G'day guys, how are you going? My name is Tech and welcome to my channel Bootlossophy. I work and live on Wajik Country in Western Australia, and I recognise the traditional custodians of this land that we share. I've bought a lot of boots on eBay, and I've reviewed some of them, and people have been asking me to roll out my eBay due diligence process, so here we go. I've reviewed quite a lot of boots on my channel which were eBay purchases, and loads of people have asked me to share what I look for when I shop on eBay to make sure I get a reasonably unworn or lightly worn boot and how to get a bargain on the price. Let's start first with a dizzying number and an array of boots that I have bought on eBay, and I'll quote the Australian dollars I paid for them, not including shipping, because that varies by crazy factors from international seller locations. So far I have bought 24 pairs of boots on eBay, and most have been lightly worn boots, and at pretty good price in my opinion at least. I have had a couple of poor choices and I'll talk about them as I go, so that's just to let you know that despite my process, I still make mistakes. Since this is not a boot review, I'm just going to rattle past the list of 24 and tell you how much I've bought them for in Australian dollars, and what they cost at least price in Australian dollars. I know you can get them discounted from time to time, but I'll quote the official listed prices converted to Australian dollars, or as sold in Australian retail shops, bearing in mind not all of these boots are available in physical stores in Australia, and you have to mail order some of them from overseas. I'm going to rattle through them quickly. The Timberland Earthkeeper, bought for $50, lists at around $300, maybe a bit under if they're on discount. It's so cheap because they have a tear in the uppers. Not a great buy, but it was cheap. Red Wing 9011 Beckman's, $200, no longer made in this format. This was a bad buy and I'll talk to you about that later. Red Wing Iron Ranges, $81.11, $350, listed at $560. Again, not another great buy and I'll explain later. Old and 403 Indies, $399 and lists at $900. Not bad, hardly anywhere. Red Wing 875 Mock Toes, $350, lists at $550. This was a great buy and practically unworn with the wage sold in perfect condition. Red Wing 3343 Blacksmiths in Copper Ruffin Tough, cost me $202 and lists at $500 with zero wear. Great buy. And the Wolverine Thousand Miles, $199, lists at $600. Pretty good value and very lightly worn. The Allen Edmonds Landon Boot, cost me $260, lists at $700, although Allen Edmonds have regular and deeply discounted sales. The R& Williams Riccabee Boot, lace-ups, bought for $250, lists at $650, totally unused pair. Redback Chelsea's, picked up at $45, lists at around $130, practically unused. Thursday Diplomats, $160, lists at $290 to $300. This was used, but very, very lightly. The Grandson Fred, $185, listed at $570. Another bargain, despite the grubby soul. The Grant Stone Edward, cost me $237, lists at over $500, lightly worn with some wear showing in the uppers. The Allen Edmonds Higgins Mill, load and suede at $258, while listing at $688, worn but really good nick. Truman Smoke Ramblers, bought for $470, lists at about $670, best pickup, totally unused. Parkhurst Nighthawk Kudu Allen Boot, $305, listed at $510 when it was available, it's no longer available. Very lightly used, great buy. White's MP in Natural Chrome XL, costs $579, but you can buy them here in Melbourne for over $900, so in my opinion it's a fantastic buy, hardly worn. White's MP again, this time in Cinnamon Wax Flesh, $609, and again over $900 in Australia, hardly used. Another White's MP in British Tan Chrome XL this time, $576, and it's before over $900 in Melbourne. Taylor Stitch Ranch Boots, bought for $100, and on their website lists at $506, hardly worn, so yeah, great buy. Another Truman in Black Rambler at $471, and would have cost me $670 new, $670 Aussie. This one is a little bit more worn, but a good pick up because it's a 360 degree storm well, which is very rare for Truman. And another Truman, this one in their classic Java Wax Flesh, bought for $471 Aussie, would have cost me about $700 new. The Wax Flesh is untouched, I put these scuffs on, and this is in the old Stitch Down construction too, which means that at least two years old, but really in excellent condition. Alan Edmonds Higgins Mill in Brown Chrome XL, you can tell by the stitch on the side there. Really good condition, I got these for $380 on their website, and certainly in Australia, they're listed for $650 Aussie. Red Wing Work Chuckets, practically unused, you can tell the tread pattern's not being touched. Very tough leather, I bought these for $200, listed on their website, and you can get them here in Australia at between $450 and $480 Aussie. Okay, that was quick. I just wanted to show you that you can get a large selection at great savings. Now, let me talk about my due diligence process. Step one is to get your mindset right. You need to approach the boot unemotionally. Yes, you are attracted to the boot, of course, you're excited even, and perhaps you're actually looking for that particular boot when you see it listed, but you should still see it as one possibility, not the boot. You need to be patient. There will be others, even if it takes a year before they pop up again. Cultivate a win-some-lose-some mindset, not a must-have mindset.  And on the other hand, you might also avoid an expensive mistake. I bought this pair of Red Wing Beckmans in Cherry Black Featherstone Leather because I did not keep that lose-some mindset. I got scared of losing out on a rare and discontinued model and ignored some of the things that I'll speak about later, so that this became probably one of my two biggest mistakes on eBay. I bought them for $200, and if new, they're no longer available, would have been about $500 Aussie Plus. The uppers were in beautiful condition, as you can see, really well cared for. The heels had some wear, but I was prepared to and I got my cobbler to put on new top-list for about $20. The Rochia Half-Sole, oh yeah, somewhere, but not worn thin by any means. But what I didn't check in my haste was the insoles. And when I got them, I found the insoles had been totally compressed into the shape of the previous owner's feet. I can wear them, but a little awkward rather than uncomfortable. I had to put a removable foam insoles inside to help flatten that compression for comfort. The truth is, if you stay patient, another one will come up. Be picky and put together a short list using eBay's Watch function. Keep your watch list short and focused or you forget the be patient part if you're overwhelmed. I once had nearly 10 boots on my short list and I was losing on some auctions and offers were getting knocked back. So I started getting overwhelmed and into a must-buy-something mindset. So I made an offer on these Timberland Earthkeepers. They were on an auction with a starting price of $50 that I didn't want them, but $50.  I won. Thank goodness it was only $50, but still, impulse by the century. Once you're watching two or three of what you're really interested in, note the time that you have left before the end of the listing so that you know what you have to play with. Okay, so targeting mode is now on and now you can spend some time on step two and do some preliminary checking. Check the obvious things like the style, the way it's described, any labels shown. You want to make sure that what you're looking at is the genuine thing. Now, there are not that many counterfeits of heritage boots, but still, if you're supposed Red Wing Iron Ranger labels don't look original, treat it with some suspicion. If it's described as shell cordovan but the photos look dull, mark it for a question. So, you know, just look for red flags that might pop up that you can check out one way or other. Put together a list of questions you have for the seller or maybe to the bootmaker. Now, having gotten an overall idea of the boots in your shortlist, it's time to visually check the wear and condition. So here I'm doing this after my initial look, not the very first thing.  This way you get a cool look before you move in for the kill. There's four things I look at closely. First, look at the condition of the uppers and stitching. Second, check out the soles and the heels. Third, check out the sole edges and the welting and stitches. And finally, check out the hardware. Let's take them one at a time. First, take a close look at the uppers in the photos. Look to see if they look dry or if they're particularly wrinkled or creased and if there are any cracks or water damage. See they look well conditioned and the right colour. My second biggest mistake was probably this pair of red-winged iron ranges. All my other checks that I'm about to tell you about all checked out. Except that I wasn't too happy about the look of the leather in the photos. For amber harness it looked wet and dark. I ignored my concerns because the price of a pair of otherwise lightly worn iron ranges was great. But when I got them I realised that they'd been totally over conditioned. They'd been used as a demo pair for a manufacturer of boot oils and leather balms and so were pulled out at every trade show and enthusiastically conditioned over and over again. The next part to focus on are the heels and the out soles. Check the photos and if there aren't any underneath the boot make a note to ask the seller for more photos of that particular area. Take a look to see whether the wear on the heel is reasonable or if you're going to have to replace the heel top lift or worse as soon as you get them. Look at the wear on the sole. How well worn are they? What's the condition of the stitching? Are there any cracks or chunks fallen out? Is the wear even? Third, make sure you look closely at the sole edging and the condition of the welt and stitching to see what kind of damage they might be. Basically what you're looking for is are you going to have to spend any money on them when you get them? Finally take a look at the hardware to check condition. Check for loss of alignment of the speed hooks any corrosion and so on. Look this sounds a lot but it's just a minute checking really a minute and again the idea is to really see what you might get not fall in love with the example on offer straight away. By now you may have found everything you need to know but you might also have a list of questions to ask the seller. It's perfectly fine to ask the seller questions. However as you might be putting in a low buyers offer later it's always good to start by making sure that you're respectful. You want to develop a rapport not a him kind of sentiment. Also as part of being respectful while you're in a hurry to seal the deal don't forget any time differences that they might be because they might be busy at work or even asleep when you're out there shopping so don't follow up with abusive messages if they haven't replied promptly. I would ask all your questions or requests in one message don't string them along one after another so that they feel you're just stringing them along. Ask short sharp direct questions don't ramble or ask for opinions. Don't be shy about asking for more or better photos. Do ask them why they're selling and if the answer is that it just doesn't fit ask what size the other boots are and how long they try to make it work. That'll give you an idea about what where to expect as they were trying to make it work. I find that you can tell from the answers how honest they are and don't forget that eBay has the opportunity for buyers to provide negative feedback about bad sellers they know this too. Once you receive your answers you can then make a decision about making an offer or a bid. Two simple things before you do number one do some research to check comfortable prices then decide on the top price you want to pay not forgetting the cost of postage and any other unfortunately crazy eBay charges. Check the listing to see if they'll send overseas if that's applicable and if they don't then add that to your queries and also your cost estimates. On the listings that provide a buy now price or a listed price not auctions you can make an offer. For items that are listed as auctions you can try to contact the seller and make an offer before the first bid is placed and see they'll accept that offer and end the auction early. If a first offer has been placed or a first bid you can only enter the bidding yourself up to your top price. Auctions are difficult to manage. Smart bidders set a level early in the auction and eBay system will inch the range upwards as other bidders come in until it reaches your top limit. eBay will then tell you and suggest you make another bid. You might think that maybe I'll put my top limit as the first bid I'll find this a little too tempting for me to then bid more at the end because I'm just being overbid a little bit. My own tactic is to put in an early bid up to say 75-80% of what I want to spend and then if I'm overbid I wait. I stalk the auction when there's maybe 20-30 minutes to the end and sometimes if the bidding goes quiet I'll swoop in with my top bid at the very last minute. If it's a listing with a listed price and they accept buyer's offers what I would do when you make your offer, particularly if it is well below the asking price is to be open, honest and rational about why you're making that offer. Tell them about the where in the heal that worries you or tell them about the level of where you see compared to others that you have seen at the prices that you've seen a man. The worst they can do is reject your offer the best that could happen is they understand your concerns and maybe they'll accept your offer. Be open to but don't invite a counter offer. Don't say for example oh if you don't like that just tell me what's the lowest that you'll accept leave the door open by saying something like hey if you don't agree with my reasons please explain so that I can have a think about and reconsider. What can happen is that they reject your offer but they make a counter offer. At that point you can decide to accept or make another offer and try to come to somewhere in between. At that point it's all about your perception of value or level of desire and if you've built a rapport you can discuss that. Remember that top price you set at the start do not go over it be okay with the one that got away it's part of the fun if you do this right you can get some of the best bargains. I've shown you some of my bad buys so let's look at some of my great buys I've got these three great pairs of whites and pea boots that are all three hardly worn the uppers are in great shape the heels and soles unnoticeably worn the hardware solid and all at around half price. Look at these Truman smoke ramblers from Truman. The soles and heels were literally untouched the solid leather midsole not yet broken in even no marks anywhere and at a 30% discount because someone might have worn them indoors a couple of times and they didn't fit. These are other two Truman's the Java Wex Flash and the black rambler were from a bootlossify watcher shout out to Typo 777 these are older models but so lightly worn I can just see some wear at the heels so there are sellers out there like Typo 777 who actively pick up bargains, renovate and clean them and resell them at a higher price. This Java Wex Flash is a now rare stitch down model in really good nick so you can get some really good bargains keep your head and be diligent at time of recording I have 70 pairs of boots 24 of them from eBay at prices averaging about half of what they would have cost new that means discounting any new ones I bought on sale my collection cost me 10% of what it would have cost if all of them were new to me that works if you're only buying 2 or 3 boots from eBay to add to your collection of 5-10 pairs it makes sense to take a look at eBay I'll put a link below to a search of boots on eBay go take a look and there you have it my buying from eBay 101 look at the end of the day boot collecting and boot wearing is about having fun so go into it with that attitude have fun don't forget to click on the like and the subscribe buttons below it'll help me out and allow me to bring you more boot videos as my channel grows until then guys take care and I'll see you soon


Army presents The Big Picture, an official report produced for the armed forces and the American people.


You get what I'm saying? And even with the rap caviar and all that, most of the joints, I'm pretty sure that be on it, be from the record labels, right? Yeah, sure. So when you are independent and you dealing with that and we got a certain amount of slots on this shit that we putting out.  Right, is we gonna take the independent artists or they say, hey, keep telling us at this record label that they trying to push this artist. Now, we gonna put this artist on there.  And we gonna spend that big of bad with y'all.  We gonna continue to rub each other's hands for sure. Absolutely. Yeah, it's for sure. With the independent nigga, you don't know if he gonna be ahead of day going to Marl, nigga.


the title for my talk, is it okay, the first? Is regulation and coordination of interest in a lot of trafficking pathways. So halfway through my organizing this conference, the mathematicians who talked with me, said that they added, we added the phrase, where is the red? Ideas and concepts. So I decided to stick to it and just talk about ideas and concepts mostly and give some examples of data. And also to put it in the context as the organizer of the rest of the conference, okay? So I'll start my talk, we'll include introduction, regulation of secretion and regulation of recycling. So what's really good, so in the introduction I just want to bring you to what does it mean regulation of interstellar trafficking. What's really good is that I don't need to give a really long introduction because you've heard everything that I'm gonna say in the introduction, you probably heard throughout these days. So the secretory pathway or the exocytic pathway takes proteins and membranes from the endoplasmic reticulum through the Golgi apparatus, through secretory vesicles to the plasma membrane. In the endocytic pathway, stuff is taken either from the outside or from the membrane through a set of endosomes to the lysosome, which is the degradative compartment of the cell. It's all gonna be full in a minute. So this was talked in length on Tuesday. You also probably know that traffic in every step is bidirectional and there is cross talk also between the endocytic and exocytic pathway. And everything between compartments is transported via vesicles between the ER and the Golgi, between the Golgi and the plasma membrane, plasma membrane to endosomes, endosomes to lysosome. So you also heard that inside compartments, Golgi, the sorting compartments, Golgi and endosomes transport is done actually by maturation. And I'll talk about these two later. That's why I wanted to. So what is vesicular transport? A donor compartment, let's say ER, you take the cargo, which can be either luminal. Luminal is inside of the compartment or membranes. And then this vesicle will form. And then it needs to fuse with the right acceptor compartment. So now this is vesicular transport, just the overview. But if you look really at the sub steps, it's much more complicated and you heard about these two. So the vesicle first has two form and there will be coats and cargo receptors. And then it will have to move. And we heard about motors, either for actin or tubulin, the cytoskeleton. And then there will sometimes be membrane remodeling. And then you heard about tethers that will bring the vesicles close to the acceptor compartment. And then you will get the snare complexes that will help the fusion of this vesicle with the acceptor compartment. Okay? So if you want to think about it simply, about regulation, so if this is the cell and this is our vesicle, this is Paris, and the vesicle, the question is who are the traffic lights of the cell? Okay? So at least some of the major traffic lights are these GTPases. Which are called YPT in yeast and RAB in mammalian cells. So you heard about RAB6. And these are really what they do. They are molecular switches. They are very small, but they can cycle by themselves from the GDP bound form to the GTP bound form. From here to here, from GDP to GDP, they exchange the nucleotide. And from GDP to GDP, they hydrolyze the GTP. And I'll explain it later. When they're in the GDP bound form, they are mostly off in the GDP bound form, they are on. So in yeast, there are nine to 11 of them. The other two we don't know yet much about them. So I'm just, I'm not sure. I'm indicated in membrane. I'll explain in a second. So, and here are the major ones. So even when we say nine, we have, for example, YPT1 in the beginning here, and YPT3132, which are sometimes called 3132, they are functional homologues, okay? And for example, we don't know much. We know about YPT5, one and two, three, but we know mostly about 51, but they are involved in the same process. So even when we say nine, it's actually less. And it's important for later. Okay. Does each one have a clear homologon in million cells or? Yes, and this is shown here. So thank you. So there are 70, about 70 MMLI and human rubs. They are also regulating the human protein trafficking pathways. So there are more, but here I'm showing for, oops. So I just wanted to point that there are really large group of FGTPases together with their friends, with their ups and regulators, and some of the downstream effectors. They form like a 200 protein group, which is about 1% of the human protein. Yes. So for example, RAP6, here you put it between the ER and the Golgi? Yeah, RAP6 is not very clear what it does. And Bruno just told you, it's like somewhere here floating. RAP1, and Alec, talk about the localization and function. It's going to get a heart attack, can you say? No, no, no, Bruno, no heart attacks here. So YPT1, the best homologue is, the close homologue is RAP1, YPT3132 is mostly RAP11. RAP6, actually the RAP6 homologue, YPT6, is also a functional homologue. YPT1 is also a functional homologue. RAP1 is a functional homologue. You can delete YPT1, put RAP1, very highly conservative, can you say? And the same is true about YPT6 and RAP6. I don't know why, we haven't figured it out. It's not essential in yeast for viability. So, and we actually focused, Bruno talks about that. On them, we focused mostly here. That's why the Golgi is so big. So I just want to give you in the introduction some idea about how we even got into where we are now. So I'll call them the phases one, two, three. So it all started in yeast. All this family was discovered in yeast. First, why yeast? Because in yeast we can do, it's the same compartments. We do cell biology the same way. We can do biochemistry. But the genetics is what separates it. And that's why we can do so much more faster, okay? Of course, in combination with molecular genetics. So in phase one, we first shown, we looked at two YPTs, really. YPT1, which is essential for viability. YPT3-1 and 3-2, which together are essential. The cell can have one or the other. So they are very similar in their functional homologues as of today. Maybe each one, they have some kind of other functions that we don't know yet, but for now, we usually delete one and then the other one becomes an essential. So this we did, how did we discover them? Somebody asked me, is by reverse genetics. Meaning that we saw, oh, this is an interesting protein. It has homology to us. It must be an oncogene and it is. But this took many years to see it. And then we went from the gene to mutant. We made mutations to phenotypes to see what's happening here. So the next thing was, or together, was to see in which transport it. So first we knew that it was a huge thing to see that no, they are not at the plasma membrane. No, they are not in signal reduction per se. So, but they are in trafficking. And then we wanted to know which transport step they, because by now we know that there is more than one, which transport step they regulate. And here again, combination of molecular genetics, genetics and cell biology. And the last thing in phase one, we already knew that it's conserved from AEs to humans, you know, the RAB1 and YPT1, by also a combination of molecular genetics and cell biology. So this is the minimalistic view of cells, exocytic pathway to plasma membrane andocytic pathway. Okay? And what we, what I'm showing here, based on function, based on mutant phenotypes, we saw that they are in the exocytic pathway. YPT1, a set of papers, we showed that it's in the early transport from ER to Golgi or Golgi2. And then the YPT3, 1 and 3, 2 are late Golgi. Exactly what they regulate, something like that. If you stop them, actually it's very fast. So I'm saying they're essential. How do we work with them? It's a good question. We have a temperature-sensitive conditional mutants. We can use different conditional mutants. The easiest one to understand, stop of trafficking transport between, we can measure ER to Golgi transport. Exactly, say we weigh the transport by just time for the auto-transfer, like that. Yeah, but we can see it's transport or not transport, but also we can see which step. By using cell biology, combination with cell biology. No, step's 1 and 2. When I say step, it's 1 and 2. Yeah, YPT1 is here. We block it, block from ER to Golgi. If we stop YPT3, 1, 3, 2, block from Golgi to plasma membrane. But why, but so, it brings, why you should stop them now? You always have a strategy. What do you mean to stop it directly? Or you've used no mutants, it's never stopped. I'll explain, okay? Why, okay? In a minute. So, because we saw it, we saw that YPT1 is an entry, entret, so this is my French, also T from the Golgi, we call them the Golgi gatekeepers, okay? Okay, in phase two, and I'm getting to your question, don't worry. So we knew that there are molecular switches. We knew that somehow they regulate vesticular trafficking, but we didn't know what's in between, okay? So the first question was, how are they regulated? What's the upstream regulation of the rubs? Who turns them on and off? So these are the people who turn off the switches, like Georgiana here, who turn on the switch. And who are they? So they are called GIFs or GIFs, so exchange of nucleotide guanine, nucleotide exchange factors to turn them on, and gaps for a GTPs activating factor to turn them off. So just to put it in perspective, I put here, this is one of the GIFs in cells, and by the way, they're very different between proteins, but it's for just YPT1, you need a core trap, which is a complex of four different proteins, five subunits, but two are identical, and this is the little YPT1 under them, that's the size. It's very small, it can interact with the GIF, it can interact with the factors, but not much more. That's why I want to argue that they are really regulators as opposed to doing something else in addition. So this is to remind you about Monday about protein complexes, and of course they play a big function, a big role in what YPT rubs do. So in addition to this after regulation by GIFs, they, as Bruno also suggested, these YPTs, the way that they are attached to membranes, they are, is by having a lepy tail, okay? So they have a lepy tail. So in the cycle between the cytoplasm and the membrane, okay? So to be in the cytoplasm, because it's a lepy tail, they have to be buried in a friend's, so there is a place where this lepy tail is inserted, and this is why they can be in the cytoplasm. It's called GDI, and then when they get on the membrane, they insert their lepy tail here, and then they can be seen by the GIF. So there are actually two for now, we are thinking of as two upstream inputs to activator rub. One is to do the membrane attachment, and the second is to turn them on with the GIF, with the activator, okay? And once they are in their GTP bound form on the membrane, this is when they are on, okay? What does it mean to be on? Oh, and the way that we think about it right now is that the gap, which turns from GTP to GTP is just required for them to be able to recycle back to the cytoplasm, which is also important, so they can function again. So we knew about the upstream regulators, regulation of YPT-1 and YPT-3-1 and 3-2, but now what happens downstream? So what happened downstream is that when they are on, they interact with these proteins, doesn't push, so I lost, oh, here, sorry. So they interact with these effectors, this means that they are on. Okay, so who are these effectors? These are the people who really do the work, unlike those activators which only turn them on and off, okay? So these are the people who really do the work. Who are they? They are all people who you already know. So I showed you this slide before, but now I just wanna say for every step, you'll see a YPT-Rab, and this is summary of work in many labs, YPT-Rab in every step, and its effector will be in red, okay? So remember, oh, and the other thing that I wanna say, a single rab can interact with multiple effectors, okay? So the first step in the formation, remember, here is the YPT-Rab, and it's one of its effector which interacts with the cargo receptor. Here, in vesicle motility, we have a motor that can be either, and Bruno already talked about myosinokinicin, depending on which cytoskeletal route they wanna go on. They can be membrane remodeling, and here are, again, a rab and its effector in vesicle docking. These are what the rabs are really famous for, and many people think of them just as sedering factors, but this is just one of their kind of effectors. And then finally, some, here the YPT and rab and its effector regulating also snare complex formation, so they also regulate vesicle fusion. So basically, all the machinery components that are required for moving a vesicle from one place to another are recruited by these rabs. Does this answer a question? No, my question is why you integrate to talk? Why you just have some protein to transport them? Well, why do you stop at normally? Okay, so let's continue to talk, okay? It's a conversation. Why do you say it? Why do you do it? I'll explain, it's coming, okay? So here we are with our peris and the vesicle and our traffic lights, and you would want, and this is partly the answer, that these traffic lights will talk with each other or will do some things so that to make the traffic go more smoothly, okay? So do YPT rabs coordinate trafficking at what levels? So now we are back to east again because there are only very few of them. We can cover the whole exocytic pathway with three rabs while in mammalian states you'll have to deal with 35. And if you think about all their interactors, the nets, the interaction nets are much smaller. So I think that this is again going back to east to try and understand this. So when I talk about regulation or coordination by YPT rabs, I'm going to talk about, first of all, coordination of multiple vesicular transports, sub steps. I told you that there are many sub steps. So if you just give the sale only the coat, but you don't, the vesicle, but you don't make sure that it also has the motor and the tethering factor, the traffic stops immediately, okay? So we have mutants that we can stop traffic. We cannot even measure it, less than one minute. It's done, stop, okay? The second one, which is a little higher regulation, is to integrate, there should be, there is a need to integrate different transport steps in the same pathway so that there will be one whole pathway smoothly going through Paris. And then also we found that they coordinate between different cellular processes and pathways, okay? So I'll try to give an example for each one of these. So we start with regulation in the secretory pathway, exocytic pathway, and I'll give you these two examples. One, coordination of sub steps, and I'll start with it, and then integration of whole pathways. So here is this example. So here is again, a vesicle forming from the donor compartment with all its friends. And if we look at formation, motility, docking and fusion, and if we look at Golgi and plasma membrane, we knew all the machinery components. We knew that YPT3132 is involved in the beginning. We knew that myosin works in motility, myosin five in this case. We knew that the tethering factor is called an exocyst. This is from work by Peter Novick's lab. And actually we knew also that there is a Jeff and this is another example of two YPTs that are needed for one transport step. The same way that you asked Bruno before, wrap six and maybe wrap eight, this is YPT3132 and sec four. This is important for just the beginning to bring sec four and then sec four takes it from there. And we also use the SNERS, here's an example, sec nine is a tether that is involved with the N. But we didn't know if there is any coordination between the sub steps, okay? So I'm gonna tell you that YPT3132 are required for vesicle formation. We showed this and then this is by using mutants, a electron microscopy. So then we see which step is, they stop it because mutants accumulate material from the step before the step in which they are blocked, okay? And then we showed by different, so whenever I say something, we showed it used by interaction, exhaustive interaction, first direct interaction and then to show, yeah, they interact in the cells, okay? And then to see what is the role of the interaction. So in this case, I'm just gonna tell you one little story. We showed that they interact, YPT3132 interacts with a myosin and we made an interaction because I think this is crucial, a interaction specific myomutant. Myomutant, because myosin five can do many things. But we made a mutant that just specifically cannot interact with YPT3132. It can interact and do jobs everywhere else, okay? And then- It's a mutation of a particular mutation of the gene, yeah? Yes, in the gene, but then it's also in the protein. It's produced by different. Yes, yes. So now we did the genetics, we replaced the myosin, we put it in cells and now we follow what happens by life cell microscopy and here what we do, we look at actin to just see. So this is budding yeast, just to remind you. Meaning that all the secretion is polarized, it's going through the bud. Actin is polarized to the bud. The vesicles we view here, just a marker for us, sec four in green and when you see them together, you get the yellow. So in wild type cells, you see them together, meaning this is a polarized transport from the mother cell very efficiently to the bud.  It's only defective in this, it's there. And then you can see that all the vesicles are here and we showed it by other, also by electron microscopy. But then, and the actin is in the right place, but the vesicles don't go to the bud. So there is no polarized secretion in this mutant. So what it means is that we already knew that YPT 3132 are important for vesicle formation for, because of interacting with other effectors, but now we show that it's also required, not just the formation, but to put on the right myosin to take them to the right place, okay? How do you build a bud without porous secretion? So the beginning of the bud probably, it just can be random, no? You don't? Okay, we can talk. Mutant does not make any bud. Well, this is a myotomeutant, it does make a bud. No, no, no, but if you inactivate the motor function. Sure, sure, sure, sure, yes. Yeah. So maybe there are other things that the myotomeutant does. No, there's another pathway. Is the excess still porous properly, because maybe. No, because the rub is rub, sec 4 is not there. Okay, we'll give it to the later. Thanks. So we showed that YPT 3132 actually couple vesicle formation and motility. Work published by Peter Novick also shows that YPT 31 or 32 bring also sec 2, which is the J for the next rub that is gonna be in this system. So actually it sets up the vesicle to a few sub steps. And I think maybe this now can answer a question that if you can start, the cargo is there, cargo coats are there, the coats are there, but the vesicle just will not, maybe it's not even gonna form this. Yeah, it will stop probably from recruiting anything. The cargo receptor included. I have a question, why? Of course it may happen. Why the cell, okay, so that's a different question. That's philosophical. You have to stop some type of transportation that are proteins. Okay, this is because in Paris, you know, there are intersection two dimensional. Oh God, can you imagine how Paris will look like if all these cars will be there without the traffic lights? It's not my subject because on two dimension it's poorly organized. Because the street cross, here they don't cross. Why you have to stop it? That's the question. And I don't know. It's absolutely wrong. Absolutely nothing to do with the cells. Two-dimensionality here, 3D, nothing in common. Why? What's the logic? Why do we have a red light? Can we? What is the function of a red light? But maybe the answer is that actually you stop only when you have a mutant. So you are in a situation. Exactly, but why normally you have a regulation and then you have a regulation? So the regulation is perhaps not to stop or put it on, it's just to make sure that the right vesicle attached to the right motor to go to the right destination. What is the right destination? In this case it's the plasma membrane. It's only one. A to B is only one destination. You don't choose. No, but it could go back. It could go back. It could go to endosomes. It could go anywhere. It could just stay in place like... Wait, wait, did you always go from A to B? Why do you always go from A to B? But there's many membranes. There's colg, er... Okay, so you choose which one. So you wanna choose plasma membrane. Which one goes to where? Yeah. But you never stop it. So there is no red light. Only there is direction. No, no. So the problem is, let's suppose I'm coming out of the plasmic reticulum and make a vesicle. So that vesicle, where would I like to take it? I would like to take it, for biological reasons, to the Golgi apparatus, right? But that vesicle could have actually gone directly to the plasma membrane. And that's a mistake. So they're not red light, just directions. Yeah. Okay, so there is no red light. They're not really red light. That's one level of revelation. Another level of revelation is the content. Which is not being discussed. Not all the guys, not all the carriers have always the same stuff. You also sort out, you segregate, right? And we're not discussing that level of complexity. Yeah, we're still normal. My point was there is no red light. There's this mutants make something very artificial. It never normally happens. So the problem, so, okay. So the other problem is, how do we biologists can study this, right? So historically, the way it has been done is to put perturbations, right? And one type of perturbation is like, shut down the pathway. You can shut it down super fast. You can shut it down slow. These are actually relatively slow. They are not super fast. Even though it's a temperature-sensitive mutant. In general, correct me on this. I don't think it's an instantaneous block. It takes a while, right? It takes less than a minute. I don't know if... No, I just said it depends on the mutant. But in, so, this is another level of complication. Oh, thank you. I understand, but I'm saying analogy. With the red light, it's completely wrong. Okay, fine. I agree. Okay, I take it back. No red lights. Because, no, the rate is important. Sometimes it goes fast. Sometimes it goes slow. How do you control the rate? Why do you make it slow? If you have some amount, it's... No, because the timing, it's responsive. Different carbons actually go different speeds.  For some time. How does it? Yes. Why would you wait? What does the cell do it? And that's... Okay, can I just try to answer this question? This is a question of evolution, and it's a little philosophical, so can we leave it to the end and please forget about the red lights, okay? Just continue to listen. Okay. If you want, you don't have to. But there is a... There is an answer. It's simply, for example, in the cell cycle, you want to have different rates of trafficking, depending on where you are and the rest of the... So really, you have excess of some production, so you don't have... If you have excess, excess, it's in some kind of... And you keep it. You don't transport it, and you wait for what? That can happen too. For example, if you don't need a certain receptor or the plasma membrane, it might still be synthesized, but it does not go to the plasma membrane until you need it at the plasma membrane. Yes. Okay, okay. This is the answer. At least we're waiting for it. In that sense, it is a red. Okay, at least we're waiting for it. I'll take it, but it's really not, because regulated secretion at the last step is different kind of regulation, but I'll take it for now. Yes. At least it's another function of the red sort of quality controller.  Make sure that everything's correct. So this is exactly what is shown here. It's like it has the motor and it has the next protein that will take it to the right place. Okay? So maybe the red lights are not good and I'm sorry that I confused you. Okay, so what about, so I just wanted to show you and give you a flavor of this one type of regulation. The other one is to look at the whole pathway. And this, we go back to the two GTPases, YPT1, YPT31 and 32. And the question here is, oh, sorry, first I wanted to say that we showed it by function, okay? I told you we showed it by mutants. More recently, we had to go back and show it by clear localization because there was in the field, there was confusion, whereas this protein and which compartment, it's also very difficult to decide which compartment, which are the compartmental markers in the Golgi. So what we did is to using a life-sale microscopy with different colors. And we first wanted, we had at least two markers for the early Golgi. We had two markers for the late Golgi that they co-localized with each other. And then we made the YPT1 or YPT31 in green and we looked at the co-localization. We confirmed everything that we saw by life-sale also by immunofluorescence microscopy. So the answer was that now when we did it very thoroughly that they actually localized to opposite sides of the Golgi. YPT1 is starting early, very, very, very low level at late in the late compartments. YPT31 is the opposite. So, and they both, about 25% of them, and it will just become a little interesting. They actually co-localize with each other and they co-localize in a compartment that is a regular, is marked by 6-7. And now just treat them. I know that Kathy Jackson likes the 6-7. It's a Rf, a Jeff, it's another GPA, but for now they are only serving and some people like Cup 1 and CHC1, but for now they are only serving us as markers, okay? So we also did some three-color IF and with all the combinations and we could show that, again, this is the point that I was trying to make earlier, YPT31 to localize about 25% of them, but 95% of this localization happens only on the 6-7 compartment, okay? So now if we make a Golgi map with the YPTs, we have Cup 1 early, we have 6-7 and CHC1 late, but we also saw some co-localization of early and late Golgi markers and we called it a transitional compartment. I'm not calling it cis-medial trans because we didn't show that they really correlate with the enzymatic activities for cis-medial trans, but that's why we called them early, transitional and late, transitional tells you, it's fast, it just comes and goes. So the transitional compartment is also, so YPT1 is on the early and transitional, 31 is in transitional and late, okay? So they co-localize it, the transitional compartment. So now I want to just branch off for a minute to Golgi's cisternal progression or cisternal maturation. We talked about it, this is what people think, how transport occurs through the Golgi. So the cargo stays in each compartment and what happened is the compartment matures and this is within the same compartment, okay? So in 2006, two groups showed in yeast. I think they provided a really good evidence for that you can see cisternal progression. The way that they did it is by looking at shifting from cup one, which is the early Golgi to six seven, which for us it's a transitional late, okay? But until then, until we came along, there was no genetic evidence that this is actually regulated. And I want to go back to what Alberto Luini said yesterday, you do not see a regulation until you just do something to it, yes? I mean, because is there a regulation or not or does it just happen, okay? So we wanted to ask this question, do YPTs, do the YPTs which are in the Golgi regulate the cisternal maturation? How do we do it? We have mutations that can affect the YPT either to be super active or to be not active, okay? So now we look to see what happens to the dynamics of the cisternal maturation that they showed, the two other groups showed, but now when we look at with these YPT mutations and we look both by collocalization, doing life cell and IF in immunofluorescence and looking at dynamics, okay? So, but we also added one more thing. We actually had now a third marker. So we looked at cup one to six seven, which is what they looked at. And we also looked at what happened with six seven to CHC one, okay? So we determined the effect of what, when we, I'll show you hyperactivation, but we also show inactivation of these YPTs on this both Golgi cisternal, Golgi proteins collocalization, snapshots, but also dynamics. And I'll show you just the dynamics. So when we look at cup one to six seven, so we watch it by looking at the dynamics of these. And I'm not gonna ask you to look at this, but just to understand what we were doing. And then we have the chemographs of tracings of these cup one to six seven. And this is in wild type cells. And we have numbers. We are looking at what happens to cup one appearance versus six seven. So cup one always appears about 15 to 20 seconds before six seven, okay? In Golgi. In the Golgi, in wild type cells. But now when we hyperactivate the YPT one, or IPT 31, we wanted to see what happens to them. So what we see, say it again. There is a mutation that we can make it super active. It's just always bound to GTP, okay? Or it looks like it has the structure that it's always bound to GTP, okay? So what we see here is that when we overactivate YPT one, but not YPT 31, it goes faster. So this step goes faster, okay? With 31, 32, it's similar to the wild type, okay? So this is our regulation of whatever was in the field, cup one to six seven. But then we also looked at what happens to six seven to CHC one. We did the same experiment. We look at the dynamics. And then we do the chemographs and the quantification. And now what happens is that YPT one does not affect it, but YPT 31 makes it go faster from 10, 12 seconds to four seconds. The effect is two or three-fold, okay? Which is significant, okay? So YPT one activation now makes the six seven go to CHC one faster. So together we can say, we can see it here. YPT one makes this step go farther, faster. YPT 31 makes this step go farther if we make the other mutant, the activating mutant, it has the effect that we expect. So in conclusion to this part of our experiment, we show that first of all, this is the first genetic evidence for systemal progression. Second, we actually divided it to two different steps and YPT one regulates the first step and YPT 31 regulates the second step. One question, sorry. Yes. So you're showing some percentages and some fraction of things going faster and slower, but what happened to the other percentage of events? In your previous slide, there was something that said 20% or 50%. No, no, no, sorry, sorry. I didn't explain it, sorry. 20% reaching the tip to the top and 50%. We are looking at the initial rate. Yeah, and what happened to the other events? Then they are together, sort of, no? What? We are looking, we are looking, we are only, it's not event. We are measuring 20% increase. I'll put it on the slide next time. Okay, let me rephrase this. Every time you see this, you have exactly the same behavior or every tracing is a little bit different. No, here is, it takes 12 seconds plus minus two seconds. That's the average. Yes. Plus minus the standard deviation. But there are events that are happening either faster or slower, right? Yes. So those, what's happening? I mean, they're not. So I don't know, I mean, we can talk about quantification and if this is enough to say that if it's 12 plus minus two or four plus minus one. Percentage of, I said percentage, sorry. It's, it's increase of the red light, the red marker to aim. In what scale? Percentage of what? On, a hundred percent is the maximum. Of what? Percentage of what? Of intensity of the light. How much of the what? It's just intensity of the light. So it was the percentage of events, right? Light being. Red or green? No, in which units? Is it the green or what? 20% meaning? It's fifth of the, of the maximum. 20? Okay, it's, it's bad. I, I, I understand. I should have written what the, what the percentages are. Aim. No, the, the, the answer is, as I understand, 100% of intensity measured whatever in the amount of dye. And in, when, and then 20% use, you mark 20% of this intensity and you say, this 20% level is reached in 12 seconds. Then you mark 50% level or this whatever. It's just two measurements of the same common ground. The same level of this intensity is reached in 10 seconds. This is what, what is the idea. Yes. Okay, I, thank you. I'll, I'll. When you get 20% and when you get 50%. This is the. And you measure intensity in which number? This I, I don't know. I don't know. So what? Which number you measure intensity? Intensity means number of molecules. Yeah, yeah. So your, your top signal is that 10 molecules, 50 molecules. I don't know. You don't know. And then each, each one. No, no, I think that intensity is measured in.  How do you feel? How do you feel? I think all the molecules are, are a, whatever each molecule maybe does it em, emits the fluorescence in a different way. But the same molecule is the same. You have one Golgi and God, let's say 10 fluorescent molecules. The next Golgi have also 10 or have 20. No, they all, so the answer to your question, they all had about the same intensity top here. About. No, there was no, no. So this is fluorescent marker, marker. Yes. This is what I, Misha, to your answer to your question, this is fluorescent marker and the intensity of the signal is the intensity of the measured fluorescent marker. There will be no lunch today. Because I. Propagation of the intensity, how often? Yes, yes. Which one? Number. This is what I guess. This is what I understand. Another, you're also going to get it. If you do it wrong, you completely need to stop. Why? This is another question. Let us continue. If you change the scale, you'll get a really different number. If you change the scale, how much? You'll go 20, have to, you have to say something. It depends on the scale. This scale, this scale, right? If nonlinear scale, you'll get a really different scale. The scale is linear. The scale is linear. Okay, why don't we continue to talk afterwards? Thank you. So the question that we are asking now, this is for Alberto, is so we know that the YPTs are important for this system of maturation and we are trying now to look at the Jeffs for YPT one, Trap One, Jeff for YPT 31, 32 to go back in the, to see if they also, first of all, to clarify that they really work in these steps and also to see what they do to go GCC steriline maturation. So the last thing that I wanted to tell you about, and I'll do it, I'll try to do it fast, not fast by talking fast, by fast by jumping over slides. So I wanna talk about autophagy. So if you look at my simple model of the cell, I wanted to add to it two recycling groups. So there is one recycling group that everybody knows which is plasma membrane recycling and we talked about recycling endosomes, et cetera. But there is another one which is autophagy that brings stuff from somewhere from all these compartments to the lysosome and lysosomes, as we know, they actually split back all the block, building blocks and then they can be built again to get back into the ER, for example. So the question is, is there coordination between trafficking and recycling? And I'm gonna jump over these, oops. I just say, how can there be one rub? And this is a question in the field that a field can take a vesicle to two different places. And the answer is, I told you that each rub can recruit different effectors, so each rub can recruit a, sorry. For example, if it will recruit effectors one, two, three, this vesicle will go to the Golgi. If it will recruit for other effectors, it will go to the lysosome. So, okay, we'll jump over this. Okay, so I wanna talk about YPT-1 because we also show that YPT-3132 are required for this loop, not just going through the Golgi, but also for this loop. Here is YPT-1, which we showed required for going from ER to the Golgi. It turns out that it's also required for autophagy. So the way that we show it, we showed it, is by using a mutant to show a role and also identifying a recycling-specific effector, an effector that doesn't have nothing to do with its role in secretion, but it is required for autophagy. So first, let me just remind you what is autophagy. It's the pathway that usually people study it under stress. And here is an example of how we look at this pathway by GFP-ATG-8, which is LC-3 in mammalian cells. And what happens is that in this pathway, an autophagosome is formed. And an autophagosome, this is to remind me to say that it's a double membrane organelle, okay? And it takes cargo, which, so the autophagosome forms around a cytoplasmic things. They can be either proteins, protein aggregates, or even whole compartments. And then they take them to the lysosome for recycling. There is also autophagy under normal conditions, growth conditions. And we have in yeast, for example, this was one available cargo that we were following. And both under stress or a normal autophagy, the process starts by formation of PAS, which is the pre-autophagosomal pathway. And PATH is a combination, a complex of about 30 proteins, which are called ATGs, and membrane, okay? And SOMI got the Nobel Prize just for showing this first step, how this is all starting. But none of these ATGs are required for the rest of the pathway. So what is the rest of the pathway? What's beyond the ATG complex? It's a membrane process. So it must have all these other machinery components that we all know. So just to tell you what is the YPT-1 connection to autophagy, how did we even get to it? We had a mutant. It's a recycling process. It is a recycling. Yes. It's stomach. It's stomach, I would say. It's iri, autoiri. Organic. Auto-phagy, okay? So that's what I was trying to say. It can happen under stress or even under normal condition. So we had a mutant in YPT-1. This is actually a very early mutant that had no effect, not major effect on secretion, but definitely it didn't allow cells to grow under stress. And stress in yeast is you just starve them, in this case for starvation, for nitrogen. Then another group came up with a subunit of TROP, also has a role specifically in this process. And then we did a yeast to hybrid screen and to our surprise, maybe we shouldn't be, have been so surprised, we got ATG-11, one of the ATGs that Osumic discovered in his screen for ATG mutants. And we got it by yeast to hybrid. And we, so I'm not gonna talk much about it. I'll just tell you that we showed that while TROP-1 is required for the role. So now I'm talking about the activators. The activator of TROP-1 takes with the YPT-1, takes cargo to the Golgi from the ER to the Golgi to the plasma membrane, while two other TROPs, TROP-3 and TROP-4, which have similar core, but different specific subunits, take it to autophagy, okay? Same YPT-1. So, and at least one Jeff. So YPT-1 is required for cell viability because of its role in secretion. It's required for stress, for autophagy under stress. No YPT-1, no stress. These TROPs, one Jeff is enough, sorry, one Jeff is enough so you need to delete both in order to see the full effect, okay? Now what about the effectors? Here again, we have YPT-1 going from the ER, a vesicle goes from the ER to the Golgi, we know what is the effector. And two, two, the- But again, why under stress, for a problem of autophagy, what is the logical effect? Because it's recycling. If you want to conserve a material under stress, you don't have any more nitrogen. You cannot, the cell cannot make any more amino acids. So it needs to eat its own proteins to make these proteins that are really essential for stress, not just extra things that are not essential now. Make sense? Okay. So what we showed, and the way that we think about it is, we're thinking about YPT-GTPAs modules. So the module has a Jeff, a specific Jeff for the specific step, a YPT-Rab, a DGTPAs, and then at least one effector, okay? So in this case, we have a module of trap three, specific subunities TRS-85, YPT-1, and at least one specific Jeff, ATG-11. So the way that we showed it is by showing interactions, collocalization, and function. And I'm gonna jump over the collocalization, and maybe I'll just show you fast the function. So how do we study function in this case? We are lucky because the- What kind of stress you're probably in use? What kind of stress? We start them for nitrogen. We start them, okay. In our cells, mammalian cells, you have to start for- Amino acids. Amino acids, thank you. So we have specific mutants which are only defective in autophagy, not in growth, okay? TRS-85 doesn't have anything to do with secretion, so we can delete it and see just the effect on this Jeff on autophagy. Same YPT-1-1, the mutant that we later showed, that it disrupts this mutation. It's a one amino acid change that disrupts the interaction of YPT-1 with ATG-11. It does not affect other functions of YPT-1. And we have, of course, ATG-11, which is by definition was isolated as specific for autophagy. So we use all these mutants to ask, what is the effect? So again, I don't have time to, I think, talk about results, but I'm just gonna tell you that in YPT-1 or TRS-85 or ATG-11, there is no pass. So pass can be seen by collocalization of two ATGs or more, if you have more. All the ATGs go to pass because I told you it's a protein complex, but in YPT-1-1, there is no pass. There is no collocalization. They don't come together, okay? So, okay. So it's true also, as I said, for the whole module. So the whole module, if we look at function, it's required for assembly of pass, okay? It's the first step of autophagy. And until now, there was no way, there was no shown regulation on it. Okay, so here we have what I call one, this is math for you, one to two to two. One YPT-Rab, two different modules, two processes. So YPT-1 with the first module is essential for cell viability, for secretion, with trap one and effector, one effector US-1. And we have another module and another process, where the same YPT with a different Jeff, with a different effector now goes to a different process. So now what we have to, when we think about, I told you in the beginning that there are two upstream inputs to activate a YPT. One is member attachment, the other one is exchange, the activation by Jeff, but I would like to add that there are actually three inputs. If you think about the possibilities, you should have also the system also has to have a way to recruit the right effector to the right module. So the YPT in one module can interact, cannot just interact freely with swimming effectors. It has to work in a module. It's a big question, how does it happen? Okay. I think that I should stop. I'll just say it in two minutes, I'm not even gonna show you the results. Thank you. No, no favor, favor is in my field. I need to stop, I'll stop. So I just wanted to say, so I wanted to tell you that we discovered a new autophagy pathway during normal growth, and it's actually quality control of ER phagee, quality control of the ER by autophagy of the ER, and the plasmic reticulum. So it's a selective autophagy pathway, and the cargo for this pathway are membrane proteins. Now, when we first discovered it, when we overexpressed, made too much of a protein, but when we found it, once we found it, we went back and looked at other ER membranes, residents, and it turns out that they, not all of them, some of them, and I'll show you who, at least two groups, some go to this pathway and some don't. Okay, so we pass through this. This is all the evidence, both. So we actually showed the stop, the block by three ways. One was by lifestyle microscopy, then we also looked by electron microscopy to see what is accumulating, and it's ER, and ER, resident proteins are there, and we also showed it that it's really ER by looking at UPR. It's an acid that shows that the ER is under stress. There is an overexpression of a protein, one protein, and it actually makes the ER stressed. So while other mutants that accumulate some structures with some of the cargo that we are looking at don't do that, okay? So this is just two more slides. So it's a new quality control of the ER. Without overexpression of proteins, we have two residents of ER, 61 is a translocone, agent G1, and these are components of getting the vesicle to the Golgi, they do not go to this pathway, to ER phagee, but these do, and about 20 to 50% of these proteins, depending on the protein, go there all the time. We just don't see it if we don't block it, okay? And then if we overexpressed a single protein, the cells are happy, there is no stress on the cells, there is no induction of general autophagy, but we just have, the ER is getting too blocked, then we get 95% of these proteins and these go now to the ER phagee, okay? So here are the other ER phagee, what happens when proteins get from the ER? So if they are native, they'll go to secretion, secretion to the Golgi to the plasma membrane. If they are misfolded heavily, they'll go through IRAD to the proteosome. There is also a micro ER phagee process, which micro ER phagee means that they do not use the normal, the ATGs, so there are ways to get to the lysosome without it, and now we added this new process which takes extra membrane proteins by this autophagy process to the lysosome and we know who participates and who regulates and the questions that you're asking now in the lab, which are more the basic questions is what I told you about the input, the three input, how does this work, if there is coordination, and just to connect to human disease, I told you the TRUB1 is the mammalian, the human homolog of YPT1, and it's actually involved both in cancer and all the generative disease. This is my connection to Friday, and thanks to everybody who helped me in my lab in beyond and stop. Sorry that I took over, we don't have to have questions. We can go have lunch and we can talk in the evening, unless you want questions. I just, I'm sorry that I... Thank you.


Oh, yo, you better chill Amanda. What do you want me to write um a five-letter word Amanda oh oh my god, that scared me What's up everyone welcome back to realistic gaming as you guys can see juniors not here today because he went to the dentist Supposedly actually saw dashing which is actually one of my favorite youtubers ever He played this game called Amanda that venture and of course it's supposed to be a rip-off of door to explore it My grandma is dying and we need to go get some magic potatoes to save her Okay, it's supposed to be scary So I wanted to check it out and see what Dora has in store for us or Amanda So let's go. Let's see how it goes by the way before we start if you can please press like share Comment and everything else. We really appreciate it And we got some links in the description below where you can find this on Instagram tick tock and everywhere else. All right, so let's get this going All right, so let's see what this game has in store for us Amanda that venture Kind of looks like a there's some VHS tapes right there. If you young ins don't know what that is That's how we used to watch movies All right, so what do I do here? Do I click on the episode one? All right? Let's put the VHS. This is how a VHS works everyone Congratulations, you have learned something today Amanda that venture Actually do like apples. Yes, I'm allergic to apple You should never be afraid to try something new but we don't even know where the store is It's right there Right behind you woman. Oh Oh, I gotta click on it. All right. Let's see we're gonna go right here. Do you know where the story? This one right there is the store Let's go Oh, I actually do gotta go to the store today There are apples, can you see apples? Apple that's not saying that that's spelling apples first off, but Good job. Now we can make apple pie. All right, let's make that apple pie baby girl. Let's go. Oh wait. What's going on? My VHS messed up Damn it. What happened? It's just gonna come out. Where'd it go? All right, what do we got to do now? Do you play a episode two or what? Now let's let's turn the TV off. I can do that. All right episode two. Let's see what's cracking with episode two Even though we didn't finish episode one, but whatever You okay, we don't have much time. Whatever you do Yeah Why are you on by the trash can The butcher oh right there We're happy to Look how he looks bro. He's looking at he's looking at everyone at the same time Is that me are those ties Well, is he what do we need I need help Oh Hey, yo, you saw Willie. He'll say no No, I don't want to tell him me. I'm gonna tell him something else. I'm gonna tell him. I'm gonna tell him a Lime Yo, she's getting mad. Yo, did you see that? All right? No, I'm not I don't like your attitude Amanda I'm gonna go with I need I need a ball. Oh, I didn't put me. I Didn't put me. I put a ball cheaters. Oh Yo, it's probably lamb. That's why that's why Willie is looking at us like oh, no, it's probably she Oh Stop cutting it in front of him like that man. Look at him Look at Amanda. Yo, she a little freak. Oh, she's scary. That's That was unsettling. It wasn't scary. It was unsettling. All right, let's see. Let's see was cracking with episode three It's dark out. Yeah, let's go home You should go inside. I don't want we had to click on the swings. I'm gonna swing Oh No, Amanda, I don't want you to go home because obviously there's something going on in your home Come on. No, I don't want to point to the house. I'm point somewhere else because I don't like your attitude Amanda Go, can I click anywhere else? She's gonna get what she wants. I don't want to give her what she wants Fine Not gonna do it. No, I'm gonna knock on the window You don't want to go inside Amanda. Just knock through the window because it's dark in there Why do you want to go in there by yourself? The window disappeared. What the heck? How are they gonna look outside now? All right, I guess I'll knock just because you told me to.  I can't say I'm scared of them.  I mean everything look everything look like Is there like any secrets here? Let's see.  Well, I guess that was it for this game.  I did get creeped out, but it wasn't like scary. You know, I wasn't like You know But that's it for today I just wanted to check the game out real quick and and yeah, it was it was interesting I'm not gonna lie But I think her and Doris should have like a like a little team up where they make a scary game together That'd be better But I said for today Hopefully you guys enjoyed that make sure you click like share Comment and all that and make sure you click the links in the description Well, you'll be able to find my links to my Instagram to my tiktok and my YouTube and you'll be able to find realistic gaming stuff Also, alright, we'll see you guys later


Hello, everyone. My name is Evelyn. I'm a staff member here at the Long Beach Public Library. I'm very excited to be crafting with you today. Before I get started, I did want to mention if you haven't signed up already for our summer reading program, make sure to do so. It's going to be filled with lots of fun activities for your summer. And then you'll be able to sign up at LongBeach.BeanStack.org. And if you haven't signed up already, join us. If you do need the code, it's going to be Nebula, where you'll be inputting that into Beanstack to make sure you get points and win prizes along the way. Okay, so let's get started. Today's craft, we're going to be making a mobile solar system. It's gonna like sell cool like this. It'll be a great addition for your room decor. And then also it could be a great gift for a family or loved one. Let's get also started talking about the supplies you're going to need. We're going to need a stick and that's mainly going to hold your solar system up. I bought this one at Home Depot and it was 50 cents. You can also go to your neighborhood, walk around. I found these branches from trees and I also went to my local park and I found this really cool one, which I really like. And then there's also smaller ones. You can make a smaller solar system. It's totally up to you. Note, all of this is completely customizable. If you want to use stuff you have at home, feel free to do so. Anything you have at home will work. This one, yours might look different from mine. And that's totally okay. So I'm going to be using, let's see, I think I'm going to be using this medium one for mine. And then we're also going to need glue. I use a hot glue gun. It's very much easier to do with the hot glue gun because it's just the yarn gets on there quicker. But if you don't have that, you can use a regular glue stick. Just know that it's going to take you a little longer. You're just going to need to hold it on there for it to dry off and then be able to hang. But that's totally okay. And then we're also going to need string. I use some leftover yarn I had at home. We're going to need nine for the planet. So we have eight planets and then our sun. So we're going to need nine strings and then one long one that's going to hang the entire thing. So regular string works. If you have leftover ribbon at home, even shoelaces, if you have about nine, that would totally work. So remember, you can customize this, check with an adult.  And then also we're going to need paper. I use paper, card stock paper, because it's just less flimsier than regular paper. If you have regular paper, you can totally get a cardboard. Just cut it up. And then that way it's not as flimsy than the card stock paper. So you can do that. And then I use some jars. And this is mainly to trace and make my circles. You can freehand that, but I'm not really great at making circles. So I use some jars, different sizes. And I even use this tiny one to make tiny planets. I did want to mention we are going to need one large circle. That's going to be our sun. We're going to need two medium planets circles. So that's Saturn and Jupiter. And then we're going to need four smaller ones, which is Venus, Earth, Uranus and Neptune. And then our two smallest planets. I'm calling these the teeny tiny ones, Mars and Mercury, because they are the smallest planets. And then for Saturn, it does have a ring around the planet.  And it'll make the ring for when we do that part. And then lastly, for our supplies, black foam paper. You can use regular card stock paper. Color that black and cut up stars. I kind of like the black foam because it kind of has a cool, soft effect. But whatever you want to do, I have all my stars right here ready. We're going to get started. This is the stick I'm going to be using. I have all of my string already cut up. As far as length, you can kind of just do one sample and see how long you want it. They don't have to all match up once you do them. You do want them kind of long. And then you can go down and cut them. That's kind of what I did towards the end. So I'm just going to start wrapping these up to just tie them. And we're just going to tie them. You can do about two knots. That's about perfect. I hung up my string. We should have one, two, three, four, five, six, seven, eight, nine. Perfect. So this is ready. I really like the little curve effect it has going on. Okay, next we're going to start painting our planets. So let's start first one. It's going to be our far left. That's going to be the sun. And let me pull out the sun. So some facts about the sun. The sun is made mostly of hydrogen and helium.  That's insane. And it also takes about eight minutes for the light to reach earth. When drawing, you can use your also supplies for crafting, which is going to be your crayons, markers, whatever you have at home. I used crayons. I don't know, I just found it easier with crayons. So I used a little yellow and orange to kind of give that hint of the natural sun. This is what mine looks like. Yours does not have to look exactly like mine. Be creative. Challenge yourself to, you know, create the sun that you think would be up in the sky. So I created this one. And then later, we're also going to add the names of the planets. And actually, I'll add them as I go. I'll just use, I'm going to be using my colors. So we have the sun. So that'll be the first one hanging. And this is when you also decide what way do you want it to go? I'm going to do it this way. And then also notes, all the planets, they're kind of wavering. They don't have to be in line exactly. Feel free to move those around however you'd like. So I'm going to put this one kind of towards the middle bottom. Next, we're going to add mercury. Here's mercury. And then some facts about mercury. Mercury is the closest planet to the sun. So that's the second planet. And then also mercury has no moons or rings. When coloring it, I did different shades of gray and kind of like striped it. And this is what we got. So we have Venus. And then let's learn some facts about Venus. Venus is the second planet from the sun and the third brightest object in the earth sky. Venus is the closest planet to earth. And then for Venus, it's different shades of orange with some grays and tans in between. We're going to be at a familiar with this one. It's earth. And let's learn some facts about earth. Earth is the largest of the terrestrial planets. It is the only planet not named after a mythological being. And 70% of earth is covered by water. And then we're going to add, you know, 70% blue, which is water, and then the rest is green. Earth is also called the red planet. Mars has huge dust storms and polar ice caps. Its moons are called phobos and demos. So because all of those dust storms and everything going on on Mars, we're going to add different shades of red. So here we go. We have lines also. See seven moons. It's the fourth brightest object in our solar system. And its great spot is an enormous storm over 300 years old. So I kind of drew kind of like the tannin spot for that. And then you're going to add light tans, a little bit of orange and grays and black on that one. It's my favorite planet, especially since we have our cool ring. So we have those seas that I told you about earlier. We're going to color those. The Saturn itself, you want to do different shades of yellow, some gray. I really like this one. I did up here. It's different shades of gray, lines, and then a really gold ring around. And you're going to glue the seas together and then grab my glue stick. And we're going to glue it on the planet. So I cut my ring here, but I didn't cut it there. I kind of like how it looks not cut. So it's totally up to you. Next we have Uranus. Some facts about Uranus. This was Uranus was discovered in 1781. It is the coldest planet in our solar system. And Uranus has 13 rings. That's very cool. Because it's the coldest planet, I did this one light blue. And then the last planet we're hanging is Neptune. And Neptune has darker shades. And I did darker lines on Neptune. It's the eighth planet from the sun. Neptune has 14 moons and three major rings named Adams, Laverre, and Galet. So cool. Looks pretty cool. Don't forget to hang the string. And we can do that right now, actually. So hanging against the wall. It should, if you turn it over, all the planets will show nicely. But I hope you have fun joining us for today's crop. This is your mobile solar system. Make sure to have fun doing this with family. And yeah, enjoy the rest of your summer. We're going to be crafting a lot in our summer reading program. We hope you join us for those. Thank you.


Hello friends, welcome to ArpitaKarwa.com India's finest online coaching for English literature. Now today we'll understand the story of one of the most famous classic novels, Withering Heights, written by Emily Bront. Now it's a Gothic novel, written in Victorian period precisely in 1847. The plot is set in late 18th and 19th century England. If we talk about the point of view, there is nothing fixed. Different characters are telling the story at different points of time. Apart from this, in this novel you will find romanticism, realism, secrets, wild landscapes and a lot of different interesting elements. And friends, in this novel the hero he is driven by passion and revenge. It adds a new dimension to the concept of suffering. And in this work Emily Bront also creates a fictional place called Eggdon Heath. Now friends, let us discuss the major characters of the novel before we dive into the story. Now first we have Mr. Lockwood. He is the tenant at Thrush Cross Grange. Second is Edgar Linden, who is the original owner of Thrush Cross Grange. And Isabella Linton, she is Edgar's sister. Mr. Earnshaw, original owner of Withering Heights. Hindley, he is Mr. Earnshaw's son. Herton is Hindley's son. Catherine, Mr. Earnshaw's daughter. Heathcliff, he is the current owner of the Thrush Cross Grange and Mr. Earnshaw's adopted son. Then Cathy, Edgar and Catherine's daughter. Linton is Heathcliff and Isabella's son. And Nelly is the housekeeper at Withering Heights. So a lot of complicated names and a lot of, you know, interconnections. So what do you do? You just give it some time and try to understand each person's connection. See in the storyboard, we have also divided it into two parts. The Thrush Cross Grange and Withering Heights for your understanding and who is where and how they are cross connected also. It's better if you photographically try to memorize this storyboard. It'll be always easier. Now once you have, you know, got a grasp of the characters, let's get into the story. So friends, the story starts with a gentleman named Mr. Lockwood. He has come to live at a place called Thrush Cross Grange on rental basis. So basic, you have to understand that after two places, Thrush Cross Grange and Withering Heights, these are the two places about which there'll be a regular mention. Now some people are staying in Thrush Cross Grange, some people are staying in Withering Heights. So this will keep happening. So just get those names clear for the two places first and then who lives where with the flow of the story. Now the name of Mr. Lockwood's landlord is Mr. Heathcliff. The landlord lives nearby in a place called Withering Heights. So his owner, the landlord, he lives in Withering Heights and the place where he rents, that is Thrush Cross Grange and who's that person? Mr. Heathcliff. Now Mr. Lockwood visits Mr. Heathcliff in Withering Heights twice. The first time he goes to meet his landlord, Mr. Heathcliff gives him a cold shoulder and does not nicely talk to him. And the second time Mr. Lockwood visits his landlord, the landlord's dog tried to attack him. So Mr. Lockwood gets scared and what does someone do when they are scared? They run away. So he also tries to run from Withering Heights but exactly then he sees some ghostly apparitions in Withering Heights. Now Mr. Lockwood is scared but he's also very curious. So there's a housekeeper who's working for Mr. Heathcliff. Her name is Nelly and Mr. Lockwood asks Nelly to tell him about the past of the house and Withering Heights. So he wants to inquire about Withering Heights basically. With this the main story of Withering Heights starts. Now listen very carefully because what we are going to discuss is the story which is told by Nelly to Mr. Lockwood. Now she tells him that there used to be two families, Earnshaw family and Linton family. Nelly first describes the Earnshaw family. The family was headed by Mr. Earnshaw, a gentleman. He was the owner of Withering Heights. He had two children, a boy named Hindley and a girl named Catherine. Mr. Earnshaw adopted a third child. His name was Heathcliff. Now the biological son of Mr. Earnshaw that is Hindley was very jealous of Heathcliff. Now you must be thinking why this jealousy because Mr. Earnshaw and Catherine used to love Heathcliff a lot. Understanding the jealousy, Hindley had for Heathcliff Mr. Earnshaw sent Hindley away to study. So after Hindley was gone, Catherine and Heathcliff they were still staying together and getting to know each other and they were getting close to each other. So I hope it's clear we have spoken about one family that is Earnshaw family in which husband wife and there were two children, a boy and a girl and an adopted son. Who is Mr. Heathcliff who is our present owner Thrush cross Grinchka. I hope I'm making sense. Now what happens Mr. Earnshaw passed away. Now after his father's death, Hindley came back and he came back with his wife. So after he came back, he started taking control of his father's property including Withering Heights. Though he came back after a lot of years, his anger and jealousy for Heathcliff was still the same. So since Hindley had powers because his father was dead and he had all the control, what he did was he stopped the education of Heathcliff and started treating him like a servant. After a while, Hindley's wife gave birth to a boy. However, Hindley's wife died during childbirth. So Hindley named the boy Hatterton. He will have a role later but for now we can keep the character away. Just remember that Hatterton is Hindley's son. After the death of his father and wife, Hindley became free. He used to drink alcohol, do gambling and ill treat and abuse Heathcliff. So basically there is a complete control by Hindley, the biological son of Mr. Earnshaw. Because Mr. Earnshaw has passed away, he's come back with a wife and now the wife is also dead. So he's basically doing all sorts of, he's creating a ruckus there. He's taking control of the property, he's gambling, he's drinking alcohol and what not and giving trouble to Heathcliff. Moving ahead, we'll talk about Linton family now because remember, Nellie was telling the story to Mr. Lockwood. Who is Mr. Lockwood? The tenant. Now Nellie tells Mr. Lockwood that Linton family was a very well-to-do family of Thrush Cross Grange. Now we are talking about Thrush Cross Grange and the Linton family. Now Linton family also had two children, a boy and a girl. Boy was Edgar, girl was Isabella. Now Catherine and Heathcliff of Earnshaw family were getting too interested in the Linton family. Especially Catherine because she had spent five weeks with the Linton family, she was drawn closer to Edgar. Basically love stories are getting made now because he was rich, handsome, educated, so she was falling for him. Now there's a twist, despite all of this like Edgar having all the qualities of, you know, eligible bachelor for marriage, she still liked Heathcliff, her adopted brother Mo. So one day Catherine was telling Nellie, the housekeeper who is narrating the story at the present moment that she cannot get married to Heathcliff because her brother Hindley has insulted him a lot. Now Heathcliff overheard this conversation and gets extremely hurt and sad. That night he runs away from Wuthering Heights. After Heathcliff ran away, Catherine got extremely lonely and she got married to Edgar and after the wedding Catherine moves to Thrush Cross Grange. Now Heathcliff ran away but not permanently. After some years, he came back to Wuthering Heights. Now he was rich, had a good status, but he also had a lot of ego. There was just one thing in his head and that was revenge. Now when Heathcliff came to Wuthering Heights, Catherine got so excited to see him, her husband Edgar tried to calm her down but she was unstoppable and got extremely happy. On the other hand, Heathcliff saw that Hindley was completely destroyed because of his gambling habits. Now to Heathcliff's surprise, Hindley welcomes him warmly to Wuthering Heights. Why? Because Hindley knows that he has money, he is powerful, so it's better that I behave properly. Now Catherine told Heathcliff that her husband's sister Isabella likes him and they should get married. However, Catherine and Heathcliff still had feelings for each other even after all those years. So when Catherine and Heathcliff meet again, they hug each other very tightly. Now her husband Edgar did not like this behaviour and he gets furious. He gave two options to Catherine. Either choose Heathcliff or choose Edgar. Catherine got very upset over this. She locked herself in a room for three days and did not eat anything.  On the same night, Heathcliff and Isabella, they ran away and got married. For the next two months, Edgar took care of Catherine. She got pregnant and remained unwell. Now what happens is, after getting married, Heathcliff ill-treated Isabella. Now you must be thinking that what did she do? You're right, she did nothing. Isabella could not even get back to Edgar. Why? Because after her marriage to Heathcliff, Edgar ended their relationship of brother and sister. And because Edgar was insecure that through Isabella, Heathcliff might want to take over his property in Trashcross Grange, so he broke all ties with his sister. So one day, Heathcliff went to see Catherine to ask about her health. Edgar came there at that exact moment and he thought there was an affair between Catherine and Heathcliff. So that night, Catherine gave birth to a baby girl and sadly, Catherine died during the childbirth. The baby was named Cathy. Catherine was buried at the place where she and Heathcliff used to play back in their childhood. Now after two days, Isabella ran away to London to get away from Heathcliff. There, she gave birth to a baby boy named Linton. Hindley had taken a lot of loans from Heathcliff. So in return, he took Wuthering Heights since Hindley was unable to pay the loan. Now the owner of Wuthering Heights is Heathcliff. Now after becoming the owner, Heathcliff started ill-treating and abusing Hindley the same way Hindley used to treat Heathcliff. So, he is just sorting everyone out. Now, 12 years have passed by. Catherine's daughter Cathy grew up to a beautiful woman. Hindley's son Herton was ill-treated just like him by Heathcliff. Linton, who was Heathcliff's son, was called back by his uncle Edgar from London. As I told you before, Linton was born in London and Heathcliff wanted Linton to stay with him whereas Edgar wanted Linton to stay with him. So, Heathcliff also wanted Linton to get close to Cathy, who was Catherine's daughter. Edgar initially did not allow the two to meet but with time Edgar's health also became bad and he allowed Cathy to meet Linton. When the two met, they came close. Heathcliff wanted Cathy and Linton to get married to each other. Meanwhile, Edgar passed away. Edgar was buried, adjacent to Catherine. Cathy got very lonely after the death of her father. She started living with Heathcliff and Linton. Now, after some time, even Linton passed away. So, a lot of deaths are happening. Heathcliff became the owner of Thrush Cross Grange also. Cathy was living with him forcefully. Herton was also living with them. Now, to the present day. With this, the story being told by Nellie to Mr. Lockwood comes to an end. Now, we will talk about the present. After hearing the story, Catherine appears in Mr. Lockwood's dream beating at a window, wailing. Let me in and blood running down her wrist. Mr. Lockwood goes to London. He comes back after six months and finds out that Cathy and Herton are in love. Even Heathcliff does not have a problem with that. Heathcliff could see him and Catherine in Herton and Cathy. There was a time when Heathcliff was poor and uneducated and still Catherine loved me. And similarly, Herton is also poor and uneducated and Cathy loves him. So, Heathcliff also dies after a while. He is buried on the other side of Catherine and in the end, Cathy and Herton get married and go to Thrush Cross Grange. So, basically, wherever a relation was not possible, that character was killed. Conveniently, whatever problem he created in his life, very conveniently, they just removed them from the scene only. Anyway, with this, the story comes to the end. Now, I will tell you some facts and quotes regarding this work. This is the only finished novel of Emily Bront and it's a romance between crude and ferocious Heathcliff and passionate Catherine, whose bond continues despite Catherine's passing away and the memories continue until the death of Heathcliff. Some important lines are, Do I want to live? Would you like to live with your soul in the grave? Be with me always. Take any form. Drive me mad. Only do not leave me in this abyss where I cannot find you. In my soul and in my heart, I'm convinced. I'm wrong. Honest people don't hide their deeds. So, these are the lines that you should remember and with this, we end this little long chapter and I hope you enjoyed it and we'll meet soon in the next one. Till the time we meet next, happy learning. Keep loving literature and stay tuned to Arpita Karwa.com


We create systems that privilege the privileged. We perpetuate a world that gives voice to the outspoken. We insist that a contextual point of view is timeless and universal. We create a God in our own image and imagine the world as a buffet of our favorite things. Or as Mary Daley said, So long as God is male, male will be God.


Hello, Chris is fish. Yes. Yeah, my name, Arnold. I recently catch maybe five, six very large fish are looking to sell you buy fish. Who's who's supply of fish? You tell me, is the boss in? Can you make a note for the boss? You write this down? Yes. That's no worries. I'm pretty sure he called back when he hear my price. So you write this down? Yes. Yeah. I have a six large fish. Yes, I think barracuda, barracuda or barramundi or both. I think maybe a little both. One is very heavy. One, I can't even lift myself. One, I need two men to lift, two whole big man to lift, right? At least 50, 60 kilo. You hear me? You write that down 50, 60 kilo, that number. I sell you premium fish. It's on ice right now. I looking at it. It's on ice in the freezer right now. I sell you 50, 60 kilo of a barracuda, $400. That one fish will last your shop four weeks. I promise. You hear? You write that down four weeks that one last. That's only one fish. We have a barramundi. Unbelievable flavor. They're still flicking around on the boat. They're still living. So they're still so fresh. And I put them on ice right now. Hala! Hala, go put that one on ice. Put it on ice with the others. Yes. That's a two now. And the other four big fish, 20 to 30 kilo. I lift myself but still very heavy. They take me three, four hour catch.  You write that down three, four hour. It's all together roughly maybe 150 kilo of fish. Fresh, straight on ice. Lying there. They're couples still flicking around. I sell you all 150 kilo. $600, $700. You make me enough. You tell him make me enough.  Dude, he's my new favorite character. I want you to beat him. I want you to beat that guy so bad. He's so good. I love him. He's still flicking around. I wonder how much of that he actually wrote down. I bet you he wrote the first bit down the 50 to 60 kilo or whatever. I wasn't sure what type it was. Barracuda or barramundi. That one had me in stitches. I reckon that's my favorite is one yet. That's my most favorite dude. You write that down. We'll see you guys next week. Yeah, we're not really the best this week. It's not been the best day, but we are the best. You write that down. We are the best. You write that down.


Welcome back, everyone. Today I'm going to show you how to identify files in Windows. So if you have a file, for example, with no extension, you still want to know what type of file it is. In, well, I can say in Linux and in Unix, there's a usually built-in command called file. And you can basically say file and then give it the actual file that you wanted to analyze. And it will use basically the file signature to identify what type of file it is. In Windows, there's nothing like that built-in. So for example, if I say, let's say, I have this photorec.ses file, which is a session file. So if I type something like file, photorec, I'll give it the configuration file. File is not a recognized internal external command. So basically the only way that I can identify this file is maybe use a hex editor or some other way to actually see the file signature of this command. But imagine that you have an extremely large file, loading an extremely large file into a hex editor could be a problem depending on your system.  And we're going to download the GNU Win32 version of file. And this is basically GNU tools for Windows. So if you go to this link, and I'll put the link on below the video. If you go to the, if you download the setup program, so get the setup program from this location, from this link. And then whenever you download that, you will get this file. The current version is 5.03 setup. So then whenever we run this file setup, just like a normal, normal program, we want to run the setup because that will install the DLLs and everything. I don't necessarily want to develop our files though. So just the binaries, definitely the binaries and the documentation if you want it. Okay, I'm going to load it into Win32 file, click next, create documents in the start folder. Okay, that's okay. And then install. Okay. Now, as soon as I click finish, should close, as soon as I click finish, then I can go to CMD. And if I run the command again right now, if I just run file, the file is still not recognized. So one thing that I need to do first is, I don't know why that's not going down. One thing that I need to do is figure out where I installed the program. So I installed it in C drive, program files x86 and GNU Win32. And then the file program is actually in the bin folder. So this is the location, full location of where I need to copy. So click on the location bar, right click, click copy. Okay, so now we've copied that. Right click on the start menu, go to system, click on advanced system settings and environment variables. And then path, edit, and then new and paste, right click and paste. And then that will basically put this location in our path. Then we click okay. Okay. Okay. Close that. Then close any command lines that you had open. Go to cmd and type file and we should see some usage information. So basically we've added file to our Windows path. That way we can just type file and Windows will know where to look for this program. Okay. So now if I type dir, I can look back at this photo rec.cfg file, which is just a text file. So I'm not really sure what's going to happen here. So if I just type file, photo rec, cfg, then okay. Yeah. So it shows up as an ASCII text file, which that's kind of what I expected. I can also run file dash I dash I photo rec cfg to see a little bit more information sometimes. So photo rec cfg text plane to plain text file. Charset US ASCII. Okay. So let's go into just to give another example. I'm not sure if I have any images on this computer, but we can try. Let's go into my documents and there's nothing in there. Okay. Okay. So I have this test PDF on my desktop. So I'm going to run file test PDF and I should obviously see I should see information about PDF basically. Yeah. So I'm going to document in the version of the PDF. I run file dash I test PDF application PDF charset binary. So this is a quick way to tell some information about a file that you're looking at without having to know the extension. Yeah. So that's that's pretty much it. That's how to install a very useful program into Windows to quickly find information, very basic information about files on your system. Thank you very much. If you like this video, please subscribe for more.