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Brian Lybeck

Type 1 Diabetes Increasing As Medical Teams Shrink

Before heading off to swim practice, Brian Lybeck of Avon tests his blood glucose level, which will tell him how much food he needs to eat and also calculates the amount of insulin he needs from a pump he programs to deliver the medication. (John Woike)
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Dr. Steiner

Dr. Donald F. Steiner, Diabetes Researcher, Dies at 84

Dr. Donald F. Steiner, a researcher whose discoveries transformed scientists’ understanding of insulin and other hormones and led to major improvements in the treatment of diabetes, died on Nov. 11 at his home in Chicago. He was 84.

A cousin, Steven Roess, confirmed the death. Until recent hip surgery, Dr. Steiner had continued to conduct diabetes research at the University of Chicago.

Dr. Steiner spent most of his career studying insulin, a hormone made by the pancreas that enables cells to take in sugar to use as fuel or to store. People who lack insulin, or cannot use it properly, develop diabetes, in which sugar builds up in the bloodstream and can cause an array of complications, including heart disease, strokes, kidney failureblindness and amputations.

About 29 million Americans have diabetes, according to the Centers for Disease Control and Prevention.

Dr. Donald F. Steiner

The disease, particularly in children, was a death sentence until the 1920s, when insulin injections became available. The hormone was extracted from the pancreases of animals, mainly pigs and cows, and daily shots saved millions of lives.

But in 1960, when Dr. Steiner became an assistant professor of biochemistry at the University of Chicago, fundamental questions about insulin had still not been answered. One concerned how it was made in the body.

Scientists knew that the insulin molecule consisted of two separate chains of amino acids, which are the building blocks of proteins. The chains were connected to one another, not end to end but crosswise at certain points along their length. Scientists wondered how the two separate chains were made.

“The thinking was that they were synthesized separately in the cell and then came together,” said Dr. Louis Philipson, a diabetes expert at the University of Chicago and a former student of Dr. Steiner’s.

But no one knew for sure. Working in a basement laboratory in an old research building, Dr. Steiner set out to find the answer.

He began working with tissue from a patient who had had surgery to remove an insulinoma — a tumor of the insulin-making cells of the pancreas. It was a rich source of human insulin and precisely the kind of cells Dr. Steiner wanted to study.

His research led to a landmark discovery, reported in a paper published in 1967: He showed that insulin started out not as two chains, but as one long chain, which was later broken into two.

This information was quickly put to use by insulin manufacturers, who were trying to purify the product made from animal pancreases.

“In the early days of insulin, people were injecting this horrible-looking mixture of stuff,” Dr. Philipson said. “It was not very pure. People would get reactions.”

Details from Dr. Steiner’s work helped the manufacturers produce much more highly purified cow and pig insulin, which was less troublesome to patients. His findings also informed later research that made it possible to produce human insulin in vats of genetically engineered yeasts or bacteria.

In addition, his work led to better ways of monitoring insulin production in patients and the body’s sensitivity to the hormone, factors important in treating diabetes and gauging its severity.

Some of the research could have been patented, but Dr. Steiner never considered doing that, said Dr. Arthur Rubenstein, a professor of medicine at and a former dean of the medical school at the University of Pennsylvania, who studied under Dr. Steiner and collaborated with him.

“There it was, one of the really, really great discoveries, and there was no patent,” Dr. Rubenstein said.

That decision was part of a pattern. “He shared everything with everybody,” Dr. Rubenstein said. Dr. Steiner, he said, gave his students ideas and time, made them first authors on scientific publications that would advance their careers, and even shared materials and data with competitors who did not always credit his contributions.

Dr. Steiner’s other passion was the arts — the Chicago Symphony, the opera and the theater. An accomplished pianist, he played classical music on a Steinway grand piano in his high-rise apartment overlooking Lake Michigan and Lincoln Park.

Donald Frederick Steiner was born in Lima, Ohio, on July 15, 1930. His father, Willis, one of five brothers who owned a machine shop that took up most of a city block, died when Donald and his older brother, Phares, were young. Their mother, the former Catherine Hoegner, was a homemaker.

Both sons studied at the University of Cincinnati. Phares became a musician and a builder of pipe organs. Donald earned a degree in chemistry and zoology and went on to the University of Chicago, where he earned a master’s degree in biochemistry and then an M.D.

Phares Steiner died last year. Besides Mr. Roess, survivors include other cousins as well as a niece and nephew.

The concept of precursor molecules had implications that extended beyond insulin to many other hormones that are also made of amino-acid chains, including some that affect growth, metabolism and signal transmission in the brain.

“It opened a window into a whole area of molecular physiology that people were not aware of,” said Dr. Rudolph Leibel, a director of the Naomi Berrie Diabetes Center at Columbia University College of Physicians and Surgeons.

Dr. Steiner’s later research involved various mutations that could disrupt insulin synthesis and cause rare forms of diabetes. He wrote hundreds of articles in scientific journals, which were cited more than 10,000 times by other researchers, according to the University of Chicago. He also received many scientific awards in the United States and other countries.

“He was very modest, and very concerned about young people — his students and his co-workers,” Dr. Leibel said. “He’s from that era, these great thinkers who were soft-spoken and gentlemanly and not in it for anything but the joy of doing the science. We don’t have as much of that now.”


Dr. Steiner

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israeli implant

Beta-O2 Testing Cure For Type 1 Diabetes

israeli implantImagine if those with type 1 diabetes no longer had to worry about insulin injections.

Posted By Abigail Klein Leichman On November 17, 2014 @ 6:00 am

The ßAir bio-artificial pancreas, developed by Israel’s Beta-O2, was recently implanted in the first of eight diabetes patients in Sweden as part of a $1 million pilot human study on this groundbreaking treatment and potential cure for type 1 diabetes (T1D).

Chairman of the Board Dan Gelvan tells ISRAEL21c that the advanced implantable system is science-fiction-come-true for people with T1D, an autoimmune disorder — also known as insulin-dependent or juvenile diabetes – in which the immune system destroys the insulin-producing islet cells of the pancreas.

T1D patients (about three million people in the United States alone) must monitor their glucose and take insulin daily to do the essential job of converting sugar, starches and other food into energy – a task normally handled by about two grams of islet cells.

“Imagine if those with type 1 diabetes no longer had to worry about insulin injections or glucose levels. They could eat what they wanted, exercise as they wished and need not measure every step they took,” says Gelvan, also managing director of life sciences at Aurum Ventures, the company’s lead investor. “This is the future that Beta-O2 envisions ßAir will help to create.”

Oxygen makes the difference

The technique of transplanting cadaver islet cells into T1D patients has been practiced for nearly 30 years, Gelvan notes. However, patients must take immunosuppressant drugs for the rest of their lives. To get around this problem, several companies have developed encapsulation techniques that protect the transplanted cells from the immune reaction to foreign matter.

Beta-O2’s encapsulation has an added, unique feature that addresses the remaining problem: getting enough oxygen into the encapsulated cells.

“Islet cells are huge consumers of oxygen. If they don’t get enough, they won’t produce enough insulin,” Gelvan says. “This company has taken an engineering approach to finding a way to make sure there is an active supply of oxygen to the transplanted cells.”

People with the ßAir would need to refill the air in the tiny device via a replenishing system with a dedicated injector, once every 24 hours.

This device delivers the needed amount of oxygen to the implant.

“Ensuring consistent supply of oxygen has been a challenge of many encapsulation systems in the past,” according to Albert Hwa, senior program scientist in the Beta Cell Therapies Program of theJDRF, which awarded a $500,000 grant toward the pilot study.

“Beta-O2 has demonstrated their device can provide long-term immune protection of islet cells in several animal models, and the addition of oxygen helps keep the cells alive and functional, all in the absence of immunosuppression.”

Mimicking the pancreas

In 2012, ßAir was implanted in a 63-year-old patient in Germany and monitored for 10 months. A report on the promising results was published  in the journal PNAS last year.

The present two-year pilot study, which will enroll eight participants at Uppsala University Hospital in Sweden, will evaluate the safety, survival and function of Beta-O2’s implanted system.

Dr. Per-Ola Carlsson, principal investigator of the ßAir study, said the first implant procedure took less than an hour. “The patient remained hospitalized for four days thereafter for observation and was then discharged. Until day 180 following implantation, the patient will, among other protocol duties, be required to return to the clinic for monthly check-ups. On day 181, ßAir will be explanted from the patient, who will continue to be followed for another 180 days.”

Because cadaver islet cells are not easy to obtain, Gelvan says the company intends to experiment with human stem cells provided by partners companies, as well as animal-derived cells.

“We can do this because the encapsulated islets are immune protected,” he stressed.

As for the lifespan of the implant, he adds: “We don’t know yet how long it lasts, but conventional islet transplants continue to function well for eight to nine years. We hope that because we’ve created a protected microenvironment fed by oxygen, it will last even longer.”

Hwa tells ISRAEL21c that if this proof of concept is successful, “we can envision using other types of islet cells in the device, and perhaps engineering an automated oxygen supply within the device.”

Gelvan explains that ßAir is entirely different than “artificial pancreas” devices that automate glucose monitoring and insulin injection, such as the Israeli product MD Logic developed at Schneider Children’s Medical Center.

“Ours is a biological device that is meant to restore the original effect of having islet cells, so you have all elements of a functioning pancreas in response to the body’s varying glucose levels,” he says. “We are actually simulating and emulating the functionality of an organ.”

The idea for the novel implant system originated with Dr. Pnina Vardi, director of the Laboratory for Diabetes & Obesity Research at Tel Aviv University. Starting in 2004, she did the initial development along with islets researcher Dr. Konstantin Bloch and serial medical-device inventor Yossi Gross. The company, based in Rosh Ha’Ayin near Tel Aviv, now is run by a professional management group.

For more information, click here.


Article printed from ISRAEL21c: http://www.israel21c.org

URL to article: http://www.israel21c.org/headlines/beta-o2-testing-cure-for-type-1-diabe…


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Brusko headshot

Dr. Todd Brusko’s Project Fully Funded on Day 1

Welcome! Today, we are going to explore an exciting field of research, potentially game-changing for the millions living with Type 1 Diabetes. We are diving into the world of Dr. Todd Brusko and his ground-breaking research. This research, fully funded on day one with a whopping $60,000, aims to engineer a patient’s immune cells, trying to halt the autoimmune attack causing Type 1 Diabetes. Intriguing, right? Let’s delve into it!

Understanding Type 1 Diabetes with Dr. Todd Brusko

Understanding Immune System’s Role

In a nutshell, Type 1 Diabetes is an autoimmune disorder where the body’s immune system mistakenly attacks the insulin-producing beta cells in the pancreas. But, what if we could tweak this misbehavior?

Symptoms and Complications

From frequent urination, constant hunger to blurry vision, the symptoms can be severe. If left unchecked, long-term complications such as heart disease and nerve damage can occur.

Dr. Todd Brusko and His Research

Research Background

Enter Dr. Todd Brusko. A respected figure in the field, Dr. Brusko has dedicated his career to understanding the role of T-cells in autoimmune diseases like Type 1 Diabetes.

The $60,000 Project

Backed by a strong team and fueled by a $60,000 funding that was fully pledged on day one, Dr. Brusko’s research has gained significant attention and momentum.

Can We Engineer Immune Cells?

Theoretical Background

But, how can we engineer immune cells to fight an autoimmune disorder? It’s like attempting to teach a dog not to fetch, right?

Mechanism and Research Findings

Actually, not quite. Dr. Todd Brusko’s research is based on a breakthrough concept of reengineering T-cells to prevent them from attacking the pancreas. Excitingly, early research findings are promising.

Implications of Dr. Todd Brusko’s Research

For Diabetes Treatment

Should Dr. Todd Brusko’s project succeed, it could potentially revolutionize diabetes treatment, turning it from management to cure.

For Autoimmune Disorders

And it’s not just diabetes. The implications could extend to other autoimmune disorders, offering hope to millions.

The Path Forward for Dr. Todd Brusko

Despite the excitement, the path forward is not without its challenges.

Potential Challenges for Dr. Todd Brusko

Scientific Challenges

The biggest hurdle is the scientific challenge. How do we make the immune cells stop their destructive behavior without suppressing their protective roles?

Regulatory and Ethical Challenges

Beyond the scientific obstacles, regulatory and ethical issues need careful navigation.

The Role of Funding

With research of this nature, funding plays a critical role.

Importance of Early Funding

This is where the $60,000 project comes in. Early funding, like the full pledge on day one, helps to kickstart the research and keep it going.

Crowdfunding and Medical Research

Crowdfunding, as demonstrated in Dr. Todd Brusko’s project, has become a game-changer in medical research funding.


Dr. Todd Brusko’s pioneering work is a beacon of hope for people living with Type 1 Diabetes. The road to a potential cure is fraught with challenges but backed by the unwavering support of donors, promising early results, and a dedicated research team, the prospect of engineering a patient’s immune cells to halt the autoimmune attack seems within reach.


  1. What is the main focus of Dr. Todd Brusko’s research?
    • Dr. Todd Brusko’s research focuses on engineering immune cells to stop them from attacking the pancreas, the cause of Type 1 Diabetes.
  2. How was the $60,000 project funded?
    • The $60,000 project was fully funded on its first day, demonstrating significant support and belief in Dr. Brusko’s research.
  3. What potential impact could Dr. Todd Brusko’s research have?
    • If successful, the research could revolutionize the treatment of Type 1 Diabetes and potentially other autoimmune disorders.
  4. What are the challenges ahead?
    • The challenges ahead include scientific hurdles, regulatory issues, and ethical considerations.
  5. What role does funding play in this type of research?
    • Funding is crucial in such groundbreaking research. It helps kickstart the project and sustains it throughout its course.


Donors were so excited to read about Dr. Brusko’s project, “Can we engineer a patient’s immune cells to stop the autoimmune attack that causes type 1 diabetes?” that they plunked down the whole $60,000 at The Diabetes Research Connection’s website launch party on Friday, 11/14/2014.

We are thrilled by this unexpected but welcome response to our website, and invite you to look at and consider supporting the other two meritorious and novel projects posted on our site under SUBMIT A PROJECT. Contributions of any amount are greatly appreciated. Let’s get these projects up and running!

Dr. Todd Brusko'

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See our approved research projects and campaigns.

Role of the integrated stress response in type 1 diabetes pathogenesis
In individuals with type 1 diabetes (T1D), the insulin-producing beta cells are spontaneously destroyed by their own immune system. The trigger that provokes the immune system to destroy the beta cells is unknown. However, accumulating evidence suggest that signals are perhaps first sent out by the stressed beta cells that eventually attracts the immune cells. Stressed cells adapt different stress mitigation systems as an adaptive response. However, when these adaptive responses go awry, it results in cell death. One of the stress response mechanisms, namely the integrated stress response (ISR) is activated under a variety of stressful stimuli to promote cell survival. However, when ISR is chronically activated, it can be damaging to the cells and can lead to cell death. The role of the ISR in the context of T1D is unknown. Therefore, in this DRC funded study, we propose to study the ISR in the beta cells to determine its role in propagating T1D.
Wearable Skin Fluorescence Imaging Patch for the Detection of Blood Glucose Level on an Engineered Skin Platform
A Potential Second Cure for T1D by Re-Educating the Patient’s Immune System
L Ferreira
Validating the Hypothesis to Cure T1D by Eliminating the Rejection of Cells From Another Person by Farming Beta Cells From a Patient’s Own Stem Cells
Han Zhu
Taming a Particularly Lethal Category of Cells May Reduce/Eliminate the Onset of T1D
JRDwyer 2022 Lab 1
Can the Inhibition of One Specific Body Gene Prevent Type 1 Diabetes?
Is Cholesterol Exacerbating T1D by Reducing the Functionality and Regeneration Ability of Residual Beta Cells?
Regeneration Ability of Residual Beta Cells
A Call to Question… Is T1D Caused by Dysfunctionality of Two Pancreatic Cells (β and α)?
Xin Tong
Novel therapy initiative with potential path to preventing T1D by targeting TWO components of T1D development (autoimmune response and beta-cell survival)
flavia pecanha