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1 s during autoimmune diabetes in the nonobese diabetic mouse.
2 creas of the interferon (IFN) gamma-nonobese diabetic mouse.
3 on of renal VDR was examined in the nonobese diabetic mouse.
4 ly class II allele expressed by the nonobese diabetic mouse.
5 itis, uveitis, and diabetes in the non-obese diabetic mouse.
6 ent type 1 diabetes mellitus in the nonobese diabetic mouse.
7 lone, is a major autoantigen in the nonobese diabetic mouse.
8 an and the orthologous I-Ag7 in the nonobese diabetic mouse.
9 betogenic CD4+ T cell clones in the nonobese diabetic mouse.
10                              In the nonobese diabetic mouse, a predominant component of the autoreact
11 activated in urothelia from a genetic type 1 diabetic mouse (Akita) by week 15.
12  of nuclear YAP localization in podocytes of diabetic mouse and human kidneys, suggesting dysregulati
13  adenine dinucleotide (NAD) depletion and in diabetic mouse and human livers.
14          GPR109A expression was increased in diabetic mouse and human retina.
15  observations have been made in the nonobese diabetic mouse and in clinical insulin-dependent diabete
16 mined the effect of exogenous SP delivery on diabetic mouse and rabbit wounds.
17 lin mRNA and protein expression in different diabetic mouse and rat models, including streptozotocin-
18 ore easily, such as those from the non-obese diabetic mouse, and display them in a more intuitive way
19 n the Toll-like receptor 4-defective C3H/HeJ diabetic mouse, arguing that the dramatic increase in co
20 ) expression in streptozotocin (STZ)-induced diabetic mouse arteries and in human coronary smooth mus
21  increased in endothelial cells of obese and diabetic mouse blood vessels.
22 ntitative analysis of PPI species present in diabetic mouse cortex and liver, and it allowed us to un
23                                         In a diabetic mouse cutaneous wound model in vivo, cell thera
24 ies in type 1 diabetes (T1D) in the nonobese diabetic mouse demonstrated that a crucial insulin epito
25 erved in TET2KO endothelium were mirrored in diabetic mouse endothelium.
26                                        Adult diabetic mouse fibroblast migration exhibited a 75% redu
27 ncrease of miR-200b/c levels was detected in diabetic mouse glomeruli and TGF-beta-treated MMC.
28                   Transcriptomic analysis of diabetic mouse glomeruli showed that cell adhesion and i
29                            The NOD (nonobese diabetic) mouse has been studied as an animal model for
30 ction of adenovirus encoding PLN-Ab into the diabetic mouse heart enhanced contractility when measure
31 sequent decrease in coronary angiogenesis in diabetic mouse heart which was rescued by ALDH2.
32                                    In 8-week diabetic mouse heart, CTGF and TGFbeta expression increa
33 ctors (AAVs) for the capacity to protect the diabetic mouse heart.
34 by which Nrf2 suppresses oxidative stress in diabetic mouse heart.
35                   Treatment of both types of diabetic mouse hearts with an INaP blocker also shortene
36 stration of the contribution of the nonobese diabetic mouse in the area of epitope identification is
37               We developed a transgenic (Tg) diabetic mouse in which eNOS is systemically overexpress
38 is is reminiscent of studies in the nonobese diabetic mouse, in which I-A(g7) is relatively unstable,
39                              In the nonobese diabetic mouse, insulin-dependent diabetes is an autoimm
40 ions, and PKCalpha activity was increased in diabetic mouse intestine.
41 t diabetic nephropathy and that the Dcn(-/-) diabetic mouse is a useful new model of progressive diab
42                                 The nonobese diabetic mouse is a widely studied spontaneous model of
43 n from insulitis to diabetes in the nonobese diabetic mouse is typically associated with Th1 pancreat
44                            The NOD (nonobese diabetic) mouse is a good animal model for human IDDM.
45                       Streptozotocin-induced diabetic mouse kidney cDNA was prepared and subtracted b
46 sentational difference analyses of cDNA from diabetic mouse kidney were performed.
47 sentational difference analysis of cDNA from diabetic mouse kidney.
48        Sgk mRNA was selectively increased in diabetic mouse kidneys.
49  to validate the presence of DMPO adducts in diabetic mouse livers.
50 ssels in the low-dose streptozotocin-induced diabetic mouse model (10 animals) was performed.
51  mitigating retinal vasculopathy in a type 1 diabetic mouse model (Akita, Ins2(Akita)).
52                We found CD44 deficiency in a diabetic mouse model ameliorates insulin resistance and
53 t reduction in a high-fat diet (HFD) induced diabetic mouse model and a genetically engineered T2DM r
54           In the present study, we used this diabetic mouse model and a proximal tubule epithelial ce
55 established the streptozotocin (STZ)-induced diabetic mouse model and examined the periodontium 8 wee
56 ogenesis in cardiac mitochondria of a type 1 diabetic mouse model and proposed that mitochondria are
57 d contractile function observed in the db/db diabetic mouse model appears to be related to decreased
58                      In vivo studies using a diabetic mouse model demonstrate that this dual-function
59 d glucose and lipid levels in an STZ-induced diabetic mouse model displaying no toxic effects on bone
60                               Furthermore, a diabetic mouse model exhibited lower FAS levels and a de
61  enable rapid reversal of blood glucose in a diabetic mouse model following glucose challenge, with s
62 lin(+) cells can suppress hyperglycemia in a diabetic mouse model for at least 6 months and regenerat
63 l or genetic suppression of tau in the db/db diabetic mouse model normalized glucose levels by promot
64             Analysis of PDGF-CC in vivo in a diabetic mouse model of delayed wound healing showed tha
65 ptide I-A(g7) dimers for use in the nonobese diabetic mouse model of diabetes.
66                                 The nonobese diabetic mouse model of human T1DM reveals that T cells
67 ession is very controversial in the nonobese diabetic mouse model of IDDM, but to our knowledge, it h
68  could fully mimic the effect of fibrin in a diabetic mouse model of impaired wound healing, demonstr
69 elayed diabetes progression in the non-obese diabetic mouse model of T1 D.
70                              In the nonobese diabetic mouse model of T1D, administration of ML351 dur
71 taneous development of disease in a nonobese diabetic mouse model of type 1 diabetes (T1D).
72  radicals (MBRs) in a streptozotocin-induced diabetic mouse model were uniquely detected by combining
73 rapeutic efficacy over wildtype hMSCs in the diabetic mouse model without replacing resident cells lo
74                              In the nonobese diabetic mouse model, beta-cell senescence largely depen
75 P2 axis in vivo, the New Zealand obese (NZO) diabetic mouse model, characterized by beta-cell loss un
76                  In a streptozotocin-induced diabetic mouse model, compound 2 potentiated the glucose
77                             Using a nonobese diabetic mouse model, here we show that heterozygous exp
78 ficiently reduced renal CHOP expression in a diabetic mouse model, providing an additional benefit to
79 rd with prior observations from the nonobese diabetic mouse model, suggesting a mechanism shared by m
80                              In the nonobese diabetic mouse model, there is new evidence that insulin
81 anilloid 1 (TRPV1) on DPN in the STZ-induced diabetic mouse model, we found that a proportion of STZ-
82    In parallel, using streptozotocin-induced diabetic mouse model, we found that treatment with oxyto
83  glucose uptake was demonstrated in a type 1 diabetic mouse model, with significant recovery after ac
84 ograft rejection in a streptozotocin-induced diabetic mouse model.
85 ractionation of an ethanolic extract using a diabetic mouse model.
86 nhibits diabetes development in the nonobese diabetic mouse model.
87 eurons ameliorated hyperglycemia in a type 1 diabetic mouse model.
88 encephalomyelitis mouse model and a nonobese diabetic mouse model.
89 igating the risk of hypoglycemia in a type 1 diabetic mouse model.
90  damage using a streptozotocin (STZ)-induced diabetic mouse model.
91 using a high-fat diet/streptozotocin-induced diabetic mouse model.
92  on bone mass and mechanical quality using a diabetic mouse model.
93 , progression, and prevention in a non-obese-diabetic mouse model.
94 vels and HbA1c in acute models and a chronic diabetic mouse model.
95 vival and number in a streptozotocin-induced diabetic mouse model.
96 evelopment of type 1 diabetes in a non-obese diabetic mouse model.
97 N neurons and a shift toward excitation in a diabetic mouse model.
98 S-IV on renal injury in db/db mice, a type 2 diabetic mouse model.
99 to normoglycemia in a streptozotocin-induced diabetic mouse model.
100 gression of diabetic nephropathy in a type 1 diabetic mouse model.
101 lcoholic steatohepatitis (NASH) in an obese, diabetic mouse model.
102 vivo and in situ in a streptozotocin-induced diabetic mouse model.
103  islet encapsulation in a chemically-induced diabetic mouse model.
104 before and after photothrombotic stroke in a diabetic mouse model.
105 nase reduced glomerular AT1R expression in a diabetic mouse model.
106  full-thickness excisional wounds in a db/db diabetic mouse model; QHREDGS showed significantly accel
107                     In diabetic patients and diabetic mouse models (streptozotocin/high-fat diet-indu
108             Moreover, inhibition of FOXM1 in diabetic mouse models (STZ-induced and db/db) results in
109                           In vivo studies in diabetic mouse models and cynomolgus macaques demonstrat
110                                     By using diabetic mouse models and human duodenal specimens, we d
111 nd that miR-7a levels are decreased in obese/diabetic mouse models and human islets from obese and mo
112 fections in type 1 (T1D) versus type 2 (T2D) diabetic mouse models and in patients with S. aureus inf
113  beta cells, islets of Txnip-deficient mice, diabetic mouse models and primary human islets.
114 toms of large-fiber DPN in type 1 and type 2 diabetic mouse models are related to alterations in musc
115 these islets in immunocompetent and nonobese diabetic mouse models are underway.
116 e agrin therapy accelerates wound closure in diabetic mouse models by engaging MMP12-YAP.
117  murine streptozotocin induced- or non-obese diabetic mouse models of T1D.
118 d "type 1" and B6.BKS(D)-Lepr(db)/J "type 2" diabetic mouse models on OCT; immunohistochemistry in ty
119 d CDDO-Me has potent anti-diabetic action in diabetic mouse models that is mediated at least in part
120 ized that superimposition of hypertension on diabetic mouse models would accelerate DKD.
121 in production was assessed directly in obese diabetic mouse models, and proinsulin biosynthesis was f
122         Similarly, in both type 1 and type 2 diabetic mouse models, SPT-siRNA attenuated the increase
123 gulated in patients with diabetes and in two diabetic mouse models, while hepatocyte-specific Sam68 d
124 at FGF1 increases islet insulin secretion in diabetic mouse models.
125 se and insulin levels in the ob/ob and db/db diabetic mouse models.
126 reptozotocin) and type 2 (obese Lepr(db/db)) diabetic mouse models.
127 t3 in the treatment of insulin resistance in diabetic mouse models.
128  diet (HFD)-induced and genetic ob/ob type 2 diabetic mouse models.
129 tein was present in pancreatic beta cells of diabetic mouse models.
130 epatic steatosis and hepatic inflammation in diabetic mouse models.
131 ivities normalizes metabolic dysfunctions in diabetic mouse models.
132  by unilateral ureteral obstruction (UUO) in diabetic mouse models.
133 ll-thickness wounds in both non-diabetic and diabetic mouse models.
134  and associated metabolic dysfunction in two diabetic mouse models.
135 DLR-N were reduced in both type 1 and type 2 diabetic mouse models.
136 ubular cells of kidneys of type 1 and type 2 diabetic mouse models.
137 s derived from three different hyperglycemic diabetic mouse models: streptozotocin-treated, high-fat
138  in a cohort of wild-type-mice (n = 5) and a diabetic mouse (n = 1).
139                              In the nonobese diabetic mouse (NOD) model, administration of IL-10/Fc f
140 he inflamed lacrimal gland (LG) of non-obese diabetic mouse (NOD), a classic mouse model of SjS.
141 ghly pathogenic CD8 T cells in the non-obese diabetic mouse, one of the best animal models for human
142 tosis and the migration and proliferation of diabetic mouse primary dermal fibroblasts and 3T3 fibrob
143  were transplanted to streptozotocin-induced diabetic mouse recipients.
144 re transplanted into the peritoneal pouch of diabetic mouse recipients.
145 sion and phosphorylation were upregulated in diabetic mouse renal proximal tubule epithelial cells, w
146 osine enhances mitochondrial turnover in the diabetic mouse retina (Ins2(Akita) males), improving cli
147 es increased the generation of superoxide by diabetic mouse retina more at night than during the day.
148 droxydocosapentaenoic acid were increased in diabetic mouse retinas and in the retinas and vitreous h
149 ned to determine whether neurons are lost in diabetic mouse retinas and whether the loss involves an
150 crease in dopaminergic amacrine cells in the diabetic mouse retinas, compared with the nondiabetic co
151                     The data suggest that in diabetic mouse retinas, neurons in the ganglion cell lay
152 se in the number of acellular capillaries in diabetic mouse retinas, which were not reversible with i
153 , and this autophosphorylation is reduced in diabetic mouse retinas.
154 nsulin receptor (IR) and PTP1B in normal and diabetic mouse retinas.
155     Further, PTP1B activity was increased in diabetic mouse retinas.
156 etic foot skin, ob/ob and diet-induced obese diabetic mouse skin, and in mouse KCs exposed to increas
157 se skin, but the level of VEGF is reduced in diabetic mouse skin, and its release from human MCs is r
158                                           In diabetic mouse skin, hyperglycaemia inhibits the express
159              Type 1 diabetes in the nonobese diabetic mouse stems from an infiltration of the pancrea
160 acerbated autoimmune disease in the nonobese diabetic mouse strain as a result of a marked reduction
161                      The model was the obese diabetic mouse strain BKS.Cg-m +/+ Lepr(db)/J, a model o
162 tect against type I diabetes in the nonobese diabetic mouse strain may, in some cases, be due to nega
163 of the CD28/B7 pathway early in the nonobese diabetic mouse strain, using CD28-/- and CTLA41g transge
164  and the other using T cells in the nonobese diabetic mouse strain, which develops spontaneous diabet
165 NOD mice compared with thymus of several non-diabetic mouse strains.
166                                       In the diabetic mouse, the laminin alpha5 chain content of the
167             p90RSK activity was increased in diabetic mouse vessels, and fluoromethyl ketone-methoxye
168 dysfunction in the heart of the Akita type 1 diabetic mouse was due to a decrease in the level of the
169 ormed in the salivary gland of the non-obese diabetic mouse, which displays chronic inflammation.
170 sphorylation of MRA and coronary artery from diabetic mouse, which was reduced by AG1478.
171  tested our hypothesis in db/db type 2 obese diabetic mouse wound infection model with Pseudomonas ae
172                  Studies based on a splinted diabetic mouse wound model confirm the efficacy for acce
173                           In delayed healing diabetic mouse wounds, both macrophage polarization and
174                      In chronically infected diabetic mouse wounds, treatment induced cytokine/chemok
175 xpression was significantly downregulated in diabetic mouse wounds.

 
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