From:
"Sukie Crandall"
Date: 2008-07-03 18:29:59 UTC
Subject: [ferrethealth] Re: What would you study?
To: ferrethealth@yahoogroups.com
--- In ferrethealth@yahoogroups.com, Bonnie <dearevolution@...> wrote:
>
> I am hoping to convince the University
> (and possibly that very same Professor) to let me do a study involving
> ferrets (I had other experience in research, but it was limiting to
> microbiology). I am only an undergrad, so who knows... they may not allow me
> squat.
*****Okay, so what you would need is a study that is within the area of
microbiology,ferret friendly, and within the capabilities of an undergrad
who has an expert mentor.*****
So, perhaps we can toss away complicated illnesses like AD (Aleutian Disease)
unless there is a way that you could build upon what has already been studied,
or unless you are interested in over-responses of the immune system. It's a
hard one to investigate, I'm afraid. Most of the damage that Aleutians does
is causes by the way that the immune system responds to the disease.
The endocrinological diseases fall mainly into two camps, and they are hard
to work with, too. Adrenal Disease is very well studied and work is currently
on-going on several possible preventative approaches. Those are post-doc
level studies.
No one knows the RATES of it, though. There had been a pers com notes
miscommunication in two places (one echoes the other) saying that there
are rates known for two years in the U.S. (which I tracked down and the
person credited with the info (Dr. Mark Finkler) said that not only did he
not give such numbers, but he has never heard of such studies here and
the numbers are not even anything like what he encounters.
So, a RATES study, getting info from vet hospitals is sorely needed.
Insulinoma is far less studied, and a RATES study is also needed for that.
The pancreas is so horridly complex. Still, one off-beat thing that maybe
has been looking promising in some diabetes research is that perhaps
neural damage of a specific type might start the ball rolling. It would
be interesting to see what those same nerves might be like in tissue
removed from ferrets with insulinoma. That might be beyond an
undergrad level, though. Ah: here you go:
BEGIN QUOTES
Cell. 2006 Dec 15;127(6):1097-9.
TRPV1+ sensory neurons control beta cell stress and islet
inflammation in autoimmune diabetes.
Razavi R, Chan Y, Afifiyan FN, Liu XJ, Wan X, Yantha J, Tsui H, Tang L,
Tsai S, Santamaria P, Driver JP, Serreze D, Salter MW, Dosch HM.
Neurosciences and Mental Health Program, The Hospital for Sick
Children, Research Institute, University of Toronto, Toronto, ON,
Canada, M5G 1X8.
In type 1 diabetes, T cell-mediated death of pancreatic beta cells
produces insulin deficiency. However, what attracts or restricts
broadly autoreactive lymphocyte pools to the pancreas remains
unclear. We report that TRPV1(+) pancreatic sensory neurons control
islet inflammation and insulin resistance. Eliminating these neurons
in diabetes-prone NOD mice prevents insulitis and diabetes, despite
systemic persistence of pathogenic T cell pools. Insulin resistance
and beta cell stress of prediabetic NOD mice are prevented when
TRPV1(+) neurons are eliminated. TRPV1(NOD), localized to the
Idd4.1 diabetes-risk locus, is a hypofunctional mutant, mediating
depressed neurogenic inflammation. Delivering the neuropeptide
substance P by intra-arterial injection into the NOD pancreas
reverses abnormal insulin resistance, insulitis, and diabetes for
weeks. Concordantly, insulin sensitivity is enhanced in trpv1(-/-)
mice, whereas insulitis/diabetes-resistant NODxB6Idd4-congenic
mice, carrying wild-type TRPV1, show restored TRPV1 function and
insulin sensitivity. Our data uncover a fundamental role for
insulin-responsive TRPV1(+) sensory neurons in beta cell function
and diabetes pathoetiology.
PMID: 17174891 [PubMed - indexed for MEDLINE]
Cell. 2006 Dec 15;127(6):1097-9.
s
Comment on:
Cell. 2006 Dec 15;127(6):1123-35.
Sensory neurons link the nervous system and autoimmune diabetes.
Bour-Jordan H, Bluestone JA.
UCSF Diabetes Center, Department of Medicine, University of
California, San Francisco, 513 Parnassus Avenue, Box 0540,
San Francisco, CA 94143, USA.
The initial factors that trigger the autoimmune response against
pancreatic islets in the nonobese diabetic (NOD) mouse are still
unknown. In this issue of Cell, propose that a defect in a subset
of sensory neurons innervating the pancreas plays a major role
in initiating the chain of events that will lead to local inflammation,
islet destruction, and autoimmune diabetes.
PMID: 17174888 [PubMed - indexed for MEDLINE]
END QUOTES
Also, I recall a PLOS article on the "birth" and development of new beta cells
in the pancreas with them occurring in large simultaneous creations, so
maybe looking at that and if an error in such genesis might play a part in
the way the insulinoma winds up so widely seeded in the pancreas of ferrets
may be of interest. I guess it is even possible that the two hypotheses
might have an over-lap.
The NIH was interested a few years ago in how changes in the Parasympathetic
Nervous System in individuals with neural crest genetic variations might affect
kidney health, and there have been studies on that into the GI system and rates
of cardiomyopathy in other species. Certainly, the rates of individual with
such genetic variations is high among pet ferrets ever since the thrust to
breed panda-heads, blaze-heads, and those with a range of body spotting
happened before the health consequences were considered.
I don't know enough about nephrology to know if it would be do-able for
a microbiology undergrad, but there are many puzzles in kidney disease
in relation to ferrets: best diet for chronic illness, rate of individuals who
get cystine uroliths on high protein diets (rare but significant enough that
multiple people here have lost ferrets to them or have to specially handle
such individuals. Rates of the types of uroliths isn't known, but many vets
don't check. (Urine pH measurements can help spot two types.) I could be
wrong but how E. coli infections cause kidney damage that crops up
later is still a mystery, I think.
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