Wednesday, April 25, 2012

Possible Cures for Type-1 in the News (April-2012)

Kamada Announces Something On Their Phase-I Trial of AAT

I know the headline is vague, but the news is vague.  This is what they said:
The trial found stabilization and even improvement in diabetes measures of the patients, and a high safety profile in the 20 children and adolescents tested.
Diabetes measures in most of the patients showed stabilization and even slight improvement.
Notice that no actual numbers are provided, and not even what they were measuring!  In my experience, this is a new high-mark in terms of vagueness.   However the safety information is nice.  AAT is already approved for another use, so it has some assumption of safety.  But, that other use is a rare one, so more safety information is important.  Here is a piece of solid news, which was also included, and which I'm happy to hear:
The company expects to publish the final report on the clinical trial in late 2012.

AAT is an anti-inflammatory drug, which the body makes naturally, and which is already FDA approved for people who have a rare condition where a person don't make enough of it on their own. In addition to this trial, there are 2 or 3 other clinical trials underway testing AAT on type-1 diabetes. And this is part of a more general anti-inflammation technique to try to cure type-1 diabetes. Most researchers believe that inflammation is a result of the body's immune attack on it's own cells. That is, the underlying immune problem causes inflammation and also causes beta cells to die (which causes the symptoms of type-1 diabetes). However, some researchers believe that the underlying immune problem causes inflammation, and that this inflammation kills the beta cells, which then causes the symptoms of type-1. The difference is that, in the second model, if you stop the inflammation you can stop the symptoms of type-1 diabetes (the high BG numbers and the low C-peptide numbers). That is a big difference. But this second model is still a minority opinion.

Previous blogging on AAT:

Diamedica Plans to Start a Human Trial of DM-199 

Diamedica has talked about starting a human trial of their DM-199 drug in the past, but I've not blogged about it, because I didn't see any activity.  However, in their most recent press release (URL below) they do say that they have submitted the IND (Investigative New Drug) paperwork.  This is the first step to starting a clinical trial.  So even though I have not seen anything on the FDA's Clinical Trials web site, I'll provide some background here.

This quote is from their web site:

DM-199 Type 1 diabetes - is a novel recombinant protein which has been found to target the three main aspects of Type 1 diabetes by increasing regulatory T cells, reducing insulitis and improving glucose control in [tissue] studies, specifically:
  • Halts autoimmune attack - significant dose dependent delay in onset of diabetes in NOD mice leading to a 12x increase in C-peptide (a primary clinical endpoint) to 5-6 nM. [Delays and reduces the onset of type-1 diabetes when given during and before the honeymoon phase.]
  • Proliferates beta cells - 1,277% increase in insulin producing beta cells, restoration of blood insulin to near normal levels. [Treated mice generate a lot more insulin of their own, almost as much as non-diabetic mice.]
  • Improves glucose control - 291% increase in peak glucose infusion rate ... and a 1.6% improvement in HbA1C (measure of blood glucose levels) in a ZDF rat model. [ZDR rats are an animal model of type-2 diabetes. Photo below.  Obviously, A 1.6 improvement in HbA1C would be a great treatment, even if not a cure, if we can do the same in type-1.]
  • Human clinical trial - proof of concept - in a Phase 2a clinical trial with first generation DM-99, glucose levels were lowered by up to 48% after a meal [I have not been able to find a description for this study, or the results, anywhere. I'm not sure if this was done on type-1 or type-2 diabetics.]

Press release:

More info on ZDR rats:


DM-199 is recombinant protein, a new and improved version of DM-99. DiaMedica has previously done research in animals on DM-99, and they believe that all those good results will also apply to DM-199. It looks to me that all future research will be in DM-199, but they will continue to cite older research on DM-99, to support DM-199 safety and effectiveness.

Here is a newspaper report and a press release based on good results (in animals) with DM-99:

And here is some literature by the company itself:

This drug is currently in phase-II trials for type-2 diabetes, but has not yet been tested in people for type-1 diabetes. The animals studies are clearly aimed at type-1 diabetes, and they claim both beta cell regeneration and lowering the autoimmune attack.

Victoza (Liraglutide) Starts Another Phase-II (but as a treatment)

Liraglutide is a GLP-1 analog which is sold under the name Victoza and is approved for use in type-2 diabetics in the USA, the EU, and elsewhere. (The most common GLP-1 analog is Byetta.) In addition, there is active research to see if this drug will help type-1 diabetics. My current option is that this research is aimed at providing a better treatment, rather than a cure for type-1. However, this posting gives a summary on the research, since there is quite a bit going on.

Here are the studies ongoing:
NCT01206101 phase-II 50 people March 2012 - Jan 2015 Novo Nordisk
NCT01536665 phase-II 42 people Feb 2012 - Sept. 2012 Novo Nordisk
NCT00993720 phase-II 30 people Oct 2009 - Oct 2010 Hvidovre University Hospital
NCT01299012 phase-I 10 people Oct 2010 - June 2011 University at Buffalo

But what do we know right now?

Here is the results section from the study:
In all fourteen patients, mean fasting and mean weekly glucose concentrations decreased significantly after one week from [an average of] 130 to 110 and from [an average of] 137.5 to 115 respectively. Glycemic excursions also improved significantly at one week. The mean S.D. of glucose concentrations decreased from 56±10 to 26±6 mg/dl (p<0.01) and the CV decreased from 39.6±10 to 22.6±7 (p<0.01). There was a concomitant fall in the basal insulin from 24.5±6 units to 16.5± 6 units (p<0.01) and of bolus insulin from 22.5±4 units to 15.5± 4 units (p<0.01).
From my point of view, the results are underwhelming.  People who already have great control (BGs of 130?  that would be great!) dropped about 20 points.  I'm not sure taking a second drug (a once a week injection) to go down 20 points is worth it.   Now, if the impact is actually 15%, that's a little different, but it's still not a big result (in my opinion).  Now the use of insulin dropped about 30%, and that is a pretty big result.



Public Citizen has officially petitioned the US FDA to remove Victoza from the market.  I would love to write up a full blog on why they think it's dangerous, and why the FDA thinks it's safe, and the trade offs and assumptions involved.  It is a great "teachable moment."  But I doubt I'll have time.  For now, Victoza is on the market.

Discussion of Phases

You might notice that of the four studies going on right now, three are phase-II and one is a phase-I, but that the phase-I study actually started after one of the phase-II studies. Furthermore, Victoza was approved for use in the USA in January 2010, so at least two of the studies could have been phase-IV ("post approval studies").  So why weren't they?  I'm not sure the official answer, but my unofficial answer is simple: researchers have great leeway to call a study phase-I, II, III, or IV as they wish.  Different researchers choose different phase numbers to try to manage expectations.

Discussion of Money

One of the interesting things about this research, was the cost.  The press release from the University of Buffalo says that the ADA is putting in about $600,000 and the study will enroll about 45 people.   For comparison, Dr. Faustman's BCG trial, cost about $10,000,000 and dosed 3 people (according to the published information).   So that means that Dr. Faustman's trial cost over 200 times as much (if compared on a dosed patient by dosed patient basis).  Remember that in both cases, the drug being used was already approved for use for another disease, and in both cases, it has already been used in type-1 clinical trials.

Can Propecia / Finasteride Cause Type-1 Diabetes?

I was recently asked if Propecia / Finasteride could cause or trigger type-1 diabetes.
Propecia is a trade name for Finasteride, and is commonly used for male-pattern baldness.  It changes the way the body processes testosterone (a "male" hormone).

I had not heard of any connection between them, and searched my "usual sources" and did not find any evidence that the drug could cause, or could trigger, type-1 diabetes.  It is sometimes given at the same time that adults are often diagnosed with type-2 diabetes, but that has nothing to do with type-1 diabetes, and there is no evidence of causality or association.  Diabetes is not listed as a possible adverse effect in drug's "package insert".  And I could not find any case reports of a link, nor any research studies showing a link in people.  I didn't check in animals.

I was able to find an FDA briefing document on Finasteride given for a kind of cancer.  This dose was five times larger than the dose for hair loss, and in a very large study (20,000 people total), the levels for "Diabetes Mellitus" for both treated and placebo groups were the same (but no separation between type-1 and type-2, unfortunately).  So again: no connection.

Side Effects:

Health Blogger Could Be Jailed for Giving Health Advice While Unlicensed
Read all about it here:

Note that this guy describes himself as a type-1 diabetic and so the reporter for "The Atlantic" does as well, but others refer to him as a type-2.  He was diagnosed in middle age, he was on Actos prior to dx (which suggests that his doctor thought he was type-2) and there is no mention of antibody tests.  On the other hand he had a BG of 700+ when diagnosed. Anyway, the gist of his blog is that carbs are bad and that nutritionists are wrong for suggesting that people eat more of them.  That's a whole can of worms in itself, but the reason I'm posting this is much more because of the "blogger might be charged with a misdemeanor crime" aspect of it, then exactly what the blogger is saying.

Notes on this Blog

I have two pieces of news about this blog:

First, I've got a large non-blog event happening in my life right now, so I'm expecting fewer blog postings in the next six months or so, compared to the number in the past. In the past, I often did 2-3 per month, but I'm expecting 1 or 2 per month, and maybe only 1 every two months for the next 6 months or so.

Second, I'm planning on turning off anonymous commenting on my blog in the next few weeks. If you just read email or by posts on internet forums, then this will not effect you, but if you read my blog directly (URL is at the bottom of this posting), then you will no longer be able to comment anonymously there.

I'm not making this change because I've gotten bad anonymous comments. If you look at my comments you can see anonymous ones that are good and that are bad. The same is true of the named, non-anonymous ones. I'm making this change because I have come to believe that anonymous comments are bad for the internet and bad for society (as the two merge). People who would never be vandals out in the open, might, if they think they are anonymous. So although my blog doesn't see a lot of that, I'm turning it off anyway. It is a statement that I think anonymity on the net is not a good thing. If you are not willing to put your name behind it, you shouldn't do it. Fake names are bad enough, but total anonymity is worse.

Joshua Levy
All the views expressed here are those of Joshua Levy, and nothing here is official JDRF or JDCA news, views, policies or opinions. My blog contains a more complete non-conflict of interest statement. 
Clinical Trials Blog:
Cured in Mice Blog:

Saturday, April 14, 2012

Three Months of New Studies

I decided to take a look at all the studies which were reported for the first time in the FDA's Clinical Trials site between January 1st and April 1st of this year.  Registration at this site is required for all studies done on people in the US, or that will be submitted for eventual FDA drug approval, and here I"m looking at all the new ones (not updates to existing ones) for a 3 month time period.  Here is a quick summary:

51 type-1 diabetes studies started, of which:
  2 Were testing new (non-insulin) treatments for type-1
  5 Artificial Pancreas studies
  2 Studies aimed at curing/delaying type-1 during the honeymoon phase.
(none were aimed a curing established type-1 diabetes)

Obviously, I'm going to discuss these nine, and especially the last two more below, but first, I want to give a very quick summary of the other 42 studies.  The largest group (14) were testing different types of insulin (Aspart 30 or 70, Degludec, Levemir, and so on). About 5 studies were aimed at complications, about 5 had psychological targets, 2 involved new ways of giving insulin, and 2 were new BG measuring techniques, 3 involved food or diet, and so on.

If I had to select the silliest study that started in the first quarter of 2012, it would be this one: "The Effect of Guided Imagery in Children With Type 1 Diabetes Mellitus on Glucose Levels and on Glycemic Control" (NCT01567254). Unfortunately, the clinical trial record doesn't say who is funding it.

New Clinical Trial of Proinsulin Peptide on Honeymooners

Proinsulin is made by beta cells, and it is later broken down into insulin and C-peptide.  These researchers hope that giving proinsulin to type-1 diabetics in their honeymoon phase will teach the immune system not to attack itself.  This is similar to how repeated injections of peanut antigens are used over time to stop allergic reactions to peanuts.  (Note that while this trial is on honeymooners, the peanut trick works on people who have been allergic to peanuts for a long time, so it is not clear to me that this general approach is limited to honeymooners.)

There have been several clinical trials aimed at giving insulin or closely related molecules to people at risk of diabetes or in the honeymoon phase to try to train the immune system not to attack the body's own beta cells.  So far, these have not cured or prevented, but a few "rays of hope" have been seen.   So the work is continuing as researchers refine their techniques and try variants that were not tried before.  This type of treatment would likely need to be combined with a beta cell regeneration technique to result in a cure for established type-1s, and maybe for honeymooners as well.

This study will run for 3 years, and will enroll 24 people.   Two groups of eight will get proinsulin at different doses, and one group of 8 will be the placebo group.  This is double blind, placebo controlled.

This trial is being done at Cardiff, Newcastle, and London in the UK, and is part of the research done by the Diabetes Vaccine Development Centre.

Clinical Trial Record:
Patient information:

New Clinical Trial of GABA on Honeymooners

GABA is sold as dietary supplement in the US, but this is the first trial I know of to test for type-1 diabetes in people.  It is being done by Dr. Lunsford at the University of Alabama at Birmingham.  They will measure C-peptides, A1Cs and change in insulin use over a 1 year period.  This study is double blind and placebo controled: A total of 30 people will be enrolled, 20 will get GABA and 10 will get the placebo.  To enroll,  patients must be within 12 weeks of diagnosis, although they haven't started to enroll quite yet.  The paper was filed in March, and said they planned to start in April.

Clinical Trial Record:

Some Discussion of GABA

One obvious question is, why does GABA work?  I'm not exactly sure.  GABA has been studied in relation to type-1 diabetes since at least 1990.  Some work suggests that it is a immunmodulator, so lowers the immune systems attack on the body's beta cells.  Other work suggests that it lowers inflammation, so if inflammation is a trigger of type-1 diabetes, then that is a mechanism for GABA be effective.  GABA and GAD are interrelated chemicals in the body, and GAD is the most common target of autoantibodies in type-1 diabetes, so there might be a mechanism there, as well.

This research provides a strong counter example to the idea that "generic drugs can't get funding for research" or "no one will work with cheap, available drugs, because there is no profit in it" or similar canards.  GABA is widely available "over the counter" (no prescription) right now.  It is not covered by a patient, and there are dozens of companies that sell it.  Yet these researchers are able to fund and run a clinical trial for it.   GABA was reported to have cured type-1 diabetes in mice in June 2011, so it looks like it will move from mice to people in a year, which is quick.  Most treatments take about 2 years to make that transition:

Artificial Pancreas Studies Starting in Q1 of 2012

I'm still trying to find a good way organize these, since there are so many.  My current thinking is to divide them by "stage"  (based on the JDRF's six stages of AP development), and then further divide them into commercial development and academic research, and then (finally) list them by research group.  So that is how they are described below.
Background blog posting:

Important note: I've tended to name the research groups after one researcher involved, but I'm not sure that is a good way to do it.  I'm sorry if these groups are named after the wrong person, and I know they are all partnerships, with many people working together, I just don't have a better way to name them right now.  The names below are not designed to slight the many other researchers involved in each project!

All of these studies are recruiting new participants.

Hovorka's Group in Cambridge, UK.  Stage 3 or 5. Academic Research
12 people total, runs from May 2012 to December 2012.  Open label (non-blind, no placebo).
This study is looking specifically at children 2-6 years old, and using deluded insulin to better support them, over a 2 day period.
Clinical Trial Record:

Group in Montreal, Canada.  Stage 4 / Stage 6.  Academic Research.
12 people total, starts in January 2012.  Open label, cross over design.
This study is using a dual-hormone AP and is comparing how well it works when the pump is told about means vs. when it needs to handle meals without being forewarned of them.
Clinical Trial Record:

Hovorka's Group in the UK.  Stage 3 or 5. Academic Research
20 people total, runs from August 2011 to August 2014.  Open Label.
This looks like a long term trial of an AP, lasting 18 months, rather than the 1-3 days as is common in other studies.
Clinical Trial Record:

Montpellier University Hospital, Montpellier, France
10 people total, runs from Feburary 2012 to March 2014. Open label.This study is testing insulin delivery which is Intraperitoneal (injected into the body) rather than just under the skin, which is normal, or into a vein, which has also been done.
Clinical Trial Record:

Dr Ward's group in Oregon, USA.  Stage 6 Academic Research
10 people total, runs from March 2012 to September 2012.  Open label.
Inpatient testing of dual hormone AP.  In previoius studies, these researchers used the same hardware but entered data by hand.  In this test, they are using a truly closed loop, without human intervention.
Clinical Trial Record:

New Treatments for Type-1

One of the studies was testing Sitagliptin as an additional (to insulin) therapy for type-1 diabetes.
This is a 30 person study which is recruiting now and is expected to finish in March 2015.  It is single blind, and is testing 3 different doses of the drug, and one placebo group.  This study is being done at the Albert Einstein College of Medicine in the Bronx, New York City, USA.
Clinical Trial Record:

The other was testing Liraglutide to see if it changes the glucagon response during low BG episodes.  (I'm not sure why this is important.)  This is a 42 person study which is recruiting now and is expected to finish in September 2012.  It is double blind, placebo controlled.  Three different groups which each get a different dose of Liraglutide for some time, and then placebo for some time.  This study is being done by Novo Nordisk in Graz, Austria.
Clinical Trial Record:
Portal to all Novo Nordisk clinical trials:

Joshua Levy
All the views expressed here are those of Joshua Levy, and nothing here is official JDRF or JDCA news, views, policies or opinions. My blog contains a more complete non-conflict of interest statement.
Clinical Trials Blog:
Cured in Mice Blog:

Tuesday, April 3, 2012

Encapulsated Beta Cells and Sernova

This blog contains two parts.  The first is a general update on encapsulated beta cells as a possible cure for type-1 diabetes, and the second is some background and an update specifically on Sernova corporation's work on encapsulated beta cells.

General Update on Encapsulated Beta Cells
The basic idea, is that you take working beta cells and wrap them in some kind of barrier (called "encapsulation"). It must allow nutrients and sugar to flow into the beta cells, and insulin to flow out of the beta cells, but must stop the body's immune cells from getting to the beta cells.  So it must not be a complete (impermeable) barrier, but a "smart" or partial barrier.  The beta cells generate insulin in response to blood sugar.  Because they are encapsulated, the body's own immune system can not attack them.  This means both that the body's broken autoimmune attack does not kill off these beta cells, but it also means that the body's natural attack on any transplanted organ doesn't happen either.  These are both good things.

For more background, the Dec-2011 Countdown (a JDRF Publication) has a good article on Encapsulation:
Obviously, it focuses on JDRF's work, but it also contains a lot of the history, complexities and past problems of using encapsulated beta cells to cure type-1.  The discussion of past problems is important.  Many people seem to assume that since encapsulation sounds like a good and simple idea, it is a good idea and simple to implement.  However, different researchers have been working on this idea for over 20 years, and a cure has not been forthcoming.  So obviously, it is not as simple as it sounds.

Below I discuss status for all the encapsulated beta cell projects that I know of.  The basic summary is that one commerical company and two academic teams are in clinical trials now:  LCT is in phase-II trials and the others are phase-I, by my standards.  Sernova hopes to start clinical trials this year, but not on encapsulation directly, and the rest are in animals trials.

Status of LCT
LCT has completed a phase-I clinical trials in Russia, and has one ongoing in New Zealand.  They have also started a third clinical trial in Argentina.  At one time, they were hoping to have commercial availability in Russia in 2011, but that did not happen.  Results in people have been mixed.  A small number of people have been cured for short periods of time, and most people see improvement in their  BG control.

Status of AZ-VUB
This is academic research with human beta cells.
A 10 person trial, started in 2011 ends in 2013, but then patients will be followed until 2018.

Status of Université Catholique de Louvain
A 15 person trial, started in 2008 and running until 2013.

Status of Sernova
I discuss this more below, but Sernova hopes to start phase-I clinical trials in the first half of 2012 [d1].
They have already completed large animal trials.
Recent Interview:

Status of Cerco
These guys are doing large animal studies now, and hope to start human trials in 2013 [d1].

Status of ViaCyte  www.­viacyte.­com
These guys are using putting embryonic stem cells into their encapsulation, which is different than the other research teams listed here, who are mostly using pig cells.  These guys have cured mice and are doing animal safety studies now, and hope to start clinical trials in 2013 [d1].

Status of Nuvilex    Cured In Mice! Nuvilex
These guys are "cured in mice".  We'll need to see what happens in people.

Background on Sernova

Sernova has a long and interesting history, which I summarize here:

It has been known for a long time, that the body's immune system does not have complete coverage within the body.  For example, the immune system is not good at attacking viral infections in the eye (for example)[d2].  One of the things that the body's immune system does not attack is your own sperm cells (or egg cells).  If you think about it, these two cells have a different genetic makeup then your body, and they might be identified as foreign invaders and attacked by the immune system.  However, this does not happen.   For sperm cells, the body has special cells, called Sertoli cells, that  are located next to the sperm cells and prevent the immune system from attacking them. [d3]

So, long ago (about 15 years) and far away (Mexico) a transplant surgeon named Rafael A Valdes-Gonzalez decided to implant into people a mixture of Sertoli cells and beta cells from pigs.  The Sertoli cells would protect the transplanted beta cells from the body's immune system. (See [d4] for discussion on pig cells, and [d5] for discussion on ethical apprvoals.)  Dr. Valdes-Gonzalez thought he was on the track to a cure, and published some promissing results [r1], but others were not so sure [r2].  Also, the standards for exotransplantation were still being created, and no where near as well formed as now.  So there was some controversy [r3].

So, when it was time to start a larger, more carefully controlled clinical trial, to resolve the doubts about the effectiveness of the treatment, the local trial review board did not give it's approval.  They pointed out that the current standard was that animal studies (preferably large animal studies) should be done prior to human studies (to assure a basic level of safety and a reasonable chance of success).  These studies had never been done.  Dr. Valdes-Gonzalez  was a transplant surgeon who was not focused on running animal trials.  As far as I know, the Mexican project has not made a lot of forward progress since then.  However, at one time around 2004, they were "open for business" at about US $35k for the operation[r4].  I don't know what the current status is.

Obviously, a lot of people were unhappy about the lack of forward progress.  One of these people was Dr. White, a Canadian researcher.   He decided to develop the Sertoli+Beta cell treatment, starting from animal trials, and worked with Sernova corporation to do so.

Sernova is working on two related projects.  The first is a pouch system which holds transplanted cells together in one place (but does not encapsulate them, there is no barrier involved).  The second is the Sertolin(tm) system, which is designed to use Sertoli cells to prevent an immune attack on the transplated cells.

Here is a quote from their web page:
Sernova, is developing two novel closely integrated proprietary platform technologies. The first is the Cell Pouch System™, a scalable device providing a natural "organ-like" environment for therapeutic cells such as insulin producing islets for diabetics and the second is Sertolin™, a cell-based technology providing an immune-privileged environment for donor cells, reducing or eliminating the need for anti-rejection drugs.
Also, their home page includes two video presentations and a power point presentation which describe what they are trying to do.

Sernova has announced that they hope to start phase-I trials for their Cell Pouch System in the first half of 2012[d1], so that is great news.  But it is limited news.  By itself, this provides no immune barrier, so it's not even part of an eventual no-rejection drug cure.  Is just a step in that direction.  Sernova has said that they are hopeful that if the pouch is successful, it means that in the future only local immune suppressive drugs would be needed.  Because the beta cells would be limited to one specific place, immune suppressive drugs would only be needed right there, also.  Since local immune suppression is safer and has less side effects than whole body immune suppression, but there's no way to know if the difference will matter.

Extra Discussion

[d1] When I use the phrase "hope to start clinical trials in ..." that means that the company or organization has said that publicly.  It does not mean it will happen; nor does it mean that I think it will happen.  Researchers in general have a strong tenancy to think they will start human trials much sooner than they actually do.

[d2] and some researchers at DRI are experimenting with transplanting cells into the eye, specifically to take advantage of this, but no human trials as yet.

[d3] After reading this, you might ask yourself, why bother with transplanting the beta cells at all?  Why not just put Sertoli cells right next to existing beta cells, and then they would protect the beta cells from the autoimmune attack.  People are working on that:
but it has not progressed to human trials, yet.

[d4] The insulin generated by pig cells does work in humans.  For decades, humans injected pig and cow insulins as standard treatment.  It is only in the last 40 years or so that we have used human insulin from genetically engineered bacteria.  Prior to that, it was all animal origin insulin.

[d5] I've read several different accounts of the ethical approvals that this research had, and what it needed.  My belief is that it did have the proper approvals from the proper authorities at the time that it started, although some have claimed that the ethical approvals were lax.


Here are a link to PubMed references for all of Dr. Valdes-Gonzalez's work:

[r1] The good results:
Three year follow up:
Four year follow up:
Long term follow up:

[r2] I doubt this is a complete list of the doubters:

[r3] This is not a complete list on the controversy, but enough to get you started:



I found this on the JDRF's "For Scientists" web site about encapsulation in general:

Joshua Levy
All the views expressed here are those of Joshua Levy, and nothing here is official JDRF or JDCA news, views, policies or opinions. My blog contains a more complete non-conflict of interest statement.
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