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Posts Tagged ‘Blood sugar’


Reporter and Curator: Dr. Sudipta Saha, Ph.D.

 

Stroke is a leading cause of death worldwide and the most common cause of long-term disability amongst adults, more particularly in patients with diabetes mellitus and arterial hypertension. Increasing evidence suggests that disordered physiological variables following acute ischaemic stroke, especially hyperglycaemia, adversely affect outcomes.

 

Post-stroke hyperglycaemia is common (up to 50% of patients) and may be rather prolonged, regardless of diabetes status. A substantial body of evidence has demonstrated that hyperglycaemia has a deleterious effect upon clinical and morphological stroke outcomes. Therefore, hyperglycaemia represents an attractive physiological target for acute stroke therapies.

 

However, whether intensive glycaemic manipulation positively influences the fate of ischaemic tissue remains unknown. One major adverse event of management of hyperglycaemia with insulin (either glucose-potassium-insulin infusions or intensive insulin therapy) is the occurrence of hypoglycaemia, which can also induce cerebral damage.

 

Doctors all over the world have debated whether intensive glucose management, which requires the use of IV insulin to bring blood sugar levels down to 80-130 mg/dL, or standard glucose control using insulin shots, which aims to get glucose below 180 mg/dL, lead to better outcomes after stroke.

 

A period of hyperglycemia is common, with elevated blood glucose in the periinfarct period consistently linked with poor outcome in patients with and without diabetes. The mechanisms that underlie this deleterious effect of dysglycemia on ischemic neuronal tissue remain to be established, although in vitro research, functional imaging, and animal work have provided clues.

 

While prompt correction of hyperglycemia can be achieved, trials of acute insulin administration in stroke and other critical care populations have been equivocal. Diabetes mellitus and hyperglycemia per se are associated with poor cerebrovascular health, both in terms of stroke risk and outcome thereafter.

 

Interventions to control blood sugar are available but evidence of cerebrovascular efficacy are lacking. In diabetes, glycemic control should be part of a global approach to vascular risk while in acute stroke, theoretical data suggest intervention to lower markedly elevated blood glucose may be of benefit, especially if thrombolysis is administered.

 

Both hypoglycaemia and hyperglycaemia may lead to further brain injury and clinical deterioration; that is the reason these conditions should be avoided after stroke. Yet, when correcting hyperglycaemia, great care should be taken not to switch the patient into hypoglycaemia, and subsequently aggressive insulin administration treatment should be avoided.

 

Early identification and prompt management of hyperglycaemia, especially in acute ischaemic stroke, is recommended. Although the appropriate level of blood glucose during acute stroke is still debated, a reasonable approach is to keep the patient in a mildly hyperglycaemic state, rather than risking hypoglycaemia, using continuous glucose monitoring.

 

The primary results from the Stroke Hyperglycemia Insulin Network Effort (SHINE) study, a large, multisite clinical study showed that intensive glucose management did not improve functional outcomes at 90 days after stroke compared to standard glucose therapy. In addition, intense glucose therapy increased the risk of very low blood glucose (hypoglycemia) and required a higher level of care such as increased supervision from nursing staff, compared to standard treatment.

 

References:

 

https://www.nih.gov/news-events/news-releases/nih-study-provides-answer-long-held-debate-blood-sugar-control-after-stroke

 

https://www.ncbi.nlm.nih.gov/pubmed/27873213

 

https://www.ncbi.nlm.nih.gov/pubmed/19342845

 

https://www.ncbi.nlm.nih.gov/pubmed/20491782

 

https://www.ncbi.nlm.nih.gov/pubmed/21211743

 

https://www.ncbi.nlm.nih.gov/pubmed/18690907

 

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Reporter: Aviva Lev-Ari, PhD, RN

Stanford’s Mike Snyder is Showing the Way With Personalized Medicine

 

11/19/12
Follow @ldtimmerman

Say the words “personalized medicine” to people from various walks of life, and you’re likely to get one of about four different reactions.

A. “Personalized medicine? What’s that?” (Usually spoken by 99 percent of patients.)

B. “Personalized medicine will bankrupt the country with expensive new diagnostic tests, and overrated targeted drugs.” (Usually spoken by health economists.)

C. “Personalized medicine is overhyped, a load of bunk.” (Usually spoken by grizzled pharma industry vets who remember the genomics crash of a decade ago, and have a financial interest in preserving the status quo.)

D. “Personalized medicine will revolutionize healthcare, moving us away from reactive sick-care and more toward predictive and preventive strategies focused on wellness.” (Usually spoken by the subset of true believers in science and the biotech industry.)

You can make arguments, buttressed with data, to support any of the last three positions. But none of these positions quite captures the truth. We are in the early days of the personalized medicine movement, and don’t know how the story will unfold. As a journalist who’s followed many different threads of this story for thelast decade, I keep getting the feeling that we’re moving further away from one-size-fits-all medicine, and more toward treatment based on extremely detailed molecular readouts on your state of health or disease. People may havesnickered at Internet pioneer Larry Smarr and his friends in the “Quantified Self” movement for being weird a couple years ago, but I can easily envision people jumping on this bandwagon sometime not too far out.

I was fascinated this past week when I had a chance to talk with Mike Snyder, a geneticist who has turned himself into a poster child for personalized medicine through his work at Stanford University. After talking with him for about a half hour last week, I hung up thinking his experience today could seem mainstream in another 10 or 20 years.

Stanford geneticist Mike Snyder

Snyder, for those who are unfamiliar, was the guy at the center of an important paper published in the journal Cell back in March. This paper described how researchers sequenced Snyder’s genome, and then really got rolling in their quest to understand his biochemical state of being at 20 different snapshots in time over a 14-month period. The scientists took blood samples from him when he was feeling fine, and a few times when he was sick with viral infections. They then ran the samples through instruments that captured an extremely detailed look at 40,000 molecular parameters in his blood. These were metabolites, proteins, RNA transcripts, self-directed antibodies. This hard-core genomic, transcriptomic, metabolomic and proteomic approach (which the scientists called an integrative personal ‘omics profile) could have been just a demonstration of technological overkill, offering very little information that could lead anyone to make better decisions about their health.

But that’s not what happened. It turned out that the results, surprisingly, showed this healthy white guy in his mid-50s was at high risk of getting Type 2 diabetes—which if it’s not controlled, it can lead down the path to blindness, amputations, stroke, or heart attack.

At the time the molecular analysis revealed this trend, it was hard to believe. Snyder had no family history of the disease, and most everybody in his family is thin. His genome said he was at low risk of obesity, and at a shade under 5-foot-10, and 160 pounds, Snyder’s general practitioner thought the idea of him becoming diabetic was far-fetched.

But just as the pan-‘omics tests had predicted, researchers saw over time that something was amiss with Snyder’s ability to control his blood sugar—especially, and oddly, when he had viral infections. When looking at two traditional blood measurements of diabetes—blood sugar concentration levels and hemoglobin A1C counts—both of those numbers progressively climbed into worrisome territory. As the sweeping ‘omics-driven analysis had predicted, Snyder was diagnosed with diabetes.

He remembers the day that word came, April 11, 2011. He decided it was time to change his health habits.

“Up until that point, I had been eating lots of sweets. I’d have ice cream all the time after dinner. It really was a pretty bad diet,” Snyder says. After the diagnosis, it took him six months to get his blood sugar levels back to normal. “I completely cut out all dessert, and have had one bite of wedding cake since,” he says. That one exception came when one of his postdocs got married, he says.

That might be how anybody in this situation would react to a diabetes diagnosis, with enough self-discipline. But what makes this story even more interesting is that when Snyder changed his diet, and ramped up his daily exercise routines, he could see how his biochemical profile changed when his behavior changed. The scientists have kept looking at measurements of 40,000 different molecules in Snyder’s blood, before, during, and after his diagnosis. Suddenly, you can see not only that bicycling 40-50 miles a week instead of 20-30 miles has helped him lose 15 pounds. You can also see the molecular warning signs of diabetes have returned roughly to normal, along with his blood sugar and hemoglobin A1c scores.

“This study is a landmark for personalized medicine,” Eric Topol, a professor of genomics at the Scripps Research Institute in San Diego, told the New York Times.

Months later, Snyder reports that even though he’s not technically cured of diabetes, he’s been able to keep it in remission through these behavior changes, without taking any drugs. That doesn’t mean he’s completely in the clear. He knows his risk will go up again as he gets older. He also knows from his genome that if he gets diabetes, and needs to take the generic drug metformin, he should take a lower-than-usual dose. But most importantly, because he’s a scientist willing to make himself a laboratory subject, he’s more likely to catch diabetes or some other ailment at an early and treatable stage.

After giving 50 samples to his research team over the past 34 months, Snyder says he expects much more interesting data to come. This wasn’t just a case of a single paper which generates some buzz, maybe a few new research ideas, and then fades into the ether. It’s really just the first step in a long-range study of Snyder at the molecular level, and what that means for his health. “I’m sure I’ll be doing this the rest of my life,” Snyder says.

No question, this is all still very much at a research stage. This kind of hard-core data-gathering approach is many years away from being reduced to practical use, or lending itself to new products for diagnosis or treatment. The Stanford team used a next-generation gene sequencing machine, and two different mass spectrometers, which are expensive pieces of equipment. The first study of Snyder’s ‘omics profile generated 50 terabytes of data, and he says the next phase of research will probably double the amount of data. It cost tens of thousands of dollars, and he doesn’t really have a full accounting that includes computer analysis and staff time. And the costs keep recurring. While the team only had to sequence his genome once—because his unique DNA signature doesn’t change over time—the battery of other ‘omic tests will probably cost at least $2,000 each time he gives blood, just for the chemical reagents required, not counting costs for analysis and staff time.

Still, every day as the costs come down, more research ideas become feasible. Snyder’s story, which got a fair bit of media attention in the spring, has inspired a number of volunteers who want to help. The Stanford team is broadening the scope of their personalized medicine vision by looking to analyze the microbes in Snyder’s gut—the microbiome—and his epigenome, which will show how his genes get expressed. Those extra analyses will add cost, but Snyder says he believes it will be soon be possible to capture a simple version of the molecular analysis for maybe $600 each time he gives blood. Once the costs get down into that range, it will be feasible to do one continuous study of 10 volunteers like Snyder, who are willing to subject themselves to all these regular blood draws, when they’re feeling well and when they’re not.

Beyond that study, Snyder says he and his team are exploring a 250-person study of people at high risk for diabetes, or who are pre-diabetic. The idea will be to take these regular personal ‘omic snapshots, connect it with a detailed picture of the person’s environmental stimuli (particularly their diet/exercise habits), and watch over a 5-year period to see whether certain biochemical pathways are truly predictive of whether a person will get diabetes. That kind of study would be clearly more informative to the practice of medicine than just one man’s experience, which could be a fluke.

Certainly, there are going to be experiments that fail, or just give us vague ideas of where an individual’s health is headed. People, being human, won’t always follow their doctor’s advice, even if they know they can stop themselves from getting diabetes. Insurance companies may use this data to their own advantage, and to the disadvantage of the individual. (In fact, Snyder says his life insurance premiums went up once he told his insurer about his diabetes diagnosis. That action is perfectly legal, he notes, because life insurance firms aren’t subject to theGenetic Information Non-Discrimination Act of 2008.)

The whole march of science, the business implications, and the ethics of this movement will surely lurch along in fits and starts over the coming decades. It will be messy. It won’t happen overnight.

But I do believe we’re going to learn amazing things that will change our behavior. And I think that within the next decade, a whole lot more people in the U.S. will have the same kind of visibility Snyder got into his individual health, because it really ought to save the whole system money if it scares people into leading healthier lives. The 99 percent of patients will no longer say “Personalized Medicine? What’s that?” People will want this information, they’ll demand it, and many will act on it. Some of today’s skeptics will turn into believers, and they’ll find ways to profit from this movement, by helping people prevent bad things from happening. As Snyder puts it, “This is what personalized medicine is all about. You can look at your altered biochemical state, and you can change things when you catch them early. It’s the name of the game.”

Luke Timmerman is the National Biotech Editor of Xconomy. E-mail him at

ltimmerman@xconomy.com Follow @ldtimmerman

SOURCE:

http://www.xconomy.com/national/2012/11/19/stanfords-mike-snyder-starts-living-the-personalized-medicine-story/2/

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Reporter: Aviva Lev-Ari, PhD, RN

Glucose in the ICU — Evidence, Guidelines, and Outcomes

Brian P. Kavanagh, M.B., F.R.C.P.C.

September 7, 2012 (10.1056/NEJMe1209429)

Just over a decade ago, a single-center Belgian study showed that normalization of blood glucose in critically ill patients lowered hospital mortality by more than 30%.1 Although subsequent studies were unable to reproduce these findings, the appeal of such a straightforward intervention was too great to resist: guidelines from professional organizations2,3 were published, and editorial commentary4 highlighted initiatives by the Institute for Healthcare Improvement, the Joint Commission on Accreditation of Healthcare Organizations, and the Volunteer Hospital Association that incorporated tight glucose control as a standard. Indeed, the prestigious Codman Award of the Joint Commission was presented in 2004 for a program of glycemic control in critical care that “saved” patients’ lives.5 Tight glucose control for critically ill patients was in vogue.

The publication in 2009 of a large international trial (the Normoglycemia in Intensive Care Evaluation–Survival Using Glucose Algorithm Regulation [NICE-SUGAR] study6) followed that of several negative trials. The NICE-SUGAR study, which involved more than 6100 patients, showed that tight glycemic control didn’t decrease mortality — it increased it. Most guidelines were hastily revised. However, in the same year a separate study by Vlasselaers et al.7 in pediatric intensive care unit (ICU) patients, most of whom had undergone cardiac surgery, showed that normalizing glucose decreased mortality from 6% to 3%, keeping open the question — at least in critically ill children.

The study by Agus et al.8 now reported in the Journal provides new key data. A total of 980 children (up to 36 months of age) admitted to an ICU after cardiac surgery were randomly assigned to usual care or tight glucose control. The results are clear — there was no significant difference in the incidence of health care–associated infections (the primary outcome) or in any of the secondary outcomes, including survival. Moreover, the rate of hypoglycemia (blood glucose level <40 mg per deciliter [2.2 mmol per liter]) in the intervention group (3%) was far less than that previously reported (25%).7 These findings contrast sharply with those of Vlasselaers et al.,7 who found that secondary infections, length of stay, and mortality were reduced. Faced with contradictory results from two large clinical trials, how does the clinician know which results are correct?

First, biologic plausibility is important in attributing a survival benefit to a specific intervention. In the first pediatric ICU study, the additional deaths in the control group did not appear to be due to causes related to hyperglycemia,7 a finding that suggests that the benefit was unlikely to be reproducible. The current authors, exclusively studying children after cardiac surgery, recognized that mortality in this population is usually due to prohibitive anatomy or surgical challenge; these are circumstances not amenable to correction by metabolic control.

Second, might differences in the target plasma glucose explain the discrepant findings? Agus et al. aimed for a higher target range of plasma glucose in the intervention group (80 to 110 mg per deciliter [4.4 to 6.1 mmol per liter]) than was targeted in the first pediatric study (infants, 50 to 80 mg per deciliter [2.8 to 4.4 mmol per liter]; children, 70 to 100 mg per deciliter [3.9 to 5.6 mmol per liter]).7 Perhaps the lower glucose target is preferable? The weight of evidence is against this, and if this target were used, the incidence and severity of hypoglycemia would have been greater, as previously reported.7 Hypoglycemia is never to a patient’s benefit, and its negative impact on neurocognitive development in children is of particular concern.

It seems that — as in adults — claims for survival benefit in critically ill children are incorrect. Furthermore, there is no reason why the effects of glucose control in children would be opposite to those in adults. In aggregate, the data do not support a basis for embarking on a pediatric megatrial.

Assuming the results of the NICE-SUGAR study6 are generalizable, we must be grateful for the future lives saved by avoiding the practice of normalizing glucose in the ICU. At the same time, we should reflect on why a large study with mortality as an end point was needed in the first place.

Perhaps the most important question from a decade of studying glucose control in the ICU is how influential practice guidelines advocating tight glucose control were developed2,3 yet turned out to be harmful — an issue noted in the lay press.9 Guideline writers, reflecting on the experience, must accept that there are multiple sources of clinical knowledge10 and must pay careful attention to trial characteristics — especially study reproducibility — in order to provide advice that genuinely helps clinicians. Clinicians in turn should use guidelines wisely, recognizing that no single source of knowledge is sufficient to guide clinical decisions.10

Is the door closed on studying glucose homeostasis in the critically ill? No, but it should be closed on the routine normalization of plasma glucose in critically ill adults and children.

Disclosure forms provided by the author are available with the full text of this article at NEJM.org.

This article was published on September 7, 2012, at NEJM.org.

SOURCE INFORMATION

From the Department of Critical Care Medicine and Anesthesia, Hospital for Sick Children, University of Toronto, Toronto.

Source:

http://www.nejm.org/doi/full/10.1056/NEJMe1209429?query=OF

REFERENCES

    1. 1

      van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl J Med 2001;345:1359-1367
      Full Text | Web of Science | Medline

    1. 2

      American College of Endocrinology and American Diabetes Association Consensus statement on inpatient diabetes and glycemic control. Diabetes Care 2006;29:1955-1962
      CrossRef | Web of Science

    1. 3

      Dellinger RP, Carlet JM, Masur H, et al. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Intensive Care Med 2004;30:536-555
      CrossRef | Web of Science | Medline

    1. 4

      Angus DC, Abraham E. Intensive insulin therapy in critical illness. Am J Respir Crit Care Med 2005;172:1358-1359
      CrossRef | Web of Science | Medline

    1. 5

      The Joint Commission. 2004 Ernest Amory Codman Award winners (http://www.jointcommission.org/2004_ernest_amory_codman_award_winners).

    1. 6

      The NICE-SUGAR Study Investigators. Intensive versus conventional glucose control in critically ill patients. N Engl J Med 2009;360:1283-1297
      Full Text | Web of Science

    1. 7

      Vlasselaers D, Milants I, Desmet L, et al. Intensive insulin therapy for patients in paediatric intensive care: a prospective, randomised controlled study. Lancet 2009;373:547-556
      CrossRef | Web of Science | Medline

    1. 8

      Agus MSD, Steil GM, Wypij D, et al. Tight glycemic control versus standard care after pediatric cardiac surgery. N Engl J Med 2012. DOI: 10.1056/NEJMoa1206044.

    1. 9

      Groopman J, Hartzband P. Why `quality’ care is dangerous. Wall Street Journal. April 9, 2009 (http://online.wsj.com/article/SB123914878625199185.html).

  1. 10

    Tonelli MR, Curtis JR, Guntupalli KK, et al. An official multi-society statement: the role of clinical research results in the practice of critical care medicine. Am J Respir Crit Care Med2012;185:1117-1124
    CrossRef | Web of Science

 

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Reported by:  Dr. Venkat S Karra. Ph.D.

Sticking yourself in the finger day after day: For many diabetics, this means of checking blood glucose is an everyday part of life. Especially for patients with Type-1 diabetes, who always have to keep a close eye on their levels, since their bodies are incapable of producing the insulin to break down the glucose in the blood. Several times a day, they have to place a tiny drop of blood on a test strip. It is the only way they can ascertain the blood glucose value, so they can inject the correct amount of insulin needed. And this pricking is not only a burdensome: it may also cause inflammation or cornification of the skin. And for pain-sensitive patients, the procedure is agony.

The daily sticking of the finger may soon become a thing of the past, thanks to a diagnostic system with Fraunhofer technology built-in. The underlying concept is a biosensor that is located on the patient’s body. It is also able to measure glucose levels continuously using tissue fluids other than blood, such as in sweat or tears. The patient could dispense with the constant needle pricks. In the past, such bioelectric sensors were too big, too imprecise and consumed too much power. Researchers at the Fraunhofer Institute for Microelectronic Circuits and Systems IMS in Duisburg have recently achieved a major breakthrough: They have developed a biosensor in nano-form that circumvents these hurdles.

Diagnostic system in miniature

The principle of measurement involves an electrochemical reaction that is activated with the aid of an enzyme. Glucose oxidase converts glucose into hydrogen peroxide (H2O2) and other chemicals whose concentration can be measured with a potentiostat. This measurement is used for calculating the glucose level. The special feature of this biosensor: the chip, measuring just 0.5 x 2.0 mm, can fit more than just the nanopotentiostat itself. Indeed, Fraunhofer researchers have attached the entire diagnostic system to it. “It even has an integrated analog digital converter that converts the electrochemical signals into digital data,” explains Tom Zimmermann, business unit manager at IMS. The biosensor transmits the data via a wireless interface, for example to a mobile receiver. Thus, the patient can keep a steady eye on his or her glucose level. “In the past, you used to need a circuit board the size of a half-sheet of paper,” says Zimmermann. “And you also had to have a driver. But even these things are no longer necessary with our new sensor.”

Durable biosensor

The minimal size is not the only thing that provides a substantial advantage over previous biosensors of this type. In addition, the sensor consumes substantially less power. Earlier systems required about 500 microamperes at five volts; now, it is less than 100 microamperes. That increases the durability of the system – allowing the patient to wear the sensor for weeks, or even months. The use of a passive system makes this durability possible. The sensor is able to send and receive data packages, but it can also be supplied with power through radio frequency.

The glucose sensor was engineered by the researchers at Noviosens, a Dutch medical technology firm. Since it can be manufactured so cost-effectively, it is best suited for mass production. These non-invasive measuring devices for monitoring blood glucose levels may become the basis for a particularly useful further development in the future: The biochip could control an implanted miniature pump that, based on the glucose value measured, indicates the precise amount of insulin to administer. That way, diabetes patients could say goodbye to incessant needle-pricks forever.

Source:

rdmag

Fraunhofer Institute

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Engineered Pancreatic Tissues Could Lead to Better Transplants for Diabetics

Reporter: Aviva Lev-Ari, PhD, RN

Wednesday, August 15, 2012
By: Kevin Hattori

Technion researchers have built pancreatic tissue with insulin-secreting cells, surrounded by a three-dimensional network of blood vessels. The engineered tissue could pave the way for improved tissue transplants to treat diabetes.

The tissue created by Professor Shulamit Levenberg of the Technion-Israel Institute of Technology and her colleagues has some significant advantages over traditional transplant material that has been harvested from healthy pancreatic tissue.

Prof Levenberg
Prof. Shulamit Levenberg

 

The insulin-producing cells survive longer in the engineered tissue, and produce more insulin and other essential hormones, Levenberg and colleagues said. When they transplanted the tissue into diabetic mice, the cells began functioning well enough to lower blood sugar levels in the mice.

Transplantation of islets, the pancreatic tissue that contains hormone-producing cells, is one therapy considered for people with type 1 diabetes, who produce little or no insulin because their islets are destroyed by their own immune systems. But as with many tissue and organ transplants, donors are scarce, and there is a strong possibility that the transplantation will fail.

The well-developed blood vessel network built into the engineered tissue is key to its success, the researchers concluded. The blood vessels encourage cell-to-cell communication, by secreting growth hormones and other molecules, that significantly improve the odds that transplanted tissue will survive and function normally.

The findings confirm that the blood vessel network “provides key survival signals to pancreatic, hormone-producing cells even in the absence of blood flow,” Levenberg and colleagues concluded in their study published in the journal PLoS One.

One reason transplants fail, Levenberg said, “is that the islets are usually transplanted without any accompanying blood vessels.” Until the islets begin to connect with a person’s own vascular system, they are vulnerable to starvation.

The 3-D system developed by the Technion researchers tackled this challenge by bringing together several different cell types to form a new transplantable tissue. Using a porous plastic material as the scaffold for the new tissue, the scientists seeded the scaffold with mouse islets, tiny blood vessel cells taken from human umbilical veins, and human foreskin cells that encouraged the blood vessels to develop a tube-like structure.

“The advantages provided by this type of environment are really profound,” said Xunrong Luo, an islet transplantation specialist at the Northwestern University Feinberg School of Medicine. She noted that the number of islets used to lower blood sugar levels in the mice was nearly half the number used in a typical islet transplant.

Islets grown in these rich, multicellular environments lived three times as long on average as islets grown by themselves, Levenberg and colleagues found.

The technology “is still far from tests in humans,” Levenberg said, but she noted that she and her colleagues are beginning to test the 3-D tissue scaffolds using human instead of mouse islets.

According to Northwestern’s Luo, the 3-D model demonstrated in the study “will have important and rapid clinical implications” if the same results can be replicated with human cells. “This model system also provides a good platform to study the details and mechanisms that underlie successful transplantation.”

The Technion-Israel Institute of Technology is a major source of the innovation and brainpower that drives the Israeli economy, and a key to Israel’s renown as the world’s “Start-Up Nation.” Its three Nobel Prize winners exemplify academic excellence. Technion people, ideas and inventions make immeasurable contributions to the world including life-saving medicine, sustainable energy, computer science, water conservation and nanotechnology.

American Technion Society (ATS) donors provide critical support for the Technion—more than $1.7 billion since its inception in 1940. Based in New York City, the ATS and its network of chapters across the U.S. provide funds for scholarships, fellowships, faculty recruitment and chairs, research, buildings, laboratories, classrooms and dormitories, and more.

 

http://www.ats.org/site/News2?page=NewsArticle&id=7567&news_iv_ctrl=1161

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