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trvelyans-archive · 4 years ago

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wanting

for @goblin-deity <3 adam and jamie being Babies !!! bc they are Babies !!! and i hope you enjoy !!!

The Detective’s hand was so soft.

How was it so soft?

Adam sighs, pushing his fingers through his hair impatiently as he stares at the dummy in front of him. In the four days that have passed since the carnival – and those four days have felt very long, even for a vampire who has lived 900 years – Jamie’s hand, the one Adam held, is all he can think about. It was so much softer than his own, so much smaller – so much stronger, too, at least in that moment, his fingers clinging onto Adam so tightly that he thought that Jamie would never let go. Like his fingerprints would be etched into Adam’s skin forever.

(Not that Adam would mind that.)

He’s has never thought much about his own hands. They’re big, wide – they can lift things, hold things together, and hit things hard enough to be sufficient in a fight. He doesn’t think much about his hands because he doesn’t need to, but he hopes that Jamie does. He hopes that Jamie wants to. And then he wonders what exactly Jamie would think about those hands doing.

(Sometimes Adam thinks about what Jamie’s hands would do to him. Sometimes he wonders if they’d still be soft when – if, he reminds himself, if – they touched all the other parts of his body.)

With a grunt, he steps forward and lashes out at the dummy with his fist before following it up with a blow to the stomach. Adam doesn’t have time for this – the Detective was distracting enough before, but now that… well, whatever it was that happened at the carnival happened, he’s going to be even harder to ignore and much harder forget. Which is exactly what Adam should be trying to do, but he can’t.

He grits his teeth and hits the dummy again, frowning hard. He thought that he would never have these feelings again – he hasn’t been with anyone since before he was turned, after all, and the 900 years he’s lived alone have passed by with little in the way of romance – but now that they’ve returned, he doesn’t know how to control them. He doesn’t know what to do to make them stop.

Perhaps there’s nothing he can do. Perhaps he can’t. And there’s nothing Adam hates more than that.

He punches the dummy again and sends it wobbling backwards a second before it topples over, hitting the ground of the training room with a hard thud. Adam growls in frustration, and a moment later, the door opens.

Of course it’s Nate. The very last person Adam wants to see right now.

Usually Adam has little qualms with confiding in Nate – not that he has none, of course – but the last thing he wants to talk about with him is the detective. Nate doesn’t understand. He understands other things, experiences they’ve shared in their times as vampires, but he doesn’t understand this. He couldn’t understand this – Adam’s apprehension, his fear, and most of all, his adoration. His complete and utter adoration for Jamie that feels like it’s straight out of a Shakespearian tragedy, a comparison that Jamie would probably like.

(Adam met Shakespeare. He didn’t like him very much.)

“Hey,” Nate says warmly, sliding into the room and shutting the door behind him. “Working hard or hardly working?” After a pause, he adds to himself, “I think that’s how the saying goes…”

Adam snorts. “Take a guess.”

“I would,” Nate replies, smiling. “But I don’t think you’d like my answer.”

With a sigh, Adam turns to Nate, bending down to grab his shirt and pull it over his head. It does little to help him maintain what’s left of his dignity, but it does enough. “What do you want, Nate?”

Nate shrugs and leans against the door. “Nothing,” he says. “I was just wondering if you wanted to talk.”

“There’s nothing to talk about,” Adam answers, his words short and clipped. “And – there’s certainly nothing I want to talk about. Unless Agent Murphy needs something, in which case –“

“Adam.” Nate nearly rolls his eyes, but stops himself at the last second. “You can’t keep avoiding this forever.”

“Avoiding what?” Adam asks even though he knows the answer very well.

“Your feelings for Jamie,” Nate says, as if it’s the simplest thing in the world. As if it isn’t tearing Adam’s heart to shreds. As if it won’t end the way Adam fears it will – as if it won’t destroy him. Because it will destroy him, one way or another.

Adam’s lip curls in a sneer. “Don’t talk about things you don’t understand,” he answers, almost immediately wincing at the defensiveness in his tone.

“I do understand.” Nate takes a step forward, his voice even and measured. “You’re scared of Jamie getting hurt, right? That you won’t always be there to save him?”

That’s exactly what he’s worried about. It’s all he can think about now when he’s not on patrol, especially after what happened with those Trappers outside of the Warehouse a few weeks ago. Still, he wrinkles his nose. “I don’t want to talk about this, Nate –“

“Adam, you don’t know how it will end.”

“I do!” he says. Nate’s eyes widen, surprised at Adam’s outburst, and Adam pauses for a moment to collect himself. “I do know, Nate. The maa-alused woman told me.”

He frowns. “What did she say?”

With a heavy sigh, Adam runs a hand over his scalp. However many weeks it’s been since their first night at the carnival, Sanja’s words echo in his head. He isn’t sure they’ll ever go away. “That even if we… embrace the light, the darkness to come will swallow us both,” he answers. “The darkness, Nate. And if I make it through that and Jamie doesn’t…”

“We’ll take care of him,” Nate assures him, though a sudden shakiness to his voice betrays that he doesn’t seem to entirely believe it himself. “You and me, Rebecca and the team. We’ll take care of him, Adam. We will keep him safe.”

“I would do anything for him,” Adam confesses under his breath. He closes his eyes, the truth nearly crushing him under the weight of it on his heavy heart. “I would do anything, Nate.”

“And I would do anything for you, old friend.” Nate claps his hand onto Adam’s shoulder, squeezing him gently. “Including telling you that you should talk to the detective, whether you want to hear that or not, and that you should let yourself have feelings for him. You should let yourself be happy, even for a little while. You shouldn’t have to deny yourself of these feelings forever. I’ll be there for you every step of the way.”

Adam sighs. “You shouldn’t have to do that,” he says. He doesn’t like relying on people, and he already relies on the team and the detective far too much for his liking. “And I can’t ask you to.”

“Well then, it’s a good thing you didn’t, and good that I’m going to do it anyway.” He smiles at Adam, his dark brown eyes sparkling. “It will be worth it. Go see him.” Before he leaves the room, he turns around on last time. “And, if you’re looking for an excuse, you could try bringing him a drink.”

“Goodbye, Nate,” Adam says, ushering his friend through the door with a tense smile before shutting it behind him.

His smile falters, however, once Nate’s footsteps fade into silence, and he leans against the door and slides onto the ground, pressing his face into his hands. How he let himself turn into such a fool, he’ll never know, but there’s nothing he can do about it now, all things considered. He’ll just have to wait and see what becomes of this – at least what becomes of this before, well, whatever darkness it is that’s awaiting them in the future…

He stays there for a few moments, collecting himself, before he stands up and heads for his room to get ready.

An hour later, Adam is standing at the foot of the detective’s apartment building, a to-go cup clutched so tightly in his fist he’s scared it’s going to crush it. That would be unfortunate – he’s wearing his cleanest white shirt, and he could do without spilling a hot drink all over it, especially considering that would require him to embarrass himself before even entering the detective’s home. After a deep breath, he strides up the front stairs and into the building.

His footsteps echo through the empty hallways, and he moves slowly in the direction of Jamie’s apartment, trying to figure out what he’s going to say. He could greet him normally and pretend there’s an Agency matter he needs to discuss with him, but – well, there isn’t, so a lie like that could cause trouble in the near future. He could say he was on patrol and wanted to stop by, but if he was on patrol then he wouldn’t have had time to go and buy Jamie a drink, so that’s out of the question. Or he could say that…

Or he could say that he just wanted to see him. After the carnival, that probably wouldn’t come as much of a surprise.

Either way, he’s knocking on Jamie’s front door before he can think twice about it.

“Hello?” Jamie calls from somewhere inside the apartment.

Even just hearing his voice makes Adam’s knees weak – it’s so familiar, so soft. Just like his hand, and just like the rest of him, probably. Adam shakes his head and clears his throat. “Hello, Detective, it’s…” He sighs. “It’s, uh, Agent du Mortain. I mean – Adam. It’s me.”

Fool.

“Oh!” There’s an awkward pause on the other side of the door and Adam frowns, unsure of how to move forward. “Uh – come in, the door should be open. I’m just changing.”

“Oh.” He closes his eyes. “It’s… Er, it’s fine, I can wait. Outside.”

He should turn on his heel and leave, really. He’s already embarrassed himself plenty.

“Adam.” He can hear Jamie laughing. “Just come in.”

Jaw clenched, Adam grabs the doorknob and reluctantly heads inside.

He’s been here enough to remember the layout. He doesn’t think he will ever forget it. From a tactical standpoint, he has counterattacks and defenses planned for and from every corner of the room – using pieces of furniture, his teammates, and himself as a means to protect the detective. He’s even spent a few distracted, aimless nights going over new tactics with every supernatural he remembers they should prepare for – that Jamie should prepare for, he always reminds himself – but it’s a long list, and he doesn’t always have time to sit down with it like he would like to.

Maybe he’ll do that instead of training whenever he’s frustrated. The Agency doesn’t have enough funds to keep supplying them with new dummies whenever he destroys them.

He places the to-go cup of earl grey on a coffee table and folds his arms over his chest, glancing around the room. It’s nicely decorated, as far as human homes go, but what catches his eye are the pictures on the bookshelves. He hasn’t examined them much before – he’s never felt the need to – but now, standing in the detective’s apartment and waiting for him to finish changing, it’s a very welcome distraction.

There are a couple of pictures of a younger Jamie, one Adam doesn’t entirely recognize at first – he has different hair, a rounder face. None of his current scars. There are a handful of framed theatre pamphlets and pictures to go along with them, as well, including a few of Jamie wearing a lopsided pair of headphones and an even more lopsided smile, and one in the middle of his bookshelf of him and Tina where her grin is wide but his is even wider, despite the harsh lighting of the hospital.

Adam clenches his fist by his sides. His heartbeat is so loud in his ears that he can’t even hear Jamie walking into the room.

“Ah, that’s one of my favourites,” Jamie says, sidling up beside Adam with his dress shirt half-unbuttoned.

Adam frowns. “Why?” he asks. He would never keep a memento of what he assumes to be a painful memory, let alone keep it on display. (Perhaps he’s just upset because he doesn’t like seeing Jamie hurt.)

Jamie shrugs, continuing to try and button up his shirt with one hand while the other grips his cane. “I don’t know,” he answers. “I just like it.”

He’s told them about the accident a few times before. He talked about it with Adam the day he drove him home after the carnival when he was nearly falling asleep in the passenger seat. It’s part of the reason Adam asked him to text him or call him whenever Jamie drives home from the Warehouse, especially at night – Adam can’t help but worry. He turns to him with a response but can’t get the words out before his eyes catch on Jamie’s fingers, struggling to finish up with the last few buttons of his shirt.

“Here,” he says in an effort to distract his mind from wandering. “Let me.”

Jamie glances towards him. “Are you sure?” he asks.

Adam stalls for a moment before nodding. “Unless you have an issue with that, in which case–“

“No,” Jamie says hurriedly. “No, I don’t mind at all.”

Adam tries to ignore the other man beaming. If he doesn’t, he’ll do something he might regret.

(Though now, with Jamie in front of him, it’s hard to regret anything. Anything leading up to this point and anything that’s going to come after.)

“So,” Jamie says, clearing his throat as Adam works slowly at his buttons. “Did you need something?”

“Hm?”

“You don’t usually drop by without texting me first,” Jamie continues. “Or, uh, getting Felix to do it.”

“Yes, well…” Adam purses his lips. He hadn’t expected that he would have to explain himself so soon, but tries not to let himself panic. (Which he shouldn’t be doing, because he’s not a man who panics. Adam du Mortain has nothing to panic about.) “I was on patrol, and thought I would stop by to check on you.”

“Mason usually patrols at this time, doesn’t he?”

Damn. That’s true. And Adam would have no reason for taking Mason’s shift – Jamie would know that very well. He pauses for a moment, considering. “Yes,” he says, “but –“

And then he sighs. “I wasn’t on patrol,” he admits. “I just… perhaps I just wanted to see you.”

“Did you now?” Jamie asks.

Adam would find that entirely un-funny if he weren’t so flustered. “Yes,” he responds simply.

“Is there a reason you came to see me?”

Adam ignores the slight hopefulness in his voice and drops his hands from the other man’s shirt, stepping away from him and gesturing towards the cup. “I brought you�� a drink,” he says. It sounds completely pathetic right now, but… perhaps that’s fitting. He feels completely pathetic right now, too, because he’s come all this way and Jamie hasn’t even said anything about what happened at the carnival.

Perhaps Adam should bring it up first…

Jamie bends down to grab the cup, lifts it to his nose, and pulls the lid away. “Oh,” he says, smiling as he sniffs it. “It’s my favourite.”

Adam nods, biting back a smile. The last thing he wants is for Jamie to know how pleased he is by that statement. “Nate said –“

Fortunately, he stops himself before he can finish, but unfortunately, it’s enough that one of Jamie’s eyebrows raises and he looks at Adam curiously.

“You were talking about me to Nate?”

Fool.

Adam splutters. “I –“ He glances away, frowning. “Do you enjoy embarrassing me, Detective?”

“Maybe,” Jamie answers. Adam doesn’t know if he’s joking or not. “But seriously - thank you, Adam, for… bringing me this. Is there, uh…” He exhales. “Is there anything else you wanted?”

Adam swallows the lump in his throat. “As I stated previously,” he begins, “I came to check on you. After everything with the maa-alused, I wanted to make sure that…” He trails off. “Now that I know you’re safe, I should… go.”

He doesn’t want to go, of course, because then he has to go back to the Warehouse, and the last thing he wants to do right now is go back to the Warehouse where he’s sure Felix will be waiting to make fun of him for leaving in the first place. Despite himself, he looks to Jamie, who says, “Or you could stay? It seems like you have something on your mind…”

“I don’t,” Adam responds.

“Yes, you do,” Jamie shoots back. Adam curses to himself. “I can tell.”

“There’s nothing to talk about,” Adam says defensively.

“Adam.”

He sighs, his shoulders tensing. “What happened the other night,” he starts uncertainly. “At the Carnival.”

Jamie crosses his arms over his chest, waiting for Adam to continue.

But he doesn’t want to, because then he’ll get confirmation on the detective’s feelings, and if Jamie feels the same way about Adam that Adam feels for him…

Then what?

Adam hasn’t been in a relationship in a long time. He doesn’t know how to be in a relationship. Human courting is so different nowadays. (Especially because they don’t even call it courting.). And besides, neither of them has the time for that, right? It would never work. It could never work.

And he knows that, so what is he doing?

“Yeah?” Jamie replies.

Adam clears his throat. “I don’t know,” he says, casting his eyes downwards. “I suppose I wanted to know your thoughts on it.”

There’s silence from Jamie. Adam glances up to see him biting his lip.

“What are your thoughts on it?” Jamie asks, his fingers running over the back of Adam’s knuckles, up the length of his thumb.

The touch is so soft. Jamie’s hand is so soft. Adam grits his teeth.

“I have none,” he says. It’s a blatant lie, but he doesn’t care how convincing it is at this point.

“That’s not true,” Jamie retorts.

“What are your thoughts, then?” Adam replies in challenge. “Detective?”

“I think you know my thoughts, Adam.”

He winds his fingers through Adam’s and squeezes his hand. Gently, but enough that Adam can feel it. Feel him from where he stands in front of him, hear his heartbeat from where he stands in front of him, the light from a nearby lamp casting handsome shadows over his face that makes Adam’s heartbeat pick up until matches pace.

It’s too much, too fast.

“I… I have to return to the Warehouse,” he says, pulling away and striding towards the door. “I’m glad you’re doing well, Detective –“

“Adam –“

“I will be in contact,” Adam continues, wringing his hands, “when I - when the Agency needs you.”

“What happened to off-kilter?”

Adam pauses at the door, clenching the doorknob hard in his fist.

He is not a soft man. He’s hardened himself to the world. He’s spent the past 900 years looking forward without giving anyone so much as a second glance, and he doesn’t want to hurt the detective. But Jamie has held Adam’s hand twice now, too, and Adam’s seen the way that Jamie looks at him – Adam is not the only one who feels that utter adoration.

It’s worth it. It’ll be worth it. He knows that.

But not now. Not today.

“I can’t talk about this right now,” Adam says finally. “I’m sorry.”

Jamie sighs behind him. “Okay,” he replies.

“But…” Adam turns around. “Another day.”

Jamie’s face lights up with a smile. “Okay,” he repeats. “Another day.”

Adam leaves without any further ceremony, opening the door and hurrying through it as gracefully as he can with his jaw clenched tight, and only when he’s down the stairs and outside once more does he raise his hand and stare down it, his fingers curling in on themselves.

Well, now he’s just going to be even more distracted. You’re a fool, Adam tells himself, running his thumb over his own palm. A fool.

But a soft smile plays on his lips, and it lingers there the whole drive home.

#my writing #my commissions #I'M SORRY FOR MAKING YOU WAIT SLKJFKLSDJFSD I PROMISED YOU TODAY AND GOD DAMN IT I WAS GONNA DELIVER #also i hope i got jamie right EEE i love them. they're iconic #what a duo !!!! two kings !!!

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borisbubbles · 6 years ago

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16. SERBIA

Balkanika - “Nova Deca” 19th place

youtube

Out of all the positive morphs I experienced this year, Serbia was the one that I suspected the least. I never hated them the way others did, but eh, I didn’t think highly of them either. Especially when the backstage clips showed them enterting the stage dressed up like members of some inauspicious fertility cult. “Oh.” I thought. “Another Genealogy. Except it won’t make the final. Whatever, NEXT”

How wrong I was though, because it did qualify and caused me to re-evaluate all I knew about life and come to the fucking conclusion that... this is really fucking good??? HOW is an exaggerated mess that has accurately been described as “Balkan Megamix Volume 3″ this great?

I actually don’t have a clear answer for this as i’m writing this down (we haven’t reached the songs I would spam the replay button on yet), but the core of it is that Balkanika tried REALLY hard to condense 900+ years worth of Balkanic musical tradition in a mere three minutes and fucking pulled it off by... striking battle poses like some Ethno-Power Rangers

GO GO BALKAN RANGERS!!!

The choreography as a whole is just so extra and beautifully overacted. The entire way through, the members of Balkanika strike poses as if in Madonna’s “Vogue”, guided on by the beguiling tunes conjured by Ljubomir’s magic whistle-wand [ed.: here’s the best gif i could make of Old Rasflutin’s background flailing, but it’s way funnier if you pay attention to his presence as you watch “Nova Deca” unfold, so SCROLL UP AND REWATCH RIGHT NAO!!!]:

Such a beautiful presence we’re not worthy of, y’all. All while the rest of Balkanika are either serving some epic 90 Percussion realness:

or chanelling some Project: Waters of Life sillyness

This could have so easily turned into a San Marinese goopy mess (which I don’t think too highly of, as you know), and briefly it looked like this would be the case; Instead, we found something better.

The plain answer however, lies in that Balkanika didn’t try to be funny and that makes a massive difference. Every piece of overacting, from Mladen’s creepy stares to Ra-Ra-Rasflutin (Serbia’s greatest love machine) prodding the action on from the background, is the product of intense belief and dedication, which... makes it hysterical, but in an endearing sort of way. Balkanika really just can’t help themselves. <3

However, as I have to take things into account other than just act, I can’t really drag Balkanika much higher than this. Their song, while cool in concept, is kinda a bit too overloaded with quirks, which are largely lost to me because you know, show-stopping staging. (lol I just realized this is such a reverse “O jardim”, how neat they will now be forever ranked next to one another in this ranking). “Nova Deca” also suffers from the fact that I already had a large slew of other faves before I started to love them. As a whole, I think they have the least to offer of those left in the ranking. Oh well, at least we’ll forever have this:

RANKING SO FAR:

16. Serbia (Balkanika - “Nova Deca”)

17. Portugal (Cláudia Pascoal - “O jardim”)

18. The Netherlands (Waylon - “Outlaw in ‘em”)

19. Ukraine (MÉLOVIN - “Under the ladder”)

20. Macedonia (Eye Cue - “Lost and Found”)

21. San Marino (Jessika ft. Jenifer Brening - “Who We Are”)

22. Sweden (Benjamin Ingrosso - “Dance You Off”)

23. Austria (Cesár Sampson - “Nobody but you”)

24. Latvia (Laura Rizzotto - “Funny girl”)

25. Azerbaijan (AISEL - “X my heart”)

26. Israel (Netta - “Toy”)

27. Norway (Alexander Rybak - “That’s how you write a song”)

28. Montenegro (Vanja Radovanovic - “Inje”)

29. Armenia (Sevak Khanagyan - “Qami”)

30. Poland (Gromee ft. Lukas Meijer - “Light me up”)

31. Greece (Yianna Terzi - “Oniro mou”)

32. Georgia (Iriao - “For you”)

33. Belgium (Sennek - “A matter of time”)

34. Italy (Ermal Meta & Fabrizio Moro - “Non mi avete fatto niente)

35. Romania (The Humans - “Goodbye”)

36. Ireland (Ryan O'Shaughnessy - “Together”)

37. Croatia (Franka - “Crazy”)

38. Belarus (ALEKSEEV - “Forever”)

39. Russia (Julia Samoylova - “I Won’t Break”)

40. Spain (Amaia & Alfred - “Tu canción”)

41. Iceland (Ari Ólafsson - “Our choice”)

42. Australia (Jessica Mauboy - “We Got Love”)

43. Czech Republic (Mikolas Josef - “Lie to me”)

FOOTNOTES (optional)

1) I decided not to credit Sanja Ilic simply because he wasn’t on the stage and I feel it’s kinda unfair to credit him just based on his merit as a composer, while Isaura composed AND performed second fiddle to Cláudia, without a letter of on-screen credit.

2) Re: Intentional vs Unintentional humour: The reason why intentional humour rarely works for me is that it comes with the built-in pressure to laugh, which... makes me less inclined to find something funny because it kinda takes away the choice element of it. Like, I think I have a fairly okay sense of humour, I can decide for myself what I find funny, you know? This is why intentional humour rarely works for me, while unintentional humour nearly always does. For reference, dial back to where I ranked Israel and Norway and Czechia and San Marino (or “Yodel it” and “Space” from last year), all acts that piggybacked on scripted humour

3) DoReDos are one of the few instances this year where intentional humour totally worked for me, although I also realize they’ve largely been hit-or-miss. But we won’t be discussing that soon.

4) Me being a history nerd, I also think the idea of “weaving a song out of literally every Serbian musical quirk ever” is a really cool song concept. It really comes close to an earnest, Balkanic version of “Swedish Smörgåsbord” <3 5) “Nova Deca” is a way more accurate representation of what actual balkan music sounds like (as opposed to the tiresome, tedious, boring Balkan Ballad). The Folk music channels in Bulgaria, for instance play “Nova Deca”-esque songs all day. 6) A funny argument between my mom and I occured during this song. My mom, who is Bulgarian, argued that Balkanika plagiarized their song from Bulgarian Polyphonic Singing. When I pointed out the song was based on the Byzantine musical traditions, she claimed that the Byzantines stole them from the Bulgarians, which is historically implausible (see note 8). This is one of many reasons I think little of ethnocentrism and nationalism, especially from the Slavs and Greeks. Everyone accuses one another of cultural appropriation (see again: Macedoniagate), when in fact, their geographical proximity exposed them to similar cultural ideas and their geopolitics (warmongering) turned it into a mutually unintelligible wash.

7) Besides, the entire point of the Balkans is that they support each other due to their cultural similarities in spite of wishing horrific, painful deaths on one another. <3

8) HISTORY LESSONS WITH BORIS #1: Polyphonic Singing. Polyphonic singing evolved as a Byzantine response to Roman Catholic liturgical chanting (instituted by Charlemagne, who as Holy Roman Emperor, took measures in making the religion more accessible to the common folk. How do we make the Bible popular? By teaching rich people how to read! What a genius. <3 ). Thus, polyphony spread as Byzantine Christianity spread, which would later become Eastern Orthodoxy after the East-West Schism in the 11th century AD. (hence why polyphony is such a big cultural benchmark all Eastern Orthodox nations, including Russia and Georgia, but not Armenia until their annexation by the Russian Empire in the 19th Century AD (since Armenian Christianity is a cadet branch of Oriental Orthodoxy, which split from Catholicism in the 4th century AD). Anyway, Bulgaria historically played a massive role in spreading Christianity and its liturgical chanting to their pagan Balkan neighbours, after the Bulgarian Knyaz (a fancy way of saying “Khan”) Boris I converted under the pressure of Byzantine Emperor Michael III. Boris (whom, as you might have guessed, I was named after) used Christianity to pacify the squabbling lords of his realm (which included both pagans and Catholics) and oversaw the creation of the Glagolitic (liturgical) and Cyrrilic scripts to speed up the spread, paving the way for Bulgaria’s Golden Age under his son Simeon. During that Golden Age, btw, much of what is now Serbia came under Bulgarian control, including Belgrade. So while the Serbs probably did learn polyphony from the Bulgarians, the Bulgarians absolutely, totally, learned it from the Byzantines, who invented the damn’ thing, in their own spin on Charlemagne’s popular church choirs. Mum, you’re WRONG. O:-)

#Eurovision #Eurovision Song Contest #Eurovision 2018 #Serbia #Balkanika #Sanja Ilic #Nova Deca

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usviraltrends-blog · 7 years ago

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New Post has been published on https://usviraltrends.com/whats-your-risk-of-kidney-disease-heart-attack-or-diabetes-a-single-molecule-can-tell-science-15/

What’s your risk of kidney disease, heart attack, or diabetes? A single molecule can tell | Science

Nate Henry (right), Nick’s identical twin, is healthy. Nick’s high levels of a molecule called suPAR may explain his illness.

Kevin Beasley

By Stephen S. HallApr. 19, 2018 , 12:15 PM

Nick Henry first experienced the symptoms of kidney disease in 2004, shortly after the 19-year-old had a severe reaction to a spider bite. “I woke up one morning, and I was just swollen from head to toe,” he recalls. But doctors managed Henry’s disease, allowing him to return to his unusually active lifestyle—including baseball, softball, basketball, flag football, golf, and fishing—in his northeast Louisiana hometown of West Monroe. Shortly after he witnessed the death of his mother in a motor scooter accident in 2012, however, Henry’s renal health took a dramatic turn for the worse. “It’s almost as if my body went into shock,” he says. “Within a couple months, boom, I started swelling up again.”

That swelling was a sign that his kidneys were no longer working normally. A biopsy confirmed that he had focal segmental glomerulosclerosis (FSGS), a severe form of kidney disease. In FSGS, the kidney’s glomeruli—the microscopic filtration units that sieve excess fluid and waste products from the blood—become overly leaky; essential proteins such as albumin seep out, disrupting blood chemistry and causing fluid to leak from the blood vessels into tissues throughout the body. Henry’s condition deteriorated so rapidly that by July 2014, his doctors in Shreveport, Louisiana, decided to remove both diseased kidneys. The next month, Henry received a transplanted kidney from his identical twin, Nate, who was healthy, even though FSGS can be genetic in origin.

Within a day of the transplant, however, Henry felt like the swelling was coming back. At first, his doctors reassured him that he was doing fine. “Once they checked my urine, saw me spilling a bunch of protein again,” he says, “they realized [FSGS] was attacking the new kidney.” Three days after the surgery, Henry’s doctors conceded that the newly transplanted kidney had already become diseased. His transplant doctor, Neeraj Singh of Louisiana State University in Shreveport, says the recurrence was “one of the most dramatic cases I’ve seen.”

The sudden failure of Henry’s new kidney is a recent chapter in a long-running medical mystery, dating to when kidney transplants became routine in the 1970s. Up to 30% of transplanted kidneys fail in FSGS patients—not because of immune rejection by the body, as doctors first suspected, but because the new organ immediately begins succumbing to the same disease process that ravaged the original ones. As he struggled to cope with that devastating turn of events (and relied on dialysis to stay alive), Henry traveled to Chicago, Illinois, to consult with Jochen Reiser, a kidney disease specialist who is chairperson of internal medicine at Rush University Medical Center there.

Ever since he learned about such transplant failures 2 decades earlier, Reiser has been convinced that “there is something in the blood circulating that attacks the kidney. And we were out to catch that.” What he and colleagues claim to have “caught,” in an elegant but still unfolding story of molecular detective work over the past 10 years, is a protein known as soluble urokinase plasminogen activator receptor (suPAR). When Reiser analyzed blood samples from the Henry twins, the results aligned with the message he has been preaching with evangelical fervor for years. Nate, the healthy brother, had relatively low levels of suPAR; Nick’s were high—a driving force, Reiser believes, of his kidney failure.

Nick Henry had a kidney transplant, but his new organ quickly deteriorated, and he spends his nights on dialysis.

Kevin Beasley

Chronic kidney disease affects 14% of the U.S. population, with estimates suggesting nearly 600 million people affected worldwide. The disease steadily erodes the kidneys’ ability to filter the blood, often leading to cardiovascular disease and premature death. Kidney disease—which can directly attack the filtration process, as in FSGS, or damage the kidney’s support structure—is particularly insidious because by the time the first diagnostic signs appear, patients have irreversibly “burned off” much of their kidney function. Historically, the leading risk factors have been high blood pressure, diabetes, and African-American ancestry. (Several mutations associated with increased risk are more common in African-Americans.)

But research by Reiser and others has dramatically challenged that traditional picture of risk. If suPAR levels are low, people with the high-risk genes are no more likely to develop kidney disease than people without those gene variants, Reiser says. If suPAR levels are high, people are at greater risk of developing the disease regardless of whether they have the mutations.

Molecular studies in animals as well as a growing number of analyses of large human populations associating suPAR with kidney disease have bolstered his confidence—and convinced him the disease could be treated by suppressing suPAR. Some other researchers aren’t convinced, noting that several clinical studies found no clear association between suPAR levels and FSGS. But on both sides of the debate there is widespread fascination with suPAR, a ubiquitous, Zelig-like bystander molecule that, at elevated levels in the blood, seems to presage many health calamities, such as heart attacks, diabetes, and premature death. Whatever suPAR’s precise role in kidney disease, the molecule appears to be a potent signal broadcast by an immune system under siege. It is exquisitely sensitive to inflammation, an accelerant for many diseases.

“What is inflammation?” asks biochemist Jesper Eugen-Olsen of the University of Copenhagen, a pioneer in suPAR research. “It’s the language of cells. It’s how cells communicate with each other. When something is going wrong, the immune system is activated. It produces suPAR … and suPAR is a voice that just shouts, ‘Get on with it! Something is going on!’”

A brash style

In neither background nor appearance does Reiser conform with the public image of the director of a major metropolitan medical center. His 10th floor office at Rush sits just behind a corridor lined with photographs of hospital administrators going back to the 19th century—stern-faced, all-knowing medical patriarchs. Inside, Reiser, 46, sports a stylish striped blue suit, fashionably stubby beard, red socks, and slick dark hair. Known among colleagues as ambitious and scientifically gregarious, he has been eager to collaborate with anyone interested in exploring suPAR biology, and his brash, full-on style extends to the conspicuous display of large-format books celebrating the history of Aston Martins (he owns one) and Porsches on the coffee table in his office. Describing the speed of data collection for a paper that several years ago ended up in The New England Journal of Medicine (NEJM), he says, “It was like going from zero to 200 in no time,” adding sheepishly, “Car analogy.”

Born and raised in the small German village of Remchingen, on the eastern edge of the Black Forest, Reiser got his medical degree and Ph.D. from Heidelberg University and did an overseas residency at Albert Einstein College of Medicine in New York City. Specializing in kidney disease, he went on to conduct research at Harvard Medical School in Boston and became chief of nephrology at the University of Miami Leonard M. Miller School of Medicine in Florida before being hired by Rush in 2012.

Reiser’s arrival in the United States in 1999 coincided with renewed interest in solving the mystery of why up to 30% of FSGS patients who receive transplants see the disease recur in the new kidney. Just 3 years earlier, a group headed by Flavio Vincenti, a transplant specialist at the University of California, San Francisco (UCSF), and Virginia Savin, at the Medical College of Wisconsin in Milwaukee, announced a major clue. They reported in NEJM that they had amassed evidence for an FSGS-promoting factor in the blood of transplant recipients who’d experienced recurrences; they couldn’t isolate the exact protein, but when colleagues later injected an extract of such patients’ blood into rodents, the animals’ kidneys became permeable and spilled protein in the urine. That mysterious “permeability factor” became “the holy grail” of the field, according to Sanja Sever, a molecular biologist who studies kidney disease at Massachusetts General Hospital in Boston.

While still in Germany, Reiser had trained his research efforts on a unique renal cell called the podocyte (so named because of its amoebic, faintly footlike extensions). That choice turned out to be fortunate. The kidney has about 1 million glomeruli, and in each one, hundreds of podocytes bridge the gap between the bloodstream and the urinary system. Their footlike extensions wrap around capillaries snaking through the kidneys and, along with two other layers of tissue, form a physical mesh of cells, like a three-ply screen door, that allows only small molecules—sodium ions, potassium ions, and metabolic wastes—to pass into the urinary tract. When the podocytes become damaged, however, they essentially lose their architectural integrity. The kidney filters then become leaky, allowing larger essential proteins such as albumin to escape from the blood and pass into the urine.

It’s like a coffee filter, Sever says. “If there are holes in your filter, then you get some coffee grounds in your urine.” Podocyte damage can be reversed early in kidney disease. But, she says, “If you keep losing them, there’s a point of no return. … You are basically walking toward end-stage renal disease.”

An organ under attack

In one scenario for a severe form of kidney disease, a blood-borne molecule called soluble urokinase plasminogen activator receptor (suPAR) disrupts the organ’s filtration units, or glomeruli, which remove waste and fluid from the bloodstream. Other molecules may intensify this attack.

A dangerous immune responseAnimal models suggest immature immune cells in the bone marrow release more suPAR when an organism is under attack. The molecule, an all-purpose marker of ill health, may be directly toxic to the kidney.A HEALTHY FILTERIn each glomerulus, the footlike extensions of cells called podocytes wrap around capillaries, fitting together tightly to create narrow “slit diaphragms.” The slits form a fine mesh that allows only small molecules to escape from the bloodstream into the urine.KIDNEY DISEASEKidneyGlomerulusFunctional unit of kidneyPodocyteGlomerular basement membraneEndothelial cellsuPARsuPARMonocyteImmature myeloid cellNeutrophilPodocyte lost to urinary spaceSlit diaphragmCapillary Albumin leakageBone marrow

What causes such damage? Reiser suspected that the mysterious blood-borne factor disrupts podocytes through receptor molecules on their cell surface. He focused on one: β3-integrin, a molecule whose activation perturbs the shape and motility of cells. When he looked for the molecular key that turned the lock of the integrin receptor, he discovered that oncologists had already been working on one such protein, urokinase PAR (uPAR), a cell surface receptor that plays a role in cancer metastasis. Reiser became even more intrigued when he learned that uPAR can be cleaved from cell surfaces and circulate in the blood—at which point it becomes a soluble cousin known as suPAR. Maybe suPAR was the mysterious kidney-destroying factor.

In 2011, Reiser and colleagues reported in Nature Medicine that in cell culture, suPAR damaged human podocytes through the integrin pathway. The researchers supplemented that evidence with three mouse models showing that rodents with elevated levels of suPAR suffered kidney damage, although sometimes more slowly than in FSGS. With human clinical data suggesting that elevated suPAR levels correlated with the recurrence of FSGS in patients, a picture emerged in which the protein triggers a pathogenic process that ultimately produces holes in the coffee filter, leading to kidney disease.

The findings both electrified and polarized the nephrology community. In a commentary for Nature Medicine, Martin Pollak of Harvard Medical School, who studies the genetics of kidney disease, and nephrologist Stuart Shankland of the University of Washington in Seattle described the findings as “paradigm shifting for our understanding of the pathogenesis of FSGS.”

But some groups could not find the same clinical association between suPAR levels and recurrent disease in FSGS patients, and other groups questioned the protocol and interpretation of the animal models. And regardless of whether suPAR actually destroys the kidney, many nephrologists thought its levels were not very informative—by the time those specialists saw patients with kidney disease, suPAR levels were already high and offered no prognostic value. With Reiser claiming to have found the “holy grail” even as several groups were reporting discordant results, says one source, “People felt very emotional.”

An omen of ill-health

By that point, another key strand of the suPAR story had emerged in Europe. There, the focus was on the molecule as a potential biomarker for a range of diseases.

The first clues came from AIDS patients. In Copenhagen, Eugen-Olsen and others examined blood collected from more than 300 HIV patients in the early 1990s, before life-saving antiretroviral therapies became available. All those patients had died, but a retrospective analysis showed their suPAR levels eerily correlated with disease progression: Higher levels were associated with an earlier death. Eugen-Olsen then spent several years collaborating with a hospital in the West African nation of Guinea-Bissau, testing suPAR levels in patients suspected of being HIV-infected. Again, higher suPAR levels predicted a quicker death among the infected. Surprisingly, however, suPAR also predicted mortality in patients who didn’t have AIDS; many turned out to have tuberculosis. That finding led him to hypothesize that suPAR might be a more general biomarker for chronic inflammation.

In 2001, Eugen-Olsen founded the company ViroGates, which began to manufacture a relatively inexpensive test to measure suPAR levels in the blood. With the test in hand, he and colleagues in Copenhagen began to look at collections of blood samples banked in large-cohort prospective studies. In one called MONICA, which monitored healthy members of the Danish population for about 13 years, elevated levels of suPAR were associated with a higher risk of cardiovascular disease, type 2 diabetes, cancer, and premature death. Two other large European populations, enrolled in the Malmo Diet and Cancer Study and the Danish Inter99 Study, showed similar associations.

The findings caught the attention of researchers at Emory University School of Medicine in Atlanta who had been looking for new and better biomarkers to predict risk of adverse cardiac events in people with heart disease. The researchers had built the Emory Cardiovascular Biobank with serum from several thousand patients. “We draw blood, and we follow them for years,” says Salim Hayek, a physician and research fellow at Emory. When two of Hayek’s colleagues, Danny Eapen and Arshed Quyyumi, delved into the biobank, they found that higher suPAR levels predicted heart attacks and death, as they reported in the Journal of the American Heart Association in 2014. (At the annual meeting of the American College of Cardiology last month, Hayek presented further evidence from the Emory group, suggesting that suPAR is a better predictor of cardiac events including heart attacks and death than any other biomarker in widespread clinical use.)

Jochen Reiser has spent years amassing evidence that suPAR mounts a powerful assault on the kidney.

Rush Production Group

In addition to serving as an omen of ill health, suPAR seems to be a remarkably sensitive indicator of lifestyle insults. Studies have shown that the protein’s blood levels typically rise with obesity and with smoking. (Eugen-Olsen, an inveterate smoker, confesses that he quits when his suPAR levels rise and resumes when they subside again.) “Just looking at the data,” Hayek says, “clearly the environment is a much larger contributor to suPAR than genetics.”

With its links to multiple diseases and environmental stresses, suPAR appears to sit at the nexus of immune signaling, chronic inflammation, and tissue damage. Among the protein’s normal sources are fat cells, immune cells, and endothelial cells, which produce low baseline levels. But a team led by Reiser and David Scadden of the Harvard Stem Cell Institute showed in 2017 that in mice, immature “stemlike” cells in the bone marrow can release a pulse of suPAR when the immune system detects an attack.

Reiser believes suPAR is an ancient and unspecific way for the immune system to send urgent signals to the major organ systems when an organism faces a severe challenge from disease or the environment. Kidney damage, he says, is the long-term cost of that vital signaling mechanism. “As one example,” he says, “you get infected, you release more suPAR, you open your kidneys up, and you can dump the big molecules out into the urine. Almost like a primitive coupling of the immune system to vital organs.” In an acute infection, he says, the body urgently needs to flush out bacterial toxins, relatively big molecules. But if that inflammatory signaling becomes chronic, it takes its toll on kidney function—a trade-off that may have been acceptable earlier in human history, Reiser suggests, but is less so now. “If you live 40 years long, you can burn off the kidney this way, no problem,” he says. “If you live to be 80, 90, 100, you might burn off your kidneys too soon.”

For Reiser, the Emory cardiac biobank offered a chance to put to rest the notion that high levels of suPAR are simply a nonspecific sign of failing kidneys, not a cause. When he saw the 2014 heart risk paper from the Emory group, he had the obvious question: Could the large databank show whether suPAR levels predicted the onset of kidney disease years later? He immediately fired off an email to Hayek.

The Emory-based group quickly agreed to conduct follow-up renal examinations in more than 1300 patients who had no evidence of kidney dysfunction when they enrolled. The team found a strong link between high suPAR levels and the later development of kidney disease. For patients with the highest levels of suPAR, the risk was three times that of patients in the lowest group, and suPAR levels could predict kidney disease up to 5 years before the first symptoms appeared. “The effect was huge,” Hayek recalls.

The association was so robust, he says, that when the group first submitted its findings for publication, “the first response we got from [NEJM] was: ‘How is that association so strong? Is that real? Something is wrong with your cohort.’” But after Hayek and Reiser found the same association in a second, unrelated cohort—the Women’s Interagency HIV Study—NEJM published their findings in 2015. “In that paper,” Reiser says, “we could show that suPAR is the strongest risk factor known in healthy people for new chronic kidney disease. Even stronger than hypertension, diabetes, black race—all of these risk factors that are known to be strong. When you adjust for those, suPAR had the strongest risk.”

In the latest piece of evidence, published last summer in Nature Medicine, Reiser collaborated with researchers at the African American Study of Kidney Disease and Hypertension, based at Johns Hopkins University School of Medicine in Baltimore, Maryland, to compare the influence of suPAR and two gene mutations known to predispose African-Americans to kidney disease. A study of about 600 participants revealed that if suPAR levels remain low, “no notable differences” in kidney dysfunction were apparent between people who had the high-risk “disease genes” and people who did not. Conversely, high levels of suPAR strongly predicted kidney disease in African-Americans, regardless of whether the individual had the genetic variants.

The proof is the cure

Yet nephrologists are still divided about whether suPAR actually attacks the kidneys—and if so, how aggressively. Doubters point to the conflicting clinical results and the slow progress of kidney damage in Reiser’s mice with elevated suPAR levels. The original 2011 animal and clinical data are “as complete as you can get,” Vincenti says. “But at some point, there has to be independent duplication of that data.”

Several unresolved issues might explain the discrepancies. Different forms of suPAR can circulate in the blood, and some variants might be more pathogenic than whole suPAR. And a team led by Minnie Sarwal of UCSF, Dany Anglicheau of Necker Hospital in Paris, and Reiser has shown that in FSGS, a second blood-borne factor, an anti-CD40 autoantibody, works with suPAR to attack podocytes. “Everyone agrees it’s more complicated” than the initial findings in 2011 suggested, Reiser concedes. “But meanwhile, the data gets stronger and stronger that suPAR is the worst toxin you can have for the kidneys.”

The data gets stronger and stronger that suPAR is the worst toxin you can have for the kidneys.

Jochen Reiser, Rush University Medical Center

The controversy may not be resolved to everyone’s satisfaction until a human trial indisputably shows that removing suPAR cures or slows the progression of kidney disease. Several groups are trying to develop a monoclonal antibody drug that would remove suPAR from the blood. One such group is Trisaq, a company Reiser and Sever founded in 2011. Vincenti said his group also has developed monoclonal antibodies to suPAR for clinical testing. “I was excited to try it in patients,” he says. “But we could not demonstrate, at least in our samples, that suPAR was a biomarker for either FSGS or recurrent FSGS. [That’s] held it back.”

The first human proof may come not from a drug, but from a medical device. Miltenyi Biotec, a company in Bergisch Gladbach, Germany, makes apheresis devices, which remove substances from plasma, and it is developing a technology that would selectively scrub suPAR out of patients’ blood. “The key question,” notes CEO Stefan Miltenyi, “is if suPAR is the cause [of] renal diseases or just a bystander molecule.” Miltenyi hopes to launch a clinical trial in 2019.

For FSGS patients such as Henry, who relies on 8-hour overnight sessions of dialysis to stay alive, a breakthrough therapy can’t come soon enough. But suPAR is already beginning to influence clinical decisions. Singh, Henry’s transplant physician, has used suPAR levels to manage the care of several kidney patients. And since 2013, every patient arriving at the emergency department at Copenhagen University Hospital Hvidovre has undergone suPAR testing to help physicians make triage and discharge decisions.

Reiser often likens suPAR to cholesterol—a key marker and disease-associated molecule that can be monitored and, perhaps, ultimately controlled. But the main lesson of suPAR, he believes, is cautionary in an age of genomics and personalized medicine. Although a huge amount of attention (and government coin) has been devoted to identifying genes associated with disease, the environment can sometimes trump them. “I think that the gene adds to the risk profile—it’s part of the picture,” he concedes. “But the environment is a way-underestimated modifier that becomes way more important, quite frankly, than the underlying gene event. And this is … a beautiful illustration of exactly that principle.”

#Science

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usviraltrends-blog · 7 years ago

Photo

New Post has been published on https://usviraltrends.com/whats-your-risk-of-kidney-disease-heart-attack-or-diabetes-a-single-molecule-can-tell-science-11/

What’s your risk of kidney disease, heart attack, or diabetes? A single molecule can tell | Science

Nate Henry (right), Nick’s identical twin, is healthy. Nick’s high levels of a molecule called suPAR may explain his illness.

Kevin Beasley

By Stephen S. HallApr. 19, 2018 , 12:15 PM

Nick Henry had a kidney transplant, but his new organ quickly deteriorated, and he spends his nights on dialysis.

Kevin Beasley

A brash style

An organ under attack

An omen of ill-health

By that point, another key strand of the suPAR story had emerged in Europe. There, the focus was on the molecule as a potential biomarker for a range of diseases.

Jochen Reiser has spent years amassing evidence that suPAR mounts a powerful assault on the kidney.

Rush Production Group

The proof is the cure

The data gets stronger and stronger that suPAR is the worst toxin you can have for the kidneys.

Jochen Reiser, Rush University Medical Center

#Science

0 notes

usviraltrends-blog · 7 years ago

Photo

New Post has been published on https://usviraltrends.com/whats-your-risk-of-kidney-disease-heart-attack-or-diabetes-a-single-molecule-can-tell-science-8/

What’s your risk of kidney disease, heart attack, or diabetes? A single molecule can tell | Science

Nate Henry (right), Nick’s identical twin, is healthy. Nick’s high levels of a molecule called suPAR may explain his illness.

Kevin Beasley

By Stephen S. HallApr. 19, 2018 , 12:15 PM

Nick Henry had a kidney transplant, but his new organ quickly deteriorated, and he spends his nights on dialysis.

Kevin Beasley

A brash style

An organ under attack

An omen of ill-health

By that point, another key strand of the suPAR story had emerged in Europe. There, the focus was on the molecule as a potential biomarker for a range of diseases.

Jochen Reiser has spent years amassing evidence that suPAR mounts a powerful assault on the kidney.

Rush Production Group

The proof is the cure

The data gets stronger and stronger that suPAR is the worst toxin you can have for the kidneys.

Jochen Reiser, Rush University Medical Center

#Science

0 notes

usviraltrends-blog · 7 years ago

Photo

New Post has been published on https://usviraltrends.com/whats-your-risk-of-kidney-disease-heart-attack-or-diabetes-a-single-molecule-can-tell-science-7/

What’s your risk of kidney disease, heart attack, or diabetes? A single molecule can tell | Science

Nate Henry (right), Nick’s identical twin, is healthy. Nick’s high levels of a molecule called suPAR may explain his illness.

Kevin Beasley

By Stephen S. HallApr. 19, 2018 , 12:15 PM

Nick Henry had a kidney transplant, but his new organ quickly deteriorated, and he spends his nights on dialysis.

Kevin Beasley

A brash style

An organ under attack

An omen of ill-health

By that point, another key strand of the suPAR story had emerged in Europe. There, the focus was on the molecule as a potential biomarker for a range of diseases.

Jochen Reiser has spent years amassing evidence that suPAR mounts a powerful assault on the kidney.

Rush Production Group

The proof is the cure

The data gets stronger and stronger that suPAR is the worst toxin you can have for the kidneys.

Jochen Reiser, Rush University Medical Center

#Science

0 notes

usviraltrends-blog · 7 years ago

Photo

New Post has been published on https://usviraltrends.com/whats-your-risk-of-kidney-disease-heart-attack-or-diabetes-a-single-molecule-can-tell-science-6/

What’s your risk of kidney disease, heart attack, or diabetes? A single molecule can tell | Science

Nate Henry (right), Nick’s identical twin, is healthy. Nick’s high levels of a molecule called suPAR may explain his illness.

Kevin Beasley

By Stephen S. HallApr. 19, 2018 , 12:15 PM

Nick Henry had a kidney transplant, but his new organ quickly deteriorated, and he spends his nights on dialysis.

Kevin Beasley

A brash style

An organ under attack

An omen of ill-health

By that point, another key strand of the suPAR story had emerged in Europe. There, the focus was on the molecule as a potential biomarker for a range of diseases.

Jochen Reiser has spent years amassing evidence that suPAR mounts a powerful assault on the kidney.

Rush Production Group

The proof is the cure

The data gets stronger and stronger that suPAR is the worst toxin you can have for the kidneys.

Jochen Reiser, Rush University Medical Center

#Science

0 notes

usviraltrends-blog · 7 years ago

Photo

New Post has been published on https://usviraltrends.com/whats-your-risk-of-kidney-disease-heart-attack-or-diabetes-a-single-molecule-can-tell-science-5/

What’s your risk of kidney disease, heart attack, or diabetes? A single molecule can tell | Science

Nate Henry (right), Nick’s identical twin, is healthy. Nick’s high levels of a molecule called suPAR may explain his illness.

Kevin Beasley

By Stephen S. HallApr. 19, 2018 , 12:15 PM

Nick Henry had a kidney transplant, but his new organ quickly deteriorated, and he spends his nights on dialysis.

Kevin Beasley

A brash style

An organ under attack

An omen of ill-health

By that point, another key strand of the suPAR story had emerged in Europe. There, the focus was on the molecule as a potential biomarker for a range of diseases.

Jochen Reiser has spent years amassing evidence that suPAR mounts a powerful assault on the kidney.

Rush Production Group

The proof is the cure

The data gets stronger and stronger that suPAR is the worst toxin you can have for the kidneys.

Jochen Reiser, Rush University Medical Center

#Science

0 notes

usviraltrends-blog · 7 years ago

Photo

New Post has been published on https://usviraltrends.com/whats-your-risk-of-kidney-disease-heart-attack-or-diabetes-a-single-molecule-can-tell-science-4/

What’s your risk of kidney disease, heart attack, or diabetes? A single molecule can tell | Science

Nate Henry (right), Nick’s identical twin, is healthy. Nick’s high levels of a molecule called suPAR may explain his illness.

Kevin Beasley

By Stephen S. HallApr. 19, 2018 , 12:15 PM

Nick Henry had a kidney transplant, but his new organ quickly deteriorated, and he spends his nights on dialysis.

Kevin Beasley

A brash style

An organ under attack

An omen of ill-health

By that point, another key strand of the suPAR story had emerged in Europe. There, the focus was on the molecule as a potential biomarker for a range of diseases.

Jochen Reiser has spent years amassing evidence that suPAR mounts a powerful assault on the kidney.

Rush Production Group

The proof is the cure

The data gets stronger and stronger that suPAR is the worst toxin you can have for the kidneys.

Jochen Reiser, Rush University Medical Center

#Science

0 notes

usviraltrends-blog · 7 years ago

Photo

New Post has been published on https://usviraltrends.com/whats-your-risk-of-kidney-disease-heart-attack-or-diabetes-a-single-molecule-can-tell-science-3/

What’s your risk of kidney disease, heart attack, or diabetes? A single molecule can tell | Science

Nate Henry (right), Nick’s identical twin, is healthy. Nick’s high levels of a molecule called suPAR may explain his illness.

Kevin Beasley

By Stephen S. HallApr. 19, 2018 , 12:15 PM

Nick Henry had a kidney transplant, but his new organ quickly deteriorated, and he spends his nights on dialysis.

Kevin Beasley

A brash style

An organ under attack

An omen of ill-health

By that point, another key strand of the suPAR story had emerged in Europe. There, the focus was on the molecule as a potential biomarker for a range of diseases.

Jochen Reiser has spent years amassing evidence that suPAR mounts a powerful assault on the kidney.

Rush Production Group

The proof is the cure

The data gets stronger and stronger that suPAR is the worst toxin you can have for the kidneys.

Jochen Reiser, Rush University Medical Center

#Science

0 notes

usviraltrends-blog · 7 years ago

Photo

New Post has been published on https://usviraltrends.com/whats-your-risk-of-kidney-disease-heart-attack-or-diabetes-a-single-molecule-can-tell-science-2/

What’s your risk of kidney disease, heart attack, or diabetes? A single molecule can tell | Science

Nate Henry (right), Nick’s identical twin, is healthy. Nick’s high levels of a molecule called suPAR may explain his illness.

Kevin Beasley

By Stephen S. HallApr. 19, 2018 , 12:15 PM

Nick Henry had a kidney transplant, but his new organ quickly deteriorated, and he spends his nights on dialysis.

Kevin Beasley

A brash style

An organ under attack

An omen of ill-health

By that point, another key strand of the suPAR story had emerged in Europe. There, the focus was on the molecule as a potential biomarker for a range of diseases.

Jochen Reiser has spent years amassing evidence that suPAR mounts a powerful assault on the kidney.

Rush Production Group

The proof is the cure

The data gets stronger and stronger that suPAR is the worst toxin you can have for the kidneys.

Jochen Reiser, Rush University Medical Center

#Science

0 notes