data amongst a host of prior data strongly suggest again strategic use of Digoxin  principally for the management of atrial fibrillation.                                                 Moving on within the realm of atrial fibrillation, we review an article published in last month's issue of Circulation Research by Yan et al. entitled Stress Signaling JNK2 Crosstalk with CaMKII Underlies Enhanced Atrial Arrhythmogenesis. In this more acellular based study the mechanism underlying atrial arrhythmogenesis associated with aging was evaluated. Yan et al. sought to figure out whether the stress response JNK in calcium mediated arrhythmias might contribute to atrial arrhythmogenesis in aged transgenic mouse models. They demonstrated significant increased activity of JNK2 and aging atria, those furthermore associated with rhythmic remodeling. This association was mediated through CaMKII and ryanodine receptor channel function, with activation of the former leading to increased calcium leak mediated by the ladder. This in turn related to increase atrial fibrillation likelihood. Identifying novel targets for atrial fibrillation therapy is critical. Given atrial fibrillation is a complex disease process related to a multitude of risk factors it can be assumed that the contribution of any single factor may be mediated through distinct mechanisms.                                                 Aging in particular as well regarded, but considered to be non-modifiable risk factor for atrial fibrillation. Identifying genes or pathways, the immediate aging associated fibrillation, may take the risk of aging as no longer a non-modifiable thing. The finding of the significance of JNK2 and associate downstream effects with AF risks and aging hearts may hold potential in offering unique therapeutic targets.                                                 Finally, within the realm of atrial fibrillation, we're viewing article by Chen et al. in last month's issue of the Journal of the American Heart Association entitled Association of Atrial Fibrillation With Cognitive Decline and Dementia Over 20 Years: The ARIC-NCS Study. Multiple studies have suggested a significant association between atrial fibrillation risk of dementia. However, these studies have limited time follow-up and were often done and predominantly white patients. Thus, the authors sought to use the data from ARIC, the Atherosclerosis Risk in Communities Neurocognitive Study, to assess the risk of cognitive decline associated with atrial fibrillation. Amongst over 12,000 participants, a quarter of whom are black and half of whom are white, they noted 2100 patients developed atrial fibrillation and 1,150 develop dementia over a 20 year follow up period.                                                 There was a significantly greater risk of cognitive decline amongst those who developed atrial fibrillation. In turn incident atrial fibrillation for the follow-up period was associated with a higher risk of dementia even after adjusting for other clinical and cardiovascular risk factors such as incidents that ischemic stroke. These data further strengthened prior evidence of a direct link between atrial fibrillation and risk of cognitive decline and dementia. Understanding this long-term risk raises the need to additionally identify approaches to prevent this occurrence, which in turn is dependent on understanding the underlying mechanisms. The finding that the risk of cognitive decline dementias independent of ischemic stroke events raises concern that either subclinical micro-embolic events or other factors may be playing a role in this risk and in turn raises question as to how best to prevent them. Until better understood, however, the question of whether the association is causal remains to be seen.                                                 Changing gears yet again, we now delve into the realm of ICDs, pacemakers and CRT. Published in last month, issue of Heart Rhythm Tarakji et al. published a paper entitled 'Unrecognized venous injuries after cardiac implantable electronic device transvenous lead extraction.' Overall risk of transvenous lead extraction includes that of potentially fatal venous laceration. The authors sought to evaluate the incidence of venous injury that may be unrecognized based on microscopic study of extracted leads. Amongst 861 leads obtained from 461 patients they noted 80 leads or almost 9%. Amongst 15% of patients showed segments vein on the lead body, most of which were transmural including the tissue layer. However, in terms of clinical significance, only 1% had need for emergent surgical intervention for clinically significant venous laceration. Risk factors for having the entire vein on the lead included age of lead, ICD leads, and the use of the laser sheath.                                                 These findings suggest that there may be a high incidence of subclinical venous injury after lead extraction though rarely resulting clinically apparent sequelae. As would be expected, venous injury, including transmural removal of portions of the vein traversed by the lead, was more common amongst older leads, which generally more often require laser sheets and ICD leads. The question is however, whether this carries any direct clinical implications. One they may be considered is the potential additive risk of an advancing new lead through the same venous channel, particularly in the setting of potential transmural venous injury that already exists.                                                 Next in last month's issue of Heart Rhythm we review an article by Sharma at al. entitled 'Permanent His-bundle pacing as an alternative to biventricular pacing for cardiac resynchronization therapy: A multicenter experience.' The use of resynchronization therapy for treatment of patients with heart failure and wide QRS has been shown to offer morbidity and mortality benefits. However, many patients maybe non-responders, and recent studies on His bundle pacing of suggested potential clinical benefits. His bundle pacing essentially only requires one pacing catheter attached within the region of the His bundle Sharma et al. sought to evaluate the safety and success rates of His bundle pacing for patients who have either failed standard resynchronization therapy or in whom most tried as a primary intervention. They noted His bundle pacing was successful in 90% of patients with reasonable myocardial and His bundle capture thresholds. Patients in both groups exhibits significant narrowing of QRS morphology and improvement in left ventricular ejection fraction from a mean of 30 to 43%. However, a total of seven patients had lead related complications.                                                 These database on a retrospective analysis of two types of patients, those failing standard biventricular therapy, and those on whom his bundle pacing was attempted as a primary modality suggest overall safety and efficacy in a handful of experienced centers. The promise of His bundle pacing is that a may allow for more effective resynchronization than standard approaches. The high rate of success suggests that His bundle pacing maybe both safe and reasonable to pursue. However randomized trials across more centers are needed to fully prove its benefit, particularly as a primary modality of treatments.                                                 Next we review ICDs and chronic kidney disease. In last month's issue of JAMA cardiology by Bansal at al. entitled 'Long-term Outcomes Associated With Implantable Cardioverter Defibrillator in Adults With Chronic Kidney Disease.' While the benefit of ICDs in patients with low EF is widely recognized, modifying factors that may increase risk of death are not as well defined. These include things like advanced age and chronic kidney disease. Bansal et al. sought to evaluate long-term outcomes and ICD therapy in patients with chronic kidney disease. In retrospective study of almost 5,900 ambulatory patients amongst whom 1550 had an ICD, they found no difference in all cause mortality. However, ICD placement was associated with an increased risk of subsequent hospitalization due to heart failure or any cause hospitalization.                                                 In light of recent studies such as DANISH the robust sense of ICD benefit is being questioned. One of the thoughts for the absence of similar benefit to prior studies lies in the improving care of ambulatory heart failure patients. In patients with chronic kidney disease several questions rises to the risk with ICD, including infectious risk in dialysis patients and the concomitant mortality risk with renal dysfunction. The author suggested in retrospective study, no incremental benefit of ICDs in patients with chronic kidney disease and perhaps some element of added risk is related to hospitalization. However, this study has several limitations. It is retrospective and many patients received ICDs may have been perceived to be sicker in some way. Thus care must be taken in interpretation, but consideration of randomized studies to adjudicate benefit are likely necessary.                                                 Finally, within the realm of devices, we reviewed an article by Tayal et al. entitled "Cardiac Resynchronization Therapy in Patients With Heart Failure and Narrow QRS Complexes.' publishing the Journal of American College of Cardiology last month. Several parameters have been stressed to identify benefit of resynchronization therapy in patients with wide QRS include cross correlation analysis with tissue doppler imaging. However, many patients may have evidence in mechanical dyssynchrony even in the absence of an apparent wide QRS thus Tayal et al. sought to evaluate the benefit of resynchronization therapy amongst 807 patients with heart failure and a narrow QRS mean criteria in a randomized study. Of the 807 46% had delayed mechanical activation. Those without delay mechanical activation had underwent we standardization therapy and were associated with worse overall outcomes likely due to new delayed mechanical activation potentially related to CRT pacing. These data support the absence of a role for resynchronization therapy in patients with a narrow QRS. This is expected as resynchronization therapy likely offers the most benefit in patients with mechanical dyssynchrony that results from electrical dyssynchrony.                                                 Since by its very nature resynchronization therapy relies on non physiologic cardiac pacing thus compared to normal cardiac activation the nature of resynchronization pacing is desynchronization. These data support the absence of a role for resynchronization therapy in patients with heart failure and narrow QRS complexes.                                                 Moving on to cellular electrophysiology we review an article by Kozasa et al. published in last month's issue of Journal of Physiology entitled 'HCN4 pacemaker channels attenuate the parasympathetic response and stabilize the spontaneous firing of the sinoatrial node.' Heart rate is controlled by an interplay between sympathetic and parasympathetic components. In turn HCN4 abnormalities have been implicated in congenital sick sinus syndrome. The authors sought to clarify the contribution of HCN4 to sinus node autonomic regulation. They created a novel gain-of-function mouse where the HCN4 activity could be modulating from zero to three times normal. They then evaluated ambulatory heart-rate variability and responsive heart rate to vagus nerve stimulation. They found HCN4 over-expression did not increase heart rate, but attenuated heart-rate variability. It also attenuated bradycardic response to vagus nerve stimulation. Knockdown of HCN4 in turn lead to sinus arrhythmia and enhanced parasympathetic response. These data suggest HCN4 attenuates sinus node response to vagal stimuli thus stabilizing spontaneous firing of the node. The clinical application of this remain to be seen but are maybe important in that they highlight a mechanism for a heretofore poorly understood mechanism for how exactly HCN4 abnormalities may lead to sick sinus syndrome.                                                 Within the realm of ventricular arrhythmias we highlighted a number of articles published this past month. The first article we review was published in last month's issue of JACC clinical electrophysiology, entitled characterization of the electrode atomic substrate and cardiac sarcoidosis: correlation with imaging findings of scarring inflammation published by [inaudible 00:41:40] et al. In patients with cardiac sarcoidosis one of the questions is how to define the electronic atomic substrate, particularly before we entered the electrophysiology laboratory. Both active inflammation and replacement fibrosis maybe be seen in patients. The authors evaluated in 42 patients with cardiac sarcoidosis, the association between an abnormal electrograms and cardiac imaging findings including PET and Computed Tomography, as well as Cardiac MRI. They noted that amongst these 40 patients, a total of 21,000 electrograms were obtained, and a total of 19% of these were classified as abnormal. Most of the abnormalities occurred in the basal paravalvular segments and intraventricular septum. They further noted that many of these abnormalities in terms of electrograms were located outside the low voltage areas, particularly as it relates to fractionation. In about 90% of patients they notice late gadolinium enhancements and they noted abnormal FDG uptakes suggesting active inflammation in about 48%.                                                 However, it should be noted that only 29 of the 42 patients underwent cardiac imaging. Segments with abnormal electrograms tended to have more late gadolinium enhancement evidence scar transmurality, and also they noted that the association of abnormal PET scan did not necessarily occur with abnormal electrograms. Thus, they concluded that in patients with cardiac sarcoidosis and ventricular tachycardia pre-procedural imaging with cardiac MRI could be useful in detecting electroanatomic map abnormalities that may in turn be potential targets for substrate ablation. However, they were more likely associated with more scar transmurality and lower degrees of inflammation on PET scanning. These data are important in that they highlight potential non-invasive means by which to understand where substrate might occur in patients with the cardiac sarcoidosis. It is well recognized that cardiac sarcoidosis is associated with increased risk of ventricular arrhythmias. These risks have increased ventricular arrhythmias, might be targetable with ablation. Newer therapies might even offer non invasive means by which to perform ablation in patients best. Thus if we could identify non based on mechanisms of identifying the substrate, this will be even more critical.                                                 The critical findings of this particular paper lie in noting that most of the abnormalities still is in intra ventricular sePtum in basal segments, and also that it is MRI in late gadolinium enhancement and associates more with the abnormal electrograms. Interestingly, the absence of inflammation correlating with the presence of more abnormal electrograms suggests that it is not so much the act of inflammation as being reflected in the endocardial map, but the existence of scar.                                                 Next, again within JACC clinical electrophysiology we review an article by Porta-Sánchez et al. entitled 'Multicenter Study of Ischemic Ventricular Tachycardia Ablation With Decrement Evoked Potential Mapping With Extra Stimulus.' The authors sought to conduct a multicenter study of decrement evoked potential base functional tech ventricular tachycardia substrate modification to see if such mechanistic and physiologic strategies could result in reduction in VT burden. It is noted that really only a fraction of the myocardium in what we presume to be substrate based on the presence of low voltage areas are actually involved in the initiation and perpetuation of VT. Thus if we can identify the critical areas within the presumed substrate for ablation, this would be even a better way of potentially honing in on our targets. They included 20 consecutive patients with ischemic cardiomyopathy. During substrate mapping fractionated late potentials were targeted and an extra stimulus was provided to determine which display decrements. All patients underwent DEEP focus ablation with elimination being correlated with VT non-inducibility after radio-frequency ablation. Patients were predominantly male, and they noted that the specificity of these decrement evoked potentials to detect the cardiac isthmus for VT was better than that of using late potentials alone. They noted 15 of 20 patients were free of any VT after ablation of these targets over six months of follow-up, and there was a strong reduction in VT burden compared to six months pre ablation.                                                 They concluded that detriment evoked potential based strategies towards ablation for ventricular tachycardia might identify the functional substrate and those areas most critical to ablation. They in turn regarded that by its physiologic nature it offers greater access to folks to ablation therapies.                                                 This publication is important in that it highlights another means by which we can better hone in on the most critical regions for substrate evaluation in patients with ventricular tachycardia. The fact is more extensive ablation is not necessarily better and might result in increased risk of harm if we think about the potential effects of longer ablations or more ablation lesions. Thus if we could identify ways of only targeting those areas that are most critical to the VT circuits, we could perhaps short and ablation procedural time, allow for novel ways of approaching targeted ablation with limited amounts of ablation performed, or perhaps even improve overall VT outcomes by knowing the areas that are most critical to ensure adequate ablation therapy provided. However, we need to understand that this is still a limited number of patients evaluated in a non randomized manner. Thus whether or not more extensive ablation performed might have been better is as of yet unclear                                                 Staying within the realm of ventricular tachycardia we review an article published in last month's issue of Heart Rhythm by Winterfield et al. entitled the 'Impact of ventricular tachycardia ablation on healthcare utilization.' Catheter ablation of atrial tachycardia has been well accepted to reduce recurrent shocks in patients with ICDs. However, this is a potentially costly procedure, and thus effect on overall long-term health care utilization remains to be seen. The authors sought to evaluate in a large scale real world retrospective study the effect of VT ablation on overall medical expenditures in healthcare utilization. A total 523 patients met study inclusion criteria from the market scan database. After VT ablation median annual cardiac rhythm related medical expenditures actually decreased by over $5,000. Moreover the percentage of patients with at least one cardiac rhythm related hospitalization an ER visit decreased from 53 and 41% before ablation respectively, to 28 and 26% after ablation. Similar changes we're seeing in number of all cause hospitalizations and ER visits. During the year before VT ablation interestingly there was an increasing rate of healthcare resource utilization, but a drastic slowing after ablation.                                                 These data suggests that catheter ablation may lead to reduced hospitalization in overall healthcare utilization. The importance of these findings lies in understanding why we do the things we do. We can provide a number of therapies to patients, but we seek two different effects. One is the individual effect of improving their particular health. The second thing is trying to avoid increasing healthcare expenditures on a population level and making sure resources are utilized. If we can reduce recurrent hospitalizations and overall healthcare expenditure in patients by providing a therapy in addition to provide individual benefit, this is the optimal situation. These data suggests that VT ablation might provide such a benefits, that in fact it reduces overall healthcare utilization while improving overall outcomes.                                                 Next and finally within the realm of ventricular arrhythmias, we review more on the basic side the role of Titin cardiomyopathy leads to altered mitochondrial energetics, increased fibrosis and long-term life-threatening arrhythmias, published by Verdonschot et al. in last month's issue of European Heart Journal. It is known now that truncating Titin variants might be the most prevalent genetic cause of dilated cardiomyopathy. Thus, the authors sought to study clinical parameters and long term outcomes related to Titin abnormalities in dilated cardiomyopathy. They reviewed 303 consecutive and extensively phenotype dilated cardiomyopathy patients who underwent cardiac imaging, Holter monitoring, and endomyocardial biopsy and in turn also underwent DNA sequencing of 47 cardiomyopathy associated genes. 13% of these patients had Titin abnormalities. Over long-term followup they noted that these patients had increased ventricular arrhythmias compared to other types of dilated cardiomyopathy, but interestingly, they had similar survival rates. Arrhythmias in those Titin abnormal patients were most prominent in those who were subjected to an additional environmental trigger, including viral infection, cardiac inflammation, other systemic disease or toxic exposure. They also noted the cardiac mass was relatively reduced in titan admirable patients.                                                 They felt that all components of the mitochondrial electron transport chain we're simply up-regulated in Titin abnormal patients during RNA sequencing and interstitial fibrosis was also augmented. As a result, they concluded that Titin variant associated dilated cardiomyopathy was associated with an increased risk of ventricular arrhythmias, and also with more interstitial fibrosis. For a long time we have reviewed all non ischemic cardiomyopathy as essentially equal. However, more recent data has suggested that we can actually hone in on the cause. In turn, if we hone in on the cause, we might be able to understand the effects of specific therapies for ventricular arrhythmias based on that underlying cause. Patchy fibrosis might not be as amenable, for example, to ablation as discreet substrate that we might see in infarct related VT. Understanding the relative benefit in very specific types of myopathies might hold benefit in understanding how to, one, risk stratify these patients, and two, understand what type of therapy, whether pharmacologic or ablative, might result in greatest benefit to the patients.                                                 Changing gears entirely now to the role of genetics, we review multiple articles in various genetic syndromes published this past month. First, we reviewed an article by Providência et al. published in the last month's issue of heart entitled 'Impact of QTc formulae in the prevalence of short corrected QT interval and impact on probability and diagnosis of short QT syndrome.' The authors sought to assess the overall prevalence of short corrected QT intervals and the impact on diagnosis of short QT syndrome using different methods for correcting the QT interval. In this observational study they reviewed the sudden cardiac death screening of risk factors cohorts. They then applied multiple different correction formulae to the ECGs. They noted that the prevalence of individuals with the QTc less than 330 and 320 was extremely low, namely less than .07 and .02% respectively. They were also more frequently identified using the Framingham correction. The different QTc correction formulae could lead to a shift of anywhere from 5 to 10% of individuals in the cohort overall.                                                 They further noted, that based on consensus criteria, instead of 12 individuals diagnosed with short gut syndrome using the Bazett equation, a different number of individuals would have met diagnostic criteria with other formulae, 11 using Fridericia, 9 with Hodges, and 16 using the Framingham equation. Thus, they noted that overall the prevalence of short QT syndrome exceedingly low and an apparently healthy adult population. However, reclassification as meeting criteria might be heavily dependent on which QT correction formula is used. The importance of these findings is that not all QTs are created equal.                                                 Depending on how you compute the QT interval in which formula to use may affect how you actually risk characterize a patient. Unfortunately, these data do not necessarily tell us which is the right formula, but this highlights that it might be relevant to in the future evaluate the role of different formulae and identifying which is the most necessary to classify a patient.                                                 Moving on to an article published in last month's issue of the journal of clinical investigation by Chai et al. we review an article entitled 'Physiological genomics identifies genetic modifiers of Long QT Syndrome type 2 severity.' Congenital Long QT Syndrome is a very well recognized, inherited channelopathy associated life-threatening arrhythmias. LQTS type 2 is specifically caused by mutations in casein to encoding the potassium channel hERG. However, even with the mutation not all patients exhibit the same phenotype. Namely some patients are more at risk of life threatening arrhythmias in spite of having the same mutation as others who do not exhibit the same severity phenotype. The authors sought to evaluate whether specific modifiable factors within the remaining genetic code might be modifying the existing mutation. Thus, they sought to identify contributors to variable expressivity in an LQT 2 family by using induced pluripotent stem cell derived cardiomyocytes and whole exome sequencing in a synergistic manner.                                                 They found that patients with severely effected LQT 2 displayed prolonged action potentials compare to sales from mildly effected first-degree relatives. Furthermore, stem cells derived from patients were different in terms of how much L-type calcium current they exhibited. They noted that whole exome sequencing identified variants of KCNK17 and the GTP-binding protein REM2 in those patients with more severe phenotypes in whom greater L-type calcium current was seen. This suggests that abnormalities or even polymorphisms in other genes might be modifying the risk attributed to by mutations in the primary gene. This showcases the power of combining complimentary physiological and genomic analysis to identify genetic modifiers and potential therapeutic targets of a monogenic disorder. This is extraordinarily critical as we understand on one level that when we sequence a monogenic disorder that there might exist variants of uncertain significance, namely they have not been classified as disease causing, but could be. In turn, we also recognize that mutations in a family might effect different relatives differently. However, why this is has been relatively unclear.                                                 If we can understand and identify those patients who are most at risk of dangerous abnormal rhythms, this will be useful in how much to follow them, and what type of therapy to use in them. The fact that other genes might modify the risk even in the absence of specific mutations, suggests that novel approaches to characterizing the risk might help for the risk modified patients classification in general. Clinical use, however, remains to be seen.                                                 Moving on from long QT, we evaluate 'The Diagnostic Yield of Brugada Syndrome After Sudden Death With Normal Autopsy' noted in last month's issue of the Journal of American College of Cardiology and published by Papadakis et al. It is well known, the negative autopsies are not uncommon in patients, however, families might be wondering how at risk they are. Thus, the authors sought to assess the impact of systematic ajmaline provocation testing using high right precordial leads on the diagnostic yield Brugada syndrome in a large cohort of Sudden Arrhythmic Death syndrome families. Amongst 303 families affected by Sudden Arrhythmic Death Syndrome evaluation was done to determine whether or not there was a genetic inherited channelopathy cause. An inherited cardiac disease was diagnosed in 42% of the families and 22% of relatives Brugada syndrome was the most prevalent diagnosis overall amongst 28% of families. Ajmaline testing was required, however, to unmask the Brugada Syndrome in 97% of diagnosed individuals. Furthermore, they use of high right precordial leads showed a 16% incremental diagnostic yield of ajmaline testing for diagnosing Brugada syndrome.                                                 They further noted that a spontaneous type 1 regard or pattern or a clinically significant rhythmic event developed in 17% of these concealed regardless syndrome patients. The authors concluded the systematic use of ajmaline testing with high right precordial leads increases the yield of Brugada Syndrome testing in Sudden Arrhythmic Death Syndrome families. Furthermore, they noted that assessments should be performed in expert centers or patients could also be counseled appropriately. These findings are important and one of the big questions always becomes how aggressively to test family members of patients or of deceased individuals who experienced sudden arrhythmic death. Many of these patients have negative autopsies, and genetic autopsy might not be possible due to lack of tissue or blood products that can be adequately tested.                                                 The data here suggest that amongst a group of 303 sudden arrhythmic death, families that Brugada Syndrome is by far the most frequent diagnosis. If an inherited cardiac disease was identified. In turn, it is not ECG alone or echo alone that helps identify them, but requires drug provocation testing in addition to different electrode placements. Whether or not this will consistently offer benefit in patients in general or my result in overcalling remains to be seen next within the realm of genetic predisposition.                                                 We view an area where we don't know if there's a genetic predisposition in article published by Tester et al. entitled Cardiac Genetic Predisposition in Sudden Infant Death Syndrome in last month's issue of the journal of american college of cardiology. Sudden Infant Death Syndrome is the leading cause of post-neonatal mortality and genetic heart diseases might underlie some cases of SIDS. Thus the authors sought to determine the spectrum and prevalence of genetic heart disease associated mutations as a potential monogenic basis for Sudden Infant Death Syndrome. They study the largest cohort to date of unrelated SIDS cases, including a total of 419 individuals who underwent whole exome sequencing and targeted analysis for 90 genetic heart disease susceptibility genes. Overall, 12.6% of these cases had at least one potentially informative genetic heart disease associated variants. The yield was higher in those mixed European ancestry than those of European ancestry.                                                 Infants older than four months were more likely to host a potentially informative gene. Furthermore, they noted that only 18 of the 419 SIDS cases hold a [inaudible 01:01:26] or likely pathogenic variant. So in other words, only 4% of cases really had a variant that they could say was distinctly pathogenic or likely pathogenic. Thus, overall, the minority of SIDS cases have potentially informative variant in genetic heart disease susceptibility gene, and these individuals were mostly in the 4 to 12 month age group. Also, only 4% of cases had immediately clinically actionable variance, namely a variant, which is well recognized as pathogenic and where we could actually say that a specific therapy might have had some effect. These findings can have major implications for how best to investigate SIDS cases in families. It might suggest that SIDS cases where the individual was older, nearly 4 to 12 months of age might have a greater yield in terms of identifying variance.                                                 While this might not affect the deceased in fit, it might affect, families are planning on having another child in whom a variant can be identified.                                                 Finally, within the realm of genetics, we review an article published in last month's issue of Science Advances by Huang. et al. entitled 'Mechanisms of KCNQ1 Channel Dysfunction in Long QT Syndrome Involving Voltage Sensor Domain Mutations'. Mutations that induce loss of function of human KCNQ1 underlie the Long QT Syndrome type 1. While hundreds of mutations have been identified the molecular mechanism by which they result in impaired function are not as well understood. The authors sought to investigate impact of 51 specific variants located within the voltage sensor domain and emphasized effect on cell surface expression, protein folding, and structure. For each variant efficiency of trafficking of the plasma membrane, impact of proteasome inhibition, and protein stability were evaluated. They noted that more than half of the loss of function mutations were seen to destabilized structure of the voltage sensor domain, generally accompanied by mistrafficking and degradation by the proteasome.                                                 They also noted that five of the folding defective Long QT Syndrome mutant sites were located in the S0 helix, where they tend to interact with a number of other loss of function mutation sites in other segments of the voltage sensor domain. They suggested these observations reveal a critical role for the S0 helix as a central scaffold to help organize and stabilized KCNQ1 overall. They also note the importance of these findings is that mutation-induced destabilization of membrane proteins may be a more common cause of disease functioning in humans. The importance of these findings lies in better understanding why specific mutations lead to appa

The theme of this year's International Women’s Day is 'Strength of a Woman: Press for Progress'. Across the world, women are making positive and empowered progress every day. All progress, however small or ordinary it may seem, is one more positive step towards reaching gender equality. In this podcast, we will be exploring the advent of female engagement teams in military situations with Major Nicki Bass, women as perpetrators of terrorist activities and the work of women in counterterrorism since 9/11 with Dr Joana Cook, and the growing importance of the study of gender relations in the military with Dr Andrea Ellner. Major Nicki Bass Nicki Bass served for 17 years in the British Army with the Adjutant General’s Corps (Educational and Training Services), retiring in September 2017 at the rank of Major. During her career, she undertook a variety of roles including managing the Army’s operational language capability and responsibility for all military education provision in the northeast of England. She also deployed on several operational tours including Bosnia, Iraq and Afghanistan. Dr Joana Cook Joana Cook recently received her PhD in the Department of War Studies and is a Senior Research Fellow at the International Centre for the Study of Radicalisation and Political Violence (ICSR). She is also a junior researcher with the Canadian Network for the Study of Terrorism, Security and Society (TSAS), and a former a Research Affiliate with Public Safety Canada's Kanishka program. Her work focuses on women in security practices, extremism, terrorism and counter-terrorism in Yemen, Canada, the US and UK. She has presented her research to senior security audiences from a number of countries. Dr Andrea Ellner Dr Ellner joined the Department as a Lecturer in Defence Studies in September 2007. Prior to this she lectured for nearly ten years on International Security Studies and related subjects at the University of Reading, where she also led the Graduate Institute of Political and International Studies for three years. In 2006/7 she served on the Committee of the University Association of Contemporary European Studies (UACES). This podcast was produced by Bisi Olulode and edited by Ivan Seifert. UPCOMING EVENTS AT KING'S COLLEGE LONDON BLASTS FROM THE PAST: ANACHRONISMS IN SECURITY STUDIES How can we conceptualise and approach anachronistic thinking in International Relations and Security Studies? What are the consequences of using present concepts to review the past and past theories to understand the present? 14th March 2018 (17:00-19:00) | Bush House NE, Room 1.03 |Strand Campus 👉RSVP: http://bit.ly/2oWzk5E IS IT GAME OVER IN THE SOUTH CHINA SEA? Massive new artificial islands, a huge leap in naval and paramilitary capabilities and relentless pressure on neighbouring states - is China swallowing the South China Sea? Meanwhile, the US Navy suffers mishaps and scandal and promised increases in capabilities are years or decades away. Is this the moment at which the United States cedes a portion of the globe to a rising power? Or are we about to enter a period of dangerous instability as existing powers try to defend the international order? 15th March 2018 (17:00-19:00)|S0.12 Strand Campus 👉RSVP: http://bit.ly/2oWzk5E THE BLACK SEA WAR OF 1914-17 THROUGH BRITISH EYES The Black Sea War focussing on the modernisation of the Ottoman navy by 1914 up to the Russian amphibious landings on the North Anatolian coast in 1916 presented by Dr Toby Ewin. 15th March 2018 (17:15-19:00) | War Studies meeting room (K6.07) 👉RSVP: http://bit.ly/2tjprok THE DOUBLE GAME: THE DEMISE OF AMERICA'S FIRST MISSILE DEFENCE SYSTEM AND THE RISE OF STRATEGIC ARMS LIMITATION The Centre for Grand Strategy will host James Cameron of the Fundação Getulio Vargas (FGV) in São Paulo, Brazil 15th March 2018 (18:00-19:30)|Pyramid Room ( K4U.04) 4th floor Strand Campus 👉RSVP: http://bit.ly/2Fo9T4a

Featured Speaker: Tamara Kleinberg, LaunchStreetWhat is your “Innovator Archetype?” Listen to our latest podcast to learn more about this theory from Tamara Kleinberg, Founder of LaunchStreet and keynote speaker at SOCAP’s upcoming 2017 Moving at the Speed of Innovation Annual Conference. Learn more about the inspiration behind Tamara launching her own company dedicated to helping businesses ignite innovation as well as her thoughts on the innovation potential of today’s customer care industry. 

To identify the greatest threats you may face, you need to know how to create a risk profile. S0, how do you develop your own risk profile? You simply ask yourself the following questions and create an honest assessment of your vulnerabilities. How to Create a Risk Profile #1) What Do I Have to Protect?… The post M4S 002: How to Create a Risk Profile appeared first on Mind4Survival.

How often do you find yourself wanting to ask for something in your relationship - more communication, more time & attention, more touch - only to find yourself holding back out of fear? Expressing (or confessing) our needs can feel scary and edgy.  If it's a 'non-negotiable need' it's easy to feel like you're threatening the relationship with an ultimatum: "I need this or I'm out". S0 do you hold back, hoping your partner will come around on their own (and getting more resentful when they don't)? Or do you bring your needs to the table and cross your fingers, hoping it all goes well? This episode will teach you how to get your needs met, without feeling  you're making a threat to the relationship. QUESTION  You speak of stating and sticking by your Non-Negotiable Needs, but you also say to never threaten to walk away from the relationship. So how do you stick up for yourself and your NNN's without the threat of walking away hanging around in the background -- isn't it implied that you'll be leaving if your NNN's aren't met? I am missing how to do this properly. THANK YOU for your help and for clearing this up! -Jessica SHOWNOTES Does having needs make you ‘needy’? [1:00] Communicating your needs to your partner in a non-threatening way [3:00] When your needs aren’t compatible with your partner’s [6:00] Getting your needs met without threatening the relationship [7:00] When you have a need for more communication and connection than he can give you [8:00] Your action step [9:30]

    10 Things a Childless not by Choice Woman Will Never Do Have you ever thought about it? There are certain things our sisters with children do, that those of us who never had children will never do! Lately I have been hearing from people who either have children or are not ready to have children yet. Some of the resounding comments include: 'I didn't know!' And 'I have always wondered about my friend/neighbor/co-worker, but did not know how to ask.' Well honestly, I would only want someone to ask if they were sincere, and then I don't know how much I would want to share with people over and over. Which is where, my podcast comes in. You get all of your questions answered without approaching someone who might not want to talk about it! Well, I am sure this episode will be an eye-opener and an all around light bulb moment for most listeners! So! Thank you for coming in and listening to another episode of 21st Century Hannah! I appreciate your taking the time to stop by! Repeat listeners, childless not by choice or not: thank you. I am truly humbled. First time listeners, childless not by choice or not, thank you! Please come back and join the family! Everyone: I hope you are telling your friends about the show. Feel free to share the show to your social media followers! I would appreciate that! S0, 10 Things a Childless not by Choice Woman Will Never Do. (this is by no means an exhaustive list):   A childless not by choice woman will never go through the 'dreaded labor' her sisters with children will go through and complain about. But she is just as strong as her sisters with children.   A childless not by choice woman will never watch her baby make a face when he or she tastes a food for the first time.   A childless not by choice woman will never watch her baby walk for the first time.   A childless not by choice woman will never stay up all night with a colicky baby. But she will choose not to stay up all night grieving that fact.   A childless not by choice woman will never stare into a crib in awe and wonder at a being she co-created. But she will pray for her nieces and nephews as they make their way into the world.   A childless not by choice woman will never get to correct a toddler who told her 'no!', shake her head at a teenager who thinks he or she knows it all, or feel the sting of disappointment from a child who made a bad decision. But she will make herself available to lend an ear to her sister or brother for those moments.   A childless not by choice woman will never feel the pride of watching her child graduate kindergarten, middle school, high school and college. But she will feel the pride in knowing she was there to help get them to that moment.   A childless not by choice woman will never feel comfortable sitting with a group of women who are chatting about their children, no matter how she may seem on the outside. But she will continue to become strong enough to do it if she must.   A childless not by choice woman will always have a little empty space in her heart. But she will be sure to fill that space with peace, joy, love, and relevance.   A childless not by choice woman has a choice to make: Live a life of bitterness and sadness, or choose to do the best with the cards that have been dealt. I know you can do it!     My contact information: Website: www.childlessnotbychoice.net and www.civillamorgan.com Facebook: booksbycivillamorgan Twitter: @civilla1 Instagram: @civilla1 Pinterest: Civilla M. Morgan, MSM LinkedIn: Civilla Morgan, MSM Until next time! Bye!            

This week the guys wanted to go down the road of a favorite stand by: Stallone! S0 they went with the 1995 action “thriller” Assassins. Where Stallone is a top assassin who ends up protecting his latest mark, Julianna Moore, from crazy newcomer to the assassin world, Antonio Banderas, who stop at nothing to kill... The post Movie Issues: Assassins first appeared on Pixelated Geek.

This week the guys wanted to go down the road of a favorite stand by: Stallone! S0 they went with the 1995 action “thriller” Assassins. Where Stallone is a top assassin who ends up protecting his latest mark, Julianna Moore, from crazy newcomer to the assassin world, Antonio Banderas, who stop at nothing to kill [...]

What use is an F-call? You're 5 and 9, or 20 over 9, or 5 and 5. It's a phrase that you'll hear regularly in amateur radio conversations as you tune up and down the bands. If we ignore for a moment the readability signal, the first number, in this case "5", which I have to confess is pretty arbitrary. My perfect readability is not going to be the same as yours. The deafer I am, the less likely you're going to get a readability score of "5", lets look at the second number. It's a signal strength. Pretty straight forward. It goes from S0 to S9 and sometimes there are extra decibels added, 10 dB over, or 20 dB over, etc. The S meter in your radio is actually a very sensitive micro ammeter. The dial displays in S-units. What is an S-unit? Well, until 1981 there wasn't a real standard. In the 1930's they'd decided that S9 means 50 microvolts at the input of the receiver, but there wasn't a standard impedance of 50 Ohm, which we take for granted today, so the number is pretty meaningless in terms of power received. In 1981 they defined it as 50 microvolts at the receiver's antenna assuming an input impedance of 50 Ohm. It gets better. The S9 is actually defined as as -73 dBm or decibel milliwatts, or 50.12 pico Watts. Each S-unit is 6dBm, so S8 is -79 dBm, or 12.6 Pico Watt, S5 is 0.2 Pico Watt. If that wasn't enough to make your head explode, radios are rarely calibrated, so one radio's S9 isn't the same as the next one's, worse still, not every radio uses 6 dB per S-unit, so S8 for one radio might be 6 dB, for the next it might be 6.5 dB. And I should add that the Automatic Gain Control in a radio affects the S-meter as well. When you next tell someone that they're 5 and 9, or 20 over 9, just be mindful that it's useful as an indication of what's happening between your station and theirs, but it's not anything that you could use as a definite resource in the future. If you want to read more, there is much to find online. Word of warning. When you read more, your head will explode more, what I've talked about here is grossly simplified and I've not even looked at the actual electronics side of things! Amateur Radio, the more you dig, the more you find. I'm Onno VK6FLAB

Aprobación del Acta de la Trigésima Novena Sesión Ordinaria del Pleno del Instituto de Acceso a la Información Pública y Protección de Datos Personales del Distrito Federal, celebrada el 26 de octubre de 2011. Aprobación del Acta de la Tercera Sesión Extraordinaria del Pleno del Instituto de Acceso a la Información Pública y Protección de Datos Personales del Distrito Federal, celebrada el 01 de noviembre de 2011. Aprobación del Acuerdo que aprueban los Criterios y Metodología de Evaluación de la información pública de oficio que deben dar a conocer los Entes Obligados en sus portales de Internet y se abrogan los aprobados mediante acuerdo 389/S0/18-09/2008. Aprobación del Acuerdo que aprueba el Informe de Resultados de la Investigación con expediente número DDP/004/2011, con sus respectivas recomendaciones. Aprobación del Acuerdo que aprueba el Informe de Resultados de la Investigación con expediente número DDP/006/2011, con sus respectivas recomendaciones. Aprobación del Acuerdo que aprueba el Informe de Resultados de la Investigación con expediente número DDP/007/2011, con sus respectivas recomendaciones. Recursos de Revisión en materia de solicitudes de acceso a datos personales: 1548, 1741 y 1733. Recursos de Revisión en materia de solicitudes de acceso a la información: 1578, 1602, 1632, 1636, 1654, 1720, 1676, 1677, 1704, 1727, 1684, 1690, 1699, 1731, 1701, 1707, 1710, 1713, 1717, 1729, 1730, 1995, 1719, 1723, 1737 y su acumulado 1738, 1745 y 1991.File Download (0:00 min / 0 MB)

AWESOME ROCKIN TIME TO COMMENCE!! TFG1Mike sat down with Dave Brenner Guitarist from Theory Of A Deadman to talk about the bands’ legacy, touring, and the brand new album The Truth Is… We find out where TOAD got their name, and how a 118 year old Canadian nursery rhyme became a song. S0 sit back ...

Transcript: Lenticular or S0 galaxies are a type of galaxy that emerged after Hubble did his work. They’re called lenticular after their lens-like appearance, and they’re intermediate in properties between spiral and elliptical galaxies. Lenticular galaxies have prominent bulges and disks without spiral arms. Their star distribution is essentially smooth. The halo is usually invisible, although as with all massive galaxies the halo contains most of the mass.

THIS WEEK'S PODCAST TRANSCRIPT: 1921: the cornerstone of the Palace of the Legion of Honor is laid ... but what was underneath? February 19, 1921 Ghosts of Lands End On this date the cornerstone for San Francisco's spectacular Palace of the Legion of Honor Museum was levered into place. The Museum was to be a vehicle for the cultural pretensions of the notorious Alma Spreckels. This social-climbing dynamo envisioned her Museum as a far western outpost of French art and culture. Drawing on the vast fortune of her husband -- sugar baron Adolph Spreckels -- she constructed a replica of the Palace of Versailles out at Lands End. Alma would stock the place with art treasures from her own vast collection -- including one of the finest assemblages of Rodin sculpture on the planet. I've already talked myself hoarse on the subject of Alma Spreckels' rags-to-riches clamber up the social slopes of Pacific Heights, but what's really interesting me today is not what's inside her museum, but what lay underneath that cornerstone in 1921. read on ...

THIS WEEK'S PODCAST TRANSCRIPT: 1869: the fashionable neighborhood of Rincon Hill is sliced in two. February, 1869 The battle for Rincon Hill is over There aren't too many people living who remember this now, but Rincon Hill was once the fanciest neighborhood in San Francisco. You know the place, right? It's south of Market Street, an asphalt-covered lump of rock with the Bay Bridge sticking out of the north-east side and Second Street running by, out to the Giants' ballpark. That's Rincon Hill. What's left of it, anyway. Exactly 140 years ago this month, the California Supreme Court gave the go-ahead to a scheme which would destroy it. San Francisco's first fashionable address As San Francisco's Gold Rush-era population explosion of tents and rickety clapboard started to settle down, the bank accounts of merchants and lucky miners started to fill up. Men were becoming civilized, acquiring culture, and the sort of women known as "wives" were moving into town. This led to a demand for a neighborhood that was distinctly separate from the barbarous Barbary Coast, and with its sunny weather, gentle elevation, and spectacular views of the Bay, Rincon Hill filled the bill. According to the Annals of San Francisco, by 1853 Rincon Hill was dotted with "numerous elegant structures" -- including the little gated community of South Park. By the 1860s, the Hill was covered with mansions in a riot of architectural styles, and had become the social epicenter of the young city. And then in 1968 (cue evil-real-estate-developer music here) a San Franciscan named John Middleton got himself elected to the California State Legislature. According to some sources, his elevation was part of a conspiracy to push through a specific radical civic "improvement". The Second Street "Cut" Here's the situation that required "improving": at the time, there was a high volume of heavy commercial horse cart traffic to the busy South Beach wharves from Market Street. Second Street provided a direct route, but -- since it went up and over the highest part of Rincon Hill -- horse carts were obliged to take the long way around via Third Street. Middleton's plan was simplicity itself: carve a deep channel through the heart of the hill, right along Second Street. He just happened to own a big chunk of property at Second and Bryant Streets, and couldn't wait to see his property values go through the roof. "But wait," you're saying, "what about the owners of those lovely homes up on fashionable Rincon Hill? Won't they object to having their front doors open up to a 100-foot canyon instead of a sidewalk? Do they even have the technology to pull this off? And what about the horrific mess the construction is going to make? We are talking high society here, right?" read on ...

This podcast posting includes five commercials produced by the Boy Scouts of America. Each commercial uses a point of the Scout Law as its theme: trustworthy, helpful, obedient, thrifty, and reverent. I hope you enjoy them as must as I did when I first saw them.

Sub-Doppler spectra of various one- and two-photon vibronic bands of benzene are discussed and analysed to determine the pathways of intramolecular relaxation for S1 benzene. New results are presented for the 14011011622 band of C6H6 and the 1401102 band of 13C6H6. The decay behaviour depends strongly on the excess energy and the rotational quantum numbers rather than on the vibrational character and symmetry of the excited state. At low vibrational excess energy the pathway for intramolecular relaxation is a coupling in the strong limit between pairs of states in S1 leading to shifts of lines, whereas at intermediate excess energy coupling in the weak limit to background states in S1 is present. These background states are strongly broadened due to a fast electronic non-radiative process. The intramolecular relaxation is found to be initiated by the coupling to the broadened S1 background states and energy can flow via these states to the T1 or S0 state. The rotationally selective disappearance of lines is believed to be due to an intricate interplay of the rotational dependence of the coupling matrix elements and accidental resonances, which lead to interference of possible decay channels.

Rotationally resolved fluorescence excitation and resonance enhanced multiphoton ionization (MPI) spectra of the 610130 one-photon band of benzene at the onset of ``channel three'' are reported. The fluorescence decay is monitored after rotationally selected excitation and a large variation of the nonradiative decay time (