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Diabetes "Cured" In Mice With Virus Therapy
phlack writes "Scientists at Baylor College of Medicine have found a way to treat diabetes in mice by using a virus (with the harmful genes removed) to trick the liver into working as a pancreas. This is still a ways away from working in humans, but it's progress, at least. Info can be found at Guardian and Science Daily."
All the need to do is invent another virus that makes some other organ function as a liver!
I've had enough abrasive sigs. Kittens are cute and fuzzy.
I have to wonder what takes the place of the liver. (Articles have been
Given the choice between a normal liver plus insulin injections, versus a "virtual pancreas" and some unknown liver treatment, I think I'd stick with the devil I knew.
More precisely, I know how my body reacts to insulin injections. Nobody knows how it would react to - ah screw it, I can't seem to express this thought coherently.
You cannot apply a technological solution to a sociological problem. (Edwards' Law)
FYI - The real question about this, and other gene therapy experiments, focueses on the safety of the vector being used. In this case an adenovirus virus was used. The virus itself is no longer virulent, but how does the target genetic material get integrated into the hosts genome? If it occurs at a specific site, then safety is maximized. If it occurs randomly, then you run the risk of knocking out genes where only a single healthy allele exists (loss of heterozygosity) and potentially, cancer.
Gene therapy holds a lot of promise, but the early cases of leukemia (remember the bubble boy cure? Two 'cured' patients subsequently developed cancer) make it prohibative. I'm an expert enough to know this a problem (in theory and in practice) but not enough of one to know how close we are to solving it.
-Sean
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I just read the Nature Medicine article and the authors speculate that they were able to induce differentiation of hepatic stem cells or hepatocytes into islet-like cells, and it looks very convincing. A potential major shortcoming of this approach is not addressed, which is that in type I ("juvenile") diabetes, the islet cells are destroyed by an autoimmune response. Thus if you generate new self "pseudo islets", you may have present the very antigens that led to their destruction in the first place. The reason that is not a problem in this experiment is that the authors artificially destroy the islets with the toxin streptozotocin. The real test would be in an animal model that mimics type I diabetes, like the non-obese diabetic (NOD) mouse. I hope and assume that is the next critical experiment.
Now the mice will have to deal with a brand new problem.. dysfunctional livers, which will then be augumented with normal livers from other 'failed' mice. I'm sure most diabetics patients will prefer the frequent needle.
"Give orange me give eat orange me eat orange give me eat orange give me you." -Nim Chimpsky
So, I can exchange taking insulin for the rest of my life with taking anti-rejection drugs for the rest of my life? What have I gained?
Clearly I'm missing a point somewhere.
You cannot apply a technological solution to a sociological problem. (Edwards' Law)
Talk about a kludgy hack!
Up to 2/3 of your liver may be destroyed (or poisoned) and it will still function correctly. I very much doubt that anything like this much will be affected by this process. Therefore it is safe to assume that there will be no percieved effects of this treatment other than the positive!
This sort of advance should work very well for people who have type I diabetes, where their bodies no long secrete insulin. I have to wonder how well it will work in people with adult-onset, type II diabetes, which is triggered by a malformed receptor that isn't sensitive enough to secreted insulin. The use of oral or injectable insulin might be eliminate, but I worry that the attendant physical ailments, such as diabetic retinopathy, will still dog those who suffer. Unfortunately, the problem of fixing those receptors may prove to be much more difficult.
C'mon, fellas... CBC's science program Quirks & Quarks
reported (over 18 months ago) that islet transplants
were suceeding in almost 90% of cases.
A further development (by a private sector co.)
reported greater success rates or fewer problems.
Let's get this story as well, eh?
I'm glad someone's helping the mice out there. We on the other hand will keep curing humans.
I've eMailed the subj program's contact eMail
to suggest that they consider sharing the news
of Islet Transplant with Australian sufferers,
but have not heard whether they have.
I suspect that Doctors (if not the program's
presenter, Dr. Norman Swan) may be quite happy
to profit from the checkup's or glitches that
come from result from regular use of insulin
by Type 1 Diabetes sufferers.
Even if they can get better vector (non-viral)which does not cause the modified cells to be eliminated, they will still have hard time to produce the right level of insulin in this way. The right insulin level is very individual thing (type II diabetics have a lot their own insulin - except that their cells ignore it).
Insulin excretion by pancreas is tightly regulated - you get a peak production about 30min-1 hour after the meal, which causes you to feel non-hungry.
High insulin levels are toxic. Intravenous insulin users can overdose easily (if they skip the meal, for example), so they usualy carry with them a source of sugar to avoid hypoglyceamia shock. Hypoglycaemia from insulin causes you to fell very tired and disoriented; you can actualy collapse and die.
I doubt that we will ever figure out - and I suspect that even if we did figure out we couldn't do much about it
Here is an excellent read on type one diabetes and stem cell research, and a comment on why study sjogren's in conjunction with diabetes (namely, the organ being damaged is much easier to get at and assess.)
Here is a great site for info- the CDC genomics site, which includes info on common and rare genetic diseases, and can give a greater array of background info. NCBI offers another set of info- an explanation of human mouse homology (thus answering the question... why mice?
I hope this helps put some extra info out there for those of you who are interested. And frankly, as one who has had to deal with the sudden "switching on" of not just one but a whole array of diseases- since my DNA happened to include the lucky strands- I'm now having my stance on animal testing completely revised...
"I'd say 'Have a good time,' but arson is still illegal.
I saw on the discovery health channel once where a man had to have his pancreas removed and they havested his beta cells and injected them into his liver so his body could produce insulin.
---- "Excuse me. Where's the children's gun section?"
I think they have surgeries that help solve part of this problem, but they come at the expense of losing your ability to park properly or find directions while driving, not to mention the all-important ability to pee whilst standing up.
One more crippling bombshell hit the already beleaguered *BSD community when IDC confirmed that *BSD market share has dropped yet again, now down to less than a fraction of 1 percent of all servers. Coming on the heels of a recent Netcraft survey which plainly states that *BSD has lost more market share, this news serves to reinforce what we've known all along. *BSD is collapsing in complete disarray, as fittingly exemplified by failing dead last in the recent Sys Admin comprehensive networking test.
You don't need to be a Kreskin to predict *BSD's future. The hand writing is on the wall: *BSD faces a bleak future. In fact there won't be any future at all for *BSD because *BSD is dying. Things are looking very bad for *BSD. As many of us are already aware, *BSD continues to lose market share. Red ink flows like a river of blood.
FreeBSD is the most endangered of them all, having lost 93% of its core developers. The sudden and unpleasant departures of long time FreeBSD developers Jordan Hubbard and Mike Smith only serve to underscore the point more clearly. There can no longer be any doubt: FreeBSD is dying.
Let's keep to the facts and look at the numbers.
OpenBSD leader Theo states that there are 7000 users of OpenBSD. How many users of NetBSD are there? Let's see. The number of OpenBSD versus NetBSD posts on Usenet is roughly in ratio of 5 to 1. Therefore there are about 7000/5 = 1400 NetBSD users. BSD/OS posts on Usenet are about half of the volume of NetBSD posts. Therefore there are about 700 users of BSD/OS. A recent article put FreeBSD at about 80 percent of the *BSD market. Therefore there are (7000+1400+700)*4 = 36400 FreeBSD users. This is consistent with the number of FreeBSD Usenet posts.
Due to the troubles of Walnut Creek, abysmal sales and so on, FreeBSD went out of business and was taken over by BSDI who sell another troubled OS. Now BSDI is also dead, its corpse turned over to yet another charnel house.
All major surveys show that *BSD has steadily declined in market share. *BSD is very sick and its long term survival prospects are very dim. If *BSD is to survive at all it will be among OS dilettante dabblers. *BSD continues to decay. Nothing short of a miracle could save it at this point in time. For all practical purposes, *BSD is dead.
Fact: *BSD is dying
... once you come up with a way of stealing underpants, the problem of generating profit will be relatively easy to get around.