So let me ask for a show of hands. How many people here are over the age of 48? Well, there do seem to be a few.
Hajde da dignete ruke. Koliko ljudi ovde ima više od 48 godina? Pa, izgleda da ih ima nekoliko.
Well, congratulations, because if you look at this particular slide of U.S. life expectancy, you are now in excess of the average life span of somebody who was born in 1900.
Čestitamo, jer ako pogledate na konkretno ovom slajdu američkog životnog veka, sada ste prešli prosečni životni vek nekoga ko je rođen 1900.
But look what happened in the course of that century. If you follow that curve, you'll see that it starts way down there. There's that dip there for the 1918 flu. And here we are at 2010, average life expectancy of a child born today, age 79, and we are not done yet. Now, that's the good news. But there's still a lot of work to do.
Ali pogledajte šta se dogodilo tokom tog veka. Ako pratite krivulju, videćete da ona počinje ovde dole. Ovde opada zbog gripa 1918. I evo nas u 2010. Prosečni životni vek deteta rođenog danas je 79 godina. I još nismo završili. To su dobre vesti. Ali ima još dosta posla da se uradi.
So, for instance, if you ask, how many diseases do we now know the exact molecular basis? Turns out it's about 4,000, which is pretty amazing, because most of those molecular discoveries have just happened in the last little while. It's exciting to see that in terms of what we've learned, but how many of those 4,000 diseases now have treatments available? Only about 250. So we have this huge challenge, this huge gap.
Na primer, ako upitate za koliko bolesti mi sada znamo tačnu molekularnu osnovu ispostavlja se da ih je oko 4000, što je zadivljujuće, jer se većina tih molekularnih otkrića dogodila nedavno. Sa stanovišta koliko smo naučili to je fantastično, ali koliko od tih 4000 bolesti danas lečimo? Samo oko 250. Tako imamo ogromni izazov, ogromni jaz.
You would think this wouldn't be too hard, that we would simply have the ability to take this fundamental information that we're learning about how it is that basic biology teaches us about the causes of disease and build a bridge across this yawning gap between what we've learned about basic science and its application, a bridge that would look maybe something like this, where you'd have to put together a nice shiny way to get from one side to the other.
Mogli biste pomisliti da to ne bi trebalo da bude previše teško, da bi jednostavno trebalo da smo sposobni da se koristimo osnovnim znanjem naučenim iz biologije o uzrocima bolesti i da sagradimo most preko zjapećeg jaza, između onoga što smo naučili o osnovnoj nauci i njenoj primeni, most koji bi izgledao nekako ovako, gde biste morali da sastavite lep svetao put kojim se prelazi s jedne strane na drugu.
Well, wouldn't it be nice if it was that easy? Unfortunately, it's not. In reality, trying to go from fundamental knowledge to its application is more like this. There are no shiny bridges. You sort of place your bets. Maybe you've got a swimmer and a rowboat and a sailboat and a tugboat and you set them off on their way, and the rains come and the lightning flashes, and oh my gosh, there are sharks in the water and the swimmer gets into trouble, and, uh oh, the swimmer drowned and the sailboat capsized, and that tugboat, well, it hit the rocks, and maybe if you're lucky, somebody gets across.
Dakle, zar ne bi bilo lepo kad bi bilo tako lako? Nažalost, nije. U stvarnosti je pokušaj prelaska od osnovnog znanja do njegove primene više nalik na ovo. Nema svetlih mostova. Više je nalik ulogu u kladionici. Možda dobijete plivača i čamac i jedrilicu i remorker koje otpratite na put i počne kiša i sevanje i o moj bože, ajkule su u vodi i plivač je u nevolji i uh, ah, plivač se udavio jedrilica se prevrnula, remorker se zabio u stene i možda, ako imate sreće, nekom uspe da pređe preko.
Well, what does this really look like? Well, what is it to make a therapeutic, anyway? What's a drug? A drug is made up of a small molecule of hydrogen, carbon, oxygen, nitrogen, and a few other atoms all cobbled together in a shape, and it's those shapes that determine whether, in fact, that particular drug is going to hit its target. Is it going to land where it's supposed to? So look at this picture here -- a lot of shapes dancing around for you. Now what you need to do, if you're trying to develop a new treatment for autism or Alzheimer's disease or cancer is to find the right shape in that mix that will ultimately provide benefit and will be safe. And when you look at what happens to that pipeline, you start out maybe with thousands, tens of thousands of compounds. You weed down through various steps that cause many of these to fail. Ultimately, maybe you can run a clinical trial with four or five of these, and if all goes well, 14 years after you started, you will get one approval. And it will cost you upwards of a billion dollars for that one success.
A kako to stvarno izgleda? Šta je uopšte to što čini nešto terapeutskim? Šta je lek? Lek je sačinjen od malog molekula vodonika, ugljenika, kiseonika, azota i još nekoliko drugih atoma, i sve to je isprepleteno u oblik i u stvari ti oblici određuju da li će određeni lek pogoditi svoj cilj. Da li će sleteti tamo gde bi trebalo? Pogledajte ovu sliku ovde - mnogo oblika pleše okolo za vas. Ono što morate da uradite, ako pokušavate da razvijete nov način lečenja autizma ili Alchajmerove bolesti ili raka, je da pronađete pravi oblik u toj mešavini koji će konačno biti od koristi i koji će biti bezopasan. I kada pogledate šta se dešava tom cevovodu, započeli ste možda s hiljadama, desetinama hiljada sastojaka. Eliminišete ih tokom različitih koraka što je uzrok da mnogi od njih propadnu. Na kraju ćete možda moći pokrenuti klinički postupak za njih četiri ili pet i ako sve bude u redu, posle 14 godina od vašeg početka dobićete jedno odobrenje. I to će vas koštati milijarde dolara, taj jedan uspeh.
So we have to look at this pipeline the way an engineer would, and say, "How can we do better?" And that's the main theme of what I want to say to you this morning. How can we make this go faster? How can we make it more successful?
Zato moramo pogledati na taj cevovod očima inženjera, pa reći: "Kako možemo raditi bolje?" I to je glavna tema o kojoj želim da vam govorim danas. Kako to možemo ubrzati? Kako to možemo raditi uspešnije?
Well, let me tell you about a few examples where this has actually worked. One that has just happened in the last few months is the successful approval of a drug for cystic fibrosis. But it's taken a long time to get there. Cystic fibrosis had its molecular cause discovered in 1989 by my group working with another group in Toronto, discovering what the mutation was in a particular gene on chromosome 7. That picture you see there? Here it is. That's the same kid. That's Danny Bessette, 23 years later, because this is the year, and it's also the year where Danny got married, where we have, for the first time, the approval by the FDA of a drug that precisely targets the defect in cystic fibrosis based upon all this molecular understanding. That's the good news. The bad news is, this drug doesn't actually treat all cases of cystic fibrosis, and it won't work for Danny, and we're still waiting for that next generation to help him.
Dozvolite da vam ispričam o nekoliko primera koji to potvrđuju. Jedan, koji se dogodio nedavno, poslednjih meseci, je uspešno odobren lek za cističnu fibrozu. Ali stići dotle zahteva mnogo vremena. Za cističnu fibrozu molekularni uzrok je otkriven 1989. u mojoj grupi i u saradnji s jednom grupom iz Toronta. Otkrili smo koja je mutacija bila u određenom genu na hromozomu 7. Vidite tu sliku? Ovde je. To je isto dete. To je Deni Biset posle 23 godine, u važnoj godini u kojoj, osim što se Deni oženio, po prvi put imamo odobrenje od FDA za lek koji precizno pogađa nepravilnost u cističnoj fibrozi i koji je zasnovan na svom tom molekularnom razumevanju. To je dobra vest. Loša vest je da taj lek ne leči sve slučajeve cistične fibroze i Deniju ne pomaže, pa i dalje čekamo sledeće generacije lekova da mu pomognu.
But it took 23 years to get this far. That's too long. How do we go faster?
Ali, da bi se dotle stiglo trebalo je 23 godine. To je predugo. Kako da idemo brže?
Well, one way to go faster is to take advantage of technology, and a very important technology that we depend on for all of this is the human genome, the ability to be able to look at a chromosome, to unzip it, to pull out all the DNA, and to be able to then read out the letters in that DNA code, the A's, C's, G's and T's that are our instruction book and the instruction book for all living things, and the cost of doing this, which used to be in the hundreds of millions of dollars, has in the course of the last 10 years fallen faster than Moore's Law, down to the point where it is less than 10,000 dollars today to have your genome sequenced, or mine, and we're headed for the $1,000 genome fairly soon. Well, that's exciting. How does that play out in terms of application to a disease?
Jedan način da se krene brže je uz pomoć tehnologije, a veoma važna tehnologija, od koje zavisimo za sve spomenuto, je ljudski genom, umeće posmatranja hromozoma, njegovo otpakivanje, vađenje DNK i mogućnost čitanja slova u tom DNK kodu, A, C, G i T slova koja su naša uputstva i uputstva za sva živa bića, a za sav taj rad je cena, koja je nekada bila stotine miliona dolara, u poslednjih 10 godina pala, brže od Murovog zakona, do svote koja je danas manja od 10.000 dolara za sekvenciranje vašeg ili mog genoma i približavamo se genomu od 1.000 dolara. Da, to je uzbudljivo, ali kako je to povezano s primenom na bolesti?
I want to tell you about another disorder. This one is a disorder which is quite rare. It's called Hutchinson-Gilford progeria, and it is the most dramatic form of premature aging. Only about one in every four million kids has this disease, and in a simple way, what happens is, because of a mutation in a particular gene, a protein is made that's toxic to the cell and it causes these individuals to age at about seven times the normal rate.
Ispričaću vam o još jednoj nepravilnosti. Radi se o veoma retkoj nepravilnosti. Ime joj je Hačinson-Gilfordova progerija i to je najdramatičniji oblik prevremenog starenja. Ovu bolest ima samo jedno u četiri miliona dece i uprošćeno rečeno radi se o tome da se zbog mutacije u određenom genu stvorio protein koji je toksičan za ćeliju i obolelim osobama uzrokuje starenje koje je oko sedam puta brže od normalnog.
Let me show you a video of what that does to the cell. The normal cell, if you looked at it under the microscope, would have a nucleus sitting in the middle of the cell, which is nice and round and smooth in its boundaries and it looks kind of like that. A progeria cell, on the other hand, because of this toxic protein called progerin, has these lumps and bumps in it. So what we would like to do after discovering this back in 2003 is to come up with a way to try to correct that. Well again, by knowing something about the molecular pathways, it was possible to pick one of those many, many compounds that might have been useful and try it out. In an experiment done in cell culture and shown here in a cartoon, if you take that particular compound and you add it to that cell that has progeria, and you watch to see what happened, in just 72 hours, that cell becomes, for all purposes that we can determine, almost like a normal cell.
Pokazaću vam snimak toga šta to radi ćeliji. Normalna ćelija, ako je pogledate pod mikroskopom ima jedro u sredini ćelije koje je lepo i okruglo, pravilnih granica i izgleda otprilike ovako. Ćelija progerije, s druge strane, zbog toksičnog proteina po imenu progerin ima ove nepravilnosti. Zato je naša želja bila, posle otkrića još u 2003., da pokušamo da nađemo način kako bi to ispravili. I opet, pošto se znalo nešto o molekularnim putevima, bilo je moguće izabrati jedan iz tog mnoštva sastojaka koji bi mogao biti koristan i isproban. U eksperimentu izvedenom u ćelijskoj kulturi i prikazanom na crtežu, ako uzmete određeni sastojak i dodate ga ćeliji s progerijom posmatrajući šta će se dogoditi videćete da posle samo 72 sata ta ćelija postaje, za sve namene koje možemo da odredimo, skoro kao normalna ćelija.
Well that was exciting, but would it actually work in a real human being? This has led, in the space of only four years from the time the gene was discovered to the start of a clinical trial, to a test of that very compound. And the kids that you see here all volunteered to be part of this, 28 of them, and you can see as soon as the picture comes up that they are in fact a remarkable group of young people all afflicted by this disease, all looking quite similar to each other. And instead of telling you more about it, I'm going to invite one of them, Sam Berns from Boston, who's here this morning, to come up on the stage and tell us about his experience as a child affected with progeria. Sam is 15 years old. His parents, Scott Berns and Leslie Gordon, both physicians, are here with us this morning as well. Sam, please have a seat.
Da, to je fascinantno, ali da li bi to zaista delovalo u stvarnom ljudskom biću? Ovo se dogodilo u periodu od samo četiri godine od časa otkrića gena do započinjanja kliničkog ispitivanja za testiranje tog određenog sastojka. Sva deca koju vidite ovde su se dobrovoljno prijavila za ovo, njih 28-oro i videćete čim se slika pojavi da je to izvanredna grupa mladih ljudi obolelih od ove bolesti, po izgledu svi nalik jedan na drugog. I umesto dalje priče o tome pozvaću jednog od njih, Sema Burnsa iz Bostona koji je ovde, da se popne na binu i da nam kaže o svom iskustvu deteta obolelog od progerije. Sem ima 15 godina. Njegovi roditelji, Skot Burns i Lesli Gordon, oboje lekari, takođe su ovde sa nama. Molim te, Sem, izvoli sesti.
(Applause)
(Aplauz)
So Sam, why don't you tell these folks what it's like being affected with this condition called progeria?
Sem, hajde reci ovom društvu kako je to biti oboleo od progerije?
Sam Burns: Well, progeria limits me in some ways. I cannot play sports or do physical activities, but I have been able to take interest in things that progeria, luckily, does not limit. But when there is something that I really do want to do that progeria gets in the way of, like marching band or umpiring, we always find a way to do it, and that just shows that progeria isn't in control of my life.
Sem Burns: Progerija me ograničava u nekim stvarima. Ne mogu da se bavim sportom ili fizičkim aktivnostima, ali bio sam u mogućnosti da se uključim u stvari koje, srećom, progerija ne ograničava. Ali kada se pojavi nešto što bih zaista želeo da uradim, a progerija tome stoji na putu, kao što je marširajući orkestar, ili sportsko suđenje, uvek pronađemo način kako da to postignem što samo pokazuje da mi progerija ne kroji život.
(Applause)
(Aplauz)
Francis Collins: So what would you like to say to researchers here in the auditorium and others listening to this? What would you say to them both about research on progeria and maybe about other conditions as well?
Frensis Kolins: I šta bi želeo da poručiš istraživačima ovde u auditorijumu i ostalima koji ovo slušaju? Šta bi im svima rekao o istraživanju progerije i još možda o drugim bolestima?
SB: Well, research on progeria has come so far in less than 15 years, and that just shows the drive that researchers can have to get this far, and it really means a lot to myself and other kids with progeria, and it shows that if that drive exists, anybody can cure any disease, and hopefully progeria can be cured in the near future, and so we can eliminate those 4,000 diseases that Francis was talking about.
SB: Istraživanja progerije su otišla toliko daleko za manje od 15 godina, što samo pokazuje kakav zalet istraživači mogu imati da dotle stignu i to zaista mnogo znači meni i drugoj deci oboleloj od progerije i pokazuje da kada takav zalet postoji otvara se mogućnost za svakoga da izleči bilo koju bolest i nadam se izlečivosti progerije u bliskoj budućnosti kao i mogućnosti eliminacije tih 4.000 bolesti o kojima je Frensis govorio.
FC: Excellent. So Sam took the day off from school today to be here, and he is — (Applause) -- He is, by the way, a straight-A+ student in the ninth grade in his school in Boston. Please join me in thanking and welcoming Sam. SB: Thank you very much. FC: Well done. Well done, buddy. (Applause)
FK: Odlično. Sem je izostao iz škole danas da bi bio ovde, a on je - (Aplauz) - On je, onako usput, odličan učenik, ima odlične ocene u devetom razredu škole u Bostonu. Molim vas pridružite mi se u zahvalnici i dobrodošlici Semu. SB: Mnogo Vam hvala. FK: Odlično je bilo drugar. (Aplauz)
So I just want to say a couple more things about that particular story, and then try to generalize how could we have stories of success all over the place for these diseases, as Sam says, these 4,000 that are waiting for answers. You might have noticed that the drug that is now in clinical trial for progeria is not a drug that was designed for that. It's such a rare disease, it would be hard for a company to justify spending hundreds of millions of dollars to generate a drug. This is a drug that was developed for cancer. Turned out, it didn't work very well for cancer, but it has exactly the right properties, the right shape, to work for progeria, and that's what's happened. Wouldn't it be great if we could do that more systematically? Could we, in fact, encourage all the companies that are out there that have drugs in their freezers that are known to be safe in humans but have never actually succeeded in terms of being effective for the treatments they were tried for? Now we're learning about all these new molecular pathways -- some of those could be repositioned or repurposed, or whatever word you want to use, for new applications, basically teaching old drugs new tricks. That could be a phenomenal, valuable activity. We have many discussions now between NIH and companies about doing this that are looking very promising.
Želeo bih samo da kažem još par stvari o toj priči i onda bih pokušao da generalizujem o tome kako bismo mogli imati priče o uspehu svuda za sve te bolesti, kako kaže Sem, za tih 4.000 koje čekaju na odgovore. Možda ste primetili da lek za progeriju, koji je sada u kliničkom ispitivanju, nije lek koji je bio za to namenjen. To je toliko retka bolest da bi kompanijama bilo teško da opravdaju stotine miliona dolara utrošenih za proizvodnju leka. To je lek koji se razvijao za rak. Ispostavilo se da nije delovao dovoljno dobro na rak, ali da ima prava svojstva, pravi oblik za lečenje progerije i tako se to dogodilo. Zar ne bi bilo bolje kada bi to radili sistematičnije? Zar ne bismo mogli da podržimo postojeće kompanije koje imaju zamrznute lekove za koje se zna da su bezopasni za ljude, ali koji nikada nisu uspeli da efektivno leče ono za šta su bili namenjeni? Sada učimo o svim tim novim molekularnim putevima - neki od lekova bi se mogli repozicionirati ili koristiti za druge namene, ili drugim rečima, dati im novu primenu, naučiti stare lekove novim trikovima. To bi mogla biti fenomenalna, vredna aktivnost. Postoji mnogo diskusija između Nacionalnog zdravstvenog osiguranja (NZO) i kompanija o tome, što je veoma ohrabrujuće.
And you could expect quite a lot to come from this. There are quite a number of success stories one can point to about how this has led to major advances. The first drug for HIV/AIDS was not developed for HIV/AIDS. It was developed for cancer. It was AZT. It didn't work very well for cancer, but became the first successful antiretroviral, and you can see from the table there are others as well.
I mogli biste očekivati da iz toga proiziđe prilično mnogo toga. Postoji priličan broj priča o uspehu koje potvrđuju da je to dovelo do značajnog napretka. Prvi lek za sidu nije se razvijao za sidu. Razvijao se za rak. To je bio AZT. Nije delovao dovoljno dobro na rak, ali je postao prvi uspešni antiretrovirusni lek i u tabeli možete videti i sve druge takve lekove.
So how do we actually make that a more generalizable effort? Well, we have to come up with a partnership between academia, government, the private sector, and patient organizations to make that so. At NIH, we have started this new National Center for Advancing Translational Sciences. It just started last December, and this is one of its goals.
Dakle, na koji način možemo takve napore šire primenjivati? Za to moramo ostvariti partnerstvo između akademskih ustanova, vlade, privatnog sektora i udruženja pacijenata. U okviru NZO smo osnovali novi Nacionalni centar za unapređivanje prevodilačkih nauka. Centar je počeo sa radom u decembru i to je jedan od njegovih ciljeva.
Let me tell you another thing we could do. Wouldn't it be nice to be able to a test a drug to see if it's effective and safe without having to put patients at risk, because that first time you're never quite sure? How do we know, for instance, whether drugs are safe before we give them to people? We test them on animals. And it's not all that reliable, and it's costly, and it's time-consuming. Suppose we could do this instead on human cells. You probably know, if you've been paying attention to some of the science literature that you can now take a skin cell and encourage it to become a liver cell or a heart cell or a kidney cell or a brain cell for any of us. So what if you used those cells as your test for whether a drug is going to work and whether it's going to be safe?
Dozvolite da kažem još nešto što bismo mogli uraditi. Zar ne bi bilo lepo kada bismo mogli da testiramo dejstvo i bezbednost leka bez rizika za pacijente, jer prvi put nismo sasvim sigurni? Kako mi znamo, na primer, da li su lekovi bezopasni pre nego što ih damo ljudima? Testiramo ih na životinjama. No, to nije sasvim pouzdano, skupo je i dugotrajno. Zamislite kada bismo mogli to raditi na ljudskim ćelijama. Verovatno znate, ako ste obraćali pažnju na neku naučnu literaturu, da danas možete uzeti ćeliju kože i podstaći je da se pretvori u ćeliju jetre ili u ćeliju srca, bubrega, mozga, za bilo koga od nas. Šta kada bismo te ćelije koristili za testiranje vašeg leka, kako deluje i koliko je bezopasan?
Here you see a picture of a lung on a chip. This is something created by the Wyss Institute in Boston, and what they have done here, if we can run the little video, is to take cells from an individual, turn them into the kinds of cells that are present in the lung, and determine what would happen if you added to this various drug compounds to see if they are toxic or safe. You can see this chip even breathes. It has an air channel. It has a blood channel. And it has cells in between that allow you to see what happens when you add a compound. Are those cells happy or not? You can do this same kind of chip technology for kidneys, for hearts, for muscles, all the places where you want to see whether a drug is going to be a problem, for the liver.
Ovde vidite sliku pluća na čipu. Ovo je nešto stvoreno na Vis institutu iz Bostona i videćemo, ako pustimo video, da su oni uzeli ćelije od jedne osobe, pretvorili ih u vrstu ćelija prisutnih u plućima i odredili šta bi se desilo kada bi im dodavali različite sastojke leka, da bi ustanovili da li su toksični ili bezopasni. Možete videti da ovaj čip čak diše. Ima kanal za vazduh. Ima kanal za krv. Između ima ćelije uz pomoć kojih vidite šta se dešava kada dodajete sastojak. Da li su te ćelije srećne ili nisu? Možete napraviti istu vrstu tehnologije čipova za bubrege, srce, mišiće, za sva mesta ako želite da ustanovite da li će lek biti problematičan za jetru.
And ultimately, because you can do this for the individual, we could even see this moving to the point where the ability to develop and test medicines will be you on a chip, what we're trying to say here is the individualizing of the process of developing drugs and testing their safety.
I na kraju, zato što to možete raditi individualno, uviđamo da se taj proces bliži fazi u kojoj će mogućnost razvoja i testiranja lekova biti na vašem čipu, odnosno šta pokušavamo reći ovde je individualizacija postupka za razvoj lekova i za testiranje njihove bezbednosti.
So let me sum up. We are in a remarkable moment here. For me, at NIH now for almost 20 years, there has never been a time where there was more excitement about the potential that lies in front of us. We have made all these discoveries pouring out of laboratories across the world. What do we need to capitalize on this? First of all, we need resources. This is research that's high-risk, sometimes high-cost. The payoff is enormous, both in terms of health and in terms of economic growth. We need to support that. Second, we need new kinds of partnerships between academia and government and the private sector and patient organizations, just like the one I've been describing here, in terms of the way in which we could go after repurposing new compounds. And third, and maybe most important, we need talent. We need the best and the brightest from many different disciplines to come and join this effort -- all ages, all different groups -- because this is the time, folks. This is the 21st-century biology that you've been waiting for, and we have the chance to take that and turn it into something which will, in fact, knock out disease. That's my goal. I hope that's your goal. I think it'll be the goal of the poets and the muppets and the surfers and the bankers and all the other people who join this stage and think about what we're trying to do here and why it matters. It matters for now. It matters as soon as possible. If you don't believe me, just ask Sam.
Dozvolite mi da rezimiram. Mi smo u značajnom trenutku ovde. Po meni u NZO za poslednjih 20 godina nikada nije bilo više oduševljenja u vezi sa mogućnostima ispred nas. Došli smo do svih tih otkrića koja teku iz laboratorija širom sveta. Šta nam treba za kapitalizaciju toga? Prvo, potrebni su nam resursi. To je istraživanje koje je jako rizično, ponekad jako skupo. Isplativost je ogromna, kako u smislu zdravlja tako i u smislu privrednog rasta. Moramo tome dati podršku. Drugo, potrebna su nam nove vrste partnerstva između akademskih ustanova, vlade, privatnog sektora i udruženja pacijenata, baš kao ona koja sam opisivao ovde, u smislu načina na koji bi mogli davati nove svrhe novim sastojcima. Treće i možda najvažnije je to da nam je potreban talenat. Potrebni su nam najbolji i najpametniji u mnogim različitim disciplinama, da dođu i da se pridruže tim naporima - svih starosnih doba, iz svih različitih grupa - jer, ljudi, sada je čas. Ovo je biologija 21. veka na koju ste čekali i imamo šansu da je prihvatimo i pretvorimo u nešto što će zaista zatreti bolesti. To je moj cilj. Nadam se da je i vaš cilj. Mislim da će to biti cilj pesnika i lutaka i surfera i bankara i svih drugih ljudi koji se pridruže na ovoj pozornici, i razmislite šta pokušavamo ovde da uradimo i zbog čega je to važno. Važno je sada. Važno je što pre je moguće. Ako ne verujete meni, pitajte Sema.
Thank you all very much.
Mnogo vam hvala svima.
(Applause)
(Aplauz)