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1 ong known to be required for diabetes in the BB rat.
2 H reduce the incidence of diabetes in the DP-BB rat.
3 processing, transport, and secretion in the BB rat.
4 studies investigated this hypothesis in the BB rat.
5 as induced by 0.5% NaCl in drinking water in BB rats.
6 is, and the inflamed pancreas of prediabetic BB rats.
7 he exocrine pancreas in these early diabetic BB rats.
8 ad to immune dysfunction and autoimmunity in BB rats.
9 e insulitis and the frequency of diabetes in BB rats.
10 on by 2.5-fold (P < 0.001) in sural nerve of BB rats.
11 tic T cells in DP vs approximately 20% in DR-BB rats.
12 T cell maturation marker found in WF but not BB rats.
13 et transplant failure in autoimmune diabetic BB rats.
14 upregulated renal AQP2 and NKCC2 in vivo in BB rats.
15 disease, including the diabetic BioBreeding (BB) rat.
16 and autoimmune diabetes in the BioBreeding (BB) rat.
17 concentration, in AVP-deficient Brattleboro (BB) rats.
18 ociated with type 1 diabetes in biobreeding (BB) rats.
20 artment, normal, athymic, and diabetes-prone BB rats all generate RT6+ intestinal epithelial lymphocy
21 type 1 diabetes--the spontaneously diabetic BB rat and the streptozocin-induced diabetic rat--have b
22 VMH of two diabetic rat models, the diabetic BB rat and the streptozotocin (STZ)-induced diabetic rat
23 were readily detectable in both untreated DP-BB rats and RT6-depleted DR-BB rats before the onset of
24 ermine the predisposition to autoimmunity in BB rats and that iddm4 is a major diabetogenic locus in
25 rs in part responsible for lymphopenia in DP-BB rats and the concomitant predisposition of these anim
28 , whereas coisogenic diabetes-resistant (DR) BB rats are disease free but can be induced to become di
32 reas transplants from the diabetes resistant BB rat (BB-DR) function indefinitely in autoimmune diabe
36 rved undergoing apoptosis in both DP- and DR-BB rats, but comprised approximately 80% of intrahepatic
39 fragmentation in freshly isolated DP- or DR-BB rat cells, but, after 24 h of culture, a higher propo
40 esent in normal, euthymic diabetes-resistant BB rats, constitutes a larger percentage of the euthymic
47 lymphopenic diabetes-prone (DP) BioBreeding (BB) rats develop spontaneous T cell-dependent autoimmuni
50 ase activity in the plasma of eviscerated DR-BB rats did not increase following injection of anti-RT6
53 the euthymic but lymphopenic diabetes-prone BB rat IEL population, and is the predominant IEL phenot
54 b subclass, whereas those in RT6-depleted DR-BB rats included both the IgG1/2a and the IgG2b subclass
55 mAb into thymectomized DR and diabetes-prone-BB rats increased soluble RT6 to levels comparable to th
56 urified immunoglobulins from RT6-depleted DR-BB rats induced abnormal pancreatic vascular leakage in
57 data suggest that T cell apoptosis in the DP-BB rat is underway in peripheral lymphoid tissues and is
60 synthesis in the spontaneously diabetic BB (BBd) rat is due to decreased levels of tetrahydrobiopter
64 perimental studies by Bartlett et al. on the BB rat model suggest that whole pancreas transplants are
67 betic (3-4 weeks, with an MDG of 2.7 mmol/l) BB rats (n = 5); and 3) moderately hyperglycemic insulin
70 rphometric analysis on pancreatic islets, DP-BB rats protected from diabetes had less severe degrees
71 eling our human studies, serum signatures in BB rats reflect processes associated with progression to
72 reas those of the exogenous insulin-injected BB rats showed moderate focal tubular atrophy and an inc
74 comparable to those observed in euthymic DR-BB rats, suggesting that HDL-bound RT6 is not derived fr
77 It is also known that the development of BB rat T-cells is recapitulated in adult thymus organ cu
78 ant role for these inflammatory mediators in BB rat T1DM and suggest that the lymphopenia due to the
80 e VMAT2-positive fiber area in the islets of BB rats that had been diabetic for only 1-2 weeks compar
81 pression of insulitis and thyroiditis in the BB rat, that Th1 lymphocytes may predominate over Th2 ly
83 OC suggested that the failure of cultured DP-BB rat thymi to generate T cells with a mature phenotype
88 bility of immunoglobulins of RT6-depleted DR-BB rats to induce pancreatic leakage, suggesting that mo
89 eripheral RT6+ T cells in diabetes-resistant BB rats using a cytotoxic monoclonal antibody is not acc
90 onically cannulated nondiabetic and diabetic BB rats was explored using the in vivo hyperinsulinemic-
91 present study, using spontaneously diabetic BB rats, we demonstrate that whereas isolated islets are
92 e gracile fasciculus of genetically diabetic BB rats, we have found that 8-10 months of streptozotoci
94 ne (BB-Ac) and streptozocin (BB-Sz) diabetic BB rats were recipients of Wistar Furth (WF) intraportal
100 on that injection of diabetes-resistant (DR)-BB rats with depleting doses of anti-RT6.1 mAb induced a
101 ) were higher in AT derived from prediabetes BB rats with destructed pancreatic beta-cells and contro
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