ECMOFOBIA, porque 14 picadelas por dia deixam qualquer um ecmofóbico...

quinta-feira, 20 de julho de 2017

Novartis-Parvus-Collaboration-Press-Release-2017-04-19.pdf

Novartis-Parvus-Collaboration-Press-Release-2017-04-19.pdf

Parvus is pioneering a breakthrough class of disease-specific biological therapeutics called NavacimsTM that are designed to halt and potentially cure autoimmune disease by restoring immune tolerance. The Company’s robust therapeutic platform is capable of generating a rich pipeline of therapeutic candidates for a wide range of autoimmune diseases. Parvus has validated two lead drug candidates to take into clinical development for Type 1 diabetes (T1D) and Multiple Sclerosis (MS), and is scaling up drug product manufacture for GLP toxicology studies.

Practical Cure Update: BCG

Practical Cure Update: BCG

Practical Cure Project Update: BCG
March 21, 2017
Summary:
  • The BCG Human Clinical Trial Program is one of twelve T1D Practical Cure projects currently in human trials.
  • A phase I trial was completed in 2012 and confirmed the safety of using BCG in patients with established T1D. An eight-year follow-up report on phase I participants is expected by the end of 2017.
  • A phase II 150 person trial hoping to demonstrate the effectiveness of BCG in reversing T1D in established adults is currently recruiting. There are 25 more patient slots available for type 1 diabetics interested in participating in the trial.
This is the second in a series of reports detailing individual research projects currently in human trials with the potential to deliver a Practical Cure. The twelve Practical Cure projects that will be profiled were identified and summarized in the 2016 State of the Cure for Type 1 Diabetes, which was published during the first week of January 2017 (Click here to view).

This report focuses on the BCG Human Clinical Trial Program at Massachusetts General Hospital and features an interview with the lead researcher Dr. Denise Faustman. The program is testing BCG (bacillus calmette-guérin), a drug currently used as a vaccine for tuberculosis, as a possible cure or permanent reversal for established type 1 diabetes. BCG is unique in that it is an inexpensive generic drug which, if approved, would be a cost-effective treatment for type 1. The trial is funded entirely by private philanthropic donations and is not supported by any for-profit research efforts or JDRF.

BCG Background

Faustman’s hypothesis is that the administration of BCG can stop the autoimmune attack in T1D and enable the restoration of near normal HbA1c values in part from beta cell regeneration. The rationale for why this works, according to Faustman, is based on an understanding of "TNF", a cell signaling protein whose presence tells the body’s immune system to stop attacking insulin-producing beta cells.

Faustman claims that people with T1D have insufficient levels of TNF, resulting in an imbalance in the immune system (too many effector T cells, which attack the pancreas, and not enough regulatory T cells, which regulate the effector T cells and identify what cells to attack and what not to attack).

In theory, administration of BCG should result in higher levels of TNF and, therefore, rebalance the immune system, stopping the auto-immune attack. “BCG is the drug that led to the discovery of TNF in 1985,” Faustman says, “it was well known that when you get vaccinated with BCG, your TNF levels went up. That was the fundamental link that drove us, alongside the ability to get into the clinic and introduce something inexpensive.”

Current Testing:

A phase II human trial is currently recruiting. It will attempt to demonstrate the effectiveness of BCG and will follow patients for five years.  Faustman underscores that these trials will focus on people with established T1D: “We are treating people who have the disease,” Faustman says, “They are five, ten, twenty years out and we are trying to reverse it. It’s a huge distinguishing point of what we do.”
Human Trials Research Design Summary (Active):
Website Link: http://www.faustmanlab.org/research/BCGTrials.html

To learn more or make a donation: www.faustmanlab.org, email diabetestrial@partners.org, or call 617-726-4048.

sexta-feira, 9 de dezembro de 2016

EPFL scientists discover cause for immune attack in type-1 diabetes

EPFL scientists discover cause for immune attack in type-1 diabetes

Type-1 diabetes occurs when immune cells attack the pancreas. EPFL scientists have now discovered what may trigger this attack, opening new directions for treatments.

Type-1 diabetes is the rarest but most aggressive form of diabetes, usually affecting children and adolescents.

The patient's own immune cells begin to attack the cells in the pancreas that make insulin, eventually eliminating its production in the body. The immune cells target certain proteins inside the insulin-producing cells. However, it is unclear how this actually happens.

EPFL scientists have now discovered that the immune attack in type-1 diabetes may be triggered by the release of proteins from the pancreas itself, as well as the package they come in. The work, which has significant implications for therapy strategies, is published in Diabetes.

(...) 

In type-1 diabetes, the patient's immune cells specifically attack beta cells, thereby disrupting the production of insulin. However, we don't actually know what causes the immune cells to attack in the first place.

Scientists from EPFL's Institute of Bioengineering, led by Steinunn Baekkeskov, have now discovered that pancreatic beta cells actually secrete proteins that are targeted by the immune attack. But it's not only the proteins that cause problems; the researchers found that it is also their packaging.

Self-destructive signals

That packaging comes in the form of small vesicles called exosomes, which are secreted by all cell types to distribute various molecules with different functions. But previous studies have shown that exosomes can also activate the immune system. Building on this, the EPFL researchers looked at exosomes from human and animal pancreatic beta cells.

The results showed that rat and human pancreatic beta cells release three proteins known to be associated with type-1 diabetes, and are in fact used by clinicians to diagnose its onset in people.

The researchers might have also discovered why the immune attack on the pancreas begins in the first place: When insulin-making beta cells were exposed to stress, they released high amounts of exosomes, which they also "decorated" with proteins that activate immune cells. These powerfully inflammatory proteins may be involved in induction of autoimmunity in the disease.

The hope is that this will lead to new directions in developing more effective treatments that focus on developing exosome mimics that contain molecules inhibiting rather than stimulating immune cells. These synthetic molecules would be taken up by the patient's immune cells and would block them from attacking beta cells.
Source:
Ecole Polytechnique Fédérale de Lausanne

quarta-feira, 28 de setembro de 2016

FDA Approves First Hybrid-Closed Loop Artificial Pancreas System, Medtronic’s 670G

FDA Approves First Hybrid-Closed Loop Artificial Pancreas System, Medtronic’s 670G

sexta-feira, 12 de agosto de 2016

Educate Your Immune System - The New York Times

Educate Your Immune System - The New York Times

Our bodies are confused
by this 21st-century world.

By MOISES VELASQUEZ-MANOFFJUNE 3, 2016

IN the last half-century, the prevalence of autoimmune disease — disorders in which the immune system attacks healthy tissue in the body — has increased sharply in the developed world. An estimated one in 13 Americans has one of these often debilitating, generally lifelong conditions. Many, like Type 1 diabetes and celiac disease, are linked with specific gene variants of the immune system, suggesting a strong genetic component. But their prevalence has increased much faster — in two or three generations — than it’s likely the human gene pool has changed.

Many researchers are interested in how the human microbiome — the community of microbes that live mostly in the gut and are thought to calibrate our immune systems — may have contributed to the rise of these disorders. Perhaps society-wide shifts in these microbial communities, driven by changes in what we eat and in the quantity and type of microbes we’re exposed to in our daily lives, have increased our vulnerability.

To test this possibility, some years ago, a team of scientists began following 33 newborns who were genetically at risk of developing Type 1 diabetes, a condition in which the immune system destroys the insulin-producing cells of the pancreas.

The children were mostly Finnish. Finland has the highest prevalence — nearly one in 200 under the age of 15 — of Type 1 diabetes in the world. (At about one in 300, the United States isn’t far behind.) After three years, four of the children developed the condition. The scientists had periodically sampled the children’s microbes, and when they looked back at this record, they discovered that the microbiome of children who developed the disease changed in predictable ways nearly a year before the disease appeared. Diversity declined and inflammatory microbes bloomed. It was as if a gradually maturing ecosystem had been struck by a blight and overgrown by weeds.

The study, published last year, was small. But for Ramnik Xavier, a molecular biologist at the Broad Institute in Cambridge, Mass., and a senior author on the study, the findings suggested for the first time that intervention might be possible. Maybe clinicians could catch and correct the microbial derangement in time to slow — or even prevent — the emergence of the disorder.

The question was how. The scientists turned to Russia for an answer. People living just over the border in Russian Karelia, as the region is known, have the same prevalence of genes linked to autoimmune disease. They also live at the same latitude and in the same climate. And yet they have a much lower vulnerability to autoimmune disease. Celiac disease and Type 1 diabetes occur about one-fifth and one-sixth as often, respectively, in Russian Karelia as in Finland. Hay fever andasthma, allergic diseases that also signal a tendency toward immune overreaction, are far less common.

So in a follow-up study, the results of which appeared last month in the journal Cell, Dr. Xavier and his colleagues followed 222 children who were genetically at risk of developing autoimmune diabetes. The newborns were equally divided among Finland, Russia and Estonia, where the prevalence of Type 1 diabetes is on the rise, but still well below Finland’s.

Autoimmune diabetes can be predicted, to some degree, by the appearance of certain antibodies in the bloodstream that attack one’s own tissues. After three years, 16 Finnish children and 14 Estonian children had these antibodies; only four Russian children did. And when the scientists compared the children’s microbiomes in the three countries, they found stark differences. A group of microbes called bacteroides dominated in Finnish and Estonian infants. But in Russia, bifidobacteria and E. coli held sway.

The scientists focused on a microbial byproduct called endotoxin, which usually spurs white blood cells into action. Both communities of microbes produced endotoxin, but not, it turned out, of equal potency. Endotoxin from Russian microbes strongly stimulated human immune cells. And when given to diabetes-prone mice early in life, it lowered their chances of developing the condition. But the Finnish endotoxin was comparatively inert. White blood cells didn’t register its presence, and it failed to protect mice from developing autoimmune diabetes.

These findings are very preliminary, but they support a decades-old (and unfortunately named) idea called the hygiene hypothesis. In order to develop properly, the hypothesis holds — to avoid the hyper-reactive tendencies that underlie autoimmune and allergic disease — the immune system needs a certain type of stimulation early in life. It needs an education.

The Russian kids evidently received this education courtesy of their distinct microbiomes. The Finns and Estonians seemingly did not.

Why was the Russian microbiome so different? The scientists aren’t sure. They controlled for diet, so it probably wasn’t food — although the Finns generally eat more packaged foods than the Russians. Differences in breast-feeding couldn’t explain it either. If anything, Finnish mothers nursed longer than Russians.

But Mikael Knip, a professor of pediatrics at the University of Helsinki and a senior author on the study, describes Russian Karelia as resembling Finland before World War II. It’s relatively poor. Many families in the study drink untreated well water. Russian kids have more fecal oral infections, such as hepatitis A, suggesting more sharing not only of pathogens, but of microbes that may benefit health. And previous studies have found that Russian homes harbor a richer and more diverse community of microbes than Finnish ones.

The hygiene hypothesis is sometimes misinterpreted as being about personal cleanliness. But it describes a much more complicated relationship with the microbial world, one that doesn’t necessarily correlate with showers or disinfectant. Lifestyle seems to be the major determinant — how the way you live guarantees (or doesn’t) exposure to a rich variety of microbes that favorably sculpt the immune system.

It’s worth noting that at 66.6 years, life expectancy in Russian Karelia is 13 years less than in Finland. Modern Nordic civilization does have its advantages.

But Dr. Knip’s hunch is that children growing up in Russian Karelia early on encounter microbes that are absent in Finland. The takeaway, in his view, is this: The human immune system most likely anticipates a microbiome that more closely resembles Russia’s because, for most of human evolution, the world was, microbiologically speaking, more like Russian Karelia than modern Finland. When we don’t encounter the attendant stimulation early in life, the immune system can become unsteady. Thus, in the past half-century, as Finland became a modern state, the incidence of autoimmune diabetes more than quintupled.

There may also be other, stranger interactions at work. Scientists think, for example, that certain infections can bring on autoimmune diseases like Type 1 diabetes, which has been linked to a common family of viruses called enteroviruses. And yet, the Russian kids probably encounter more enterovirus infections than the Finns, but develop Type 1 diabetes less often.

What gives? One possibility is that toughening the immune system early in life alters how we respond to hits later, making those viral infections less likely to provoke autoimmunity. Another is that the kind of microbiome you have when the virus arrives determines how you respond. And yet another is that when you first encounter viral infections determines how dangerous they are. If they arrive when infants are protected by their mothers’ antibodies, as they probably do in Russian Karelia, no problem. But if they arrive after that protection has waned, they can push you toward autoimmunity.

Scientists have borrowed this theoretical framework from polio. One popular theory holds that if the poliovirus arrives in infancy, it produces mild if any symptoms. But if it arrives in childhood or adulthood, it can cause the feared paralysis. In retrospect, the polio epidemics that began striking Europe in the 19th century probably signaled improving conditions, not a new pandemic. Children were imbibing less human waste, and encountering the poliovirus later and later.

THIS same dynamic may apply to another disease many consider autoimmune: multiple sclerosis. In M.S., the immune system is thought to strip the insulation, called myelin, off neurons, leading to progressive disability. The condition is linked to a herpes virus called Epstein-Barr, which establishes a lifelong, though generally asymptomatic, infection. M.S. hardly seems to occur without Epstein-Barr infection happening first. And yet nearly everyone has the virus by their late 30s. What determines who gets M.S.?

Alberto Ascherio, an epidemiologist at Harvard, thinks that, even more so than with polio, when you’re exposed to Epstein-Barr influences your fate. Studies on migrants suggest that a childhood in the developing world, where infection with Epstein-Barr generally occurs early, lowers one’s risk of M.S. But acquiring Epstein-Barr in adolescence or adulthood, when it can causemono — infectious mononucleosis, the “kissing disease,” as American teenagers call it — more than doubles the risk of M.S.

The implication is that, by delaying exposure to once-common infections, improvements in societal hygiene may increase the prevalence of autoimmune diseases. Paradoxically, until we have a vaccine that confers lifelong immunity to Epstein-Barr, the best way to reduce one’s risk of M.S., says Dr. Ascherio, may be deliberate exposure to the virus while young. That’s unlikely to happen, he concedes, but it jibes with an overarching theme of this research.

The world today is very different from the one our immune system evolved to anticipate — not just in what we encounter, but in when we first encounter it. Preventing autoimmune disorders may require emulating aspects of that “dirtier” world: safely bottling the kinds of microbes that protect the Russian kids, so we can give them to everyone and guide the “postmodern” immune system along a healthier path of development.

Moises Velasquez-Manoff is the author of “An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Disease.”

domingo, 31 de julho de 2016

State of the Cure 2015

2015 State of the Cure, the fourth annual edition of this report, which
takes stock of the past year’s progress toward a Practical Cure for type 1 diabetes.


'At this time, there are four broad research pathways that have the potential to result in
a Practical Cure within the next 15 years. While each pathway has the potential to deliver
a Practical Cure on its own, it is also possible that a complete solution will require
a combination of multiple pathways.


THE FOUR PRACTICAL CURE PATHWAYS:

1. Islet Cell Transplantation involves implanting insulin-producing islet cells into a person
with type 1 diabetes. It has three major components:
• Cell protection: The islet cells must be protected from immune attack after they
have been implanted in the body. Various encapsulation approaches have been
tested in humans with no breakthrough to date. Immune-suppressing drugs are
another alternative, but current side effects would have to be reduced to qualify
as part of a Practical Cure.
• Cell supply: The only existing source of Islet cells is cadavers, which have very limited
availability. Only about 100 islet cell transplantations can be done annually in
the United States due to limits in cell supply. Research into deriving a sustainable
supply from human stem cells has seen recent advances. Two well known examples
of cell supply research are Viacyte’s work with progenitor cells, currently in
human trials, and Douglas Melton’s work at Harvard University, which produces
beta cells from an embryonic stem cell line but is several years away from human
trials.
• Site selection: Islet cells require large supplies of oxygen and nutrients to survive.
The current protocol is to transplant islet cells into the liver, where the majority do
not survive. Other transplantation sites, including the stomach lining and the area
under the skin, are being tested as alternatives.


2. Immune System Modification would use drugs or treatments to stop the body’s
immune system from attacking the insulin-producing beta cells. There are three modification
approaches: 1) blocking, 2) retraining, or 3) balancing. Blocking would most
likely use a drug to stop the autoimmune attack. Retraining refers to approaches that
seek to correct the autoimmune response, for example, through exposure to properly
functioning T Cells. Balancing seeks to restore a healthy ratio between the immune system’s
Killer T cells and Regulatory T cells. To date, there has been only limited progress
along this pathway.


3. Glucose-Responsive Insulin, aka “smart insulin,” is chemically activated in response
to changes in blood glucose. Once injected under the skin, “smart insulin” acts as a
biological artificial pancreas, maintaining even blood sugars with no other intervention
required. Insulin is bound to a protein structure that acts as a gate for insulin release,
closing when blood sugar is low and opening as blood sugars rise. To qualify as a Practical
Cure, smart insulin would have to last long enough to require no more than a single
injection per day. Additionally, the risks of having excess insulin (present but not yet
activated) in the body must be well understood. The best known example of this pathway
is the Merck project, which has been in human trials for over a year, but utilizing
a study design that still needs multiple injections per day. In the current study format,
it does not yet fulfill the Practical Cure vision but we are hopeful that it will iterate and
progress. We will address any changes to this outlook in future reports.


4. A Device that Mimics the Pancreas, often referred to as an artificial pancreas, is under
development at several commercial and academic centers. To be a Practical Cure,
a device that mimics the pancreas would require an exceptionally reliable closed-loop
system that adapts to each individual. It also must be small enough to be forgotten
about. The most well know projects are the Artificial Pancreas work led by JDRF and
the Bionic Pancreas work led by Ed Damiano at Boston University. Progress on the
devices has been encouraging with some excellent results in human trials. However,
several important hurdles remain, including a proven shelf-stable glucagon, adequate
fail-safe back-up systems, and a device size that is truly small enough to be worn without
bother.'


http://thejdca.org/

terça-feira, 8 de março de 2016

Doenças autoimunes: descoberto mecanismo-chave | ALERT® ONLINE - PT

Doenças autoimunes: descoberto mecanismo-chave | ALERT® ONLINE - PT



Doenças autoimunes: descoberto mecanismo-chave

23 fevereiro 2016
Investigadores do Canadá descobriram um novo mecanismo que impede o ataque do sistema imunológico e desenvolveram uma nova classe de fármacos que utiliza este mecanismo para o tratamento de várias doenças autoimunes, como a diabetes tipo 1 e a esclerose múltipla, sem comprometer todo o sistema imunitário, dá conta um estudo publicado na revista “Nature”.

“Esta descoberta é muito importante, porque agora sabemos como impedir as doenças autoimunes de uma forma altamente específica sem comprometer a imunidade em geral”, revelou, em comunicado de imprensa, um dos autores do estudo, Pere Santamaria.

Nas doenças autoimunes, um tipo de células imunitárias, os leucócitos, que habitualmente são responsáveis por afastar invasores estranhos, como bactérias e vírus, por vezes atacam erradamente as próprias células do organismo, o que causa a sua destruição. Cada doença autoimune resulta de um ataque contra milhares de fragmentos proteicos no órgão-alvo, como é o caso das células produtoras de insulina na diabetes tipo 1.

Neste estudo, os investigadores da Universidade de Calgary, no Canadá, demonstraram que as nanopartículas decoradas com alvos proteicos que atuam como “isco” para os leucócitos causadores de doenças podem ser utilizadas para reprogramá-los e suprimir a doença. Esta nova classe de fármacos explora um processo que ocorre naturalmente e que envolve a ativação do sistema imunológico para proteger o organismo contra doenças autoimunes.

O estudo demonstrou que este mecanismo e as nanopartículas que o exploram podem ser aplicadas a várias (e potencialmente a todas as) doenças autoimunes nos animais, ao modificar simplesmente o “isco” nas nanopartículas.

(...)
ALERT Life Sciences Computing, S.A.

sábado, 30 de janeiro de 2016

New Stem Cell Treatment "Switches Off" Type 1 Diabetes | IFLScience

New Stem Cell Treatment "Switches Off" Type 1 Diabetes | IFLScience


...



'The MIT researchers decided to modify the chemical structure of the alginate capsules in as many different ways as possible to try and build a better shield for the beta cells. “We made all these derivatives of alginate by attaching different small molecules to the [large molecule] chain,” said Arturo Vegas, lead author of the study and an accompanying paper in Nature Biotechnology, in astatement. They hoped that one of the 800 alginate derivatives would have “the ability to prevent recognition by the immune system.”
Luckily, one variant did indeed prove to be effective, in both mice and nonhuman primates. Known as triazole-thiomorpholine dioxide (TMTD), this variant was shown to be able to hide from white blood cells within hyperglycemic mice with a very strong immune system. Following the transplant, these beta cells began to immediately produce insulin, and brought the blood sugar levels down to healthy levels for a remarkable 174 days, a significant length of time considering their lifespan.

domingo, 20 de dezembro de 2015

Updated List of Practical Cure Research in Human Clinical Trials



This is the semi-annual review of T1D research in human clinical trials. The review identified 361 open trials that focus on T1D and only 11 initiatives have the potential to deliver a Practical Cure.
Over the three years that we have been tracking T1D projects in human trials, the story has remained more or less unchanged: there are very few Practical Cure projects. We strongly believe that more qualifying projects in human trials would significantly increase the chances of a successful outcome.
Since the last update in November 2014, there has been only small changes in the Practical Cure project list. The number of qualifying initiatives has moved from 8 to 11, with the addition of two new projects and one returning. The returning project, ATG/GCSF,recently started Phase II trials, after over two years of inactivity. No project has been removed since November.

The chart below lists the Practical Cure projects in human trials as of June 2015. A more detailed record of the Practical Cure research in human trials can be located on the clinicaltrials.gov website using the NCT numbers listed in the chart.






Glu : Lilly Plans to Take Locemia Solution’s Needle-free Glucagon to Market

Glu : Lilly Plans to Take Locemia Solution’s Needle-free Glucagon to Market


Nasal-Glucagon-in-Hand

How we—you and T1D Exchange—played a role in advancing intranasal glucagon

We want to congratulate two of our member companies, Lilly and Locemia Solutions, on some exciting news!
Lilly has acquired Phase III Intranasal Glucagon from Locemia Solutions. Intranasal glucagon is a potential treatment for severe hypoglycemia in people with diabetes who use insulin and could be the first needle-free rescue treatment for severe hypoglycemia. (Learn more about severe hypoglycemia and intranasal glucagon below.)
This announcement highlights the important collaborations that are happening every day to improve outcomes in type 1 diabetes.
And you are part of this exciting collaboration. How? Our T1D Exchange community participated in advancing intranasal glucagon in the following ways:

Question of the Day

  • In 2013, the Glu community answered a Question of the Day about the complexities of using injectable rescue glucagon and about severe hypoglycemia preparedness. Our community’s real-world experiences helped Locemia Solutions define the challenges of injectable glucagon in discussions with the FDA, which ultimately led to clinical studies of an intranasal form of glucagon.

T1D Exchange Clinic Expertise

  • Locemia Solutions partnered with T1D Exchange to:
    • Design clinical protocols and conduct two multi-site clinical studies. Our highly qualified clinical investigators conducted these studies.
    • Recruit participants from the T1D Exchange Clinic Registry to participate in clinical studies.
“When you’re looking for that special population of people with diabetes, access to the expertise, and the investigators who can run the special procedures like that, T1D Exchange offers something that just is unavailable anywhere [else] in the world…” —Dr. Claude Piché, CEO of Locemia Solutions

 Collaborating for Improved Outcomes: A Case Study

The potential of bringing intranasal glucagon to market to relieve the burden of severe hypoglycemia has been a case study in partnership and collaboration, including:
  • Initial funding from The Leona M. and Harry B. Helmsley Charitable Trust and Locemia Solutions
  • Real-world evidence about complexities of the glucagon rescue kit from the Glu community.
  • T1D Exchange works with Locemia Solutions to design and run phase III clinical studies and recruits participants from its Clinic Registry
  • Lilly is now leveraging its global expertise and heritage in diabetes to bring this product to market.
Read more about this announcement from Lilly.

Background on Severe Hypo and Intranasal Glucagon

In type 1 diabetes, a severe low can cause confusion, seizures, or unconsciousness. It requires medical intervention right away from someone other than the person with T1D. It might be a spouse, parent, or friend. It can be a teacher, coach, or babysitter—most often, it’s from someone who has no medical training.
IMglucagon
Today’s life-saving hypoglycemia rescue kit is complex. It contains a powdered form of glucagon that needs to be reconstituted into a liquid, drawn into a needle and injected in the person’s thigh. No easy task under the best of circumstances—and certainly not while a loved one or friend is seizing or unconscious.
Intranasal glucagon could be the first needle-free rescue treatment for severe hypoglycemia.
Intranasal glucagon uses a proprietary glucagon nasal powder formulation that is delivered in an emergency situation using a single-use, ready-to-use device. The caregiver presses a small plunger on the bottom of the device to release the glucagon as a puff in the nose, where the glucagon is absorbed in the nasal passages.
Congratulations to our members, Lilly and Locemia Solutions, and to the entire T1D Exchange patient community!
—Dana Ball
Co-founder and Executive Director, T1D Exchange