วีดีโอ

Very interesting!

Ma'am how to get admission in interm university

Are you available?

This is Claudius

Alejandro is so handsome!😍😍😍

My professor 🤍

They reference a previous #stateofthescience showing users how to use the HumanIslet platform: th-cam.com/video/-XdD84gfZdA/w-d-xo.html

Thank you

If i just have antibodie Is tix100 can prevent disease?

Oğlum için bu tedaviyi çıkarın ve diğer çocuklar için lütfen

Ok and what are your thoughts that China is claiming they cured Diabetes.?

Awesome research kudos

Very interesting! Great job Dr. Chang. Congratulations.

The environmental causal graphic at 3:20 is interesting. Goes against some of the popular rnarrative.

One of the largest problems with diabetes today is the poor diet advice given to our population. I am shocked that this video does not have thousands of Likes.

Very informative

Are mouse and human beta cells different in redox sensitivity or mRNA decay?

Solid hope

When can I buy levicure?

Not all.. I use a pump 780G manusl and use regular for Protein (110g), Fat (160g) and less than 10 g of carbs. A1C 4.5 - 5 last 10 years. 68 years old 47 years T1D and Low Carb Bernstein 10 years Keto 5 years and Ketovore/Carnivore last 10 years.

It's so exciting to hear the doctor's and researchers working in this arena talking about their discoveries!

TTP399 CAN BE THE CURE OF DIABETE TYPE 1 ? And when is gonna be in the market This year 2023 or after 20 years from now ?

Interest topic Thank you sir

Great Talk! :)

Thank you Klaus Kaestner for driving study on diabetes and thank you Sugar Science for bringing people together to share their research. I think you are really doing someting wonderful here. Wonderful to hear about different endotypes and different ethnicities being addressed. Nice work!

so happy for you Kalpana

Thanks for opening my eyes to new information.

After a life time of diagnosed with Bad breath , I got cured with the help of Dr Abumere remedy whom I met on TH-cam . It was wonderful taking his herbs as there was improvement during the process which I felt and after taking his herbal dosage I was completely cured and till now I'm free .. glad to share this and you can get his herbs on too.th-cam.com/channels/lduhp9Qc6amd5KFTi6Q6Qg.html

Dr. khiria herbal medicine on th-cam.com/channels/akmsTFQWIWtUVIkQaGUK6g.html cure my chronic diabetes ,

p̴r̴o̴m̴o̴s̴m̴ 💐

Ulf for the Win!

Will it be available for t1des soon?

What's the dose of each of the drugs in Triple therapy ?

Fantastic talk by Dr Wang and Dr Eizirik; there need to be more studies with generic meds. I wonder is there a 510k equivalent for medications for fast track approval? If there is a way to incentivize pharma to study generics, that could be a way to get more momentum in terms of research and reduction in time to market

Proud of you doctor as a an azerbaijani turk🙏

Please accelerate your research to an urgent implementation🙏as a mom of t1d boy I must say that we are suffering😥we really pray the cure come our without any delay🙏

Great work

Great work by Kulkarni lab 👏👏

Is the cure close?

How to good news world daibities.. M1D and M2D pls come to new research medicine

Is there any treatment, vaccine or implantation for T1D? my 7 year son is diabetic for last one year.

I wish u fond for our pancréas médicament ✌🏻🙄🙄🙄🙄 diabities type 1 since 2005 i have 35old i had my glecemy clucose down perheps and no help from my country algeria no tecnologie we dont have free style libre 2 to check sugar and test everytime automatic night and day with alarm i cant live alone i have test sugar on finger ☝🏻☝🏻☝🏻☝🏻☝🏽 because everytime down sugar in blood very crazy time i want help it is since 2005

I am diabetes from algeria type one 😣😣😣😣 i want that share expérience of your search and expérience my diabet was since 2005 i was all my life in emergency my sugar down much coma i wish be healthy

Fenofibrate might also be helpful in t1 b/c it inhibits first pass hepatic extraction of insulin.

More likely imo is that an infectious agent hijacks the secretory system to its own end. long story short pathogen breaks the golgi. also the pathogen in question (coxsackie b?) could persist and be a latent infection. some people go off the deepend and believe diabetes re-activates ancient viruses embedded in the dna...sounds like a good fairy tale, but im not ready to go to the rubber room yet.

good will bless u

please give us regular updates on diabetes

Thank you 'weinerdad' for your detailed and thought-provoking feedback and questions. We agree fully that the maturity of both the immune system and the pancreas are likely to be key components in the age-dependent effects we observe. This is an area that we, and many others in the field, are investigating and is still far from understood. In addition to pancreas studies, there are multiple lines of evidence, suggesting that there may be different forms/ sub-types of T1D. As alluded above, these could well be linked to immune system and/or pancreas maturity. Several examples include: the appearance of insulin autoantibodies as an initial response, is often associated with younger onset whereas antibodies to GADA tend to appear first in those with older onset; both responder and non-responder populations are seen in many immunotherapy trials; and differences in the progressive loss of endogenous beta cells (measured by c-peptide decline) varies among individuals. Collectively these findings highlight that the underlying disease mechanisms could be different. We know that complete beta cell loss occurs rapidly in many younger children and appears to be driven by a more aggressive immune attack. By contrast, among individuals diagnosed at older ages, the immune attack is less intense, and beta cell dysfunction is likely to play a bigger role in the insulin insufficiency as beta cells can be retained many years after diagnosis. The two very different underlying disease profiles seen in the target organ are likely to require different therapeutic approaches. We want to better understand these differences and find ways of identifying who will have which form of the disease to help with better management and more effective and targeted treatment options in the future. It is, of course, key to gain a better understanding about WHY such differences are observed. Our pancreas studies are designed to reveal how age-dependent differences in immune system and pancreas maturity might translate into the distinct immune cell profiles observed in the pancreas. A second fundamental question is why beta-cells are killed more effectively by a "B cell high (CD20Hi)" type of infiltration than a "B cell low (CD20Lo)" profile. We need to understand what the CD20+ B cells contribute to the immune-medicated destruction and why they are there. Thirdly, we are asking why the beta cells are still present in individuals diagnosed in their teens or above but are not working as they should? Regarding your comments about LADA. I want to emphasise that our studies, so far, have been completed on donor pancreata from individuals predominantly diagnosed <30, most <20y. Therefore it is very hard for us to comment specifically on what happens in LADA (diagnosed>35y). There are very, very few recent-onset pancreata available from such donors worldwide, however, in the few that we have examined, a large number of residual beta cells are retained at onset and low levels of inflammation are found in the islets. Moreover, only a proportion of the insulin-containing islets are inflamed. LADA patients with longer duration of disease also retain some insulin-containing islets. So, these features appear very similar to those seen in the pancreases of teenage/ young adult (T1DE2) donors. But I have to stress the numbers are very small and more work is required on this also. In summary, our goal is to understand the mechanisms mediating beta-cell death/ dysfunction and to establish how this might be prevented. We fully expect that the differences may arise due to immune system or pancreas maturity, but we need to understand each of these more fully in order to better predict progression and to improve the choice and effectiveness of future immunotherapies.

Really love that you all are having this conversation, and in a public forum. But the one broad question that seems to be skipped over, which I have: Could the difference in the rate of beta cell destruction be explained by a common general difference between youth and adults? Like, adults may have developed a more "mature" immune system, which can better balance out the auto-immune attack, slowing it down. Or the inverse, that something is wrong in the thymus, and since children have a much more active thymus, perhaps the damage is ramped up in younger patients as opposed to older patients who have a smaller, less active thymus? I was hoping to see more conclusive data, but even that plot chart of the two distinct groupings, shows exactly that the curve seems largely related to age. So, instead of blaming it on some distinct difference in the underlying disease, is it possible that there the difference is in children's immune systems vs. adults immune systems? Maybe it is genetic, but in families hit with T1D multiple times, it is observable that some are in multiple younger people, while others are split between children and adults (LADA) -- so, how is that a distinct difference? You have both "juvenile" and "LADA." Even in monozygotic twins who both develop T1D, there is a period of discordance that can be many years. Just seems like, whatever the combo of influences is that triggers the process, the "honeymoon" time period seems more based on the "maturity" of person's immune system; and not much evidence actually points to different disease processes. It feels like they are intentionally looking for a distinct difference in disease processes, and so what they are finding in bits and pieces kind of supports their hypothesis, but not really a proven conclusion (or provable?) for various reasons. Don't want to demean their research, but community discussions are being driven to claim that childhood Type 1 is distinctly different from LADA, leading to this separating notion of "Type 1.5." That adult onset is somehow a mixture of Type 1 and 2, and that it "masquerades" as Type 2 -- all of which seem preposterous given that adult patients simply aren't tested for antibodies very often at time of diagnosis; and children almost always are. Wish one of your many brilliant researchers could address that, as I've never seen it even discussed: The general difference between the immune systems (or the pancreases) of children and adults, and how that might be related to the length of time in which beta cell destruction occurs. Also, on the same topic, how many newly diagnosed adults have a very rapid beta cell destruction -- "classic T1D" expectation vs. more gradual "LADA." And what about this youth version of extended honeymoon, "LADY" -- how often is that actually occurring?

Keep it up 👏🏻👏🏻👏🏻👏🏻👏🏻