Yes, so So today what I'm going to tell you about is genome and it is data integration genome by transcriptome by emr But it's on the way to genome by transcriptome by encode to emr So I'm I'm here to learn more about using every all the new tools in encode just like the rest of you and The purpose for me is is all about The genetic component to common disease I think data integration is one of those things that is extremely helpful and getting us to the Just the few remaining questions we have on the role of genetic variation and disease like what what are the genes What are the mechanisms? What are the directions of effects and Where are those reverents so We've spent a lot of time in my group Trying to get at functional genomics at the function of genome variation most specifically and I think You know so so most of what we have worked on is this sort of Pathway where we start with genome variation Oops, let's see Yeah, start with genome variation and And assume that genome variation has an effect on transcript levels in some cases Now of course things besides genetics influence transcript levels and so we get some distribution around that genetically determined effect and and we presume beyond some threshold of Of expression in some genes you can become affected and so that's a sort of a generic model within GTX people have used creative ways to Characterize to sort of look at how regulatory variation Concentrates heritability so this is the heritability with Gcta for type 1 diabetes using all SNPs that are interrogated in the welcome trust case control Consortium GWAS for type 1 diabetes, so you see about So about 48 percent heritability for type 1 about 50 percent heritability for Crohn's disease but Concentrated with just the few thousand SNPs that are characterized as eqtls and adipose You see almost 40 percent of that heritability in Just a few thousand SNPs that are eqtls and adipose or heart or lung or muscle And and so across the board for type 1 diabetes. You see this regulatory architecture concentrating heritability and and this is Indeed essentially the same set of SNPs regulating the same set of genes in a set of So it's shared regulatory architecture across all of these tissues But for Crohn's disease, it's a completely different pattern. You see Concentration of heritability in whole blood which has of course all those cells that are so important in inflammatory disease But you don't see much concentration of heritability across all these other cell types So a key take-home message is yes, you get this concentration of heritability, but it's not eqtl this per se Because it's the very same set of eqtls Concentrating heritability here for type 1 diabetes and failing to concentrate heritability for Crohn's disease and So it's a feature of the genetic architecture this ability to concentrate heritability and regulatory elements and our colleagues at Harvard and the Broad did us one better so with Alka's price Alka's prices groups paper at the end of the year in 2014 where they combined 11 common diseases together as disease and compared it with controls and used basically n-code annotations to show that yeah about 40 percent of heritability of All the heritability that you get with all variants can be concentrated into The the variants that you directly interrogate that lie in DNA swan hypersensitivity sites But if you use the imputed data this is closer to 80 percent of the common variant heritability is Concentrated in SNPs that map to DNA swan hypersensitivity sites, which is remarkable and and Yes, it varies by disease. So this is a concatenation of a bunch of diseases and it's heavily representing Autoimmune disorders for example, so but so this this does vary, but whether it's 60 percent or 80 percent that's a remarkable concentration of the common variant heritability into what we see as DNA variation that must be in a sense regulatory and probably regulatory at the level of transcriptomes and so that that led us to think about The analysis of this data in a different way of these data in a different way Think of it as a missing data problem so if we really believe that a substantial fraction of The genome variation affecting risk of common disease is regulatory Why not focus our analysis on endophenotypes that that are more direct measures than what we really want? so the genetically determined part of transcript levels and instead of testing individual SNPs or Test testing individual SNPs and asking after the fact are they regulatory? Let's aggregate those variants into SNP based predictors of transcript levels and then test these predicted transcript levels directly for association with disease or relevant quantitative traits So this is the brainchild of a talented young faculty member at the University of Chicago that I sincerely hope will be Talented young faculty member at Vanderbilt soon. She's a really out-of-the-box thinker, and this is now to the box idea it takes a while to wrap your mind around the notion of of testing Calculated endophenotype genetically predicted expression and the the manuscript describing the method and and initial applications Is in press and nature genetics now as a GTX companion paper, but but if you think about a Decomposition of measured transcript levels some part of it is completely genetically determined a Substantial part of it is of course all those non-genetic factors that influence what we measure as transcript levels and over a lifetime the environmental influences on transcript levels and the lifetime of genetically determined transcript levels lead us to have certain diseases that feed back and and and Chaint the diseases you have changes your measured transcript levels as well Which is why it's been so confounding to try to use measured gene expression to figure out what drives disease because if we you know measured transcript levels in Blood cells and kids with asthma and kids without there are thousands and thousands of genes Differentially expressed between cases and controls most of that as a consequence of disease not a cause but here We're going to focus on just the genetically Determined part of transcript levels and and look at the association of that Phenotype with our disease that finesses this problem, so we don't we don't have the confound And it's very similar to the ideas in Genome imputation very analogous to genome imputation So with genome imputation we use thousand genomes as the reference panel to learn the correlations between DNA variants due to linkage disequilibrium and then use that information so that when we've Genotyped just a subset of the total sequenced variants in thousand genomes with some genotyping chip we can impute Millions of additional variants here. We're going to use GTX as our reference panel and Learn the the relationship between the genome variation and the measured transcript levels We can store that those the weights from these prediction equations and then basically in Any data set where we have genome interrogation At at least the common variant level so that can be whole genome sequencing, but it can just be a GWAS as well You can basically impute transcript levels in all tissues measured in GTX and use that as an endophenotype to do a gene-based test on trans on whether Genetically determined transcript levels are associated with your phenotype of interest now of course Heritability represents the upper limit on how well you could do with such a method right because we're using only the genome variation to impute the transcript levels Fortunately, there are plenty of transcripts that have very high heritability So what you what you see here is the prediction performance are squared so this is an out of sample comparison of the predicted transcript level to the directly measured transcript level and And and we're showing this by the heritability the GCTA based mixed model linear mixed model based Heritability the trait so the black line Is the actual measured estimated heritability the red dots are the is the R squared prediction performance So the more highly heritable the trait is the the better the prediction performance is and For any given tissue there are a substantial number of genes with quite reasonable Heritabilities right so so all the genes down here. You're not going to do very well predicting But in some tissues those genes will be up in this part of the curve most of them and so the On average so we see the significance of the correlation between predicted and directly measured expression levels Have Q values Less than 0.05 for 40 to 50 percent of genes less than 0.1 for 60 to 70 percent of genes So the significance of that correlation 80 percent of genes have a correlation between predicted and measured expression greater than 0.1 and 50 percent of genes have a correlation between the Predicted and the directly measured greater than 0.2 and a substantial number of genes have that correlation greater than 0.5 0.6 there's plenty with with with that correlation being greater than 0.8 Which is a remarkable set of genes where the environment is hardly impinging on the expression of those genes and yet the population Has wide range of variability completely genetically determined I mean essentially completely genetically determined It's a really interesting from an evolutionary perspective set of genes that the the prediction models that turn out to be the best probably tell us something about the genetic architecture of Sys regulatory variation because with the sample size and GTX now we're still using just the sys Regulatory variants so polygenic prediction did not do as well as lasso or elastic net the Suggesting that this is mean a more penalized models More sparse models actually do a better job than polygenic prediction as your sample size increases It makes less and less different switch predictor predictive model you use But but right now we've been using elastic nest net because it's the most robust so regardless of which Genotyping product used in your GWAS and and the quality of your imputation the elastic net tends to be more robust in terms of the Prediction the idea the advantages of the framework is that we're we're iteratively using more and more of what we do know All of this information on how genome variation relates to transcript levels to learn what we most want to know What are the genes? We get genes with this test right. It's a gene-based test. We get directions of effects It's a much more natural way to move into pathway and network analyses So so the discovery level information is better So The other thing we're looking at is using this in the analysis of whole genome sequence data as a way to combine Unify the common and rare variant contributions because you're getting the gene level information You can imagine combining the common variant gene level information on the regulatory end of things with the rare variant information on the functioning of the protein itself and so now I'm going to tell you about the Integration with the electronic medical records so ever since we worked with under jet ski on this cell paper where Andre used 130 million electronic medical records to show that each Common disease has a characteristic set of Mendelian diseases that are over represented Among the common diseases. He called it a Mendelian barcode. And so ever ever since we've worked on that paper. I've been obsessed with understanding the continuum between Mendelian and complex common diseases and the continuum between loss of function mutations deleterious amino acid polymorphisms and just reduced expression of genes and so So now We've been thinking about how we can use predict scan in this context To potentially validate and prioritize rare variant discoveries. So so the idea is predict scan itself involves an integration of transcriptome and genome variation So Using g-tex for example as a reference panel to really make this this relationship to Validate and prioritize rare variant discoveries You have to do further integration with what I'd call a phenome reference panel and Having moved to Vanderbilt. Have I got a phenome reference panel for you? so they at Vanderbilt, there's The clinical data warehouse is called the synthetic derivative and so you get a Deidentified and continuously updated image of the electronic medical record with now 2.3 million subjects Vanderbilt built their own EMR more about 30 years ago And so you have a really longitudinal set of data in addition they until Just this year. They had an opt-out procedure for collecting samples So they their biobank has more than 200,000 subjects. They they moved to prospective consenting By as per NIH requirements now, but they're really not there's really no change in the rate of sample accrual with the prospective consents because with the opt-out we removed a Random set of individuals to make sure that nobody knew who was in or out of the database and now we don't have to do that So it ends up being a wash in terms of the rate of recruit the rate of accrual Right now. There's about 20,000 samples with GWAS level data 42,000 with exome chip But by by the end of 2015 or beginning of 2016 There will be more than 2.5 million subjects in the synthetic derivative Will have dense genotype or whole genome sequencing on more than a hundred thousand with with exome chip data on all of those individuals exome chip interrogation and That's a dandy phenome reference panel. So you guys are all familiar with the idea of GWAS But with bio view you can do a fee was so a phenome wide Association study and the way they've done that in the past is to use Individual functional variance or individual variants that were say the top signal for atrial fibrillation And then you can look at what other phenotypes? Across the entire medical record are associated with that apparently functional SNP So what besides atrial fibrillation? Is associated with the top SNP for atrial fibrillation and to do fee was you have to have a very large cohort of patients with both genotype data and many Different diagnoses the idea with bio view now though is that we can use predict scan to do gene-based fee was across the entire cohort and gene-based fee was for For different expression of genes in different tissues so cardiac tissues for heart disease brain for Neuropsychiatric phenotypes and that that really makes bio view into a phenome reference panel so the given my obsession with the Questions around Mendelian disease genes the natural question was what phenotypes are associated with? Reduced genetically regulated expression of Mendelian disease genes the heart our hypothesis was if this is going to work You would expect the entire spectrum of the Mendelian disease to be represented in individuals Across bio view who just have reduced expression of these genes so the so Of course, it's all even though we've got 20,000 with genotype data It's on all different GWAS products and the quality of the imputation Wasn't quite where it needed to be so we're still we're re-imputing So that these analyses have been done on just the 5,000 bio view subjects done with the aluminum 1m Which is the largest number of individuals done with any given single GWAS product and we focused just these preliminary studies on the The the genes where all the SNPs in the prediction equation are directly Interrogated on that product in either a whole blood predictor Which we actually built from the depression gene network data because it's bigger than what we have in GTex now It's more than 900 or the cardiac tissue. So that's I Think I used left ventricle Built for more than 300 individuals in GTex. So we have 125 genes. So that's that's the data said I'm showing you But it's already really interesting. So pex 19 is one of a set of 12 genes from this gene family where recessive mutations lead to a Paroxysomal biogenesis disorder called the Zellweger syndrome spectrum of Mendelian phenotypes So the kids with this disease are born with Hypotonia they have seizures they have what's called bony stippling in the patella and the long bones showing bone Resorption in those areas on on on X-ray you see Kidney and liver cysts the liver cysts lead to coagulopathies the kidney cysts and also kidney stone formation lead to renal failure um pex 19 actually is is One of the rarest causes of the Zellweger syndrome because it the kids are I mean, it's a the most severe form of this Zellweger syndrome spectrum and so we looked at what bio view phenotypes are associated with reduced genetically determined expression of pex 19 because all of the snips in the predictor for pex 19 were directly genotyped and So what you see are the top association is with an ICD-9 code given to kids that they think need a Screen for chromosome anomaly or genetic disorder So they the kids probably have hypotonia maybe have seizures at birth, but you see Kidney failure hypertensive heart arena disease hypertensive chronic kidney disease epilepsy kidney replaced by transplants of kidney failure um Fracture of the patella. So again this bone resorption of the patella is seen partial epilepsy Eplot recurrent seizures. So so essentially all of these features you're seeing as associated with reduced genetically determined expression. You also see the Disorders of calcium and phosphorus metabolism Hyperparathartism disorders of pyra pyra the proxosomes are a calcium store in cells and if Kids with Zellweger syndrome lived long enough. They would probably have these disorders. So my Mendelian experts tell me so really interesting set of phenotypes associated with reduced expression of pex 19 but because of the work that's been done on the genes that regulate Paroxysomal biogenesis genes we actually know what to expect for increased expression of pex 19 and you'll actually see exactly the phenotypes that you would expect associated with increased expression of this gene as well. So you see primarily cancer phenotypes Metabolic syndrome associated with increased expression of pex 19. So again pretty much exactly in line with expectations another Mendelian disorder that we looked at is a leads to a mitochondrial A mitochondrial depletion syndrome. It's a DNA synthetase for mitochondria. So you basically don't Don't replicate DNA. So you lose mitochondria rapidly over time The the kids are born often with the droopy eyelids They have the inability even to move their eyes after a while They lose the ability if they ever walk they lose the ability to walk even to breathe so that they lose the ability to really use muscles recent study in Finland on a series of patients there suggested that they have increased fractures although The paper said they didn't know if that would be because they fall down more because of the muscle weakness Or they actually have bone weakness due to mitochondrial depletion and bone. And so what are we seeing in Bio of you with reduced expression. We actually see the ptosis of the eyelid. So you see the ptosis of the eyelid which is a Sort of the canonical thing. We see fractures everywhere skull fractures tibial fractures rib fractures femur fractures, so Really interesting potential It's possible they just fall down more, but I think It'll be interesting to test and I got a guy who is very interested in mitochondrial diseases Working on the possibility that bones really are more fragile Increased expression of this same gene is associated with periprotonemia and multiple myeloma and So that would be unexpected But a really interesting idea for what might happen if you have mitochondria on steroids able to reproduce more rapidly than than Expected and so so we're looking at this as well in a much larger series in multiple myeloma This raises a question of whether altered expression increased or decreased of Mendelian disease genes might contribute Disproportionately to common disease so you saw kidney failure with Pex 19 a lot of Mendelian disease genes have kidney failure as part of their spectrum and if reduced expression of Those genes leads to kidney failure that may be a substantial contributor to what we see is garden variety kidney failure in addition for some so for some genes some Mendelian disease genes we see additional phenotypes Hemochromatosis we think you know we think of as being associated with certain phenotypes and we see some of those phenotypes Associated in individuals in bio view the cardiomegaly for example and But we see additional phenotypes so most people with hemochromatosis in the US have Mutations as a cause as opposed to loss of function Mutation so they just have a poly more amino acid changes that are deleterious that lead to The disease but in bio view we see really strong associations with kidney failure We know that actually iron does accumulate in kidneys and people with hemochromatosis It's not reported to cause kidney failure, but Significantly reduced expression of this gene may lead to kidney failure And that's something we'll be looking at as we go forward Just I'll just close with a few examples of so So we think that if if but with Mendelian diseases if you if reduced expression of Mendelian diseases are essentially reproducing the Mendelian phenotypic spectrum then You could use something like bio view to refine phenotypes of Existing Mendelian diseases and characterize new ones basically predict what the Mendelian phenotype will look like When went as you know with the undiagnosed diseases program and the Mendelian diseases programs Go forward. We'll have a way to match things up with these undiagnosed diseases programs where you've got an individual with a Set of phenotypes that suggest strongly that there's a genetic Basis for the disease they have but nobody knows what it is when you do exome sequencing you often have half a dozen or a dozen Genes that could be the driver we could go into bio view when we have more than a hundred thousand subjects Genotyped we can go into bio view and look at what which of these dozen genes have the set of phenotypes most similar to For reduced expression of the genes most similar to what we see in the individual and of course with many of the sequencing studies That we're doing even today so in type 2 diabetes for example with very large numbers of exome sequences done We don't have many new Findings we can find some of the things we already knew about but we have a lot of genes that are close to being Genome-wide significant we can take those genes into bio view and look at Which ones show with reduced expression reduced genetically predicted expression show Evidence of being associated with diabetes Glucose traits insulin traits you know across the board BMI. So so it's another way to help Prioritize the rare variant discoveries we think There's a few just a few others what that I was going to show you that are kind of fun to look at so these are not Mendelian disease genes Some of them were just genes like this one that I had some idea what phenotypes should be associated with a colocystic ion and receptor so indeed biliary disease is associated with Reduced genetically expression. Oh, sorry increased predicted expression of this Gene, but what was what was kind of intriguing was to see the Other association so this is a receptor not just for regulatory peptides in the gastrointestinal tract But also in the brain and you do see a few other interesting suicidal ideation post traumatic stress disorder Hard to know what that means in just these 5000 samples, but when we have more than a hundred thousand That's going to be a really interesting thing to keep an eye on There's a there was a gene greek 5 that looks like an eye super gene so increased expression of greek 5 was associated with retinal detachment cataracts glaucoma of various sorts Disorders of the vitreous body other retinal disorders. So and again, that's increased predicted expression Which of course Makes it ideal as a drug target for for developing a therapeutic reduced predicted expression of this gene which is Import it's so it's one of those genes that acts as a chaperone for proteins from the endoplasmic reticulum to the Golgi Was associated with schizophrenia with Psychosis with other non with other non psychotic or transient mental disorders Psychogenic and somatiform disorders and epilepsy but It has an interesting pattern of association with other things too. So you see transient alteration of awareness thyrotoxicosis, which can sometimes be I Mean that's delusions and people thought to have thyroid disease Lack of normal physiological development failure to thrive alteration of cons consciousness and meningitis So it looks like it just makes brains more sensitive to any kind of insult. So again You know, I wouldn't make much of it now, but when we have a hundred thousand This is going to be an interesting one to look at so so what I've shown you is just a little bit of a flavor So this is the results of our studies in five thousand in bio view with the predictions built only through statistical methods So we're modifying those now to use n-code annotations which should improve the quality of the predictors Within a few weeks we'll have results with this improved methodology on all genes in so we have a hundred twenty five genes now all genes in twenty thousand and then In a year or so we'll have results in more than a hundred thousand With all genes. So I think it's going to be really fun to use this as a general discovery tool But to really try to get an understanding of whether altered expression of Mendelian disease genes really does Contribute disproportionately to human diseases So these are our members of our g-tex team and I need to especially point out hockey m and eric gamazon who have I hope hockey will be I'm signing on the dotted line to come and sing in our new Nashville group So with that I need to acknowledge my g-tex college colleagues. It's a really fantastic project I'm Many of you that work in n-code know how much fun it can be to work with Like-minded group of of people on these big projects, but I'm happy to take questions now Well, I don't think the mic is on but it should be Probably have some interesting data also Taking into account sexual dimorphisms in Expression levels. Yeah, so there's a whole group in g-tex working on context specificity with respect to sex So barbers strange that we had we got a one of those Supplements to really study sex Context specificity in g-tex and they've really been doing a ton of work on it. It's One of the things that's Challenging with respect with respect to context specificity Sex and even the cis trans thing is how you choose to normalize because actually The the normalization process and even the way we use peer factors to Prior to general analysis can remove a lot of the sex effects can remove Trans effects clearly also and so So I think there's a lot of kind of deep thinking and diving in The exact best way to do this to make sure that we find the sex effects that you know are there But I think there's some really interesting preliminary studies out already from other groups Suggesting that the x chromosome is a very Is a much more interesting chromosome with respect to Sex effects in transcription then Then we I mean not that we should be surprised but but really disproportionately interesting I am catalysus that from pen So for the predicts can so In my reading the g-tex you find two kind of EGs or e-snips one that are shared and the others are Cell type specific so do you use that separately? And then the other question is if you take now the cell type specific e-snips you actually see enrichment for Diseases that are associated for that specific issue. Yeah, so So it's definitely true that This is a feature of genetic architecture. So for some diseases if you don't use The regulatory variation identified very specifically in the right Cells and tissues you don't see anything and and so There's a lot of examples for neuropsychiatric diseases where you really have to have the regulatory variation from brain in order to see effects Not true for all but probably for 80 90 percent of Neuropsychiatric disorders. That's true and and this cross tissue versus Single tissue architecture is important as well. So what we've been doing is building both tissue specific Predictors as well as a cross tissue predictor and that's true. So for brain. We're building a so there's several Brain regions sampled in g-tex. So we're building brain specific predictors, but also a general cross brain predictor because there's definitely shared architecture And when you use that shared architecture across multiple tissues from the same set of individuals You improve your power and and your resolution for the predictions. So when What you want to study is the cross regulatory architecture using The this cross tissue sort of predictor is going to be a better idea When you really need to hone in on the Specificity you want to use the tissue specific and of course at some point Through collaborations with the single cell consortium. We hope we'll have even cell types specific and you can get that for some cell types now but but But for now that the tissue definitely helps for diseases that have that sort of architecture Okay, so I have a few announcements and I'll do these in reverse order We need to be back here at 10.05 for our next talks. So please be back a few minutes early We'll have coffee if you go outside and back to the left. I think there will be signs that say how to get there So we'll be on break for coffee and join me again in thanking our keynote speaker and ansi cox for next one talk


The Nigerian army forces says it has saved the nation the loss of 173,985,650 Naira worth of crude oil in the south-south oil-rich region of the country. The DMO have been consistent in briefing the press bi-weekly, also said that it last two weeks saw a total of 1,332 terrorists and their family members comprising 222 adult males, 411 adult females and 699 children, surrendering to troops at different occasions within the theater of operations. Troops of the joint task force of the Nigerian Delta team and other operations in the south-south region of the country have continued to sustain the war against oil debt, illegal refinery and criminal activities in the Niger Delta through addressing patrols. Hello, hope you enjoyed the news, please do subscribe to our YouTube channel and don't forget to hit the notification button so you get notified about fresh news updates. Thank you. Thank you.


So my beautiful people, I am back with another out-of-the-ring video. Today I'm going to showcase to you guys how you can get the Arborich wizard lock in amazing armor skin for all you mages out there. This is what you need in your life. Check that out. How cool is that people? How cool is... you know you want this and it's so easy to get. It's unreal. How's it going guys? My name's DPJ and if you do enjoy the video leaving a like who helps out and if you like what you see and want to see more be sure to subscribe. So any early to medium player can get this quite straightforward. I'm not going to lie and it is looking absolutely incredible. Those gems those red are diamonds I don't even know what they are. I can see purple, I can see blue, I can see red, I can see pink, I can see all sorts. It's like a black version of Gandalf's costume. Look at the gauntlets as well. Incredible guys it really is. So I'll show you the stats before I show you where it's located. I mean this may be something a lot of people are looking for. Don't want to look cool as well. It's having these kind of stats which obviously help their magicians out there. So yeah this is what we have here. So yeah you want to pause the video and read through this properly you can. Well here we go guys. So the only real thing you have to do is to get this is defeat. One small bus really. It's not even yeah a small bus as well as having a dectus medallion because you need to get up to here. Simple as that. So dectus medallion. One half you get from a guy here. Another half I believe is from a fort around this area. If you search dectus medallion guide on youtube it's straightforward people. You shouldn't have a problem. Upon getting that you come to this part here the grand lift of dectus. Activate the medallion and you'll come up to this area. From here guys follow this path right here. Come around here. Come around here. And here guys you'll have a guy on the horseback. It's not hard to beat whatsoever. I basically one bombed him.  And you follow the route around and I'll show you this. I believe I get to about this checkpoint. It's around this checkpoint. Yeah but either way you'll see the route on screen now to exactly where you go. Just pick this up.  No buffs in a way. Nothing guys. Just grab this thing and you are good to go people. You are good to go. And there we have it people. That is how you get some amazing arbor rich wizard costume. I think that looks so cool. It's unbelievable. It really is. So yes guys enjoy the rest of the video. I hope it helps you out. If it doesn't leave a like really helps me out. If you're new until I want to see more out of the ring be sure to subscribe. And hopefully people I will see you on that next one.


What's up everyone it's your girl Kenzie here from Layton Sports Cards and I'm ripping a personal for Nathan S We've got two of the 2020-21 Panini Mosaic basketball team all-in-dition boxes best of luck your Nathan Thanks for hopping in for the red and gold waves shot ferret I don't know about that. That thing bit me. I don't know what I'd do. I'm never really a big fan of ferrets Shaq we've got red wave Jalen Smith for the Suns Patrick Williams Dave blue you red wave debook for the Suns Yeah more group breaks tomorrow night everyone for 10 box Tuesday starting at 4 p.m.. And then we've got museum Collection baseball Wednesday day breaks. Those are posted on the site Mason Plumlee Red We've got half case pick your team formats with Magic Matt over on the LSE baseball and random team half Half case breaks with forest over on the sports up Jason Jason Tate We've got national pride Lamello ball red wave. Nice one there for you, Nathan So dual streams on release day there Got mosaic Duncan Robinson and red wave of Miles Bridges Lamello ball debut and got Siddiq Bay rookie and Goldwave Gordon Dragich And rust For hanging in there for what three quarters almost Okay, do you we've got red wave finals MVP Kawhi letter? You went back to school like Billy Madison Tyree Tala Burton red wave Robin Lopez. He spent one year with Urban Meyer and Jackson. I was like, ah I want to go back. It's a Stuart red wave Steph Curry Yeah, Steve Bay red wave rookie debut James Weisman another nice rookie there Trey Jones red wave Spencer Dinwiddie and Last pack of box one here for you Nathan We'll get in the box too One more Stevens and Goldwave little Bobon for the mass Watching Trevor Lawrence play in person at that preseason game like he did not look good He was overthrowing under throwing passes I don't know ant-man on the NBA debut red wave Jamal Murray And you'll quickly rookie red wave of Lori market Tyrese Maxi on the rookie base silver Rigo bear and red wave rookie Isaiah Joe Lajewan red wave Kent Baysmore Killian Hayes we've got a red wave of Norman Powell Jerry West on the red wave that it's not a serious Chris Paul red wave of Jordan Clarkson Pazzo we've got Goldwave Kevin Love Cass He didn't play in the game versus Jacksonville that I went to Dario He just played in the very last preseason game got red wave the Andre Jordan. He did all right Way too much I think just one half red wave rookie debut Payton Pritchard Then it was also revealed that he was battling a foot injury, so There's that too silver Paul George and red wave rookie Payton Pritchard But all I know is we are screwed if he gets hurt Let me tell you because Anthony McFarlane junior and Benny Snell are not do it for us One of them got cut. I think Snell got cut or was it McFarlane one of the two is on the practice squad now No be CJ LB. We've got red wave rookie of Desmond Bain and another red wave a Zubak for the clippers two red waves in that last pack Alrighty Nathan that'll do it for your boxes. Congrats and thanks for helping in we'll get these right out to you


So, we will look at application of first law to psychrometric processes where we will look at both flow as well as non-flow processes. Although flow processes are probably more common in HVAC because if you want to heat or cool a building normally you have the refrigeration power plant perhaps on the roof of the building and then the plant is connected to the rooms through ducts and so on. Flow examples are more common although non-flow examples are also non-flow situations or applications are also there. So, we will look at both of them. Now, application of first law to psychrometric process is quite straight forward. The simplicity is that you know we are simply treating moist air as a mixture of two components, two ideal gases dry air and water vapor. So, that is where the simplicity comes from. So, you know really application of first law to psychrometric process is just like application of first law using ideal gases, mixture of ideal gases that we have done before. So, it is no different from that. What the two points that we need to note is that the change in internal energy of dry air is calculated assuming that dry air is a calorically perfect gas. So, we assume CV to be constant and the specific internal energy of water vapor, this is for non-flow process specific internal energy of water vapor is usually approximated like this that it is just equal to the specific internal energy of saturated vapor at the same temperature. Although we can probably look up the value from the table for engineering purposes, this is simply not what the trouble and we simply approximate as u g of t. So, u v of t comma p is simply taken as u g of t. Even though we may know the partial pressure of the water vapor and the temperature, we simply just take it as specific internal energy as u g of t. So, we looked at an example before which was something like this where moist air at 25 degree Celsius and one atmosphere was compressed in a polytropic process up to state 2 to 5 times its initial pressure and then it was cooled at constant volume. So, what we are asked to determine now is the amount of heat removed during the cooling process. So, if we simply apply first law to the cooling process, we get delta e equal to delta u equal to q minus w. There is no change in there are no kinetic or potential energy changes. So, delta e equal to delta u and w is 0 because it is a constant volume process, no displacement work and there are no other forms of work also. So, w is 0. So, q is equal to delta u and delta u itself consists of delta u of dry air plus delta u of the water vapor. So, we may write this as delta u of dry air plus delta u of water vapor. And the delta u of dry air may be written as m a times c v a times t 3 minus t 2. And the delta u for water vapor may be written as mass for the water vapor times u 3 minus u 2. Notice that what we are doing here? So, basically delta u of water vapor would be mass of water times change in its internal energy, but mass of water remains the same and that is equal to m v 1.  And by using the definition of omega 1, remember omega 1 is equal to m v 1 divided by m a.  So, then the expression becomes something like this. And u 2 is simply equal to u g at 138 degree Celsius. The temperature was 138 degree Celsius after the compression process. So, we can get this from the temperature table. And the dryness fraction was evaluated to be, so the dryness fraction was evaluated to be 0.3955. So, the specific internal energy of the mixture at state 3 may be evaluated as u f plus x times u g minus u f. So, that is 1016.04. What is that? The specific internal energy of the, if it is just vapor, then the specific internal energy of the vapor alone is approximated as u g at that temperature. If it is a saturated mixture, then we need to evaluate it in the same manner as we have always done. So, we take CV of dry air to be 717.86 joule per kg Kelvin throughout. And if you substitute the known values, we get q to be minus 101 kilojoules. So, that is the, that is application of first law to psychrometric problem, which as we can see is no different from what we have done before. Only important things that you need to keep in mind are these sorts of things, mass of vapor. So, for example, if you look at this expression, delta u for water vapor itself would have been equal to m of water, let us say H 2 O times delta specific of the water, which itself may be written as, say in the final state, we have mixture of liquid plus water, I am sorry liquid plus vapor. So, we say m H 2 O times u 3 minus m, now instead of writing m H 2 O, we can simply write this as mass of vapor, because initially we have only vapor.  And this is only vapor. So, we approximate this as u g of T 2. So, you need to keep track of these sorts of things vapor, if the water condenses, then you have to take into account the mass of the condensate. The mass of the condensate may be small, but specific internal energy is of the order of few 1000 kilojoules per kilogram. So, that actually can be a significant quantity, mass times the specific internal energy. If it is just mass, then in certain applications, you may simply neglect the mass of the water vapor that has condense without any impact on the accuracy, but for specific internal energy, that will not be there. Or for internal energy, that will not be the case. So, you just need to keep track of these masses of vapor and liquid in the water quite accurately in psychrometric applications. Let us look at the next example, 2 kg of air at 25 degrees Celsius, one atmosphere, and 25 percent relative humidity is compressed isothermally until the volume becomes one-fifth of the initial volume. Determine the amount of water that condenses, if any, and the heat that is removed. So, basically you may think of a piston cylinder mechanism like this. This contains moist air and it is compressed until the volume becomes one-fifth of the initial volume. We are asked to determine any water or the amount of water that may condense and the heat that is removed. So, the relative humidity is given as 25 percent at state 1 and the temperature is also known. So, at state 1, as you can see from here, 25 degrees Celsius, one atmosphere and 25 percent relative humidity. So, we may look up P sat of 25 from the temperature table and we get the partial pressure of water vapor to be 0.79 225 kPa. So, that state is indicated here. Now, it is being compressed isothermally. So, that means we are following this line here. Now, if you cross the saturated vapor line during the process, then obviously the water will condense. So, we need to find out the pressure, temperature is already known. So, we need to find out the pressure at which the process line crosses the saturated vapor line. Since the compression process is isothermal, the final pressure is 5 times 101.325 kPa. So, basically what we are saying is the final pressure of the contents of the cylinder is 5 times the initial pressure which is 101.325. So, 5 times 101.325 is the final pressure of the contents of the cylinder because it is an isothermal process. Now, the partial pressure of the water vapor is basically, notice that the partial pressure of water vapor can only go up to. So, here is the isobar. So, the partial pressure of water vapor can go only up to p sat of 25 which is equal to, as we just looked it up, p sat of 25 is 3.169. So, once the partial pressure of water vapor exceeds that, water begins to condense. Since we have said that, you know, the pressure is 5 times that much and the volume is also going to be one-fifth of that. So, we have to be careful. But the important point is the partial pressure of the water vapor can increase only up to 3.169 which is just about 4 times its initial pressure. So, at the at the instant when the process line crosses the saturated vapor line, the partial pressure of water vapor becomes 3.169 which is 4 times the initial value, initial partial pressure of the water vapor. So, once it reaches there, the partial pressure of the water vapor remains constant because phase change begins to take place. Water vapor begins to condense. So, the partial pressure of the water vapor remains at 3.169 kilopascal, while the mixture pressure continues to increase as the contents of the cylinder are compressed. So, that is a very, very subtle point. So, the water pressure, partial pressure of water vapor can go only up to 3.17 and then it remains constant. So, the pressure increases from here to here and then remains constant. Whereas, the mixture pressure continues to increase until it is 5 times the initial pressure. So, the specific volume of water vapor at the initial state, it is slightly superheated. So, we will assume that it is an ideal gas and use the ideal gas equation of state and calculate it to be 173.74. The final specific volume is one-fifth of the initial specific volume V1 divided by 5 and the initial specific volume itself is equal to VV1 because it is in the vapor form. So, the final specific volume comes out to be 34.748 meter cube per kilogram. And we may evaluate the dryness fraction, once this is known, we may evaluate the dryness fraction as 0.8014. Using the definition of dryness fraction, we may evaluate the mass of water that has condensed to be 1.94 grams, just like what we did before. Note that using the definition of the dryness fraction, we may write the mass of liquid water as mw equal to 1 minus x times mv1. Remember, dryness fraction is defined as mass of vapor divided by mass of the mixture and mass of vapor itself may be written as mass of the mixture minus mass of liquid divided by mass of mixture. So, if you rewrite this, you get mass of liquid to be m times 1 minus x where m is the mass of the saturated mixture. Now, remember, we had certain amount of water vapor initially and out of that water vapor some amount has condensed and some remains as water vapor. So, the mass of the mixture is equal to the mass of vapor that we started out with. So, m in this case is equal to mv1. So, that is how we end up with this expression. Application of first law to the isothermal compression process gives delta E equal to delta U, no ke or pe changes, q minus w and w is a displacement work. So, that is p1 v1 natural log v2 over v1 where p is the mixture pressure and v is the volume occupied by the mixture.  Delta U for dry air is 0 because it is an isothermal process and we have assumed dry air to be calorically perfect gas. In delta U for water is nothing but so delta U for water is mass of water times U2 minus U1. And mass of water is mv1 because there is a total amount of vapor that was present and part of which is condensed now. So, this may be written as mv1 times U2 minus U1. So, this was initially superheated. So, we approximate this as Ug of T1 and U2 itself may be evaluated like this 1951.3 using the temperature table. And the initial volume, remember we are using the Dalton's model. So, the initial volume is written like this. The initial volume is written like this because we are using Dalton's model and the components occupy the entire volume that is available. They are different pressures, same temperature and same volume. So, we may evaluate the initial volume as m volume occupied by vapor divided by the specific volume of the vapor. So, if you take the mass of the vapor outside, we may write it in terms of omega and mass of the mixture and after substituting the values we get Q to be minus 4.4736 kilojoules. So, this again illustrates how application of first law to a psychrometric process is carried out. And once again you must keep track of the mass of different phases in these problems especially when condensation takes place. If condensation does not take place then it is relatively straightforward mass of the individual components remains the same and we can just go ahead. If phase change takes place, phase change for the water takes place then we need to keep track of the amount of water that condenses and the amount that is remaining in the vapor phase. So, the next set of examples that we are going to discuss or steady flow examples we have seen non-flow examples so far. Next we will look at steady flow example and as I mentioned earlier HVAC involves unit operations like heating, cooling or dehumidification. So, we will try to look at examples involving these operations. Since these are steady flow applications we will encounter the enthalpy or specific enthalpy of individual components and not specific internal energy and the enthalpy of the mixture is calculated like this. It is the sum of the enthalpy of dry air plus water vapor. And as just like what we did earlier for specific internal energy the specific enthalpy of the vapor is approximated as Hg of T. Earlier we said U of the vapor specific internal energy was Ug of T. This one is Hg of T and the specific enthalpy of the air itself is written as Cp times T where we take Cp to be 1.005. So, we are assuming as I said before the dry air to be calorically perfect. So, the specific enthalpy of dry air is written as Cp times T. So, the first example reads like this ambient air at 5 degree Celsius, 1 atmosphere pressure and 85 percent relative humidity is to be heated as it flows steadily in a duct. So, that the relative humidity becomes 25 percent. The volume flow rate is 100 meter cube per minute at the inlet determine the rate of heat addition and assume pressure remains constant that is mixture pressure remains constant at 1 atmosphere. So, the inlet state is completely fixed. We know the temperature, relative humidity, volume flow rate at the pressure at exit relative humidity is given. We are asked to determine how much heat is being added. So, relative humidity is given at the inlet temperature is also known. So, we may evaluate P sat of 5 degree Celsius from the temperature table and evaluate the partial pressure of water vapor at the inlet to be 0.74205 kilopascal. And the humidity ratio may also be evaluated as 4.59 grams of vapor per kilogram of dry air. At the outlet the mixture pressure remains the same and since no water is added or removed the partial pressure of water vapor also remains the same. So, Pv2 equal to Pv1 equal to this and omega2 is equal to omega1. So, because no water is added or removed and the relative humidity value is also given. So, using the definition of relative humidity we may evaluate P sat of T2 to be 2.9682 kilopascal and from the temperature table we can then work out that the exit temperature is 24 degree Celsius. Now, we apply steady flow energy equation to the duct and this gives us q dot minus Wx dot plus m dot times h1 minus h2 equal to 0 and there is no work in this case. So, Wx dot is 0 and we may write h1 is nothing but so m dot times h1 may be written as m dot A times h1 or we may write m dot times h1 minus h2 we can split that into two things and write it as m dot A times hA2 minus hA1 plus m dot B times hV2 minus hV1. So, we treat this as two streams and hA2 minus hA1 itself may be written as Cpa times T2 minus T1. What is that m dot B may be replaced using the definition of omega. So, omega equal to m dot V over m dot here. So, we may write m dot V equal to omega times m dot A. So, we write like this and hV2 because it remains in the vapor state and does not condense hV2 may be approximated as hG of T2 hV1 may be approximated as hG of T1. Now, m dot A remember it is given that the volume flow rate is 100 meter cube per minute at the inlet. So, volume mass flow rate of dry air may be evaluated using this information V1 dot divided by its own specific volume which we may evaluate using the ideal gas equation of state. So, this works out to 126.072. What is that the partial pressure of air is used here to calculate the mass flow rate of air. So, that is the correct way of doing this P a1 which is equal to P1 minus P V1. So, notice that again we are using Dalton's model. So, the volume flow rate that is given although it is not specifically given that is volume flow rate of dry air that is understood because we are using the Dalton's model. So, volumetric flow rate is given. Once I use the partial pressures correctly I should be able to use the same value of volume because the entire volume as I said is occupied by all components of mixture only the pressures are different temperature and volume are the same. So, we can get hG at the inlet state and hG at the exit state from the temperature table and if you substitute the value we get Q dot to be 40.458 kilowatts. The next example that we are going to look at involves moist air but in this case we are actually going to cool and dehumidify coolant. So, we are going to cool the air remove the water vapor. So, in the previous case we actually heated the air in this case we are going to cool the air. So, here we have written mass of liquid water to be equal to 1 minus x times mv1. So, where we have used the definition of the dryness fraction. So, dryness fraction is defined as mass of vapor divided by mass of mixture and mass of vapor itself may be written as m minus mass of water divided by mass of mixture. So, that mass of water is equal to 1 minus x times mass of the mixture. So, we started out with the certain amount of water as you can see from here. So, we started out with the certain amount of water vapor at state 2 and now part of it has condensed as liquid and part of it remains as vapor. So, the mass of the mixture at state 3 is equal to the mass of water vapor that we started out with. So, we may then write mass of the mixture as 1 minus. So, this may be written as 1 minus x times mass of vapor at state 2 or I am sorry mass of vapor at state 1 is also okay because the vapor quantity of vapor remains the same. So, we may write this as mass of vapor at state 1 also.


Ireland, what are you doing? Well, sure. OK, I was originally from Connecticut, but I came here in 1966 for a Peace Corps training. And then after a Peace Corps on the Marshall Islands, I went back, got my MD in University of Connecticut, did some training in emergency medicine in California, and then ended up on the Big Island 25 years ago. And working in the Kona Hospital, I was vice chief of staff there when I left. And then I went back to school and actually got a degree in psychology and was halfway through a program in mental health counseling. So I've had a lot of psychology courses as well as medical training. I think that's important for this issue because it's not just medication. It's the psychology of dying. And so many people don't want to talk about death and dying and planning in advance. And your letter, which we will post, your letter was so good and it dealt with all of those issues that we have to deal with prior to making a decision about medical aid and dying. You want to tell us about that or how you came to this issue? Well, I should say, this is Representative Richard Kreegan. Oh, yes, I'm sorry. I'm in Ireland so you can make low the thirds to show who he is. Yeah, I represent Richard Kreegan. Thank you. And this issue has been on the table for some time. Doctors deal with this issue all the time in hospitals. They're controlling people's pain, but that control of pain often results in them dying. And they call that a dual effect. But I mean, you don't do this to patients without their consent, but they say, you tell them, look, we're going to help your pain. But if we control your pain, we give you enough medication to control your pain, you're likely to stop breathing. And they'll say, I'm good with that. So this isn't something that's foreign to physicians. It's part of our duty as physicians to help people not only to live, but help to have a peaceful death. So physicians have been doing this not in the sense of euthanasia, but in the sense of helping people to die a peaceful death. And I think this is just recognizing that we're all going to die someday, that most people, if you ask them how they want to die, at least many of them will say, I'd just like to die in my sleep.  We give them, put them into a deep sleep.  And it's a very peaceful way to go. It's peaceful for the patient, but it's also very peaceful for the family. Too many people in our society are forced to take their lives by very violent means. We talk about gun violence and homicides. There's one and a half gun suicides for every gun homicide. Now, not all these people are dying, but many of them are older people who are ill and are looking for a way out of a tortured life or a very painful life.  Some of the things that happen outside, we don't like to talk about those things either. But they do happen. So this is a way, a better way, of helping people to deal with the fact that they're dying and to allow them to have a choice. Not anyone has to make this choice, and most people are not going to make this choice. But the people who do want to make this choice, and I think it's an excellent choice for some people, I would like to have that choice. I don't know if I would use it. It's kind of scary thinking about dying, right? I mean, you're here and then you're not here. As a physician, the transition for most people is very peaceful. They just stop breathing. That's it, and they're gone. And in this method, that's what happens. You just stop breathing, and then you're no longer there. But if you're with the people that love you and that you love, it's such a, in my view, a much better way of going. And it's not at the hospital usually. It's usually at home, with your family, your dogs, your pets, in the place you love. I mean, I don't want people in Hawaii have to go to Oregon or California to seek this. I think we should be able to have it here. Do you think that the bill will pass this year? Do you have a feeling about that? I think it's very likely. I'm extremely likely. But it's very likely it will pass. The Speaker introduced it. He believes in it. Four of our governors are supporting it. I think most of the people in the House and Senate support it. But it's one of these issues that has a lot of moral loading for people. And people sometimes are hesitant to vote on bills like this. So we had the same kind of trepidation about same-sex marriage. So I think there was a lot of that trepidation whenever it was 10 years ago, when it almost passed. And some of the religious organizations came up very strongly and scared some people into not voting for it. Hopefully, that won't happen this time. Now, I feel that if you are a Catholic or a Mormon or whatever, and your religion says you don't do this and you chose to follow that religion, then all means you don't do that. But for the rest of us, should have the option that should not stand in the way of other people who do not belong to those religious traditions, organizations, that they should not be able to stand in the way of other people. That's my feeling how if we are a democracy then how can a religion stand in the way of the rest of the population?


The Acting Secretary of the Army and the Sergeant Major of the Army visited Research Triangle Park in North Carolina, June 29th, to learn about Army science and technology investments in the future force. Acting Secretary Robert M. Speer and Sergeant Major of the Army Daniel A. Daly met with scientists and engineers and learned about the mission of the Army Research Laboratory from its director, Dr. Philip Percanti. So when we look at the totality of where the Army wants to go and what concepts we're thinking about, the first thing we do is we ask ourselves, what are the knowledge gaps? And that's how we get after our foundational research programs to address those knowledge gaps. What we call it is use-inspired research. Scientists also showcase their partnership with the Defense Advanced Research Projects Agency or DARPA to explore solutions to help soldiers in need of prosthetic devices. Research Triangle Park is where the lab's Army Research Office acts as a guiding hand for university research that may uncover the next big thing in technology to make soldiers stronger and safer. The critical thing that ARO brings is access to the tremendous resource we have with university professors. I think the Secretary left going very optimistic with an increased even more enthusiastic understanding and appreciation of what long-term basic research brings to the Army's fight current and future. The leaders told the researchers that the work done at the laboratory is held in high esteem. So it's great to see the excitement and the results and or the thought processes going on. So I wanted to come down here and at least on the way thank you guys and let you know it's appreciated. From Durham, North Carolina, David McNally, ARL TV.


This is your girl, Sewit with Britt and welcome back again to my YouTube channel. Long time no see everyone, it is so good to be back after such a long break from posting content. Anyways, I am back and today we are going to learn the basic bodice block by Helen Joseph Armstrong. To those who are not familiar with Helen Joseph Armstrong, she is the author of Pattern Making for Fashion Design and I must say this book is by far one of the best pattern making books out there in the market and I recommend that you guys get this book. I will put the link down below where you could buy pattern making for fashion design. Before we move on to the tutorial, please be a doll and make sure to hit that subscribe and bell button and if you are new to my channel, make sure to check out my other tutorials as well. So without further ado, let's get this tutorial started. Here are the materials that we need for this tutorial. Pen, not sure for patterns, pencil for drafting, measuring tape, measurements from the model or dress form, fashion rulers, pattern paper and of course your model or dress form. Before we draft our basic bodice, we need to take all of these measurements from our dress form or our model. Please pause this video and copy these required measurements. First, let's take the circumference measurements from our model. Number one, around the bust. Make it sure to position your measuring tape around the largest part of the bust. Number two, around the waist. This is the smallest part of the waist. Number three, abdomen. This is three inches below the waist. Number four, around the hip. Largest part of the hip area, this is usually eight to nine inches from waist, sizes medium to large and six to seven inches from waist, sizes extra small to medium. Important marks for the armhole. Mead armhole. The mead armhole is the same level with the plate screw. Make it sure to pin mark the back and the front. Armhole depth. To locate the armhole depth, measure down from the shoulder tip passing through armhole plate and add four eighths inches and pin mark this location. Next measurements, the front vertical measurements. Number five, front center length. Mark this measurement on the center line from neck to waist. Number six, front full length. Mark this measurement from shoulder at neck going to the waistline parallel to the center line. Number seven, front shoulder slope. Mark this from the center line at the waist to the shoulder tip. Number nine, bust depth or point. Mark this from the shoulder tip going to the largest part of the bust or the nipple area. Next measurements, the back vertical measurements. Number five, back center length. Mark this on the center line from the nape going to the waist. Number six, back full length. Mark this measurement from shoulder at neck going to the waistline. Number seven, back shoulder slope. Mark this from the center line at the waist to the shoulder tip. Number eight, then use trap. Place the tip of the measuring tape at the corner of shoulder at neck to bottom of the waistband at the side seam and record. Next, the front horizontal measurements. Number 10, bust span. Measure the point to point of the bust and divide this measurement by two. Number 14, front across shoulder. From the tip of the shoulder going to the center front neck. Number 15, front across chest. Center front to one inch above mid arm hole. Number 17, bust arc. From center front over bust point ending two inches below arm plate at side seam. Number 19, front waist arc. From center front waist to the side waist seam. Number 20, front dark placement. From center front waist to side front or the princess line of the dress form. For the model, minus five eighths inches from bust span. Number 22, abdomen arc. From center front to side seam starting three inches down from waist. Number 23, front hip arc. From center front to side seam. Number 25, hip depth eight to nine inches from waist or six to seven inches from waist. Next, the back horizontal measurements. Number 12, back neck. From center back neck to shoulder at neck. Number 14, back across shoulder. Same as front. Number 15, back across chest. Same as front. Number 18, back arc. Same as front. Number 19, back waist arc. From center back waist to side waist seam. Number 20, back dark placement. From center back waist to the side front or the princess line of the dress form. Number 22, back abdomen arc. Same as front. Number 23, back hip arc. Same as front. And number 25, back hip depth. Same as front. Next, and the final measurements. The side measurements. Number nine, bust radius. Measure from bust point ending under bust mound. Number 11, side length. Mark below arm plate at side seam to side waist. Number 13, shoulder length. From shoulder tip to neck. Number 26, side hip depth. From side waist to the hip depth line. We are done taking up measurements from our dress form or our model. And these measurements are the measurements that I got from my dress form. Now that we got our measurements, we can now move on to drafting. First step, draw an extended horizontal line. Next, draw an extended vertical line perpendicular to the horizontal. Label the horizontal line B. B to A. Mark up the front full length plus one eighth inches from B. Label this A. C to A. From A, extend the horizontal line and mark in across shoulder less one eighths inches and label this C. From C, square down three inches. B to D. Mark up front center length and label it D. And square a horizontal line from D. D to E. Mark in bust arc plus two eighths inches and label it E. From E, square up 11 inches. B to G. Mark in shoulder slope plus one eighths inches from B. G should touch the C line. G to H. From G, mark in the bust depth or point and label this H. G to I. Mark in the shoulder length and label it I. J to K. Square a horizontal line at the bust point or H. Label it J. From G, mark in the bust span plus two eighths inches and label it K. D to L. Get the measurement from D to J divided by two and square this measurement from D. Label it L. L to M. Mark in front across chest plus two eighths inches and label it M. B to F. From B, mark the front dark placement. On that mark, mark down three sixteenths and label it F. Next draw a slight curve from F to B. I to N. From I, mark the measurement of new strap plus one eighths inches. Intersect this line to E line and label it N. N to O. From N, mark up the side length measurement and label it O. From O, mark in four eighths inches guideline. N to P. Mark out seven eighths inches or one to eight inches from N and label it P. Here's a chart for the bus cop formula. P to O. Connect the mark to O and make it sure that P to O is equal to N to O. Next, extend the guideline from P to F. P to Q. This is the waist arc plus two eighths inches east and minus the measurement from B to F or front dark placement. Mark this measurement from P and label it Q. On the Q mark, mark down three sixteenths and draw a slight curve from Q to P. Q and F to K. Draw the dart legs going to K. From K, mark down five eighths inches and redraw the dart legs on the five eighths mark. Using the French curve, connect G to M, M to O and this is the armhole. Last, connect I to D and this is the front neckline. Label the chest line, bust line, bust point and waist line and we are done with the front but it. Okay, let's now move on to the back bodice drafting. For the back bodice, label the horizontal line B. B to A. Mark up the back full length and label it A. A to C. Square a horizontal line from A. Mark in the back across shoulder and label it C. From C line, square down three inches. B to D. Mark up back center length and label it D. Square a horizontal line from D line. From B, mark in four eighths inches and this will be the new B or line. New B to E. Mark in back arc plus six eighths inches E and label it E. From A line, square up 11 inches. A to F. Mark in back neck plus one eighths inches from A line and label it F. New B to G. Mark up the back shoulder slope plus one eighths inches and label it G. G line should touch the C line. F to H. Mark the shoulder length plus four eighths inches from F and this will pass through the G mark. Label it H. New B to I. Mark in the back guard placement measurement from UB and label it I. New B to J. Mark in waist guard measurement plus one and a half dark intake and two eighths inches E and label it J. I to K. Mark in the dark intake which is one and a half inches. Label the center L and label the dart leg K. J to M. Mark down three sixteenths. Next, mark down one eighths inches past I and K. Next, draw slide curves from I to New B and K to M. M to N. Mark in the side length and label it N. From N, mark in four eighths inches guideline. L to O. Square up the same length as M to N and label it O. Connect I and K to O to complete the back guard. Next, divide F to H and mark the center and label it P. Draw a guideline from P to O for the back shoulder dart. P to Q. Square down three inches from P and label it Q. This is the length of the shoulder dart. Mark two eighths inches on both sides of P and label it R. Next, mark up one eighths inches on both arm marks. Slightly connect to F and H and complete the dart. D to S. Get the one foot measurement of D to B and mark this measurement from D and label it S. S to T. Square a horizontal line from S and mark in the across back plus two eighths inches and label it T. Next, using the French curve connect H to T and T to N and this is the back arm hole. Next, connect F to D and this is the back neckline. New B to S. Connect QB to S. Label chest and waist and back and we are done with the back bodice y'all. And here you go guys. We have completed the front and back bodice. Congratulations guys and we can finally try this on our model or our dress form. So here I am. I am just using another pattern paper to trace my front and back bodice and transfer it on a fabric to see if there are alterations needed for this bodice. So as you guys can see I need to make some little alterations here and there but this pattern looks pretty neat to me and since there are added ease we cannot avoid altering our pattern but that's okay. I am satisfied with the bodice that I made and I hope you guys are too. Anyways you guys thank you for watching and again don't forget to subscribe to my youtube channel SewItBitBit and be part of our growing community. I'll see you guys again on the next tutorial. Bye!


I'm Mix Kaneda, I will now begin the presentation of a relationship between onomatopoeia and physical properties when pressing a soft object. First, please look at this. Which one do you think is booba and which one is kiki? Most people would say that the one on the right is booba. Booba and kiki are a kind of onomatopoeia. In this way, onomatopoeia can share meaning. And even in Japanese, there is onomatopoeia which can express minor differences in softness. For example, this video uses onomatopoeia to express punipuni on the left and mochimochi on the right. If you are a native speaker of Japanese, you can share the meaning. Therefore, we decided to conduct an experiment to clarify the relationship between onomatopoeia which expresses softness and physical properties. Because we thought that if we could share the meaning, we could write them to changes in physical properties. Using 12 different gels, we conducted experiments under 3 conditions. Visual, visual tactile, and tactile conditions. As shown in the video, the experiment involves separating the fear of the gel by touching or licking at it. The variations are naturalist, viscosity, elasticity, and onomatopoeic responses. We had 12 participants. We have found that many forenames vary with hardness in all 3 conditions. For example, in hard samples, the first consonant is often G. In intermediate hardness to soft samples, P is often used. In soft samples, M is used. We also used the Recreation Theory 1 to conduct our analysis. This table shows the significance probability when onomatopoeia is used as an exploratory variable. The results show that the consonants and boards in the pressed mora are common to these conditions and have a significance probability of less than 5%. This could be important in the representation of onomatopoeia. We found that there are subtle differences between the conditions. For example, in the visual tactile and tactile conditions, the significance probability of constructed sounds in the second mora is less than 5%. While in the visual condition, the significance probability of other than penetration is not less than 5%, suggesting that the factors that are important in onomatopoeic expression may change depending on the condition. Here is the summary. Thank you very much.


Watching slaughterhouse footage is a way of bearing witness but nothing comes close to being at that truck and looking the animals in the eyes feeling their energy saying I'm sorry I see you and we're trying and welcome like there's something welcoming about pushing childlike beings into a gas chamber What's your name bro? Richard. How long have you been coming here for? Almost a year and a half. A year and a half and you said you've noticed something with the trend of trucks coming in what's been happening? There's been less and less over time we've come like every two weeks or so and then there used to be sometimes like 15-16 trucks and now average is around 8 or 9 or 10 and they're not full capacity anymore and then there's a guy who works here who's been here for like 18-19 years and he said there was a day a few weeks ago where they didn't kill anything and he said he's never seen that happen the entire time he's worked here. Wow see in a year and a half gradually there because you'd think if meat consumption was increasing these guys would be kicking goals wouldn't they? It's going down for pigs sheep and lamb in this country but chickens is going up and they own like spam and chilips all like lunch and meat and meat and stuff so so pretty big industry yeah really big company one of the biggest one of the bigger companies like Danish bacon which is like a big thing in England. Wow so whoever says the save movement doesn't work this is evidence that us standing out in front of these slaughterhouses bringing images out bringing videos out of these animals is working okay because meat consumption is is going down because consumers are getting becoming aware of the horror story that's inside okay so the save movement is working. Just the wheat pigs yourself? Sorry? Just the wheat pigs yourself after working here for so long? Very rare. Very rare. I can have salesy off of me but I don't even have it anymore.  Well it does a bit.  A squeal. Like dogs squeal when you kick them and stuff like that type of squeal. A yelp. Yeah dogs yelp when you kick them so that's it's kind of like their yelp. Yeah I mean what more can you say about that it's just terrified childlike beings being pushed into this dungeon and suffocated with gas and they're burning from the inside out. People who've been following my channel for a while now know how terrifying and horrific gas chambers actually are. We just stopped a truck out the front and real infant like pigs in there they're really gentle and really young maybe five or six months old and now they've been subjected to this horror inside of here. Ah that's interesting that's interesting uh do you say I don't know if I could work here for so long and still think that they're their food actually. Have you seen images from inside that have they showed your footage of inside the gas chambers? I've worked here I've worked every day. So you've seen the pigs go down and struggle in the cage and stuff?  So you've seen them get processed and gutted and yeah do you think you're desensitized to it now? Like you're like no I don't think it doesn't make you feel the same way as it did when you first seen it. I know it's pretty hard to come to terms with but this is the reality of it this is what they go through billions every single week. I think it's it's important as an activist to come and listen to their screams to suffer with them to bear witness to them. One of the most powerful forms of activism I've ever done for me as an activist is suffering with animals so you know why you're fighting. Here they are the victims of the holocaust in here look at their faces look at these beautiful animals faces prisoners in here. Does it bother me you can't let it bother you if you want to work here?  I've seen a number of people that follow me and watch my videos still eat pigs still eat animals and this is what you're eating you're eating the suffered body of an animal that didn't want to be pushed into these places these animals are going in against their will and you're eating their bodies you're eating that you're eating all of that all of that violence all of that fear all of that suffering I couldn't think of anything more horrific to put inside my body than the body of someone who struggled for their last breath. It's like a used to bring kids here all right well for a tour yeah that was a long time ago full of 20 school kids and a few hundred minibosses what they took him through the processing line I can't believe that that's a good way to turn everyone vegan actually. Plus it's never come to a pig is it in the trail the supermarket because a lot of kids not when they go to a pig farm are they so where are they going to see them at the slaughterhouse exactly I can't believe that I can't believe that I think it was just showing like how the stuff that's on the supermarket shelf gets there.  Many people out there have children too and you're feeding your children these suffered bodies of children these are children in here they have the same intellect the same you know level of awareness the same intelligence as a child you're feeding these dead children to your children ham sandwiches bacon sandwiches sausages we have vegan options for all of that you're putting that inside your child's body and they don't know about it the children you're feeding these pork chops to do not know what happens in here show them let them let them listen to a gas chamber the most humane method for stunning pigs in the world this one here let your children listen to it all those Christians out there who think god wants this let your children see what happens in these places and tell me if they think it's okay you know that's an indicator of whether or not this is our natural food or not because if we can't show our children how it's produced and it makes them sick that's just showing us that it's not food god created your children god doesn't want this trust me this is a hellhole if you think about it a baby yeah that's interesting there because a true natural carnivore would see that and not not blink or not they'd get hungry they'd be like oh a suffering animal human beings i think it's when it's a baby or a young guy and that gets it seems to affect kids more six month old pigs are still basically infants yeah yeah i mean they used to be nine month old you know about the world health organization and stuff yeah bacon causes cancer and well we'll get all sorts of uh oh yeah they've been coming in for a couple of years now like at least you know about it anyway of you know you know more than most people in society and i think like if everyone had your job a lot of people wouldn't be eating them that's for sure i feel sorry for the guys who have to wake up in the morning and stab pigs in the throat that's for sure so another thing i want to talk about is that the workers in here don't wake up in the morning and say hey i want to go work in a slaughterhouse they don't grow up as a little child and say hey i want to kill animals every day for the rest of my life but these people that are working in these places are suffering trauma okay and the only reason they're working in these horrific conditions is because consumers want to eat animal bodies okay so we're subjecting humans to these disgusting working conditions subjecting innocent child-like animals to horrific horror stories like a gas chamber all because you want a fleeting taste in your mouth that we can get from plant-based sources now think about that think about what we're subjecting humans and non-humans to just for a burger just for a sandwich that we can get vegan alternative sports and they drop them into the gas yeah in the cages yeah is this a gondola so it's like a roller coaster with yeah how many cages are 15 or 10 how many how many how many pigs in a cage well there's three in a cage hey not six in a cage oh six in a cage and how many cages okay apparently the call of the ferris wheel of death that'd be scary hey that'd be scary we've got footage we've got footage of pigs screaming and you know the gas chambers in melbourne diamond diamond valley pork a guy used to work cleaning out the bottom of the gas chambers he found about 50 hoofs so hoofs that the pigs had ripped off of their own limbs trying to escape the cages this screaming and suffering and yeah yeah really they're not always tuning the gas correctly and they're burning and suffering and so i guess this is just a plea to people who are still eating these animals and to vegans who aren't active yet this is what's going on every single day every second of every hour of every day okay and if you're not active and you're vegan you're allowing this to happen okay these animals are being condemned to slaughterhouses because people aren't awake yet they're unconsciously purchasing these products and if you're vegan and you're not speaking out against it you're complicit in this you have a level of complicity because you know this happens okay you know this happens and you're not doing anything about it okay that's why we need to all be active as vegans the vegans that we have on earth right now need to be active to speak up against this because a majority of people they don't know about this and if they knew about this they would think twice about it trust me especially the horror that goes on in these gas chambers especially this okay the powers in our hands okay we need to be the voice for them okay and end these industries we need to end it this year all of us together this year 2018 okay let's do it i'll talk to you a bit after bro thanks mate shut coming in all right so if you guys can see really scared little five or six month old pigs in here they look like puppy dogs or something hey all right so the killer out 2800 here a day about 14 000 a week and this makes any human genocide look about this big we're talking billions of week billions of animals a week eight trillions a year sea animals ripped out of the ocean pigs pushed in gas chambers chickens hung upside down and dragged through electrical bars and had their throat sweat open you tell me this isn't a holocaust you tell me this isn't a massacre yeah so that last truck was really hard and i just kept looking at their little bodies and i just thought to myself that that's the reason why they're in the back of those trucks because human beings want to rip the flesh off of their bodies their flesh and i just looked at their little wires and how scared they were and i just thought why are they doing this to them you know why are we doing this to them hello hello sweetie i'm no sweetie i know you're scared darling they're so beautiful nothing has given me fuel to do what i do more than suffering with the animals it's a very hard thing to do and it really gives you perspective it gives you perspective and the animals perspective and we can never know what they're going through truly because we are not them but we can have a level of understanding that will help us be ambassadors for them hello hello darling i'm really sorry about this and so do the local people you know they're just kind of used to it yeah the local people are probably used to it well let's get it on yeah so it's all the normal normal something a bit weird has it deterged you from eating peaks at all has it made you think about eating peaks at all you don't eat peaks at all no is that because all is that because of hearing no sounds if you kill them in the right way what is the right way doing that what is the right way in your opinion but it's not right where is the real it's no right way to take someone's life from them if they want to live well yeah that's up to you that's it i don't i don't know well we we look at it from the victim's point of view from the animal's point of view yeah i can understand you don't get right into it like that no is it easier for you just to sort of block it out your mind and pretend it doesn't exist we realize that by us paying for the the animal products we're condemning them to death you know that's a 22 day vegan challenge yeah they mentor you on facebook they give you heaps of good tips and it's all free i don't think there's anything more powerful than showing either slaughterhouse footage or an animal about to be slaughtered okay saying hey these are the victims of your dinner plate this is what they look like hey vegans these are the animals you're supposed to be speaking up for okay they're getting driven into this slaughterhouse day after day second after second they're getting slaughtered okay nothing's more powerful to get people active to give you that fuel that fire to stop people from eating them and the things that come out of them the save movement it's changing the world it's just upsetting isn't it can you imagine what they go through if you can imagine uh you know what would be like then if that was you would you would want someone to come and help yeah like if there were dogs in there people would want us to save them you know and they're no different in the way they want to live and yeah appreciate that brother


Hello, Seesaw Nation. My name is Robin Schumacher. I am a second grade teacher and differentiation coach at Altitude Elementary in Colorado. You can follow me on Twitter at Robin underscore SCHUH. I'm going to jump into a quick and fun activity. I've done for four years now with Seesaw. It is called a friend a day in May. Every year I do a little something different depending on my class and what they create, but I will share that with you right now. So what we do to start our a friend a day in May as we end the year with a bang, I hang up the number of balloons for the number of students. Every day we pop a balloon and inside each balloon is a student's name. We celebrate that student for that day in Seesaw. You could also do this with name of wheels in Google. You could do it with just drawing kids names out of a hat each day. So we celebrate those students in Seesaw by taking a smiling picture of them. We usually have a friend do this and then that student and child get to add in their name. They get to choose their label style and add one emoji in about them. Then we put the iPad or computer at the back of the room and every student comes up and creates one label for that student.  They can even add an emoji for younger students. In my past years what I've done is put out a list of character traits for those students. When they get done with all the students adding one kind word about their friend they get to hit the check mark and turn it in. So there's a few ways you can access this activity. You can go into the activity library where I have the activity called a friend a day in May. Or every day you can simply pick a kid and click on the photo button and create your labels about that student. To add to this fun project or to turn it into a lasting memory you can create a mini memory book by printing out the images from seesaw and handing it out at the end of the year. You can add a teacher recording to each image and get the item QR and seesaw to print and share with your kids. You could also save the images from seesaw and create a mini movie for the students to watch in seesaw or even just to send home on a disc if you want to to share with them. Thank you. If you have any questions you can find me at robin underscore s-c-h-u-h on twitter. My emails are schumacher at cherry creekschools.com. You can also check out my activity library and I'm always adding lots of fun and creative stuff in there. Thank you for tuning in. I hope you have a great day or a great evening. Thanks.


working as an assistant professor in computer science and engineering department at Volchian Stop Technology, Sola. Today, we are going to discuss about the buffer pool scenarios. As we have seen in our previous videos, we have already covered what is meant by buffer, what is buffer cache, what is buffer pool and hash cube and we have also covered the gate block scenario one. So, now today we are going to see the gate block scenario second and third in Unix operating system. At the end of this lecture, our session student will understand the concepts of gate block scenarios two and three and the gate block algorithm for the same. Now, now basically I will just give you the review, it means what actually we are going to do or what we are actually going to learn in this session like the algorithms for reading and writing the disk blocks uses the algorithm gate block to allocate the buffer from the pool. There are typically five scenarios the kernel may follow in gate block to allocate a buffer for a disk block. Now, we have already covered the scenario first in our previous video. So, now today we will see the scenario second and third. Now, scenario two the block could not be found on the hash cube. So, a buffer from the free list is allocated and now in the scenario third block could not be found on the hash cube and allocating a buffer from the free list, but that buffer is marked as a delayed write is allocated. The kernel must write the delayed write buffer to the disk and allocate the another buffer means what basically the delayed write is a one more concept in these buffer scenarios. We will see this delayed write in the scenario three when we are going to explain in detail. So, now basically we will see the some examples how actually this scenario second and third is going to be work. We have already seen this diagram in our previous videos. So, now here we will have the hash cube headers, we will have the total four blocks block number 0, 1, 2, 3 and we will have the maximum four blocks. So, that is why our in a hashing function the n number is 4. So, now here we will have the 28, 4, 64 are the buffers in this way we have this diagram. So, now we will see how actually the scenario two is going to be work. Now, scenario two is nothing but the like block could not be found on the hash cube. So, a buffer from the free list is allocated means there is one process that process is going to search for the block 18. So, now while searching that process what actually it will perform that process what we will do that process will send the request to the kernel like requesting for the block 18. So, then kernel what will do it will perform the hash function on the block 18 to get the exact address of that block. So, now here they are going to use the block number mod n that is the hash function. Now, here we are searching for the block 18. So, what we will do 18 mod 4 here what we will get we will get the reminder as a two. So, what we will do we will search for that two search for that block in block number two. So, now when we will look at this block number two will have 98, 50 and 10 in our buffer pool, but we do not have that 18. So, now here means block could not be found on the hash cube means 18 is not found in the hash cube. So, now here we need to allocate that buffer to the free list allocate that buffer from the free list. So, now here in our free list will have the 3, 5, 28, 4, 97, 10 these are the links will have the free list. So, now what we will do as we have explained previous video to achieve or to allocate this free buffer we are going to use the list recently used buffer. Now, here we will identify the list recently used buffer is third. So, now here what we will do in the next slides what we have done we have removed the first block from the free list and assigned it to the 18. So, now we will get the list of buffers like in block number two 98, 50, 10 and 18 in this way we will remove the buffer from the free list and assigned to the 18. So, now that is nothing but our scenario two, but now here one more thing here we need to update the free list again because we had removed the three as we have seen in the previous slide that three buffer will remove from the free list and as make it as a 18 and we will give the link the first buffer in this free list is 5. So, now in this way it will work. Now, we will go for the next slides. Now, here the block could not be found on the hash queue. So, the buffer from the free list is allocated as we have seen in the previous block. Now, process is now looking for the block 18, but that block 18 is not present in the hash queue the kernel allocate the buffer on the free list. Now, remove the third block from the free list and assign to the block 18 all these steps we have already discussed in the previous slides. So, now we will go for the scenario third. Now, block could not be found on the hash queue and when allocating a buffer from the free list a buffer marked delayed write is allocated. Then the kernel must write the delayed write buffer to the disk and allocate the another buffer means what basically here we need to understand the what is the delayed write. The delayed write is the term used to describe the method in the Unix kernel uses to write the disk block back out to the physical media means when any process is requesting for some block and that block is currently not available on the hash queue. Then what we will do we will allocate the buffer from the free list, but now that free list is marked as the delayed write means that particular block has been already updated by some other process and still that block data is not updated back it means or written back on to the disk means that recent data is not maintained on the disk. So, now here we cannot overwrite that buffer because it is a delayed write means here we cannot allocate that buffer to the requested requested by that process. So, now here let us take the example now here block 3 and 5 are the delayed write block on the free list or look into the diagram. Now, what we will do here we will search for the block 18 as previously we have seen that one. Now here searching for the block 18 now delayed write block on the free list. Now in the scenario 2 we have already seen the block 18 is not present on the hash queue then we need to allocate that third buffer to the 18, but now here third is already a delayed write marked as a delayed write and then we need to find out the next buffer. Now next buffer is our fifth but again that fifth is again the delayed write means the data from the third buffer and the fifth buffer needs to be written right back on to the disk. So, now here we need to find out the next free buffer now here we will get the next free buffer as a 4. So, now look into the buffer what we will do we will allocate that buffer and we will make the changes in the free list header like third and fifth are the delayed write. So, need to remove that buffers from the free list because currently we are writing that data back to the disk from the third and fifth. So, now in this way we will update the list now here if you look into the diagram here we will get the 28 is the next free buffer then 97 then 10 and then the next pointer of the 10 is the free list header. So, now in that way we will allocate that 18 block into the block number 2. So, now this is nothing but the delayed write. So, now if we look into the diagram sorry algorithm here we will searching for the buffer till the buffer is not found now while buffer not found the loop is continued if the block not in a hash queue then what we will do it will come into the next if buffer mark for the delayed write that is scenario third then what we will do the asynchronous write buffer to the disk and then continue means we are not going to perform any action on that particular buffer till that buffer is going to be written back on to the disk now that is nothing but the scenario third now on to the scenario 2 means what if the block is not in a hash queue and if it is not marked as a delayed write then what we will do remove that buffer from the old hash queue and put buffer on to the new hash queue and written the buffer that is nothing but our scenario 2. Now think and write what is delayed write pause the video and write your answer here the answer is delayed write is the term used to describe the method the Unix kernel uses to write the disk block back on to the physical media references are we have referred the design of Unix operating system book by the author of Moorish J batch. Thank you.