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      "author": "cheetah",
      "body": "Hi! I am a robot. I just upvoted you! I found similar content that readers might be interested in:\nhttps://steemit.com/cryptocurrency/@simonsayz/don-t-miss-this-new-altcoin-exchange-arriving-shortly-low-fees-and-a-great-team",
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      "author": "dfv219",
      "body": "<html>\n<p><img src=\"https://steemitimages.com/0x0/https://steemitimages.com/DQmbwKb2fP67edBBXrL2VA96AnvpaB5Yr4RnHvZVrqEt5rG/altcoinexchange_steemit_simonsayz.png\" width=\"1680\" height=\"614\"/></p>\n<p>&nbsp;Hi Steemian's</p>\n<p>I'm not one to normally post referral links (other than in my signatures), but this new exchange looks like is has the goods! I personally use Bittrex. This new site hasn't launched yet, but you can register your email and be the first to know. I think this is going to be a great platform as the team behind it have a lot of experience and have built it for all skill sets of traders from novice through to expert, I will be interested to view their roadmap and find out what tools they have on the site when it launches.</p>\n<p>Anyway as always , do your own due diligence and do not treat this as financial advice.</p>\n<p>In addition to launching soon , it will only apparently have 0.1% fees!!!</p>\n<p><a href=\"http://www.altcoinexchange.com?kid=H4NAJ\"><strong>Join Here</strong></a><br>\nSign up here today: <a href=\"http://www.altcoinexchange.com?kid=H4NAJ\">http://www.altcoinexchange.com/</a></p>\n<p><strong>Why ACE?</strong><br>\nOne of the highlights of the team for me is that they have Andrew Gazdecki onboard.</p>\n<p>He comes from a technical background with experience building scalable software platforms. In 2017, he was awarded Inc. Magazine's 30 Under 30. I suggest you do some research into his businesses, I truely believe he will help make this exchange the \"big\" go to Exchange for the future. : source: <a href=\"http://www.altcoinexchange.com?kid=H4NAJ\">http://www.altcoinexchange.com/</a></p>\n<p>Check out the rest of their team on the link I have provided, I believe you too will be impressed, it will be great to have faces and know who is behind the exchanges we deal with!</p>\n<p><strong>Here is a copy of their Company Mission</strong>&nbsp;</p>\n<p><img src=\"https://steemitimages.com/0x0/https://steemitimages.com/DQmZaHfn2WqrDsVwLPyMXjZzzEGfEikNJ1cvwsXe3Yh1DAE/altcoinexchange_company_mission_steemit_simonsayz.png\" width=\"1680\" height=\"632\"/></p>\n<p>&nbsp;source of information and images: <a href=\"http://www.altcoinexchange.com?kid=H4NAJ\">http://www.altcoinexchange.com/</a></p>\n<p>&nbsp;Until next time, happy speculating!&nbsp;</p>\n<p><br></p>\n</html>",
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      "body": "![](https://steemitimages.com/DQmQGG7PULc5CqomwFor2vxvEd2qpSp4iaNgy2UcoieHYh9/image.png)\nMaking breakfast your main meal and skipping snack time helps avoid weight gain, study shows.\n\nEating a good breakfast and letting go of your snacking habits may provide the key to leading a healthier life and preventing weight gain, a new study shows.\nUnhealthy weight gain is a problem that many Americans have to tackle and which state-led programs promoting wholesome dietary habits seek to prevent. According to the Centers for Disease Control and Prevention (CDC), [36.5 percent](https://www.cdc.gov/obesity/data/adult.html)\nof adults, and around [17 percent](https://www.cdc.gov/obesity/data/childhood.html) of children in the United States live with obesity.\n\nExcess weight also puts people at an [increased risk](https://www.cdc.gov/obesity/data/adult.html) of developing serious conditions or diseases, including [heart disease,](http://www.medicalnewstoday.com/articles/237191.php) type 2 [diabetes,](http://www.medicalnewstoday.com/info/diabetes/type2diabetes.php)\nand some types of [cancer.](http://www.medicalnewstoday.com/info/cancer-oncology/)\n\n\nResearch into [nutrition,](http://www.medicalnewstoday.com/articles/160774.php) healthy eating habits, and how our diet impacts our day-to-day lives is conducted on a regular basis, with new discoveries being reported all the time. For instance, an analysis recently covered by Medical News Today suggests that some [biomarkers](http://www.medicalnewstoday.com/articles/318335.php) could predict the effectiveness of weight loss diets.\n\nA new study on the link between the impact of meals and their frequency to weight gain has now been conducted by Dr. Hana Kahleova, from the Loma Linda University School of Public Health (LLUSPH), in California. She collaborated with colleagues from her own institution, as well as from the Institute for Clinical and Experimental Medicine and the Institute of Endocrinology, both based in Prague, Czech Republic.\n\nTheir [results](http://jn.nutrition.org/content/early/2017/07/12/jn.116.244749.abstract?sid=39dc4717-c136-41ed-be77-4d617b43852d) were published in The Journal of Nutrition, and they were co-written by Prof. Gary Fraser, from LLUSPH. Dr. Kahleova will present the findings at the International [Conference](https://www.pcrm.org/icnm2017)\non Nutrition in Medicine, in Washington, D.C., on July 29.\n\n# Participants with peculiar eating habits\nResearchers worked with participants from the [Adventist Health Study-2](http://publichealth.llu.edu/adventist-health-studies/about) (AHS-2), an endeavor monitoring the health lives of 96,000 Seventh-day Adventists from the U.S. and Canada.\n\nThe AHS-2 considers that the Adventist population is situated at a lower risk of developing conditions and diseases such as [hypertension,](http://www.medicalnewstoday.com/articles/150109.php)\nheart disease, cancer, or [diabetes.](http://www.medicalnewstoday.com/info/diabetes/)\nThis, researchers suggest, may be thanks to their specific eating habits.\n\nLed by Dr. Kahleova, the study included 50,660 adult individuals from this population, all aged 30 or older. The focus was on the possible link between when and how often people eat, and their body mass index [(BMI).](http://www.medicalnewstoday.com/info/obesity/what-is-bmi.php)\n\n\nThe participants had various body types and sizes, the researchers specify, and their eating habits and health outcomes were monitored for an average period of 7 years.\n\nAt the outset, the participants were asked to fill in a questionnaire, detailing their medical history, eating practices, physical activity, and other relevant information. As the study went on, they filled in follow-up forms declaring any major health events. The final follow-up questionnaire reported how often participants had normally taken their meals, and at what times of the day.\n\n# Breakfast is good, dinner less so\nThe study had several main findings. In the first place, it showed that people who regularly ate only one or two meals per day had a decrease in BMI. Conversely, those who ate more than three meals a day increased their BMI, and the more meals they ate, including snacks, the greater the weight gain.\n\nThe researchers also found that people who had breakfast regularly tended to lose more weight than people who chose to skip breakfast.\n\n###### More importantly, the participants whose largest meal of the day was breakfast experienced a large BMI decrease, in contrast with those who made lunch or dinner their largest meal.\n\nAdditionally, the researchers found that skipping dinner altogether and having a long, 18 or 19-hour, overnight fast contributed to weight loss.\n\nOther good eating practices, the researchers observe, include leaving 5 or 6 hours between breakfast and lunch, and abstaining from snacks throughout the day.\n\nThese findings confirm what previous [studies](http://ajcn.nutrition.org/content/early/2014/06/04/ajcn.114.083402) conducted on smaller population samples also inferred. The importance of breakfast to our diet and its impact on our general health have long been appreciated, yet this is the first recent analysis to be conducted on such a large, unrestricted population sample.\n\n# Age affects BMI\nThe researchers also highlighted that there is a strong link between BMI and advancing age. According to them, participants younger than 60 tended to gain more weight, whereas those over 60 tended to experience a loss in BMI.\n\nIn this context, they note that people under 60 with more mindful dietary habits, who eat breakfast as their main meal, tend to avoid the weight gain that is to be expected in their age category.\n\n\"Before age 60 years, those eating [calories](http://www.medicalnewstoday.com/articles/245588.php)\nearlier in the day had less weight gain,\" says Prof. Fraser. \"Over decades, the total effect [of regularly eating a large breakfast] would be very important,\" he adds.\n\nAt the same time, the study observes that people over 60, who naturally lose more weight, will be similarly affected by this regime, which could lead to negative health outcomes in some cases.\n\nA clearer understanding of the impact that meal frequency and the importance that meals have on BMI levels could, therefore, help us make better, more informed decisions about our individual health and dietary needs.\n\nRead about the link between colorectal cancer and a [high-fat diet.](http://www.medicalnewstoday.com/articles/318301.php?bl)\n\n\n[Source](http://www.medicalnewstoday.com/articles/318448.php)",
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      "body": "![](https://steemitimages.com/DQmSxKAJ6cw8Hd5Vtt6ETpYSy4eATcGpDWkxy1uu4FAPyUr/image.png)\nA giant asteroid impact probably won’t wipe life off our planet.\n\nBy Giorgia GuglielmiJul. 14, 2017 , 5:00 AM\n\nA giant asteroid crashing into our planet would instantly kill off millions of animals. But the aftermath of such an impact would be even more disastrous: Tsunamis, earthquakes, and vast clouds of dust blocking out the sun would lead to crop failure and mass extinction.\nLink: http://www.sciencemag.org/news/2016/07/here-s-how-world-could-end-and-what-we-can-do-about-it\nSixty-five million years ago, just such an event killed off 75% of species on Earth. But to really wipe life off the planet, it would take an astrophysical event so powerful that Earth’s oceans would literally boil away, according to a new study. The heat and cosmic radiation would make Earth inhospitable even to tardigrades, among the hardiest organisms ever discovered.\n\n“They’ve taken a grand question—how resilient is life?—and turned [it] into a well-posed calculation, by focusing on the energy required to boil Earth’s oceans,” says Joshua Winn, an exoplanets expert at Princeton University, who was not involved in the study. “It’s an awful lot of energy.”\n\nResearchers first calculated the amount of energy it would take to bring all Earth’s water above 100°C: 6 x 1022 joules, about a hundred times more than total annual energy consumption by humans, or a trillion times the energy needed for the space shuttle to lift off. Translated into cataclysms, it would take the energy given off by the impact of an asteroid the size of Vesta or Pallas,\nLink: https://www.nature.com/articles/s41598-017-05796-x\namong the solar system’s biggest, they report today in Scientific Reports. Other options: exploding stars known as supernovae or gamma ray bursts, highly energetic explosions in outer space.\n\nBut none of these is very likely. Asteroids of the right size exist, but “they’re not heading in our direction,” says study author and astrophysicist Avi Loeb of Harvard University. And although the heat given off by a supernova could make all the water on Earth evaporate, such an explosion would have to be “just next door,” cosmically speaking. That’s 0.13 light-years away, or about 30 times nearer to our solar system than the closest supernova candidate. Finally, there’s almost zero chance that gamma ray bursts would happen at a distance capable of stripping Earth of its seas. “It really is pretty hard to sterilize a planet,” says Gregory Laughlin, an astronomer at Yale University who was not involved in the study.\n\nThe researchers turned to tardigrades—microscopic, water-dwelling creatures that can endure temperatures as cold as -272°C and as hot as 150°C—as the Earth animals most likely to survive when all others are dead. Tardigrades, also known as water bears, can live for days in the vacuum of outer space.\nLink: http://www.sciencemag.org/news/2008/09/water-bears-survive-earth-orbit\nThey can also withstand pressure up to six times that at the bottom of the ocean and levels of radiation thousands of times the lethal human dose, thanks to a yet-unknown mechanism that allows them to repair their DNA. But they wouldn’t be able to survive prolonged exposure to severe heat and cosmic radiation without water—or endless time in space.\n\nThe findings have implications for more than just earthlings. They could inform our search for creatures on alien worlds, says study author David Sloan, a cosmologist at the University of Oxford in the United Kingdom. “This really broadens the range of places where we should be looking for life.” That’s because the sturdiest organisms on Earth—not only tardigrades, but also microorganisms that thrive in extreme conditions\nLink: http://www.sciencemag.org/news/2016/10/alien-life-could-feed-cosmic-rays\n—may resist a wide range of catastrophes, including humanmade ones such as global warming or nuclear wars. “I have an optimistic view about life,” Loeb says. “It may be able to survive all the mistakes we’ll make in politics in the future.”\n\nPosted in: Earth\nDOI: 10.1126/science.aan7105\n\nSource:\nhttp://www.sciencemag.org/news/2017/07/what-it-would-take-kill-all-life-earth",
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      "body": "@dfv219\nNice Post!\nThanks for sharing this.",
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      "body": "Hi! I am a robot. I just upvoted you! I found similar content that readers might be interested in:\nhttp://www.chefkoch.de/rezepte/313001112708050/Clints-Chili-con-Carne.html",
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      "body": "![](https://steemitimages.com/DQmV4qZq8a81eC1TL3vvP6CEbn1MevExChHr4kme3bvxchH/image.png)\n\nZutaten\n\n1 \t         Gemüsezwiebel(n)\n1 \t         Paprikaschote(n), grüne\n1               Zehe/n Knoblauch\n4 EL        Öl\n500 g\tRinderhackfleisch\n4 \t        Tomate(n)\n1 Dose\tKidneybohnen, 250 g Abtropfgewicht\n1 Dose\tMais, 140 g Einwaage\n6 EL\tTomatenmark\n1 \t        Chilischote(n), rote scharfe, oder Peperonischote\n1 TL\tBasilikum\n1 TL\tCayennepfeffer\n1 TL\tZucker\n3 TL\tPaprikapulver, rosenscharf\n \t        Salz\n\n\nZubereitung\n\nArbeitszeit: ca. 10 Min. / Koch-/Backzeit: ca. 1 Std. / Schwierigkeitsgrad: simpel / Kalorien p. P.: ca. 666 kcal\n\nDie Zwiebel fein würfeln, die Knoblauchzehe fein hacken, die Paprikaschote und die Tomaten in Würfel schneiden. Die Kidneybohnen in ein Sieb geben und abspülen. Die Chilischote aufschneiden und die Kerne entfernen, anschließend in kleine Streifen schneiden. \n\nDas Öl in einer großen Pfanne oder einer Kasserolle heiß werden lassen und das Hackfleisch scharf anbraten, bis es grau und krümelig ist. Nun die zerkleinerte Zwiebel, Paprikaschote und Knoblauchzehe dazugeben und alles so lange braten, bis das Fleisch etwas angebräunt ist. Jetzt die Kidneybohnen, den Mais mit dem Maissaft aus der Dose, dem Tomatenmark, den gewürfelten Tomaten und etwas Wasser hinzufügen und bei mittlerer Wärmezufuhr zugedeckt etwa 20 Minuten weiter schmoren. \nAnschließend die Chilischote mit den anderen Gewürzen hinzufügen und alles unter ständigem Rühren etwa 10 Minuten offen köcheln lassen, bis die gewünschte Konsistenz erreicht ist. Das Chili mit Salz abschmecken und heiß servieren. \n\nDazu gibt es Weißbrot oder Ciabatta.\n\n\nQuelle: \nhttp://www.chefkoch.de/rezepte/313001112708050/Clints-Chili-con-Carne.html",
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      "body": "nice info thx",
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      "author": "cheetah",
      "body": "Hi! I am a robot. I just upvoted you! I found similar content that readers might be interested in:\nhttp://www.livebitcoinnews.com/promising-cryptocurrencies-buy-2017/",
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      "body": "The Most Promising Cryptocurrencies To Buy In 2017\n\nBy Dr Tamer Sameeh Published on  April 15, 2017 at 6:09 BST\n![](https://steemitimages.com/DQmUz8KgHp8ShwkcSsy2Ud3MMnLRLdDhCmcDfcNR2Y1QEHL/image.png)\n\nThe year 2017 kicked start with a booming bullish wave that pushed the price of bitcoin and many altcoins up to unprecedented levels. Bitcoin recorded its all time high a few weeks ago, as it exceeded the $1300 price level for the first time ever since the genesis block was mined. This rise in the market capital of bitcoin, ethereum, monero and others was fueled by uncertainty towards the fiat economy secondary to Trump’s winning of the US Presidential elections, Brexit and the unrest in the Middle East.\n\nThroughout this article, we will point out the most promising cryptocurrencies that have the potential to grow massively and hence, can represent good investment opportunities in 2017.\n\n \n\nEthereum:\nEthereum is a unique cryptocurrency that presents a distributed computing platform that features the “smart contract” functionality. Many crypto-enthusiasts think that ethereum is undervalued at the moment and others believe that its real value is even greater than that of bitcoin. Ethereum is by far the most promising coin to invest in this year. During the past couple of months, ethereum has been witnessing a bullish wave that led to more than %300 rise in its price in March. Even more, ethereum has recorded last March its all time high of $54. In my opinion, ethereum has the potential to be worth more than $100 by the end of this year.\n\n \n\nMonero:\nMonero is one of the most promising altcoins that will definitely witness enormous gains in 2017. Apart from most other cryptocurrencies, Monero’s transactions are anonymous, thanks to its CryptoNote protocol that relies on ring signatures. Similarly to ethereum, monero’s price spiked, recording more than 100% gains during the past few weeks. Interestingly enough, monero has also recorded, in the later half of last March, its all time high of $25. Monero has the potential to grow to over $50, especially after AlphaBay, one of the major darknet marketplace, has chosen to add monero as a payment method late in 2016. Oasis, another darknet marketplace, also started to accept monero payments, and more markets are expected to do so too, during 2017, which will take the price of monero to the moon.\n\n \n\nDASH:\nDASH currently represents the third biggest cryptocurrency by market capitalization. Similarly to monero, DASH’s transactions are anonymous via a unique coin mixing service known as “PrivateSend”.\n\nThe year started with a bullish wave that has been controlling DASH’s market since then.  The bullish  wave climaxed later in March by scoring DASH’s price all time high of around $116. DASH was the second cryptocurrency to be added as an accepted payment method on darknet’s marketplaces. It has the potential to grow to over $200 this year, especially that DASH is by far the cryptocurrency with highest anonymity levels.\n\n \n\nOther Coins:\nThere are other coins that hold great potential for growth in 2017. Augur is a promising altcoin as it is presenting a new concept for decentralized market predictions. STEEM also holds enormous potential as it is by far the most successful decentralized social network. MaidSafeCoin’s price can also skyrocket during the upcoming months as it is supporting a new concept of crowd-sourced internet. GameCredits also hold great potential for growth during 2017, especially that it is introducing a new concept for online gaming markets.\n\n\nSource:\nhttp://www.livebitcoinnews.com/promising-cryptocurrencies-buy-2017/",
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      "author": "cheetah",
      "body": "Hi! I am a robot. I just upvoted you! I found similar content that readers might be interested in:\nhttp://www.mantouchong.com/2017/07/a-stem-cell-transplant-helped-beat-back-a-young-doctors-cancer-now-its-assaulting-his-body/",
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      "author": "dfv219",
      "body": "By Jon CohenJul. 12, 2017 , 9:00 AM\n![](https://steemitimages.com/DQmSuY8S2cNtUGpvUDsf1rCMyqjpUBmJfR1w7gq6Tz2kXeg/image.png)\n\nST. LOUIS, MISSOURI—A few months before completing medical school in 2003, Lukas Wartman was diagnosed with acute lymphoblastic leukemia (ALL), a blood cancer that's particularly lethal when it strikes adults. So began a battle to stay alive that has involved more than 70 drugs, two rounds of cell transplants, and a staggering series of twists and turns.\n\nWartman immediately received aggressive chemotherapy, which drove the cancer into remission and enabled him to graduate from Washington University School of Medicine (WUSM) in St. Louis in Missouri. He then embarked on a career of clinical care and lab research focusing on leukemia, the disease that had almost killed him. But 5 years later, ALL returned.\n\nAnother round of chemotherapy again knocked the cancer back to undetectable levels. Doctors also used chemicals and radiation to obliterate his bone marrow, the source of all his blood cells—a crude but effective strategy to destroy any cancerous ones that survived chemotherapy. Then they infused him with a bone marrow transplant from his brother. Stem cells from his brother's marrow reconstituted his blood cells, including immune system cells, and within a year, Wartman was working full time and running regularly. \"I was almost back to my baseline,\" he says, as his runs gradually lengthened and his speed improved. But in 2011, \"all of a sudden I hit a wall.\" Leukemia had returned, and his prognosis was bleak. \"The outcomes with patients who relapse a second time with ALL are abysmal,\" he says.\n\nChemotherapy this time did nothing for his leukemia and almost killed him. But then a cutting-edge technique came to the rescue. A genetic analysis performed at WUSM's genome center, where Wartman worked, pinpointed a hyperactive gene, and a drug for advanced kidney cancer happened to inhibit the protein that gene produces. He went into remission for the third time. A front-page story in the 8 July 2012 issue of The New York Times on the promise of targeted cancer treatments highlighted the success. \"While no one can say that Dr. Wartman is cured, after facing certain death last fall, he is alive and doing well,\" the story said.\n\nConcerned that the drug by itself might not keep his aggressive cancer at bay, Wartman opted for a second transplant—this time with stem cells isolated from peripheral blood from an unrelated donor. He steadily regained his health and returned to seeing patients and working on leukemia experiments in mice. Daily walks with his two dogs again became part of his routine, as did a 6.5-kilometer Saturday run.\n\nToday, Wartman, now 39, remains in remission, but in the cruelest twist of all, he's struggling to survive the cure.\n\nA dearth of options\nSitting barefoot in the living room of the immaculately restored 1897 brick home he shares with his partner, Wartman unfolds a pair of socks. \"All right, let's see if I can put these on,\" he says. He slides one of them onto a curved piece of plastic called a Sock Aid that has two ropes attached, a device octogenarians commonly use. He slowly wiggles a sock onto each foot. He then lifts one leg and moves it atop a Nike running shoe. \"I can touch my ankle, but I can't reach my toes,\" he says, wedging his foot into the shoe with the help of a half-meter-long shoehorn.\n\nWartman has a chronic form of graft-versus-host disease (GVHD), a debilitating consequence of blood stem cell transplants. It occurs when immune system cells from the donor proliferate and attack the host's tissues. That immune attack inflamed and weakened Wartman's muscles so much that a fall in January cracked his skull. Necrosis of the blood vessels that feed his hips have caused one to collapse, leaving one leg several centimeters shorter, and he has a slow, limping gait. His eyes are so dry that he must put in drops every 20 minutes, and he has painful sores in his mouth. His skin has become leathery in some places. So far, GVHD has spared his organs, but it could damage his liver, lungs, gastrointestinal tract, and genitals. The steroids he takes to calm his transplanted immune system have bloated his face and put him at high risk of infection and osteoporosis.\n\n\n\n![](https://steemitimages.com/DQmWpcprPHj5ZNr5KqQ7PgXLMjCqfYigEBMX9EsKhYwTRG4/image.png)\nWartman in his lab in March 2011 (left), before he developed chronic graft-versus-host disease, and last month at a physical therapy session (right).\nPHOTOS: (LEFT TO RIGHT) LUKAS WARTMAN; WHITNEY CURTIS\n\nWartman's condition is severe but not unusual. GVHD affects up to half of the more than 30,000 people worldwide each year who receive an immune system transplanted from a donor, as either bone marrow or peripheral blood stem cells. The number of transplants—and cases of GVHD—are increasing, yet treatments have not kept pace. Steven Pavletic, who heads the Graft-versus-Host and Autoimmunity Section at the National Cancer Institute in Bethesda, Maryland, says the standard treatments—corticosteroids such as prednisone—\"carpet bomb\" the immune system, causing a host of side effects and weakening the immune response to potentially deadly infections.\n\nMajor recent advances in understanding GVHD's underlying biology, improved animal models, better targeting of interventions, and more systematic clinical trials are finally moving beyond \"accumulated sketchy information,\" Pavletic says. Still, no GVHD treatment has yet received regulatory approval, and with a limited market and a long history of failed clinical trials, drugmakers are leery of getting involved.\n\nThe urgency of his case has turned Wartman into one of the world's few patients who advocate for GVHD research, prevention, and treatment. \"Most people it affects suffer quietly,\" says Wartman, who has written journal articles and given presentations and media interviews about his condition. \"They're grateful they're alive, and they're beaten down. It's the paradox of being cured and dying of the cure. Even if you can get past that, you don't have the energy to advocate, and that's really tragic.\"\n\nImmunologic mayhem\nCell transplantation to treat leukemias began with bone marrow transplants in the 1950s and '60s. But those early attempts routinely failed because, unless the donor was an identical twin, the host's immune system attacked the foreign stem cells before they became established. Advances in immunology in the late '60s improved the ability to identify closely matched siblings who were not twins, expanding the pool of potential donors. That, coupled with improved management of GVHD and other complications, led success rates to climb dramatically by the mid-1970s.\n\nMore recently, physicians have learned how to harvest blood-forming stem cells from a donor's blood and transplant them into a patient, sidestepping the need for an operating room and a needle stick into the pelvis to extract bone marrow. New immunosuppressive drugs also have made it possible to transplant bone marrow or peripheral stem cells from a donor less closely matched to the host. And changes to the conditioning regimens that wipe out the host's cells have extended transplants to leukemic patients older than 55, who previously were excluded because they couldn't handle the toxic effects.\n\nAs a result, cell transplants have become more common and more successful. The Worldwide Network for Blood & Marrow Transplantation has documented a 57% jump in using cell transplants to treat otherwise highly lethal blood cancers from 2006 to 2012. Up to half of the cancer patients with intermediate level disease who received transplants survived longer than 3 years. Some 70% of transplants are now done with peripheral blood, even though that approach has a slightly higher risk of triggering GVHD. All told, those trends have increased the incidence of this medically created condition, which kills 15% to 20% of people who develop it.\n\nGVHD can occur in two stages. Within 100 days of the transplant, up to half of patients develop an \"angry\" skin rash, nausea, vomiting, diarrhea, and liver abnormalities. That acute phase begins with the conditioning regimen, which damages tissue, leading to a storm of immune messengers called cytokines; trauma to the gut causes extra problems as it leaks bacteria into the bloodstream. In response, the graft's T cells, the pit bulls of the immune system, go haywire. The cytokines speed up T cell cloning and knock down regulatory T cells, which put the brakes on the cloning process. Antigen-presenting cells add to the mayhem by displaying pieces of host antigens and bacteria from the gut to the T cells, further driving their expansion.\n\nAcute GVHD is \"entirely a T cell–mediated disease, most people would agree,\" says Paul Martin, an oncologist and transplant veteran at the Fred Hutchinson Cancer Research Center (the Hutch) in Seattle, Washington. Those battalions of cells bombard tissues that make up the gut, liver, and skin, attacking them as \"foreign.\"\n\nIn about one-third of cases, immunosuppressive treatment resolves the acute phase of GVHD within 45 days, while the body's normal checks and balances eliminate the T cells doing the damage, leaving populations that \"tolerate\" the new host. That's what happened with Wartman when he received his brother's bone marrow. But, as occurred with his second transplant, acute GVHD symptoms can morph into the chronic form of the disease. (About one-third of people who develop chronic GVHD never go through an acute phase.)\n\n![](https://steemitimages.com/DQmUQKdMTGcywtq7j9SNVYusQD5PhBfUSuzoaDXMn8t9pi5/image.png)\n\nThe biology of chronic GVHD remains murky. On top of the T cell abnormalities, chronic GVHD involves antibody-producing B cells and scavenger cells called macrophages. Accumulating evidence suggests that, like T cells, donor B cells are over-produced, pumping out high levels of antibodies that can attack the body's own tissues. Separately, the high levels of a type of T cell called Th17 cells secrete gobs of interleukin-17 (IL-17), expanding macrophage populations. The antibodies also make matters worse by attaching to receptors on the macrophages, which in response spit out transforming growth factor β, an immune messenger that activates collagen-producing fibroblasts, leading to fibrosis of tissues.\n\nResearchers trying to tamp down GVHD have to deal with a major complication: Some graft-versus-host response is good. Convincing evidence for that came in 1979 from a team at the Hutch led by E. Donnall Thomas, who later won the Nobel Prize in Physiology or Medicine for his pioneering work. His Hutch team found that leukemia patients who received bone marrow transplants from an identical twin had far higher relapse rates than people who used a closely matched, but not identical, sibling. The reason is that some cancer cells remain even after the strongest conditioning, and the graft's attack on the host can mop up the stragglers.\n\nThe need to preserve some graft-versus-leukemia (GVL) effect has hampered attempts to fight chronic GVHD. \"If you're aggressive against the complication, you compromise the therapeutic effect of the transplant,\" Pavletic says. \"That's been the core challenge from the beginning, and it's still a core challenge today.\"\n\nStruggling for balance\nAlong with steroids, the mainstay of GVHD treatment today is drugs that turn down the production of IL-2, a cytokine that helps T cell populations expand and diversify. Wartman stabilized his GVHD with high doses of prednisone and the IL-2–dampening drug tacrolimus, but that wasn't enough suppression to resolve his symptoms. And because GVL depends on T cells, oncologists hesitate to suppress them completely. \"There's a price to pay if you prevent too much,\" says Leo Luznik, an oncologist and hematologist at Johns Hopkins University School of Medicine in Baltimore, Maryland, \"and unfortunately we don't have a thermostat that we can turn up or down\" to get the T cell suppression right.\n\nLuznik and colleagues have sought the right balance by giving high doses of cyclophosphamide, a chemotherapy drug with immunosuppressive effects, shortly after transplantation. That approach, which shuts down the hyperactive donor T cells when they first arrive, has not only allowed patients to tolerate grafts from increasingly mismatched hosts but, in several recent studies, has also cut rates of severe acute and chronic GVHD to less than 15%. Although some researchers worry about increased risk of relapse, the treatment has steadily won over skeptics.\n\nAnother approach to taming the donor graft relies on a mixture of anti–T cell anti-bodies called antithymocyte globulin, which is produced in horses or rabbits. Given to the patient shortly before the transplant, the infusion of antibodies theoretically reduces the host's residual T cells, minimizing the risk of graft rejection while eliminating T cells from the donor to thwart GVHD. But the approach is controversial. \"For every study where there's a benefit, there's a study where there's no benefit,\" says pediatric oncologist James Ferrara, who studies GVHD at the Icahn School of Medicine at Mount Sinai in New York City.\n\nA more targeted approach depletes a specific cell population in the graft: naïve T cells, which have not yet differentiated into specific types. A team led by the Hutch's Marie Bleakley and by Warren Shlomchik of the University of Pittsburgh School of Medicine in Pennsylvania removes naïve T cells from grafts with a magnetic system that uses monoclonal antibodies bound to iron beads. In a 2015 report, they said that although the approach had no impact on acute GVHD in 35 patients who received peripheral blood stem cell transplants, it sharply reduced the risk of the disease's chronic form. Relapse rates were unchanged. \"That's definitely a step forward,\" says Geoffrey Hill, a transplant hematologist and researcher at Royal Brisbane and Women's Hospital in Australia.\n\nHill's lab has focused on a different bad actor: overproduction of IL-6, which causes Th17 cells to proliferate. Hill and colleagues treated 48 transplant patients with tocilizumab, a monoclonal antibody approved to treat rheumatoid arthritis that blocks the IL-6 receptor on cell surfaces. Only 12% developed acute disease, they reported in 2014, although the intervention had no discernible impact on rates of chronic GVHD. A second independent group reported similar results, and animal experiments suggest that the treatment has no impact on the GVL effect. Neither tocilizumab nor naïve T cell depletion has yet proved its worth in randomized studies, however.\n\nAnd in work that has not yet reached the clinic, the Hutch's Leslie Kean and her team built on their discovery that patients with GVHD have high levels of a molecule called OX40 on the surface of T cells. In experiments on monkeys, they combined an antibody to OX40 with the drug rapamycin, which slows production of IL-2, and saw \"total control\" of GVHD: Five of five animals had no signs of the disease 100 days after a graft from a highly mismatched donor.\n\nSoon, Ferrara says, better ways to identify who is most likely to develop GVHD will markedly improve options for people who receive cell transplants. In search of early warning signs of the disease, he and co-workers studied almost 700 transplant recipients, comparing protein levels in the blood of patients who developed GVHD with those who did not. This year, his team showed that patients with elevated levels of proteins known as ST2 and REG3α were more likely to suffer severe GVHD and die. Such biomarkers, he says, could eliminate use of prednisone, a risky steroid, in patients not likely to develop GVHD and could signal the need for aggressive treatments in people at high risk. More important, the biomarkers could help researchers choose the best participants for clinical trials.\n\nPromising possibilities\nUntil some of those treatments prove themselves, Wartman and other patients with chronic GVHD face an endless series of drugs that are approved for other conditions or still stuck in experimental limbo. Wartman, in consultation with his primary doctor, WUSM hematologist and oncologist John DiPersio, has tried many unproven interventions and is still searching for others. \"It's a challenge taking care of him because he insists on doing stuff his own way,\" DiPersio says. \"But he's one of the smartest guys around. And it's been painful for me to see him get weaker over the past 5 years. It has been slow but inexorable. It's profoundly annoying not to be able to come up with some brilliant approach to turn things around for this guy.\"\n\nWartman tried the voodoo-sounding extracorporeal photopheresis, which involved implanting a catheter in his chest to run blood twice a week through a machine that filtered out white blood cells, killed them with chemicals and ultraviolet light, and then returned the blood to his circulation. Although that procedure relieved some of his chronic GVHD symptoms, the benefits waned and he stopped after about 60 treatments. The rheumatoid arthritis drug etanercept, which inhibits a key cytokine that leads to inflammation, also had no effect.\n\nIn July 2015, his muscles wasting away, Wartman joined a clinical trial of a drug, ibrutinib, approved to treat specific blood cancers. The drug inhibits a tyrosine kinase enzyme that helps antibody-producing B cells mature, and in the trial it seemed to help many participants. But not Wartman. \"He initially tolerated it well and it seemed like he was having a response, but after about 3 months, he had an adverse reaction to the drug and he just wanted to stop it,\" says Iskra Pusic, a GVHD specialist at WUSM who helps with his care.\n\nAfter that, Wartman began taking the drug ruxolitinib, which is on the market to treat a bone marrow disorder that leads to anemia. (The drug costs about $10,000 per month, and he had to appeal to his insurance company to cover its off-label use.) It inhibits two tyrosine kinase enzymes called Jak1 and Jak2, which rev up production of immune cells. Researchers in DiPersio's lab showed in a mouse model that the drug can reduce GVHD without compromising the GVL effect. Wartman continues to take ruxolitinib to this day in combination with steroids.\n\nLast year, the U.S. Food and Drug Administration recognized the promise of both drugs, designating them \"breakthrough therapies\"—ibrutinib for chronic GVHD and ruxolitinib for the acute disease. (Clinical data don't yet exist for its use in chronic cases like Wartman's.) Those drugs may soon become the first approved treatments for GVHD.\n\nWith Wartman's GVHD in a holding pattern, he keeps searching for other drugs to try off-label or in clinical trials. \"Unless we find something to take my inflammation down a notch, things will just continue to progress,\" Wartman says. He remains optimistic that even if a new drug cannot undo the damage from GVHD, it will improve his quality of life. \"I may be able to get back to doing some of things I'm not able to do now,\" he says, such as simply walking his dogs.\n\nNeither DiPersio nor Wartman regrets the decision to undergo a stem cell transplant, accepting the chronic GVHD as the tradeoff for an increased GVL effect. \"My leukemia couldn't have been cured unless this immunological onslaught was allowed to occur,\" Wartman says.\n\nHe adds that he is grateful his professional connection to the disease has given him the best options for dealing with the devastating consequences of his cure. \"I take care of patients who are going through terrible, terrible complications who deal with them without any recourse,\" Wartman says. \"These are people I often consider have lives that are more worthwhile than mine. I've taken care of so many patients in their early 20s to early 40s who have productive careers in the workforce or are raising children, and their lives are cut short not by the disease but by the cure. As a group, transplant physicians feel they're doing something to save people's lives and underestimate the impact of a transplant. But I don't.\"\n\n\n\n\nSourche:\nhttp://www.sciencemag.org/news/2017/07/stem-cell-transplant-helped-beat-back-young-doctor-s-cancer-now-it-s-assaulting-his\nPosted in: HealthCancer topic\nDOI: 10.1126/science.aan7079",
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      "title": "A stem cell transplant helped beat back a young doctor’s cancer. Now, it’s assaulting his body"
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